An Atlas and Practical Guide
MULTIDETECTOR CT IN NEUROIMAGING Evelyn M Teasdale • Susan Aitken
CLINICAL PUBLISHING
An Atlas and Practical Guide
MULTIDETECTOR CT IN NEUROIMAGING Evelyn M Teasdale BSc MBChB MRCP FRCR Consultant Neuroradiologist Department of Clinical Neuroradiology Institute of Neurological Sciences South Glasgow University Hospital, Southern General Hospital Glasgow, UK
Susan Aitken DCR(R)(T), BA Superintendent for CT Department of Clinical Neuroradiology Institute of Neurological Sciences South Glasgow University Hospital, Southern General Hospital Glasgow, UK
CLINICAL PUBLISHING OXFORD
Clinical Publishing an imprint of Atlas Medical Publishing Ltd Oxford Centre for Innovation Mill Street Oxford OX2 0JX UK Tel: +44 1865 811116 Fax: +44 1865 251550 Email:
[email protected] Web: www.clinicalpublishing.co.uk Distributed in USA and Canada by: Clinical Publishing 30 Amberwood Parkway Ashland OH 44805 USA Tel: 800-247-6553 (toll free within US and Canada) Fax: 419-281-6883 Email:
[email protected] Distributed in UK and Rest of World by: Marston Book Services Ltd PO Box 269 Abingdon Oxon OX14 4YN UK Tel: +44 1235 465500 Fax: +44 1235 465555 Email:
[email protected] © Atlas Medical Publishing Ltd 2009 First published 2009 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Clinical Publishing or Atlas Medical Publishing Ltd. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. A catalogue record of this book is available from the British Library ISBN-13 978 1 904392 68 2 ISBN e-book 978 1 84692 596 2
The publisher makes no representation, express or implied, that the dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publisher do not accept any liability for any errors in the text or for the misuse or misapplication of material in this work. Printed by Henry Ling Ltd, Dorchester, Dorset, UK
Contents Preface
vi
General note
vii
Image display
vii
Contributor
vii
Bibliography
viii
Abbreviations
viii
1 Routine noncontrast brain imaging
1
2 Contrast enhanced brain imaging
11
3 Orbital pathology
27
4 Visual failure
35
5 Pituitary imaging
45
6 Cranial nerve palsies 3–6
53
7 Intracranial imaging in stroke: ischaemic
61
8 Vascular imaging in ischaemic stroke and TIA
69
9 Acute haemorrhagic stroke
81
10 Variations in arterial anatomy
93
11 Venous pathology and variations in venous anatomy
101
12 Cranial nerve palsies 7–12
113
13 Spinal imaging
121
Concluding comments
139
Index
141
vi
Preface
Multidetector computed tomography (MDCT) offers new and exciting opportunities for imaging patients suspected of afflictions of the nervous system. Achievement of this benefit requires an understanding of its full potential in displaying the features of the spectrum of relevant diseases. It also depends upon employing an approach that ensures that it is applied to best effect by tailoring the technique of examination to the patient's clinical problem. We hope that this account, distilling the conceptual and technical lessons gained from our extensive experience of MDCT, will provide practical guidance to radiologists, whether general or specialist, and their team of radiographers/technicians that will enable them to take full advantage of the opportunities offered by MDCT in brain and spine imaging. This will enrich their practice and expand the benefits they can bring to their patients. The advantages of MDCT include its ability for routine sub-millimetre scanning of large areas at acceptable radiation doses. The enhanced postprocessing techniques and the rapidity and ease with which they can be obtained mean that they can be applied with no limitation on throughput or reporting times. Although magnetic resonance imaging (MRI), with its ability to differentiate soft tissues has many applications, computed tomography (CT) remains the appropriate first-line investigation for most patients with an acute cerebral event and for those who still cannot undergo MR for one reason or another (approximately 1 patient in 5). MDCT has many technical benefits over single-slice CT but when a small area is to be covered, e.g. the orbit and the cavernous sinus, a single slice scanner is acceptable and a 4slice MDCT can be almost as effective as a 64-slice CT. In contrast, when a large area is to be covered, a scanner with
16 or more detectors is optimal and single slice imaging precluded by technical limitations and the radiation dose it would give. MDCT provides new opportunities to improve the standard of routine brain examinations and to expand CT techniques into new areas. The techniques we describe can be adapted to any MDCT system for any similar clinical situation In most radiology textbooks a systematic approach is followed. The appearances of specific pathologies, e.g tumours, trauma, and degenerative disease, are classified, described and inclusively illustrated. In practice, most patients present with a combination of symptoms and signs which must be investigated in order that pathology can be either excluded or identified and managed. This book adopts such a problem-based approach and is intended to be a supplement to the standard disease-based texts. Our approach is based on the concept that the information from the clinical referral can be used to define a tailored MDCT technique which will optimize the likelihood of correctly identifying or excluding causative pathology. The commonly held belief that a single CT brain protocol is appropriate in all situations is no longer realistic, appropriate, or tenable. The illustrations are intended to convey how the CT techniques applied affected diagnosis or management in a range of common clinical scenarios. They show how MDCT can be used in a routine service role in a way that maximizes its potential, and how knowledge of that potential enables its use to be extended to unexpected applications. The illustrations are not inteded to be a comprehensive catalogue of abnormalities, but to convey why such images should be obtained and how to get the most from them. Protocols are given in detail so that radiographers or technicians, with the
Preface vii
guidance of the radiologist, can apply them in any specialist or nonspecialist department. Detailed imaging of a patient suspected of disease of the brain or other parts of the nervous system need no longer be the prerogative of a specialist neuroradiology unit. Using the approaches we describe, detailed, highly focussed, highly informative and clinically influential investigation can be practised in any radiology department where there is a need and desire to provide quality brain and spinal CT imaging. This book will appeal to many kinds of reader and at different stages of their careers. It will be an invaluable companion to trainee and trained radiologists in their daily
study and work. Radiographers/technicians will find the reasons that a specific protocol is chosen will enhance their knowledge and understanding and make their work more interesting and fulfilling. Clinicians will gain insight into the radiologists mind: how and why they make decisions and why specific techniques are chosen. Most of the common neurological and neurosurgical conditions are covered so that a review of the images will be a valuable exercise in preparation for the ordeals of post-graduate examinations!
General note
Image display
The authors work in the Regional Department of Clinical Neuroradiology at the Institute of Neurological Sciences, Southern General Hospital, Glasgow. This is a busy tertiary referral neurological and neurosurgical unit for the 3 million people in the west of Scotland. The neuroradiology department has had computed tomography (CT) experience since the second only commercial EMI CT scanner was installed there in 1973. CT scanning remains a pivotal part of the acute imaging service and regular upgrading of the scanners has allowed the unit to keep abreast of technological developments; the department currently has one 4-slice and one 64-slice multidetector (MDCT) scanner. The contents of this book are intended to show what can be achieved with MDCT in current neuroimaging. The book details the actual protocols used in the authors’ unit but these principles adopted by another unit will need to be tailored to the technical specification of the local scanner. Achieving the quality of imaging presented requires work, practice, and experience.
• The legends make it clear on which side lies any pathology but none of the images have a printed left/right. • Axial images are displayed in standard body mode with the patient’s right on the left side of the image. • Coronal reconstructions are displayed as if facing the patient, that is, with the patient’s right on the left side of the image. • Axial volume rendered 3D images are displayed as if looking down on the patient from the top of the head, so the right side of the patient is on the right of the image • No window centre/window width is printed on the images. Examples are given in the techniques sections and the illustrations show the optimal level of contrast.
Evelyn M Teasdale Susan Aitken
Contributor Leighton J Walker MA MBChB MRCP FRCR Consultant Diagnostic Neuroradiologist Institute of Neurological Sciences South Glasgow University Hospital Southern General Hospital Glasgow, UK
viii
Bibliography We have included below a list of useful standard neuroimaging and clinical texts as well as some new books which offer descriptions of MDCT technology, data storage and image manipulation. At the end of each chapter is a list of books for further reading specific to the topic of the chapter. Baker M. Current issues in MDCT: radiation dose, data flow and arrangement, data interpretation and presentation, and new clinical applications. In: The Year in Radiology. Special Issue: Advances in MDCT. Saini S, Bonomo L, Teasdale E, White R (eds). Clinical Publishing, Oxford, 2005 pp. 238–245. Bonomo L, Foley D, Imhof H, Rubin G (eds). Multidetector Computed Tomography Technology. Royal Society of Medicine Press, London, 2003. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology, 4th edn. Lippincott, Williams & Wilkins, Philadelphia, 2001.
Hoffer M. CT Teaching Manual, 3rd edn. Georg Thieme Verlag, New York, 2007. Hosten N, Liebig T. CT of the Head and Spine. Georg Thieme Verlag, New York, 2002. Kalender WA. Computed Tomography: Fundementals, System Technology, Image Quality, Applications, 2nd edn. Publicis Corporate Publishing, Erlangen, 2005. Lipson S. MDCT and 3D Workstations: a Practical Guide and Teaching File. Springer Science+Business Media, Philadelphia, 2006. Osborne A. Diagnostic Neuroradiology – A Text/Atlas. Elsevier Mosby Saunders, St Louis, 1994. Sartor K, Haehnel S, Kress B. Direct Diagnosis in Radiology. Brain Imaging. Georg Thieme Verlag, New York, 2008.
Abbreviations ACTH adrenocorticotrophic hormone AVM arteriovenous malformation BBB blood–brain barrier CBF cerebral blood flow CBV cerebral blood volume CSF cerebrospinal fluid CT computed tomography CTA computed tomography angiography DAVF dural arteriovenous fistula DSA digital subtraction angiography ECST European Carotid Surgery Trial IAM internal auditory canal ICA internal crotid artery IIH idipoathic intracranial hypertension IV intravenous MCA middle cerebral artery MDCT multidetector computed tomography MDCTA multidetector computed tomography angiography MDCTV multidetector computed tomography venography
MIP maximum intensity projection MPR multiplanar reformation MR magnetic resonance MRA magnetic resonance angiography MRI magnetic resonance imaging MTT mean transit time NASCET North American Symptomatic Carotid Endarterectomy Trial PACS picture archive and communication system PICA posterior inferior posterior cerebrellar artery ROI region of interest SAH subarachnoid haemorrhage TIA transient ischaemic attack TTP time to peak US ultrasound vHL von Hippel-Lindau (disease) VR3D volume rendered 3D (image) VRT volume rendered technique WC window centre WW window width
Chapter 1
1
Routine noncontrast brain imaging
Introduction Using a modern multidetector computed tomography (MDCT) system, ‘routine’ brain scanning should usually be performed using incremental techniques. Scanning incrementally, rather than helically, gives high quality imaging while affording a lower radiation dose than scanning helically. The radiation dose from an incremental scan is typically 25–30% lower than for a similar volume scanned helically. Additionally, if a patient moves during an incremental scan, only one block of data is corrupted. Many more slices are corrupted for a helical scan. Scanning incrementally also allows the scanner gantry to be angled to avoid the lens of the eye and to reduce the length of scan required to image the brain. Scanning helically usually means that the gantry cannot be angled, meaning a higher volume is scanned and the lens of the eye cannot be avoided. With the speed of acquisition currently available there can be no reason not to apply a detailed technique. It is, however, disappointing to observe that when a hospital acquires a new scanner, and after the company demonstrator leaves, the brain imaging technique regresses to one similar to that of the old scanner with thick slices and high contrast images. Radiologists should ensure that thin slices are acquired which are combined to provide images with better spatial resolution and signal to noise, but they can also be reprocessed into the acquired thickness to provide good multiplanar reformation (MPR) if necessary. On a modern scanner, it is possible to reconstruct the combined data down to the acquired submillimetre sections for detailed analysis if necessary, whilst thicker combined sections are sent to the institutional picture archive and communication system (PACS). If a lesion is seen on a routine scan and the decision to give contrast is made, the following contrast scan should be acquired with a helical technique as described in Chapter 2, or as an angiographic study as appropriate.
In specific situations, where scan information is used as a regular or repeated clinical update, it is possible to use a limited scan of a few thick slices with a markedly reduced radiation dose. This is specifically for follow-up of head injured/postoperative patients and those for intraventricular drainage monitoring. This should be used rarely outwith an interactive neurosurgical environment.
Indications • • • • • • • • • • •
Headache. Epilepsy/seizure. Head injury. Stroke. Subarachnoid haemorrhage. Deteriorating conscious level. Dementia. Confusion. Unexplained coma. Any acute presentation. Anything else that is justifiable.
Technique Table 1.1 presents the parameters for a routine scan of the brain. Figure 1.1 is a surview for routine and follow-up brain scans. Incremental, not helical, scanning allows an angulation of the gantry parallel to the floor of the anterior fossa to avoid irradiating the lens of the eye.
The follow-up brain scan Table 1.2 presents the parameters for a follow-up brain scan.
2
Routine noncontrast brain imaging
Reconstruction and reformation Usually only the simple, axial plane reconstructions are necessary (1.2). To obtain the reverse temporal lobe angle for the assessment of the hippocampus in possible Alzheimer’s disease, take a sagittal plane through the temporal horn then angle the axial plane parallel to the temporal horn (1.19).
Pathology and illustrations Some illustrations of disease/conditions will be given (1.3–1.19) but clearly almost any pathology could be shown and the vast majority of such examinations in the above clinical situation will be normal. A negative head scan can be a very reassuring examination and the anticipated and desired clinical result.
Table 1.1 Parameters for a routine scan of the brain
Patient position
Supine
Surview
Lateral
First slice
1 cm below foramen magnum Angle parallel to floor of anterior fossa
Last slice
Vertex
Field of view
~250 mm
Slice width
2.5 mm fused to 5 mm
Slice increment
2.5 mm
Collimation
16 × 0.625 mm
Rotation time
1.5 sec
kV/mAs
120 kV/300 mAs
Resolution
Standard
Filter
Soft tissue with bone/brain correction if available
Reconstructive zoom
To cover whole head
Windowing
WC 40 WW 100
1.1 Surview for routine and follow-up brain scan.
Table 1.2 Parameters for a follow-up brain scan Patient position
Supine
Surview
Lateral
First slice
1 cm below foramen magnum Angle parallel to floor of anterior fossa
Last slice
Vertex
Field of view
~250 mm
Slice width
10 mm
Slice increment
10 mm
Collimation
16 × 0.625 mm
Rotation time
1.5 sec
kV/mAs
120 kV/150 mAs
Resolution
Standard
Filter
Soft tissue with bone/brain correction if available
Reconstructive zoom
To cover whole head
Windowing
WC 40 WW 100
Dose
50% of the routine brain technique
Routine noncontrast brain imaging 3
1.2 (A–D) Representative images of a normal patient scanned with the routine brain protocol.
A
B
C
D
1.3 Grey matter migration abnormalities can be seen with MDCT. (A) This is a deep right frontal sulcus (schisencephaly) with thickened abnormal grey matter surrounding it. (B) shows ectopic grey matter on the lateral walls of the lateral ventricles. Either can be associated with epilepsy.
A
B
4
Routine noncontrast brain imaging
A
B
1.4 This is a very typical severe head injury with left temporal haemorrhagic contusions and an overlying thin subdural (A). This is easy to show (B) without changing the viewing factors because of the improved resolution of the thin acquired slices.
1.5 The right frontal haemorrhagic contusion shows different episodes of bleeding; the most recent bleed (arrow) is posterior to the retracted hyperdense clot. It is of lower attenuation because it is still liquid. The thin subdural (left) and the tiny bilateral contusions are well defined, as is the midline shift and the diffuse low attenuation in the left temporoparietal region. All these lesions will have an effect on the patient’s final outcome. (4-slice scan.)
Routine noncontrast brain imaging 5
A
B
C
1.6 The massive acute subdural haematoma in (A) and (B) shows mixed attenuation within it. The low attenuation areas are the most recent heamorrhges. The midline (arrows in [B]) is displaced more than 2 cm and there is abnormal dilatation of the posterior horn of the left lateral ventricle due to compression at the foramen of Munro. This sign correlates with the clinical signs of brain stem compression. The medial temporal lobe has herniated through the tentorial hiatus (arrow in [A]) and compresses the brainstem. There is also a linear haemorrhage in the midbrain (short arrow). This is a Duret haemorrhage due to the tearing of the perforating arteries secondary to the inferior displacement of the midbrain by the supratentorial mass. Note also the loss of grey/white matter differentiation in the compressed right hemisphere due to secondary ischaemia. In contrast is the moderately large subdural haematoma in (C) which has minimal mass effect because of the underlying atrophy.
1.7 The subtle haemorrhages associated with primary diffuse axonal injury are better defined now with the improved spatial resolution. This parasagittal image shows small high midbrain lesions (arrows) and scattered subcortical lesions (arrowheads) diagnostic of this primary brain trauma. Occasionally only low attenuation oedema identifies the site of the brain injury and this is much better appreciated with thin slice acquisition.
6
Routine noncontrast brain imaging
A
B
1.8 The thin slices offer less artefact from metal penetrating objects and can show the intracranial injury despite the signal drop out (black streak in [A]). This was a self inflicted wound with a crossbow. (B) This is a sagittal image from an angiographic study (helical) to assess any vascular injury following this orbital penetrating injury with a wooden handled brush. Angiography is recommended in the assessment of all penetrating trauma and MDCTA can often suffice.
A
B
1.9 Suspect a penetrating injury when there is a linear contusion/haemorrhage as in (A) (arrow). The VR3D (B) is from the subsequent angiographic study but it confirms the slit-like knife wound (arrow). Not all patients are keen to tell the truth about exactly what happened to them!
Routine noncontrast brain imaging 7
A
B
C
1.10 This student was admitted in December in coma. The initial scan (A) shows very subtle loss of density in the globus pallidus (arrows) bilaterally, more obvious on the left. This is indicative of carbon monoxide poisoning which was confirmed on the scan the next day (B) (arrows). The late follow-up shows the focal damage and more generalized atrophy and ventriculomegaly (C). A faulty heating system was discovered to be the cause of the poisoning.
A
B
1.11 This patient, admitted in coma, had been found with signs of a soft tissue neck injury; assumed strangulation. The scan shows low attenuation ischaemia of the entire brain stem, midbrain, and supratentorial structures. The dense tissue outlined in (A) is a combination of the vital cerebellum and tentorium. The high attenuation material around the midbrain (arrows) in (B) is not SAH but reflects the pia and arachnoid material against the low attenuation ischaemic brain, the so called ‘reversal sign’.
8
Routine noncontrast brain imaging
1.12 One of the commonest reasons for brain CT is possible SAH. While a heavy blood load is easy to identify, subtle changes are easy to miss. One give away is the presence of slight hydrocephalus as shown by the dilated temporal horns as in this case. The arrow points to a little SAH in the Sylvian fissure. Similar appearances can also be seen with meningitis so lumbar puncture or good clinical judgement is necessary.
A
1.13 This patient has a complex alcohol and drug abuse problem and had this scan after an episode of confusion and ‘collapse’. The low attenuation centrally within the pons (arrow) is diagnostic of central pontine myelinolysis secondary to rapid correction of a sodium imbalance.
B
1.14 Coma can be due to acute occlusion of the arteries to the brain stem. Always review the attenuation of vertebral and basilar arteries. In (A) the right vertebral artery (arrow) is of much higher attenuation than the left and this reflects acute thrombus within that artery. In (B) the thrombosed basilar artery (arrow) is denser than the internal carotid (arrowhead).
Routine noncontrast brain imaging 9
1.15 Stroke is a common indication for routine brain scanning. Thin cuts of the posterior fossa are necessary to define accurately any ischaemia such as the low attenuation PICA infarct here (A); it is important not to overlook this in the expectation of, or presence of, A supratentorial ischaemia (B) where there is bilateral occipital ischaemia and a subtle infarction in the left thalamus (arrow). (See also Chapter 7.)
B
1.16 This patient presented with a seizure and confusion. The diffuse haemorrhage in the white matter is very suggestive of venous infarction and the sagittal reformation shows the hyperdense acute thrombosis (arrows) in the sagittal sinus.
1.17 There is an irregularly calcified lesion with no mass effect and no enhancement with IV contrast. This is a large cavernoma, a type of capillary/venous vascular malformation which can present with brain haemorrhage or seizures.
1.18 One major problem caused by the increased availability of scanning is the demonstration of incidental pathology which is of no consequence. Here is a small pineal cyst (arrow). It is essential that patients are not worried by such findings and that repeated examinations, usually MR, do not reinforce a belief that the cyst may cause harm.
10
Routine noncontrast brain imaging
A 1.19 Patients with Alzheimer’s dementia have loss of B volume of the hippocampus. From a standard scan, axial reformations are planned from the sagittal MPR along a line parallel to the temporal horn (A). The width of the hippocampus opposite the midbrain should be 10 mm or greater when normal. Here it measures only 6 mm (B).
Learning points • This technique provides a rapid high resolution examination of the entire brain and reduces radiation to the orbits. • It suffices for most of the common reasons for head scanning. • Small lesions are much better identified than with single slice CT. • Fused thin sections improve spatial and contrast resolution especially in the posterior fossa. • Spatial resolution is best with incremental scans. • If the diagnosis is to be made from axial sections and not on MPR views then incremental scanning is best.
Further reading Frisoni GB, Geroldi C, Beltramello A, et al. Radial width of the temporal horn: a sensitive measure in Alzheimer’s disease. AJNR 2002;23:35–47. Gadda D, Carmignani L, Vannucchi L, Bindi A. Traumatic lesions of corpus callosum: early multidetector findings. Neuroradiology 2004;46:812–16.
Jobst KA, Smith AD, Szatmari M, et al. Detection in life of confirmed Alzheimer’s disease using a simple measurement of medial temporal lobe atrophy by CT. Lancet 1992;14:340(8829);1179–83. Jones TR, Kaplan RT, Lane B, Atlas SW, Rubin GD. Single versus multidetector row CT of the brain: quality assessment. Radiology 2001:219(3):750–5. Roos JE, Desbiolles LM, Willmann JK, Weishaupt D, Marincek B, Hilfiker PR. Multidetector-row helical CT: analysis of time management and workflow. Eur Radiol 2002;12:680–5. Rubin GD. Data explosion: the challenge of multidetectorrow CT. Eur Radiol 2000;36:74–80. Yama N, Kano H, Kurimoto Y, et al. The value of multidetector row computed tomography in the diagnosis of traumatic clivus epidural haematoma in children: a three year experience. J Trauma 2007;62:898–901.
Chapter 2
11
Contrast enhanced brain imaging
Introduction Since the development of brain CT in the early 1970s, intravenous iodinated contrast enhanced brain imaging has been recognized as providing additional information. It improves the definition of normal brain anatomy by showing clearly the position of the vessels and dura and enhances the definition of areas of blood–brain barrier (BBB) breakdown found in tumours and other pathologies. MDCT makes it possible to acquire of volume of data with sub-millimetre slices and to reformat images in any standard or curved plane with isotropic voxels. Volume rendered reformations are possible from any volume acquisition and can provide a unique display of pathology or anatomy so useful in communicating information to clinicians. Current workstations provide such rapid reconstructions that they are now used routinely in many situations. This MDCT technique challenges the standard features of MR and offers more flexibility in image manipulation than MR. The technique described below is the optimal sequence for the demonstration of any lesion within the cranium or craniocervical junction when specific vascular information is not required. It may be used with limited coverage for the investigation of possible posterior fossa pathology, e.g. facial pain, deafness, ataxia, cough impulse headache. When bone detail is also required the same data can be reprocessed with a bone filter and viewed on bone windows. This protocol may also be used without intravenous (IV) contrast in place of the routine brain study described earlier, if this is thought clinically more appropriate. This technique is the advanced workhorse of CT brain imaging. If there is doubt about the clinical diagnosis or a clinical observation, then this gives the highest likelihood of identifying any structural abnormalities in any plane.
Parenchymal lesions The degree of contrast enhancement can be optimized and increased by giving a large dose of iodine (e.g.100 ml of 300 or 350 mg/ml or 60 ml of 400 mg/ml) and waiting 5 minutes before scanning starts. As contrast crosses a deficient BBB the more iodine given and the longer the delay (up to a point!) the more will accumulate in the abnormal tissues. In this way enhancement, equivalent in most respects to MR, can be obtained. CT can therefore be used with confidence in any patient in whom MR is contraindicated or impossible, routine follow-up of malignant brain tumours, or in any situation where optimal CT brain scanning is required.
Extra-axial lesions This protocol is equally effective in the demonstration of extra-axial masses, i.e. meningiomas, neuromas. In these situations, as in metastatic neoplasia, contrast enhancement is due to the natural gaps in the walls of the capillaries as there is no BBB to break down. The clear simultaneous demonstration of any associated bone abnormality, e.g. hyperostosis or destruction, is advantageous. Since many of these lesions involve the skull base and the parasellar region, examples will be found in subsequent chapters.
Ventricular lesions These are uncommon but the high resolution and multiplanar reformations will enable correct identification that the lesion is intraventricular. The craniocervical junction and the aqueduct between the third and fourth ventricles can be easily assessed when MR is not possible. It is also useful in the assessment of congenital or acquired hydrocephalus.
Contrast enhanced brain imaging
12
Indications • • – – – –
Follow on from an abnormal routine examination. Used as the first examination for: Possible posterior fossa disease. Malignant brain tumour follow-up. Exclusion/proof of metastatic disease. Focal epilepsy as the chance of finding a causative lesion is relatively high. – Progressive neurological deficit +/- papilloedema. – Assessing a cause of/treatment for hydrocephalus.
Table 2.1 Patient preparation
• The patient should be given 100 ml of contrast IV by hand or pump injection at 2 ml/sec • A full 5 min delay from the end of injection before scanning gives time for optimum enhancement of cerebral tumours/abscesses as contrast leaks out across the damaged BBB
Table 2.2 Protocol parameters for a ‘catch-all’ study
Technique Applying different algorithms or reconstructive zooms to focal areas of interest (e.g. orbits, internal auditory meati, pituitary) allows detailed examination from the one data set. The same protocol can be performed without contrast for simple structural imaging, e.g. the craniocervical junction. Table 2.1 presents optimal patient preparation, and Table 2.2 the protocol parameters. Figure 2.1 shows the surview.
Reconstruction and reformation Usually simple axial, coronal, and sagittal reformations are sufficient but curved and oblique ones will allow a clearer depiction in an asymmetrical head. All reformations can be achieved at right angles to each other and the skull base by rotating the axial plane along the line of the skull base initially. Focused review is easily achieved to give more detail of a small region, e.g. orbit, parasellar area, posterior fossa. The raw data can also be reprocessed to focus on a smaller area and this slightly improves the resolution over simple photographic resizing.
Patient position Surview First slice
Supine Lateral Through spinous process of C1 Last slice Vertex Field of view Whole head (~230 mm) Slice width 0.9 mm Slice increment 0.45 mm Pitch 0.683 Collimation 64 × 0.625 mm Rotation time 0.75 sec kV/mAs 120 kV/300 mAs Resolution Standard Filter Soft tissue with bone/brain correction if available Reconstructive zoom To include whole head Windowing WC 40 WW 100 Contrast 100 ml by hand or pump at 2 ml/sec Wait full 5 min before scanning
Pathology and illustrations Parenchymal lesions Intrinsic parenchymal tumours: primary and secondary infratentorial supratentorial Infection
Other conditions: developmental anomalies demyelination granuloma cavernoma
Contrast enhanced brain imaging 13
Extra-axial lesions
Intraventricular lesions and hydrocephalus
Meningioma: infratentorial supratentorial Neuroma Skull/dural metastasis
Tumour Cyst Chiari malformations
A
B
2.1 Surview (A). The base images can be combined into a required thickness to give the desired image appearance (B); e.g. contiguous 5 mm slices with multiplanar reformats in the coronal and sagittal planes to demonstrate clearly the position and extent of a mass.
A
B
2.2 This technique is excellent for the assessment of tumours which extend from one area, e.g. the cranial cavity, to another area, e.g. the face and infratemporal fossa. Full assessment of this chondrosarcoma requires MPR review in sagittal (A) and coronal (B) planes in addition the standard axial reconstructions.
14
Contrast enhanced brain imaging
2.3 Posterior fossa lesions are well demonstrated with this technique. Patient A, B: these postoperative scans show the craniectomy and the recurrent intra-axial A B ependymoma lying lateral and inferior to the fourth ventricle. Patient C has a typical cystic haemangioblastoma at the craniocervical junction with irregular marginal enhancement; haemorrhage into the cyst can be seen from the hyperdense fluid layering posteriorly C D within it. The tumour is causing progressive compression on the medulla resulting in quadriplegia and bulbar nerve palsies. Patient D: sagittal MIP with a recurrent solid haemangioblastoma in a patient with precipitating von Hippel-Lindau (vHL) disease. Note also the small enhancing lesion in the pituitary stalk (arrow). This is also a haemangioblastoma in the commonest supratentorial site in vHL.
B 2.4 (A, B) The large complex peripherally-enhancing secondary deposit in the midline cerebellar vermis is clearly shown. The smaller deposit in the tectal plate is A also visualized in both planes (arrows). Both lesions cause obstruction to the CSF outflow so causing secondary hydrocephalus. (4-slice scan.)
Contrast enhanced brain imaging 15
A
B
2.5 (A, B) Here there are multiple supra- and infratentorial secondary deposits of varying sizes demonstrated in two planes.
A
B
2.6 (A, B) This secondary deposit is from breast cancer. They often have this homogeneous enhancement pattern with minimal oedema. A contrast-only scan is simplest, quickest, and most informative in suspected secondary tumour, the noncontrast scan can be omitted. Note the large deposit in the left internal capsular region passes across in the region of the anterior commisure and there is another deposit in the midline outflow of the fourth ventricle (foramen of Magendie) (B, arrow).
16
Contrast enhanced brain imaging
2.7 (A, B) This patient presented with a right 3rd nerve palsy and bilateral deafness. The MDCT shows enhancing masses in both IAMs, a small enhancing lesion in the right pons (B, arrow) and diffuse enhancement over the surface of the vermis and a deposit engulfing the calcified pineal gland: this is diffuse meningeal secondary tumour.
B
A
C
A
D
B
C
2.8 It is often thought erroneously that metastatic disease is always accompanied by oedema and that MR is needed to detect those small lesions. MDCT with thin sections and delayed contrast acquisition will demonstrate these in planar section (A and B, arrows) and the superficial location demonstrated on surface rendered 3D (C, arrowhead).
Contrast enhanced brain imaging 17
2.9 Complex solid and necrotic irregularly enhancing primary glioblastoma WHO grade 5 in axial (A) and coronal (B) section. The other patient (C, D) was referred with a malignant glioma as he had confusion and recent onset of seizures. However, the characteristic subfrontal location of the lesions (C, D) combined with the relative lack of mass effect, slight high attenuation within the enhancing rings, and the left frontal low attenuation subdural hygroma, all indicate that the lesions are resolving haemorrhagic contusions and not glioma.
A
B
D
C
C 2.10 This is a superficial intra-axial lesion within the brain. It should not be confused with an extra-axial lesion outwith the brain, as brain tissue can be seen surrounding the mass in the coronal (B) and sagittal (C) planes.
B A
18
Contrast enhanced brain imaging
2.11 This tumour (A, B) with poor differentiation from the normal brain, minimal enhancement inferiorly, and thick sheets of calcification is a typical low-grade oligodendroglioma with malignant transformation inferiorly. This contrasts with the low-grade astrocytoma (C, D) which is of diffuse low attenuation with no barrier breakdown and subtle mass effect.
A
B
D
C 2.12 (A, B) Show an intraventricular meningioma: the commonest intraventricular tumour after glioma. (C, D) This is an intraventricular lymphoma; note how the temporal horn on the left is engulfing the mass confirming its intraventricular location.
B A
D C
Contrast enhanced brain imaging 19
A
B
C
D
E
F
2.13 With a large meningioma like this (A, B) the displaced grey matter is difficult to distinguish but the enhancing veins over the surface of the tumour mark the boundary of the tumour and the brain. The enhancement pattern is typically homogeneous but cysts and fatty deposits are all possible. The adjacent hyperostosis can confirm the diagnosis in peripheral tumours. (C) This meningioma has a low attenuation centre (likely necrotic but could be a cholesterol variant) and was malignant on histology. (D) This meningioma shows bone erosion and invasion, classical but not as common as hyperostosis. (E) This meningioma with a calcified rim arises from the under surface of the tentorium and displaces the 4th ventricle but does not cause hydrocephalus. (F) This meningioma arises from the falx.
B 2.14 (A, B) This suprasellar and temporal tumour is large but has little mass effect. This, in addition to the modelling of the pituitary fossa and fatty attenuation (-27HU), combine to prove that the lesion is a developmental dermoid tumour.
A
20
Contrast enhanced brain imaging
2.15 (A, B) Well demarcated thin regular wall enhancing lesions, clustered together as in this cerebellum are typical of abscesses. Lesions like this should always be identified as possible abscess as cure is likely with biopsy/drainage. (4-slice CT.)
B
A
A
B
C
D
2.16 This is another abscess (A, B). Note the slightly higher density in the middle of it; this is inspissated pus. Note also the soft tissue in the left mastoid. Most abscesses are the result of adjacent sinus infection or are blood-borne in septicaemia as in (C). Occasionally an abscess is found in relatively avascular tissue as here in the corpus callosum (D). (E) Even very small abscesses can be easily demonstrated with MDCT.
E
Contrast enhanced brain imaging 21
2.17 This partly calcified enhancing (A) complex lesion is due to Aspergillus. (B) One of two symetrical fungal abscesses in a girl with leukaemia.
B A 2.18 Postcontrast CT scans. (A) This patient from South America presented with a seizure. In this population cysticercosis is the presumed diagnosis and CT shows the typical enhancing ring and spot appearance of a live scolix. (B) Infection with toxoplasmosis is common in immunosupressed individuals. This patient with medial temporal basal enhancement, proven to be due to Toxoplasma, had Waldenstrom’s macroglobulinaemia.
A 2.19 This is a large chronic subdural abscess. They are usually small and difficult to identify (see 3.10D). They classically have a strongly enhancing dural margin against the brain.
B
22
Contrast enhanced brain imaging
2.20 This is a deep brain stimulator inserted for the treatment of Parkinson’s disease. You can see the low attenuation collections parallel to it and the enhancing collection against the burrhole, indicative of infection.
A
B
2.21 The slightly hyperdense fluid in the dependent posterior ventricular horns (arrows) is pus in this patient with ventriculitis.
C
2.22 Meningitis can be a very severe disease with widespread low attenuation ischaemia secondary to involvement of the basal arteries and veins with the infection (A). The serpiginous enhancement in the cortex is due to barrier breakdown in ischaemic grey matter and some meningeal enhancement (B, C).
Contrast enhanced brain imaging 23
B
A
C
2.23 This is a very classical hyperdense cyst (proteinaceous fluid) at the foramen of Munro; a colloid cyst. It does not show contrast enhancement and typically presents with bilateral lateral ventricular enlargement and small 3rd and 4th ventricles. Here all the ventricles are normal.
2.24 This patient presented with enlargement of the lateral ventricles only and a colloid cyst was suspected from the standard unenhanced referral CT. MDCTA showed arterial enhancement in the mass at the foramen of Munro (A) and the sagittal MIP (B) confirmed this to be a large basilar aneurysm.
B
A 2.25 Within the low attenuation lesions it is difficult to make out any focal pathology on the unenhanced image (A) but two large enhancing lesions are evident in (B). Both have an outer more intensely enhancing margin and are within the white matter. This appearance is typical of acute demyelination. The lack of mass effect makes tumour unlikely.
A
B
24
Contrast enhanced brain imaging
A
B
C
2.26 There are multiple nonspace-occupying lesions with and without calcification and showing some enhancement. These are multiple cavernomas, a lesion now shown to be common as it is very visible on MR because of the associated haemosiderin. Calcification is the CT marker for this developmental vascular anomaly. Multiple lesions are commonly familial (see 1.17). 2.27 Three illustrations here have IV contrast, one does not (B), but all are thin (2 mm) midline MPRs and must be so to ensure that partial volume artefact does not mask the aqueduct. (A) The normal aqueduct is a 2 mm channel between the third and fourth ventricles (short arrow). The floor of the third ventricle (arrowhead) and the mamillary body A B (long arrow) are normal. (B) Despite the Hounsfield artefact the Chiari 1 malformation is evident with the tonsil lying at the level of the spinous process of the atlas. There is no normal surrounding CSF so this may well be the cause of the patient’s headaches. (C) This shows a communicating hydrocephalus: the floor of the enlarged third ventricle is depressed (arrow) but the aqueduct is widely patent as is C D the foramen of Magendie (arrowhead). (D) This patient was referred as possible SAH and the CTA shows a mass (arrowhead) in the roof of the aqueduct which is causing mild lateral and third ventricular hydrocephalus. The floor of the third ventricle is depressed and lies against the basilar artery tip and this lies close to the mamillary body (arrow) so making surgical treatment with ventriculostomy impossible.
Contrast enhanced brain imaging 25
Learning points
A
• Scan thin (0.6 mm) but view thick (3–5 mm) is the basic principle when using MDCT. • Delay the scan start by 5 minutes to optimize the effects of contrast enhancement. • Look carefully at the base data and routinely review MPR and volume reconstructions. • If the initial routine scan (Chapter 1) reveals an abnormality requiring a postcontrast examination, then use this technique with a high contrast dose and do not repeat the routine one after 50 ml of contrast, as is all too often the usual practice. • In the investigation of any mass lesion, this technique is sufficient for patients in whom MR is not possible, i.e. about 20% of patients. • Routinely review MPR views.
Further reading
B 2.28 (A) This VR3D image of the surface of a normal brain is achieved by subtracting the bone data. This is possible with any volume data set without rescanning the patient. The gyral pattern can aid in the planning of epilepsy and other types of surgery. The definition of the gyri has been shown to equate to surface MR images. The gyral pattern is irregularly and poorly defined in (B) because of the oedema associated with the multiple metastatic deposits. There are five visible; can you spot them all? One is very small!
Drevelegas A (ed). Imaging of Brain Tumours with Histological Correlations. Springer-Verlag, 2002. Gadda D, Vannucchi, Niccolai F, et al. CT in acute stroke: improved detection of dense intracranial arteries by varying window parameters and performing a thin-slice helical scan. Neuroradiology 2002;44:900–6. Hirano T, Tanabe S, Brando M, et al. Evaluation of threedimensional enhanced brain surface imaging using CT (3D surface CT angiography) and magnetic resonance imaging (3D surface MR angiography). Nippon Hoshasen Gijutsu Gakkai Zasshi 2002;58:1622–31. Lonser R, Butman J, Kiringoda R. et al. Pituitary stalk haemangioblastomas in von Hippel-Lindau disease. J. Neurosurgery 2009;110(2):350–3. Mezrich R. Sixteen-section multidetector row CT scanners: this changes everything. Acad Radiol 2003;10:351–2 Rathi V, Thakur LC, Sarikwal A. Noncontrast-enhanced four-detector multisection CT for the detection of ring lesions in seizures. Clin Radiol 2006;61:1041–6. Saini S, Bonomo L, Teasdale E, White R (eds). The Year in Radiology: Advances in MDCT, Vol 1. Oxford Clinical Publishing, Oxford, 2005. Saski T, Saski M, Hanari T, et al. Improvement in image quality of noncontrast head images in multidetector row CT by volume helical scanning with a three-dimensional denoising filter. Radiat Med 2007;25:368–72.
Chapter 3
27
Orbital pathology
Introduction
Technique
The Royal College of Radiologists of the United Kingdom affirm that CT is the optimal investigation for orbital pathology because of the good spatial resolution and inherent contrast of soft tissues with orbital fat. Diseases affecting the orbit are considered according to the anatomical compartment in which they originate; intraconal: within the muscle cone; conal: involving the muscle cone; and extraconal: outwith the muscle cone, e.g. sinus, bone, lachrymal gland. In general, extraconal pathology produces globe proptosis with an early presentation with diplopia. Intraconal or conal lesions produce proptosis with restricted eye movement. Diplopia without proptosis indicates retro-orbital or midbrain pathology (see Chapter 6). Globe disease is well assessed by clinical visual inspection and ultrasound, rarely is CT necessary. Thin section helical scanning is best; IV contrast is not necessary in primary screening as most orbital masses enhance to the same extent as the muscles so, therefore, there is no differential enhancement to assist in making a tissue specific diagnosis. If there is a history of pulsatile exophthalmos then a MDCT angiogram (MDCTA) protocol is required. As with most neurological disease, it is necessary to have an accurate history and examination to enable CT to provide an optimal examination. The orbit links onto other important skull base areas and pathology in these areas overlaps clinically; therefore, illustrations may overlap with those in other chapters including visual failure, pituitary, and the cavernous sinus.
Patient preparation is described in Table 3.1 and a surview in figure 3.1A.
Reconstruction and reformation The images can be presented in the axial, coronal, and sagittal planes if required. The multiplanar reformats can be done with 2 mm slice width/2 mm interspace to show all structures clearly (3.1B), with the axials angled along the optic nerves in a line taken from the posterior clinoid through the globe (3.1C). MPR curved planes are occasionally useful. Protocol parameters are presented in Table 3.2.
Pathology and illustrations Intraconal Vascular abnormalities: congenital/acquired Optic nerve tumours (see Chapter 4) Pseudotumour/granuloma Abnormal fat (dysthyroid) Metastases/lymphoma
Conal Dysthyroid disease Primary and secondary tumour Myopathy Metastases/lymphoma
28
Orbital pathology
Extraconal Lachrymal gland tumour/granuloma Bone disease: congenital, e.g. fibrous dysplasia tumour, e.g. meningioma infection Sinus disease
Table 3.1 Patient preparation
• The patient should be instructed to hold a downward gaze for the main sequence • Doing this will ‘stretch’ the optic nerve for optimum visibility on the images and keep the eyes still • Care should be taken to ensure that, when doing this, the patient does not tilt the whole head down after the surview and sequence plan has been done. This may result in the area required being out of the field
A
Table 3.2 Protocol parameters for orbital scanning
Patient position Surview First slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
Supine Lateral To clear lower border of orbital cavity To cover orbital roof ~180 mm 1 mm 0.5 mm 0.563 mm 40 × 0.625 mm 0.75 sec 120 kV/250 mAs Standard Soft tissue with bone/brain correction if available As appropriate to show orbital cavity WC 60 WW 360 100 ml if required. Can be injected by hand or pump at 2 ml/sec
B
C 3.1 (A) Surview for the orbit. (B) Sagittal display for axial reformat – the angle taken is from the anterior clinoid through back of globe. (C) Axial reformat of orbital cavity.
Orbital pathology 29
A
B
3.2 (A) MIP of the ophthalmic artery. This vessel is only 1 mm in diameter; its location, below the optic nerve in the optic canal, is evident as is its subsequent course curving over the optic nerve to lie above it in the mid orbital position. This visualization has only become routine with the advent of MDCTA. (B) This shows the size of the normal superior ophthalmic veins in 3D.
A
B
C
3.3 This patient presented with pulsatile exophthalmos. MDCTA shows markedly abnormal and enlarged ophthalmic veins (A, 3D). The base image (B) accurately located the site of the fistula (arrow) through which a balloon was manipulated, inflated with contrast (C) and detached, so closing the caroticocavernous fistula and resolving the patient’s symptoms and signs.
A
B
3.4 This patient with hyperthyroidism has proptosis due to a large amount of abnormal intraconal fat. The coronal image clearly shows the soft tissue strands within the fat. There has been a left orbital decompression carried out with removal of the orbital floor but proptosis persists. Cytotoxic drug therapy is sometimes required to control this complication.
30
Orbital pathology
3.5 (A, B) (4-slice MDCT.) This is typical dysthyroid muscle involvement of the inferior rectus muscles bilaterally, worse on the left. Maximum width for a normal rectus muscle is 8 mm. B Note the typical sparing of the muscle insertion into the sclera. This is contrary to involvement of the muscle and its insertion in orbital granuloma. This distinguishes it from the expansion of the whole length of the muscle in orbital granuloma (3.6).
A
A B
C 3.6 (A) This diffuse mass occupying the intraconal space and spreading through D the superior orbital fissure into the left cavernous sinus is orbital granuloma (pseudotumour) . This is an extreme example and could not be differentiated from any other intraconal tumour. (B, C) The more typical appearance with a mass located towards the orbital apex associated with diffuse enlargement of the (typically) medial rectus muscle which involves the whole length of the muscles. A metastatic or lymphomatous deposit would look very similar but without the muscle thickening. Note also the enlarged medial rectus muscle in the right orbit (B). (D) This is a very mild case. There is only infilling and loss of the apical orbital fat on the left with some thickening of the length of the medial rectus muscle and slight proptosis.
Orbital pathology 31
A
B
3.7 (A–C) The diffuse soft tissue mass within the superior and medial rectus muscles on the left and the superior rectus muscle on the right also invades through the left superior orbital fissure. It has destroyed the left medial orbital wall and spread in to the ethmoid air cells. Careful examination also reveals intracranial tumour spread (B, C, arrows). This was an aggressive lymphoma.
C
3.8 (A, B) This patient’s right eye is displaced inferiorly. The 3D image shows the distortion of the roof of the right orbit and the diffuse abnormal frontal bone. The midline MPR defined the thickened clivus, frontal and occipital vault with the typical ‘cysts’ and amorphous abnormal bone of fibrous dysplasia. Progressive proptosis is a common consequence of this condition.
A
A
B
B
C
3.9 (A–C) This patient also has an eye displaced inferiorly. There is also distortion of the orbital roof here but this is due to expansion of the right frontal sinus and destruction of the orbital roof by a mucocoele secondary to chronic sinusitis. The marked bone destruction is evident in the 3D view (C). Extraconal masses typically displace the globe, resulting in diplopia as an early sign.
32
Orbital pathology
3.10 (A, B) This is a preseptal periorbital abscess secondary to sinusitis. (C, D) This orbital abscess is in the postseptal space, between the superior rectus muscle and the orbital roof. It is associated with a small epidural abscess (D).
A B
C
D
A
B
3.11 There is extensive preseptal cellulitis and soft tissue inflammation associated with osteitis in the thickened and irregular anterior wall of the frontal sinus (A, B). Another patient with chronic sinusitis and osteitis has pus extruding into the forehead soft tissues through holes in the frontal bone (C, arrowheads) and there is also a large oroantral fistula (arrow).
C
Orbital pathology 33
Learning points • The high resolution, inherent high contrast resolution, and speed of MDCT offer optimal orbital imaging. • Millimetre or submillimetre sections are essential. • Remember to check the connected paraorbital regions. • Review the optic nerve in reconstructions angled along its long axis. • In diplopia without proptosis think of a retro-orbital/brain stem lesion.
Further reading 3.12 This patient had a repair of a blow-out fracture of the orbital floor. Unfortunately the eye remained fixed in position postoperatively. CT shows adhesions inferior to the globe involving the inferior rectus muscle and the elevated bony fragment which is sited a little higher than the rest of the floor.
A
B 3.13 (A) Curved MPR. This patient with bilateral proptosis has diffuse tumour spread along the optic nerves which also involves the muscles. This was lymphoma. Note the benign scleral calcification most prominent on the left (B).
Chen CC, Chang PC, Shy CG, et al. CT angiography and MR angiography in the evaluation of carotid cavernous sinus fistula prior to embolisation: a comparision of techniques. AJNR 2005;26(9):2349–56. El Ouafi N, Rafai MA, Fadel H, et al. Bilateral idiopathic orbital myositis. Rev Neurol (Paris) 2006;162:750–2. Park WC, White WA Woog JJ, et al. The role of highresolution computed tomography and magnetic resonance imaging in the evaluation of isolated orbital neurofibromas. Am J Ophthalmol 2006;142:456–63. Royal College of Radiologists. Making the Best Use of a Radiology Department: Guideline for Doctors. Royal College of Radiologists, London, 2007. Sheikh M, Abalkhail S, Doi SA, et al. Normal measurements of orbital structures: implications for the assessment of Graves’ ophthalmopathy. Australas Radiol 2007;51:253-6. Shields JA, Shields CL, Scartozzi R. Survey of 1264 patients with orbital tumours and simulating lesions: The 2002 Montgomery Lecture, part 1. Ophthalomolgy 2004;111:997–1008. Terui K, Koskimichi S, Nakao N, et al. Radiographic characteristics of fibrous dysplasia of the clivus: a case report and review of the literature. No Shinkei Geka 2007;35:895–9. Yan J, Wu Z, Li Y. The differentiation of inflamatory pseudotumour from lymphoid tumours of orbit: analysis of 319 cases. Orbit 2004;23:245–54. Yeh S, Foroozan R. Orbital apex syndrome. Curr Opin Ophthalmol 2004;15:490–8.
Chapter 4
35
Visual failure
Introduction
Technique
A patient with visual failure is a relatively common referral to neuroradiology from many clinical specialities. The site of the pathology affecting the visual pathway can be predicted from its anatomy and so an accurate description of the visual complaint and clinical findings are essential if imaging is to be optimized. Site in turn predicts the differential diagnosis. For example, monocular visual loss reflects retinal or optic nerve disease. Bitemporal hemianopia reflects pathology affecting the optic chiasm. Homonymous hemianopia is a disorder of the visual cortex. Unfortunately we are not always given such detailed information and sometimes it is not possible to obtain it from the patient. The combination of visual failure and cranial nerve palsies 3, 4, or 6 will help to localize the pathology to the superior orbital fissure or cavernous sinus (Chapter 6). Colour vision abnormalities point to an optic nerve problem, while the onset of confusion can be due to bilateral occipital infarction causing cortical blindness. It is possible to provide one single CT technique which will enable all parts of the visual pathway to be examined in sufficient detail that any causative structural pathology will be shown. Opinion may be divided between those who advocate MDCT for orbital and parasellar pathology and those who advocate MR because of its superior soft tissue contrast. However, what cannot be denied is that if there is any urgency in the investigation of visual failure then a CT scan performed properly will exclude or identify any structural cause and any delay awaiting an MR is inappropriate. What is important is that the supervising radiologist is able to perform diagnostic studies in all patients.
The CT examination is a helical study of the entire visual pathway within the brain. It incorporates the anatomy of the orbital cavity, the optic chiasma, pituitary, and visual cortex. From the base data, multiplanar reformats of each of the above areas with appropriate reconstructive zooms can be created. This gives a high quality CT image of each area to diagnose pathology in the patient presenting with visual failure. Patient preparation is presented in Table 4.1 and a surview in figure 4.1. Protocol parameters are presented in Table 4.2.
Reconstruction and reformation Presentation of images is done from multiplanar reformats of each area: orbital cavity, the pituitary/optic chiasma, and whole head to show the visual cortex.
Orbital cavity (4.1B) The angulation is a line from the posterior clinoid through midglobe along the line of the optic nerve as shown in Chapter 3 (Orbital pathology) with 12 images. Slice width is 2 mm/interspace 2 mm. Note the enlarged left lacrymal gland.
Pituitary region and optic chiasma (4.1C) The coronal images should show good arterial enhancement around the pituitary. 12 images with slice width 2 mm/interspace 2 mm.
36
Visual failure
Visual cortex (4.1D) Whole head reformat to show most importantly the visual cortex. 12 images, slice width 6 mm/interspace 6 mm. These three main areas of interest are displayed in multiplanar reformations.
Pathology and illustrations
Table 4.1 Patient preparation
• The patient should be prepared as for CT angiography with an 18 or 20 gauge venflon in the antecubital fossa • The patient should be instructed to hold a downward gaze during the scan in order to ‘stretch’ the optic nerves
Globe Retinal detachment Vitreous/subhyloid haemorrhage Trauma Central retinal artery/vein occlusion
Table 4.2 Protocol parameters for visual pathway imaging
Optic nerve Demyelination Meningioma Glioma Trauma
Patient position Surview First slice Last slice
Optic chaism Pituitary tumour Suprasellar meningioma Aneurysm Craniopharyngioma Rathke cyst Metastasis
Optic tract/radiation and visual cortex Infarction Demyelination Malignant tumour Extra-axial mass Examples of a variety of pathology in all parts of the visual pathways are included.
Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter
Reconstructive zoom
Windowing Contrast
Supine Lateral Bottom border of cavernous sinus To cover orbital roof and occipital cortex posteriorly ~250 mm 0.9 mm 0.45 mm 0.685 64 × 0.625 mm 0.5 sec 120 kV/300 mAs Standard Soft tissue – special bone/brain interface filter if available Zoom partial images to orbits/chiasma region initially (see below) WC 60 WW 360 High pressure pump injection 100 ml contrast media, 4 ml/sec, 60 sec scan delay
Visual failure 37
A
B
4.1 (A) The surview for visual pathways must include the occipital cortex for a complete study. (B–D) These show the multiplanar formats for this technique. The acquired data set has a reconstructive zoom over the area of the orbital cavity and chiasma, which is then reformatted to optimize the optic nerves in the axial plane (B) and the chiasma in the coronal plane (C: optic chiasma, arrow; pituitary stalk, arrowhead). The base data is then reconstructed with a full head field of view and reformats done in the axial plane C 5 mm slice width/5 mm interspace to clearly show the occipital cortex and whole brain (D).
D
B 4.2 (A) Axial, (B) curved coronal reconstructions. Clinically on direct visualization of the optic nerve head, papilloedema can be confused with a benign condition when there is calcification in the optic nerve head but it is buried beneath the surface causing enlargement of the A nerve head. This buried drusen is very obvious on CT (arrows; bilateral in this case) but in this patient there is also a meningioma (arrowheads) so there may be both papilloedema and buried optic nerve drusen.
38
Visual failure
4.3 (Axial). This patient suffered sudden partial monocular right-sided visual loss. CT shows an abnormal soft tissue lesion within the right globe (arrows) and a filling defect within the major superior ophthalmic vein (arrowhead). The exudate/haemorrhage within the globe is secondary to thrombosis of the superior ophthalmic vein.
4.4 The left globe was punctured during an accident and the collapsed globe contains higher attenuation haemorrhage with an adjacent lateral haematoma. (4-slice scan.)
4.5 (Sagittal.) This patient has been blind in the right eye for some time and abnormal soft tissue can be seen inside the globe and the higher attenuation lens is dislocated. This patient also has a pituitary adenoma which is compressing the chiasm (arrow) and which is responsible for the new complaint of loss of peripheral vision in the other good eye.
4.6 There are many forms of orbital prostheses; most are smaller and denser (left) than the normal globe. Some are only half shells. (This was an incidental finding in a CT of the paranasal sinuses.)
Visual failure 39
A
B
4.7 (A) Axial, (B) sagittal. The normal optic nerve complex should measure in the order of 5 mm. It can be enlarged by an increase in the CSF that ensheaths the nerve, which occurs when there is raised intracranial pressure (as in this case), and clinically papilloedema is seen (compare with optic nerves in 3.1C).
A
4.8 Two small enhancing lesions are noted on the retina on the left; unfortunately the larger of these metastatic deposits (arrow) involves the fovea just lateral to the optic nerve head so producing visual failure early in this disease process.
B 4.9 (A) Axial, (B) sagittal. The left optic nerve is thickened here because there is a tumour of the nerve sheath; a C meningioma. This typically gives ‘tram-line’ parallel enhancement (B) while an optic nerve glioma has a more uniform appearance (C). Both may enlarge the optic canal and grow into the optic chiasm (arrows) as the right-sided glioma demonstrates here.
40
Visual failure
A
B
4.10 (A) Sagittal, (B) curved coronal. This lady complained of retro-orbital headache. MDCTA proved the lesion was not an aneurysm as suggested by routine contrast enhanced CT, but a meningioma associated with bony blistering of the anterior clinoid (arrow) and tumour extension along the optic nerve.
A
B
4.11 (A) Axial, (B) coronal. This patient had trans-sphenoidal pituitary surgery and radiotherapy 20 years previously. She now complains of visual disturbance in the right eye. Axial MDCT shows the radiation induced meningioma medial and anterior to the right carotid artery, within the optic canal and spreading anteriorly over the planum sphenoidale. There is the usual postoperative intrasellar cisternal herniation and the residual pituitary gland is seen separate from the meningioma in the floor of the pituitary fossa (arrow).
4.12 (A) Axial, (B) sagittal. The commonest parasellar mass to cause visual failure is a pituitary macroadenoma, most commonly a homogeneously enhancing mass expanding the sella (unlike suprasellar masses); the pituitary A B stalk is part of the mass (arrow) and not separate from it (compare with the suprasellar meningioma, 4.13). As with MR it is often not possible to distinguish the optic chaism from the tumour when it is very large, as in this case.
Visual failure 41
4.13 (A) Coronal, (B) sagittal. The pituitary gland is normal but there is a homogeneous mass between it and the optic chiasm (arrows) which is in direct contact with the mass. This patient presented with the classical chiasmal compression sign of A B bitemporal hemianopia. This lesion is a suprasellar meningioma. In (B) note the clearly different attenuation of the pituitary and the suprasellar mass confirming that the mass is not a pituitary macroadenoma (see 4.12B). The pituitary stalk is also clearly visualized in both planes.
4.14 4-slice MDCT, (A) axial and (B) sagittal. This uniformly enhancing mass involving the chiasm and spreading along the right optic nerve is a chiasmal glioma in a patient with neurofibromatosis. There is a small cyst on the upper tumour surface seen in (B).
A
B
4.15 (A) Coronal, (B) sagittal. This complex mass lesion lies directly above and distinct from the pituitary gland but it cannot be separated from the chiasm or the pituitary stalk. Notice the shape of the pituitary fossa which has been flattened and the anterior and posterior clinoid displaced A B laterally and posteriorly respectively. This indicates a chronic lesion. This lesion was a low-grade pilocytic astrocytoma of the hypothalamus.
42
Visual failure
A
B
C
4.16 A craniopharyngioma typically comprises solid tumour with cystic and calcified components. The calcification is very specific on CT (A, axial; B, sagittal). A hyperintense proteinaceous cyst is characteristic on MR (C) in which the calcification is difficult to recognize. The overall diagnostic capabilities are similar with CT and MR as evidenced on these images; the aqueduct, the tectal plate and the corpus callosum are equally well displayed on the CT as on the MR.
A
B
4.17 (A, B) This patient was referred for surgery with a craniopharyngioma diagnosed on MR at the referring hospital. However, it seemed likely that the diagnosis was incorrect and the dual phase examination allowed good vascular imaging to show the lesion to be a calcified, mainly thrombosed, carotid-ophthalmic artery aneurysm. The small residual lumen (arrows) is well shown (4-slice CT examination).
Visual failure 43
A
B
C
D
4.18 This girl had a craniopharyngioma (A, MR preoperative) resected, and at the time of operation a tear in the anterior cerebral artery was repaired with an aneurysm clip. A similar clip was tested in vitro for MR compatibility and found to be safe, but the amount of clip artefact destroyed all local information as seen on the sagittal MR (B). However, MDCT clearly showed the residual enhancing suprasellar tumour despite some clip artefact (C, coronal; D, sagittal).
A
B
4.19 (A) Coronal, (B) 3D angio. Unusually, this patient has a nasal field cut on the left. The cause is a left carotid aneurysm compressing the upper part of the left side of the chiasm. Note the pituitary stalk medial to the carotid superiorhypophyseal artery aneurysm in (A). The VR3D shows the intrasellar location of the medially pointing aneurysm. (4-slice scan.)
44
Visual failure
4.20 There is a calcified suprasellar craniopharyingioma which was treated with radiation therapy 5 years previously. The new complaint of recent visual deterioration is due to radiation induced demyelination in the optic tracts bilaterally, shown here as low attenuation (arrows).
4.21 This patient presented with a short history of confusion and falls. There is established bilateral acute (48 hours or so) infarction of the occipital lobes, slightly more mature on the left than the right. The patient may not appreciate that she is blind as the blindness is cortical.
4.22 This patient developed a field cut over several weeks. The appearances are typical of a highgrade malignant glioma.
Learning points
Further reading
• Timely CT is preferable to delayed MR. • One 10 second MDCT can provide all the information required in all possible pathological sites. • Isotropic MPRs are essential. • Look carefully at, and identify all, the normal/abnormal parasellar structures. • Bitemporal hemianopia is not always due to a macroadenoma; look and think: is this a suprasellar mass?
Boulos PT, Dumont AS, Mandell JW, et al. Meningiomas of the orbit: contemporary considerations. Neurosurg Focus 2001;15:10(5):E5. Hershey BL. Suprasellar masses: diagnosis and differential diagnosis. Semin Ultrasound CT MR 1993;14:215–31. Massry GG, Morgan CF, Chung SM. Evidence of optic pathway gliomas after previously negative neuroimaging. Ophthalmology 1997;104:930–5. Miller NR. Primary tumours of the optic nerve and its sheath. Eye 2004;18:1026–37. Rennert J, Doerfler A. Imaging of parasellar lesions. Clin Neurol Neurosurg 2007;109:111–24.
Chapter 5
45
Pituitary imaging
Introduction
Indications for pituitary imaging
Magnetic resonance imaging is an excellent imaging modality for pituitary and optic chiasmal disease. However, MDCT is a proven accurate alternative if and when MR is not possible, or cannot be accessed urgently in a patient with acute visual failure. MDCT has been shown superior to MR in assessing the lateral extent of an adenoma and the sellar floor. The purpose of imaging is to identify the presence or absence of a functioning/nonfunctioning adenoma or any parasellar pathology causing a hormonal abnormality. The effect of any lesion on the adjacent chiasm and the anatomy of the parasellar vessels will all determine future management. An axial helical scan provides isotropic images in all planes and so is superior to angled direct coronal incremental scanning. Careful review of all adjacent structures and the pituitary infundibulum (stalk) is an integral part of pituitary imaging, as disease of the stalk or hypothalamus can produce hormone abnormalities that mimic primary pituitary disease. Presurgical assessment requires comments about the gland, the cavernous sinus, the carotid arteries, and the sphenoid sinus so good vascular contrast is necessary. Dual bolus contrast acquisition allows time for the normal pituitary tissue to enhance and the second contrast bolus optimizes the vascular data. Single phase scanning is also acceptable but vessels are less well defined.
Hormonal Hyperprolactinaemia Acromegaly Cushings syndrome Thyroid stimulating hormone excess Suspected pituitary stalk compression (moderately elevated prolactin) Hypopituitarism Apoplexy Hypogonadism
Structural Bitemporal hemianopia (nonfunctioning adenoma/suprasellar mass) Incidentally found enlarged sella on skull radiograph
Technique Protocol parameters for pituitary imaging are shown in Table 5.1 and surview is shown in figure 5.1A. Multiplanar reformations in the axial, sagittal, and coronal planes can then be done from the data set. Twelve or 14 images in each plane at slice thickness 2 mm/interspace 2 mm covers the parasellar region. The images below show an example of each and also the reconstructive zoom used for this study.
46
Pituitary imaging
Reconstruction and reformation Axial (5.1B) coronal (5.1C), and sagittal (5.1D) reformations are standard. Typical macroadenoma is shown here.
Pathology and illustrations These will include examples from the list of indications above, including hormonal and structural pathology.
Table 5.1 Protocol parameters for pituitary imaging
Patient position Surview First slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
Supine Lateral Lower edge of cavernous sinus Through lateral ventricles ~180 mm 0.9 mm 0.45 mm 0.639 mm 40 × 0.625 mm 0.5 sec 120 kV/300 mAs Standard Soft tissue with bone/brain correction if available To include pituitary and orbits WC 70 WW 250 Dual bolus technique 80 ml at 3 ml/sec Pause for 1 min 50 ml at 4 ml/sec 25 sec delay to scan start
A
B
C 5.1 (A) Surview for pituitary study. Axial (B) coronal (C), and sagittal (D) reormations. In each of these (B–D) the intra- and suprasellar lesion appears well enhanced from the first contrast bolus. Similarly, from the second bolus, the adjacent vessels are very well defined.
D
Pituitary imaging 47
5.2 (A) Sagittal and (B) coronal reformations. This is an arterial phase acquisition and it shows that the normal pituitary tissue has not yet enhanced, the contrast within the stalk is in the hypophyseal portal system, and the focal intrapituitary enhancement, the ‘tuft’, should be central. It can be displaced by a small microadenoma and so can be an indirect sign of such pathology.
A
B
5.3 (A) Sagittal and (B) coronal reformations. The pituitary gland and stalk are normal in this dual phase examination. Note the large vein running between the cavernous sinuses (arrows). This can cause heavy bleeding during trans-sphenoidal pituitary surgery.
A
5.4 This macroadenoma, i.e. >10 mm in diameter, is typical in that it shows less enhancement than the residual pituitary tissue in the far left side of the fossa. Note the displacement of the stalk from right to left, the convex upper gland surface, and the lateral displacement of the right carotid artery. There is no cavernous sinus invasion and trans-sphenoidal surgery can be curative. The optic tracts just emerging from the optic chiasm can be seen on either side of the stalk (arrows) so this patient will not have visual disturbance. This could be any hormonally active tumour; ACTH producing tumours tend to be much smaller at presentation because of the obvious clinical problems. Be sure to view the examination with low contrast as, if not, important structures, e.g. the optic structures, will not be visualized.
B
48
Pituitary imaging
5.5 This large macroadenoma expands superiorly to contact the right side of the optic chiasm. Note the medial position of the right ICA to which the surgeon must be alerted.
5.6 When there is massive elevation of the serum prolactin then a very large tumour is anticipated. Although a benign tumour, the adenoma can be very aggressive and grow laterally into the temporal lobe causing seizures, or down through the skull base as is seen here.
5.7 (A, B) This patient presented with headache and galactorrhoea. The headache may be because the 8 mm prolactinoma lies within the right cavernous sinus causing dural stretching. The adenoma enhances less than the normal cavernous sinus or pituitary tissue (arrow) and the carotid arteries are identified separate from the pituitary and the adenoma. The sagittal cut is through the right cavernous sinus and the low A B attenuation adenoma lies superior and posterior to the carotid artery. Surgical treatment in this situation is not possible.
A
B
5.8 The MIP coronal (A) and axial (B) MDCTA shows an aneurysm arising from the left internal carotid artery and lying within the left lateral pituitary gland (arrows). This is why it is best to use dual phase contrast studies when assessing the pituitary fossa as the neurosurgeon must be made aware of this potentially disastrous situation if trans-sphenoidal surgery is contemplated.
Pituitary imaging 49
5.9 This study is not dual phase (4-slice MDCT) so the vessels are less well defined. The pituitary gland itself is normal but the stalk is markedly enlarged; normal is 2 mm. This patient presented with hypopituitarism due to this sarcoid granuloma.
5.10 Hypopituitarism in this patient with lung cancer was thought to be due to malignant meningitis with deposits (arrows) over the pituitary and stalk and behind the dorsum. The focal intrapituitary low attenuation may be an incidental pituitary cyst (found in 5% of autopsies), an adenoma, or even a secondary deposit; the radiology is not specific.
5.11 This elderly man presented with confusion and biventricular hydrocephalus which, from the referring hospital CT, was thought to be due to an intraventricular colloid cyst. He was found to be hyponatraemic and this scan shows a uniformly enhancing mass in continuity with the pituitary stalk, extending into the hypothalamus (floor of the third ventricle) and then becoming intraventricular and obstructing the foramen of Munro. Sadly he died soon after admission and no final histological diagnosis was made.
5.12 This girl had delayed development of secondary sexual characteristics. She was claustrophobic and would not tolerate MR without a general anaesthetic. CT shows a low attenuation nonenhancing suprapituitary tumour with the compressed enhancing pituitary along the floor of the fossa. The basilar artery is also displaced posteriorly. The fossa shows signs of enlargement with an abnormally flattened and sloping anterior wall (‘fish hook sella’) indicating a long-standing/developmental cause. The cause was a slowly growing craniopharyngioma. Compare with the case illustrated in 4.15B.
50
Pituitary imaging
5.13 Hypopituitarism was secondary to calcified tuberculous meningitis in this patient. Typical location and appearance of the ‘popcorn’ calcification and enhancing thickened meninges.
A
5.14 Hypopituitarism can be due to an intrapituitary tumour, usually an inactive pituitary adenoma or a secondary deposit. This ill-defined enhancing centrally placed intrapituitary mass is a secondary tumour from a lung primary. More commonly secondary tumours causing hypopituitarism are in the stalk.
B
5.15 This mass of the pituitary stalk was an incidental finding in a patient presenting with headache (A). A developmental hamartoma should be the likeliest diagnosis, especially in association with the bony deformity of the dorsum sellae (B); however, a hamartoma would not show enhancement as this lesion does so a low-grade tumour is the best guess; follow-up may be enlightening!
Pituitary imaging 51
A
B
5.16. This patient presented with sudden severe headache and was thought to have suffered an SAH. The axial plain CT (A) shows abnormal high attenuation material in the expanded pituitary fossa and in the left cavernous sinus. This is haemorrhage into a previously undiagnosed pituitary macroadenoma. Image (B) is a coronal view from the emergency pretrans-sphenoidal surgical assessment of the adjacent vessels and sphenoid sinus. There is chiasmal compression in this patient with pituitary apoplexy.
5.17 This patient was referred with a diagnosis of pituitary macroadenoma made from MR scan. MDCT shows a normal enhancing pituitary and stalk lying above the less enhancing mass in the sphenoid sinus which has destroyed the fossa floor and the dorsum. This tumour arises in the sphenoid; the pituitary is normal. Biopsy confirmed sphenoid sinus carcinoma.
52
Pituitary imaging
Learning points • MDCT provides imaging data equivalent to that of MR, but it needs to be examined carefully. • Differentiation of sellar from suprasellar/parasellar pathology requires careful analysis of the size/shape of the fossa, the position of the pituitary stalk, the attenuation of any mass compared to the pituitary tissue, and the status of the planum sphenoidale. • Thin acquired slices and isotropic MPR are essential. • Don’t miss the gland enlargement in apoplexy in an acute presentation. Radiologists are often the first to suggest this diagnosis.
Further reading Abe T, Izumiyama H, Fujisawa I. Evaluation of pituitary adenomas by multidirectional multislice dynamic CT. Acta Radiol 2002;43:556–9. Bonnevill J-F, Cattin F, Dietemann J-L. Computed Tomography of the Pituitary Gland. Springer-Verlag, 1986.
Chanson P, Salenave S. Diagnosis and treatment of pituitary adenomas. Minerva Endocrinol 2004;29:241–75. Gruber A, Clayton J, Kumar S, et al. Pituitary apoplexy: retrospective review of 30 patients – is surgical intervention always necessary? Br J Neurosurg 2006;20:379–85. Gutenberg A, Hans V, Puchner MJ, et al. Primary hypophysitis: clinical-pathological correlations. Eur J Endocrinol 2006;155:101–7. Miki Y, Kanagaki M, Takahashi JA, et al. Evaluation of pituitary macroadenomas with multidetector-row CT (MDCT): comparison with MR imaging. Neuroradiology 2007;49:327–33. Rennert J, Doerfler A. Imaging of the sellar and parasellar lesions. Clin. Neurol Neurosurg 2007;109:111–24. Ruscalleda J. Imaging of parasellar lesions. Eur Radiol 2005;15:549–59. Sergides IG, Minhas PS, Antoun N, et al. Pituitary apoplexy can mimic subarachnoid haemorrhage clinically and radiologically. Emerg Med J 2007;24:308.
Chapter 6
53
Cranial nerve palsies 3–6
Introduction
Technique
Palsies of the 3rd to the 6th nerves can be caused by pathology anywhere along the length of the nerve from the superior orbital fissure or the foramen ovale, through the cavernous sinus and the basal cisterns, to their nuclei in the mid brain (3 and 4) and pons (5 and 6). Any palsy can occur in isolation or in combination. The volume of brain and skull involved is only about 6 cm in depth and so it is easy to use a short CT technique to examine all the possible sites of disease. There are obvious anatomical overlaps in imaging of this busy part of the skull and brain and so you may need to refer to the chapters on the orbit, visual failure, and the pituitary to find illustrations of pathology in these sites which could be associated with a palsy of the 3rd to the 6th nerves. The multiple sites and number of pathologies possible make this a most challenging (and most rewarding) area for the radiologist. Getting a rare diagnosis or detecting a subtle abnormality here could make your reputation! It is essential to give IV contrast and use a submillimetre helical scan to achieve best resolution and tissue differentiation. The contrast timing depends upon the likely clinical cause. If an aneurysm is suspected (e.g. isolated painful 3rd nerve palsy with pupillary involvement) then MDCTA as for the Circle of Willis is best. If cavernous sinus (multiple palsies) or skull base pathology (facial pain) seems most likely, then a venous timed scan is best (see Chapters 11 and 12). If in doubt, do an MDCTA and plan a duplicate scan to follow at venous timing (60 seconds delay) or at 5 minutes delay if the first processed scan suggests a nonvascular mass (see Chapter 2). It is necessary to include the skull base from the hard palate to the orbital roof, as invasive tumours of the nasopharynx can spread along the nerves into the cavernous sinus and beyond.
The scan set up is as for the ‘visual failure’ protocol (Chapter 4) using a submillimetre helix with the timing of the contrast dependent upon the above clinical considerations. This is why it is so important to understand the exact nature of the clinical question being asked and why good clinical understanding and interactions are essential for optimizing neuroimaging. It is important to be present to supervise and direct these examinations to ensure maximum information from minimum scanning.
Reconstruction and reformation Axial, coronal, sagittal, and oblique MPR views are often necessary with volume rendered 3D (VR3D) angiogram and maximum intensity projection (MIP) for assessing vascular causes.
54
Cranial nerve palsies 3–6
Pathology and illustrations Superior orbital fissure associated with proptosis (Orbital apex syndrome) Orbital granuloma Neuroma Nasopharyngeal malignancy with perineural spread
Cavernous sinus Neuroma Meningioma Nasopharyngeal malignancy with perineural spread Aneurysm/fistula (see Chapter 3) Cavernoma Thrombosis (see Chapter 11) Infection: bacterial, fungal Secondary tumour Lymphoma
Pituitary (see Chapter 5) Adenoma Apoplexy
Basal cisterns Aneurysm Neuroma Metastatic tumour Meningitis
Mid brain and pons Demyelination Infarction Tumour Encephalitis False localizing sign secondary to a mass lesion
Sphenoid sinus/clivus Infection Tumour: primary and secondary Midline granuloma
6.1 This uniformily enhancing mass in a patient with left sided 3rd, 4th, 5th and 6th nerve palsies is a meningioma; this is one of the commonest causes of such a clinical scenario. However in view of its location over the petrous apex and into the foramen ovale, a neuroma of the 5th nerve is also a reasonable differential.
Cranial nerve palsies 3–6 55
6.2 This patient presented with sudden onset of a right 3rd nerve palsy. CT shows an intrasellar mass with extension into the right cavernous sinus (A, B) and posterior extension between the posterior cerebral (pca) and the superior cerebellar (sca) arteries (C), exactly the A location of the 3rd nerve. This is pituitary apoplexy, the first presentation of the pituitary tumour in this young man.
B
C
A
B
6.3 This young patient was investigated with MR for rapid onset 3rd nerve palsy. MR could not distinguish between a solid enhancing mass and an aneurysm so CT angiography was advised. MDCTA confirmed no aneurysm and defined the presence of a small lesion (A, B, arrows), not enhancing in this angiographic study. The position of the mass lateral and adjacent to the curve of the posterior communicating artery (A), the anatomical site of the 3rd nerve, indicates that the mass is most likely to be a neuroma of that nerve.
6.4 This patient presented with left-sided facial pain. The lesion outlined (arrowheads) is thought to be a meningioma with a long intracranial course from just above the internal auditory canal region (A) up to the free edge of the tentorium (B) A B involving the route of the 5th nerve. Frequently masses in this region are followed with serial imaging as operative biopsy can be hazardous and surgical excision is likely to worsen the neurological deficit.
56
Cranial nerve palsies 3–6
A
6.5 Coronal (A) and axial (B) venous phase CT. This patient with neurofibromatosis had a slowly progressive isolated left 6th nerve palsy. The mass in the left cavernous sinus is most likely to be a 6th nerve neuroma. The well defined low attenuation structures in the right cavernous sinus are the
B
normal cranial nerves, most probably 3 and 4.
6.6 This 15-year-old boy developed painful left 3rd, 4th, and 6th nerve palsies over a few days associated with a headache and general malaise. CT shows sphenoid sinusitis, a low attenuation linear structure in the left cavernous sinus adjacent to the sphenoid sinus wall, and a thickened intermediate attenuation in the cavernous sinus associated with a small globule of gas. The interpretation is that there is an abscess (low attenuation) in the cavernous sinus with overlying sinus thrombosis with air, indicative of infected thrombus. It resolved after a course of antibiotics.
A
B
6.7 A young Chinese business man developed right-sided facial pain and a squint. CT shows a mass occupying the right foramen ovale, spreading into the cavernous sinus. The location of the pathology in an oriental male is almost pathognomic of neural spread of a nasopharyngeal carcinoma. This was the case and in fact his father had died of the same disease.
Cranial nerve palsies 3–6 57
6.8 This unfortunate 32-year-old woman complained of diplopia and retro-orbital headache worsening over a 4 week period. CT shows a mass in the right cavernous sinus spreading anteriorly along the inferior rectus A B muscle (B), inferiorly through the inferior orbital fissure into the pterygoid fossa, and also along the calvarial extradural space (A, short arrows). It is associated with bone erosion (A, arrow), therefore granuloma is most unlikely. This was neural spread of a salivary gland tumour (adenoid cystic carcinoma). The patient died 6 months later.
6.9 One of the commonest causes of a painful 3rd nerve palsy is a terminal carotid aneurysm. The pupil is usually involved because there is compression on the pupillary fibres which lie superficially on the nerve. This aneurysm (A) arises from the posterior wall of the ICA and, in this case, the neck involves the origin of the posterior communicating artery (arrow). Occasionally a large basilar tip aneurysm (B), or superior cerebellar artery aneurysm, will cause the palsy. MDCTA can replace DSA in the diagnosis of possible aneurismal 3rd nerve palsy.
A
6.10 (A, B) An aneurysm of the intracavernous carotid artery frequently presents with a 6th nerve palsy as the 6th nerve lies within the carotid sheath within the cavernous sinus. This was the case here with a narrow necked (A, arrows) carotid aneurysm, later treated with coil embolization (see also 6.11). The cessation of the pulsation is believed to remove the pressure on the nerve and allow it to heal despite the presence of the coils filling the aneurysm sac.
A
B
B
58
Cranial nerve palsies 3–6
A
B
6.11 (A, B) More frequently an intracavernous aneurysm produces multiple nerve palsies and typically the patient is an elderly female. Severe facial pain due to involvement of the 5th nerve is also common and is the main indication for any treatment. This giant aneurysm is more than 50% thrombosed and the location of the calcified margin (arrowheads) shows the aneurysm to be much larger than the patent lumen (arrows) filling with contrast would suggest. These aneurysms tend to have a wide neck so treatment involves a combination of stenting with coil occlusion or carotid occlusion. Accurate assessment of the neck of the aneurysm on MDCTA enables accurate noninvasive treatment planning. (See also cavernous sinus fistula, figure 3.3.)
A
B
6.12 Sudden onset of ptosis and a small pupil are likely to reflect a Horner’s syndrome where there is no associated diplopia. In this case the Horner’s was due to dissection of the left internal carotid artery with the false aneurysm at the skull base (A, arrow) and the dissection flap evident in the base images (B, arrowhead). The sympathetic fibres of the 3rd nerve run in the carotid sheath and damage to them causes the syndrome.
Cranial nerve palsies 3–6 59
6.13 This elderly lady had severe facial pain which was thought to be trigeminal neuralgia, but she had loss of sensation in the mid face which mitigated against this condition. CT showed abnormal enhancement within the pons and along the 5th nerve into the ganglion and cavernous sinus. The likely cause is lymphoma or a metastatic deposit.
Learning points • Choosing the correct contrast timing is very important. • Look carefully along the whole length of the nerve(s) involved. • Parenchymal brain disease is better shown with MR and may be invisible on CT, e.g. demyelination. • Review the skull base for subtle bone destruction or tumour especially invading from the nasopharynx. • Multiple palsies with proptosis indicate orbital apex pathology; and without: cavernous sinus/skull base disease. • Sudden onset of an isolated painful 3rd nerve palsy is most commonly due to an aneurysm.
Further reading Bone I, Hadley D. Syndromes of the orbital fissure, cavernous sinus, cerebello-pontine angle, and skull base. J Neurol Neurosurg Psychiatry 2005;76(Suppl lll):iii29–iii38. Borges A. Trigeminal neuralgia and facial nerve paralysis. Eur Radiol 2005;15:511–33.
Borges A, Casselman J. Imaging the cranial nerves: Part 1: methodology, infectious and inflammatory, traumatic and congenital lesions. Eur Radiol 2007;17:2112–25. Borges A, Casselman J. Imaging the cranial nerves: Part 11: primary and secondary neoplastic conditions and neurovascular conflicts. Eur Radiol 2007;17:2332–44. Eisenkraft B, Ortiz AO. Imaging evaluation of cranial nerves 3, 4, and 6. Semin Ultrasound CT MR 2001;22:488–501. Castillo M. Imaging of the upper cranial nerves I, III-VIII, and the cavernous sinuses. Neuroimaging Clin N Am 2004;14:579–93.Go JL, Kim PE, Zee CS. The trigeminal nerve. Semin Ultrasound CT MR 2001;22:502–20. Mathew MR, Teasdale E, McFadzean RM. Multidetector computed tomographic angiography in isolated third nerve palsy. Ophthalmology 2008;115(8):1411–5. Weninger WJ, Prokop M. In vivo 3D analysis of the adipose tissue in the orbital apex and the compartments of the parasellar region. Clin Anat 2004;17:112–7.
Chapter 7
61
Intracranial imaging in stroke: ischaemic
Introduction ‘Stroke’ is a clinical diagnosis characterized by a sudden onset of acute neurological symptoms of presumed vascular origin. This chapter illustrates some of the common and not so common appearances in acute ischaemic stroke. The role of CT in the modern medical setting has become imperative with the advent of thrombolytic treatment for ischaemic infarction of under 3 hours’ duration. There are three principle goals in stroke imaging and MDCT is useful in each area: 1 The characterization of the type of underlying pathology directs immediate and ongoing management. Routine incremental scanning (Chapter 1) will define ischaemic infarction, intracerebral haemorrhage, or subarachnoid haemorrhage (SAH) (Chapter 9), or other lesions presenting as, or being confused with, clinical stroke, e.g. tumour, encephalitis. Additional contrast enhanced volume scans may be required for clarification. 2 Confirmation of infarction and identification of potentially salvageable brain parenchyma may be done by dynamic CT perfusion. 3 Vascular imaging is required to confirm or exclude local vascular disease (Chapter 8 and Chapter 9). This section will cover the first two of the above issues. It is not the intention simply to illustrate this with case after case of acute ischaemic infarction (this is well covered in standard neuroradiological texts), but rather to show how MDCT can offer benefits in certain aspects of infarction identification. Up to 75% of trial patients with proximal MCA occlusion have identifiable ischaemic changes on CT at 3–6 hours after the stroke onset.
It may be difficult to identify the very early changes of ischaemia on CT. If the eyes are included on the scan and they are deviated to one side, it is more than likely that the patient has a total anterior circulation stroke affecting the hemisphere towards which the eyes are deviated. When identified, look extra carefully for either a dense artery sign, or subtle loss of the grey matter definition in the insula and/or basal ganglia, on the ipsi-lateral side. Always look for a hyperdense artery. This is most regularly reported in the MCA, but it can be identified in any first or second order vessel including the ICA, branch MCA, basilar, and posterior cerebral arteries. Thin section acquisition, e.g. 1–2 mm, has been shown to increase the identification of vessel occlusion and early ischaemic loss of grey/white matter differentiation, so this should be used routinely if possible. One of the new exciting and useful benefits of MDCT is the ability to offer routine perfusion brain imaging. The role of perfusion imaging in the management of acute stroke is still under debate. In our centre it is currently used as a troubleshooting tool. Presently, all patients receive an immediate CT brain scan. In cases where there is doubt as to the patency of the vessels, MDCTA is performed. This is probably the most appropriate additional technique. CT perfusion is used when there is doubt as to the time of onset of symptoms or where a second infarct or extension of the first infarct may have occurred. We currently operate on a 3 hour time limit for thrombolysis, but this is likely to increase to 6 hours as more data become available. It is not within the remit of this book to give a full technical description of perfusion CT. The essential technique is to scan the same volume of brain repeatedly
62
Intracranial imaging in stroke: ischaemic
during a high infusion rate injection of iodinated contrast. The aim is to generate sequential images which contain precontrast, arterial uptake, and washout before recirculation can occur. This is then postprocessed, usually with a deconvultional technique to obtain perfusion parameters on a voxel by voxel basis. The parameters in routine clinical use are the mean transit time (MTT), cerebral blood flow (CBF), time to peak (TTP), and cerebral blood volume (CBV). These are intimately related on a physiological level. Again, a conclusion on which parameters are ‘best’ or most suitable has not been reached. Interested readers are directed to the many articles on the topic, of which a few starter papers are given in the References section. Most current techniques use a single slab of tissue, in the region of 4 cm width for a 64-slice scanner. This allows for
Table 7.1 Perfusion scanning parameters for standard (nonjog) mode. This allows 2 cm of brain to be examined with a 4-slice CT and 4 cm with a 64-slice CT
Patient position Surview First slice Last slice Field of view Slice width Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
No. of cycles Cycle time
Supine Lateral skull Mid basal ganglia Selected from routine brain 250 mm 5 mm 64 × 0.625 mm 0.4 sec 120 kV/200 mAs Standard Soft tissue Whole head WC 60 WW 360 50 ml contrast High-pressure pump; 5 ml/sec; 9 sec delay 30 2 sec
a very short interval between scans and allows an attempt at quantitative imaging. Recently, ‘jog’ or ‘shuttle’ modes have been introduced, wherein after the initial scan, the gantry moves to an adjacent slab, another scan is performed, the gantry returns to the original position and the sequence is repeated. This allows qualitative scanning over a large volume (up to 8 cm width). Unfortunately the interscan interval is prolonged. The quantitative data are therefore unreliable and should not be used. If a purely qualitative assessment is required then the jog/shuttle mode is fast and reliable. If more detailed qualitative data are required then standard perfusion techniques should be utilized. Processing of the studies is fast and simple, but practice and patience are necessary. If the technique is not used frequently there is the danger of being insufficiently skilled, as in all radiological techniques.
Table 7.2 Perfusion scanning parameters (jog mode). This allows 8 cm of brain to be examined with a 64-slice CT
Patient position Surview First slice Last slice Field of view Slice width Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
No. of jog cycles Cycle time
Supine Lateral skull Immediately above petrous bone Above lateral ventricles 250 mm 5 mm 64 × 0.625 mm 0.4 sec 80 kV/200 mAs Standard Soft tissue Whole head WC 60 WW 360 50 ml contrast High-pressure pump 5 ml/sec; 9 sec delay 15 1.8 sec
Intracranial imaging in stroke: ischaemic 63
Technique The techniques for the noncontrast, postcontrast, arterial, and venous studies are given elsewhere (Chapters 1 & 2; 8 & 9; 11, respectively). Perfusion technique parameters are described below (Tables 7.1, 7.2). Figure 7.1 shows the positioning for perfusion study (jog mode; 0 mm cover), and 7.2 shows axial perfusion images.
Venous (See Chapter 11)
Pathology and illustrations By definition pathology here is limited to ischaemia but the illustrations include:
Arterial Internal carotid;middle cerebral and branch infarction Posterior circulation infarction Vessel hyperdensity Diffusion abnormalities (See also examples in Chapter 1) 7.1 Positioning for perfusion study (jog mode; 80 mm cover).
A
B
C
D
E
F
7.2 Sample of axial perfusion images (standard 40 mm cover; jog mode: 80 mm cover).
64
Intracranial imaging in stroke: ischaemic
7.3 Acute infarct in the left paracentral lobule (arrows) on CT (A) and diffusion weighted MR (B). Even though the infarct is tiny, it is still visible on CT as a low attenuation and slightly swollen gyrus. It is essential to have an understanding of neuroanatomy and functional areas when diagnosing infarction.
A
B
7.4 Low attenuation change is present within the left superior and middle frontal gyri (arrowheads) in a patient with acute weakness in the right arm and leg. Note the poor definition of the grey matter when compared to the right hand side. The clinical situation sugested a lacunar syndrome. High cortical infarcts are easily forgotten and often overlooked, even when extensive as in this case.
A
B
7.5 Low attenuation within the right side of the pons on CT (A, arrow) in a patient who presented with marked hemisensory loss with hemiplegia. Ischaemia in the pons, midbrain and brainstem can often be difficult to demonstrate on CT, masked by the Hounsfield artefact. This patient also had MR scanning (B) which shows a zone of restricted diffusion in the same location confirming the acute ischaemia.
Intracranial imaging in stroke: ischaemic 65
A
B
7.6 Clinically a total right anterior circulation syndrome. The CT (A) shows loss of the clear definition of the right lentiform nucleus and insula with swelling and reduction in the CSF spaces of the right Sylvian fissure indicating early changes of ischaemia. Twenty-four hours later, the repeat CT (B) shows infarction in the lentiform nucleus, head of caudate, internal capsule, and frontal cortex extending to the midline. This must therefore be due to occlusion of the terminal right ICA, MCA, and anterior cerebral arteries.
7.7 Patient with acute onset left hemispheric stroke with rapid decline in conscious level. The CT demonstrates a large basal ganglia haemorrhage (often hypertensive in origin) with extension into the ventricular system and subsequent hydrocephalus. It is not possible to predict ischaemic from haemorrhagic stroke on clinical grounds.
7.8 This axial slice includes the eyes, which are looking towards the right. The gaze palsy associated with anterior circulation infarct means that the patient ‘looks’ towards the damaged hemisphere. On close inspection the hyperdense MCA and the loss of grey/white matter differentiation throughout the cortex can be seen on the right.
66
Intracranial imaging in stroke: ischaemic
A
B
C
D
7.9 The hyperdense vessel sign may be seen at any site, and not just of the classical MCA so frequently reported. (A) Routine axial CT shows hyperdensity in the proximal right MCA. The images were reprocessed back to the base 0.65 mm thickness and a coronal MIP was done (B), which demonstrates fresh hyperdense thrombus in the terminal ICA and proximal ACA in addition to the MCA. This reduces the likelihood of the effectiveness of thrombolysis. (C) The very dense dot in the left Sylvian fissure is calcific thrombus detached from a carotid plaque. (D) The spots of hyperdensity arrowed were confirmed as fresh thrombus in the posterior cerebral artery on MDCTA. (E) The rather subtle serpiginous hyperdensity in the right parietal region (arrow) was confirmed as fresh thrombus on MDCTA.
E
7.10 One advantage of MDCTA in acute stroke is that the base images can be reformatted to 5 mm cuts and often the poorly perfused infarct will then show more prominently as demonstrated in this small left posterior capsular infarction (arrow) not identified on the routine plain CT.
Intracranial imaging in stroke: ischaemic 67
7.11 The graph top left shows the arterial inflow/outflow in red and venous in blue.These allow a numerical value to be given for cerebral blood flow (CBF) and cerebral blood volume (CBV). The axial brain slices illustrate the absolute measured parameters (CBF/CBV) and the relative parameters (mean transit time [MTT] and time to peak [TTP]) with the colour chart applicable to each, for two brain levels from a perfusion data set. Studies have shown that the absolute CBV (with a threshold at 2.0 ml x 100 g-1) most accurately reflects the acute infarct core. The mismatch between the area of abnormal CVB and the relative MTT (with a threshold of 145%) gives the most accurate delineation of the tissue at risk of infarction. This pattern is displayed schematically in the two images on the extreme right where the core had been shown in red and the penumbra, potentially salvageable tissue, in green. The extent of the final infarct depends upon whether or not the occluded vessel reopens.
Learning points • Stroke is a clinical, not a pathological, definition. • Stroke may be arterial, venous, or a result of another disease mimicking stroke, e.g. brain tumour. • Look carefully at the attenuation of the insular cortex and the basal ganglia. • Review the posterior fossa structures and high frontal and parietal cortices.
• A hyperdense acutely thrombosed artery can be seen in many sites. • Eye deviation should stimulate a careful review of the hemisphere they are looking towards.
68
Intracranial imaging in stroke: ischaemic
Further reading Hill M, Rowley H, Eliasziw M, et al. Selection of acute ischaemic stroke patients for intra-arterial thrombolysis with pro-urokinase by using ASPECTS. Stroke 2003;34:1925–31. Konig M. Brain perfusion CT in acute stroke: current status. Eur J Radiol 2003;45 (Suppl 1):S11–22. Miles K, Eastwood JD, Konig M (eds). Multi-Detector Computed Tomography in Cerebrovascular Disease: CT Angiography and Perfusion Imaging. Informa Healthcare, 2007. Muir K. A clinical perspective on MDCT in acute stroke. Advances in MDCT: Head and Neck 2007;3:1–9. Muir K, Buchan A, von Kummer et al. Imaging in acute stroke. The Lancet 2006;5:755–68. Murphy BD, Fox AJ, Lee DH, et al. Identification of pernubra and infarct in acute ischaemic stroke using CT perfusion-derived blood flow and blood volume measurements. Stroke 2006;37:1771–7. Nabavi D, Kolska S, Nam E, et al. Multimodal stroke assessment using computed tomography: novel diagnostic approach for the prediction of infarction size and clinical outcome. Stroke 2002;33:2819–26.
Pexman J, Barber P, Hill M, et al. Use of the Alberta Stroke Program Early CT Score (ASPECTS) for assessing CT scans in patients with acute stroke. AJNR 2001;22:1534–42. Smith WS, Roberts HC, Chuang NA, et al. Safety and feasibility of a CT protocol for acute stroke: combined CT, CT angiography, and CT perfusion imaging in 53 consecutive patients. AJNR 2003;24:688–90. Wintermark M, Flanders AE, Velthius B, et al. Perfusion CT assessment of infarct penumbra: receiver operating characteristics (ROC) curve analysis in 130 patients suspected of suffering from acute hemispheric stroke. Stroke 2006;37:979–85. Wintermark M, Reichhart M, Cuisenaire O, et al. Comparison of admission perfusion computed tomography and quantative diffusion- and perfusionweighted magnetic resonance imaging in acute stroke. Stroke 2002;33:2025–31.
Chapter 8
69
Vascular imaging in ischaemic stroke and TIA
Introduction Acute brain ischaemia is the expression of primary vascular, and not brain, pathology. Accurate diagnosis of the vessel pathology is urgent and essential if appropriate timely treatment is to be given. This chapter includes details and examples of vascular imaging in patients presenting with acute ischaemia and those attending with a presumed transient ischaemic attack (TIA). The technique is identical and many of the imaging findings are similar. In all cases vascular imaging is required as soon as possible after the event. The risk of further events is highest soon after the initial event. Treatment for the underlying vascular cause should be performed as soon as possible to have maximal future protective effect. In the past, imaging has been concentrated upon an assessment of the common carotid bifurcation. This is due to the data from the European and American studies comparing medical and surgical treatment of carotid territory stroke in the ECST and NASCET trials. In these, digital subtraction angiography (DSA) was the only vascular imaging used. The advent of MDCT, and especially 64-slice CT, now offers a new and exciting method of assessing the entire cerebral vasculature, from arch to Circle of Willis in only 6 seconds. This is also important as reanalysis of the earlier trials shows that aortic disease can be responsible for ongoing ischaemic events. Posterior circulation ischaemia, increasingly recognized as a cause of stroke in young adults, was largely ignored in previous studies. Doppler ultrasound, a commonly used screening examination, covers little of the necessary vessels, and is of limited value. MDCTA provides a new solution to all these imaging requirements. Good vascular imaging can be achieved with a 4-slice
MDCT scanner. The acquisition with a 64-slice scanner provides a significant improvement in the imaging because of improved temporal resolution and relative lack of jugular venous superimposition. With a slice thickness of 0.65 mm compared to 1.25 mm with the 4-slice scanner, the spatial resolution is also markedly improved. All scans are triggered from the contrast density in the ascending aorta with the faster 64-slice scanner. With the 4-slice system the scan was triggered from the pulmonary artery in patients under 50 years to ensure the slower scanner did not miss the contrast bolus. The number of technical failures with 64-slice systems is very low. It is now possible to confirm or exclude vascular disease in any vessel supplying the brain. The time for an experienced radiologist to perform this total assessment is 15–20 minutes which compares favourably with the 30 minutes required for Doppler ultrasound assessment. The issue of radiation dose is not relevant in patients in the age group usually affected. Our dose for MDCTA is actually just a little more than that of our helical head protocol. It is necessary to ensure secure intravenous cannulation to avoid potentially hazardous contrast extravasation. Previously venous reflux and in-flow contrast venous contamination were problematic and could mask pathology at the root of the neck. This is largely resolved by using smaller volumes of contrast, 60 ml compared to 100 ml, and following that with a large bolus of saline. The right arm is preferred for venous access to minimize artefact from incoming contrast. If the left arm is used, beam hardening artefact from contrast remaining the brachiocephalic vein, which passes anterior to the origins of the great vessels, can destroy details of the vessel origins or cause artefactual stenoses.
70
Vascular imaging in ischaemic stroke and TIA
Technique
Table 8.1 Patient preparation for bolus tracking
Bolus tracking This protocol uses 60 ml of contrast (Xenetix 350 or equivalent) injected via dual headed high-pressure pump and flushed with 30 ml saline, both given at 5 ml/sec. Bolus tracking links the optimal cardiac contrast output to the beginning of data acquisition to ensure best arterial contrast density with minimal venous contamination. The locator scan for the positioning of the bolus tracking triggering region of interest should be planned approximately 1.5 cm below the carina on the AP surview (8.1A). The locator scan is a 10 mm slice (30 mAs). Table 8.1 presents optimal patient preparation, and the protocol is presented in Table 8.2.
Reconstruction and reformation VR3D images provides a rapid overview of the vessels, but base image or MPR review is necessary to measure accurately the degree of stenosis either as a percentage of diameter or, more accurately, the area of the carotid artery.
• The patient should be prepared for this examination with an 18 or 20 gauge Venflon in the right cubital fossa • The right side is the preferred site of injection for optimum post processing. Injections into the right arm prevent artefact that occurs from the brachiocephalic vein crossing the arch of the aorta • The patient should be instructed not to swallow during the clinical scan as movement artifact from this can simulate stenosis around the carotid bifurcation
Table 8.2 Protocol parameters to show aortic arch/great vessel origins, cervical carotid, vertebral arteries, and the Circle of Willis in vascular ischaemic stroke
Patient position Surview
Pathology and illustrations Vascular Atheroma is by far the commonest focal causative pathology and is illustrated at many sites. Dissection: spontaneous traumatic Vasculitis: large vessel, e.g. aortitis, Takayasu intracranial
Cardiac Arhythmias, e.g. atrial fibrillation Right to left shunt, e.g patent foramen ovale Tumour, e.g. atrial myxoma
First slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
Supine – chin slightly raised Anteroposterior from below carina to mid cranium 1 cm above carina To cover Circle of Willis ~300 mm 0.67 mm 0.33 mm 0.875 64 × 0.625 mm 0.75 sec 120 kV/400 mAs Standard Soft tissue As appropriate to show vessel origins WC 60 WW 360 Bolus tracking technique is used for this protocol 60 ml at 5 ml/sec Trigger 150 HU
Vascular imaging in ischaemic stroke and TIA 71
8.1 (A) Surview for carotid study. The position of the locator can be seen below the carina. Above that is the planned clinical scan. (B) The locator scan showing position of trigger point (150 HU) in the ascending aorta.
A
B
8.2 VR image of the aortic arch. This technique for analysing the arch allows assessment within seconds. In this case, the arch and origins of the great vessels are normal.
8.3 This patient has extensive atheroma affecting the arch. The ulcerative soft atheroma in the base image (A) is displayed as the irregular ‘solid’ outer wall of the vessel on the VR3D using the standard filter settings (B). Aortic atheroma in excess of 4 mm is an independent risk factor for cerebrovascular events. This is easily assessed on base images. A
B
72
Vascular imaging in ischaemic stroke and TIA
8.4 VR3D aortic arch. This patient has gross aortic calcification. This pattern of external calcification is common in diabetic patients. The technique incorporates the calcium on to the surface image and so will hide any underlying pathology. This makes review of the base reconstructions or MPR images essential.
8.5 VR3D of the vertebral artery origins. In this illustration, the lower part of the cervical spine and upper part of the thoracic spine were removed, while retaining the vertebral artery origins which are viewed from behind. In this projection stenoses and calcification are easily visualized. Doppler US is unlikely clearly to define this vascular region.
8.7 Curved MPR of the vertebral artery origin. This study, performed on a 4-slice system, is degraded by artefact. Note that the diagnostic quality is not materially affected. The study is sufficient to show a heavy atheroma load (arrows) occluding the proximal subclavian artery extending to involve the vertebral artery origin with subsequent stenosis. 8.6 VR3D of the subclavian arteries; viewed from behind as in 8.5. This patient has bilateral subclavian stenoses (arrows on left; arrowheads on right) proximal and distal to the vertebral artery origins and this is associated with occlusion of the right vertebral artery. This technique is useful in patients with suspected subclavian steal.
Vascular imaging in ischaemic stroke and TIA 73
8.8 Assessment of the carotid bifurcations is rapid using a combination of axial images and VR3D images, which help the clinicians appreciate the disease process. This is a nearly normal internal carotid artery – there is only minor irregularity of the vessel, without stenosis.
8.10 This study (4-slice scan) shows extreme tortuousity at the carotid bifurcations. It is easy to see how the internal and external carotid arteries can be confused with Doppler US.
8.9 In this patient, the vessels are very tortuous and slightly dilated (ectatic). The appearance seen in the internal carotid arteries is often described as a ‘tonsillar loop’ because of the proximity of the cervical tonsils. This anatomical pattern makes characterization using Doppler US extremely difficult. MR techniques based on time of flight sequences cannot adequately demonstrate anatomy or pathology in such tortuous vessels.
8.11 MPR images are used for the quantification of a stenosis. The technique utilizes seed points defined on the vessel, either from the axial base data or from the VR3D from which a semi-automatic curved MPR is generated. Of the current algorithms available, no manufacturer has developed an entirely reliable technique. This image shows the ‘centre-line’ generated by the algorithm. It is essential that this line is examined before any measurements are made to ensure the validity of the curved MPR. This image demonstrates calcification and small amounts of soft atheroma within the proximal internal carotid artery.
74
Vascular imaging in ischaemic stroke and TIA
8.12 This patient with recurrent TIAs has a severe, moderate length stenosis. The material giving rise to the stenosis is ‘soft’; the attenuation measurements are similar to the soft tissues of the vessel wall and neck. Note that the outside of the vessel is easily visible (arrow), contrasted against the fat in the carotid sheath. Even when other tissues abut the vessel, the outside is almost always visible. Like any other aspect of this technique, practice is required to detect the described features. The degree of stenosis, as determined by NASCET measurements, has for some time been used as the primary indicator of stroke risk. It is probable that the effect of the degree of stenosis is not as great as previously thought. The nature of the internal surface of the atheroma may be as or more important. Specifically, are there areas of ulceration? This is probably the main detectable indicator of an unstable plaque.
8.13 This curved MPR (A) shows a normal position of the external surface of the internal carotid artery (arrows) with soft atheroma internally. Note that the atheroma is very irregular with numerous areas of ulceration.
8.14 This patient (A) presented with an acute infarct. The ICA is occluded within the bulb and does not refill (small, lower arrow). Note that a small vessel is seen in the expected path of the ICA (large, upper arrow). This is the ascending pharyngeal artery (APA) which arises from the proximal external carotid artery and usually lies on the ICA for most of its course. It can be mistaken for the ICA so care must be taken and it is essential to review the axial data. A helpful hint is to check the carotid canal in the skull base: if there is a vessel there then the ICA cannot be occluded. This was done in patient (B) and most unusually there was a collateral from the APA to the occluded ICA (long arrow). The short arrow identifies the opening of the carotid canal.
A
B
Vascular imaging in ischaemic stroke and TIA 75
8.15 This VR3D image (A) demonstrates a severe stenosis within the left ICA in a patient presenting with a TIA. The most important clinical aspect of a TIA is the timing of the event. The best surgical outcomes appear to be in those who have immediate surgery. At 6 weeks after a TIA, the risk of subsequent events appears to have fallen greatly. The curved MPR (B) demonstrates a short, tight (NASCET 90%) internal carotid artery stenosis (arrow). This causative lesion is ideal for surgical treatment. Unfortunately, the patient went on to have further TIAs which prompted the postendarterectomy MDCTA (C). The distended and irregular carotid bulb is typical of a postendarterectomy vessel.
8.16 This 41-year-old woman had intermittent dysphasia for 2 hours before admission. Brain CT was normal and in view of the patient’s minimal symptoms thrombolytic treatment was in doubt. MDCTA showed incomplete occlusion of the left common carotid artery There is increase in the overall diameter of the distal relative to the proximal common carotid artery (arrows indicate walls) associated with irregular luminal stenosis. This is dissection of the common carotid artery; an unusual location for dissection, confirmed at emergency embolectomy.
A
B
C
8.17 The identification of the outside of the vessel wall, often reflected in the line of the APA, can be essential in the diagnosis of ICA dissection. This patient presented with an acute infarct with synchronous neck pain. Curved MPR demonstrates irregular narrowing of the internal carotid artery (small arrows) with vessel wall thickening and an intraluminal thrombus (large arrow). The APA is clearly seen (arrowheads). These patients should be identified on admission as they benefit from a period of anticoagulation treatment lasting several months.
76
Vascular imaging in ischaemic stroke and TIA
8.18 Follow-up imaging is required after vessel dissection to determine if the vessel has returned to normal, remained irregular or occluded, or a pseudoaneurysm has formed, as it has in this case (arrow). There is a persistent increased risk of distal embolic events which may necessitate stenting or occlusion of the artery.
8.19 This healed dissection was an incidental finding. VR3D shows that two irregular channels have been retained (A) and the dissection flap (arrow) is clearly seen in the base image (B).
A
B
A
B
8.20 Assessment of the posterior circulation is often seen as a less important task, mainly due to lack of knowledge of its importance and of proven treatment options. In this patient (A), the left vertebral artery is occluded throughout much of its length. It refills in at the level of the third cervical vertebra (arrow) and calcification is visible here. The lateral view (B) demonstrates the collaterals (arrows) from the occipital and ascending cervical arteries. Occluded vertebral arteries frequently reconstitute in this way. Note also the symptomatic 90% right carotid stenosis.
Vascular imaging in ischaemic stroke and TIA 77
8.21 The features seen in carotid dissection are also seen in vertebral dissection. In this case the vessel is markedly thickened, with expansion of the vessel wall and irregular eccentric stenosis of the vertebral artery as it passes into the subarachnoid space in this oblique slab MIP. The arrows demonstrate the outer vessel wall. Urgent anticoagulation is also required to prevent distal embolization.
8.23 This patient presented with an acute left hemispheric syndrome. You have seen his ICA occlusion in 8.14 and this intracranial VR3D confirms intracranial ICA occlusion (arrow) with clot also occluding the MCA and proximal anterior cerebral artery. This extent of thrombosis rarely responds to thrombolytics and intra-arterial treatment may be more effective.
8.22 The MDCTA technique described allows full definition of the intracranial circulation on modern systems. This study was performed on a 4-slice system but still demonstrates well the irregular vertebrobasilar system with areas of stenosis (arrows). Characterization of basilar artery disease can be vital in the correct treatment of acute basilar thrombosis. Notice also the unusual aneurysm on the terminal right vertebral artery and the disease of the terminal left vertebral artery.
8.24 This patient presented with acute right hemispheric symptoms. The proximal or M1 segment of the middle cerebral artery is normal (A, arrowheads). The major branch of the MCA is occluded (arrow). Branch occlusion in the nondominant hemisphere tends to predict a favourable outcome. Vessel cut-off in the second order segments of vessels are easily detected by MDCTA. The other patient (B) has an acute occlusion of the P2 segment of the left posterior cerebral artery (arrow).
A
B
78
Vascular imaging in ischaemic stroke and TIA
8.25 The Circle of Willis and the intra/extracranial anastamoses serve to maintain cerebral blood flow in the presence of obstruction. In this patient, the right internal carotid artery is occluded from its origin. The right middle cerebral artery fills via an enlarged ophthalmic artery (arrowheads). The patient’s presentation of left hemispheric TIAs are probably haemodynamic and not embolic. Carotid Doppler scanning would be unable to reveal this abnormality.
A
B
8.27 Treatment for MCA stenosis (the left MCA origin is stenosed; coronal VR3D viewed here from behind) can be with an astomosis between the superficial temporal artery, through a craniectomy with a distal MCA branch. Patency, as in this case, or occlusion, can be shown by MDCTA obviating the need for DSA. (4-slice scan.)
8.26 This patient (A) presented with a posterior circulation TIA. CT brain showed a small acute left midthalamic infarct. CTA was normal with the exception of this tight stenosis of the proximal basilar artery, the cause of which does not appear to be atheroma and so dissection must be considered. The lesion was treated by intravascular stenting. CTA is adept at detecting these stenoses, identifying causative intracranial vascular disease despite normal extracranial vessels. In patient (B), although the carotid bifurcation was normal, sagittal MIP shows two severely stenosed segments of the ICA in the skull base (arrows) deemed responsible for the patients TIAs.
8.28 This patient has bilateral terminal ICA stenosis, worse right than left, with multiple abnormal collateral vessels: these cause the classic ‘puff of smoke’ or ‘moyamoya’ appearance on DSA. In this case, the stenosis was secondary to radiotherapy for a childhood brain tumour. Coronal thin slab MIP in this MDCTA shows the numerous small abnormal vessels characteristic of these conditions.
Vascular imaging in ischaemic stroke and TIA 79
8.29 Intracranial vasculitis is an uncommon cause of stroke but one which can be reversed. The diffuse irregular beaded stenoses, most prominent in the middle cerebral arteries in this slab MIP, are typical findings of vasculitis (arrows). In this case, they resolved after 6 months’ treatment with cyclophosphamide.
8.30 This patient (A) has a large vessel vasculitis, Takayasu disease. There is complete occlusion of both subclavian arteries (arrows) and the left vertebral origin is occluded. There was an attempt to revascularize the subclavian vessels by grafts from the common carotid arteries but this VR3D shows that they have both subsequently occluded (arrowheads). Fibromuscular dysplasia (FMD) is reported to occur in about 2% of people. In our experience it is much less common. In this case (B) the ‘string of beads’ is shown in the distal right ICA (arrow) and the left reflects a symptomatic but now healed dissection with aneurysm formation (arrowheads). FMD is a recognized cause of dissection. A 8.31 This intracranial VR3D demonstrates a combination of vessel occlusions (arrows) in some territories and aneurysm formation in others (arrowheads). This vessel damage has resulted from multiple emboli from an artial myxoma in this young man with repeated strokes.
B
80
Vascular imaging in ischaemic stroke and TIA
8.32 This patient presented with a typical left-sided total anterior circulation stroke. The scanogram for the routine MDCTA showed a lung mass, so chest CT followed the CTA. The source of his embolic stroke was a previously undiagnosed tumour shown growing from the lung, through the pulmonary vein and into the left atrium.
Learning points • Review the dataset with VR3D images but measure with base images or MPRs. • Check the intracavernous carotid – curved MPR is best. • Dissection segments can be quite short so check all base images. • Remember there may be significant disease outwith the carotid bifurcation. • Look at all sites of possible disease.
Further reading Bartlett E, Walters T, Symons S, et al. Quantification of carotid stenosis on CT angiography. AJNR 2006;27:1319. Bartlett E, Walters T, Symons S, et al. Quantification of carotid near occlusion using CT angiography. AJNR 2006;27:632–7. Bash S, Villablanca J, Jahan R, et al. Intracranial vascular stenosis and occlusive disease: evaluation with CT angiography, MR angiography, and digital subtraction angiography. AJNR 2005;26:1012–21.
Berg M, Zhang Z, Ikonen A, et al. Multi-detector row CTA in the assessment of carotid artery disease in symptomatic patients: comparison with rotational angiography and digital subtraction angiography. AJNR 2005;26:1022–34. Chuang YM, Chao AC, Teng MM, et al. Use of CT angiography in patient selection for thrombolytic therapy. Am J Emerg Med 2003;21:167–72. Chen CJ, Tseng YC, Lee TH, et al. Multisection CT angiography compared with catheter angiography in diagnosing vertebral artery dissection. AJNR 2004;25:769–774. Debernardi S, Martincich L, Lazzaro D, et al. CT angiography in the assessment of carotid atherosclerotic disease: results of more than 2 years’ experience. Radiol Med (Torino) 2004;108(1–2):116–27. Fleishman D. Principles of contrast medium delivery for computed tomography angiography. Saini S, Bonomo L, Teasdale E, White R (eds).The Year in Radiology. Special Issue: Advances in MDCT. Clinical Publishing, Oxford, 2005, 207–18. Klingebiel R, Busch M, Bohner G, et al. Multislice CT angiography in the evaluation of patients with acute cerebrovascular disease: a promising new diagnostic tool. J Neurol 2002;249:43–9. Rothwell PM, Giles MF, Chandratheva A, et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet 2007;370:1432–42. Saba L, Caddeo G, Sanfilippo R, et al. CT and ultrasound in the study of ulcerated carotid plaque compared with surgical results: potentialities and advantages of multidetector row CT angiography. AJNR 2007;28(6):1061–6. Silvennoinen HM, Ikonen S, Soinne L, et al. CT angiographic analysis of carotid artery stenosis: comparison of manual assessment, semiautomatic vessel analysis and digital subtraction angiography. AJNR 2007;28(1):97–103. Yoon D, You S, Choi C, et al. Multi-detector row CT of the head and neck: comparison of different volumes of contrast material with and without a saline chaser. Neuroradiology 2006;48(12):935–42.
Chapter 9
81
Acute haemorrhagic stroke
Introduction Haemorrhagic stroke is less common than occlusive ischaemic stroke. About 15% of stroke is due to primary haemorrhage which can be SAH, subdural, parenchymal, intraventricular, or any combination. Vascular imaging is essential in SAH and in many cases of parenchymal haemorrhage where a structural cause is likely on imaging criteria or if urgent surgical evacuation is planned. MDCTA is now accepted (almost univerally) as the primary investigation of acute SAH if it is available. It has been proved to be accurate and acceptable to patients and DSA is only occasionally required as a diagnostic tool if MDCT is not available, or normal and a vascular cause remains likely. Cerebral aneurysms are the commonest cause of SAH, but MDCTA must be good enough to include the accurate diagnosis of the other causes including arteriovenous malformation (AVM), dural fistula, vascular dissection, and other rarer causes. MDCTA is almost as good as rotational DSA in the display of vascular and aneurysm anatomy necessary for treatment planning. Such DSA requires selective carotid/vertebral artery catheterization, which limits it to dedicated neuroradiological sites. The technique is also useful in the immediate postoperative phase or in delayed referral when secondary vasospasm requires vascular imaging in addition to transcranial Doppler ultrasound assessment. It can also be used to assess aneurysms clipped with titanium clips, or aneurysms at other locations in patients treated with other types of clips or coils. MDCTA is also used extensively as a first examination in the investigation of spontaneous parenchymal haemorrhage and, because of its ease of use, it is applied even if an underlying vascular cause is not very likely. It must always be remembered that venous thrombosis
can also present as an acute haemorrhagic stroke (see figure 1.6 and Chapter 11).
Technique CT angiography of the Circle of Willis The field of view selected routinely covers only the Circle of Willis from C1 to above the ventricles. Other centres will routinely include the whole head. In any case, if there is an intracerebral haematoma, the field of view must cover it completely. Table 9.1 presents optimal patient preparation, Table 9.2 presents the parameters for CTA of the Circle of Willis, and 9.1 shows surviews for a bolus tracking Circle of Willis study. As the patient is likely to go for interventional treatment of many of the vascular abnormalities found, in all patients aged 60 or over the scan should begin at C6 to include the carotid bifurcation and so aid DSA planning. The trigger for bolus tracking is set to 150 Hounsfield units (HU). A sufficient post-threshold delay should be anticipated to allow for the distance between tracker and clinical scan starting position (usually 4 seconds for a 4-slice scanner). The initial routine CT should be reviewed prior to setting up the MDCTA to ensure that any parenchymal haematoma will be completely included in the scan. If there is a large clot, marked hydrocephalus, or the patient is in a very poor clinical grade, it is better to forego bolus tracking in favour of a scan delay of 22 seconds from the start of the injection. If there is increased intracranial pressure there will be a delay to the intracranial vessel filling, which is not allowed for with cardiac dependent bolus tracking.
82
Acute haemorrhagic stroke
Reconstruction and reformation
Pathology and illustrations
Base image review should be followed by a VR3D review of all likely aneurysm sites. This usually gives the best appreciation of the shape and vascular relationships of any aneurysm. Measurements must be made on base images or MIP/MPR reformations. Surface VR3D often aids in the understanding of a superficial AVM.
Aneurysm AVM/fistula Intracerebral vessel dissection Fragile collaterals: atheroma moya-moya Mycotic aneurysm Tumour Bleeding/coagulation disorder Venous thrombosis (see Chapter 11) Many of the above causes will be demonstrated with the emphasis on aneurysm assessment.
Table 9.1 Patient preparation for CTA
• Patients must be completely still throughout this scan as even slight movement during the sequence renders the volume data useless for postprocessing • The agitated patient should be supported in the scanner if possible to avoid the need to repeat examinations • A venflon (18 or 20 gauge) should be placed in the antecubital fossa in preparation for the highpressure pump injection • A careful explanation of the effects of the highpressure injection should be explained to conscious patients to avoid movement during the scan due to discomfort
Table 9.2 Protocol parameters for CTA of the Circle of Willis
Patient position Surview First Slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom
Windowing Contrast
Supine Dual – AP/LAT Spinous process C1 To cover Circle of Willis ~180 mm 0.67 mm 0.33 mm 0.685 mm 64 × 0.625 mm 0.5 sec 120 kV/300 mAs Standard Soft tissue with bone/brain correction if available To include Circle of Willis, anterior cerebral arteries, pericallosal arteries, and basilar artery with associated vessels (see figure 9.1) WC 60 WW 360 60 ml contrast High-pressure pump injection at 5 ml/sec Bolus tracking – trigger 150 HU on ascending aorta
Acute haemorrhagic stroke 83
A
B
C 9.1 (A) Lateral and (B) AP surviews showing the position of the clinical and the locator scans. (C) Locator slice showing region of interest (ROI) over the ascending aorta. (D) Zoomed image from data set acquired with the dual surview technique. The frontal area should be included in the reconstructive zoom to allow the pericallosal arteries to be included.
D
84
Acute haemorrhagic stroke
A
B
9.2 Patient (A): VR3D with most of the extraneous detail removed, reveals a moderate sized aneurysm at the origin of the pericallosal artery from this azygous anterior cerebral artery (arrowhead) and a smaller aneurysm of the left middle cerebral artery bifurcation (arrow). Patient (B): VR3D showing a 7 mm ICA aneurysm arising in relation to the origin of the posterior communicating artery. The purpose of MDCTA in SAH is to identify the underlying cause and plan the best treatment by analysis of the sac/neck ratio, neck size, and adjacent vessel involvement. A ruptured aneurysm will often have a nipple to indicate the bleeding point as seen here. Patient (C): sagittal 12 mm slab. This projection is ideal for assessing the anterior cerebral arteries and branches. This patient has had a SAH from a pericallosal artery aneurysm. No cause for the adjacent calcification was determined. Patient (D): VR3D 12 mm slab, uncommon distal pericallosal aneurysm. Peripheral aneurysms are more likely to be mycotic in origin but those are not at branching points. Patient (E): VR3D 4-slice system displayed in a posteroanterior coronal projection. A rounded left ophthalmic aneurysm region (large arrowhead), and smaller medially orientated rupture superior hyposphyseal artery aneurysm (small arrowhead) lying anterior to the posterior communicating artery (arrow).
C
D
E
Acute haemorrhagic stroke 85
B
A 9.3 Patient (A): the more rapid acquisition with the 64-slice CT means that the intracavernous carotid artery is no longer hidden within the enhancing cavernous sinus, so aneurysm of this segment can now be identified (arrows). Patient (B): it is often helpful to leave bony detail in place. This patient has bilateral ophthalmic artery region aneurysms. On the right (arrowhead) the aneurysm projects above the anterior clinoid process. This aneurysm is amenable to either surgical or coil treatment. The left sided aneurysm (arrow) is hidden beneath the anterior clinoid process and is much more suitable for coiling. Patient (C): this patient has a large peripheral aneurysm on the right arising from the mid portion of the right posterior cerebral artery (arrow). The great majority of aneurysms at these sites are due to dissection. Patient (D): this patient has an irregular ruptured broad necked aneurysm of the left middle cerebral artery bifurcation. The neck involves the MCA branches, so surgery will be the best treatment. Patient (E): posterior circularion aneurysms are surprisingly well defined despite the dense skull base as this posterior inferior cerebellar artery (PICA) aneurysm shows.
C
D
E
86
Acute haemorrhagic stroke
9.4 In patients with SAH who are aged over 60, we routinely perform MDCTA to include the carotid bifurcation to show the vascular approach prior to coiling. (A) The soft plaque at the bifurcation (short arrows) precluded safe coiling of the aneurysm (long arrow). (B) This patient had a history of prior femoral artery stenting and claudication. MDCTA showed no possible femoral artery access for catheter treatment so the aneurysm was treated surgically.
A
B 9.5 This patient had an anterior communication artery aneurysm clipped 10 years previously and presents now with new SAH. CTA shows a recurrent/new aneurysm arising adjacent to the clip. MDCTA can identify such an aneurysm if a titanium clip has been used.
A
B
9.6 The acute left hemiparesis in this patient was due to expansion of the larger right sided giant aneurysm. A giant aneurysm is 25 mm diameter or greater. Many such aneurysms contain thrombus and so the VR3D images (A) do not tell the whole truth as it demonstrates only the patent lumen. These aneurysms grow by repeated haemorrhage into the wall so expanding the outer margins (arrows) assessed on standard axial reconstructions (B).
Acute haemorrhagic stroke 87
9.7 Axial image of a giant left middle cerebral artery aneurysm. The aneurysm is entirely filled with thrombus. Volume rendered imaging in aneurysms like this may show only distortion of the normal arteries with a minor irregularity at the aneurysm neck.
A
B
9.8 This giant aneurysm arising from the intracavernous carotid artery, contains no thrombus. This patient presented with a painful 3rd nerve palsy and in view of the high risk of SAH due to the size of the aneurysm, treatment was achieved using an intravascular stent and intra-aneurismal coiling.
C
9.9 (A–C) The 3 plane-slab MIP from this MDCTA examination has failed to demonstrate any underlying arterial or venous cause and despite the large amount of oedema, no tumour was found at follow-up. MDCTA has become a routine emergency examination to inform prior to surgical clot evacuation.
88
Acute haemorrhagic stroke
A
B
9.10 This large clot in the left basal ganglia (A) was thought to be typical of a spontaneous hypertensive bleed, but the small, more medially placed clot was a little suspicious of a possible underlying cause. We were surprised to discover the cause was the large irregular aneurysm of the terminal left ICA (B)
A
B
C
9.11 This is a large peripheral haematoma but the MIP shows a small focus of enhancement (A) at the end of a very faintly delineated artery (B, arrows). Such a distal aneurysm is typically secondary to an infected embolus (mycotic aneurysm). Conversely, in (C) no arterial connection could be identified and the enhancement represents contrast extravasation (arrow), a sign shown recently to correlate with an unstable haematoma.
Acute haemorrhagic stroke 89
9.12 Amyloid angiopathy typically causes repeated large lobar haemorrhages in the elderly, often with a fluid level or clot of different ages as illustrated here: (A) March 2003, (B) July 2007. CTA does not demonstrate any vessel pathology so is not required.
A
9.13 This young man presented with a large intraventricular haemorrhage caused by rupture of one of the multiple, tiny, pathological collateral vessels induced by severe idiopathic stenosis of the terminal ICA, the proximal anterior, and middle cerebral arteries (moyamoya). Collaterals from atheromatous stenosis can also cause SAH.
B
9.14 Dissection of the terminal vertebral artery, basilar artery or the PICA can all cause SAH so diagnosis must be possible from routine MDCTA. This VR3D shows diffuse irregular stenosis (arrowheads) of the terminal right vertebral artery and aneurismal dilatation (arrow) of the PICA; the appearances are typical of dissection. It can be difficult to understand complex vascular pathology like this without interactive image manipulation.
90
Acute haemorrhagic stroke
A
B
9.15 The base image from the CTA (A) identifies the parenchymal midbrain bleed (arrow) and associated oedema (arrowhead) directly associated with abnormal enlarged venous sacs. The VR3D reconstruction (B) shows the chain of abnormal venous sacs to arise from a single point on the free edge of the tentorium (arrow). This is a fairly typical intracranial dural arteriovenous fistula, which often present with a combination of SAH and subdural or parenchymal haemorrhage.
A
B
9.16 An AVM can present with bleeding into the brain, the ventricles, or the subarachnoid space. This VR3D angiogram of the right hemicranium (A) has been selected to show the AVM nidus and the draining veins with venous aneurysms noted on the transverse sinus. To aid surgical excision the surgeon requested a surface brain image reformation (B) to show only those vessels which would present on the brain surface.
Acute haemorrhagic stroke 91
9.17 MDCTA can assist in determining the risk of rupture in an AVM. This oblique cut away VR3D shows a large AVM supplied mainly by the MCA, but it is at increased risk of rupture because of the stenosis (arrow) of its main drainage channel, the sagittal sinus.
Learning points • Triggered submillimetre MDCTA is optimal. • Look very carefully in all possible aneurysm sites with VR3D and MIP. If a vascular cause cannot be found, another radiologist should be asked to review the examination independently. Two heads are better than one. • Remember to look for an AVM/fistula; look beyond the Circle of Willis. • Venous thrombosis and arterial dissection can also cause sudden headache.
Further reading Bittles MA, Sidhu Mk, Sze RW, et al. Multidetector CT angiography of pediatric vascular malformations and haemangiomas: utility of 3-D reformatting in differential diagnosis. Pediatric Radiol 2005;35:1100–6. Chappell ET, Moure FC, Good MC. Comparison of computed tomography with digital subtraction angiography in the diagnosis of cerebral aneurysms: a meta-analysis. Neurosurgery 2003;52:624–31.
Coenen VA, Dammert S, Reinges MHT, et al. Imageguided microneurosurgical management of small cerebral arteriovenous malformations: the value of navigated computed tomographic angiography. Neuroradiology 2005;47:66–72. Enterline DS, Kapoor G. A practical approach to CT angiography of the neck and brain. Tech Vasc Interv Radiol 2006;9:192–204. Gatscher S, Brew S, Banks T, et al. Multislice spiral computed tomography for paediatric intracranial vascular pathophysiologies. J Neurosurg 2007;107:203–8. Gazzola S, Avai R, Gladstone D, et al. Vascular and nonvascular mimics of the CT angiography ‘spot sign’ in patients with secondary intracerebral haemorrhage. Stroke 2008;39(4):1177–83. Han M-H, Kim Y-D. Role of multislice computerized tomographic angiography after clip placement in aneurysm patients based on comparison with three dimensional digital subtraction angiography. J Korean Neurosurg Soc 2007;42:103–11. Hoh B, Cheung A, Rabinov J, et al. Results of a prospective protocol of CTA in place of catheter angiography as the only diagnostic and pre-treatment planning study for cerebral aneurysms by a combinatined neurovascular team. Neurosurgery 2004;54:1329–42. Lubicz B, Levivier M, Francois O, et al. Sixty-four-row multisection CT angiography for detection and evaluation of ruptured intracranial aneurysms: interobserver and intertechnique reproducibility. AJNR 2007;28:1–7. Tsuchia K, Makita K, Furui S. Moyamoya disease: diagnosis with three-dimensional CT angiography. Neuroradiology 1994;36:432–4. Wada R, Avai R, Fox A, et al. CT angiography ‘spot sign’ predicts haematoma expansion in acute intracerebral haemorrhage. Stroke 2007;38(4):1257–62. Wu J, Chen X, Shi Y, et al. Noninvasive three-dimensional computed tomographic angiography in preoperative detection of intracranial arteriovenous malformations. Chin Med J (Engl.) 2000:113:915–20. Yoon DY, Lim KJ, Choi CS, et al. Detection and characterization of intracranial aneurysms with 16channel multidetector row CT angiography: a prospective comparison of volume-rendered images and digital subtraction angiography. AJNR 2007;28:60–7.
Chapter 10
93
Variations in arterial anatomy
Introduction MDCTA offers a new appreciation of arterial and venous anatomy. All arteries and veins will show complete ‘filling’ or enhancement which, if the protocol is correctly timed, gives effective blood pool imaging. MDCTA therefore does not suffer from flow effects which can cause artifact in both magnetic resonance angiography (MRA) and DSA. With catheter DSA, dilution in a vessel due to the influx of blood not opacified by contrast agent limits its value in anatomical demonstration. This is most commonly illustrated in the complete assessment of the anterior communicating arterial complex in the Circle of Willis, which requires bilateral selective carotid catheterization with or without contralateral carotid compression with DSA, and even then may fail to demonstrate the complete anatomy. Conversely, if flow information is important, then MDCTA is not the ideal choice. Information about likely flow direction can only be inferred from MDCTA. The ability to rotate a three dimensional angiographic image in any direction enables determination, for example, of the completeness of the Circle of Willis, the optimal view in which to coil an aneurysm, what a surgeon will meet on the approach to an aneurysm or an AVM. Many of the projections available with MIP and 3D CTA are not possible with standard biplane DSA. This facility also makes it easier to appreciate arterial fenestrations (partial fusions remaining from earlier embryological situations), and other common and uncommon vascular variations. The details of the acquisition angiographic techniques will be found in Chapters 8 and 9. Anatomical examples are given here and others are listed and identified as incidental in other chapters. Some anatomical variations will influence the manifestations of disease, e.g. if the posterior cerebral artery
arises from the carotid and not the basilar artery as is usual, then carotid atheroma could cause occipital infarction. Included are examples of anomalies for the great vessels, the cervical carotid and vertebrobasilar systems, in addition to intracranial variations.
Illustrations Vascular variations are seen routinely as the number of noninvasive vascular studies keeps increasing, expanding our exposure to many more vessels than we had seen with catheter angiography or from earlier pathological studies. Some examples are included, all obtained from standard MDCTA techniques.
94
Variations in arterial anatomy
10.1 The right vertebral artery arises unusually from the right common carotid artery and there is an aberrant right subclavian arising distal to the left subclavian artery.
A
B
10.2 The aberrant right subclavian here gives rise to the right vertebral artery and there is a common origin of the right and left common carotid arteries.
C
10.3 (A) The left vertebral artery arises directly from the aortic arch proximal to the left subclavian in about 5% of people; however, here it arises unusually beyond the left subclavian. This vertebral artery enters the vertebral canal at the usual level of C6, however the nondominant right vertebral enters at C4. (B) Both vertebral arteries enter the canals at C5, the left arising directly from the arch proximal to the left subclavian origin. (C) Here the right vertebral enters the canal at C6 and the left at C4. The proximal vertebral arteries are therefore very variable but this is not associated with any pathology.
Variations in arterial anatomy 95
A
B
C
10.4 (A) This patient with a large aneurysm of the right cervical ICA has a rare true duplication of the left vertebral artery. The straighter anterior extraosseous vessel arises directly from the arch and fuses with the ‘normal’ vertebral artery, which arises from the subclavian artery, at the C4 level. (B, C) Typical and common fenestrations of the D E vertebral artery (between arrows in C). Nerves and small vessels pass through the small gap. (D) This unique leftsided variation reflects the way the branchial arches fuse to form the terminal vertebral and its branches. (E) This shows fusion of the two vertebral arteries just at a point where the posterior inferior cerebellar arteries arise. Note also the two large vessels coming from the posterior aspect of the right carotid artery (arrows); the lower one is the posterior communicating artery and the distal is a combined medial temporal and anterior choroidal artery.
96
Variations in arterial anatomy
A
C
B
D
A
B
10.5 (A) Both vertebral arteries lie in a groove on the upper surface of C1. (B) There is a partial canal for the left vertebral artery. (C) A canal is present on the left and a groove on the right. (D) Both vertebral arteries lie within a canal. These are all common variations and it is unlikely that there is any increased risk of vertebral dissection due to vessel restriction if it lies within a canal rather than a groove as has been suggested.
C
D
10.6 The branching of the external carotid artery is very variable. (A) This is the most common pattern. The meningeal artery is not visualized once it lies within the bone and cannot be separated from it. (B) Here the common conjoined lingual and facial artery trunk is present (arrow). (C) The large facial branch (large arrow) with the small medial lingual branch actually arises from the common carotid artery. The external/internal bifurcation lies distally and there is calcific stenotic atheroma affecting the origin of the internal carotid (small arrow). (D) The superior thyroid arises from the common carotid in this patient with severe bifurcation atheroma. (E) The occipital artery arises from the internal carotid here.
E
Variations in arterial anatomy 97
A
B
C
10.7 VR3D (A) shows a very rare anomaly (only two cases are reported in the literature) with separate origins of the left internal and external carotid arteries directly from the aortic arch. In (B) and (C) there is an aberrant left ICA (incidence as much as 1%). The ICA has been replaced by the enlarged inferior tympanic branch of the ascending pharyngeal artery resulting a high and vertical ‘common carotid’ bifurcation. Note that the aberrant vessel enters the skull base through the jugular bulb and not the (absent) carotid canal (B). Coronal MPR (C) shows that the aberrant vessel lies in the middle ear cavity where it can be, and has often been, confused with a glomus tympanicus tumour – a potentially disastrous error!
A
B
10.8 (A) There are two parallel branches to both MCA: this is MCA duplication. (B) 4-slice MDCTA. This is a more complex left MCA duplication with the vessel arising from the A1 segment of the anterior cerebral artery with a linking vessel mid MCA. (Did you spot the large left sided carotid aneurysm?)
98
Variations in arterial anatomy
A
B
C
10.9 (A) There is a short fused segment of the two A2 segments of the anterior cerebral artery. (B) The long A2 fusion is called an azygous (unpaired) anterior cerebral. (C) Here there E is a pericallosal artery aneurysm on an azygous anterior cerebral vessel. (D) The arrow points out a duplication of the A1 segment. (E) This is the classical two anterior cerebral arteries linked by a small communication artery. The A1 segments are frequently asymmetrical as seen here. Note also F the bilateral (fetal) posterior cerebral arteries arising from the carotid arteries, not the basilar tip as is usual. This is a normal developmental situation in the fetus before the basilar system ‘steals’ the posterior cerebral arteries, with a vestigial connection to the carotids remaining as the posterior communication arteries. These are very variable in size. (F) The presence of three A2 segments is another common anterior cerebral anomaly; here associated with an aneurysm.
D 10.10 The Circle of Willis is very variable. The anterior communicating artery is absent, the left posterior cerebral is fetal in type, and the P1 segment of the posterior cerebral is consequently absent; the right posterior communicating artery is of the adult type communicating with the posterior cerebral artery but smaller than it.
Variations in arterial anatomy 99
10.11 (A) This persistent (left-sided) trigeminal artery (arrow) is the commonest persistent fetal connection between the carotid artery and the basilar artery (incidence 1%). There are bilateral fetal posterior cerebral arteries and another vessel arises from the intracavernous carotid on the left, swings posteriorly and inserts into the basilar artery proximal to the superior cerebellar arteries. The remainder of the basilar artery is a tiny thread. (B) Another example on the right. It is more obvious because the intracavernous carotid artery is displaced laterally by a meningioma (not visualized on this reformation). The basilar artery here is only slightly reduced in size. (C) This shows a patient with bilateral trigeminal arteries (T) with the superior cerebellar arteries (SC) and posterior cerebral arteries (PC) identified. The terminal left carotid and the left fetal posterior cerebral artery are occluded by clot and so not visualized. This caused an acute stroke which was the reason for the examination.
B
A
C
10.12 The aberrant hypoglossal artery is the second commonest persistent embryonic carotid/basilar connection with an incidence about one-sixth that of the trigeminal artery. VR3D of the ICA (A) shows an unusual large branch (arrow) (the ICA has no such extracranial branches), which enters the skull base medial and proximal to the carotid canal. This is the hypoglossal canal, the normal left, which transmits the hypoglossal nerve, is marked (asterisk). Viewed from inside the cranium (B), this persistent hypoglossal artery anastamoses with a branch from the small terminal vertebral to form the basilar artery (arrow). (16-slice acquisition from Royal Alexandra Hospital, Paisley; postprocessed on the Philips workstation.)
*
A
B
100
Variations in arterial anatomy
Learning points • Look closely and you will be surprised just how many variations you will identify. • Variations of the Circle of Willis can have important effects on treatment planning in stroke or SAH. • An overlying vein can mimic a duplication.
Further reading Albayram S, Gailloud P, Wasserman BA. Bilateral arch origin of the vertebral arteries. AJNR 2002;23:455–8. Goldstein JH, Woodcock R, Do HM, et al. Complete duplication or extreme fenestration of the basilar artery. AJNR 1999;20:149–50. Goray VB, Joshi AR, Garg A, et al. Aortic arch variation: a unique case with anomalous origin of both vertebral arteries as additional branches of the aortic arch distal to left subclavian artery. AJNR 2005;26:93–5.
Hoh BL, Rabinov JD, Pryor JC, et al. Persistent nonfused segments of the basilar artery: longitudinal versus axial nonfusion. AJNR 2004;25:1194–6. Jayaraman MV, Mayo-Smith WW. Multi-detector CT angiography of the intra-cranial circulation: normal anatomy and pathology with angiographic correlation. Clin Radiol 2004;59:690–8. Lasjaunias P, Berenstein A, Ter Brugge KG. Surgical neuroangiography. Volume 1. Clinical Vascular Anatomy and Variations. Springer-Verlag, 2001. Lemke AJ, Benndorf G, Liebig T, et al. Anomalous origin of the right vertebral artery: review of the literature and case report of the right vertebral artery origin distal to the left subclavian artery. AJNR 1999;20:1318–21. Tuccar E, Yazar F, Kirici Y, et al. A complex variation of the vertebrobasilar system. Neuroanatomy 2002;1:12–13.
Chapter 11
101
Venous pathology and variations in venous anatomy Introduction Venous disease of the brain has been underestimated and under recognized but the ease and accuracy with which MR and multidetector computed tomography venography (MDCTV) can display the veins has raised awareness and appreciation of this previously overlooked entity. MDCTV is the only technique which is not affected by flow, filling all veins everywhere equally, and so it displays the complete venous anatomy. Variations in cerebral venous anatomy are more prevalent than arterial variations, and as neurosurgeons are becoming more aware of the complications secondary to venous occlusion, they frequently request MDCTV prior to complex surgery. The full extent of congenital or acquired venous stenosis/occlusion is only demonstrable with MDCTV, as with DSA only part of the venous system is filled from each artery injected. Cerebral venous thrombosis is now recognized as a common disease with a much better prognosis than was reported when the diagnosis depended upon invasive DSA. Plain unenhanced CT will demonstrate acute thrombus in the veins and MDCTV the extent of the new and pre-
existing thrombosis. The possibility of venous disease must always be kept in mind in the setting of acute stroke and in assessing any cerebral haemorrhage or thunderclap headache. MDCTV also has a new useful role to play in the assessment of idiopathic intracranial hypertension. Simple enhanced CT is not a substitute for CT venography which requires this specific technique if errors are to be avoided.
Technique Table 11.1 presents optimal patient preparation, and the protocol is presented in Table 11.2. A surview for CT venography is shown in 11.1. The series of axial scans can be displayed as seven combined images to give a manageable number for viewing either on film or PACS system. The window centre and width can be adjusted to show the contrast in the venous sinuses throughout the brain.
Table 11.1 Patient preparation for MDCTV
• The patient should have a venflon (18 or 20 gauge) in a cubital vein in preparation for a high-pressure pump injection • Injection should be at the rate of 5 ml/sec
102
Venous pathology and variations in venous anatomy
Reconstruction and reformation
Anatomy, pathology, and illustrations
Base image review with wide windows, e.g. 350 window; 100 level to allow differentiation of venous sinus enhancement from the adjacent bone; this is essential as it is possible to diagnose venous thrombosis on axial image review without any more complex reformations (11.1 B–D). MIP and VR3D are also useful.
Some examples of venous pathology are shown in other chapters, e.g. caroticocavernous fistula (Chapter 3); cavernous sinus disease (Chapter 6). Other entities are shown here under the headings: Normal venous display Aberrant veins Venous abnormalities: congenital acquired including dural arteriovenous fistula Venous thrombosis Tumour planning Idiopathic intracranial hypertension
Table 11.2 Protocol parameters for MDCTV
Patient position Surview First slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
Supine Lateral Through spinous process of cervical vertebra 1 Vertex ~250 mm 0.9 mm 0.45 mm 0.673 64 × 0.625 mm 0.5 sec 120 kV/300 mAs Standard Soft tissue with bone/brain correction if available Whole head WC 150 WW 450 100 ml using high-pressure pump; 5 ml/sec with a scan delay of 60 sec
Venous pathology and variations in venous anatomy 103
A
C
B
D
E
11.1 (A) Surview for MDCT venography. (B–E) Four axial images demonstrating clearly the venous sinuses (WC 150, WW 450: can be adjusted for optimum visibility of venous sinuses against skull bone).
104
Venous pathology and variations in venous anatomy
A
B 11.2 MIP angiogram of the normal deep and superficial cerebral veins, lateral (A) and oblique (B). This can be used prior to surgery to show dominance of a sinus and whether or not the straight sinus drains into the torqula as in (B) or selectively into one transverse sinus. The VR3D (C) shows the veins which lie on the surface only and can guide the surgeon to avoid and preserve those which are large and important.
C
A
B
11.3 These VR3D surface views show the variations in the anatomy of the superficial veins, left (A) and right (B) sides. Their relationship to certain sulci or pathology informs the surgeon about a safe approach to avoid veins or to identify pathology in relationship to the veins. (4-slice CTV.)
Venous pathology and variations in venous anatomy 105
11.4 Large veins can overlie the basilar tip and have been misinterpreted as an aneurysm. (A) The basal vein of Rosenthal (arrows) lies parallel and superior to the posterior cerebral artery and can be confused with it. These risks can be reduced with faster scanning (64- versus the 4-slice scanner used in this study) and more accurate arterial timing for acquisition (see Chapter 9). (B) There is no development of the anterior sagittal sinus and the frontal regions are drained by long cortical veins parallel to the falx, joining the sagittal sinus in its mid portion. Note the normal asymmetry of the transverse sinuses. The patient in (C) has a developmental cavum septum pellucidum which has separated the septal veins. (D) 64-slice scanner: the temporal vein on the right drains inferiorly medial to the carotid artery into the cavernous sinus (arrow); the normal drainage into the basal vein is present on the opposite side.
11.5 This patient has a developmental venous dehiscence with a large venous ‘aneurysm’ thinning the petrous bone (A). The MIP (B) shows the aneurysm and an adjacent normal pacchionian granulation visible as a filling defect (arrow). This dehisence may present clinically with tinnitus.
A
B
D
C
A
B
106
Venous pathology and variations in venous anatomy
A
B
11.6 The massive abnormal veins (B) are indicative, not of an AVM, but of acquired or congenital venous outflow obstruction at the level of the sigmoid sinuses and jugular bulbs. Note the huge temporal and superior ophthalmic veins (A) which are a main drainage route for this patient’s cerebral veins.
11.7 Axial projection. Congenital bilateral jugular bulb occlusion with aneurysmal dilatation of the torqula. Note again the ophthalmic venous diversion. (4-slice scan.)
11.8 This is a large developmental venous anomaly. There are no abnormal arteries so it is not an AVM, it runs from the ventricular margin to the brain surface and drains normal brain. They are very common but are rarely as large as this. They can also be associated with a cavernoma. (Volume MIP.)
Venous pathology and variations in venous anatomy 107
A
B
C 11.9 The normal cavernous sinus (A) has small filling defects of the 3rd, 4th, 6th, and 5th cranial nerves (see also 6.5). The sinus is closely applied to, but of less density than, the enhancing carotid artery. With thrombosis there is only arterial filling (B, C) where the enhancing dural walls of the cavernous sinuses are highlighted (C, arrows). The bilateral thrombosis is secondary to sphenoid sinusitis in both examples. In (D) the sinuses are poorly defined but expanded due to the nonenhancing clot. In this case, an expanded thrombosed superior ophthalmic vein (arrow) is also present. (E) This thrombosis is complicated by extensive deep and superficial venous thrombosis in the neck (arrowheads). Note the elongate clot filling defect in the right jugular vein (arrow).
D
E
108
Venous pathology and variations in venous anatomy
A
B
C
D
11.10 (A, B) Routine noncontrast enhanced CT. With acute venous thrombosis the vein or sinus is hyperdense as with the sagittal sinus in (A, B) (arrows). Haemorrhage in the white matter is common in venous infarction seen with acute thrombosis. CT venography shows a dark filling defect of clot (arrows) within the sagittal sinus (C) and also note the lack of enhancement and swelling of at least two thrombosed cortical veins (arrowheads). The follow-up CT venogram (D) shows partial re-established patency of the sagittal sinus but no recanalization of the previously thrombosed cortical veins.
Venous pathology and variations in venous anatomy 109
A
B
11.11 This patient presented with sudden severe headache while returning from a two-week holiday in Spain. (A) Sagittal MPR of a venogram shows normal enhancement for most of the sagittal sinus except for slightly less dense acute clot at the torqula and extending into the straight sinus (arrowheads). (B) The following day there has been extension of the clot at the torqula and a new ‘skip’ clot in the anterior sagittal sinus (arrow). Note how the original clot is now of lower attenuation as it ages. (C) This shows the surface view in VR3D with involvement of the left transverse sinus and thrombus within the distended vein of Labbé (arrow).
C
11.12 It is essential to know of any involvement of the venous sinuses by an adjacent tumour prior to surgery. (A) This squamous carcinoma erodes through the skull but is still extradural and displaces but does not invade the sagittal sinus. (B) This recurrent meningioma is invading the sagittal sinus (arrows) making surgical cure impossible.
A
B
110
Venous pathology and variations in venous anatomy
A
B
C
D
11.13 (A, B) Prelumbar puncture; (C, D) postlumbar puncture; similar angled coronal and sagittal MIPs. Idiopathic intracranial hypertension (IIH) is a syndrome with headache and papilloedema, but no causative mass lesion or hydrocephalus: IIH has been found to be associated with bilateral transverse sinus stenosis (A, arrows) although there is disagreement as to whether this is causative of, or secondary to, the raised intracranial pressure. Postlumbar puncture and removal of some CSF: this patient developed a low pressure headache clinically; repeat CTV showed reversal of the bilateral transverse sinus stenosis (C) and enlargement of the inferior sagittal and straight sinuses (D). These changes reflect the expansion of the venous compartment in response to CSF volume reduction. It also indicates that in this case, as in most cases, the bilateral transverse sinus stenosis is secondary to, and not causative of, the raised ICP.
Venous pathology and variations in venous anatomy 111
A
B
11.14 This patient presented with headache and possible SAH. The MDCTA (A) shows filling of the left jugular bulb (arrow) to arterial concentrations but the proximal sigmoid sinus (arrowheads) is not yet enhanced. This rapid filling is due to multiple abnormal communications between branches of the external carotid artery and the jugular vein. Note particularly in (B) the large occipital artery branch which ‘disappears’ into the bone (arrow). Any time you see this, suspect that a dural fistula is present, as in this case. However, with no evidence of arterialization of the veins in the subarachnoid space the fistula is incidental to, and not the cause of, this patient’s SAH.
Learning points
Further reading
• Venography is not just a contrast enhanced routine brain scan: venous identification requires a vascular study and thin slice helical acquisition. • Venous variations are easiest to identify on the VR3D reconstructions. • Base image review with a window width which shows the venous contrast separate from the bone means that you can diagnose venous thrombosis without the need for fancy reconstructions. • Look out for arterial enhancement in veins, and remember to look at the veins in MDCTA in patients with possible SAH. • The clinical consequences of venous ischaemia are much more reversible than those of arterial ischaemia.
Casey SO, Alberico RA, Patel M, et al. Cerebral CT venography. Radiology 1996;198:163–70. Higgins J, Tipper G, Varley M, et al. Transverse sinus stenoses in benign intracranial hypertension demonstrated on CT venography. Br J Neurosurg 2005;19:137–40. Khandelwal N, Agarwal A, Kochhar R, et al. Comparison of CT venography with MR venography in cerebral venous thrombosis. AJNR 2006;187:1637–43. Krishnan A, Mattox DE, Fountain AJ, et al. CT angiography and venography in pulsatile tinnitus: preliminary results. AJNR 2006;27:1635–8. Leach JL, Fortuma RB, Jones BV, et al. Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls. Radiographics 2006;26:Suppl1:S19–41.
112
Venous pathology and variations in venous anatomy
Linn J, Ertl-Wagner B, Seelos KC, et al. Diagnostic value of multidetector-row CT angiography in the evaluation of thrombosis of the cerebral venous sinuses. AJNR 2007;28:946–52. McGonigal A, Bone I, Teasdale E. Resolution of transverse sinus stenosis in idiopathic intracranial hypertension after L-P shunt. Neurology 2004;62(3):514–5. Meckel S, Lovbald K, Abdo G, et al. Arterialization of cerebral veins on dynamic MDCT angiography: a possible sign of a dural arteriovenous fistula. AJNR 2005;184:1313–31.
Rodallec MH, Krainik A, Feyed A, et al. Cerebral venous thrombosis and multidetector CT angiography: tips and tricks. Radiographics 2006;26:Suppl 1:S5–18; discussion S42–3. Suzuki Y, Ikeda H, Shimadu M, et al. Variations of the basal vein: identification using three-dimensional CT angiography. AJNR 2001;22:670–6. Taksem M, Casey S, McKinney A, et al. Anatomy and frequency of pontomesencephalic veins on 3-D CT angiograms of the circle of Willis. AJNR 2003;24:1598–601.
Chapter 12
113
Cranial nerve palsies 7–12
Introduction
Applied techniques
The cranial nerves 7–12 arise in the brainstem, medulla, or upper cervical spine and exit the cranium from the posterior fossa. Clinically they present with a variety of different signs and symptoms. The facial nerve can be involved in pathology in the petrous bone, infratemporal fossa and face as it passes anteriorly towards and within the parotid gland so necessitating bone and soft tissue information. One common referral for MR imaging is the patient who presents with unilateral deafness or tinnitus as it can exclude even a very small intracannicular acoustic schwannoma on the 8th nerve. CT is poor at defining such a small tumour within a bony canal, but can detect tumours as small as 6 to 8 mm which extend beyond the internal acoustic porus if MR is contraindicated. The 9th, 10th, and 11th cranial nerves exit medial to the jugular vein in the jugular foramen and, therefore, often present with a constellation of complaints including difficulty in swallowing, hoarseness, and weakness of neck and shoulder movement. As much of their function is involved with innervation of glands, heart, and digestive tract, clinical signs can be sparse. A neuroma of a nerve can present as a face or neck mass with minimal or no abnormal neurology. The hypoglassal nerve exits though a canal anterolateral to the foramen magnum and disease here will cause a palsy of the tongue on the same side. As many of these cranial nerves have a long path through extracranial soft tissues it is necessary to include the craniocervical junction, face and neck in the examination. MDCT has completely changed the way disease of the cross-over area between these regions is assessed routinely. The ability of CT to show high resolution bone, soft tissue, and blood vessel, and review them in any plane or combination, is unique and why MDCT is of such benefit.
1 If the presentation involves the 7th, 8th, or 12th nerves then a thin section helical contrast enhanced scan (Chapter 2) with reprocessing with both bone and soft tissue filters should suffice. The facial area should be included for facial nerve assessment, so the scan is started at the level of C3. 2 If disease of the jugular bulb is suspected, and here it is necessary to include patients with tinnitus or audible bruit because of the likelihood of a glomus tumour, then it is best to use an angiographic technique. The MDCTA technique as described in Chapter 8 is used, but with a delay of 40 seconds from the start of the injection, rather than an aortic triggered start, to ensure some venous filling. This technique is also used for pre-surgical assessment of vessels adjacent to a tumour in the posterior fossa or skull base.
Reconstruction and reformation Thin section MPR (e.g. 2 mm) in orthogonal and curved planes with angiographic MIP and VR3D are usually all employed in addition to review of the base images. A wide window setting is necessary to distinguish vessels and vascular tumour from adjacent bone (e.g. 150 WC/450 WL as for venography). Specific presurgical questions must be clearly defined before the examination is performed to ensure that it will be answerable from the scan.
114
Cranial nerve palsies 7–12
Pathology and illustrations Intra-axial Demyelination Brain stem tumour Extra-axial Meningioma Metastatic tumour Arachnoid cyst Epidermoid tumour Nerve Neuroma Schwannoma Paraganglioma Glomus tympanicum Glomus jugulare Carotid body tumour
Vascular Aneurysm, AVM Bone Dysplasia Infection Cholesterol granuloma Tumour: primary /secondary Soft tissues Tumour Many of the pathologies listed above are demonstrated in previous chapters and will not be repeated here. Those specific to the clivus, jugular bulb, and foramen magnum and extension into the neck will now be considered.
B
A 12.1 This patient presented with a right facial palsy. MDCT demonstrated a bony metastatic deposit on the outside of the skull which had grown through the bone (A, C) into the extradural space and spread over the petrous bone (B) to involve the facial ganglion (arrow). The C 3D skull image defines the extent of the bone involvement, including the little skip deposit posterosuperior to the main deposit.
Cranial nerve palsies 7–12 115
A
B A
C 12.2 Axial (A) and coronal (B) images in a patient with an odd sensation in the left side of his mouth/tongue, show benign expansion of the facial canal (arrowheads) compared to the normal right side (arrows). There is as yet no pathology confirmation but this is thought to represent enlargement from a slowly growing facial neuroma. (C) shows a small tumour (arrow) of the deep lobe of the parotid gland as the cause of the patient’s left sided lower motor neuron facial palsy.
B
C 12.3 Acoustic schwannoma. It is useful to remember that modern CT will show small acoustic tumours which extend out of the IAM a little way (A, axial; B, coronal). (C) Shows erosion of the bony spur separating the 7th from the 8th nerves within the left IAM. (See also 2.7.)
12.4 This patient had MR for right-sided deafness and was diagnosed as having a carotid aneurysm. CTA correctly identified the expansile nonenhancing mass in the pertous apex which has eroded the medial wall of the carotid canal and compressed the ICA as a typical cholesterol granuloma. Because of its propensity to bleed into itself, it can be confused with an aneurysm on MR and MRA.
116
Cranial nerve palsies 7–12
L
A 12.5 This patient has a large left-sided acoustic neuroma. The surgeon wanted to know if it was safe to sacrifice the left transverse sinus to gain access. B This surgical planning venogram shows an unusually vascular tumour with a large draining vein medial to it (A). The left transverse sinus is dominant so sacrifice is not advisable. Note also the bilateral sinus stenosis (arrows) secondary to the raised intracranial pressure (B, viewed posteroanterior VR projection).
A A
B 12.6 Presentation: bilateral 12th and 6th nerve palsies. This shows a secondary renal tumour expanding and replacing the normal clival marrow. The 6th nerve has a long intracranial course adjacent to the clivus and is a good marker for clival pathology (see also Chapter 6).
B 12.7 This patient presented with a right 12th nerve palsy. The right-sided destructive clival mass was a plasmacytoma (A). On the coronal reconstruction (B) the loss of the normal hypoglossal canal is evident when compared to the left side (arrow).
Cranial nerve palsies 7–12 117
A 12.8 This was diagnosed on MR as an enhancing meningioma. The heavy calcification of the tumour was an unwelcome surprise to the surgeon. The exact site of origin from the skull base is well shown by CT.
12.9 CTA (A) was requested to assess B the vascularity and adjacent vessel involvement of this craniocervical junction meningioma. The VR3D (B) confirms a vascular tumour with only slightly less attenuation than the vertebral arteries in this angiographic acquisition, and that these arteries and the PICAs are displaced, not encased, by the tumour.
12.10 A cherry red mass was noted deep to the tympanic membrane, and base images from the angiographic sequence confirm the mass filling the middle ear cavity (A and B, A B arrows) enhances to the same degree as the carotid artery as it lies in the carotid canal. This is a glomus tympanicus tumour. DSA used to be required to confirm this diagnosis. Note the incidental sigmoid sinus dehiscence in (B).
12.11 This is a VR3D of the bony skull base from an angiographic acquisition. Looking from below, the left jugular fossa (arrowhead) is normal in size and shape. The right shows expansion of both the anterior neural segment and the posterior venous segment. This could be due to a large normal jugular vein, a glomus tumour, a neuroma, or even a meningioma.
118
Cranial nerve palsies 7–12
B
A
C
12.12 This patient has pulsatile tinnitus and the MDCTA shows a mass in the expanded right jugular fossa enhancing to the same degree as the carotid artery (A). The coronal reformation shows that the jugular vein adjacent to the tumour enhances to a much greater extent (arrows) than the left jugular vein (B). This is secondary to the shunting of blood/contrast through the vascular tumour. These appearances are confirmed on the VR3D (C). This is a glomus jugulare tumour.
A
B
C
12.13 This patient, also with pulsatile tinnitus, was diagnosed with a glomus tumour by MR. MDCTA was requested to decide if preoperative embolization would be possible. The right jugular fossa is expanded. There is no enhancement within the jugular bulb (A, axial; B, coronal; C, VR3D). This tumour is a typical hypovascular neuroma with associated jugular vein occlusion. Both a neuroma and a glomus tumour will appear similar on standard contrast enhanced CT or MR, but the difference with the MDCTA appearances offers a simple differentiation.
Cranial nerve palsies 7–12 119
A
B
12.14 Both a hypervascular glomus tumour (A) and an ‘avascular’ neuroma (B) can present with an enhancing mass in the neck on standard postcontrast CT or MR. Arterial vascular imaging can clearly differentiate between the two. (A, 4-slice scan.)
A
B
C
12.15 Tumour spread assessed on vascular CT. Occasionally a glomus tumour will spread within the venous system. In (A) the enhancing tumour has expanded and spread down within the jugular vein. (B, C) This patient has a partly excised supratentorial meningioma which has spread within the right transverse (long arrow) and superior petrosal (short arrows) sinuses. The meningioma, which is relatively poorly enhancing (C, arrows), has also spread within and expanded the right jugular vein to the level of the superior vena cava.
120
Cranial nerve palsies 7–12
Learning points R
L • Careful examination of the acquired thin section cuts or of the MPR reconstructions will demonstrate most pathology. • Angiographic appearances are essential as delayed postcontrast studies will not necessarily differentiate pathology. • If there is clinical doubt then an arterial and delayed scan (which may not be performed) can be planned at the start of the study. • VR3D images are useful in surgical planning.
Further reading
12.16 This patient presented with an 8 month history pulsatile tinnitus and a neck mass: possible glomus tumour. MDCTA with coronal thin slab MIP shows the very dense left ICA (arrow) tapering imperceptibly with the large mass with a lower attenuation, similar to that of the distal left ICA (L). The distal right ICA (R) is of a normal arterial attenuation. The interpretation is that there has been dissection of the left ICA which has caused the aneurysm mass; the neck is formed by a long dissection flap so the aneurysm fills and empties slowly such that the high percentage of unopacified blood mixed with a little contrast results in the abnormally poor arterial opacification. The referral scan acquired at usual postinjection timing, e.g. 2–3 minutes, did not show any differential enhancement as the iodine concentrations equalize with time. The tinnitus was due to an ipsilateral dural fistula similar to that shown in 11.14B.
Alaani A, Chavda S, Irving R. The crucial role of imaging in determining the approach to glomus tympanicum tumours. Eur Arch Otorhinolaryngol 2008;265:1199–203. Bone I, Hadley D. Syndromes of the orbital fissure, cavernous sinus, cerebello-pontine angle, and skull base. J Neurol Neurosurg Psychiatry 2005;76(Suppl lll):iii29–iii38. Gandhe AJ, Hill DL, Studholme C, et al. Combined and three-dimensional rendered multimodal data for planning cranial base surgery: a prospective evaluation. Neurosurgery 1994;35:463–70. Larson TC 3rd, Aulino JM, Laine FJ. Imaging the glossopharyngeal, vagus, and accessory nerves. Semin Ultrasound CT MR 2002;23:238–55. Leong JL, Batra PS, Citardi MJ. Three-dimensional computed tomography angiography of the internal carotid artery for preoperative evaluation of sinonasal and intraoperative surgical navigation. Laryngoscope 2005;115:1618–23. Suzuki Y, Matsomoto K. Detection of the venous system of the skull base using three-dimensional CT angiography (3D-CTA): utility of the subtemporal approach. No Shinkei Geka 2000;28:17–22.
Chapter 13
121
Spinal imaging
Introduction The established view of the pre-eminence of MRI in spinal imaging is now being challenged by the growing appreciation of the value of MDCT. This is obvious in the assessment of spinal trauma but experience is showing its value in many acute and subacute spinal presentations. Because MDCT can examine large spinal volumes rapidly, it is of great value in the assessment of possible spinal cord compression. Experience has shown that benign, malignant, and infective compression can be shown well with MDCT. This is important because many patients with spinal compression have their imaging delayed waiting for MR, and then up to 20% are excluded on safety grounds or find MR impossible to tolerate because of pain and the need to lie supine for a long time. MDCT can examine patients in any position they find acceptable in a matter of seconds. Accurate surgical localization is possible and the bone detail provides definitive information on spinal stability. Degenerative disease of the cervical spine is simplest if examined with MR but MDCT will show soft disc and osteophytes well and any associated root compression. Primary or relapsed postoperative lumbar disc disease is also well shown in a CT examination tolerated despite severe pain or obesity. MDCT is often very useful in the acute situation when pain and lumbar spasm necessitates a quick accurate examination. The entire lumbar spine can be imaged to exclude or confirm a clinical diagnosis of spinal claudication, giving excellent bone, disc, and ligamentous definition where MPR can straighten out any rotational scoliosis common in the elderly degenerate spine. The standard three planes of MR greatly limit this full assessment. Mass lesions at the
craniocervical junction are optimally examined with MDCT as has been illustrated in Chapter 12. In acute trauma, multiple noncontiguous fractures are common so it is essential to include all suspected levels of injury, or a complete spinal region, with a thin section helix to provide a complete assessment. MDCTA is easily incorporated with the bone assessment if vessel injury is likely or suspected (see Chapter 8). Low-dose techniques can be effective in the cervical region. For suspected spinal compression the basic technique is for very thin slice acquisition following rapidly after 100 ml of IV contrast given by hand or at 2 ml/sec. This increases the definition of the spinal cord, enhances the venous plexus to contrast with disc prolapse or osteophyte compression, and enhances infective/inflammatory/tumour tissue, differentiating it from the neural structures. Spinal dural fistula and other vascular lesions can be accurately defined by MDCTA which is now able to replace diagnostic spinal angiography if surgical treatment is planned for a fistula, or guide and shorten a diagnostic or therapeutic spinal catheter angiogram. For ease of understanding, the variety of different CT techniques applied to the spine, which are determined by the clinical site and possible pathology present, will be considered first. The pathologically based illustrations will follow to include all spinal areas.
122
Spinal imaging
Technique CT for lumbar disc disease
Spinal stenosis
Table 13.1 presents optimal patient preparation, and the protocol is presented in Table 13.2. A surview is shown in 13.1.
When clinical history is suggestive of spinal stenosis (neurogenic claudication), the same parameters can be used to scan a larger area from the top border of L1 to the lower border of S1 (13.2). A series of MPRs parallel to the discs is made, with one axial slice at the level of the pedicles and one through the disc of each level from L1 to S1 as illustrated (13.2A, B). Additional reconstructions can be made if an additional disc prolapse or other bone pathology is found.
Multiplanar reformations The dataset is used to create 8 axial multiplanar reformats parallel to each disc space using a slice width of 2.5 mm and a slice interspace of 2.5 mm; if the patient is very large a thicker slice (3–5 mm) will improve image quality.
Cervical/thoracic disc For cervical or thoracic disc assessment the technique for spinal cord compression (see later) is best, but limited to the area of clinical interest. The contrast given enhances the epidural veins to aid the identification of small lesions.
Table 13.1 Patient preparation for CT lumbar spine in disc disease
Table 13.2 Protocol for CT lumbar disc disease
• The patient should be positioned supine with knees flexed in order to minimize lumbosacral curve • If the patient has had surgery to the affected area more than 6 weeks or less than 10 years ago an injection of contrast media is required to distinguish between residual disc and fibrous tissue • 100 ml of contrast should be injected either by hand or pump (2 ml/sec). No special timing is needed – the patient is scanned when the injection is finished
Patient position Surview First slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs Resolution Filter Reconstructive zoom Windowing Contrast
Supine Lateral Mid body of L3 (upper border of L1 for stenosis) Lower border of S1 ~250 mm 1 mm 0.5 mm 0.875 64 × 0.625 mm 1.5 sec 120 kV/300 mAs Standard Soft tissue As appropriate to include vertebral body WC 60 WW 360 See Table 13.1
Spinal imaging 123
A
B
13.1 Surview and cover for lumbar disc disease (A). (B, C) Axial MPRs through disc spaces L3/L4 and L5/S1 from the base data. This is done for each of the three lower disc spaces examined. Sagittal plane MPRs (c. 12 images) are also done – slice width 3 mm and interspace 3 mm.
C
B
A
C
D
13.2 (A) Surview and coverage for spinal stenosis. (B–D) The angled 2.5 mm MPR axial reformats as described for L1 and L2. All levels are appropriately angled. Slice width 2.5 mm and interspace 17–20 mm depending on size of vertebrae.
124
Spinal imaging
Extended spinal area examinations
CT for cord compression
Table 13.3 presents optimal patient preparation and Table 13.4 presents the parameters for CT spine. The parameters and techniques for CT scanning of the spinal column are broadly similar, the only differences being in the use of suitable filters, contrast administration, and timing. AP and lateral surviews for planning a thoraco-lumbar study are shown in 13.3. It should be extended if the cervical spine is to be included and/or reduced if only upper motor neurone features are present. If possible, dual projections are useful for spinal planning to ensure correct levels. For complete thoracic cover start the scan at C6. In many situations the whole spine should be examined from the foramen magnum to the coccyx. If there is any doubt about the level of the possible pathology it is better for the scan to be inclusive and not exclusive.
Plan the scan appropriate to the clinical findings and put the scanner to the start position. Give IV contrast: 100 ml by rapid hand injection, or 100 ml at 2 ml/sec by high-pressure pump and scanning immediately after the end of injection. Remember the site of any compressive lesion will be at or above the clinical level, never below it, and so as a general rule scan the whole spine or at least six spinal segments higher than the presumed site of pathology. Resolution: standard Filter: soft tissue in first acquisition with postreconstruction with bone filter
Table 13.4 Basic parameters for spinal CT
CT for spinal trauma The minimum cover is one vertebral level above to one level below the fractured vertebrae; however, multiple level fractures are common and the extent of injury not always clear on in initial clinical assessment and, increasingly, with the efficiency of MDCT, complete spinal areas are examined. Resolution: high mAs: 150 Filter: bone
Patient position Surview First slice Last slice Field of view Slice width Slice increment Pitch Collimation Rotation time kV/mAs
Resolution
Table 13.3 Patient preparation for spinal CT
Filter Reconstructive zoom
• For any patient experiencing pain it may be worthwhile to get the ward staff to administer strong pain relief before the examination to enable the patient to cooperate throughout the scan • For CT myelography the patient should be prepared and consented for lumbar/cervical puncture
Windowing
Contrast
Supine Dual surview if possible, AP and lateral Top border of vertebra above area of interest Lower border of vertebra below area of interest ~250 mm 0.9 mm 0.45 mm 0.875 64 × 0.625 mm 1.5 sec 120 kV/350 mAs If looking only for bony injury mAs can be kept low, i.e. 150 mAs See notes for examination required See notes for examination required As appropriate to include vertebral bodies WC 250 WW 1500 or other bone windows See notes for examination required
Spinal imaging 125
A
B
C
13.3 AP (A) and lateral (B) surviews for a thoracolumbar study. (C) Sagittal MPR. CT mylogram of a patient with clinically severe cervical myelopathy; a pacemaker precluded MR.
CT myelography
CT spinal angiography
Contrast: intrathecal contrast via lumbar or cervical puncture, e.g. 5 ml 300 mgI% of contrast licensed for intrathecal use. The patient is then tilted to allow the contrast to run over the entire spine. There should be enough time allowed for this – at least 15 minutes but up to 2 hours. If there is no contrast in the intrathecal space at the area of interest, the examination will be useless and the patient will have received a significant dose of radiation for no benefit. It is therefore useful to perform one single test slice through the area of interest (low dose) before starting the main scan to ensure opacification of the cerebrospinal fluid (CSF). Resolution: standard Filter: this is basically a high contrast examination so a bone filter prevents flaring from areas of high contrast accumulation
Contrast amount and timing for CT spinal angiography are crucial for good demonstration of the vascular pattern. Rotation time: 0.75 sec Resolution: standard Pitch: 0.703 Filter: soft tissue Contrast: 100 ml with saline chaser injected at 5 ml/sec A bolus tracking technique is used. The trigger point is the descending aorta (150 HU) as illustrated in 13.4. The tracker has a postinjection delay of 5 seconds and the clinical scan a post-threshold delay of 6 seconds.
Reconstruction and reformation MPR, especially curved coronal, are usually most helpful. VR3D gives surgical localization (e.g thoracic disc) and a better appreciation of fractures and dislocations. Careful review of axial slices at an angle along the line of the disc is required to ensure the integrity of the pedicles and laminae (trauma, tumour).
126
Spinal imaging
13.4 (A) AP surview showing locator position. (B) Trigger point on descending aorta for bolus tracking spinal CTA.
A
Pathology and illustrations Pathology will be considered under the following headings: Disc disease: lumbar/cervical/thoracic (13.5–13.11) Trauma (13.12–13.17) Infection (13.18–13.22) Tumour (13.23, 13.24) Vascular lesions (13.25–13.29)
B
Disc disease
A
B
C
13.5 (A) The sagittal MPR from the volume data set provides similar data to MR spinal images where the disc prolapse is traced from right to left and into the root axilla. The degenerative spondylolysthesis at L3/L4 is noted with a soft disc prolapse to the left confirmed on the axial scan (B). The calcified smaller prolapse at L5/S1 is clearly seen tucked into the root exit zone compressing the left S1 root (C). Such calcification indicates a chronic disc prolapse and helps the surgeon plan the operation. This calcification can be difficult to recognize with MR.
Spinal imaging 127
A
B
C
13.6 The lower roots can be seen fanning out towards the sacral canal below the large soft tissue compressive disc at the L5/S1 level ([A] curved coronal MPR, [B] sagittal) . The axial scan (C) confirms the mainly right-sided location and compression. A very large disc prolapse can be difficult to identify with either MDCT or MR.
A
B
13.7 (A, B) When a patient is too large to fit into an MR scanner, thick slice reconstruction (4–5 mm) with MDCT can be effective without the need for intrathecal contrast. These images are noisy but diagnostic of the large left sided L5/S1 disc prolapse (arrows) in this obese patient.
128
Spinal imaging
A
A
B
13.8 (A, B) This patient, 4 days post disc surgery, developed urinary retention. MR was unsuccessful due to movement artefact. To be sure of getting a diagnostic test, 5 ml of intrathecal contrast (Iopamidol 300 mg%) was injected prior to MDCT, which showed the large recurrent/residual posterior disc prolapse as a large extradural filling defect compressing the contrast column.
B 13.9 The cervical venous plexus lies medial to the exiting roots so contrast enhancement outlines the venous plexus (arrows) to show the nerves as negative filling defects (A); it enhances the dura surrounding the cord (arrow) (B) and shows the small left-sided disc/osteophyte bar compressing the left root zone.
A 13.10 Soft disc (A) and calcified B cervical disc/osteophyte material (B) are easily shown in the cervical spine above level of the shoulder artefact. Cord compression is shown in this sagittal MPR due to prolapse of the C4/C5 disc (C).
C
Spinal imaging 129
Trauma MDCT is now the examination of choice in polytrauma and this includes the spine. 20% of all spinal fractures are multiple and all require assessment for stability and cord compression. Sagittal and coronal MPR cannot yet replace the review of axial cuts. Interactive VR3D increases the physician’s understanding of the complexity of the 3D bone abnormalities.
A
B
13.11 (A) The great majority of thoracic disc prolapse are calcified and so easily shown by CT (especially with sagittal MPR) including its effect on the cord. The same data set can be viewed in VR3D (B, different patient) to confirm the exact level (arrow) and allow minimal and accurate surgical exposure by correct identification of the rib anatomy pre- and perioperatively.
13.12 Even thick slice CT done for abdominal/thoracic injury as seen here with sagittal MPR (A) and axial base image review (B) can often suffice.
A
B
C
D
13.13 (A) This MDCT done with 0.65 mm slice width shows a Dennis 3 column unstable lumbar burst fracture. Note the fracture A B of the spinous process and the associated haematoma (arrows) increasing the effect of the bony compression on the cauda equina. (B) Similar thin slice scan in possible cervical trauma confirms no bone injury, no acute disc prolapse, and no cord compression or swelling. Note how well the cord can be visualized in the cervical and thoracic areas in slender patients. (C) The tiny bony fragment avulsed from the left occipital condoyle is visible surrounded by thickened ligaments while the associated extradural haematoma which extended to the level of C5 is seen to displace the thecal sac and cord posteriorly and to the right at the C2 level (D).
130
Spinal imaging
A
B
C
13.14 (A–C) This examination can provide all the necessary data to assess in full this complex lateral flexion compression injury with two nonadjacent unstable lumbar fractures. Low-dose MDCT will allow the entire spine to be covered in major trauma to determine all spinal fractures safely.
A
B
13.15 Coronal (A) and sagittal (B) MPRs show the transpedicular screw and plate fixation of this unstable T4 thoracic fracture. Metalwork in all dimensions is best assessed with CT. Note also the distant T12 fracture.
13.16 (Opposite) The craniocervical junction and cervical spine are particularly vulnerable to injury due to the shallow apophyseal joints and the necessary physiological mobility. Instability carries devastating clinical consequences and accurate CT assessment is paramount. Patient (A): this unusual extradural haematoma, anterior to the medulla, was not associated with fracture but with ligamentous injury that allowed dislocation at the foramen magnum causing medullary contusions but without medullary compression. Patient (B): the oblique MPR along the length of the pedicle clearly shows a superior facet fracture dislocation (arrow) with a vertical fracture through the vertebral body. Patient (C, D): VR3D illustrates the displacements of the fractures of the left lateral mass of C2 (C), and a right sided fracture through the vertebral canal. (D) The lateral shows the displaced laminar fracture. Patient (E, F): the rotatory subluxation of C2 on C1 is increasingly recognized. VR3D viewed optimally from below, clearly shows the right lateral mass of C2 rotated posteriorly out of alignment with the C1 articular surface (E). The postfixation position (F) shows some reduction of the rotation but it is now fixed and so can sublux no farther. Vertebral artery injury is possible as the rod passes through the right vertebral canal. Patient (G, H): fracture of the dens will not heal if not immobilized. It will remain unstable and moving between extension (G) and flexion (H), where it causes compression and ongoing cord damage. Note that the cord is clearly visible in the upper cervical spine CT.
Spinal imaging 131
A
E
B
F
C G
D
H
132
Spinal imaging
13.17 This man was stabbed in the back and presented with a hemicord syndrome. MR was not possible in case small metal fragments from the knife had been retained. MDCT shows the skin entry point and the haematoma within the muscles (A, arrowheads) and the focal haemorrhage in the right anterior cord (A, arrow). The coronal reconstruction (B) illustrates the high A B C attenuation of subarachnoid haemorrhage outlining the cord and conus and shows the intramedullary clot. The small bony injury is clear on the VR3D (C, arrow).
Infection Increasingly spinal infection is being managed nonsurgically, with long-term antibiotics and follow-up imaging after CT guided biopsy and confirmation of the infecting organism and its drug sensitivity. Immediate CT enables this management in the most time effective way. Epidural abscess requiring surgical decompression should
be evident on good quality MDCT carried out post IV contrast, but if it does not give the answer, you must proceed to urgent MR. MR is optimal for abscess definition, but patients often find it too painful to lie in the MR and nondiagnostic images are unfortunately common.
13.18 (A) Coronal curved MPR of the pathological fracture of the infected L1 with the associated bilateral psoas abscesses. (B) The severe compression of the cauda equine is visualized on the sagittal view. Cervical discitis (C) with a large soft tissue swelling anterior to the spine with diffuse granulamatous dural/epidural thickening anterior (arrows) and posterior to the cord, causing diffuse cord compression. Potential spinal A B C instability is also evident (greater than 2 mm posterior shift C4 on C5) secondary to inflammatory softening of the ligaments.
Spinal imaging 133
13.19 Sometimes in chronic discitis the affected vertebral bodies are sclerotic on either side of the destroyed disc. Soft tissue calcification and the left-sided psoas granuloma confirm the continuing disease activity.
13.20 Sclerotic but healed discitis with no abnormal soft tissue component.
13.21 IV drug abuser with neck pain. Midline MPR shows an epidural fluid collection (abscess) behind the dens with some compression on the medulla, secondary to osteitis of the dens shown on the bone window reconstruction of the same image. An epidural abscess is much more difficult to identify on CT from C6 to T5 because of artifact from the shoulders.
13.22 In this patient with rheumatoid arthritis there is pannus and secondary degenerative disease at the C1–C2 level, but the cord compression is at the C5/C6 level and is due to anterior subluxation.
134
Spinal imaging
Tumour Spinal cord compression from tumour is shown well by CT and since the whole spine can be covered in a few seconds with MDCT, and with an acceptable radiation dose, there is no need to wait for MR. Cord compression can improve with emergency treatment and improvement is greatest when the compression is relieved early when there are only minor clinical signs. CT can demonstrate isolated soft tissue lesions causing cord compression, as well as bone and mixed bone and soft tissue causes. The detail of the bone involved will determine any instability more easily than MR.
13.23 Patient (A–C): soft tissue, centred around the right D9 pedicle (A) compresses the cord and has spinous process involvement and is potentially unstable (B). It is shown to be amenable to CT guided biopsy on the axial base image (C). Patient (D–F): curved coronal MPR (D) shows a pathological fracture, which involves the pedicles, and with an adjacent soft tissue component (E) and an associated mediastinal mass, visible on the axial slice. VR3D (F) shows a rib metastasis (arrow) and old fractures (arrowheads). The ability of CT to review the whole body is a definite advantage over MR which is limited to the spine only.
A
B
C
E
D
F
Spinal imaging 135
G
H
I
K
J Patient (G, H): the bilateral soft tissue dural/intradural mass at the cervicothoracic level are well shown L M on the curved MPR (G) with no associated bony abnormality and the cord compression on axial images (H). Lymphoma is the likeliest diagnosis. For MDCT to confirm soft tissue only compression, the scan is best done with 100 ml of IV contrast (see Technique) as in this example. Patient (I): oblique VR3D demonstrates the malignant bone destruction involving the body, pedicle, and spinous process: an unstable situation. Patient (J–L): 4-slice MDCT (J). Pathological fracture and tumour invasion of the adjacent lower vertebral body with soft tissue cord compression. (K) The spine was stabilized with a vertebral body replacement but unfortunately there was little effective reduction in the compressive mass outlined by the arrows (L). Patient (M): the majority of intraspinal meningiomas are calcified and easily detectable with MDCT. This patient also has severe osteopenia. As with calcified thoracic discs, CT acts as an excellent perioperative localizer.
136
Spinal imaging
Vascular lesions MDCT spinal angiography has surprisingly proved of great benefit in the identification of the arterial supply, and accurate location, of spinal malformations. The artery of Adamkiewicz can now be identified in up to 60% of patients prior to aortic aneurysm repair so spinal complications can be avoided. The demonstration of the relationship of the vertebral arteries to spinal and foramen magnum tumours can improve surgical planning and preoperative pathology determination.
13.24 MR scan identified a lateral mass compressing the root and cord on the right. CT was requested to better define the structure of the mass: it proved to be a benign otherwise unclassified calcified lesion!
A
B
13.25 The request was for preoperative localization of the vertebral artery. The benign erosion and widening of the exit foramen with the soft tissue neurofibroma are shown on the MPR (A) and the anterior and medial displacement of the uninvolved but displaced vertebral artery (B).
13.26 (4-slice MDCT.) This patient had intermittent dizziness and drop attacks. VR3D demonstrates the calcified degenerative lump displacing and compressing the right vertebral artery at the C3 level (arrow).
Spinal imaging 137
A 13.27 The oblique MIP shows the two branches of the thyrocervical trunk passing through adjacent intervertebral foramina to supply the intradural spinal AVM. Spinal MDCTA therefore simplifies time consuming catheter spinal angiography and treatment planning.
A
B
13.28 (4-slice MDCT.) MDCT angiography can now be done over the entire spine with a slice thickness of 0.6 mm. The studies obtained demonstrate the intercostal arteries and paired veins (A) and feeding vessels (B) to the commonest type of spinal AVM, the spinal dural fistula, as in this case. The feeding intercostal branch and fistula (arrow) always lie under the pedicle, with the enlarged vein passing from a lateral position to fill the abnormally distended coronal venous plexus.
B
13.29 The MR scan diagnosed a neuroma at the C1 level. MDCTA was done to assess the relationship of the vertebral artery to the neuroma. However, CTA demonstrated a very vascular tumour inconsistent with a neuroma with a large short arterial supply from the V3 vertebral artery segment (B, arrow). Haemangiopericytoma was the diagnosis given by CT, therefore preoperative embolization was recommended. Haemangiopericytoma was confirmed at pathology.
138
Spinal imaging
Learning points • MDCT can replace MR in all acute situations if MR is not available/contraindicated, especially if structural pathology is suspected, e.g. tumour, infection. • The speed of the examination confers great benefit to a patient with an acute painful cord compression state. • Acquired thin slices are essential with sagittal and coronal reconstruction. • In cord compression always scan at least six spinal levels above the clinical level; the pathological level may be higher but never lower than the clinical level. • Spinal MDCTA is of great value in assessing vascular spinal pathology either tumour, dissection, or arteriovenous malformation (AVM).
Further reading Antevil J, Sise M, Sack D, et al. Spiral computed tomography for the initial evaluation of spine trauma: a new standard of care? J Trauma 2006;61:328–7. Boll DT, Bulow H, Blackham K et al. MDCT Angiography of the spinal vasclature and the artery of Adamkiewicz. AJR 2006;187:1054–60. Cassar-Pullicino V, Imhof H. Spinal Trauma – An Imaging Approach. Georg Theme Verlag, 2006. Griffey RT, Ledbetter S, Khorasani R. Changes in thoracolumbar computed tomography and radiography utilization among trauma patients after deployment of multidetector computed tomography in the emergency room. J Trauma 2007;62:1153–6. Hur J, Yoon CS, Ryu YH, et al. Efficacy of multidetector row computed tomography of the spine in patients with multiple myeloma: comparison with magnetic resonance imaging and fluorodeoxyglucose-positron emission tomography. J Computer Assist Tomogr 2007;31:342–7. Kropil P, Fenk R, Fritz LB, et al. Comparison of whole body 64-slice multidetector computed tomography and conventional radiography in staging multiple myeloma. Eur Radiol (Published on line) Oct 2007. Kubota T, Yamada K, Ito H, et al. High-resolution imaging of the spine using multidetector-row computed tomography: differentiation between benign and malignant compression fractures. J Computer Assist Tomogr 2005;29:712–19.
Mann FA, Cohen WA, Linnau KF. et al. Evidence-based approach to using CT in spinal trauma. Eur J Radiol. 2003;48:39–48. Mulkens TH, Marchal P, Daineffe S, et al. Comparison of low-dose with standard-dose multidetector CT in cervical spine trauma. AJNR 2007;28:1444–50. Munera F, Cohn S, Rivas L. Penetrating injuries of the neck: use of helical computed tomographic angiography. J Trauma 2005;58:412–12. Nakayama Y, Awai K, Yanaga Y, et al. Optimal contrast medium injection protocols for the depiction of the Adamkiewicz artery using 64-detector CT angiography. Clinical Radiology 2008;63:880–7. Padayachee L, Cooper J, Irons S, et al. Cervical spine clearance in the unconscious traumatic brain injury patients: dynamic flexion–extension fluoroscopy versus computed tomography with three-dimensional reconstructions. J Trauma 2006;60:341–5. Torina P, Flanders A, Carrino J, Burns A, et al. Incidence of vertebral artery thrombosis in cervical trauma: correlation with severity of cord injury. AJNR 2005;26:2645–51. Tsuchiya K, Katase S, Aoki C et al. Application of multidetector row helical scanning to post myelographic CT. Eur Radiol 2003;13:1438–43. Van Goethem JW, Maes M, Ozsariak O et al. Imaging in spinal trauma. Eur Radiol 2005;15:582–90. Zampakis P, Santosh C, Taylor W, Teasdale E. The role of noninvasive computed tomography in patients with suspected dural fistulas with spinal drainage. Neurosurgery 2006;58:686–94.
139
Concluding comments
• A referral for a radiological examination is a referral for a consultant radiological opinion; this may, or may not, include the examination requested. • A clinician can request, not order, a radiological examination. • The clinical information on the request card can only be fully interpreted by a medically trained radiologist and should be sufficient to allow the choice of the most appropriate examination to be determined. If not, there should be a discussion with the referrer to clarify the issues. • The expression of a valid opinion on an examination can only be made by a radiologically trained doctor. A list of differential diagnoses is not a substitute. • The choice of technique can be guided by protocols, but it is essential that a radiologist is available to review the examination before the patient leaves the CT suite. To divorce the radiologist from the acquisition process means that vital information may not be acquired. • The clinically based protocols given and illustrated in this book give a sound framework for improving the imaging and diagnosis for your patients and referring clinicians.
141
Index
abscess 20, 21, 32, 56, 133 Alzheimer’s 2, 10 amyloid angiopathy 89 aneurysm 79, 84 anterior communication artery 86 basilar 23 basilar tip 57, 105 carotid artery 43, 57, 97, 115 carotid-ophthalmic 42, 85 cerebral artery bifurcation 84, 85, internal carotid artery 84, 88 intracavernous 58, 85, 87 intrasellar 43 mycotic 88 ophthalmic artery region 85 pericallosal artery 84, 98 posterior communicating artery 84 posterior inferior cerebellar 85 superior hyposphyseal artery 84 terminal carotid 57 vertebral artery 77 anterior circulation stroke 80 anterior clinoid, bony blistering of 40 aortic atheroma 71 apoplexy, pituitary 51, 55 artery 8, 63, 65, 93, 94–99 anterior cerebral 77, 97, 98 anterior choroidal 95 aortic arch 71, 72, 94, 97 ascending cervical 76 ascending pharyngeal artery (APA) 74, 75 azygous anterior cerebral 84, 98 basilar artery 23, 77, 78, 99
artery (continued) cervical artery collaterals 76 common carotid 75, 94, 96, 97 external carotid 96, 97, 111 facial 96 femoral 86 hypoglossal 99 intercostal 137 internal carotid see internal carotid artery (ICA) lingual 96 medial temporal 95 meningeal 96 middle cerebral see middle cerebral artery (MCA) occiptal 96 ophthalmic 29, 78 posterior cerebral 77, 85, 98, 99, 105 posterior circulation 76, 78, 85 posterior communicating 84, 95, 98 posterior inferior cerebellar (PICA) 95 subclavian 72 superior cerebellar 57, 99 superior thyroid 96 superior vena cava 119 thyrocervical trunk 137 trigeminal 99 vertebral 72, 76, 94, 95, 96, 136 arteriovenous malformation (AVM) 90, 91, 137 artial myxoma 79 atheroma aortic arch 71
atheroma (continued) bifurcation 96 common carotid artery 96 internal carotid artery 73, 74, 96 vertebral artery 72 atrophy, brain 7 basal cisterns 54 basal ganglia 65, 88 bifurcation atheroma 96 bitemporal hemianopia 41 blow-out fracture repair, orbital floor 33 bolus tracking 70, 82, 126 branchial arches 95 calcification aortic arch 72 cervical disc 126, 128 proximal internal carotid artery 73 scleral 33 stenotic atheroma 96 Sylvian fissure 66 caraoticocaverous fistula 29 carbon monoxide poisoning 7 cardiac pathology 70 carotid artery 71, 98, 99, 117 aneurysm 43, 57, 97, 115 birfurcation 73, 86 intracavernous 85 right stenosis 76 stenotic atheroma 96 cauda equina 129, 132 cavernoma 9, 106
142
Index
cavernous sinus 54, 56, 107 cavum septum pellucidum 105 central pontine myelinolysis 8 cerebral blood flow (CBF) 67 cerebral blood volume (CBV) 67 cerebral venous thombosis 101 cervical disc 122, 126, 128, 132, 133 cervical trauma 129 cervicothoracic mass 135 Chairin 1 malformation 24 chiasmal compression 38, 41, 51 chiasmal glioma 41 cholesterol granuloma 115 Circle of Willis 78, 81, 98 clivus 54 colloid cyst 23 coma 1, 7, 8 confusion 1, 8, 9, 17, 44, 49 congenital bilateral jugular bulb occlusion 106 cord compression 124, 128, 132 cortical veins, thrombosed 108 craniocervical junction 117, 130–131 CT mylogram 125 cysts 42, 49 deafness, bilateral 16 dementia 1 demyelination 23, 44 Dennis 3 column fracture 129 dens 130–131, 133 diplopia 31, 57 disc disease 126–129 disc prolapse 126, 127, 128 dissection carotid artery 58, 75, 76 intracranial 85, 89 vertebral artery 77 dorsum sellae: deformity 50 dural fistula 90, 111, 120 Duret haemorrhage 5 dysphasia 75 dysthyroid muscle involvement 30 embolic stroke 80 embolus, infected (mycotic aneurysm) 88
epidural abscess 32, 133 epilepsy 1, 3 extra-axial pathology 11, 13, 114 extraconal pathology 28, 31 facial pain 59 facial palsy 58, 114, 115 fibromuscular dysplasia (FMD) 79 fibrous dyslasia 31 fish hook sella 49 foramen magnum, disclocation 130–131 galactorrhoea 48 gaze palsy 65 globe, pathology 36 granuloma, orbital 30 grey matter migration 3 gyrus 64 haematoma basal ganglia 65 brain 9 diffuse axonal injury 5 extradural 130–131 intraventricular 89 orbital 38 parenchymal 87, 88 right anterior cord 132 spinal fracture 129 subdural 5 haemorrhagic contusions 4, 17 haemorrhagic stroke, acute 81–82, 82–91 hamartoma 50 head injury 1, 4 headache 1, 56, 109, 110, 111 helical scans 1 hemicord syndrome 132 hippocampus 11 hormonal abnormalities 45, 47 Horner’s syndrome 58 Hounsfield artefact 24, 64 hydrocephalus 8, 14, 24, 49, 65 hyperdense cyst (proteinaceous fluid) 23, 42 hyperdense thrombus 66
hyperdensity arteries 66 veins 9 hyperostosis I9 hyperthyroidism 29 hypoglossal canal 116 hypopituitarism 49, 50 hypothalamus 41 idiopathic intracranial hypertension (IIH) 110 infarction acute 64, 65, 67, 74, 75, 78 bilateral acute 44 carotid 65 cerebellar 9 gyral 64 left posterior capsular 66 occipital 9 pons 64 thalamic 9, 78 venous 9 infection Aspergillus 21 cellulitis, preseptal/postseptal 32 cysticercosis 21 discitis 133 fungal 21 orbital abscess 32 osteitis 32 psoas abscess 132 psoas granuloma 133 sclerotic discitis 133 septicaema 20 sphenoid sinusitis 107 spinal imaging of 132–133 subdural abscess 21 toxoplasmosis 21 see also abscess internal carotid artery (ICA) 73, 88, 96 abberrant 97 aneurysm 51, 84, 88 atheroma 73, 74, 96 calcification 73 dissection 76, 120 intracavernous carotid artery 85, 87, 99
Index 143
internal carotid artery (ICA) (continued) multiplanar reformation 74, 75 occlusion 65, 74, 77, 78 pseudoaneurysm 76 stenosis 75, 78, 89 tortuous and dilated vessels (ectatic) 73 variations in anatomy 97, 99 intervertebral disc prolapse 128 intraconal orbital pathology 27 intracranial injury 6 intracranial pressure, raised 39 intracranial vasculitis 79 intradural spinal AVM 137 intra/extracranial anastamoses 78 intrasellar cisternal hernation 40 intraventricular lesions and hydrocephalus 13 intraventricular lymphoma 18 intraventricular meningioma 18 ischaemic stroke: intracranial imaging 9, 61–63, 63–67, 68 ischaemic stroke: vascular imaging 69–70, 70–80 jugular fossa 117 lens, disclocated 38 ligaments: inflammatory softening 132 lumbar disc disease 122, 123 lumbar fractures, unstable 130–131 medial rectus: enlargement 30 medistinal mass 134 medulla 130–131, 133 meninges, enhancing thickened 50 meningioma I9, 37, 39, 40, 109 5th nerve 55 causing cranial nerve palsies 54 foramen magnum 117 suprasellar 40 venous invasion 109, 119 meningitis 8, 22, 49 middle cerebral artery (MCA) 89 aneurysm 84, 85, 87 duplication 97
middle cerebral artery (MCA) (continued) hyperdense 65, 66 occlusion 77, 78 stenosis 78, 79 middle ear cavity 97, 117 moyamoya 78 mucocoele 31 neurofibroma 136 neurofibromatosis 41, 56 neuroma 54, 55, 56, 115, 118, 119 ocular lesions 38 oedema 16, 87 optic chaism, pathology 36, 37 optic nerve 36, 37, 39, 40 orbital granuloma 30 orbital pathology 27–28, 28–33 orbital penetrating injury 6 oroantral fistula 32 osteopenia 135 pacchionian granulation 105 palsies see cranial nerve palsies pannus 133 papilloedema 37, 39, 110 paracentral lobule, acute infarct 64 parenchymal lesions 11, 12 parenchymal midbrain bleed 90 Parkinson’s disease 22 pathological fracture 134, 135 pedicles: pathological fractures 134 penetrating injury 6, 132 perfusion imaging 61–62, 63 periorbital abscess 32 persistent fetal connections 99 PICA see posterior inferior cerebellar artery pineal cyst 9 pituitary adenoma 38, 50 apoplexy 51, 55 imaging 45–46, 46–51, 52, 54 intrapituitary tumour 50 macroadenoma 40, 48, 51 microadenoma 47
pituitary (continued) prolactinoma 48 tumour 55 pons 54, 59, 64 popcorn calcification 50 postendarterectomy vessel 75 posterior inferior cerebellar artery (PICA) infarction 9 preseptal cellulitis 32 prolapsed disc 126, 127, 128 proptosis 29, 30, 33 pseudoaneurysm 76 ptosis 58 pulsatile exophthalmos 29 pulsatile tinnitus 118, 120 raised intracranial pressure 110, 116 retina, metastic deposits 39 retro-orbital headache 57 reversal sign 7 rheumatoid arthritis 133 rib metastasis 134 sarcoid granuloma 49 schisencephaly 3 scleral calcifcation 33 secondary ischaemia 5 seizures 1, 9, 17, 21, 48 sinus stenosis, bilateral 116 soft disc 128 sphenoid sinus 51 spinal angiography CT 125 spinal AVM 137 spinal cord compression 134–135 spinal dural fistula 137 spinal imaging 121, 124, 127–137, 138 disc disease 122, 126–129 infection 132–133 stenosis 122, 123 techniques 122, 123–126 trauma 124, 129–132 spondylolysthesis, degenerative 126 stenosis 74 bilateral terminal ICA 78 bilateral transverse sinus 110, 116 common carotid artery 75
144
Index
stenosis (continued) diffuse irregular 79, 89 left internal carotid artery 75 middle cerebral artery 79 sagittal sinus 91 secondary 78 spinal 123 subclavian 72 transient ischaemic attack 75 vertebral artery 72 strangulation 7 string of beads 79 stroke see haemorrhagic; ischaemic subarachnoid haemorrhage (SAH) 1, 8, 51, 86, 111, 132 superior facet fracture disclocation 130–131 superior orbital fissure 54 Takayasu disease 79 thecal sac and cord, displaced 129 thoracic disc 122, 129 thrombus, hyperdense artery 66 vein 9 tram-line parallel enhancement 39 transient ischaemic attack (TIA) 74, 75, 78 trauma: spinal imaging 129–132 tuberculous meningitis, calcified 50 tumour acoustic neuroma 116 acoustic schwannoma 115 adenoid cystic carcinoma 57 brain 13, 14, 16, 18, 19 breast cancer 15 carcinoma 51, 56, 57, 109 chondrosarcoma 13 cystic haemangioblasta 14 craniopharyngioma 42, 43, 44, 49 dermoid 19 diffuse meningeal secondary 16 ependymoma 14 glioblastoma 17 glioma 17, 39, 41, 44 glomus 117, 118, 119, 120 haemanglioblastoma 14
tumour (continued) haemangiopericytoma 137 high-grade malignant glioma 44 infratentorial secondary deposits 15 intraspinal meningioma 135 intrapituitary 50 lymphoma 18, 31, 33, 59, 135 malignant bone destruction 135 malignant menigitis 49 meningeal secondary 16 metastasis, rib 134 metastic deposits 14, 15, 16, 39, 59, 134 nasopharyngeal carcinoma 56 oligodendroglioma 18 parotid gland 115 pilocytic astrocytoma, low-grade 41 pituitary 55 plasmacytoma 116 salivary gland (adenoid cystic carcinoma) 57 secondary brain 15 secondary renal 116 spinal 134–135 squamous carcinoma 109 suprapituitary 49 suprasellar 9, 19, 43, 49 suprasellar craniopharyingioma 44 suprasellar meningioma 41 vein 101–102, 111–112 anatomical variations 103–106 basal vein of Rosenthal 105 cerebral 104 cervical venous plexus 128 coronal venous plexus 137 jugular 107, 111, 117, 118, 119 jugular bulb 97, 106, 111 pathology 107–111 sagittal sinus 91, 105, 108, 109, 110, 125 sigmoid sinus 106, 111, 117 sinuses 31, 32, 56, 104, 107 straight sinus 109, 110 superior ophthalmic 29, 38, 107 temporal 105 torqula 106, 109
vein (continued) transverse sinus 90, 105, 110 vein of Labbé 109 vena cava, superior 119 venous aneurysm 90, 105 venous plexus, cervical 128 venous sinuses 103 venous anomaly 106 venous dehiscence 105 venous infarction 9, 108 venous outflow obstruction 106 venous pathology 101–112 venous sacs, abnormal enlarged 90 venous thrombosis 107 ventriculitis 22 ventriculomegaly 7 vertebral canal 95 vertebral artery dissection 77 vertebrobasilar system, stenosis 77 vessel dissection, follow-up imaging 76 visual failure 35–36, 36–44 von Hippel-Lindau (vHL) disease 14 Waldenstrom’s macrogloulinaemia 21
