Learning Imaging Series Editors: R. Ribes · A. Luna · P. Ros
R. Ribes · J. C. Vilanova (Eds.)
Learning Musculoskeletal Imaging
Ramón Ribes MD, JD, PhD Platero Martinez 19 14012 Córdoba Spain
[email protected] Joan C. Vilanova , MD, PhD University of Girona Chief MRI Unit Clínica Girona Lorenzana, 36 17002 Girona Spain
[email protected]
ISBN: 978-3-540-87999-2
e-ISBN: 978-3-540-88000-4
DOI: 10.1007/978-3-540-88000-4 Springer Heidelberg Dordrecht London New York Library of Congress Control Number: 2010921306 © Springer-Verlag Berlin Heidelberg 2010 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag. Violations are liable for prosecution under the German Copyright Law. The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Cover design: eStudioCalamar, Figueres/Berlin Printed on acid-free paper 9 8 7 6 5 4 3 2 1 Springer is part of Springer Science+Business Media (www.springer.com)
“To Manuel Sánchez Gálvez, my first hero.” Ramón Ribes “To my wife Cris and my children
Cristina and Eduard for their love and for accommodating the sacrifices of personal time.” Joan C. Vilanova
Preface
Musculoskeletal (MSK) radiology is a radiological subspecialty that has expanded its knowledge base and imaging capabilities with the advent of MRI, multi/detector CT, ultrasound, and PET. Prior to the advent of MRI, MSK radiologists used plain film X-rays and arthrograms as their primary tools. The subspecialty has progressed from primary imaging of osseous structures and indirect imaging of joint spaces, to direct imaging of soft tissue structures with direct visualization and fine definition of MSK structures. A specialized MSK radiologist requires a sound knowledge of anatomy, pathophysiology, orthopedic surgical techniques, and advancements in imaging modalities. MSK imaging involves all aspects about anatomy, function, disease states, and aspects of interventional radiology appertaining to the MSK system including imaging in orthopedics, trauma, rheumatology, metabolic and endocrine diseases, as well as aspects of pediatrics, oncology, and sports imaging. Subspecialty training in MSK radiology must ensure competence to obtain experience in the following techniques: plain radiography, ultrasonography, CT, MRI, nuclear medicine, bone densitometry, and fluoroscopic procedures including arthrography. MSK radiologists must be aware of the strengths and weaknesses of the different imaging methods in each pathological condition and choose the appropriate imaging technique and/or the appropriate sequence in the investigation of specific clinical problems. A MSK radiologist should be prepared to assure an in-depth understanding of disease of the MSK system and understand the role of imaging in the diagnosis and treatment of MSK disease. Moreover, because of innovation and new medical imaging modalities, there are increasingly demanding requirements by clinical specialists. If radiologists do not or cannot keep up with increasing demands for MSK interpretations, clinicians will be forced to compete with radiologists in providing interpretations. From the beginning of the subspecialty in the 1970s with the foundation of the International Skeletal Society, multiple multidisciplinary or dedicated skeletal radiology societies have been founded and organized from international or national societies. We will try to expand the development of MSK radiology through complete prepared radiologists, in order to develop the ability to transmit the knowledge and assume the continuity and evolution of radiological diagnosis in the field of MSK radiology. Córdoba, Spain Girona, Spain
Ramon Ribes Joan C. Vilanova
Contents
1 Infection and Arthritis José A. Narváez, Matias De Albert, and Joan C. Vilanova . . . . . . . . . . . . . . . . . . . . . . .
Case 1.1 Femur Osteomyelitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 1.2 Rheumatoid Arthritis of the Cervical Spine. . . . . . . . . . . . . . . . . Case 1.3 Ankylosing Spondylitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 1.4 Enthesitis in Psoriatic Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . Case 1.5 Calcium Pyrophosphate Crystal Deposition Disease. . . . . . . . . Case 1.6 Muscular Abscess. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 1.7 Septic Arthritis of the Pubic Symphysis. . . . . . . . . . . . . . . . . . . . Case 1.8 Facet Joint Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 1.9 Cellulitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 1.10 Pyogenic Spondylodiscitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1 2 4 6 8 10 12 14 16 18 20 22
2 Tumors Guadalupe Garrido-Ruiz, Antoino Luna-Alcalá, and Joan C. Vilanova . . . . . . . . . . .
Case 2.1 Osteoblastoma of the Rib. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.2 Ewing’s Sarcoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.3 Intraosseous Lipoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.4 Giant Cell Tumor of Bone. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.5 Skeletal Muscle Metastases. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.6 Synovial Sarcoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.7 Synovial Hemangioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.8 Brown Tumor. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.9 Intramuscular Myxoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 2.10 Soft-Tissue Liposarcoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
23 24 26 28 30 32 34 36 38 40 42 44
3 Tendons and Muscles Rosa Mónica Rodrigo, Mario Padrón, and Eugenia Sanchez-Lacalle . . . . . . . . . . . .
Case 3.1 Tennis Leg Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 3.2 Hamstring Muscle Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 3.3 Indirect Rectus Femoris Strain Injury . . . . . . . . . . . . . . . . . . . . . Case 3.4 Adductor Muscle Strain Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 3.5 External Hip Rotator Muscle Injury . . . . . . . . . . . . . . . . . . . . . . . Case 3.6 Chronic Avulsion of the Ischial Tuberosity . . . . . . . . . . . . . . . . . Case 3.7 Acute Avulsion of the Anteroinferior Iliac Spine. . . . . . . . . . . . . Case 3.8 Patellar Tendinopathy: Partial Tear. . . . . . . . . . . . . . . . . . . . . . . . Case 3.9 Posterior Tibial Tendon Dysfunction. . . . . . . . . . . . . . . . . . . . . . Case 3.10 Partial Rupture of the Aquilles Tendon with Tendinosis. . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
45 46 48 50 52 54 56 58 60 62 64 66
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Contents
4 Bone Marrow Joan C. Vilanova, Mercedes Roca, and Sandra Baleato . . . . . . . . . . . . . . . . . . . . . . . .
67
Case 4.1 Bone Metastasis of Melanoma in the Femoral Head Mimicking Avascular Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 4.2 Bone Marrow Necrosis Due to Nonhodgkin’s Lymphoma. . . . . Case 4.3 Systemic Mastocytosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 4.4 Bone Crisis in Gaucher’s Disease. . . . . . . . . . . . . . . . . . . . . . . . . . Case 4.5 Non-Hodgkin’s (Diffuse Large B-Cell) Lymphoma. . . . . . . . . . . Case 4.6 Shoulder Arthropathy Secondary to Gaucher’s Disease. . . . . . . Case 4.7 Multifocal Osteonecrosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 4.8 Multiple Myeloma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 4.9 Bone Metastases. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 4.10 Regional Migratory Osteoporosis. . . . . . . . . . . . . . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
68 70 72 74 76 78 80 82 84 86 88
5 Spine Eva Llopis, Victoria Higueras, Elena Belloch, and María Vañó . . . . . . . . . . . . . . . . .
Case 5.1 Congenital Scoliosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.2 Herniated Disc Migration with Spontaneous Regression . . . . . Case 5.3 Ligamentum Flavum Cyst. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.4 Primary Vertebral and Epidural Lymphoma. . . . . . . . . . . . . . . . Case 5.5 Osteoid Osteoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.6 Meningioma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.7 Myeloma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.8 Fracture Dislocation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.9 Spondylodiscitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 5.10 Sacral Chordoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
89 90 92 94 96 98 100 102 104 106 108 110
6 Shoulder Fernando Idoate-Saralegui, and Joan C. Vilanova. . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
Case 6.1 Adhesive Capsulitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.2 Parsonage: Turner Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.3 Bankart Lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.4 Perthes Lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.5 Alpsa + Hill–Sachs Lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.6 Glad Lesion and Calcified Loose Body. . . . . . . . . . . . . . . . . . . . . Case 6.7 Slap Lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.8 Posterior Labral Tear + Paraglenoid Labral Cyst . . . . . . . . . . . . Case 6.9 Ambrii + Bilateral Labral Tears. . . . . . . . . . . . . . . . . . . . . . . . . . . Case 6.10 Posterosuperior Impingement (Throwing Shoulder + GIRD) . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
112 114 116 118 120 122 124 126 128 130 133
7 Elbow, Hand, and Wrist Juan de Dios Berná, Ana Canga, and Luis Cerezal . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
Case 7.1 Slac Wrist. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136 Case 7.2 Scaphoid Avascular Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
Contents
Case 7.3 Intraosseous Ganglia of the Lunate (“Pseudo-Kienböck” Disease). . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 7.4 Glomus Tumor in the Thumb. . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 7.5 Carpal Boss. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 7.6 De Quervain Tenosynovitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 7.7 Distal Biceps Tendon Rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 7.8 Posterior Dislocation of the Elbow. . . . . . . . . . . . . . . . . . . . . . . . Case 7.9 Occult Fracture of the Radial Head. . . . . . . . . . . . . . . . . . . . . . . . Case 7.10 Pigmented Villonodular Synovitis of the Elbow. . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
140 142 144 146 148 150 152 154 156
8 Hip and Pelvis Ara Kassarjian, José Martel-Villagrán, and Ángel Bueno-Horcajadas . . . . . . . . . . 157
Case 8.1 Postpartum Sacral Fracture. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 8.2 Acute Avulsion Fracture of the Ischial Apophysis. . . . . . . . . . . . Case 8.3 Transient Osteoporosis of the Hip. . . . . . . . . . . . . . . . . . . . . . . . . Case 8.4 Osteolysis Associated with Total Hip Arthroplasty. . . . . . . . . . . Case 8.5 Osteomalacia with Looser Zones. . . . . . . . . . . . . . . . . . . . . . . . . . Case 8.6 Femoroacetabular Impingement (Predominantly Cam Type) . Case 8.7 Pubalgia Due to Common Adductor Tendon Microavulsion . . Case 8.8 Osteopoikilosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 8.9 Rapidly Destructive Osteoarthritis. . . . . . . . . . . . . . . . . . . . . . . . Case 8.10 Osteonecrosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
158 160 162 164 166 168 170 172 174 176 178
9 Knee Joan C. Vilanova, Sandra Baleato, and Joaquim Barceló . . . . . . . . . . . . . . . . . . . . . . . 179
Case 9.1 Case 9.2 Case 9.3 Case 9.4 Case 9.5 Case 9.6 Case 9.7 Case 9.8 Case 9.9
Lipoma Arborescens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pigmented Villonodular Synovitis. . . . . . . . . . . . . . . . . . . . . . . . . Spontaneous Osteonecrosis of the Knee. . . . . . . . . . . . . . . . . . . . Discoid Meniscus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Osgood-Schlatter Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chondromalacia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Meniscal Tear . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Osteochondritis Dissecans. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mucoid Degeneration of the Anterior Cruciate Ligament with Ganglion Bone Cyst. . . . . . . . . . . . . . . . . . . . . . . . Case 9.10 Acute Meniscal and Ligament Tears of the Knee. . . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
180 182 184 186 188 190 192 194 196 198 200
10 Ankle and Foot Xavier Tomas and Ana Isabel Garcia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
Case 10.1 Case 10.2 Case 10.3 Case 10.4 Case 10.5
Osteochondral Talar Lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Calcaneal Fracture. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Complete Achilles Tendon Tear. . . . . . . . . . . . . . . . . . . . . . . . . . . Lateral Collateral Ligament Sprain. . . . . . . . . . . . . . . . . . . . . . . . Syndesmotic Ankle Sprain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
202 204 206 208 210
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Case 10.6 Plantar Fasciitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 10.7 Plantar Fibromatosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 10.8 Tarsal Tunnel Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 10.9 Diabetic Foot. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Case 10.10 Intermetatarsal Bursitis and Morton’s Neuroma. . . . . . . . . . . . Further Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
212 214 216 218 220 222
Contributing Authors
Sandra Baleato Department of Radiology CHOP Complexo Hospitalario de Pontevedra Pontevedra Spain
Luis Cerezal Diagnóstico Médico Cantabria (DMC) Manuel Cacicedo 91 39012 Santander Spain
Joaquim Barceló Department of Radiology Clínica Girona-Hospital Sta. Caterina Girona Spain
Matias de Albert Department of Radiology Hospital Universitario de Bellvitge Hospitalet de Llobregat Barcelona Spain
Elena Belloch Department of Radiology Hospital de la Ribera Carretera de Corbera km1 46600 Valencia Spain
Ana Isabel García Radiology Department Muscle-Skeletal Unit Hospital Clínic Barcelona Spain
Ángel Bueno-Horcajadas Hospital Universitario Fundación Alcorcón Alcorcón (Madrid) Spain
Guadalupe Garrido-Ruiz Hospital Vall d’Hebron Barcelona Spain
Juan de Dios Berná-Mestre Department of Radiology Virgen de la Arrixaca University Hospital 30120 El Palmar (Murcia) Spain
Victoria Higueras Department of Radiology Hospital de la Ribera Carretera de Corbera km1 46600 Valencia Spain
Ana Canga Department of Radiology Marqués de Valdecilla University Hospital Radiologic Anatomy 39008 Santander Spain
Fernando Idoate-Saralegui Department of Radiology Clínica San Miguel Pamplona Spain
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Contributing Authors
Ara Kassarjian Massachusetts General Hospital Boston, MA USA Eva Llopis Department of Radiology Hospital de la Ribera Carretera de Corbera km1 46600 Valencia Spain Antonio Luna-Alcalá Clínica Las Nieves Sercosa 23007 Jaén Spain José Martel-Villagrán Corades, S.L. Majadahonda (Madrid) Spain Rosa Mónica Rodrigo Resonancia Bilbao Bilbao Spain José A. Narváez Department of Radiology Hospital Universitario de Bellvitge Hospitalet de Llobregat Barcelona Spain Mario Padrón Radiology Department Clínica Cemtro Madrid Spain
Mercedes Roca Ciberer. Instituto Aragonés de Ciencias de la Salud I+D+I Zaragoza Spain Eugenia Sanchez-Lacalle Radiology Department Clínica Cemtro Madrid Spain Xavier Tomas Radiology Department Muscle-Skeletal Unit Hospital Clínic Barcelona Spain Maria Vañó Department of Radiology Hospital de la Ribera Carretera de Corbera km1 46600 Valencia Spain, Joan C. Vilanova University of Girona Chief MRI Unit Clínica Girona Lorenzana, 36 17002 Girona Spain
Infection and Arthritis José A. Narváez, Matias De Albert, and Joan C. Vilanova
1
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J. A. Narváez, M. De Albert, and J. C. Vilanova
Case 1.1 Femur Osteomyelitis
Fig. 1.1.1
Fig. 1.1.2
Fig. 1.1.3 Fig. 1.1.4
Fig. 1.1.5
Infection and Arthritis
A 9-year-old boy presented with a 3-week history of left hip pain. Four weeks prior, the patient had suffered a superficial injury to his abdomen, which required a subcutaneous suture. At admission, he had intermittent fever. He was reluctant to bear weight on his left limb and had gait disturbances. Plain-film pelvic radiographs performed in the emergency room were suspicious for a bone tumor of the left ischium. CT, bone scintigraphy, and MRI examinations were requested to rule out bone tumor.
Acute hematogenous osteomyelitis usually occurs during skeletal growth when the growth plate is open. Early detection of osteomyelitis is essential to enable therapy to be started before bone devitalization. Hematogenous osteomyelitis may not be evident on plain films until at least 10 days after the onset of symptoms. The evolution of the infection can manifest radiographically as soft-tissue swelling with obliteration of adjacent muscle planes, subperiosteal calcification, and resorption of bony trabeculae. Bone scintigraphy is highly sensitive for the diagnosis of osteomyelitis. Bone scintigraphy scans are sensitive indicators of altered osteoblastic activity, but local disturbances in vascular perfusion, clearance rate, permeability, and chemical binding also affect imaging. CT should be used only as a third-line technique for visualizing bony destruction, gas within the bone, or bony sequestration. MRI is highly sensitive as an indicator of disease because pathological findings are evident much earlier in the course of the disease. The MRI diagnosis of osteomyelitis is based on its capability to detect bone marrow abnormalities within the physis. Active osteomyelitis foci appear as low signal intensity areas on T1-weighted images and high signal intensity areas on T2-weighted images, fat-suppression, or STIR sequences. MRI is an excellent technique for the detection of osteomyelitis and the depiction of its extent. It is important to understand the limitations of each imaging technique to avoid delays in the diagnosis and management of osteomyelitis and prevent possible complications. The differential diagnosis of pelvic osteomyelitis in children should include septic arthritis, Legg-Calve-Perthes disease, toxic synovitis, and less commonly, collagen-vascular diseases, neoplasms involving bone, and retroperitoneal abscess.
Comments
Plain film of the pelvis (Fig. 1.1.1) shows no pathologic findings for bone infection in the left femur. A swollen left ischiopubic synchondrosis was found incidentally (open arrow) and was at first interpreted as the reason for the patient’s complaint. Bone scintigraphy (Fig. 1.1.2) scan shows increased uptake within the left femoral head (arrow) and slight uptake in the left ischiopubic synchondrosis (open arrowhead). CT (Fig. 1.1.3) shows a round annular area in the left femoral head corresponding to the focal site of infection. Axial T1-weighted MRI (Fig. 1.1.4) shows diffuse low signal intensity within the proximal metaphysis of the left femur. Coronal STIR MRI (Fig. 1.1.5) reveals high signal intensity in the bone marrow of the proximal femoral growth plate, with edema in the surrounding soft-tissues. Note the hypertrophy of the ischiopubic synchondrosis (arrowhead).
Imaging Findings
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J. A. Narváez, M. De Albert, and J. C. Vilanova
Case 1.2 Rheumatoid Arthritis of the Cervical Spine Comments
A 58-year-old woman with a 10-year history of rheumatoid arthritis (RA) presented hyperreflexia and neck pain unresponsive to conventional treatment. No sensory or motor deficits were found at neurologic examination. Radiographs and MRI of the neck were requested to rule out cervical spinal canal compromise.
The cervical spine, particularly the craniocervical junction, is one of the most common sites of RA involvement. The prevalence of cervical spine lesions of any kind among RA patients ranges from 43 to 86%. Cervical spine involvement can lead to severe pain and disability, as well as a variety of neurological complications. RA attacks the synovium; the atlantoaxial joint, where most of the synovial tissue in the cervical spine is located, is where the disease is most prevalent and
Fig. 1.2.2 Fig. 1.2.1
Fig. 1.2.3
Fig. 1.2.4
Infection and Arthritis
where characteristic changes are most evident at imaging. Atlantoaxial joint synovitis erodes the transverse ligament that holds the odontoid process to the atlas and causes laxity, resulting in anterior atlantoaxial subluxation. This is the most common pattern of atlantoaxial instability. Radiographs are the initial imaging method in these cases. The normal anterior atlantoodontoid interval is less than 3 mm. Anterior atlantoaxial subluxation may be not detected in radiographs obtained in a neutral position, and lateral views with the neck flexed should be obtained. When the anterior atlanto-odontoid interval is greater than 9 mm, the risk of cord compression increases. A more severe manifestation of atlantoaxial rheumatoid disease is vertical subluxation, in which the odontoid process migrates upward, protruding into the foramen magnum. This condition results from destruction of the lateral atlantoaxial joints or of bone around the foramen magnum. Subaxial (below C2 level) involvement is less common in RA. In this cervical spine segment, the most common rheumatoid manifestation is anterior subluxation, caused by apophyseal joint destruction. An anterior vertebral body displacement greater than 3 mm is diagnostic of anterior subaxial subluxation. End-plate erosions, sclerosis, and destructive changes are apparently due to extension of the inflammatory process from adjacent neurocentral joints (the joints of Luschka, which are lined by synovium) into the discovertebral area Magnetic resonance imaging (MRI) is the imaging modality of choice for assessing involvement of the cervical spine in RA. It permits evaluation of the anatomical relationships of the occiput, atlas, and axis, and it is therefore useful to define the extent of subluxation of this spinal segment. It also permits direct visualization of periodontoid synovitis formation, spinal cord, and brainstem. MRI of the cervical spine is mandatory when spinal cord compression is clinically suspected. In asymptomatic patients, MRI of the cervical spine should be considered when radiographs show vertical subluxation, an anterior atlanto-odontoid interval greater than 9 mm, a posterior atlanto-odontoid interval of 14 mm or less, or a subaxial canal diameter of 14 mm or less.
Lateral view of the cervical spine in neutral position (Fig. 1.2.1) shows a normal anterior atlanto-odontoid interval (open arrow). Disc space narrowing, end-plate erosions, and subchondral erosions are seen in the anterior region of C3–C4; the rest of the disc space is spared and no associated osteophytes, which correspond to discovertebral rheumatoid involvement, are present. Lateral view of the cervical spine with the neck in flexion (Fig. 1.2.2) reveals anterior atlantoaxial subluxation (anterior atlanto-odontoid interval of more than 3 mm) (arrows). Sagittal T1-weighted (Fig. 1.2.3) and T2-weighted (Fig. 1.2.4) MRIs show periodontoid synovitis, which presents low signal intensity on T1-weighted and high signal intensity on T2-weighted images (open arrows). Periodontoid synovitis causes a mild mass effect on the anterior thecal sac (arrowheads), but there is no cord compression. MRI was performed in the neutral position, so the anterior atlantoaxial subluxation is not evident. Note the small erosions and subchondral low signal intensity changes (open arrowheads) in the anterior region of the C3–C4 disc space.
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Case 1.3 Ankylosing Spondylitis Comments
A 47-year-old man presented with long-standing low back pain and stiffness. Several years earlier, he was diagnosed with “probable degenerative disc disease.” Radiographs of the lumbar and cervical spine and pelvis were obtained.
Ankylosing spondylitis is a chronic inflammatory disorder that mainly affects the axial skeleton. It is more common in males, with a male-to-female ratio of 5:1. It is seen predominantly between the ages of 15 and 35 years.
Fig. 1.3.2
Fig. 1.3.1
Fig. 1.3.3
Fig. 1.3.4
Infection and Arthritis
The most common and characteristic initial symptoms are chronic, inflammatory low back pain, and stiffness. Occasionally, back pain is too mild to impel the patient to seek medical care, or it is misdiagnosed as sciatica due to degenerative disc disease, as occurred in our case. Ankylosis spondylitis is characterized by bilateral sacroiliac and spinal involvement. The sacroiliac joint is the first joint involved. The disease initial involves the spine in the thoracolumbar junction and progresses to the lumbar and thoracic spine. Cervical spine involvement is less frequent. Radiographs are the initial imaging technique in these patients. Radiographic signs of sacroiliitis are included in the diagnostic criteria of ankylosing spondylitis. Small erosions are the initial radiographic abnormality, initially on the iliac side and then on the sacral side. Usually, erosions are surrounded by subchondral sclerosis. The anterior, synovial aspect of the joint ankyloses relatively early, but ankylosing of the posterior, ligamentous aspect of the joint is common. When radiographic findings are normal or inconclusive, CT can demonstrate these destructive and reparative changes better. Initially, radiographs of the spine show erosion of the anterior corners of the vertebral body with secondary reactive sclerosis and a “squared” appearance of the vertebral body. Ossification of the longitudinal ligaments is called syndesmophyte and involves the spine in a symmetrical fashion. Spine ankylosis is associated to disc calcification. Ankylosing of the apophyseal joints and ossification of the interspinous ligaments may be present. The resulting appearance is called “bamboo spine.” The axial distribution and the bone reparative changes with progression to ankylosis in a short period of time allow a confident diagnosis in most cases. In the last decade, MRI has been increasing used to study the inflammatory process in ankylosing spondylitis and the other spondyloarthropathies. In contrast to radiographs and CT, which detect destructive and reparative changes as mentioned above, MRI can detect inflammatory changes at joints before these destructive-reparative changes take place. MRI signs of early sacroiliitis are subchondral bone marrow edema and increased signal on T2-weighted images and increased contrast-enhancement of the joint cavity, corresponding to synovitis. Bone marrow edematous changes at the ligamentous insertions (entheses) in the spine are the hallmark of early disease.
Radiograph of the pelvis (Fig. 1.3.1) reveals complete ankylosis of both sacroiliac joints. Ossification of the ligaments in the posterior superior portion of the joints is called the “star” sign (open arrows). Radiographs (AP and lateral views) of the lumbar spine (Figs. 1.3.2 and 1.3.3) demonstrate bilateral, succinct syndesmophytes. Note also disk calcification and partial ankylosis of the apophyseal joints. Radiograph (lateral view) of the cervical spine (Fig. 1.3.4) shows anterior syndesmophytes at some disc spaces (closed arrows), disc space calcification, and partial ankylosis of the apophyseal joints.
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Case 1.4 Enthesitis in Psoriatic Arthritis
Fig. 1.4.2
Fig. 1.4.1
Fig. 1.4.3
Infection and Arthritis
A 26-year-old man complained of a painful left heel for several months. Pain did not subside with rest. Conservative treatment with relative rest, nonsteroidal antiinflammatory drugs, and a soft rubber heel pad was ineffective. Initially, radiographs were obtained. MR imaging study was requested to better evaluate the soft-tissue structures of the heel.
The enthesis is the point where a tendon, ligament, or joint capsule attaches to bone. Inflammation at the enthesis, or enthesitis, is considered the hallmark of the spondyloarthropathies, which are a group of inflammatory arthropathies that share some common genetic, pathologic, and clinical features. This group includes ankylosing spondylitis, psoriatic arthritis, reactive arthritis (e.g., Reiter syndrome), arthritis associated with inflammatory bowel disease (e.g., Crohn disease or ulcerative colitis), and undifferentiated spondyloarthritis. Psoriatic arthritis has been defined as an inflammatory arthritis associated with psoriasis. Peripheral enthesitis is a common manifestation of psoriatic arthritis. The most common locations are at the enthesis of the Achilles tendon and plantar fascia in the calcaneus. Enthesitis is usually bilateral and may be the initial manifestation of the disease. Radiographs show erosions and bone proliferations at the enthesis of the Achilles tendon and plantar fascia, creating irregular and ill-defined spurs. The spurs tend to point upward toward the calcaneus rather than downward along the course of the plantar aponeurosis as occurs in normal heel spurs. MRI not only identifies the destructive and reparative changes, but it also reveals the inflammatory changes at the entheses. MRI signs of enthesitis include edematous changes in the bone marrow adjacent to the insertion of the tendon or fascia and in the Achilles tendon and plantar fascia themselves, which show increased signal intensity and variable thickening. Edematous changes are also seen in the adjacent soft-tissues. Erosions are seen as irregularity and defects of the bony margins, and sclerosis shows low signal intensity on all pulse sequences. Precisely the aim of the MRI study is to identify enthesitis before erosions and reparative sclerosis appear, making it possible to start effective treatment as early as possible.
Comments
Lateral view plain-film radiograph of the ankle (Fig. 1.4.1) shows erosion and bone formation at the attachment of the Achilles tendon (open arrow). There is also sclerosis and formation of a calcaneus spur (closed arrow), which points upward toward the calcaneus. T1-weighted (Fig. 1.4.2) and STIR (Fig. 1.4.3) MRI demonstrates extensive edematous changes in bone marrow at the insertions of the Achilles tendon and plantar fascia (open arrowheads). Note also the edematous changes in the adjacent soft-tissues, with small retrocalcaneal bursitis (closed arrowheads).
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Case 1.5 Calcium Pyrophosphate Crystal Deposition Disease
Fig. 1.5.1
Fig. 1.5.2
Fig. 1.5.3
Fig. 1.5.5
Fig. 1.5.4
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A 73-year-old man complained of inflammatory cervical pain for 1 month. Cervical pain increased progressively and required fentanyl treatment. After radiographs of the cervical spine were inconclusive, a CT study of the cervical spine was requested.
Calcium pyrophosphate dehydrate (CPPD) crystal deposition is characterized by a constellation of clinical manifestations, which can be grouped in five discrete patterns: pseudogout, pseudoosteoarthritis with synovitis, pseudoosteoarthritis without synovitis, monoarthropathy, and pseudorheumatoid arthritis. CPPD crystals may be deposited as soft-tissue masses, a condition known as tophaceous pseudogout. Commonly affected sites of deposition include the temporomandibular and atlantoaxial joints, ligamentum flavum, and the finger joints. Involvement of the atlantoaxial joint is primary related to ligamentous CPPD crystal deposition, which is associated with periodontoid synovitis and bony erosions and cysts, mainly in the odontoid process. Erosion of the odontoid process can produce a pathologic fracture. Retrodental synovial masses with calcification can cause cervical cord compression. This syndrome of acute neck pain associated with calcification surrounding the odontoid process has been described as “crowned dens syndrome.” Symptomatic spinal involvement of the ligamentum flavum of the cervical and lumbar spine has been reported. Ligamentous calcification can be detected by radiographs, but CT is usually necessary to identify calcifications in the periodontoid synovial masses, allowing a correct diagnosis. MRI is useful to assess the relationships between these periodontoid masses and the cervical cord.
Comments
Lateral view radiograph of the cervical spine (Fig. 1.5.1) shows small calcifications located below the anterior rim of the atlas (open arrow), with ill-defined erosions of the odontoid process. Axial CT scans (Figs. 1.5.2 and 1.5.3) demonstrate calcified deposits (closed arrow) and odontoid erosions (open arrowhead). Coronal multidetector CT reconstruction of the cervical spine (Fig. 1.5.4) shows the periodontoid calcifications. Coronal multidetector CT reconstruction of the pelvis (Fig. 1.5.5) demonstrates a linear calcification of the symphysis pubis as well as irregular calcifications at the adductor muscle insertions (closed arrowheads).
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Case 1.6 Muscular Abscess
Fig. 1.6.2 Fig. 1.6.1
Fig. 1.6.3
Fig. 1.6.4
Infection and Arthritis 13
A 52-year-old alcoholic man presented at the emergency department with disorientation and depressed level of consciousness. Signs of malnutrition, hypotension, and generalized edema were detected. Laboratory tests showed pancytopenia. Blood cultures were positive for Streptococcus equisimilis, though no clear source of infection was identified. Five days after admission, a cellulitic plaque appeared on his right thigh. He underwent ultrasonography and CT.
Although most bacterial infections in the soft-tissues remain localized, depending on the immunologic status of the patient, these infections can extend and may form an abscess. The most commonly isolated pathogen in soft-tissue abscesses is S aureus, especially methicillin-resistant S aureus. Ultrasonography plays a major role in the detection and management of superficial abscesses, but deeper fluid collections usually require MRI or CT. MRI and CT are the ideal techniques to display the soft-tissue abnormalities and can be quite specific and helpful in detecting the presence and extent of infection, which generally is suspected clinically on the basis of physical and laboratory findings. At ultrasonography, soft-tissue abscesses are demonstrated as an irregular fluid-filled anechoic or diffusely hypoechoic area with posterior acoustic enhancement containing a variable amount of echogenic debris. Color Doppler imaging may be used to demonstrate hyperemia at the periphery of the mass and absence of flow in its center. CT shows a well-demarcated fluid collection, with a peripheral pseudocapsule showing rim enhancement. MRI shows a well-demarcated fluid collection that is hypointense on T1-weighted images and hyperintense on T2-weighted and STIR images, surrounded by a pseudocapsule with low signal intensity in all sequences and peripheral rim enhancement after intravenous administration of gadolinium-based contrast material. Needle aspiration biopsy is mandatory if an abscess is suspected. Abscesses are treated with antibiotics and percutaneous drainage.
Comments
Ultrasonographic image of the posterior compartment of the right thigh (Fig. 1.6.1) shows a well-circumscribed hypoechoic subcutaneous cavity (open arrow) with internal echoes (arrow) displacing the fat lobules (open arrowhead). The echogenic material filling the abscess fluctuated on compression. Power Doppler ultrasound image (Fig. 1.6.2) shows hyperemic blood flow within the abscess wall (open arrow). No flow was seen in the center. CT (Fig. 1.6.3) shows septations of the subcutaneous fat (open arrow), skin thickening (arrow), and a small rim-enhancing, well-demarcated fluid collection adjacent to the biceps femoris muscle (open arrowhead). Coronal MPR CT (Fig. 1.6.4) shows the intramuscular location of the abscess, inside the biceps femoral muscular fibers (open arrow).
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Case 1.7 Septic Arthritis of the Pubic Symphysis
Fig. 1.7.1
Fig. 1.7.3
Fig. 1.7.2
Fig. 1.7.4
Infection and Arthritis 15
An 82-year-old man, who had undergone prostatectomy 2 months before, presented at the emergency department with a temperature of 38°C and history of two days of nausea, and vomiting. He reported lower abdominal pain centered on the suprapubic region. The white blood cell count was 20,100 cell/mm3. An exploratory CT examination was performed.
Septic arthritis of the pubic symphysis is a rare and painful condition that may become apparent 1 month or longer after a pelvic procedure or surgery, especially after surgery to correct incontinence in women, prostate surgery, and surgery on pelvic malignancies. Plain films are relatively insensitive, especially early in the course of disease. The radiographic appearance includes mild to severe pubic symphysis thickening and subchondral bony irregularity, usually in both pubic bones. In advanced stage disease, bone sclerosis can also be observed. CT scans show the classical findings of septic arthritis and include joint effusion with synovial enhancement and bone erosions around the joint. An MRI is more sensitive in the detection of early changes in septic arthritis, revealing signal intensity abnormalities in the bone narrow and soft-tissues, both of which have edema-like signal intensity (i.e., are hypointense on T1-weighted images and hyperintense on fat-suppressed T2-weighted images and STIR images). Extension of infection from the joint space into surrounding tissue is also easily recognized on both CT and MRI. This rare disease must not be confused with the more common osteitis pubis, a sterile, inflammatory condition of the pubis occurring after pregnancy, trauma, or gynecologic or urologic surgery and also seen in athletes, characterized by pubic pain radiating to the groin, waddling gait with adductor spasm, sclerosis, and rarefaction of the pubic symphysis on imaging studies. Osteitis pubis in athletes is usually a noninfectious, chronic pubic periostitis that appears with overuse injuries of muscles inserting on the symphysis.
Introduction
Plain film of the pelvis (Fig. 1.7.1) shows doubtful thickening of the pubic symphysis (open arrow). CT of the pelvis at the level of the pubic symphysis (Fig. 1.7.2) in soft-tissue window shows a small collection (open arrow) with peripheral rim enhancement, (arrow) corresponding to an abscess. CT at the same level with bone window (Fig. 1.7.3) shows cortical thinning (open arrow) and erosion of the anterior portion of the symphysis. Sagital MPR CT (Fig.1.7.4) shows, in a more clear view, cortical thinning (open arrow) with some small erosion (arrow) in the anterior portion of the symphysis.
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Case 1.8 Facet Joint Arthritis
A 47-year-old female patient with a past history of moderate alcoholism and cutaneous discoid lupus erythematosus treated with chloroquine presented 16 days after the onset of acute back pain not relieved with nonsteroidal antiinflammatory treatment. Blood and urine
Fig. 1.8.3
Fig. 1.8.1
Fig. 1.8.4
Fig. 1.8.2
Fig. 1.8.5
Infection and Arthritis 17
cultures were positive for S. aureus. Radiographs of the lumbar spine were obtained and Technetium-99 bone scintigraphy, CT, and MRI of the lumbar spine were requested.
Pyogenic facet joint infection is a rare and underrecognized clinical entity that is poorly documented to date. Clinically, it is characterized by inflammatory low back pain and fever; neurologic impairment is seen in nearly half the cases. Patients often present systemic predisposing factors, including diabetes mellitus, malignancies, or alcoholism. In one third of cases, one or more concomitant infectious processes due to the same microorganism are found, mainly arthritis, skin and soft-tissue infections, endocarditis, and urinary tract infections. Staphylococcus aureus is the most common etiologic microorganism. Radiographs are usually of no value in the first stages of the disease. Technetium-99 scintigraphy shows increased tracer uptake at the level of the affected vertebra. Unlike spondylodiscitis, tracer uptake is usually oriented more vertically than horizontally, although it is difficult to distinguish between the two conditions based only on the scintigraphic findings. CT abnormalities include loss of subchondral bone associated with the facet joint, loss of ligamentum flavum density, and obliteration of fat planes. Contrast-enhanced CT can also detect phlegmonous changes and/or fluid collections in paraspinal soft-tissue; however, MRI depicts soft-tissue structures better than CT. CT is also useful for image-guided biopsy in selected cases. MRI is the modality of choice for diagnosing pyogenic facet infection. MRI is both sensitive and specific in diagnosing pyogenic facet joint infection as early as 2 days after the onset of symptoms, and it can rule out involvement of the disc space and vertebral body. Moreover, it is especially effective for evaluating the neural structures of the spine (i.e., the spinal cord and nerve roots) and the spread of infection to the epidural space and/or paraspinal soft-tissues. Paraspinal and/or epidural extension is a frequent finding, and the use of gadolinium contrast is required to better delineate the extent of the process and to differentiate nonenhancing abscesses from phlegmonous changes. It is important to understand the limitations of each imaging technique to avoid delays in the diagnosis and management of pyogenic facet joint infection and prevent possible complications.
Imaging Findings
Bone scintigraphy (Fig. 1.8.1) shows increased tracer uptake at the right L5 level. CT (Fig. 1.8.2) shows erosions of the right L5-S1 facet joint. Note the juxta-articular enhancing phlegmonous reaction in the posterior paraspinal muscles as well as in the spinal canal (open arrows). Axial T2-weighted (Fig. 1.8.3) and axial contrast-enhanced T1-weighted (Figs. 1.8.4 and 1.8.5) MRI show edematous bone marrow changes and loss of the low signal intensity of the joint abscess. Note posterior paraspinal (closed arrows) and epidural (open arrowheads) abscesses, which present high signal intensity on the T2-weighted image and appear as a nonenhancing collection surrounded by thick enhancing walls.
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Case 1.9 Cellulitis
A 46-year-old man presented at the emergency department with pain, swelling, and functional impotence of the right lower limb from the thigh to the foot. He was morbidly obese and had hypertension. He had a fever (up to 40°C) with shivering in the 3 days before admission but no other symptoms. At physical examination, his temperature was 37.3°C and a large area of cellulitis
Fig. 1.9.1 Fig. 1.9.2
Fig. 1.9.3
Fig. 1.9.4
Infection and Arthritis 19
occupied nearly the entire limb; he had skin ulcers in the first and second toes of the right foot and adjacent to the peroneal malleolus. After emergency ultrasound examination and suspicion of necrotizing fasciitis, we performed a CT study.
Cellulitis or superficial nonnecrotizing fasciitis is an acute infection of the dermis and superficial subcutaneous tissue that does not involve the epidermis or the deep fascia. It is commonly found in clinical practice and, in most cases, the causative agents are group A Streptococcus pyogenes or S. aureus. It causes pain, erythema, edema, and warmth. Its origin may be cutaneous, by contiguity, or bacteremic. The cutaneous type occurs more frequently (bites, sores, cracks, trauma, previous surgery, etc.). Patients with peripheral vascular disease or diabetes are especially susceptible to this type of infection since minor skin injuries facilitate infection. It is usually managed clinically and does not normally require radiological studies. Imaging studies are required when necrotizing fasciitis is suspected and to assess the depth of the infection or the presence of bone infection or abscess formation. Ultrasound may have an important role, especially for differentiating cellulitis from an abscess and distinguishing the latter from other soft-tissue masses. Ultrasound shows an irregular ill-defined hyperechoic appearance of fat and blurring of tissue planes, progressing to hypoechoic strands reflecting edema. Color and power Doppler imaging may help clinical diagnosis by depicting a hypervascular pattern. CT may demonstrate skin thickening, septation of the subcutaneous fat, and thickening of the underlying superficial fascia. If the infection spreads to deeper tissues, deep cellulitis, myositis, necrotizing fasciitis, or osteomyelitis can occur, all of which can be ruled out with CT. After injection of intravenous contrast material, diffuse increased enhancement is present in the same areas that are abnormal on unenhanced CT. Lack of involvement of the deep fascia allows fasciitis to be differentiated from necrotizing cellulitis. MRI shows skin thickening with low signal on T1-weighted images and high signal on T2-weighted images, with a reticular (lace-like) pattern in the subcutaneous fat.Additionally, MRI may show fluid collections and other complications. The main limitation of MRI is its limited availability in emergency departments.
Comments
Ultrasound image over the pretibial region (Fig. 1.9.1) shows enlargement and fluid distension of all septa (open arrows) of the subcutaneous tissue. Note the fat lobules, which appear as individual structures (arrow) separated by the intervening fluid. Axial CT scan (Fig. 1.9.2) shows skin thickening (open arrow) and septation of the subcutaneous fat with thickening of the superficial fascia (arrow). Note the severe fatty atrophy of muscle due to the patient’s extremely sedentary lifestyle (open arrowhead). Coronal 3D volume-rendered CT images (Fig. 1.9.3) show a noticeable increase in the diameter of the right lower limb compared with the contralateral side (open arrows). Coronal CT multiplanar reconstruction (Fig. 1.9.4) shows the extension of the process and how it affects practically the entire right leg and ankle (open arrows).
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Case 1.10 Pyogenic Spondylodiscitis
A 66-year-old man presented with insidious nonmechanical back pain of 3 weeks’ evolution. He reported an episode of fever and night chills 2 weeks prior. No neurologic signs were evident at physical examination. Laboratory tests showed mild leukocytosis (white blood cell count of 13,100 cell/mm3.) and elevated eryt\spine.
Fig. 1.10.1
Fig. 1.10.2
Fig. 1.10.3
Fig. 1.10.4
Infection and Arthritis 21
Infectious spondylitis appears in 2–4% of cases of skeletal infection. A spinal infection may become established by hematogenous spread from distant septic foci, direct inoculation, or direct extension from septic foci in adjacent soft-tissue. The lumbar region is most often affected, followed by the thoracic spine and the cervical spine. MRI is currently the modality of choice for the evaluation of potential spinal infection. Advantages of MRI include its capabilities for multiplanar imaging, direct evaluation of the bone marrow, and simultaneous visualization of the neural structures. Imaging patterns indicative of spinal infection include decreased disk height with fluid-like signal intensity and low signal intensity on T1-weighted images, with a loss of definition and erosion of the vertebral endplate and of the adjacent vertebral bodies and high signal intensity on T2-weighted and STIR images. After administration of gadolinium, enhancement is evident in the disc and in infected bone marrow. However, early stages of spondylodiscitis may be difficult to differentiate from degenerative abnormalities (especially Modic 1 abnormalities), fractures in seronegative spondyloarthropathy (Andersson lesion), and less frequently encountered diseases such as amyloidosis. Because of the difficulties of noninvasive imaging techniques in diagnosing or excluding spondylodiscitis, some authors recommend CT-guided core biopsy of intervertebral discs and adjacent endplantes prior to treatment. CT allows definition of the extent of bone and disc destruction and of paravertebral and intraspinal involvement. Gas may be identified in the infected soft-tissue. MRI provides better definition of epidural extension of the inflammatory process and compression of the spinal cord and dural sac than CT does. Most cases are successfully managed with conservative measures, including an appropriate antibiotic and spinal bracing. Surgical intervention is warranted in only a few specific circumstances (neurologic signs, spinal instability, vertebral collapse, etc.)
Comments
Axial T1-weighted MRI (Fig. 1.10.1) at the level of the infected area shows decreased signal intensity in the T6–T7 disk (open arrow) and a hypointense mass surrounding it, corresponding to paravertebral inflammatory extension (arrow). Axial contrast-enhanced fat-suppressed T1-weighted (Fig. 1.10.2) image at the same level as in Fig. 1.10.1 shows enhancement in paravertebral and epidural tissue (open arrow), corresponding to a phlegmon. Sagittal contrast-enhanced fat-suppressed T1-weighted (Fig. 1.10.3) image shows marked enhancement of all the infected areas, i.e., both vertebral bodies (open arrow) and the intervertebral space, whose height is diminished (arrow). Note the epidural phlegmon encompassing all of T6 and T7 (open arrowhead). Sagittal CT multiplanar reconstruction (Fig. 1.10.4) 3 months later shows changes in the bony ankylosis between the two vertebral bodies (open arrow).
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Further Reading Books Artritis in black and white. Brower AC, Flemming DJ (1996). Elsevier, Amsterdam Bone and Joint Imaging. 3rd ed. Resnick D, Kransdforf MJ (2005). Elsevier, Saunders, Richmond Kelley´s Textbook of Rheumatology. 8th ed. Firestein GS, Harris ED, Ruddy S (2008). Elsevier, Saunders, Amsterdam, Philadelphia Imaging of arthritis and metabolic bone disease. Weissman B (2009). Mosby, London Rheumatology. 2d ed. Klippel JH, Dieppe PA (1998). Mosby, London
Web-Links http://www.rad.washington.edu/academics/academic-sections/ msk http://www.learningradiology.com/ http://www.indyrad.iupui.edu/public/ddaven/main.htm http://www.gentili.net/ http://chorus.rad.mcw.edu/index/6.html
Articles Aliabadi P, Nikpoor N, Alparslan L. Imaging of neuropathic arthropathy. Semin Musculoskelet Radiol 2003; 7:217–225 Azer NM, Winalski CS, Minas T. MR imaging for surgical planning and postoperative assessment in early osteoarthritis. Radiol Clin North Am 2004; 42:43–60 Bennett DL, Ohashi K, El Khoury GY. Spondyloarthropathies: ankylosing spondylitis and psoriatic arthritis. Radiol Clin North Am 2004; 42:121–134 Boutry N, Morel M, Flipo RM, Demondion X, Cotten A. Early rheumatoid arthritis: a review of MRI and sonographic findings. AJR Am J Roentgenol 2007; 189:1502–1509 Braun J, Sieper J, Bollow M. Imaging of sacroiliitis. Clin Rheumatol 2000; 19:51–57 Fayad LM, Carrino JA, Fishman EK. Musculoskeletal infection: role of CT in the emergency department. Radiographics 2007; 27:1723–1736 Hayes CW, Conway WF. Calcium hydroxyapatite deposition disease. Radiographics 1990; 10:1031–1048 Hermann KG, Althoff CE, Schneider U et al. Spinal changes in patients with spondyloarthritis: comparison of MR imaging
and radiographic appearances. Radiographics 2005; 25: 559–569 Lacout A, Rousselin B, Pelage JP. CT and MRI of spine and sacroiliac involvement in spondyloarthropathy. AJR Am J Roentgenol 2008; 191:1016–1023 Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR imaging findings in spinal infections: rules or myths? Radiology 2003; 228:506–514 Leigh MS, Rafii M. Advanced imaging of tuberculosis arthritis. Semin Musculoskelet Radiol 2003; 7:143–153 Llauger J, Palmer J, Roson N, Bague S, Camins A, Cremades R. Nonseptic monoarthritis: imaging features with clinical and histopathologic correlation. Radiographics 2000; 20 Spec No:S263–S278 McGonagle D, Gibbon W, Emery P. Classification of inflammatory arthritis by enthesitis. Lancet 1998; 352:1137–1140 Monu JU, Pope TL Jr. Gout: a clinical and radiologic review. Radiol Clin North Am 2004; 42:169–184 Narvaez J, Nolla JM, Narvaez JA et al. Spontaneous pyogenic facet joint infection. Semin Arthritis Rheum 2006; 35:272–283 Narvaez JA, Narvaez J, Roca Y, Aguilera C. MR imaging assessment of clinical problems in rheumatoid arthritis. Eur Radiol 2002; 12:1819–1828 Preidler KW, Resnick D. Imaging of osteoarthritis. Radiol Clin North Am 1996; 34:259–271, x Restrepo S, Vargas D, Riascos R, Cuellar H. Musculoskeletal infection imaging: past, present, and future. Curr Infect Dis Rep 2005; 7:365–372 Salaffi F, Carotti M, Guglielmi G, Passarini G, Grassi W. The crowned dens syndrome as a cause of neck pain: clinical and computed tomography study in patients with calcium pyrophosphate dihydrate deposition disease. Clin Exp Rheumatol 2008; 26:1040–1046 Sheldon PJ, Forrester DM, Learch TJ. Imaging of intraarticular masses. Radiographics 2005; 25:105–119 Sommer OJ, Kladosek A, Weiler V, Czembirek H, Boeck M, Stiskal M. Rheumatoid arthritis: a practical guide to state-ofthe-art imaging, image interpretation, and clinical implications. Radiographics 2005; 25:381–398 Steinbach LS. Calcium pyrophosphate dihydrate and calcium hydroxyapatite crystal deposition diseases: imaging perspectives. Radiol Clin North Am 2004; 42:185–205, vii Tehranzadeh J, Ashikyan O, Dascalos J. Advanced imaging of early rheumatoid arthritis. Radiol Clin North Am 2004; 42:89–107 Watt I. Basic differential diagnosis of arthritis. Eur Radiol 1997; 7:344–351 Wilson DJ. Soft tissue and joint infection. Eur Radiol 2004; 14(suppl 3):E64–E71
Tumors Guadalupe Garrido-Ruiz, Antoino Luna-Alcalá, and Joan C. Vilanova
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Case 2.1 Osteoblastoma of the Rib
Fig. 2.1.2
Fig. 2.1.1
Fig. 2.1.3
Fig. 2.1.4
Tumors 25
An 18-year-old man consulted for recurrent attacks of left back pain during the previous year. The episodes were occasionally associated with abdominal pain, mainly localized in the left hypochondrium. At physical examination, tender swelling was noted below the left scapula. After chest X-ray, a bone tumor was suspected at the level of the left fifth rib and CT and MRI studies were requested.
Osteoblastoma is a rare benign osteoid-producing bone neoplasm accounting for approximately 1% of primary bone tumors. Conventional and aggressive types of osteoblastoma have been described. Osteoblastomas are commonly located in the posterior elements of the spine (34%) and long bones (30%). The ribs are only affected in 4% of cases. Most lesions are intramedullary; however, intracortical and periosteal tumors can occur. The lesion is observed most frequently in individuals younger than 30 years of age. Local pain is a common manifestation. Worsening of pain at night and amelioration with salicylates are inconstant clinical features. The diagnosis of osteoblastoma may be suggested by direct visualization on X-ray or CT studies of an expansile, circumscribed lytic lesion with variable reactive sclerosis and central calcification. Cortical expansion, cortical destruction, and periosteal reaction can occur. MRI provides information on the extent of the lesion, but the MRI appearance of low signal intensity on T1- and mixed to high signal intensity on T2-weighted images is also nonspecific. MRI is the most accurate technique in evaluating the surrounding edema, which may be prominent. Scintigraphic bone scans show intense focal radiotracer accumulation. Other diagnoses that share similar clinical and radiographic features with conventional osteoblastoma include osteoid osteoma, giant cell tumor, and fibrous dysplasia. Osteoid osteoma and osteoblastoma are thought to be variant manifestations of the same osteoblastic process. The tendency of osteoblastoma to form a less sclerotic, more expansile mass and its size (by definition greater than 2 cm) are the two major differences between these two entities. Aggressive osteoblastomas may disrupt cortex and have a soft-tissue component, mimicking malignant tumors, such as osteosarcoma.
Comments
Chest X-ray shows an expansile lytic lesion with well-demarcated margins and some cortical erosion involving the posterior shaft of the left fifth rib (Fig. 2.1.1). On each side of the tumor, the rib is broadened and sclerosed. Internal calcifications are seen within the lesion (open arrow) (Fig. 2.1.2). CT scan (Fig. 2.1.3) confirms the presence of a well-circumscribed osteolytic lesion with surrounding sclerosis. Central ossification is prominent. The posterior cortex of the rib is diffusely thinned with an expanded contour and focal disruption, but no soft-tissue mass is observed. Axial STIR MR image (Fig. 2.1.4) demonstrates a well-demarcated intermediate signal intensity lesion with central calcifications. Prominent reactive marrow edema (open arrow), solid anterior periosteal reaction (arrow), and mild surrounding soft-tissue edema (open arrowhead) are also observed.
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Case 2.2 Ewing’s Sarcoma
Fig. 2.2.1
Fig. 2.2.3
Fig. 2.2.2
Fig. 2.2.4
Tumors 27
A 22-year-old man presented with pain in his right knee 1 year after anterior cruciate ligament reconstruction with a patellar tendon autograft.
Ewing’s sarcoma is the sixth most common malignant tumor, accounting for approximately 11–12% of all malignant bone tumors. The tumor is derived from red bone marrow. Ewing’s sarcoma usually occurs in young people (4–25 years) and the mean age of presentation is 13 years. The tumor has a decisively male predominance. Patients typically present systemic symptoms (fever, anemia, and leukocytosis) and a painful mass. Ewing’s sarcoma can occur in both long (60%) and flat (40%) bones. The long bones are more commonly affected in younger patients. The most common sites are the femur, tibia, and humerus. The most commonly affected flat bones (typically in older patients) are the pelvis and the ribs. In the long bones, the tumor almost always affects the metaphysis or the diaphysis. Although Ewing’s sarcoma presents multiple radiological appearances, it is typically based within the medullary cavity, metadiaphyseal in location, and poorly delineated, with aggressive periosteal reaction and a large associated soft-tissue mass. Commonly, there is a permeative lytic pattern. MRI is essential to evaluate the bone marrow and soft-tissue extent of the tumor. The typical MRI appearance of Ewing’s sarcoma includes low signal on T1-weighted sequences, high signal on T2-weighted sequences, and heterogeneous contrast enhancement. MRI provides useful information for preoperative planning and posttreatment follow-up. The differential diagnosis should include osteomyelitis, lymphoma, chondrosarcoma, Langerhans cell granuloma, and osteosarcoma. It is important to remember that age is the most important factor for narrowing the differential diagnosis for bone tumors.
Comments
Lateral plain-film radiograph of the distal femur (Fig. 2.2.1) shows a permeative lytic pattern of bone destruction. Sagittal T1-weighted MRI demonstrates the intraosseous and extraosseous extent of the tumor and the disruption of the cortex (open arrow) (Fig. 2.2.2). The tumor has lower signal intensity than normal marrow fat in this pulse sequence. Notice the hyperintensity of the patellar tendon from which the ACL graft was taken. Coronal fat-suppressed T2-weighted MRI shows a heterogeneous high signal intensity lesion within the medullar cavity and a soft-tissue mass (arrow) (Fig. 2.2.3). Axial fat-suppressed T2-weighted MRI (Fig. 2.2.4) shows the intramedullary lesion and the soft-tissue mass extending to the cortex.
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Case 2.3 Intraosseous Lipoma
Fig. 2.3.2
Fig. 2.3.1
Fig. 2.3.3
Fig. 2.3.4
Tumors 29
A 51-year-old man presented with a 6-month history of intermittent localized right heel pain, sometimes exacerbated by activity. Physical examination revealed tenderness at the medial aspect of the right heel, but no swelling. Plain-film radiographs of the right heel showed a lytic lesion in the calcaneus and a CT scan was done to characterize the lesion.
Intraosseous lipoma is a rare benign primary bone tumor. Lipomas are categorized by their relation to bone as either intraosseous, intracortical, or parosteal. Intracortical lipoma is extremely rare. Multiple osseous lipomas have been described in patients with type IV hyperlipoproteinemia. Intraosseous lipomas may be diagnosed at any age, but they are most common in the fourth through sixth decades. No significant sex predominance has been noted. While these tumors may be asymptomatic, localized pain and/or soft-tissue swelling is reported in up to two-thirds of patients. The long tubular bones are most commonly affected. The fibula (20% of cases), femur (15%), and tibia (13%) are frequently involved. Another common site of involvement is the calcaneus, which accounts for 15% of cases. Other reported sites include the ilium, skull, mandible, maxilla, ribs, spine, sacrum, coccyx, and the bones of the hands and feet. Plain films can suggest the diagnosis of intraosseous lipoma when a well-circumscribed radiolucent lesion with a thin sclerotic border is visualized in the calcaneus. A central ossified nidus may be present and lobulation or internal osseous ridges can often be seen. Cortical bone and periosteum are preserved. CT scans confirm the fat density of the mass and may demonstrate the central ossified component, if present. MRI can also be used to confirm the fatty nature of the mass, which displays fat signal intensity on all pulse sequences. Chemical shift imaging may be helpful. The diagnosis of an intraosseous lipoma in the calcaneus can be suggested by the plainfilms. However, its radiographic appearance may be similar to unicameral bone cysts, which usually appear in the same location as lipomas, in the anteroinferior portion of the calcaneus, an area free from the main stress lines. The differential diagnosis may also include normal variations of the trabecular pattern of the calcaneus, which may produce the appearance of “pseudotumor of the calcaneus,” secondary to atrophic bone trabeculae. Other, less frequent, entities that should be considered in the differential diagnosis include posttraumatic cyst, chondroblastoma, fibrous dysplasia, giant cell tumor, osteoblastoma, and desmoplastic fibroma.
Comments
Plain-film radiographs of the right heel (Figs. 2.3.1 and 2.3.2) show a well-circumscribed lytic lesion with a thin, sclerotic border and a lobulated appearance in the calcaneus. No cortical destruction or periosteal reaction is present. Lateral projection shows the location of the lesion in the triangular region of the calcaneus, between the major trabecular stress lines (Fig. 2.3.2). CT scan (Fig. 2.3.3) confirms the well-circumscribed hypodense mass, with negative Hounsfield unit values (Fig. 2.3.4), suggesting a fatty lesion.
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Case 2.4 Giant Cell Tumor of Bone
Fig. 2.4.2 Fig. 2.4.1
Fig. 2.4.3
Fig. 2.4.4
Tumors 31
A 43-year-old man presented with localized pain in his left knee that was exacerbated with movement. He had no history of trauma. At clinical examination, local swelling and tenderness were noted. Radiographs, CT, and MRI of the left knee were performed.
Giant cell tumor of bone (GCT) accounts for approximately 5–9% of primary bone tumors and 20% of benign bone tumors. GCT occurs only after the epiphyseal plates have closed. It most commonly presents in patients between the ages of 25 and 40 and has a slight female predominance. GCT can arise in any bone of the skeleton, but is most frequently detected around the knee (50%); it involves the epiphyseal regions of the distal femur and proximal tibia, although it originates in the metaphysis. GCT is a locally aggressive, generally benign lesion; however, 10% are malignant with local spread or metastases, generally to the lungs. On radiologic study, typical GCT is usually easily distinguished from other bone tumors. GCT is lytic, subarticular, and eccentric, and often lacks a sclerotic rim. Prominent trabeculation may be seen. No internal mineralization is present. CT usually adds little diagnostic information to the radiographic findings, although it is useful in regions with complex anatomy, such as the vertebrae or pelvic bones. Marginal sclerosis, cortical destruction, and soft-tissue masses are better assessed with CT scans than with radiographs. Fluid-fluid levels are seen occasionally, but are nonspecific. MRI characteristics include low to intermediate signal intensity on T1-weighted images and heterogeneous high signal intensity on T2-weighted images. Fluid levels may be demonstrated within the tumor. Peritumoral edema is uncommon in the absence of a fracture. The tumor usually enhances heterogeneously with intravenous administration of contrast medium. MRI is sensitive for the detection of soft-tissue changes, intraarticular extension, and marrow changes. MRI is the best method for assessing subchondral breakthrough and extension of tumor into an adjacent joint. The diagnostic accuracy of MRI is high, especially when it is interpreted in conjunction with plain radiographs. Bone scintigraphy is not usually required, except for the evaluation of suspected multicentric GCT. Some conditions such as aneurysmal bone cyst, intraosseous ganglion, chondroblastoma, osteosarcoma, and giant cell reparative granuloma may resemble GCT on plain-film radiographs and should be considered in the differential diagnosis.
Comments
Plain-film radiographs of the left knee (Figs. 2.4.1 and 2.4.2) show a well-defined expansile eccentric radiolucent lesion in the proximal lateral tibia condyle. No sclerotic margins or periosteal reaction is present. CT scanning (Fig. 2.4.3) demonstrates a large osteolytic lesion with marked thinning of the cortex. MRI shows a well-circumscribed lobulated lesion of low to intermediate signal intensity on T1-weighted images (not shown) and high signal intensity on T2-weighted images (Fig. 2.4.4).
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Case 2.5 Skeletal Muscle Metastases
Fig. 2.5.1
Fig. 2.5.2
Fig. 2.5.3
Fig. 2.5.4
Fig. 2.5.5
Tumors 33
A 56-year-old man diagnosed with stage IV cholangiocarcinoma 2 months before presented with a palpable mass in the posterior aspect of his left thigh. The mass was painful at palpation and surrounding soft-tissue inflammation was noted. Plain-film radiographs of the thigh showed no abnormalities. Axial T1- and T2-weighted, axial and coronal STIR, and dynamic contrast-enhanced MRI sequences were obtained. Subsequently, contrastenhanced thoracoabdominal CT scanning was carried out to evaluate and restage the primary tumor.
Skeletal muscle is a rare site of metastasis. Most muscle metastases occur in the abdominal, pectoral, deltoid, psoas, and thigh muscles. The neoplasms with the highest incidence of metastasis to muscle are carcinoma, leukemia, and lymphoma. Muscle metastases are often considered a sign of generalized tumor spread; the number and the location of the lesions are important for the patients’ clinical outcome. An intramuscular mass is first suspected to be a primary tumor rather than a metastasis. In oncologic patients with pain in large muscles and no radiographic or scintigraphic evidence of bone metastasis, soft-tissue metastases are suspected. The imaging approach to a suspected soft-tissue mass begins with a plain-film radiograph to exclude a bone lesion or deformity that could simulate a soft-tissue tumor. On unenhanced CT, muscle metastases can appear hypodense or isodense with the surrounding muscle and may only be noticed as a muscle asymmetry when compared with the opposite side. After intravenous contrast administration, muscle metastases usually present rim enhancement with central hypodensity. The advantages of MRI over CT for evaluating soft-tissue masses include multiplanar acquisition and better soft-tissue contrast resolution. MRI findings of multiple muscle lesions displaying low to intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images can suggest the diagnosis of skeletal muscle metastases, but are not pathognomonic. The use of intravenous gadolinium facilitates differentiation between tumor, muscle, and edematous tissue, and provides information on tumor vascularity. The differential diagnosis includes soft-tissue sarcomas, hematomas, and abscesses. MRI findings, together with the clinical history, should point to the correct diagnosis.
Comments
Axial T2-weighted MRI (Fig. 2.5.1) shows two soft-tissue masses, one intramuscular mass located between the vastus lateralis muscle fibers in the anterolateral aspect of the left thigh (open arrow) and the other penetrating the superficial fascia of the posterolateral aspect of the left thigh (arrow). Both lesions are surrounded by extensive edema, highlighted in the STIR image (Fig. 2.5.2). Dynamic contrast-enhanced MRI (Figs. 2.5.3 and 2.5.4) shows strong, early rim enhancement (open arrows). Contrast-enhanced abdominal CT (Fig. 2.5.5) shows a nodular lesion with rim enhancement and central hypoattenuation in the left psoas muscle (open arrow). Other nodular lesions were depicted in the right psoas and in the abdominal wall muscles (not shown); these findings supported the initial diagnosis.
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Case 2.6 Synovial Sarcoma
Fig. 2.6.2
Fig. 2.6.1
Fig. 2.6.3
Fig. 2.6.4
Tumors 35
A 39-year-old man presenting with a tender, palpable mass in the anterior aspect of the right leg and ankle that had gradually increased in size over 10–12 months and moderate weight loss over the same time period underwent MRI on a 1.5-T unit. Synovial sarcoma is a malignant neoplasm of mesenchymal origin that accounts for 8–10% of all soft-tissue sarcomas. It is the fourth most common type of soft-tissue sarcoma and usually occurs in adolescents and young adults. It predominantly affects the extremities (80– 95% of cases), usually the lower limbs, and particularly the popliteal fossa in the knee. Despite its name, the lesion occurs primarily in the para-articular regions, usually close to tendon sheaths, bursal structures, and joint capsules. Patients usually present with a slow-growing palpable soft-tissue mass or swelling. Pain and/or neurogenic dysfunctions can occur. The duration of symptoms before diagnosis varies widely, with an average of 2–4 years. Radiographic findings of a soft-tissue mass near, but not within, a joint in a young patient are very suggestive of synovial sarcoma, particularly if calcification is present. Typical cross-sectional imaging features of synovial sarcoma include multilobulated morphology and marked heterogeneity. The most common CT appearance is a soft-tissue mass isodense or slightly hypodense to muscle. CT is especially useful for detecting softtissue calcifications and cortical bone involvement. MRI findings of synovial sarcoma often include a well-defined juxta-articular mass with mainly intermediate signal intensity on T1-weighted images and intermediate to high signal intensity on T2-weighted images. Marked heterogeneity, consisting of hyperintense, hypointense, and isointense intermixed areas (the “triple signal” sign), with presence of fluid levels, hemorrhage, and septa (the “bowl of grapes” sign) on T2-weighted images is the rule in large lesions. Intense but heterogeneous enhancement is seen after intravenous gadolinium injection. Although it is not possible to make a specific diagnosis with MRI, this technique is the optimal imaging modality for assessing the extent and intrinsic characteristics of synovial sarcomas. Scintigraphic evaluation of synovial sarcomas may show increased radiotracer uptake, revealing their hypervascularization. The differential diagnosis of synovial sarcoma should mainly include other sarcomas such as soft-tissue chondrosarcoma, parosteal osteosarcoma, and malignant fibrous histiocytoma. Other disorders such as myositis ossificans, pigmented villonodular synovitis, or juxtacortical chondroma should also be considered. It is important to remember that smaller, welldefined, homogeneous lesions are more prone to mimicking cystic or solid benign lesions.
Comments
Axial (Fig. 2.6.1) and sagittal T1-weighted images (Fig. 2.6.2) show a heterogeneous multilobulated mass isointense to muscle tissue with areas of high signal intensity consistent with hemorrhage (open arrows). A pseudocapsular appearance is seen at the superior margin of the lesion (arrow). On T2-weighted images (Fig. 2.6.3), the lesion appears heterogeneous, with hyper-, hypo- and isointense areas relative to fat, creating the triple signal sign. Hemorrhagic components and fluid-fluid levels are also detected. MRI sequence acquired after intravenous injection of contrast material (Fig. 2.6.4) shows heterogeneous enhancement of the mass.
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Case 2.7 Synovial Hemangioma
Fig. 2.7.3
Fig. 2.7.1
Fig. 2.7.4
Fig. 2.7.2
Fig. 2.7.5
Tumors 37
A 23-year-old woman underwent MRI to investigate longstanding pain in the medial compartment of her right knee.
Synovial hemangiomas are rare. As in this case, the clinical history usually includes pain or other longstanding joint symptoms. Synovial hemangiomas typically present during early childhood, adolescence, or young adulthood. They most commonly involve the knee, followed by the elbow and wrist. They may appear in bursa adjacent to a joint, although hemangiomas not confined by a synovial structure should be excluded from this group, as should those arising from tendon sheaths or the intramedullary compartments of bone or skeletal muscle. The origin and pathogenesis of synovial hemangiomas are related to those of true neoplastic vascular proliferations or to the late stages of a posttraumatic lesion. The most common histological subtype is cavernous. Synovial hemangiomas are a common cause of intraarticular bleeding, which can lead to an appearance similar to pigmented villonodular synovitis or hemophilia-related arthropathy. Preoperative assessment with MRI and arthroscopy allows accurate classification and appropriate management. Wellcircumscribed masses can be excised arthroscopically, but a wide, open excision is necessary in cases of diffuse synovial hemangioma. Like hemangiomas in other locations, synovial hemangiomas typically show serpentine vascular spaces, intratumoral fat content, and increased vascularization. Focal limb enlargement due to increased vascularization has been reported in some cases of synovial hemangioma. Plain films may be unremarkable or show subtle changes like capsular thickening, phleboliths, soft-tissue density, or bone erosion. Angiography has proven useful in the evaluation of this vascular lesion, allowing the identification of fine-caliber vessels with contrast pooling in dilated vascular spaces and early visualization of venous structures. Embolotherapy has proven effective in treating synovial hemangioma. Although CT is able to detect intratumoral fat, calcifications, and enhancement, MRI’s superior soft-tissue contrast makes it the preferred imaging modality for the detection and characterization of synovial hemangiomas. Histological analysis remains necessary to confirm the diagnosis. The imaging differential diagnosis of synovial hemangioma includes pigmented villonodular synovitis, nonspecific synovitis, and lipoma arborescens. MRI is able to differentiate between these entities in most cases.
Comments
MRI shows a 50-mm intrasynovial anteromedial mass with well-defined borders and multiple internal septa. On T2-weighted sequences (Fig. 2.7.1), the mass is hyperintense with low signal septa; on fat-suppressed T1-weighted TSE sequences (Fig. 2.7.2), it showed intermediate signal intensity. After contrast administration (Fig. 2.7.3), the mass shows intense heterogeneous enhancement. In the high b-value diffusion-weighted MRI (Fig. 2.7.4) and apparent diffusion coefficient map (Fig. 2.7.5), the mass shows moderate restriction of free water movement. No hemorrhage, fat content, or infiltration of adjacent structures was demonstrated. Intraarticular fluid and enhancing synovial hypertrophy were additional features. Histological analysis confirmed the imaging suspicion of synovial hemangioma.
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Case 2.8 Brown Tumor
Fig. 2.8.1
Fig. 2.8.3
Fig. 2.8.5
Fig. 2.8.2
Fig. 2.8.4
Fig. 2.8.6
Tumors 39
A 47-year-old man with a history of giant cell reparative granuloma in his left patella resected 2 years before presented progressive pain at the symphysis pubis.
Brown tumors are expansile bone lesions typically associated to hyperparathyroidism. Their most frequent locations are the mandible, pelvis, ribs, and femora, although potentially any bone may be involved. Intratumoral hemorrhage, necrosis, and cyst formation are the hallmarks of these tumors. Brown hemorrhage stroma and giant cell formation are also common pathological findings. Recently, a progressive increase in echo time on T1-weighted sequences has been used to detect magnetic susceptibility artifacts secondary to the hemorrhagic content of brown tumors. Brown tumors appear as expansile lytic lesions with slight trabeculation, uncommon periosteal reaction, and increased activity on scintigraphic bone scans. Nowadays, it is uncommon for brown tumors to be detected as the first sign of hyperparathyroidism, as in the case presented. These tumors are destructive and may be associated to pathological fractures. They usually heal with new formation of dense bone after removal of the cause of hyperparathyroidism. Brown tumors cannot be differentiated from reparative giant cell granuloma on the basis of histological and imaging findings. In this clinical setting, correlation with analytical and clinical features to rule out hyperparathyroidism is critical for correct diagnosis and therapeutic management. This is not uncommon when dealing with bone tumors or even soft-tissue tumors, as histological analysis does not always ensure the correct diagnosis. Radiologists should be aware of this fact and integrate imaging findings with clinical and analytical data. In this case, the presence of several lytic lesions is the differentiating feature, as reparative giant cell granulomas are rarely multiple and they have not been reported in pelvic bones.
Comments
An expansive lytic lesion was detected in the right superior pubic ramus at plain-film (not shown). CT (Fig. 2.8.1.) confirmed a multiseptated expansive lytic lesion with cortical rupture and detected another lytic lesion in the posterior aspect of the contralateral superior pubic ramus. MRI showed hypointensity on both T2-weighted sequences (Fig. 2.8.2) and T1-weighted (Fig. 2.8.3) sequences, with moderate enhancement after contrast administration (Fig. 2.8.4). Additional features seen on MRI were absence of soft-tissue extension and another lytic lesion in the right femoral head. The presence of multiple lytic lesions and the personal history of reparative giant cell granuloma raised the suspicion of brown tumors. Laboratory tests showed hypercalcemia; later, primary hyperparathyroidism and the diagnosis of multiple brown tumors were confirmed. Review of the pathological specimen from the previously resected patellar tumor concluded that it also corresponded to a brown tumor. After resection of a parathyroid gland adenoma, the brown tumors partially regressed and showed a more fibrotic appearance, as seen in the 5-year follow-up MRI (Figs. 2.8.5 and 2.8.6, axial pre- and postcontrast T1-weighted TSE sequences, respectively).
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Case 2.9 Intramuscular Myxoma
Fig. 2.9.1
Fig. 2.9.2
Fig. 2.9.3
Fig. 2.9.4
Tumors 41
A 47-year-old man presented nonspecific progressive posterior thoracic pain during the nine months prior to consultation.
Intramuscular myxoma (IM) is a benign intramuscular neoplasm composed of fibroblasts and abundant myxoid stroma. This tumor usually arises in the proximal large muscles of the extremities. It is more prevalent in women and most commonly presents in the fourth and fifth decades. Clinically, it usually presents as a nonpainful palpable mass. At histological examination, it appears macroscopically as a well-circumscribed, loculated, gelatinous mass; most lesions are less than 10 cm in diameter. The classic histological description is a hypocellular, hypovascular tumor with no mitoses, composed of bland spindle cells embedded in a rich myxoid extracellular matrix. This tumor lacks a true capsule. An excisional biopsy is necessary for definitive diagnosis, since it is difficult to make an accurate evaluation with fine-needle aspiration due to its scant cellularity and nonspecific cytologic features. The association between IM and fibrous dysplasia is known as Mazabraud´s syndrome. MRI features for IM include intramuscular location, well-circumscribed margins, homogeneous hypointense signal compared to muscle on T1-weighted images, homogeneous hyperintense signal on T2-weighted images, and inhomogeneous enhancement. This tumor usually shows fine linear stranding within the tumor, representing thin fibrous septa. It is also common to find perilesional edema, which represents portions of the tumor merged into the adjacent muscle separating the fibers, which become atrophic. Another frequent finding is the presence of fat around both poles of the lesion; this finding correlates with histological findings of fatty muscle atrophy due to the infiltrative pattern of slow growth of IM. Postcontrast images commonly show a rim of peripheral enhancement, although most reported cases evaluated with contrast media had either heterogeneous internal enhancement or peripheral enhancement with occasional fine internal septa. Areas without any internal enhancement are present in about 50% of cases, corresponding to cystic areas. A complete absence of internal enhancement is possible but rare.
Comments
CT (Fig. 2.9.1) shows a well-defined hypodense mass (open arrow) located in the left thoracic paravertebral soft-tissue. MRI confirms the presence of the mass (arrow), which is hyperintense on T2-weighted sequences (Fig. 2.9.2) and homogeneously hypointense (open arrowhead) on T1-weighted sequences (Fig. 2.9.3). After contrast administration, heterogeneous internal enhancement indicates its solid nature (Fig. 2.9.4). Additional detectable features were peritumoral edema in the adjacent soft-tissue and fat around the lesion. Histological examination after resection confirmed the diagnosis of IM.
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Case 2.10 Soft-Tissue Liposarcoma
Fig. 2.10.1 Fig. 2.10.2
Fig. 2.10.3
Fig. 2.10.4
Tumors 43
A 22-year-old man presented with a painless tender mass in the upper left supraclavicular region.
Liposarcoma is a malignant tumor of mesenchymal origin. The term liposarcoma does not imply that the tumor is derived from fat, but rather that the tumor contains differentiated adipose tissue. Liposarcoma is the second most common soft-tissue sarcoma seen in adults (10–18%) after malignant fibrous histiocytoma. Liposarcomas are classified into four histologic subtypes: well-differentiated, myxoid, round cell, and pleomorphic. Well-differentiated liposarcoma is synonymous with atypical lipoma. Between 40 and 65% of liposarcomas of the extremities occur in the thigh. Other common sites, in order of descending frequency, are the upper arm and shoulder, popliteal fossa and lower leg, buttocks, and forearm. Clinically, these tumors manifest as painless masses. The radiological features of a liposarcoma depend on its histologic type and tend to reflect its degree of differentiation. CT or MRI findings for well-differentiated liposarcomas closely resemble those of subcutaneous fat or a simple lipoma. They are frequently composed of more than 75% fat, while the other types usually have less than 25%. On CT, a well-differentiated liposarcoma may appear as a well-delineated mass, with attenuation values equal to those of simple fat, mimicking a benign lipomatous tumor. On MRI, a well-differentiated liposarcoma shows some thickened linear or nodular softtissue septa that enhance after intravenous administration of contrast material. These small nonlipomatous components have low signal intensity on T1-weighted images and increased signal intensity on fat-suppressed T2-weighted images. Features for discriminating a well-differentiated liposarcoma from a simple lipoma include a deep (intramuscular) rather than subcutaneous location, a size of more than 10 cm in maximum diameter, the presence of nodular nonadipose components or thick septa, high signal intensity of septa or nodular soft-tissue areas on T2-weighted fat suppression or STIR images, and contrast enhancement of nonadipose components (best seen on fat-suppressed T1-weighted images).
Comments
MRI is the most specific modality for diagnosing liposarcoma. Figure 2.10.1 shows an axial T1-weighted image of a large mass located in the left supraclavicular region, posterior to the sternocleidomastoideus muscle and medial to the scalene muscles and brachial plexus. The tumor is predominantly isointense to subcutaneous fat. Multiple thickened septa extend throughout the tumor (open arrow). Axial T2-weighted MRI (Fig. 2.10.2) shows the tumor with signal intensity similar to that of subcutaneous fat and the presence of thick, low signal intensity septa (arrow). Coronal STIR MRI (Fig. 2.10.3) shows the nonadipose areas with increased signal intensity relative to fat (open arrowhead). Axial fat-suppressed T1-weighted MRI (Fig. 2.10.4) obtained after contrast administration shows moderate heterogeneous enhancement of the nonadipose areas (arrowhead).
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Further Reading Books Bone and Joint Imaging. 2nd ed. Resnick D (1998) W.B. Saunders, Philadelphia, PA Imaging of Bone Tumors and Tumor-Like Lesions. Techniques and Applications. Davies AM, Sundaram M, James SLJ (2009) Springer, Berlin Imaging of Soft Tissue Tumors. 2nd ed. De Schepper AM, Parizel PM, De Beuckeleer L, Vanhoenacker F (eds) (2001) Springer, Berlin Radiology Review Manual. 6th ed. Dähnert W (2007) Lippincott Williams & Wilkins, Philadelphia, PA Soft Tissue Tumors. 3rd ed. Enzinger FM, Weiss SW (eds) (1995) Mosby St Louis, Mo
Web-Links http://www.auntminnie.com// http://www.eurorad.org// http://www.bonetumor.org// http://www.emedicine.medscape.com// http://www.umdnj.edu/tutorweb
Articles Alyas F, James SL, Davies AM, Saifuddin A. The role of MR imaging in the diagnostic characterisation of appendicular bone tumours and tumour-like conditions. Eur Radiol 2007; 17:2675–2686 Berquist TH, Ehman RL, King BF, Hodgman CG, Ilstrup DM. Value of MR imaging in differentiating benign from malignant soft-tissue masses: study of 95 lesions. AJR Am J Roentgenol 1990; 155:1251–1255 Binkovitz LA, Berquist TH, McLeod RA. Masses of the hand and wrist: detection and characterization with MR imaging. AJR Am J Roentgenol 1990; 154:323–326 Bodner G, Schocke MFH, Rachbauer F et al. Differentiation of malignant and benign musculoskeletal tumors: combined color and power doppler US and spectral wave analysis. Radiology 2002; 223:410 Brown KT, Kattapuram SV, Rosenthal DI. Computed tomography analysis of bone tumors: patterns of cortical destruction and soft tissue extension. Skeletal Radiol 1986; 15:448–451 Crim JR, Seeger LL, Yao L, Chandnani V, Eckardt JJ. Diagnosis of soft-tissue masses with MR imaging: can benign masses be differentiated from malignant ones? Radiology 1992; 185:581–586 Dalinka MK, Zlatkin MD, Chao P, Kricum ME, Kressel HY. The use of magnetic resonance imaging in the evaluation of bone and soft-tissue tumors. Radiol Clin North Am 1990; 28:461–470
Hayes CW, Conway WF, Sundaram M. Misleading aggressive MR imaging appearance of some benign musculoskeletal lesions. RadioGraphics 1992; 12:1119–1136 Kransdorf MJ. Benign soft-tissue tumors in a large referral population: distribution of specific diagnoses by age, sex, and location. AJR Am J Roentgenol 1995; 164:395–402 Kransdorf MJ. Malignant soft-tissue tumors in a large referral population: distribution of diagnoses by age, sex, and location. AJR Am J Roentgenol 1995; 164:129–134 Kransdorf MJ, Murphey MD. Radiologic evaluation of soft-tissue masses: a current perspective. AJR Am J Roentgenol 2000; 175:575–587 Llauger J, Palmer J, Monill JM, Franquet T, Bague S, Roson N. MR imaging of benign soft-tissue masses of the foot and ankle. RadioGraphics 1998; 18:1481–1498 Ma LD, Frassica FJ, Scott WW, Fishman EK, Zerhouni EA. Differentiation of benign and malignant musculoskeletal tumors: potential pitfalls with MR imaging. RadioGraphics 1995; 15:349–366 May DA, Good RB, Smith DK, Parsons TW. MR imaging of musculoskeletal tumors and tumor mimickers with intravenous gadolinium: experience with 242 patients. Skeletal Radiol 1997; 26:2–15 Miller TT. Bone tumors and tumor-like conditions: analysis with conventional radiography. Radiology 2008; 246:662–674 Murphey MD, Robbin MR, McRae GA, Flemming DJ, Temple HT, Kransdorf MJ. The many faces of osteosarcoma. RadioGraphics 1997; 17:1205–1231 Narvaez JA, Narvaez J, Aguilera C, De Lama E, Portabella F. MR imaging of synovial tumors and tumor-like lesions. Eur Radiol 2001; 11:2549–2560 Nomikos GC, Murphey MD, Kransdorf MJ, Bancroft LW, Peterson JJ. Primary bone tumors of the lower extremities. Radiol Clin North Am 2002; 40:971–990 Panicek DM, Gatsonis C, Rosenthal DI et al. CT and MR imaging in the local staging of primary malignant musculoskeletal neoplasms: report of the Radiology Diagnostic Oncology Group. Radiology 1997; 202:237–246 Salamipour H, Jimenez RM, Brec SL, Chapman VM, Kalra MK, Jaramillo D. Multidetector row CT in pediatric musculoskeletal imaging. Pediatr Radiol 2005; 35:555–564 Schoenberg NY, Beltran J. Contrast enhancement in musculoskeletal imaging. Radiol Clin North Am 1994; 32:337–352 Stacy GS, Mahal RS, Peabody TD. Staging of bone tumors: a review with illustrative examples. AJR Am J Roentgenol 2006; 186:967–976 Sundaram M, McLeod RA. MR imaging of tumor and tumor-like lesions of bone and soft tissue. AJR Am J Roentgenol 1990; 155:817–824 Vilanova JC, Woertler K, Narváez JA et al. Soft-tissue tumors update: MR imaging features according to the WHO classification. Eur Radiol 2007; 17:125–138 Zimmer WD, Berquist TH, McLeod RA et al. Bone tumors: magnetic resonance imaging versus CT. Radiology 1985; 155:709–718
Tendons and Muscles Rosa Mónica Rodrigo, Mario Padrón, and Eugenia Sanchez-Lacalle
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Case 3.1 Tennis Leg Injury
Fig. 3.1.1
Fig. 3.1.2
Fig. 3.1.3
Fig. 3.1.4
Tendons and Muscles 47
A 22-year-old male professional basketball player felt a sharp burning pain in the mid-calf, associated with a snapping sensation during training.
Tennis leg is a common injury in tennis, basketball, and soccer players, but it can also occur in middle-aged people during daily activities such as hurried running, walking, or climbing stairs. It is often related to an indirect mechanism (extension of the knee and forced dorsiflexion of the ankle). The medial (MG) and lateral (LG) heads of the gastrocnemius converge in the middle of the calf through a myotendinous junction (MTJ) into a broad flat tendon. The tendon of the gastrocnemius becomes the attachment of the underlying aponeurosis of the soleus muscle. The tendons of both muscles (gastrocnemius and soleus) are parallel to each other for a distance until they narrow and form the Achilles tendon about 15 cm above the heel. The plantaris muscle (absent in 7–20% of limbs) consists of a small muscle that originates from the lateral supracondylar line just superior and medial to the lateral head of the gastrocnemius muscle and a long slender tendon that follows an oblique course between the medial head of the gastrocnemius and soleus muscle and is inserted into the calcaneus, just anteromedial to the Achilles tendon. The pathogenesis of tennis leg is more commonly related to the distal MTJ rupture of the medial gastrocnemius (complete or partial) and is less commonly related to soleus or plantaris muscle ruptures. These muscle tears in the calf involving the MG and soleus typically occur along their attachment to the aponeuroses and are also known as muscleaponeurosis avulsion. Magnetic resonance imaging (MRI) and ultrasonography are both good tools to diagnose this entity. MRI is also useful in differentiating between other serious causes of calf pain, such as deep vein thrombosis, compartment syndrome, and Achilles tendon rupture. The most common finding is a serous-sanguineous fluid collection between the aponeuroses of the MG and soleus muscles. The amount of fluid can inexplicably increase with time. The fluid often surrounds the gastrocnemius bellies (MG more frequently) and edema is usually seen in the ruptured muscle. A capsulated hematoma sometimes develops and a laminar fibrous scar is often seen as the result of this rupture, which can be symptomatic on occasions.
Comments
Axial inversion recovery-weighted FSE MRI (Fig. 3.1.1) shows fluid (open arrow) separating the fascial planes between the medial gastrocnemius (MG) and soleus, as well as edema (arrow) in the MG muscle (as a result of a complete distal myotendinous tear). At a more caudal level (Fig. 3.1.2), note the fluid surrounding the MG muscle (empty arrow) and edema within the muscle itself (arrow). Sagittal T2-weighted fat-suppressed FSE MR image at the MTJ of the MG (Fig. 3.1.3) reveals a total tear surrounded by fluid (open arrow) and an elevated GM muscle (arrow). MRI acquired in the same sequence and plane after 1 month of inadequate treatment (Fig. 3.1.4) shows that the lesion has developed into a capsulated fluid collection (open arrow) that needs to be drained.
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Case 3.2 Hamstring Muscle Injury Comments
A 30-year-old male professional basketball player consulted for acute posterior thigh pain (10 cm below the gluteal fold) that started when trying to make a catch during a game; the lesion swelled and he was forced to abandon the game immediately.
The hamstring muscle (HM) complex is one of the most frequently injured muscles in the general population (as they increase their level of fitness) and in athletes (especially soccer and basketball players). HM strains and tears typically occur during running. Risk factors for this strain include, among others, increasing age and a prior history of posterior thigh pain (hamstring strain or back pain). Thorough knowledge of the relevant anatomy is essential to enable accurate diagnosis. The HM complex consists of the semimembranosus (SM), semitendinosus (ST), and biceps femoris (BF) muscles. At MR, two different rounded areas of low signal intensity can be seen at the ischial tuberosity (IT); these represent the conjoined tendon (ST/BF) arising
Fig. 3.2.1
Fig. 3.2.2
Fig. 3.2.3
Fig. 3.2.4
Tendons and Muscles 49
from the inferomedial aspect of the IT and the SM tendon arising from its superomedial aspect (anterior to the conjoined tendon). The bulbous ST muscle is the first muscle seen (just below the IT), with the SM tendon (the largest of the HM complex) lying anterior to it. The SM muscle originates beneath the proximal half of the ST muscle, and its distal tendon is attached to the posteromedial tibia in several locations. The BF muscle (long head) occupies the most lateral compartment in the posterior thigh, beside the ST muscle, and its main distal attachment is inserted in the head of the fibula. The ST muscle continues to the anteromedial aspect of the proximal tibia, joining the gracilis and sartorius, to be inserted as the pens anserine complex. It is important to note that the MTJ, which is the weakest link in the HM complex and the most frequently overstretched component, is a very extensive area in these muscles (as each HM has a tendon extending, completely or almost completely, down the length of the muscle); thus, injuries can occur not only in the proximal or distal MTJ, but also in the intramuscular MTJ. The proximal MTJ and BF are the most frequently injured and it is even more common to have more than one HM injured. MRI provides excellent visualization of HMC injuries, and an accurate diagnosis is easily obtained, even of low grade strain injuries (which can be missed at US). A feathery pattern of intramuscular edema is seen in grade 1 strains. Grade 2 injuries are partial tears of the MTJ without retraction, with intramuscular edema, distortion of the well-defined black tendon, perifascial fluid beyond the muscle margin, and frequent hematomas (the appearance of which varies according to its age) within the muscle or outside the epimysial covering (fascia) between the muscles. Grade 3 represents a complete disruption with retraction of the musculotendinous elements. Axial fat-suppressed T2-weighted FSE MR images at different levels show this grade 2 BF strain injury in the proximal MTJ. At the IT level (Fig. 3.2.1), the proximal SM tendon remains attached to the anterior IT (empty arrow), the conjoined ST/BF tendon remains normal at its posterior attachment (full arrow), and perifascial edema (empty arrowhead) is seen between muscular planes. An image obtained below the IT level, at the proximal MTJ of the HM complex (Fig. 3.2.2), shows a blurred and ruptured conjoined BF/ST tendon with intramuscular edema in the BF and ST (open arrow) muscles, a normal SM tendon (empty arrowhead), and perifascial fluid surrounding the HMC and the normal sciatic nerve (arrowhead). Intramuscular edema is also seen in the adductor magnus and gluteus maximus. An image acquired at a more caudal level (Fig. 3.2.3) shows a hypointense hematoma (empty arrow) between the SM tendon (arrow) and the sciatic nerve (empty arrowhead), a thicker defined conjoined BF/ST tendon (arrowhead), intramuscular edema, and a fluid collection surrounding the HMC. An image acquired using the same sequence and plane (at the same level as in the previous figure) 1 month later (Fig. 3.2.4) shows that the hematoma (open arrow) has become smaller and isointense to fluid; the perifascial fluid has disappeared (although some intramuscular edema remains), and some high signal intensity areas have been replaced by areas of low signal intensity (arrow). The low signal areas correspond to fibrosis and blood products, which partially envelop the sciatic nerve (open arrowhead) and alter its morphology. This player complained of temporary sciatic pain for some time.
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Case 3.3 Indirect Rectus Femoris Strain Injury Comments
A 20-year-old male professional soccer player (Figs. 3.3.1 and 3.3.2) complained of progressive pain when kicking and sprinting while training.
Rectus femoris (RF) muscle injuries are common in soccer players. Unlike hamstring and tennis leg injuries, RF muscle injuries are not related to age. They occur due to an indirect mechanism during
Fig. 3.3.2 Fig. 3.3.1
Fig. 3.3.3
Fig. 3.3.4
Tendons and Muscles 51
activities with eccentric contraction, such as sprinting and kicking. Predisposing factors include muscle fatigue, insufficient warm-up exercises, and a previous tear, among others. Thorough knowledge of the anatomy of the MTJ of the RF is essential to understand the different injuries to this muscle. The RF is a long, fusiform muscle on the anterior superficial portion of the quadriceps muscle group. It has two proximal tendinous insertions above the hip: the direct (straight) head, arising from the anterior inferior iliac spine (AIIS) and the indirect (reflected) head, arising more inferiorly and posteriorly from the superior acetabular ridge and hip joint capsule. Both heads form a conjoined tendon a few centimeters below their origins. The direct head, forming most of the anterior part of the conjoined tendon, blends more distally with the anterior fascia of the RF. The indirect head, which forms most of the posterior component of the conjoined tendon, becomes intrasubstance and forms a long intramuscular MTJ, extending approximately along two thirds of the length of the muscle. Indirect (reflected) tendon injuries are usually clinically classified as a contracture because the pain is usually progressive and players usually complain of a sharp pain when kicking and sprinting. A hard cord is usually palpated along the length of the intramuscular MTJ. MRI is extremely useful in the diagnosis of an indirect tendon injury. Different degrees of edema are seen surrounding the central indirect tendon on fat-suppressed T2-weighted images. A “bull´s eye” pattern of injury is commonly seen in axial images and a “featherlike” pattern is usually seen in coronal images. As the degree of injury increases, a different amount of hemorrhage and fluid are usually seen surrounding the muscle below the fascia or through the fascia, even between intermuscular planes. A “muscle into a muscle” tear pattern has also been described, as the hemorrhage surrounds the indirect head tendon and separates it from the rest of the RF muscle. These indirect injuries usually respond to conservative therapy; afterwards, an irregular focal scar of the indirect tendon is frequently seen where the rupture was more evident.
Axial fat-suppressed T2-weighted FSE MR image of a professional soccer player (Fig. 3.3.1) shows a grade 1 injury with increased signal intensity (open arrow) surrounding the indirect MTJ of the left RF (described as an “acute bull’s eye” pattern) and a tiny focal discontinuity in the tendon (full arrow) with no fascial hemorrhage. Coronal fat-suppressed T2-weighted FSE MR image (Fig. 3.3.2) shows increased signal intensity surrounding part of the long length of the indirect MTJ (open arrow) of the RF in a “feather-like” pattern. Axial fat-suppressed T2-weighted FSE MR image of a different 20-year-old professional basketball player (Fig. 3.3.3) shows a more serious lesion (grade 2) in a swollen left RF, with huge muscular edema surrounding the indirect MTJ and hemorrhage separating this indirect MTJ (open arrow) from the rest of the muscle, in a “muscle into a muscle” lesion pattern. Hemorrhage is seen beyond the fasciae of the rectus and vastus lateralis (on the anterior border of these muscles) and between the intermuscular plane with the sartorious (arrow). The same sequence and plane 40 days later (Fig. 3.3.4) shows no fascial hemorrhage and a dark line (empty arrow) of hemosiderin and fibrous tissue (surrounding the indirect MTJ) with faint residual edema.
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Case 3.4 Adductor Muscle Strain Injury
Fig. 3.4.1
Fig. 3.4.3
Fig. 3.4.2
Fig. 3.4.4
Tendons and Muscles 53
A 25-year-old male professional soccer player complained of a stabbing inner thigh pain during a match, which later became more diffuse with swelling and bruising.
Adductor strain injuries are most frequently seen in hockey, tennis, and soccer players. The injury usually occurs when a strong eccentric contraction of the adductor musculature is required, such as during rapid acceleration (sprinting), side to side movements, sudden stops and changes of direction, and rapid movements of the leg against resistance (such as kicking a ball). Risk factors include periods of prolonged overuse, a sudden increase in the amount or intensity of activity, and insufficient adductor muscle strength, among others. The adductor musculature is divided into short adductors, which go from the pubis to the femur (the pectineus, adductor brevis, and adductor longus), and long adductors, which go from the pelvis to the knee (gracilis and adductor magnus). The most commonly injured muscle is the adductor longus (ABL) muscle, which connects the anterior pubic ramus to the linea aspera of the femur. ABL injury usually occurs at the MTJ or at the junction between the tendon and pelvic bone, with acute adductor strain commonly occurring at the MTJ and chronic injuries being more frequent in the junction between the tendon and pubic ramus. MRI enables accurate diagnosis and classification of ABL strain MTJ injuries. In Grade 1, intramuscular edema is found. In grade 2 (partial rupture), blurring of the MTJ, intramuscular edema, intermuscular fluid, and sometimes hematoma are seen. In grade 3 strain injuries, total discontinuity of the MTJ is present together with all the above signs.
Comments
Axial fast gradient-recalled (FGR) MR image at the MTJ of the adductor longus (just below its insertion) (Fig. 3.4.1) shows a left adductor MTJ (open arrow) (clearly seen in the inner part of the ABL muscle) and a blurred and partial torn right ABL MTJ (arrow) with edema surrounding it. Below the previous slice (Fig. 3.4.2), a small hematoma (empty arrow) between the ABL muscle and the fascia defines this as a grade 2 lesion; a better-defined tendon remains with edema surrounding it, and extramuscular perifascial fluid is seen surrounding the MTJ medially (arrow). A closer view (FOV 24) of axial fat-suppressed T2-weighted FSE MR image at the same level (Fig. 3.4.3) shows the MTJ edema, the blurred tendon, and a less clearly defined hematoma (open arrow) than in the previous FGR MR image, which is more sensitive for blood. Perifascial edema surrounds the ABL muscle below the fascial plane, which is seen as a fine black line (arrow), and outside the fascia. The same sequence and plane (at the same level) 44 days later (Fig. 3.4.4) shows the fascia joined to the muscle (as the hematoma and perifascial liquid have disappeared), less intramuscular edema, and some fibrosis and blood products (arrow) surrounding the MTJ. It is interesting to note that although some edema was still seen at this time, the player was ready for the first match and full training the day after this MRI.
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Case 3.5 External Hip Rotator Muscle Injury
Fig. 3.5.1
Fig. 3.5.3
A 23-year-old male professional soccer player complained of acute pain in the groin (without ecchymosis or swelling in the area) that caused him to withdraw from the match.
Fig. 3.5.2
Fig. 3.5.4
Tendons and Muscles 55
External hip rotator muscle strain injuries are an uncommon sports injury, seen mostly in soccer players. Although these lesions are uncommon, it is important to have knowledge of them, as they can be serious and require a long recovery period for soccer players. These injuries usually occur with the adduction and rotation of the hip, which occur frequently during training in soccer players. The pain is usually first diagnosed as an adductor strain injury. However, although the adductor stress test provokes vague pain, unlike adductor strain injuries, external hip rotator muscle strain causes pain in the gluteal area and occasionally in the groin area (as the external hip rotator muscles are in tension) on the internal rotator hip test. A more careful physical examination and an MRI study are needed if these lesions are suspected. The external hip rotator muscles are the quadratus femoris muscle, obturator externus and internus muscles, piriformis muscle, and inferior and superior gemellus muscles. The most frequently injured are the quadratus femoris and obturator externus muscles. The quadratus femoris extends from the lateral border of the IT and inserts in the intertrochanteric crest on the posterior surface of the femur between the trochanters. The obturator externus extends from the medial side of the obturator foramen and the obturator membrane and inserts distally as a tendon in the trochanteric fossa, where the greater trochanter joins the neck on the posterior surface of the femur. MRI is an excellent tool for the evaluation of injuries to the external hip rotator muscles. Ultrasonography can miss lesions to these muscles because they are located deep within the hip. Grade 1 injuries are seen as diffuse intramuscular edema and grade 2 injuries are seen as intramuscular edema, perifascial fluid beyond the muscle margin, and hematomas. Grade 3 injuries are uncommon in this group of muscles.
Comments
Axial fat-suppressed T2-weighted FSE MR image (Fig. 3.5.1) shows a grade 1 injury of the right obturator externus muscle, with intramuscular edema in the obturator foramen and obturator membrane insertion (open arrow), with no edema in the distal portion of the muscle (arrow). Coronal fat-suppressed T2-weighted FSE MR image (Fig. 3.5.2) shows diffuse edema within the medial aspect of the belly of the right obturator externus muscle (open arrow) without hematoma. Coronal fat-suppressed T2-weighted FSE MR image of both thighs in a different 20-year-old professional soccer player who complained of right groin pain during training (Fig. 3.5.3) shows intramuscular edema in the right obturator externus muscle near the trochanteric fossa (open arrow) with some perifascial fluid (arrow) surrounding it. Axial fat-suppressed T2-weighted FSE MR image in a different 17-year-old semiprofessional soccer player who complained of acute subgluteal posterior thigh pain during a match (Fig. 3.5.4) shows edema in the belly of the right quadratus femoris (open arrow) without hematoma and with a large amount of perifascial edema in the intermuscular plane. This sequence also shows lesions of the obturator internus and adductor magnus muscles (arrow) and a partial avulsion of the right ischial apophysis as a disruption in the cortex of the IT (open arrowhead) with edema and hemorrhage in the surrounding softtissue. The ischiotibial tendons are free of lesions, and the sciatic nerve, running immediately posterior to the quadratus femoris muscle (arrowhead), appears normal.
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Case 3.6 Chronic Avulsion of the Ischial Tuberosity
Fig. 3.6.1
Fig. 3.6.2
Fig. 3.6.3
Fig. 3.6.4
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A 17-year-old male soccer player presented with pelvic pain several months after experiencing repeated pain in the gluteal fold region.
Avulsion injuries occur at several sites in the pelvis, the most common of which is the ischial tuberosity (IT), where the hamstrings (HMs) insert. Avulsions occur before closure of the apophysis. Acute injuries are caused by extremely active contraction of the hamstrings during sprinting. Patients typically present with pain in the buttock region and inability to walk. Chronic avulsion injuries are the result of repetitive microtrauma or overuse and usually occur during sporting activities. At radiography, healing avulsions may have an aggressive appearance resulting from new bone formation and may resemble neoplastic or infectious processes. CT may be helpful in diagnosis and in planning treatment. Surgical excision of malunited or hypertrophic fragments may relieve pain.
Comments
Anteroposterior radiograph of the pelvis shows overgrowth and widening of the right ischium with new bone formation together with lytic and sclerotic areas with no periosteal reaction and adjacent soft-tissue calcification (Fig. 3.6.1). Coronal T1-weighted MR image shows a left ischium bony protuberance with broad insertion of the right HMs (Fig. 3.6.2). Coronal fat-suppressed proton density-weighted images show a bony irregularity at the tendon insertion with fluid-filled signal intensity surrounding the new bone formation (Figs. 3.6.3. and 3.6.4). The hamstring insertion is intact and no changes in signal intensity are evident in the adjacent bone.
Findings
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Case 3.7 Acute Avulsion of the Anteroinferior Iliac Spine
Fig. 3.7.1 Fig. 3.7.2
Fig. 3.7.3
Fig. 3.7.4
Tendons and Muscles 59
An 18-year-old male soccer player presented with sudden groin pain and gait dysfunction after an “air kick.”
Avulsion injuries are common lesions among adolescents participating in organized sports. Acute injuries result from extreme, unbalanced, and often eccentric muscular contraction and may be associated with avulsed bone fragments. Most often, the injury is abrupt and a clear history is available. The patient presents with severe pain and loss of function. Avulsion fracture of the anteroinperior iliac spine (AIIS) is common in young soccer players; it results from forceful extension at the hip and is very common after a failed kick at the ball. The AIIS is the origin of the straight head of the RF muscle. The proximal RF has two tendinous origins: the direct (straight) head arising from the AIIS and the indirect (reflected) head arising slightly more inferiorly and posteriorly from the superior acetabular ridge and hip joint capsule. The two heads form a conjoined tendon a few centimeters below their origins. Injured patients typically present with groin pain, an antalgic gait, or inability to walk. A nondisplaced avulsion of the AIIS appears as a curved, sharply margined piece of bone adjacent to its origin. Patients with injuries of this type tend to respond well to conservative treatment such as several days of bed rest and restricted activity over the next 6 weeks. If the fragment is displaced more than two centimeters, however, fibrous union may occur resulting in extended disability.
Comments
Coronal fat-suppressed proton density-weighted MR image shows a fracture line with high signal intensity at the insertion of the direct head of the RF with preserved tendon integrity and slight displacement of the bony attachment (Fig. 3.7.1). Contiguous sagittal fat- suppressed proton density-weighted MR images show the fracture line, tendon integrity, and adjacent soft-tissue damage (Figs. 3.7.2 and 3.7.3). Axial fat-suppressed proton density-weighted image shows mild displacement of the AIIS with fluid signal intensity in surrounding soft tissues due to edema and hemorrhage (Fig. 3.7.4)
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Case 3.8 Patellar Tendinopathy: Partial Tear
Fig. 3.8.1 Fig. 3.8.2
Fig. 3.8.3
Fig. 3.8.4
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A 20-year-old male athlete complained of anterior knee pain and tenderness at palpation with the knee at full extension and relaxed patellar tendon (Basset sign).
The patellar tendon is vulnerable to overuse-type injuries. In adolescents, Osgood Schlatter disease and Sinding-Larsen-Johansson syndrome are traction-type injuries affecting the tibial tubercle and proximal end of the patellar tendon, respectively. These two conditions have a good prognosis and resolve with conservative management. Patellar tendinopathy was first related to jumping and was commonly referred to as “jumper’s knee.” The term tendinopathy has been accepted by most orthopedic and sports-related physicians and can be used to describe both acute and conditions and those resulting from overuse. Histological study reveals mucoid and myxomatous degeneration and regeneration with increased cellularity and neovascularization of the proximal tendon. The probable mechanism of injury is impingement of the tendon by the inferior pole of the patella. The pathogenesis of patellar tendinopathy is complex, and exactly how extrinsic (repetitive mechanical overload) and intrinsic (malalignment, impingement of the inferior pole) factors combine to trigger the degeneration of the patellar tendon has yet to be established. Patellar tendinopathy can be assessed with US and MRI. Characteristic sonographic features include focal or diffuse hypoechogenicity, tendon thickening, irregularity of the tendon envelope, swelling of surrounding structures, and increased vascularity on color Doppler. Calcifications are not uncommon. On MRI, the tendon shows increased signal intensity on T1-weighted images and on fluid-sensitive pulse sequences. Focal or fusiform thickening of the tendon is another typical finding. Focal discontinuity with the signal intensity of fluid has been associated with partial tears. The injury usually affects the osteotendinous junction. Findings typically occur in the deep posterior portion of the patellar tendon adjacent to the lower pole of the patella. Imaging techniques still have some limitations in the evaluation of tendinopathy, so further research is needed.
Comments
Sagittal proton density-weighted and gradient-echo MR images show marked thickening of the patellar tendon with increased signal intensity in the proximal third of the tendon due to tendinopathy and partial tear in the midsubstance of the tendon (Figs. 3.8.1 and 3.8.2). US correlation shows decreased echogenicity along the tendon substance and a focal area of hypoechogenicity with increased neovascularization that corresponds to the partial tear (Figs. 3.8.3 and 3.8.4).
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Case 3.9 Posterior Tibial Tendon Dysfunction
Fig. 3.9.1
Fig. 3.9.2
Fig. 3.9.3
Fig. 3.9.4
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A 76-year-old woman diagnosed with sprain after a fall presented 2 months later because her ankle was still swollen; physical examination showed selective pain and tenderness on palpation of the posterior tibial tendon.
Partial or complete rupture of the posterior tibial tendon is a relatively frequent syndrome in women in their fifth or sixth decades; the left side is affected more often. Posterior tibial tendon rupture has also been reported in young athletes (soccer, tennis, ice-hockey, and gymnastics). It may present as a painful mass in the medial aspect of the foot, swelling, or tenderness, associated with progressive flat-foot deformity. Posterior tibial tendon rupture can be caused by trauma, degenerative changes, inflammatory arthritis, seronegative spondyloarthropathies, infections, or abnormal insertion in an accessory navicular. Typically, the mid-portion of the tendon is affected at the level of or immediately distal to the medial malleolus; this area corresponds to a zone of relative hypovascularity. Three types of posterior tibial rupture have been described: Type I: the tendon is thickened, with longitudinal tears producing a striated appearance on MR images. Type II: the tendon is markedly attenuated with variable intratendinous signal intensity changes on MR images. Type III: a complete tear seen as discontinuity with a low to intermediate signal intensity fluid-filled gap on MR images; subtendons are present in partial tears. Associated peritendinous inflammatory changes can be present in all three types. In cases with associated tenosynovitis, hyperintense fluid with degeneration and tendon tears are seen. Other findings associated include hypertrophy of the medial navicular tubercle, abnormal talonavicular alignment, accessory navicular, loss of the longitudinal arch, and, less commonly, dislocation associated with disruption of the flexor retinaculum.
Comments
Sagittal T1-weighted MRI (Fig. 3.9.1) shows a thickened tendon, with an intermediate signal intrasubstance; fat-suppressed proton density-weighted image shows a longitudinal split (Fig. 3.9.2). Axial fat-suppressed proton density-weighted image (Fig. 3.9.3) shows several subtendons and hyperintense fluid within the tendon in a type II posterior tibial tendon tear; a hyperintense signal within the peritendinous fat is also present. On axial T1-weighted images (Fig. 3.9.4), the tendon is enlarged and attenuated at the level of the medial malleolus.
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Case 3.10 Partial Rupture of the Aquilles Tendon with Tendinosis
A 32-year-old male professional soccer player complained of acute Achilles tendon pain that forced him to withdraw from training. Although he had been previously asymptomatic during that season, he had complained of discomfort and stiffness in the Achilles region in previous seasons (3 years before).
Comments Achilles tendon injuries are commonly associated with strenuous physical activities such as running and jumping. Achilles tendon injuries are classified as either noninsertional or insertional. Noninsertional tendinopathy (located 2–6 cm from the tendon insertion within the hypovascular watershed zone) ranges from tendinosis (noninflammatory pathology) to partial and full-thickness tears. Insertional tendinopathy includes insertional tendinosis and retrocalcanear bursitis, which often coexist. It is interesting to point out that terms like “tendinitis,” “tendonitis,”
Fig. 3.10.1
Fig. 3.10.2
Fig. 3.10.3
Fig. 3.10.4
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“degenerative changes,” “chronic tendinopathy,” and “achillodynia” all involve changes in the Achilles tendon that can be defined as “tendinosis.” Although most patients who sustain a spontaneous rupture have never had any symptoms in the Achilles tendon before the rupture, histopathologic studies on ruptured tendons have shown that almost all subjects have clear degenerative changes. The terms “tendinosis” and “partial rupture” are difficult to distinguish, especially in patients with longstanding symptoms, where the clinical and imaging findings are frequently identical. Partial rupture is most often associated with a sudden onset of pain, whereas in tendinosis pain increases gradually. However, a condition in which tendon pain increases gradually might have started with a minor partial rupture; therefore, tendinosis and partial rupture may in fact be coexisting or may possibly be regarded as the same condition. The Achilles tendon is the strongest, largest, and thickest tendon in the human body; it is formed by collagen fibers running from the two heads of the gastrocnemius and deeper soleus muscles. The tendon is enclosed in a paratendon (fibrous tissue with blood vessels), which provides nutrition to the tendon, allows it to stretch up to several centimeters in length, and provides some degree of tendon gliding. The insertion site of the Achilles onto the calcaneus is an enthesis and is intimately related to the only true anatomic bursa in the ankle, the retrocalcaneal bursa. Although the patient’s history and a careful clinical examination will verify the diagnosis of Achilles tendon injury, both ultrasound (US) and MRI help in defining the condition and in monitoring clinical progress. US is also useful for administering platelet-rich therapies like the infiltration of preparation rich growth factors (PRGF) to stimulate tissue healing; this treatment has been used for tendinosis and more commonly for partial Achilles tendon tears. Tendon imaging abnormalities usually persist even after patients have recovered function; consequently, imaging appearance should not be used to guide whether or not an athlete is fit to return to competition after Achilles tendinopathy. Sagittal T1-weighted MR image 1 month after the onset of acute pain (Fig. 3.10.1) shows a dark, homogeneous, thickened Achilles tendon with increased signal intensity (open arrow); the parallel anterior and posterior margins of the tendon have been obliterated. Sagittal fat-saturated T2-weighted image (Fig. 3.10.2) is more sensitive to detect the mucoid degeneration combined with interstitial tear (open arrow) inside this tendon. Findings of paratendonitis are also seen, such as minimal edema in Kager’s fat pad (arrow) and posterior to the tendon (empty arrowhead). Axial image in the same sequence (Fig. 3.10.3) also shows the loss of the normal anterior concave margin (open arrow) and the external location of the injury. This tendon lesion was treated with rest, massotherapy, and finally US-guided PRGF infiltration in the external part of the tendon in the first session and in the perilesional zone in the second session a week later. Sagittal fat-saturated T2-weighted image in a different 22-year-old male professional soccer player (Fig. 3.10.4) who complained of tenderness in the Achilles region 5 days after an excessive training session with inappropriate training shoes, shows peritendinosis with a huge edema in the anterior Achilles tendon fat (open arrow) and a smaller edema posterior to the tendon (arrow). The tendon itself remains unchanged. The same injury developed in the contralateral Achilles tendon 4 days later (not shown).
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Further Reading Books Atlas of Imaging in Sports Medicine. 2nd ed.Anderson A, Read J (2007) Mc Graw/Hill, New York Diagnostic Imaging Orthopaedics. 1st ed. Stoller D, Tirman P, Bredella M, Beltran S, Branstetter R, Blease S (2008) Amirsys, Salt Lake City Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. Stoller DW (2006) Lippincott Williams and Wilkins, Philadelphia Orthopaedic Pathology. 2nd ed. Vincent J, Vigorita MD (2007) Lippincott Williams & Wilkins, Philadelphia Patologia muscular en el deporte. Diagnostico, tratamiento y recuperación funcional. 1st ed. Ramón B (2004) Masson, Elsevier, Paris
Web-Links www.radsource.us www.wheelessonline.com. Wheeless’ Textbook of Orthopaedics www.cmeinfo.com/store_temp/Sports_Medicine_Imaging__296. asp http://books.google.es/books?id = 1FSLoxkWe7YC&printsec = frontcover#PPP1,M1 Magnetic resonance imaging in orthopedic sports medicine. Pedowitz PD, Resnick R, Chung CB. 2008 www.essr.org
Articles Alfredson H, Lorentzon R. Chronic achilles tendinosis: recommendations for treatment and prevention. Sports Med 2000; 29(2):135–146 Brien SD, Bui-Mansfield LT. MRI of cuadratus femoris muscle tear: another cause of hip pain. AJR Am J Roentgenol 2007; 189:1185–1189 Connel DA, Scheneider-Kolsky ME, Hoving M, Hoving JL, Malara F, Buchbinder R, Koulouris G, Burke F, Bass C. Longitudinal study comparing sonographic and MRI assesments of acute and healing hamstring injuries. AJR Am J Radiol 2004; 183:975–984 Cross TM, Gibbs N, Houang MT, Cameron M. Acute cuadriceps muscle strains. Magnetic resonance imaging features and prognosis. Am J Sports Med 2004; 32(3):710–719 Delgado GJ, Chung CB, Lektrakul MD et al. Tennis leg: clinical US study of 141 patients and anatomic investigation of four cadavers with MR imaging and US. Radiology 2002; 224:112–119 Gyftopoulos S, Rosenberg ZS, Schweitzer ME, BordaloRodriguez M et al. Normal anatomy and strains in deep musculotendinous junction of the proximal rectus femoris: MRI
features. AJR Am J Roentgenol 2008; 190:w182–w186 (web exclusive article) Hasselman CT, Best TM, Hughes C, Martinez S, Garret W. An explanation for various rectus femoris strain injuries using previously undescribed muscle architecture. Am J Sports Med 1995; 23:493–499 Hsu JM, Fischer DA, Wright RW. Proximal rectus femoris avulsions in national football league kickers. A report of 2 cases. Am J Sports Med 2005; 33(7):1085–1087 Hutchinson PH, Stieber J, Flynn J, Ganley T. Complete and incomplete femoral stress fractures in the adolescent athlete. Orthopedics 2008; 31:604 Jansen JA, Mens JM, Backx FJ, Stam HJ. Diagnostics in athletes with long-standing groin pain. Scand J Med Sci Sports 2008; 18:679–690 Järvinen TAH, Kannus P, Paavola M, Järvinen TLN, Józsa L, Järvinen M. Achilles tendon injuries. Curr Opin Rheumatol 2001; 13:150–155 Khan KM, Forster BB, Robinson J, Cheong Y, Louis L, Maclean L, Taunton JE. Are ultrasound and magnetic resonance imaging of value in assessment of Achilles tendon disorders? A twoyear prospective study. Br J Sports Med 2003; 37:149–153 Koulouris G and Connel D. Evaluation of the hamstring muscle complex following acute injury. Skeletal Radiol 2003; 32: 582–589 Koulouris G, Connel D. Hamstring muscle complex: an imaging review. Radiographics 2005; 25:571–586 Lovell M. The management of sports-related concussion: current status and future trends. Clin Sports Med 2009; 28:95–111 Matt M. Biomechanics of muscle strain injury. Lecture 2002. Sports Medicine and Scine NZ Conference Montalvan B, Parier J, Brasseur JL, Le VD, Drape JL. Extensor carpi ulnaris injuries in tennis players: a study of 28 cases. Br J Sports Med 2006; 40:424–429 Ouellete H, Thomas BJ, Nelson E, Torriani M. MR imaging of rectus femoris origin injuries. Skeletal Radiol 2006; 35:665–672 Peltola K, Heinonen OJ, Orava S, Mattila K. Quadratus femoris muscle tear: an uncommon cause for radiating gluteal pain. Clinical J Sport Med 1999; 9:228–230 Schweitzer ME, Karasick D. MR imaging of disorders of the achilles tendon. AJR Am J Roentgenol 2000; 175:613–625 Silva RT, De BA, Laurino CF, Abdalla RJ, Cohen M. Sacral stress fracture: an unusual cause of low back pain in an amateur tennis player. Br J Sports Med 2006; 40:460–461 Smet AA, Best TM. Best MR imaging of the distribution and location of acute hamstring injuries in athletes. ARJ Am J Roentgenol 2000; 174:393–399 Smigielsky R. Management of parcial tears of the Gastro-Soleus complex. Clin Sports Med 2008; 27:219–229 Weishaupt D, Schweitzer ME, Morrison WB. Injuries to the distal gastrocnemius muscle: MR findings. J Comput Assist Tomogr 2001; 25(5):677–682 Willick SE, Lazarus M, Press JM. Quadratus femoris strain. Clini J Sport Med 2002; 12:130–131
Bone Marrow Joan C. Vilanova, Mercedes Roca, and Sandra Baleato
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Case 4.1 Bone Metastasis of Melanoma in the Femoral Head Mimicking Avascular Necrosis
Fig. 4.1.1
Fig. 4.1.2
Fig. 4.1.3
Fig. 4.1.4
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A 43-year-old white man presented right hip pain for approximately 10 months related to nonspecific trauma. Findings at physical examination were normal. Ten years earlier, a pigmented skin lesion resected from his shoulder was diagnosed as melanoma (Level I on Clark’s classification and 2.5 mm on Breslow’s classification).
The incidence of malignant melanoma is increasing faster than any other cancer in humans. The incidence of melanoma peaks in the fourth decade of life, and the head, neck, and lower limbs are most frequently affected. Although the prognosis for lesions less than 0.76 mm thick is excellent, metastases occur in 2–8%. Skeletal metastases are found in 17% of melanoma patients at computed tomography and in 23–57% during autopsy. The appearance of melanoma on CT is nonspecific, but on magnetic resonance imaging (MRI), amelanotic cells can produce a different pattern than the common melanincontaining tumors. Metastasis from malignant melanoma should be included in the differential diagnosis even when the depth of the primitive tumor is low.
Comments
Plain-film radiograph (Fig. 4.1.1) of the right hip shows a sharply lytic lesion on the right femoral head surrounded by a sclerotic rim (open arrow), raising suspicion of avascular necrosis. MRI shows a lesion with low signal intensity on T1-weighted images (Fig. 4.1.2) and mixed signal on T2-weighted images (Fig. 4.1.3). The patient underwent hip replacement surgery and chemotherapy. MRI follow-up 1 year later (Fig. 4.1.4) shows a polylobulated pseudoencapsulated (arrow) soft-tissue mass with high signal intensity on T2-weighted images within the gluteus muscles near the prosthesis. At histological examination, the femoral head and soft-tissue lesions were both consistent with infiltration by amelanotic epithelioid malignant melanoma.
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Case 4.2 Bone Marrow Necrosis Due to Nonhodgkin’s Lymphoma
Fig. 4.2.1
Fig. 4.2.2
Fig. 4.2.3
Fig. 4.2.4
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A 53-year-old woman presented with a mass in her right underarm 2 months after it appeared. She had no general symptoms or history of illness. Physical exam found a 60-mm axillary mass and a second 12 mm mass in the groin. Blood tests, including LDH, were normal.
Bone marrow necrosis (BMN) is a rare entity characterized by fever and bone pain; hypercalcemia and increased LDH are usually found in blood tests. Bone marrow aspirate contains amorphous eosinophilic material, with isolated cells in different degrees of necrobiosis. These findings appear in up to 19.8% of all autopsies, mostly after hematological malignancies with proliferative features (acute leukemia, lymphoma). BMN is generally regarded as a sign of poor prognosis. Magnetic resonance imaging (MRI) is useful for evaluating bone marrow involvement in this condition. Histological examination of bone marrow aspirate shows poor cellularity, with different degrees of necrobiosis on a stippled background. The clinical picture in this case was interpreted as BMN secondary to non-Hodgkin’s lymphoma.
Comments
MRI showed diffuse spongy marrow involvement in the lower spine, sacrum, and pelvic bones. A nonhomogeneous variegated pattern of infiltration was detected in all vertebral bodies (Figs. 4.2.1 and 4.2.2), pelvic bones, and femoral head (Figs. 4.2.3 and 4.2.4). Multiple foci of low signal on T1-weighted images and high signal on T2-weighted images are characteristic of nonhomogeneous mottled or variegated pattern.
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Case 4.3 Systemic Mastocytosis
Fig. 4.3.1
Fig. 4.3.3
Fig. 4.3.2
Fig. 4.3.4
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A 29-year-old woman with bone pain, fever, diarrhea, and sweating underwent plain-film radiography of the pelvis and humerus.
Systemic mastocytosis (SM) is a rare disorder (less than 10% of mastocytoses) that usually affects adults. The clinical symptoms resemble those of lymphoma or leukemia. Many organs are involved, including the liver, spleen, lymph nodes, skin, and bone marrow. SM follows a malignant course and can lead to death within a few years. Skeletal abnormalities are seen in 70% of cases. There is a special tropism for the axial skeleton. This proliferation is commonly silent, although 28% of patients complain of pain. Mast cell proliferation into bone marrow stimulates fibroblastic activity and a granulomatous reaction, which leads to trabecular destruction and replacement with adjacent new bone formation. MRI features related to medullary infiltration by mast cells in SM are nonspecific. However, MRI is an excellent technique for assessing the degree of medullary infiltration in these patients.
Comments
Changes are depicted on plain-film radiographs as a sclerotic lesion with diffuse distribution (Figs. 4.3.1 and 4.3.2). MRI shows hypointense signal on T1-weighted images (Fig. 4.3.3), similar to that of other sclerotic bone lesions, such as metastases (from breast or prostate cancer) or end-stage Paget’s disease; infiltration is shown as a nonhomogeneous diffuse pattern including the epiphysis. Microscopic examination of biopsy specimens (Fig. 4.3.4) shows mast cell infiltrates in bone marrow as focal cell aggregates with granuloma-like shape and paratrabecular distribution.
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Case 4.4 Bone Crisis in Gaucher’s Disease
Fig. 4.4.1
Fig. 4.4.3
Fig. 4.4.2
Fig. 4.4.4
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A 31-year-old white woman first diagnosed with type 1 Gaucher’s disease at the age of 4 (genotype N370S/W-4X) and receiving enzyme replacement since 1992 presented with mild pancytopenia, liver and spleen enlargement, and acute severe pain in her right hip and knee of several weeks’ evolution. Her right knee was swollen. She improved after 1 month of treatment with NSAIDs, steroids, and opioids. Skeletal MRI diagnosed a new bone crisis.
Gaucher’s disease is the most common lysosomal storage disorder. Type 1 is characterized by splenomegaly, hepatomegaly, pancytopenia, and osteolytic and osteopenic changes in the skeleton. Clinical symptoms of the disease are variable and can be apparent during the first weeks of life or can remain undetected until the eighth decade of life. Type 1 affects all races, but is especially common among Ashkenazi Jews. The pathogenesis of bone crisis is not clear, but the process appears to cause acute infarction of a large segment of bone. This event, also called pseudo-osteomyelitis or aseptic osteomyelitis occurs in 23–37% of patients with Gaucher’s disease. Laboratory tests usually find marked leukocytosis, but findings at plain-film radiography are usually normal. Osteonecrosis is probably the most disabling bone complication of Gaucher’s disease; it can appear at any age and the femoral head is involved in 50% of patients. Bone marrow infiltration by Gaucher cells is thought to be a critical step in the development of focal and local disease, with the increase in intraosseous pressure leading to ischemia and necrosis. Bone marrow infiltration may induce the release of inflammatory mediators such as cytokines from osteocytes and macrophages into the stromal microenvironment, leading to the dysregulation of osteoblastic/osteoclastic (formation/resorption) activity and pathological bone turnover. Plain-film radiography is useful for the diagnosis of long-bone and spinal infarction as well as focal lesions such as osteolysis and osteosclerosis, but has a poor sensitivity for overall patterns of focal disease. It is therefore not an optimal monitoring method. MRI is the method of choice for assessing bone marrow burden; it is also very sensitive for the detection of bone crisis, acute bone infarction, infection, and avascular necrosis.
Comments
Focal hyperintense signal in both femoral heads and extended marrow edema in both distal diaphyses are shown (Figs. 4.4.1 and 4.4.2). Some sclerotic foci corresponding to old lesions are also seen on T1-weighted images (Fig. 4.4.3). The vertebral bodies have an entirely normal signal with no changes suggestive of marrow infiltration by Gaucher cells (Fig. 4.4.4).
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Case 4.5 Non-Hodgkin’s (Diffuse Large B-Cell) Lymphoma
Fig. 4.5.1
Fig. 4.5.3
Fig. 4.5.2
Fig. 4.5.4
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A 55-year-old white woman underwent MRI for left groin pain. She had traveled around a tropical country in the previous month. Findings at clinical examination and blood tests were normal. After MRI and bone biopsy, she was diagnosed with non-Hodgkin’s lymphoma (diffuse large B-cell lymphoma, DLBCL).
The incidence and mortality of all the major lymphomas except Hodgkin’s lymphoma is rising in all European regions; this trend is more accentuated in the Western and Northern European countries than in Eastern European countries. New technology to study gene expression offers new opportunities to identify different clinical subsets; for example, DLBCLs, the most common lymphoid malignancies, are clinically and genetically heterogeneous disorders. Although DLBCL is a chemo-responsive tumor, many patients will not be cured with conventional empiric treatment regimens. Gene expression profiles by microarray analysis of specific genetic abnormalities and functional assays have been used to develop comprehensive molecular signatures of tumors that share similar features and rely upon common survival pathways. These studies are leading to the identification of subtype-specific rational therapeutic targets and associated inhibitors for clinical investigation. Related to different subtypes according to the REAL-WHO classification, the morphologies with the highest survival were cutaneous lymphoma and other specified lymphomas, followed by small lymphocytic leukemia/chronic lymphocytic leukemia (SLL/CLL), follicular lymphoma, and lymphoplasmacytic lymphoma. Morphologies with low survival were lymphoblastic, diffuse B, other T cell, Burkitt’s, and mantle cell/centrocytic. Three geographical areas were compared: EUROCARE west (France, Germany, Italy, the Netherlands, Spain, Switzerland, Iceland, Malta), EUROCARE east (Czech Republic, Estonia, Slovakia, and Slovenia), and SEER (US registries). For each morphological group, survival does not usually differ significantly between the three geographic areas. Exceptions are cutaneous lymphoma, follicular lymphoma, small lymphocytic NHL together with SLL/ CLL, and mantle cell/centrocytic lymphoma, for which 5-year survival in EUROCARE east (EU) is significantly lower than in SEER (USA); for follicular lymphoma, survival is also significantly lower in EUROCARE west than SEER.
Comments
Plain-film radiograph (Fig. 4.5.1) fails to show the bone marrow infiltration; trabecular bone is preserved on both the femoral head and neck. Pelvic MRI showed a low signal area in the left femoral neck on T1-weighted images (Fig. 4.5.2). After gadolinium administration, the peripheral margins enhanced (Fig. 4.5.3). Multiple foci were detected in pelvic bones (open arrows) on fat-suppressed images (Fig. 4.5.4).
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Case 4.6 Shoulder Arthropathy Secondary to Gaucher’s Disease
A 49-year-old white man diagnosed with type 1 Gaucher’s disease at the age of 10 years (and prior splenectomy) and receiving enzyme replacement therapy (ERT) for 18 months, presented with diffuse bone pain of several weeks’ evolution. After plain-film X-ray and MRI examinations, severe shoulder arthropathy was diagnosed.
Fig. 4.6.1
Fig. 4.6.2
Fig. 4.6.3
Fig. 4.6.4
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Bone abnormalities affect the vast majority of untreated patients with Gaucher’s disease; these abnormalities often lead to progressive skeletal manifestations like osteonecrosis, osteosclerosis, focal cortical thinning and long-bone deformity, and generalized osteopenia and osteoporosis. These symptoms can arise alone or in combination in both children and adults at any time during the course of disease, and they are consistently reported as the most disabling and debilitating complication of type 1 Gaucher’s disease. Patients who have undergone splenectomy, particularly at a younger age, may be more susceptible to the most severe bone changes. Gaucher bone manifestations are very often associated with a significant degree of pain, pathological bone fractures, and a risk of “bone crises,” where patients suffer episodes of “excruciating” bone pain. The effects of Gaucher’s disease on the skeleton therefore have a heavy impact on patients’ quality of life. Between 15 and 20% of patients have limited mobility as a result of Gaucher bone manifestations. The following diagram shows a protocol for the diagnosis and monitoring of Gaucher bone manifestations related to bone tissue and bone marrow: Two therapeutic options are available for patients with mild-to-moderate type 1 Gaucher’s disease: ERT with imiglucerase (Cerezyme®; Genzyme Corporation) and substrate reduction therapy (SRT) with miglustat (Zavesca®; Actelion Pharmaceuticals). ERT, which is based on the replacement of the deficient enzyme, b-glucocerebrosidase, in Gaucher patients was first introduced in 1991 in the form of a modified human placentalderived product (alglucerase). This was later replaced by imiglucerase, a recombinant DNA analogue of the human enzyme, which is indicated for the long-term treatment of symptomatic children and adults with type 1 Gaucher’s disease. Both enzyme preparations must be administered by intravenous infusion. SRT is a relatively new treatment aimed at reducing the accumulation of glucosylcer amide to a level that allows the residual activity of deficient glucocerebrosidase in Gaucher patients to act more effectively. Miglustat is a glucose analogue that competitively inhibits glucosylceramide synthase, the enzyme that catalyses the first committed step in glycos phingolipid synthesis. It is indicated for the treatment of adults with type 1 Gaucher’s disease for whom ERT is not a therapeutic option (e.g., due to constraints such as allergy, hypersensitivity, or poor venous access).
Comments
Plain-film radiographs (Figs. 4.6.1 and 4.6.2) show complete destruction of the humeral head. The distal clavicle appears intact, and the scapula shows osteoporosis and changes in the trabecular bone architecture. Coronal T2-weighted (Fig. 4.6.3) and axial T1-weighted (Fig. 4.6.4) MRI can detect associated bone infarcts and bone marrow infiltration secondary to type 1 Gaucher’s disease. T1-weighted images show decreased marrow signal secondary to marrow infiltration by Gaucher cells. T2-weighted images are used to assess ischemia or vascular obstruction during episodes of acute bone pain as well as osteomyelitis or intraosseous/subperiosteal hemorrhage.
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Case 4.7 Multifocal Osteonecrosis
Fig. 4.7.1
Fig. 4.7.2
Fig. 4.7.3
Fig. 4.7.4
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A 26-year-old woman presented with bilateral knee pain.
Multifocal osteonecrosis is uncommon; it is usually found in the following clinical settings: corticosteroid administration, connective tissue disorders (e.g., rheumatoid arthritis and systemic lupus erythematosus), dysbarism, hemoglobinopathies, Gaucher’s disease, pregnancy, inflammatory bowel disease, and alcohol abuse. Other rarer contexts are HIV infection, transplantation (kidney, heart, or bone marrow), and cancer treatment. In these patients it is often difficult to isolate a single causative agent, because the underlying disease process, corticosteroids, chemotherapy, or radiation therapy may be responsible, either alone or in combination with one another. Corticosteroids are the single most frequent cause of osteonecrosis. Alcohol abuse has rarely been reported as a secondary cause of multifocal osteonecrosis, although it is not uncommon as a cause of osteonecrosis of the femoral head. A high index of suspicion is required, and treatment remains expectant and symptomatic. Early recognition of this condition can significantly prevent morbidity. It is necessary to detect involvement of other areas like the knee or elbow in alcohol-induced osteonecrosis.
Comments
T1-weighted whole-body MRI (Fig. 4.7.1) shows necrotic lesions on both femoral heads (open arrows) and within the knee joint (arrows). STIR sequence whole-body MRI (Fig. 4.7.2) shows a low signal intensity lesion from the sclerotic subchondral necrosis of the hip and high signal intensity from the necrosis of the femur and tibia of both lower limbs. Multifocal necrosis extends to both elbows (open arrowheads) on coronal T1-weighted image (Fig. 4.7.3). Bone scintigraphy (Fig. 4.7.4) confirms the osteonecrosis in both legs and elbows, although the necrosis in both hips is not depicted due to lack of current osteogenic activity.
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A 51-year-old male complained of lumbar back pain.
Case 4.8 Multiple Myeloma
Fig. 4.8.1
Comments
Multiple myeloma is a generalized bone marrow disease caused by an infiltration of plasma cells. It is characterized by expansive growth of malignant plasma cell clones with consecutive destruction of the bony architecture. It accounts for 10–15% of all hematological malignancies and 1–2% of all cancers. The incidence of multiple myeloma varies by race and age. Clinically, approximately 10–40% of patients are asymptomatic at diagnosis, although bone pain is the most common symptom. Predilection sites are the axial skeleton (spine and pelvis), but also the ribs, the shoulder region, skull, and proximal femurs – thus, the need for whole-body imaging to adequately assess the extent of disease.
Fig. 4.8.2
Fig. 4.8.3
Fig. 4.8.4
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In patients with myeloma, the basic diagnostic work-up in many institutions includes radiographic examinations of the skull (two planes), the rib cage, the upper arms, the spine (two planes), the pelvis, and the upper legs. Typical radiographic findings include punchedout lytic lesions without any reactive sclerosis in the flat bones of the skull and pelvis. In the long bones, there is a range of appearances from endosteal scalloping, to discrete small lytic lesions, to larger destructive lesions. This diagnostic approach is still represented in the classic Salmon and Durie staging system of the disease, which assesses radiographic, immunohistochemical, and serological factors of the disease to determine the best therapy. Plain-film radiographs are routinely used for skeletal surveys; however, they are not sensitive enough to detect early osteolytic lesions. Newer imaging techniques like multislice CT, MRI, and whole-body PET offer improved diagnostic accuracy, enabling more precise staging and better management of this disease. Modified diagnostic criteria published in 2006, the Durie-Salmon Plus Staging System, integrate whole-body MRI, FDG-PET, and CT into routine staging. The role of imaging in the management of myeloma is to assess the extent of intramedullary bone disease, to detect extramedullary foci, to evaluate the severity of disease at presentation; to identify and characterize complications, and to evaluate the response to treatment. MRI has proven valuable for initial screening and follow-up in almost all types of myeloma patients. MRI has the advantage of enabling bone marrow involvement to be evaluated and therefore plays an important role in clinical decision making for patients with myeloma. Whole-body MRI has the potential to visualize the bone marrow directly and to determine abnormalities in bone marrow cell composition with high anatomic resolution. Whole-body MRI is performed using sagittal T1-weighted spin-echo sequences of the entire spine, coronal fat-suppressed T2-weighted short tau inversionrecovery (STIR) and diffusion-weighted imaging of the head, thorax including the upper limps, abdomen, pelvis, and thighs. Abnormalities in the bone marrow due to myeloma typically show low signal intensity on T1-weighted sequences and high signal intensity on STIR or T2-weighted sequences. Diffuse involvement is best detected on unenhanced T1-weighted SE sequences, where it manifests as homogeneous signal reduction. Myeloma lesions on diffusionweighted images present restricted diffusion. The differential diagnosis includes metastases, lymphomas, myeloproliferative disease, or atypical hemangiomas. Treatment of multiple myeloma is complex and can include chemotherapy, radiation, and transplant.
Sagittal T1-weighted FSE MRI (Fig. 4.8.1) shows diffuse low signal from the vertebral bodies with some expansion at the T12 level (open arrow). Bone scintigraphy shows no abnormal uptake (Fig. 4.8.2). Diffusion-weighted whole-body MRI (Fig. 4.8.3) with inverted gray scale shows multiple lesions in the ribs, spine, pelvis, and femurs (arrows). The corresponding STIR sequence (Fig. 4.8.4) from the whole-body MRI study shows the same lesions and the extension to both femurs (open arrows).
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A 31-year-old woman underwent plain-film radiography and MRI for left hip pain of 1 month’s evolution.
Case 4.9 Bone Metastases Comments
Bone is a common site of metastasis for many primary malignant tumors; indeed, it is the third location after the liver and lungs. Metastases are the most frequent cause of bone tumors, accounting for 25% of cases. Furthermore, the spine represents the most frequent site of skeletal metastasis. Most metastatic lesions in the skeleton are encountered in middle-aged and elderly patients. Malignant cells can disseminate to the spine by various mechanisms: through the arterial system, through venous drainage, by cerebrospinal fluid, or by direct extension. With the vertebrae’s rich blood supply, the hematogenous route is the most common of these pathways. Back pain is the most frequent initial complaint in patients with spinal metastatic disease. Pain, pathological fractures, and hypercalcemia are the major sources of morbidity of patients with bone metastases. The diagnosis of bone metastasis is crucial to determine the prognosis and to optimize therapy. Imaging of
Fig. 4.9.1
Fig. 4.9.2
Fig. 4.9.3
Fig. 4.9.4
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spinal metastatic disease may include radiography, myelography, bone scintigraphy, CT, and MRI.99mTc-phosphonate-based skeletal scintigraphy is the standard method for the initial staging of bone tumors; its sensitivity ranges from 62 to 89%. MRI and PET can identify bone metastases. MRI is the only imaging technique that allows direct visualization of the bone marrow and its components. Technical advances have enabled whole-body MRI examination using fast gradientecho, T1-weighted, STIR, and diffusion-weighted sequences in less than an hour. Metastatic bone lesions can be described as osteolytic, osteoblastic, or mixed. On T1-weighted sequences, tumor spread is identified by replacement of normal marrow, resulting in an isointense or hypointense signal compared to muscle tissue. On STIR sequences, increased water content within tumor cells readily reveals bone tumors as lesions hyperintense to the surrounding normal marrow. In osteoblastic metastases, areas of low signal intensity on T1-weighted turbo SE images correspond to areas of low signal intensity on T2-weighted turbo SE images. On STIR sequences, the appearance of osteoblastic metastases ranges from no signal in very dense sclerotic metastases to hyperintense signal in cases where more cellular components are present. Unfortunately, T2-weighted and STIR sequences do not differentiate intracellular water signal intensity due to malignant disease from the interstitial water signal due to fracture edema. In diffusion-weighted sequences, these differences can be used to characterize tissue pathology. Diffusion-weighted MRI highlights areas with restricted diffusion, such as occurs in many malignant primary and metastatic tumors, and provides outstanding visualization of lymph nodes. Diffusion-weighted MRI also provides functional information and can be used to detect and characterize bone metastases. Diffusion-weighted sequences typically demonstrate increased signal intensity for tumor areas, edema, infections, highly cellular lymph nodes, as well as for lytic metastases. Complete osteoblastic metastases are not shown on diffusion-weighted images. Whole-body MRI allows the diagnosis of spinal metastasis and appears to be a powerful tool for differentiating posttherapeutic changes from tumor recurrence. Treatment for bone metastases is normally palliative. The indications for surgical treatment of spinal metastases are intractable pain, the onset of neurological deficit (caused by compression of the myeloradicular structures by the tumor mass or by pathological fracture of the vertebra), and instability of the affected spinal segment that causes ingravescent mechanical pain and/or neurological deficit.
Plain-film radiograph of the pelvis (Fig. 4.9.1) shows a radiolucent lesion in the left acetabulum and another lytic bone lesion in the right femur (open arrows). These lesions appear as greatly increased signal on coronal fat-suppressed T2-weighted MRI (Fig. 4.9.2). Coronal diffusion-weighted whole-body MRI with inverse grayscale intensity scale (Fig. 4.9.3) demonstrates a large apical right pulmonary mass as a low intensity area (open arrow), left pulmonary metastases (arrow), and bone metastases from the pelvis (open arrowheads). Corresponding coronal T1-weighted image (Fig. 9.4.4) depicts the primary neoplasm in the right lung (open arrow).
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Case 4.10 Regional Migratory Osteoporosis
Fig. 4.10.2 Fig. 4.10.1
Fig. 4.10.3
Fig. 4.10.4
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A 49-year-old woman with a history of lateral meniscectomy in her left knee 1 year earlier, complained of pain in the lateral compartment of her left knee. Four months later, she had pain in her left hip. After conservative treatment, she reported pain in her right hip. Six months later, she had pain in her left foot.
Regional migratory osteoporosis (RMO) is a feature of bone marrow edema syndrome (BMES). BMES also includes various transient clinical conditions, such as transient osteoporosis of the hip (TOH) and reflex sympathetic dystrophy (RSD). The pathogenic mechanism of BMES is unknown. Typical MRI features include ill-defined hyperintensities on fat-suppressed T2-weighted images and on STIR images and areas of decreased signals on T1-weighted images. The bone marrow edema pattern seen on MRI is a nonspecific finding that has been described in several conditions; thus, it is necessary to distinguish between reversible and irreversible lesions. BMES is a transient condition that usually requires no active intervention: TOH, RMO, and RDD are self-limiting, and surgical treatment is not necessary. RMO is an uncommon condition characterized by migrating arthralgia involving the weight-bearing joints of the lower limb. RMO may occur in patients of either sex and at all ages from late adolescence onwards. The hips are the most commonly affected primary joint; involvement of secondary joints typically occurs within 6 months of presentation. It regresses spontaneously, with restoration of normal function and bone density over a period of 6–12 months. Plain-film radiographs may initially be normal but eventually demonstrate demineralization in the affected joint with preservation of the joint space after 3–6 weeks. Bone scintigraphy shows increased uptake in the affected joints; bone scintigraphy usually shows abnormal findings before changes are detected on plain-film radiographs and may also precede the onset of arthralgia at other sites. MRI shows diffuse bone marrow edema involving the epiphysis of the affected joints, with high signal intensity on T2-weighted and STIR sequences and low signal intensity on T1-weighted sequences. Joint effusion may also be present. MRI findings are seen within 48 h after the onset of symptoms and resolve 4–11 months after presentation. Conservative treatment with limited weight-bearing and analgesia is thought to be effective.
Comments
Coronal STIR MRI (Fig. 4.10.1) demonstrates an ill-defined area of high signal intensity compatible with bone marrow edema in the lateral femoral condyle of the left knee. Four months later, the patient developed pain in her left hip. Coronal T1-weighted FSE MRI (Fig. 4.10.2) shows bone marrow edema in the left femoral head and neck. Six months later, new onset symptoms developed in the right hip. Coronal T1-weighted FSE MRI (Fig. 4.10.3) demonstrates complete resolution of the left femoral edema with low signal intensity in the right femoral head, neck, and intertrochanteric region on T1-weighted sequences. Seven months later, the patient complained of right ankle pain. Sagittal T2-weighted fat-saturated MRI (Fig. 4.10.4) demonstrates bone marrow edema in the talus.
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Further Reading Books Gaucher disease: molecular, genetic and enzymological aspects. Grabowski GA, Horowitz M (1997) In: Gaucher’s Disease, Zimran A (ed). Balliere Tindall, London, 635−636 Musculoskeletal MRI. Phoebe K, Clyde H, Mark WA, Robert D, Nancy M (2001) Elsevier, Amsterdam Myeloproliferative disorders. Resnick: Diagnosis of Bone and Joint Disorders 2ed, vol 4. Resnick D, Haghighi P (1996) WB Saunders, Philadelphia, 633 IRM Ostéo-articulaire et musculaire.Imagerie Médicale Diagnostic Railhac JJ, Sans N. (2004) Masson, Paris Resonancia Magnética en Enfermedades Hematológicas. Giraldo P, Roca M, Rubio-Felix D (2001) Aula Médica Ediciones, Madrid
Web-Links www.skeletalrad.org. The Society of Skeletal Radiology www.internationalskeletalsociety.com. International Skeletal Society www.sfr-radiologie.asso.fr. Societé Francaise de Radiologie www.mrrc.yale.edu. Magnetic Resonance Research Center www.em-consulte.com. Elsevier Massom EM/consulte
Articles Barceló J, Vilanova JC, Riera E, Balliu E, Pelaez I, Martí J et al. RM de todo el cuerpo con técnica de difusión (PET virtual) para el cribaje de metástasis óseas. Radiología 2007; 49(6):407–415 Charrow J, Andersson HC, Kaplan P et al. The Gaucher registry: demographics and disease characteristics of 1698 patients with Gaucher disease. Arch Intern Med 2000; 160:2835−2843 Cox TM, Schofield JP. Gaucher’s disease: clinical features and natural history. Baillieres Clin Haematol 1997; 10:657−689 Delgado P, Giraldo P, Roca M, Alvarez R. [Magnetic resonance imaging in the early diagnosis of bone marrow necrosis]. Sangre (Barc) 1999; 44(1):65–69 García Erce JA, Giraldo Castellano MP, Roca Espaiu M. Alteraciones radiológicas en la mastocitosis sistémica. Radiología 1998; 40:424–425 Glockner JF, Sundaram M, Pierron RL. Radiologic case study. Transient migratory osteoporosis of the hip and knee. Orthopedics 1998; 21(5): 600, 594–596 Hermann G, Pastores GM. Abdelwahab IF. Gaucher disease: assessment of skeletal involvement and therapeutic responses to enzyme replacement. Skeletal Radiol 1997; 26:687–696
Jones DN. Multifocal osteonecrosis following chemotherapy and short-term corticosteroid therapy in a patient with small-cell bronchogenic carcinoma. J Nucl Med 1994; 35:1347 Karantanas AH, Nikolakopoulos I, Korompilias AV, Apostolaki E, Skoulikaris N, Eracleous E. Regional migratory osteoporosis in the knee: MRI findings in 22 patients and review of the literature. Eur J Radiol 2008; 67:34–41 Korompilias AV, Karantanas AH, Lykissas MG, Beris AE. Bone marrow edema syndrome. Skeletal Radiol. 2009; 38(5): 425–436 LaPorte DM, Mont MA, Mohan V, Jones LC, Hungerford DS. Multifocal osteonecrosis. J Rheumatol 1998; 25:1968–1974 Moon JG, Shetty GM, Biswal S, Shyam AK, Shon WY. Alcoholinduced multifocal osteonecrosis: a case report with 14-year follow-up. Arch Orthop Trauma Surg 2008; 128:1149 Pastores GM, Einhorn TA. Skeletal complications of Gaucher disease: pathophysiology, evaluation, and treatment. Semin Hematol 1995; 32(3 suppl 1):20–27 Patten RM, Shuman WP, Teefey S. Metastases from malignant melanoma to the axial skeleton: A CT study of frequency and appearance. AJR Am J Roentgenol 1990;155:109–112 Roach R, Miller D, Griffiths D. Multifocal osteonecrosis predominantly affecting the knees secondary to chronic alcohol ingestion: a case report and review. Acta Orthop Belg 2006; 72:234 Roca M, Mota J, Alfonso P, Pocoví M, Giraldo P. S-MRI Store: a simple method for assessing bone marrow involvement in Gaucher disease. Eur J Radiol. 2006;62:132–137 Schmidt GP, Schoenber SO, Schmid R, Stahl R, Tiling R, Becker CR et al. Screening for bone metastases: whole-body MRI using a 32-chanel system versus dual modality PET-CT. Eur Radiol 2007; 17:939–949 Sevinc A, Kalender ME, Pehlivan Y, Sari I, Camci C. Thrombotic thrombocytopenic purpura and bone marrow necrosis as the initial presentation of lung cancer. Clin Appl Thromb Hemost 2007; 13(4):449–452 Sidransky E. Gaucher disease: complexity in a “simple” disorder. Mol Genet Metab 2004; 83:6−15 Tall MA, Thompson AK, Vertinsky T, Palka PS. MR imaging of the spinal bone marrow. Magn Reson Imaging Clin N Am 2007; 15(2):175–198 Tang MY, Jeavons S, Stuckey Smiddleton H, Gill D. MRI features of bone marrow necrosis. Am J Roentgenol 2007; 188(2): 509–514 Toms AP, Marshall TJ, Becker E, Donell ST, Lobo-Mueller EM, Bar`ker T. Regional migratory osteoporosis: a review illustrated by five cases. Clin Radiol 2005; 60:425–438 Vilanova JC, Barceló J. Diffusion-weighted whole-body MR screening. Eur J Radiol 2008; 67(3):440–447 Weinreb N, Barranger J, Packman S et al. Imiglucerase (Cerezyme) improves quality of life in patients with skeletal manifestations of Gaucher disease. Clin Genet 2007; 71:576−588
Spine Eva Llopis, Victoria Higueras, Elena Belloch, and María Vañó
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Case 5.1 Congenital Scoliosis
A 5-year-old child born with craniosynostosis and multiple congenital vertebral abnormalities was evaluated for spinal deformity. Full spine plain-film radiographs showed a complex deformity with double-fixed left thoracic and right lumbar curves. MDCT was performed to evaluate bone congenital abnormalities and full spine MRI was performed to rule out cord abnormalities.
Fig. 5.1.2
Fig. 5.1.1
Fig. 5.1.3
Fig. 5.1.4
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Congenital scoliosis is defined as scoliosis due to bony abnormalities of the spine present at birth. Patients with congenital scoliosis must be monitored clinically and radiographically with full spine films. The embryonic development of the vertebra is closely related with that of the spinal cord; these two structures develop at the same time, so MRI is necessary to rule out neural axis lesions. Spinal MRI should look for cord abnormalities such as Chiari malformation (cerebellar tonsil extension below the foramen magnum), syringomyelia (cavity within the spinal cord extending for more than two vertebral body segments), tethered cord syndrome with or without associated lipoma (includes thick filum terminale, dorsal and caudal position of the conus of the conus medullaris), and diastematomyelia (cord split over a portion of its length). The cleft that divides the cord in diastematomyelia might be associated with a fibrous or osteocartilaginous spur or septum. The cleft is located below T8 in 85% of cases and involves only the lumbar spine in 60% of cases. Usually, the cord reunites after the cord. In diastematomyelia, the gray matter of each hemicord usually forms a dorsal and a ventral horn. MDCT should be used as a complementary technique to evaluate bone deformities, especially complex ones in which there are a jumble of abnormalities that are difficult to depict and understand on conventional plain-film radiographs. Reformatted images provide a more complete picture of the patient’s deformity. Congenital deformities can be divided into two basic groups based on the embryologic development: segmentation defects and formation defects. Segmentation defects can be symmetric or asymmetric; asymmetric defects take the form of unilateral, unsegmented, solid bars with bone fusing on two or more segments. This defect closely correlates with progressive spinal curvatures. Formation defects occur secondary to a lack of embryonic material for normal vertebral development. Hemivertebra, one of the most common formation defects, is defined as the complete failure of a vertebra to form one side. The severity of the resultant scoliosis is related to the degree of segmentation associated.
Comments
Figure 5.1.1 Plain-film radiographs of the entire spine show a complex deformity with multilevel deformities and double-fixed kyphoscoliosis (left thoracic, right lumbar). Figure 5.1.2 MRI shows a double neural tube separated by a bony spur (open arrow). The complex kyphoscoliosis has caused the spur to rotate and cross the spinal canal. The spur inserts into an externally rotated lamina and creates significant asymmetry in the two hemicanals. Low cerebellar amygdala, diagnostic of Chiari malformation, and low conus medullaris completed the spectrum of pathologic conditions affecting the neuroaxis. Figure 5.1.3 Axial volume-rendered MDCT clearly shows the lateral bone spur dividing the spinal canal into two hemicanals (open arrow). Figure 5.1.4 Volume-rendered MDCT reconstruction shows the complex vertebral abnormalities with a segmentation defect of the anterior arch of C1 (open arrow), a complex formation defect, unilateral bars at the cervicothoracic junction (C6-C7-T1) (solid arrow), a large unilateral left bar segmentation defect on T4–T9, and complex associated rib alterations (arrowhead).
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Case 5.2 Herniated Disc Migration with Spontaneous Regression
Fig. 5.2.1
Fig. 5.2.3
Fig. 5.2.2
Fig. 5.2.4
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A 25-year-old woman presented with acute sciatic pain. MRI showed a herniated disc with cranial extrusion. She was provided conservative treatment, and a follow-up MRI 3 months later showed a marked decrease in the size of the hernia.
Herniated disc migrates either superiorly or inferiorly but remains confined to the left or right anterior epidural space by a midline septum adjacent to the posterior longitudinal ligament. A standardized nomenclature and classification system now classifies disc herniations as protrusions, extrusions, and sequestrations. Disc herniation is classified as protrusion when the protruding portion involves the majority of the disc; as extrusion when the protruding portion is wider than the neck connecting the cap to the bulk of the disc in the interspace; and as sequestration when a fragment of the disc becomes separated from the remaining parent disc. Differentiation between protrusion and extrusion might be of clinical significance because 52% of asymptomatic patients have a bulging disc, 27% have a protruded disc, and only 1% has an extruded disc. Spontaneous disc herniation reduction is well known clinically and was also demonstrated on CT and also on MRI by Bozzao et al. About 70% of herniated discs reduce their size spontaneously in patients treated conservatively. Pain relief is thought to be due to subsidence of root sleeve edema and of inflammatory and fibrotic changes around the disc material. Although the exact mechanism is unknown, dehydration and shrinkage of the disc material, probably related to the inflammatory response, are thought to be the main factors involved. The only imaging findings associated with the amount of regression are the size of the herniation and rim enhancement. Thoracic disc and cervical disc herniation have been studied less and their rate of regression is lower. One of the reasons for lower regression rates in thoracic herniation is the presence of calcification within the disk.
Comments
Figure 5.2.1 Sagittal T1-weighted FSE MRI shows obliteration of the normal epidural fat in the left lumbar recess by an oval soft-tissue mass connected with the L5-S1 intervertebral disc, consistent with superiorly migrated herniated material (solid arrow). The lesion is slightly hyperintense compared to fluid and normal intervertebral disc (open arrow), and this is associated with a subacute process. Figure 5.2.2 Sagittal T2-weighted FSE MRI shows the migrated herniated disc (open arrow) with irregularity and edema in the adjacent endplates (arrow). Figures 5.2.3 and 5.2.4 Three-month follow-up MRI study: Sagittal T1-weighted FSE MRI and T2-weighted FSE MRI show the marked regression in the size of the herniated disc (open arrow).
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Case 5.3 Ligamentum Flavum Cyst Introduction
A 70-year-old man presented with posterior right lower limb pain of 2 months’ evolution; pain become persistent and severe about 2 weeks before the MRI exam. The diagnosis was confirmed at spinal surgery.
Facet and juxtafacet cysts are cystic lesions originating in the facet joint or its surrounding structures. Synovial cysts and ganglia are distinguished by the presence or absence of synovial lining, which cannot be differentiated on MRI. Synovial cysts originating in the facet joint are called facet cysts and those originating in the ligamentum flavum are called
Fig. 5.3.1
Fig. 5.3.3
Fig. 5.3.2
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ligamentum flavum cysts. These cysts are usually located in the lumbar spine and L2-L3 is the most common site. Juxtafacet cysts of the lumbar spine are associated with degenerative facet and ligamentum flavum process due to degenerative disc disease together with facet microinstability and hypermobility. Up to 50–70% have spondylolisthesis. Clinically, these lesions are a well-recognized cause of lumbar radicular pain and neurogenic claudication. Symptoms are related to acute compression or the inflammatory process surrounding the cyst. Diagnosis of a juxtafacet cyst of the lumbar spine is relatively easy with MRI because of its high contrast resolution. The diagnosis can also be suggested on CT, where calcium and vacuum phenomena are better depicted. At MRI, they appear as posterior epidural lesions with low to intermediate signal intensity on T1-weighted MRI. On T2-weighted MRI, the cyst capsule appears as a hypointense line, well demarcated from the high-signal-intensity intrathecal CSF, representing a fibrous capsule with hemosiderin deposits or thin calcification. The content of the cyst varies; therefore, it usually has the signal intensity of fluid, but it can be heterogeneous with low signal intensity on T2-weighted images due to the presence of proteinaceous material, hemorrhage (causing acute symptoms), calcification, and the vacuum phenomenon. Rim enhancement is seen after gadolinium injection. The location of the cyst and its relations to other structures are the key to differentiating between facet cyst and ligamentum flavum cyst. The connection between the lesion and the facet or ligamentum flavum can be demonstrated by tailoring the study. Medially located lesions (from 2 to 5 o’clock on the right and from 7 to 10 o’clock on the left) adjacent to the ligamentum flavum with less degenerative changes of the facet are diagnostic of ligamentum flavum cysts, whereas laterally located, more inferior lesions with degenerative changes and fluid within the facet joint are characteristic of facet cysts. Hemorrhage within the cyst is slightly more common in ligamentum flavum cysts than in facet cysts. These imaging findings, especially the anatomical location, can suggest the diagnosis. The differential diagnosis includes other processes that can affect the facet, such as septic arthritis (when hemorrhagic deposits are seen with high signal intensity on T1-weighted images), pigmented villonodular synovitis of the facet joint, posterior migration of a sequestrum from a herniated disc (although these very rarely extend the ligamentum flavum), perineural cyst (these are usually associated with the nerve root sleeve in the neural foramen and are separate from the facet), or cystic schwannoma (these are usually intradural and lack a hypointense rim).
Figure 5.3.1 Sagittal T1-weighted FSE MRI shows a hyperintense posterior epidural lesion located in the mid-lateral canal at the L2-L3 level. Figure 5.3.2 Sagittal T2-weighted FSE MRI shows a hyperintense heterogeneous lesion with a hypointense rim (solid arrow). Figure 5.3.3 Axial T1-weighted MRI after gadolinium injection shows the right centrally located posterior epidural lesion, connected with the ligamentum flavum and moderate rim enhancement (solid arrow).
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Case 5.4 Primary Vertebral and Epidural Lymphoma Introduction
A 75-year-old woman presenting with intermittent and progressive pain in the upper thoracic spine associated with weakness and paresthesias in both arms underwent spinal CT and MRI. The diagnosis was confirmed by CT-guided biopsy.
Primary bone lymphoma is an uncommon malignancy that accounts for less than 5% of all primary bone tumors. Primary lymphoma is defined as lymphoma with no evidence of systemic disease at the time of the presentation. The radiological appearance of primary bone lymphoma is variable and without reliable characteristics for a firm diagnosis; however, several features together might suggest the diagnosis.
Fig. 5.4.1
Fig. 5.4.2
Fig. 5.4.3
Fig. 5.4.4
Fig. 5.4.5
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Primary bone lymphoma has also been called reticulum cell sarcoma, malignant lymphoma of the bone, and more recently osteolymphoma. The vast majority of cases are of the non-Hodgkin’s type. There are three main types of lymphoma: B cell, T cell, and Hodgkin’s disease. The differential diagnosis is readily resolved by immunohistochemical analysis. Primary bone lymphoma occurs in a broad range of patients and is most prevalent among patients in the sixth to seventh decades. The femur is the most common site, followed by pelvis, humerus, and tibia. Vertebral involvement is not unusual, and the thoracic spine is the most common site in the spine. It is important to obtain a specific diagnosis for bone lymphoma because this tumor has a better response to therapy and a better prognosis than other lymphomas. The radiological appearance is variable; the most frequent appearance is an aggressive lytic lesion with permeative bone destruction or more rarely osteosclerosis, and bone lymphoma forms part of the differential diagnosis of “ivory vertebra”. Typically, bone lymphoma shows permeated cortical bone without significant gross destruction, limited periosteal new bone formation, and a very large soft-tissue mass. Lymphoma does not have a bone or cartilage matrix. Expansion of the involved bone is unusual. The disc spaces are usually preserved, but can become widened in rare cases. Extension into the spinal canal is frequent, as are paraspinal soft-tissue masses; the extraosseous component is often homogeneous. Epidural masses cause cord compression more often than vertebral collapse in spine lymphoma. On plain-film radiographs and CT, primary lymphoma of the spine may be lytic, sclerotic, or mixed with associated partial or complete vertebral compression. MRI not only permits early identification but also depicts the extent of soft-tissue involvement and can be used to assess the outcome of treatment.
Figure 5.4.1 Unenhanced CT shows a coarse permeative and trabecular pattern in the body of T3, with periosteal preservation (open arrow) without significant cortical destruction. A large soft-tissue mass extends to the prevertebral space and spinal canal (solid arrow). Findings at chest CT were normal, without pulmonary nodules or adenopathies. Figure 5.4.2 Axial T1-weighted FSE MRI shows a low signal intensity mass in the T3 vertebral body, with preservation of the cortical periosteal bone (open arrow) and a large hypointense soft-tissue mass extending into the prevertebral and epidural spaces, as well as into the vertebral foramen, where it involves the spinal cord (solid arrow). Figure 5.4.3 Sagittal T2-weighted FSE MRI shows the mass isointense to the T3 vertebral body and posterior elements; the spinal cord is compressed by the epidural anterior and posterior soft-tissue mass (open arrow). The soft-tissue mass is slightly hyperintense compared to the spinal cord and extends posteriorly. Figure 5.4.4 Coronal T1-weighted FSE MRI clearly shows the right paravertebral softtissue extension (open arrow) as well as the preserved cortical bone and intervertebral space (solid arrow). Figure 5.4.5 Sagittal fat-saturated T1-weighted FSE MRI after gadolinium injection reveals the highly intense homogenous enhancement of the vertebral body, posterior elements, and soft-tissue mass.
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Case 5.5 Osteoid Osteoma
A 13-year-old boy presented with low back pain of 2 months’ evolution; the pain was predominately nocturnal and accompanied by right radicular pain. Plain-film radiographs and MRI of the lumbar spine showed sclerosis and bone marrow edema in the sacrum, so a dedicated study of the sacrum was performed.
Fig. 5.5.2
Fig. 5.5.1
Fig. 5.5.3
Fig. 5.5.4
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Osteoid osteoma of the spine accounts for 10% of all osteoid osteomas, but only 2% of spinal osteoid osteomas are found in the sacrum. Osteoid osteomas affect men two to three times more often than women, usually between the ages of 10 and 20 years. Most axial osteoid osteomas are located in the posterior elements of the vertebra (pedicles, articular facets, and laminae), and only 7% are located in the vertebral body. The remaining cases involve the transverse and spinous processes. The lumbar spine is most commonly affected, followed by the cervical, thoracic, and sacral segments. These benign osteoblastic lesions contain a central nidus characterized by osteoid and highly vascular fibrous tissue. Histologically, the nidus of an osteoid osteoma is a small (<1.5–2.0 cm in diameter), round mass of pink-to-red tissue; the color of the lesion reflects its vascularity. The nidus is usually less than 1 cm in size and is surrounded by a zone of reactive sclerosis. On plain-film radiographs, a central radiolucent lesion less than 2 cm in diameter represents the nidus and is surrounded by marked perifocal sclerosis. Central calcification may be observed within the osteolytic nidus. CT is highly specific for the diagnosis. The usefulness of MRI in detecting the nidus is unclear; when an osteoma is detected, signal intensity is generally low with an isointense central nidus on T1-weighted images and intermediate to high signal intensity on T2-weighted images. Bone-marrow edema and soft-tissue edema are conspicuous on T2-weighted fat saturation images. In some patients, the nidus is undetectable as a result of marrow edema, soft-tissue edema, or surrounding sclerosis. The enlarged transverse process together with soft-tissue edema might be responsible for radicular pain. The differential diagnosis for a dense pedicle includes osteoblastoma (which is larger than 1.5–2 cm), osteoblastic metastasis, enostosis (bone island), unusual infection, lymphoma, and reactive sclerosis caused by abnormalities of the facets.
Introduction
Figure 5.5.1 Coronal MDCT MPR reconstructions show enlarged and markedly sclerotic right S3 process; the central nidus is clearly shown as a small central radiolucent lesion measuring 7 mm (less than 2 cm) without central calcification (open arrow). Figure 5.5.2 Axial T1-weighted FSE MRI shows hypointensity in the sclerotic area (open arrow) and a central area that is isointense-slightly hyperintense to the muscle nidus (solid arrow). Figure 5.5.3 Axial STIR MRI shows hyperintensity in the central nidus (open arrow), a slightly hypointense sclerotic area surrounding it, and marked soft-tissue edema extending to the right piriformis muscle (solid arrow) and into the right foramen, where it involves the right neural root. Figure 5.5.4 Coronal T1-weighted fat saturation FSE MRI after gadolinium injection shows strikingly high arterial phase uptake in the nidus due to its high vascularity and enhancement of the surrounding tissue (open arrow). Radiofrequency ablation of this lesion achieved a good outcome.
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Case 5.6 Meningioma
Fig. 5.6.1
Fig. 5.6.3
Fig. 5.6.2
Fig. 5.6.4
101 Spine A 67-year-old woman presented with low back pain, left radicular pain, weakness of the lower limbs, instability, and paresthesias. MRI performed to rule out spinal compression suggested the diagnosis of meningioma, which was confirmed at surgery.
Meningioma is the second most common tumor of the spine, accounting for approximately 25% of spinal canal tumors. There is a strong female preponderance (80%), with peak age in the fifth and sixth decades. The most common location is the thoracic spine, followed by the cervical spine; meningiomas in the lumbosacral spine are rare. Meningiomas are extramedullary lesions. Because they have a dural attachment, most spinal meningiomas (approximately 90%) are intradural, only 5% are extradural, and another 5% have combined intradural and extradural components.
Introduction
The typical clinical scenario is a middle-aged woman with signs and symptoms of cord or nerve root compression. The radiological diagnosis is often suggested by its intraspinal extramedullary location and association with the nerve root sleeve. CT might show calcification, although this finding is uncommon. At MRI, the tumor typically appears as a well-circumscribed lesion isointense or slightly hypointense to the spinal cord on T1- and T2-weighted sequences, with homogeneous gadolinium enhancement. However, in meningiomas with an extradural component, the extradural component only enhances minimally. The “dural tail sign”, consisting of dural enhancement adjacent to the dural attachment, can be detected, although is not specific and might also be present in some metastases, lymphoma, or sarcoidosis. The differential diagnosis should include neurinomas, which are the most common intraspinal intradural extramedullary tumors. Neurinomas are usually more hypointense on T1-weighted images and hyperintense on T2-weighted images, and they are more likely to widen the neural foramen than meningiomas. Other, less frequent, entities in the differential diagnosis are filum terminale ependymoma, drop metastasis, sarcoidosis, and lymphoma. Surgical excision is the treatment of choice in most cases, and recurrence is uncommon.
Figure 5.6.1 Sagittal T2-weighted FSE MRI shows a well-defined solid mass at the T11–T12 level, isointense with the spinal cord (open arrow). Figure 5.6.2 Sagittal T1-weighted FSE MRI shows the extramedullary lesion isointense to the cord. Figure 5.6.3 Coronal T1-weighted FSE MRI after gadolinium injection shows homogeneous enhancement with a broad dural attachment (open arrow) and normal-sized neural foramen; the spinal cord is displaced to the right (solid arrow). Figure 5.6.4 Sagittal fat-saturated T1-weighted MRI after gadolinium injection demonstrates strong and homogeneous enhancement.
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Case 5.7 Myeloma
Comments
Fig. 5.7.1
A 57-year-old patient presented after 2 years’ chronic progressive lumbar pain refractive to conservative treatment and 2 weeks’ lower limb weakness. Plain-film radiographs of the lumbar spine revealed multiple lytic lesions, and the diagnosis was reached with spinal MRI, CT-guided biopsy, and bone marrow biopsy. He was treated with radiotherapy, chemotherapy, and steroids; the response to treatment was good (decreased size of the soft-tissue mass and of the lytic lesions). Eighteen months later, the patient developed progressive paresthesias and bilateral motor deficit. MRI showed myelopathy and a lesion with ring enhancement; on the basis of these findings and clinical and laboratory analyses, the diagnosis of late postradiotherapy progressive myelopathy was reached.
Myeloma is the most common primary bone malignancy and one of the most common hematologic malignancies. The diagnosis is based on laboratory tests (monoclonal paraprotein in serum or urine), bone marrow aspiration, biopsy (greater than 10% of atypical plasma cells), and the typical radiological appearance of lesions. There are multiple classification systems, but the most widely used is Durie-Salmon classification, which includes plain-film findings in addition to laboratory analyses. An update incorporated MRI or PET/CT in the Durie-Salmon PLUS classification to determine the number of focal lesions and extent of the diffuse infiltration. Stage IA: Normal skeletal or a single lesion. Stage IB: Less than five focal lesions or mild diffuse disease. Stage IIA/B: 5–20 focal lesions or moderate diffuse disease. Stage IIIA/B: More than 20 focal lesions or severe diffuse disease. Subclasses A and B: (A normal renal function and B abnormal).
Fig. 5.7.2
Fig. 5.7.3
Fig. 5.7.4
103 Spine Solitary plasmocytoma is uncommon and occurs in only approximately 5% of patients with plasma cell myeloma; by strict definition, the diagnosis requires histologic confirmation of a monoclonal plasma cell infiltrate in one lesion, absence of other bone lesions, and a lack of marrow plasmacytosis. Often plasmocytoma is present for a year or more as an isolated lesion before the laboratory evidence of multiple myeloma manifests. Multiple myeloma develops in most patients in a few years. Plain-film radiography shows focal osteolytic lesions and diffuse inhomogeneous osteopenia. Sclerotic lesions are rarely seen, though they are more frequent after treatment. Several MRI patterns have been described, including from normal bone marrow signal to focal involvement, diffuse bone marrow infiltration, or combined focal and diffuse (salt and pepper) pattern. MRI studies should combine T1-weighted FSE sequences with fat-suppressed T2-weighted or STIR sequences. Focal lytic lesions can be large and there may be a soft-tissue mass with cord compression. On MRI, the soft-tissue mass appears as an expansile lesion that is hypointense on T1-weighted images and hyperintense on T2-weighted images. Recently, a pattern on axial MRI referred to as a “mini brain” was reported to be characteristic of vertebral plasmocytoma. In this pattern, curvilinear structures with low signal intensity on all imaging sequences extend partially through the vertebral body; these curvilinear structures result from the compensatory hypertrophy of the residual trabecular bone in the lytic vertebra that is responding to weight-bearing stress. The differential diagnosis includes metastasis, lymphoma, myeloproliferative disease, or atypical hemangiomas. Treatment includes biphosphonates to reduce fractures, chemotherapy, radiotherapy, and transplantation. Evaluation of the response to treatment should include the following parameters: serum or urine monoclonal gammopathy, reduction of plasma cell infiltration, reduction of the soft-tissue mass, and no increase in the size or number of lytic lesions. Progressive myelopathy is an uncommon complication of radiotherapy. The following three criteria must be fulfilled for the diagnosis: (1) inclusion of the spinal cord in the area irradiated; (2) location of the main lesion in the irradiated segments of the cord; (3) exclusion of other causes of compression. Radiation myelopathy normally becomes evident 6 months to 2 or 3 years after radiation therapy. Spinal MRI shows hyperintensity along the irradiated cord on T2-weighted FSE images and variable enhancement after gadolinium injection.
Figure 5.7.1 Sagittal T1-weighted FSE MRI shows an expansile lytic lesion in T8 with a softtissue mass (open arrow) extending toward the posterior elements and the superior and inferior vertebral bodies; the soft-tissue mass involves the epidural space and compresses the spinal cord, which is posteriorly displaced. Other small lytic lesions are also depicted. Figure 5.7.2 Corresponding sagittal STIR sequence shows a large hyperintense softtissue mass with pathological fracture on T8. Figure 5.7.3 Follow-up sagittal STIR image obtained 3 months later shows marked reduction in the size of the soft-tissue spinal mass (open arrow) and of the rest of lytic lesions. The bone marrow signal is diffusely lower due to fat infiltration. Figure 5.7.4 One year later, sagittal T2-weighted FSE image shows progressive reduction in the size of the lytic mass in T8 (open arrow) and ill-defined hyperintensity within the spinal cord, indicative of progressive myelopathy (solid arrow).
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Case 5.8 Fracture Dislocation
A 41-year-old patient presented at the emergency department after falling from a height of 4 m. Neurological exam revealed complete paraplegia of the lower extremities. Plain-film radiographs of the spine showed L1–L2 fracture dislocation with associated bilateral facet fracture. MDCT and MRI were performed to depict the relationships among the structures and the spinal canal and to evaluate injuries to the spinal cord and organs of the chest and abdomen.
Fig. 5.8.1
Fig. 5.8.2
Fig. 5.8.3
Fig. 5.8.4
105 Spine Vertebral bodies are joined by the intervertebral disc, and the posterior portions of adjacent vertebrae are connected by a ligament complex (supraspinous and interspinous ligaments, posterolateral joints, and ligamentum flavum). This ligament complex ensures spinal stability and avoids luxations. Sagittal-translation fractures are rare, occurring in approximately 3% of vertebral fractures. These complex fractures result from combined flexion and rotation forces: the posterior complex ruptures and the upper vertebrae swing on the lower. In the cervical region, pure dislocation occurs because of the horizontal orientation of its articular processes. In the lumbar region, the articular processes are oriented more vertically; thus, it is more common for them to undergo fracture and subsequent dislocation rather than pure luxation. On plain-film radiographs, bony anatomy may be obscured by overlying structures. Nevertheless, lateral views can demonstrate wedge deformity of the vertebral body, sagittal translations, and separation of the spinous processes. The AP view may identify lateral shift of the articular processes. Radiographic indicators of instability of vertebral fractures include the presence of translational components, compression greater than 50% of vertebral body height, fracture of the posterior elements, and increased interpeduncular distance. Fracture dislocations are therefore unstable by definition. MDCT, with its capability for multiplanar reconstructions in the coronal and sagittal planes, has changed the diagnostic approach to vertebral fractures. MDCT can precisely depict all the elements involved in the fracture and the status of spinal canal. MRI evaluation provides information about the integrity of soft tissues: posterior ligaments, discs, and spinal cord and extra-axial collections (epidural hematomas). Fat saturation T2-weighted images and STIR sequences may also reveal soft-tissue and bone edema, as well as spinal cord damage. Proton density-weighted images are best for assessing ligamentous integrity.
Introduction
Figure 5.8.1 Axial CT at L2 level demonstrates vertebral body fracture with retropulsion of the cortex of the posterior vertebral body and narrowing of the spinal canal. Note the fracture of right pedicle (arrow). Figure 5.8.2 MDCT with sagittal volume rendering reconstruction of the thoracolumbar spine confirms the fracture of the superior endplate of L2, with loss of vertebral body height anteriorly, and anterior luxation of L1 on L2. Reformatted images demonstrate widening of the spinous processes between L1 and L2, with associated fracture of the spinous process of L1 (open arrow). There is a small fracture of T12 superior endplate (solid arrow). Figure 5.8.3 Sagittal T1-weighted MRI of the lumbar spine shows L1–L2 luxation, fracture of the anterosuperior endplate of L2 (open arrow), and increased distance between the spinous processes with disruption of the interspinous ligament. Anterior and posterior (solid arrow) longitudinal ligaments are elongated without rupture. There is a small hyperintense epidural collection related to hematoma (arrowhead) as well as compression of the conus medullaris and cauda equina nerve roots. Figure 5.8.4 Sagittal STIR MRI shows marked high signal in the soft tissues (open arrow) and anterior disruption of the interspinous ligament (solid arrow). Bone-marrow edema is seen in the T12, L1, and L2 vertebral bodies, related to trabecular fractures.
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Case 5.9 Spondylodiscitis
a
b
Fig. 5.9.1
Fig. 5.9.3
Fig. 5.9.4
Fig. 5.9.2
Fig. 5.9.5
107 Spine A 76-year-old woman presented with an 8-week history of persistent low back pain despite analgesic treatment and constitutional symptoms. She had a previous history of recurrent urinary tract infections and diabetes. At physical examination, her temperature was 37.5° and tenderness over lumbar vertebrae was noted. Laboratory tests revealed increased C-reactive protein without leukocytosis. Comparing plain-film radiographs obtained in the emergency room with those obtained 1 month before suggested discitis; MRI and CT-guided biopsy confirmed the diagnosis.
Clinical History
Infectious discitis is an infl ammatory process of the intervertebral disc that usually involves the discovertebral junction and may extend into the epidural space, posterior vertebral elements, and paraspinal soft tissues. Spondylodiscitis accounts for 2–4% of all osteomyelitis. It may occur spontaneously, by hematogenous spread from distant septic foci, direct inoculation from spinal surgery or penetrating trauma, or direct extension. The most common causative organism is Staphylococcus aureus. Most patients present with back pain. Other symptoms, such as fever, anorexia, and weight loss may be present. Laboratory tests might reveal leukocytosis, but can be normal in tuberculous infection and in immunocompromised or older patients. C-reactive protein is the most reliable test because erythrocyte sedimentation rate (ESR) is variable, especially in older patients. Plain-fi lm radiographs of the spine are normal in the early stages of infection, and alterations are rarely seen before 2–4 weeks. MRI is the noninvasive method of choice for the diagnosis in the early stages space. Imaging fi ndings include decreased signal intensity of the intervertebral disk and adjacent vertebral body marrow on T1-weighted images, and high signal intensity on T2-weighted images. After intravenous administration of gadolinium, discs can show homogeneous, patchy, or peripheral enhancement. Adjacent bone marrow also enhances diffusely. The differential diagnosis of infectious discitis includes degenerative changes, ankylosing spondylitis, SAPHO syndrome (combination of synovitis, acne, pustulosis, hyperostosis, and osteitis), and neuropathic spine.
Introduction
Figure 5.9.1 Plain-film radiographs acquired in the emergency department (b) and 1 month before (a) show progressive destruction of the T12–L1 endplate, with erosion and kyphosis (open arrow in (a) and solid arrow in (b)). Marked degenerative changes in the rest of the spine are also evident. Figure 5.9.2 Sagittal MDCT multiplanar reconstructions clearly show the erosions and permeative pattern of the superior and inferior vertebral bodies adjacent to the T12–L1 disc space. Figure 5.9.3 Sagittal T1-weighted MRI shows decreased signal intensity of the subchondral bone marrow and marked erosion of the endplates adjacent to the T12–L1 intervertebral disc (open arrow). Degenerative L4-L5 spondylolisthesis (solid arrow) and small disc herniation in L3–L4 are also shown (arrowhead). Figure 5.9.4 Sagittal STIR MRI shows increased signal intensity with erosion of the vertebral bodies and fluid signal intensity in the T12–L1 intervertebral disc (open arrow). Figure 5.9.5 Contrast-enhanced sagittal fat-suppressed T1-weighted image reveals diffuse enhancement of the vertebral bodies without abscess (open arrow).
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Case 5.10 Sacral Chordoma
Fig. 5.10.2
Fig. 5.10.1
Fig. 5.10.3
Fig. 5.10.4
109 Spine A 54-year-old man had severe low back pain of several weeks’ duration that radiated to both legs. His medical history and physical examination were unremarkable.
Chordoma is the most common primary malignant sacral tumor; it accounts for 2–4% of malignant osseous neoplasms. Chordomas arise from the notochord, which is normally replaced by mesodermal tissue by the 7th week of development. Scattered vestiges of notochord may be found in the nucleus pulposus and can be present at any level from the base of the skull to the coccyx. Fifty to sixty percent of chordomas develop in the sacrococcygeal region. These tumors are found at all ages. The mean age at diagnosis is the sixth decade. Chordoma affects males twice as often as females. The classic appearance of chordoma is a destructive, lytic lesion, commonly with internal calcifications (30%). A large presacral soft-tissue component is usually present. These tumors are capable of extending across the adjacent disk space and the sacroiliac joint. Chordoma shows heterogeneous low signal intensity on T1-weighted images and prominent heterogeneously increased signal intensity on T2-weighted images, reflecting the high water content of the lesions. Contrast enhancement at MRI is common. The differential diagnosis includes other primary tumors (sarcoma, giant-cell tumor, and, rarely, ependymoma). Metastases are the most common sacral neoplasm. Total surgical resection provides the best hope for cure. MRI has proven highly accurate for evaluating the extent of disease. Most patients succumb to locally recurrent tumor because chordoma is relatively radioresistant, although patients with chordoma often survive many years after surgery. The 5-year survival in patients treated with radiation therapy is 50%.
Comments
Figure 5.10.1 Plain-film radiography of the sacrum is nonspecific and might reveal a lytic lesion, with obliteration of the cortex (open arrow). Figure 5.10.2 CT is useful to detect the internal calcifications (arrow) and the extent of the destructive soft-tissue mass within the sacrum. In this case, the mass extends across the sacral canal and the anterior neuronal foramina. Figure 5.10.3 MRI is the best imaging technique, showing low signal intensity on sagittal T1-weighted images and marked enhancement with a peripheral septal pattern after contrast administration (open arrowhead). Figure 5.10.4 T2-weighted MRI shows a heterogeneously (due to the presence of septa) hyperintense sacral mass with a presacral and soft-tissue component within the canal.
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Further Reading Books Clinical biomechanics of the spine. White A, Panjabi MM (1990). Lippincott Williams and Wilkins, Philadelphia Diagnostic Imaging: Spine. Ross JS, Brant-Zawadzki M, Chen MZ, Moore KR (2005). Elsevier, Philadelphia Imaging of the Musculoskeletal System. Pope TL, Bloem HL, Beltran J, Morrison W, Wilson D (2008). Saunders, Philadelphia Moe’s Textbook of scoliosis and other spinal deformities. Moe JH, Bradford DS (1995). WB Saunders, Philadelphia MR Imaging of the Spine and Spinal Cord. Uhlenbrock D (2004). Thieme, Stuttgart, NY
Web-Links http://www.srs.org/ http://www.asnr.org/spine_nomenclature/ http://myeloma.org/main.jsp?type = article&id = 889 http://www.essr.org http://www.serme.org/
Articles Baur-Melnyk A, Buhmann S et al. Role of MRI for the diagnosis and prognosis of multiple myeloma. Eur J Radiol 2005; 55(1):56–63 Bernstein MP, Mirvis SE et al. Chance-type fractures of the thoracolumbar spine: imaging analysis in 53 patients. AJR Am J Roentgenol 2006; 187(4):859–868 Bozzao A, Gallucci Met al. Lumbar disk herniation: MR imaging assessment of natural history in patients treated without surgery. Radiology 1992; 185(1):135–141 Costello RF, Beall DP. Nomenclature and standard reporting terminology of intervertebral disk herniation. Magn Reson Imaging Clin N Am 2007; 15:167–174, v–vi. Fardon DF. Nomenclature and classification of lumbar disc pathology. Spine 2001; 26: 461–462 Frymoyer JW. Back pain and sciatica. N Engl J Med 1988; 318: 291–300 Gallucci M, Bozzao A et al. Does postcontrast MR enhancement in lumbar disk herniation have prognostic value? J Comput Assist Tomogr 1995; 19(1):34–38
Gallucci M, Limbucci N, Paonessa A, Splendiani A. Degenerative disease of the spine. Neuroimaging Clin N Am 2007; 17: 87–103 Hiwatashi A, Danielson B, Moritani T, Bakos RS, Rodenhause TG, Pilcher WH et al. Axial loading during MR imaging can influence treatment decision for symptomatic spinal stenosis. AJNR Am J Neuroradiol 2004; 25:170–174 Imhof H, Fuchsjager M. Traumatic injuries: imaging of spinal injuries. Eur Radiol 2002; 12(6):1262–1272 Jackson RP, Cain JE Jr., Jacobs RR, Cooper BR, McManus GE. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus: II. A comparison of computed tomography (CT), myelography, CT-myelography, and magnetic resonance imaging. Spine 1989; 14:1362–1367 Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002; 137:586–597 Jensen MC, Brant-Zawadzki MN et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331(2):69–73 Keynan O, Smorgick Y et al. Spontaneous ligamentum flavum hematoma in the lumbar spine. Skeletal Radiol 2006; 35(9): 687–689 Koeller KK, Rosenblum RS et al. Neoplasms of the spinal cord and filum terminale: radiologic-pathologic correlation. Radiographics 2000; 20(6):1721–1749 Krishnan A, Shirkhoda A et al. Primary bone lymphoma: radiographic-MR imaging correlation. Radiographics 2003; 23(6): 1371–1383; discussion 1384–1387 Malfair D, Beall DP. Imaging the degenerative diseases of the lumbar spine. Magn Reson Imaging Clin N Am 2007; 15:221–238, vi Modic MT, Ross JS. Lumbar degenerative disk disease. Radiology 2007; 245:43–61 Mulligan ME. Myeloma update. Semin Musculoskelet Radiol 2007; 11(3):231–239 Scavone JG, Latshaw RF, Weidner WA. Anteroposterior and lateral radiographs: an adequate lumbar spine examination. AJR Am J Roentgenol 1981; 136:715–717 Schwarzer AC, Wang SC, O’Driscoll D, Harrington T, Bogduk N, Laurent R. The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine 1995; 20:907–912 van Tulder MW, Assendelft WJ, Koes BW, Bouter LM. Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies. Spine 1997; 22:427–434 Vilanova JC, Barcelo J. Diffusion-weighted whole-body MR screening. Eur J Radiol 2008; 67:440–447 Wilmink JT. CT morphology of intrathecal lumbosacral nerveroot compression. AJNR Am J Neuroradiol 1989; 10:233–248
Shoulder Fernando Idoate-Saralegui, and Joan C. Vilanova
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Case 6.1 Adhesive Capsulitis
Comments
A 44-year-old right-hand-dominant woman presented shoulder pain and dysfunction for 20 weeks. Pain started insidiously in the cervical spine 1 year previously and progressed to the right shoulder. Pain and stiffness were aggravated by all movements of the shoulder, but were most severe at rest. The intensity of pain and stiffness increased over time, and she complained of not being able to move her left arm and having difficulties in dressing and washing herself. At physical examination, both active and passive ranges of motion were severely restricted. She had no history of acute trauma, dislocation, previous shoulder surgery, or arthritis. No abnormalities were found at cervical MRI 2 months before. Previous physical therapy and antiinflammatory medication failed to improve her symptoms. We performed shoulder MR arthrography.
Adhesive capsulitis is a poorly defined entity. Codman coined the term “frozen shoulder” in 1934 to describe an entity characterized by slow onset of shoulder pain, inability to sleep on the affected arm, restriction of both active and passive elevation, and external rotation. In 1945, Neviaser described characteristic synovial changes in the glenohumeral joint in patients with frozen shoulder and suggested the term “adhesive capsulitis.” The estimated prevalence of adhesive capsulitis is 2–6%; it commonly affects women between the ages of 40 and 70 years. The pathogenesis of adhesive capsulitis is still unknown. It may be idiopathic, or it may occur after trauma or in association with diabetes mellitus or conditions such as Dupuytren’s disease or heart surgery. The course of
Fig. 6.1.1
Fig. 6.1.2
Fig. 6.1.3
Fig. 6.1.4
113 Shoulder idiopathic frozen shoulder syndrome is considered benign. Most authors state that symptoms resolve from 6 weeks to 10 years after presentation. Contralateral shoulder involvement occurs in up to 20–30% of patients. Nevasier described the three arthroscopic stages of adhesive capsulitis, supporting the hypothesis that the underlying pathological change is synovial inflammation with subsequent reactive capsular fibrosis. The most common diagnostic criteria are clinical; these include painful stiff shoulder for at least 4 weeks, severe shoulder pain that interferes with daily living activities or work activities, night pain, and painful restriction of both active and passive elevation to less than 100% and of external rotation (at the side) to less than 50%. Other causes must be excluded. Findings at plain-film radiography are usually normal, except for some decreases in bone mineral density during acute and secondary adhesive capsulitis. Arthrography has been the examination of choice for years and has even been proposed as a therapeutic alternative. Decreased joint capacity, obliteration of the axillary recess, and variable filling of the biceps tendon sheath have been considered essential for the correct diagnosis. Conventional MRI has been proposed as a noninvasive method of evaluation. MRI may show abnormal signal and thickness of the synovial membrane of the shoulder joint. However, MR arthrography is more reliable for visualizing capsular thickness and locating the anatomical region of inflammation associated with frozen shoulder, i.e., the rotator cuff interval and the coracohumeral ligaments. In 2004, Mengiardi et al. described thickening of the coracohumeral ligament and the capsule at the rotator cuff interval and complete obliteration of the fat triangle under the coracoid process (subcoracoid triangle sign) as characteristic MR arthrographic findings for frozen shoulder. MRI and MR arthrography also make it possible to rule out other causes of shoulder pain. Therapeutic options include physical therapy, mobilization and stretching, intraarticular corticosteroid injection, closed mobilization with anesthesia, and capsulotomy.
We performed shoulder MR arthrography, discontinuing the injection when the patient complained of pain and we felt a strong resistance through the syringe; we were able to inject 10 mL of 1 mmol/L diluted gadopentate dimeglumine (Magnevist; Schering, Berlin, Germany). Oblique coronal T1-weighted MR arthrogram (Fig. 6.1.1) shows considerable thickening of the joint capsule and synovium at the axillary pouch (open arrows); note the normal appearance of the supraspinatus tendon. Axial T1-weighted MR arthrogram (Fig.6.1.2) shows a marked decrease in the volumes of the axillary recess and posterior joint cavity (open arrow). The images reflect capsular retraction. Some contrast solution is seen outside the capsule (solid arrows); extracapsular contrast solution may be secondary to capsular rupture due to overdistension. Sagittal (Fig. 6.1.3) and axial (Fig. 6.1.4) T1-weighted MR arthrograms show a synovitislike lesion of intermediate signal intensity (open arrows) located at the subcoracoid fat triangle, obliterating the fat. The limits of the triangle are defined anterosuperiorly by the coracoid process (arrow), superiorly by the coracohumeral ligament (open arrowhead), and posteroinferiorly by the joint capsule (arrowhead). This obliteration of subcoracoid fat is a characteristic sign of adhesive capsulitis.
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A 30-year-old right-hand-dominant woman complained of sudden onset of severe pain and progressive weakness affecting her right shoulder and upper arm. Clinical examination revealed impaired shoulder abduction. There was some sensory disturbance along her lateral arm. Acute rotator cuff tendon rupture was suspected. Plain-film radiography showed no subacromial calcification. Shoulder ultrasonography excluded rotator cuff tear and subacromial bursitis. Findings at dedicated MRI of the shoulder were consistent with isolated involvement of the suprascapular nerve without compression of the structures at the suprascapular notch, as opposed to at the supraglenoid fossa. Electromyography found selective axonal neuropathy.
Case 6.2 Parsonage: Turner Syndrome
SS IS
SE
TM Fig. 6.2.3
Fig. 6.2.1
Fig. 6.2.4
Fig. 6.2.2
Fig. 6.2.5
115 Shoulder Parsonage-Turner syndrome (PTS), also known as acute brachial neuritis and neuralgic amyotrophy, is an uncommon clinical problem consisting of an idiopathic self-limiting neuropathy involving the brachial plexus that causes intense acute pain and progressive neuromuscular weakness. The exact cause of PTS is unknown. Many factors have been proposed to cause the neuritis, including trauma, infection, viral disease, heavy exercise, recent surgery, immunization, and autoimmune conditions. PTS is relatively rare, with a reported incidence of 1.64 cases per 100,000. It appears to affect males more often than females, with a peak in incidence in patients in their third and seventh decades. There does not seem to be any relationship to hand dominance. Bilateral involvement occurs in up to 30% of patients. The clinical presentation can be confusing, and there is considerable overlap of the typical signs and symptoms with a broad range of alternative diagnoses such as cervical spondylosis, rotator cuff tear, shoulder impingement syndrome, and acute calcific tendonitis. The classic clinical presentation is described as the sudden onset of severe shoulder pain followed by profound weakness with no known cause. The pain subsides over a few weeks, but weakness increases. No specific diagnostic test has been established, but a characteristic pattern of muscle signal change has been reported on MRI. The MRI findings of PTS are thought to reflect denervation injury, mainly diffuse high signal intensity involving one or more muscles innervated by the brachial plexus depicted on T2-weighted images. T1-weighted MR images may also show atrophy of the affected muscle(s). The pattern of muscular involvement should match the distribution of one or more peripheral nerves originating from the brachial plexus. Muscles innervated by the suprascapular nerve (supraspinatus (SS) and infraspinatus (IS) muscles) are most commonly affected, although other muscles around the shoulder may be involved. These findings are also nonspecific and may be seen in other myopathies or compression neuropathies. MRI allows the presence of ganglion cyst and masses or other compressive structures at the supraglenoid notch to be excluded. These are important distinctions to make, because treatment of PTS is conservative, whereas suprascapular nerve compression caused by a ganglion located at this fibro-osseous tunnel warrants surgical exploration. The diagnosis must be confirmed by electromyography showing denervation affecting muscles innervated by brachial plexus. Recovery generally occurs over the course of a few months but may take several years.
Comments
Sagittal T1-weighted depicts shoulder anatomy (Fig. 6.2.1). Sagittal STIR (Figs. 6.2.2 and 6.2.3) images show diffusely increased signal intensity (arrows) involving the IS and SS muscles; note the normal signal intensity of the subscapular (SE) and teres minor muscles (TM). Neither muscle atrophy nor fatty changes are noted on T1-weighted images. Oblique coronal T2-weighted fast spin-echo MRI (Fig. 6.2.4) shows diffuse high signal intensity throughout the SS muscle. Axial T2-weighted GRE image (Fig. 6.2.5) shows diffuse high signal intensity in the IS muscle (arrows). Note the absence of compressive structures at the suprascapular notch (solid arrows in Fig. 6.2.4) and spinoglenoid notch (solid arrows in Figs. 6.2.5). Rotator cuff tendons show no abnormalities and there are no signs of subacromial impingement. These MRI findings reveal what is probably neurogenic edema.
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Case 6.3 Bankart Lesion
A 27-year-old left-hand-dominant male soccer player presented 7 days after an initial anterior dislocation of his left shoulder successfully was reduced by the team physician at the field. He was treated with physical therapy and NSAIDs; 3 months later, he referred recurrent left shoulder pain and a painful popping. At physical examination, the range of motion was normal but with great apprehension,
Fig. 6.3.1
Fig. 6.3.2
Fig. 6.3.3
Fig. 6.3.4
117 Shoulder particularly in abduction and external rotation. He referred two other previous episodes 4 years before and provided a shoulder MRI done 2 years earlier. MR arthrography was done to evaluate the glenoid labrum, glenohumeral capsule, and rotator cuff. Arthroscopic evaluation showed an extensive detachment of the anterior, superior, and posterior labrum, which were repaired arthroscopically.
The classic labral injury described by Bankart is a complete detachment of the anteriorinferior labrum from the glenoid associated with a rupture of the scapular periosteum, without tear of the anterior band of glenohumeral ligament. The Bankart lesion represents the most common form of labroligamentous injury in patients with first-time traumatic dislocations of the shoulder. Due to the lost contact with the periosteum, the lesion shows no tendency to heal, and commonly a Bankart lesion will lead to recurrent subluxation, dislocation, or multidirectional instability. Surgical treatment (Bankart repair) consists of reattachment of the labro-ligamentous complex to the glenoid, either arthroscopically or during an open procedure. Although MRI may depict labral abnormalities, its accuracy is low. MR arthrography typically shows a deformed anteroinferior labrum, which is completely separated from the glenoid and therefore is “floating” in the anterior capsular recess adherent to the anterior band of the inferior glenohumeral ligament. In many cases, the torn periosteum can be visualized on axial MR arthrograms. The Hill–Sachs lesion is a posterosuperolateral notch defect in the humeral head created by a compression injury of the posterolateral humeral head against the anteroinferior aspect of the glenoid rim that develops during anteroinferior dislocation. The incidence of this lesion at arthroscopy varies considerably (from 47 to 100%) among different series of patients with first-time traumatic dislocations. The initial defect may become larger with repeated subluxations or dislocations. The Hill-Sachs lesion can be well seen in all routine imaging planes and is accurately depicted on MRI. On axial sequences, it is seen on the first three to four slices, at or above the level of the coracoid. Below this, there is a normal flattening of the posterior aspect of the humeral head.
Comments
Axial fat-saturated T1-weighted GRE (Fig. 6.3.1) performed 2 years before the current injury shows an irregular focus of high signal intensity in the anterior labrum (open arrow), interpreted as a probable labral tear. However, it was not possible to evaluate the degree of labral attachment to the glenoid. MR arthrography revealed severe detachment of the labrum. Axial T1-weighted SE (Fig. 6.3.2) MR arthrogram shows contrast medium between the glenoid rim and the detached labrum (open arrow) consistent with complete detachment of the anteroinferior labrum (Bankart lesion) and posterior labral tear (solid arrow); oblique sagittal fat-saturated T1-weighted image (Fig. 6.3.3) shows the extent of the anteroinferior labral injury (open arrows). Coronal fat-saturated T1-weighted MR arthrogram (Fig. 6.3.4) demonstrated a longitudinal tear posterior to the base of the attachment of the long head of the biceps tendon (SLAP) (open arrow). A mild Hill-Sachs deformity is observed (open arrowheads in Figs. 6.3.2 and 6.3.4).
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Case 6.4 Perthes Lesion
Fig. 6.4.1
Fig. 6.4.2
Fig. 6.4.3
Fig. 6.4.4
119 Shoulder A 25-year-old left-hand-dominant female competitive water polo player presented right shoulder pain since a traumatic injury 3 years earlier in a bike accident; she also referred two later episodes of anteroinferior shoulder luxations that she reduced by herself. She showed full active and passive range of motion and normal strength. At physical examination, the orthopedic surgeon observed pain during the apprehension test and positive Jobe and O’Driscoll tests. MR arthrography was performed to evaluate structural anomalies associated to instability.
The Perthes lesion is a variant of the Bankart lesion, which also occurs due to anteroinferior glenohumeral luxation and is associated to anterior instability. In the Perthes lesion, first described by the German surgeon Perthes in 1905, the anteroinferior labroligamentous complex is detached from the glenoid, but unlike in the Bankart injury, the scapular periosteum remains intact and stripped medially, resulting in an incomplete avulsion of the labrum from the glenoid margin. Therefore, unless only loosely attached, the labrum may remain in its normal anatomic position. The integrity of the periosteum allows partial “healing” of the labrum, which might also become resynovialized and may appear indistinguishable from a normal labrum on arthroscopic inspection. On conventional MRI, Perthes lesions can look normal and may be impossible to differentiate from a normal labrum. MR arthrography may reveal contrast medium extending between the glenoid and the base of the anteroinferior labrum, indicating a loose labrum and the loss of the stabilizing function. Nondisplaced Perthes lesions can also be difficult to detect at MR arthrography because scar tissue can prevent contrast material from entering the labral tear. Additional imaging with the arm in abduction and external rotation (ABER position) can at times help to visualize nondisplaced Perthes lesions by separating the base of the anteroinferior labrum from the glenoid and allowing the contrast media to enter. In the case presented, although the tear is still demarcated by contrast media in the ABER position, it is more conspicuous on the conventional axial section. Therefore, the surgeon should be aware of MRI findings that indicate the possibility of a Perthes lesion, because they may alter treatment planning.
Comments
Oblique sagittal T1-weighted MR arthrogram (Fig. 6.4.1) shows a labral tear that involves the anterior labrum (open arrows). Axial fat-suppressed T1-weighted MR arthrogram (Fig. 6.4.2) depicts detachment and slight displacement of the anterior labrum from the glenoid (open arrow); the labrum remains attached to the intact scapular periosteum (arrow). These findings are consistent with a Perthes lesion. Axial T1-weighted spin-echo MR arthrogram located inferior to the previous image (Fig. 6.4.3) shows a thin line of increased signal intensity (open arrow) under the attachment of the anterior labrum to the bony glenoid, consistent with a nondisplaced labral tear. Note the prominent Hill-Sachs defect (arrows). T1-weighted spin-echo MR arthrogram with fat saturation obtained in the ABER position (Fig. 6.4.4) shows partial detachment of the anterior labrum from the glenoid. Note the increased signal (open arrow) at the labral insertion to the glenoid.
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Case 6.5 Alpsa + Hill–Sachs Lesion
Fig. 6.5.2
Fig. 6.5.1
Fig. 6.5.4
Fig. 6.5.3
Fig. 6.5.6
Fig. 6.5.5
Fig. 6.5.7
121 Shoulder A 27-year-old left-hand-dominant male amateur handball player had his left shoulder dislocated by downward traction. When reduction on the field was unsuccessful, plain-film radiographs were acquired and the shoulder was reduced under conscious sedation. Seven days later, MRI to evaluate the capsulolabral complex showed hemarthros and anteroinferior labral tear. He declined to undergo surgery and opted for conservative therapy. Six months later, he suffered an anteroinferior reluxation of the shoulder. MR arthrography was performed to reevaluate the labrum.
ALPSA (anterior labroligamentous periosteal sleeve avulsion) lesion is an avulsion of the anteroinferior labrum from the glenoid with periosteal stripping, which leads to medial displacement and inferior rotation of the labroligamentous complex together with the intact periosteum in a sleeve-like fashion, thereby causing incompetence of the inferior glenohumeral ligament and anterior instability. As a result, the labrum is displaced medially near the scapular neck. ALPSA lesions were described by Neviaser as a variant of the Bankart lesion. In chronic ALPSA, the lesion may heal and resynovialize in this abnormal position and be covered by fibrous tissue formation and adjacent synovial proliferation. This may produce a pseudo-normal anterior labrum, which can be missed at arthroscopy. ALPSA is more common in patients with recurrent traumatic dislocations of the shoulder than with first-time dislocations. MR arthrography shows the medial and inferior displacement of the deformed labroligamentous complex; this is best seen on axial and coronal oblique images. The glenoid edge typically lacks a normal labrum; contrast medium often outlines a crease or cleft between the glenoid and the nodular-shaped fibrous tissue located medially on the glenoid neck. Transformation of the ALPSA lesion into a Bankart lesion by dissection of the complex from the glenoid followed by anatomic refixation (Bankart repair) is the treatment of choice. ALPSA lesion is often associated to Hill–Sachs defects.
Comments
The initial radiologic evaluation (Fig. 6.5.1) shows an anteroinferior luxation of the humeral head; the humeral head (open arrow) is not in the glenoid fossa (solid arrow). Axial T2-weighted (Fig. 6.5.2) and sagittal T1-weighted (Fig. 6.5.3) GRE images show hemorrhagic articular distension (note the isointense SI of articular fluid in the T1-weighted image). Sagittal image shows the absence of labrum at the anterior glenoid (arrow in Fig. 6.5.3); the anterior labrum is medially displaced (arrow in Fig. 6.5.2). These findings were consistent with labral disruption and possible ALPSA lesion. MR arthrography was performed after relaxation of the shoulder. Axial T1-weighted MR arthrogram (Fig. 6.5.4) shows the anterior-inferior labrum partly avulsed from the glenoid and located medial to the glenoid (open arrows); it remains attached to an intact scapular periosteum. Oblique coronal MR arthrogram (Fig. 6.5.5) shows inferior displacement of the labroligamentous complex (open arrow). A Hill–Sachs fracture with subjacent bone sclerosis and marrow edema in the posterolateral humeral head is demonstrated (open arrowheads at Figs. 6.5.6 and 6.5.7).
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Case 6.6 Glad Lesion and Calcified Loose Body
An elite male rugby player with a previous history of shoulder injuries (two clinically reported anteroinferior subluxations) and no complete shoulder dislocations reported a resubluxation (he fell onto his outstretched arm with the ball underneath his forearm and a player landed on top of his shoulder). The athlete described global and persistent shoulder pain without relief of symptoms after physiotherapy.
Fig. 6.6.1
Fig. 6.6.2
Fig. 6.6.3
Fig. 6.6.4
123 Shoulder Physical examination showed a marked reduction in the range of movement of the affected shoulder, mainly due to pain, and some impingement but no shoulder instability. A superior labral anterior-to-posterior tear (SLAP) was initially suspected and shoulder MR arthrography showed a nondisplaced superficial tear of the anteroinferior labrum adjacent to an area of articular cartilage erosion. After the MR arthrogram, a shoulder CT was performed.
The GLAD (glenolabral articular disruption) lesion as described by Neviaser is a superficial tear of the anteroinferior labrum that is held in place by an intact periosteum, in combination with an articular cartilage lesion (fibrillation and erosion) of the anterior inferior quadrant of the glenoid. The injury is thought to result from impaction of the humeral head onto the glenoid caused by forced adduction injury to the shoulder with the arm in abduction and external rotation. The labral component of the abnormality typically represents an inferior-based flap tear without evidence of capsuloperiosteal stripping; it is important to note that the anterior labroligamentous structures and the periosteum remain intact, so there is no displacement of the labrum and usually no anterior instability. The degree of articular cartilage damage is variable and ranges from softening and fibrillation to deep surface defects. When a GLAD lesion is seen at MRI, loose bodies should be sought and should not be misinterpreted as air bubbles (which appear at nondependent locations). MRA allows the labral flap tear to be seen by distending the joint and filling it with contrast material. The chondral defect also allows the integrity of the anteroinferior paralabral periosteum and IGHL to be evaluated. In a patient with a typical injury and no signs of instability, the GLAD lesion should be considered the cause of persistent pain. Identification of the lesion facilitates appropriate treatment, usually arthroscopic debridement of the labrum and adjacent chondral injury.
Comments
Fat-saturated T1-weighted GRE arthrogram (Fig. 6.6.1) reveals a nondisplaced labral tear; high signal gadolinium is tracked into the labrum (open arrow) showing a full-thickness defect of the adjacent glenoid cartilage (solid arrow). Axial T1-weighted SE MR arthrogram (Fig. 6.6.2) slightly caudal to Fig. 6.6.1 shows a full-thickness chondral defect of the anterior glenoid associated to subchondral sclerosis (open arrow). These findings correspond to a GLAD lesion. Fat-saturated T1-weighted GRE arthrogram (Fig. 6.6.3) shows a rounded intraarticular low signal intensity structure located in dependent regions of the anterior articular space near the glenoid insertion of the capsule, consistent with a loose body (open arrow). Inadvertently injected air bubbles are visualized in nondependent regions (solid arrow); note the blooming artifact, characteristic of air on GRE images. Corresponding shoulder CT (Fig. 6.6.4) confirms the presence of calcified loose bodies (open arrow) adjacent to the coracoid process (solid arrow).
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Case 6.7 Slap Lesion
Comments
A 21-year-old professional soccer goalkeeper presented with nonspecific shoulder pain that was particularly intense with overhead motions. He also complained of popping, clicking, and catching sensations, some weakness, and some pain on throwing. The patient referred a fall onto his outstretched arm with the shoulder in abduction during a match. He had undergone physiotherapy without improvement. On clinical examination, he had a full range of active and passive movements, but he referred pain in full abduction. Cuff examination was normal. The palm-up test was positive but he had no pain on palpation of the long head of the biceps tendon. Findings at examination of the acromioclavicular joint were normal. MR arthrography was performed.
SLAP tears, first described in 1990 by Snyder, are an abnormality of the superior labrum usually centered on the attachment of the long head of the biceps tendon. SLAP lesions occur at and posterior to the bicipital long head insertion into the superior labrum and
Fig. 6.7.1
Fig. 6.7.2
Fig. 6.7.3
Fig. 6.7.4
125 Shoulder usually affect athletes. Repetitive overhead motion or falling on an outstretched arm is the most frequent mechanism of injury. Recently, a study in cadavers confirmed the peel-back theory of SLAP lesions; in the abducted and externally rotated shoulder, the biceps tendon assumes a more vertical and posteriorly directed orientation, which transmits a force to the superior labrum, causing it to peel off the glenoid. The clinical diagnosis of a SLAP lesion is difficult. Nonspecific shoulder pain, particularly with overhead or cross-body motion, is the most common clinical presentation. Several examinations can be performed, including the anterior slide test, the O’Brien test, the Crank test, and the Speed test, although their accuracy is limited. SLAP lesions can lead to shoulder instability or be consequence of it. Imaging plays a key role in the diagnosis. MR arthrography has proven superior to conventional MRI at identifying SLAP lesions; MR arthrography is reliable in assessing the stability of the biceps anchor and detecting associated injuries. Distending the glenohumeral joint outlines the intraarticular and synovial surfaces and shows leakage of contrast through the labral tears, making the pathology more conspicuous and depicting the superior labrum and its relationship with the long head of the biceps tendon attachment to the glenoid. Four different types of SLAP lesions were described in Snyder’s original classification: Type I is degenerative fraying of the superior labrum with no instability of tendon; Type II is avulsion of the superior labrum and biceps anchor from the glenoid, causing an instable anchor; Type III is a bucket-handle tear of the superior labrum with preserved biceps anchor; and Type IV is similar to type III with extension of the tear into the long head of the biceps tendon. Several additional types of lesions have been described; these mainly represent combinations of the most common forms: the type II SLAP lesion with other injuries of the labrum, medial glenohumeral ligament, or rotator cuff. In practical terms, a description of the extent of the abnormality is sufficient, and the original Snyder classification is widely accepted. One of the major challenges of MR arthrography is the differentiation of SLAP lesions from capsulolabral anatomic variants such as sublabral recess and sublabral foramen. Numerous concurrent pathologies may be seen in association with SLAP lesions; these include tears of the glenohumeral ligaments, partial tears of the rotator cuff, Hill-Sachs defects, Bankart lesions, chondral loose bodies, and paralabral cysts.
Oblique coronal T1-weighted MR arthrograms (Figs. 6.7.1 and 6.7.2) show high signals throughout the superior labrum, extending anteriorly and posteriorly due to a tear (open arrows). The tear has a vertical and an additional horizontal contrast interface, which separate the avulsed superior labrum as a triangular-shaped fragment from the intact biceps tendon; these findings are consistent with a type III SLAP tear (bucket-handle tear). Most SLAP lesions are best depicted on MR arthrograms oriented in the oblique coronal plane. Oblique sagittal (Fig. 6.7.3) and axial (Fig. 6.7.4) planes show extensively high signals throughout the superior labrum, extending anteriorly and posteriorly (arrowheads) to the biceps anchor (solid arrow).
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Case 6.8 Posterior Labral Tear + Paraglenoid Labral Cyst
A 35-year-old male amateur tennis player complained of pain localized in the posterior aspect of the right shoulder of 3 years’ evolution. The patient also referred shoulder fatigue and clicking with activity, and these symptoms increased during the previous year. No pervious history of traumatic shoulder dislocation was referred. At physical examination, external rotation of the arm was significantly limited, while flexion and internal rotation were remarkably normal. Pain and sense of instability were elicited when the arm was held in the position of forward flexion,
Fig. 6.8.1
Fig. 6.8.2
Fig. 6.8.3
Fig. 6.8.4
127 Shoulder adduction, and internal rotation. The posterior drawer/relocation test showed posterior translation of the humeral head onto the glenolabral rim (clunking without locking). Preliminary X-rays were normal. MR arthrography was done.
Posterior instability is less frequent than anterior instability, accounting for only 2–5% of all cases of shoulder instability patterns. Its etiology is generally threefold, consisting of a major injury, a repetitive minor trauma, and a virtually atraumatic process. Common causes of posterior instability include traumatic posterior dislocation (usually during violent muscle contraction resulting from seizures or electrical shock), a redundant posterior capsule, and microinstability associated with overhead arm sports involving abduction, flexion, and internal rotation (weightlifters, baseball pitchers, racket sport athletes, footballers, and swimmers).The lesions associated with posterior instability can be identified in detail with MRI, particularly MR arthrography, allowing proper treatment planning. Findings at MR arthrography include an excessively retroverted or hypoplastic glenoid, a detached posterior capsule, posterior labral tear, and reverse Hill-Sachs lesion. Similar to anterior labral tears, posterior tears at MR arthrography are seen as fluid extending into the substance of the labrum. Paralabral cysts are associated with glenoid labral tear; a paralabral cyst is diagnosed when MRI shows a well-defined focal fluid collection within 1 cm of the glenoid labrum. The mechanism involved in paralabral cyst formation is similar to that of meniscal cyst formation, with extrusion of joint fluid through labrocapsular tears into adjacent tissue planes. Extraarticular extension of a labral cyst into the spinoglenoid notch or suprascapular notch can produce suprascapular nerve entrapment, which is a cause of shoulder pain that can be evaluated with MRI. Paralabral cysts may be difficult to identify on MR arthrography unless a T2-weighted sequence is performed. Cyst aspiration may result in temporary relief of symptoms, but an untreated labral tear should be suspected if cysts recur.
Comments
Axial T1-weighted MR arthrogram (Fig. 6.8.1) shows a posterior labral tear (open arrow); note the normal shape and signal intensity of the anterior labrum (solid arrow). A round structure of intermediate signal intensity is seen at the spinoglenoid notch (arrowheads) adjacent to the posterior labrum; this structure is also visualized on the coronal fat- saturated T1-weighted MR arthrogram (arrows in Fig. 6.8.2); it is not filled with gadolinium contrast material. After the usual arthrographic T1-weighted sequences, oblique coronal T2-weighted (Fig. 6.8.3) and sagittal STIR (Fig. 6.8.4) sequences performed to evaluate the posterior paralabral mass demonstrate the cystic characteristic of the mass (high signal intensity content) and enable the diagnosis of paralabral cyst. The cyst is located between the suprascapular and spinoglenoid notches near the 9 o´clock position of the posterior labrum (arrowheads), but no indirect signs of neural compression are seen (normal signal intensity of deltoid and rotator cuff muscles on STIR images).
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Case 6.9 Ambrii + Bilateral Labral Tears
A 15-year-old girl, a competitive kayaker, presented with recurrent bilateral shoulder pain, which was more intense in the right shoulder, where she referred a painful popping sensation. The patient had no history of acute trauma or dislocation but noted exacerbation of symptoms (mainly pain) while kayaking. Physiotherapy had failed to improve her symptoms. Pain disappeared after she stopped kayaking, but recurred after she started again. On physical examination of the right shoulder, no atrophy or tenderness to palpation was noted. She had markedly laxity in both shoulders with a positive sulcus sign in both shoulders. The patient had full active and passive range of motion. Cuff examination was normal. Biceps signs were negative. Findings at examination of the acromioclavicular joint were normal. Apprehension test was positive. MR arthrogram showed an anterior labral tear and a voluminous glenohumeral capsule. One year later, an MR arthrogram of the left shoulder for exacerbation of pain during training showed findings equivalent to the contralateral side.
Fig. 6.9.2 Fig. 6.9.1
Fig. 6.9.3
Fig. 6.9.4
129 Shoulder The term “instability” constitutes a spectrum of disorders, which includes hyperlaxity, subluxation, and dislocation. Instability of the shoulder is defined as abnormal or symptomatic motion, usually translocation of the humeral head with respect to the glenoid. Laxity, however, describes the passive motion characteristics of the joint. Shoulder instabilities can be divided into traumatic (TUBS from traumatic, unidirectional, bankart lesion, surgery), atraumatic glenohumeral instability (AMBRII from atraumatic multidirectional, bilateral, rehabilitation, inferior capsular shift, interval closure), and microtraumatic glenohumeral instabilities. Congenital or acquired hyperlaxity, microinstability, and traumatic instability can overlap, particularly in athletes engaged in overhead sports. Atraumatic glenohumeral instability is typically multidirectional and usually evident in individuals with congenital hypermobility syndrome. This instability permits abnormal motion in two or three planes, generally, anterior-inferior and posterior-inferior. The incidence of multidirectional instability peaks in the second and third decades of life, and most patients are younger than 35 years old. On clinical examination, these athletes exhibit bilateral, symmetric increases in shoulder laxity in association with generalized hyperlaxity of ligaments and joints. The increased baseline level of laxity can be advantageous for several types of sports, but also harbors a high risk of long-term injury with damage to intra- and periarticular structures. The two anatomic lesions associated with multidirectional instability are deficiency of the rotator interval and a redundant inferior capsular pouch. A voluminous inferior capsular pouch can lead to instability in all three directions. MR arthrography’s ability to distend the glenohumeral joint and its improved soft-tissue contrast makes it the procedure of choice to evaluate the capsular volume, labroligamentous complex, and articular surface of the rotator cuff. In most nonathletic AMBRII patients, MR arthrography shows increased capsular volume; in symptomatic athletes, laxity of the capsule is frequently associated with secondary damage to the labrum (which may be hypoplastic or torn, but can also appear swollen and show increased signal intensity due to more or less extensive degenerative change), the rotator cuff, the labrum, and the biceps anchor. MR arthrography can help with therapeutic decisions by identifying or ruling out significant intraarticular pathology that might represent an indication for surgical repair in addition to capsular reduction. If conservative management fails, multidirectional instability is usually treated surgically by inferior capsular shift and closure of the rotator interval.
Comments
Postarthrogram sagittal (Fig. 6.9.1) and axial (Fig. 6.9.2) T1-weighted images of the right shoulder show capsular laxity. There is a patulous anterior, inferior, and posterior joint capsule distended by the intraarticular contrast (open arrows); note the prominent capsule at the rotator interval (solid arrow). A small labral tear is shown (open arrowhead). MR arthrogram of the left shoulder 1 year later shows a voluminous anterior, posterior, and inferior capsular pouch attached to the capsule medially (arrows in Fig. 6.9.3). Axial (Fig. 6.9.3) and sagittal (Fig. 6.9.4) MR images show an anterior labral tear extending from 2 o’clock to 4 o’clock (arrowheads). These findings are consistent with atraumatic glenohumeral instability associated to bilateral labral tears.
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Case 6.10 Posterosuperior Impingement (Throwing Shoulder + GIRD)
Fig. 6.10.1 Fig. 6.10.2
Fig. 6.10.3
Fig. 6.10.5
Fig. 6.10.4
Fig. 6.10.6
131 Shoulder A 24-year-old right-hand-dominant elite professional handball player was referred for pain in his right shoulder. After his shoulder was caught down by a defender, he experienced severe pain during throwing. He referred mild chronic shoulder pain prior to the episode when throwing (mainly late cocking-acceleration phase) and a progressive decrease in throwing velocity over the previous 4 months. At clinical examination, he had almost full range of active and passive movement, with pain at 160° flexion and abduction. The Jobe test was positive. The palm-up test was also positive. Positive posterior translation was found. The Napoleon sign and lift-off test were negative. The acromioclavicular joint was normal. Shoulder ultrasound, MRI, and MR arthrography were performed.
Internal shoulder impingement syndromes result from the impingement of the soft tissues of the rotator cuff and joint capsule between the glenoid and the humerus. Posterosuperior glenoid impingement (PSI) was first described in 1993 by Walch et al in normal shoulders in the ABER (abduction external rotation) position when the posterosuperior rotator cuff comes into contact with the posterosuperior labrum. This shoulder entrapment may become pathologic in throwers and overhead athletes, such as baseball pitchers, tennis players, swimmers, javelin throwers, and handball players, in whom it usually affects the dominant shoulder. Posterosuperior impingement presents with acute or chronic posterior shoulder pain. It is thought to result from repetitive microtrauma during the late cocking and acceleration phases of the throw. A typical pattern of injuries develops (the so-called “kissing lesions”), which includes corresponding lesions of the undersurface of the rotator cuff, the posterosuperior labrum, the greater tuberosity, and the superior bony glenoid. Two etiologic theories have been postulated to explain this syndrome. Jobe et al postulated that chronic microtrauma of the anterior capsule (repetitive stretching) can provoke anterior microinstability, which causes anterior subluxation of the humeral head in abduction and external rotation during overhead movements and thus allows excessive contact between the rotator cuff and the posterosuperior glenoid. Burkhart and Morgan first developed a model of posterior-inferior capsule contracture, which changes the glenohumeral contact point in the late cocking position and leads to progressive stretching of the anterior capsule. These changes intensify what would otherwise be gentle pinching of the labrum, cuff, and joint capsule between the greater tuberosity and glenoid rim, as well as cause twisting shear stress tears of the posterior cuff and labrum. The evidence for this second theory is that many athletes with pathologic internal impingement have a clinically significant glenohumeral internal rotation deficit (GIRD) compared with the contralateral shoulder, presumably due to a tight posterior-inferior capsule. Although ultrasonography can depict rotator cuff tears, MRI, and especially MR arthrography are the techniquesof choice to depict intraarticular injuries to guide therapeutic decisions. MRI findings of posterior impingement in the throwing shoulder reflect the structural abnormalities after microtraumatic glenohumeral instability; these changes are best depicted by MR arthrography and include cortical irregularities, sclerosis and subchondral cyst formation in the posterior humeral head, laxity of the anterior capsule, labral injuries ranging from degeneration and fraying to tearing and detachment, SLAP (superior labral anterior to posterior) lesions, and articular surface tears of the rotator cuff. Unlike in patients
Comments
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with subacromial impingement, the supraspinatus lesion usually involves the posterior part of the tendon. Conservative treatment is usually called for in athletes with minor structural abnormalities, whereas surgical debridement and repair (eventually in combination with capsular plication) are indicated in the presence of relevant rotator cuff and labral lesions.
Imaging Findings
Coronal ultrasound scan (Fig. 6.10.1) of the supraspinatus shows an intrasubstance focus of hypoechogenicity (fiber defect) consistent with partial tear (open arrows) affecting the middle and articular thirds of the tendon. Coronal T2-weighted image (Fig. 6.10.2) shows subacromial-subdeltoid bursal thickening and fluid; the preinsertional fibers of the posterior supraspinatus tendon show a linear hyperintensity on the articular side of the tendon, suggesting a partial tear (“rim rent” tear) (open arrow). Oblique coronal T1-weighted MR arthrogram (Fig. 6.10.3) shows a tear in the articular surface and contrast accumulation in the undersurface of the substance of the tendon (open arrow); the arthrogram shows extension of the intraarticular gadolinium to the subacromial-subdeltoid bursa, consistent with complete tear; axial projection demonstrated a small “gap” consistent with a full-thickness supraspinatus tendon tear (open arrow in Fig. 6.10.4). A SLAP lesion with involvement of anterior labrum is also shown (solid arrows in Figs. 6.10.4 and 6.10.5). There are cortical irregularities in the posterior corner of the humeral head (open arrowheads in Fig. 6.10.6). Note the prominent axillary and anterior recesses of the glenohumeral capsule (solid arrowheads) in contrast to the thickened posterior capsule at the posterior capsular labral junction (open arrow at Fig. 6.10.6), which are associated with GIRD.
133 Shoulder
Further Reading Books Imaging of the Shoulder; Techniques and Applications. 1 ed. Baert AL (2006). Springer, Berlin Internal Derangements of Joint. 2 ed. Resnick D (2007). Saunders, Philadelphia Magnetic Resonance Imaging in Orthopedics and Sports Medicine. 3 ed. Stoller DW (2007). Lippincott Williams & Wilkinson, Philadelphia Magnetic Resonance Imaging in Orthopedic Sports Medicine. 1 ed. Pedowitz R, Chung CB, Resnick D (2008). Springer, Berlin The shoulder. 4 ed. Rockwood C (2009). Saunders, Philadelphia
Web-Links http://www.wheelessonline.com/ http://www.radiolopolis.com/ http://chorus.rad.mcw.edu/ http://www.secec.org/ http://www.jshoulderelbow.org/
Articles Armfield DR, Stickle RL, Robertson DD, Towers JD, Debski RE. Biomechanical basis of common shoulder problems. Semin Musculoskelet Radiol 2003; 7(1):5–18 Carroll KW, Helms CA. Magnetic resonance imaging of the shoulder: a review of potential sources of diagnostic errors. Skeletal Radiol 2002; 31(7):373–383 Chang D, Mohana-Borges A, Borso M, Chung CB. SLAP lesions: anatomy, clinical presentation, MR imaging diagnosis and characterization. Eur J Radiol 2008; 68(1):72–87 Chung CB, Corrente L, Resnick D. MR arthrography of the shoulder. Magn Reson Imaging Clin N Am. 2004; 12(1):25–38 Connell D, Padmanabhan R, Buchbinder R. Adhesive capsulitis: role of MR imaging in differential diagnosis. Eur Radiol 2002; 12(8):2100–2106 De Maeseneer M, Van Roy P, Shahabpour M. Normal MR imaging anatomy of the rotator cuff tendons, glenoid fossa, labrum, and ligaments of the shoulder. Magn Reson Imaging Clin N Am 2004; 12(1):1–10 Elsayes KM, Shariff A, Staveteig PT, Mukundan G, Khosla A, Rubin DA. Value of magnetic resonance imaging for muscle denervation syndromes of the shoulder girdle. J Comput Assist Tomogr 2005; 29(3):326–329 Gaskin CM, Helms CA. Parsonage-Turner syndrome: MR imaging findings and clinical information of 27 patients. Radiology 2006; 240(2):501–507
Grainger AJ. Internal impingement syndromes of the shoulder. Semin Musculoskelet Radiol 2008; 12(2):127–135 Harish S, Nagar A, Moro J, Pugh D, Rebello R, O’Neill J. Imaging findings in posterior instability of the shoulder. Skeletal Radiol 2008; 37(8):693–707 Hodler J. Technical errors in MR arthrography. Skeletal Radiol 2008; 37(1):9–18 Jost B, Gerber C. What the shoulder surgeon would like to know from MR imaging. Magn Reson Imaging Clin N Am. 2004; 12(1):161–168 Mengiardi B, Pfirrmann CW, Gerber C, Hodler J, Zanetti M. Frozen shoulder: MR arthrographic findings. Radiology 2004; 233(2):486–492 Moosikasuwan JB, Miller TT, Burke B. Rotator cuff tears: clinical, radiographic, and US findings. Radiographics 2005; 25(6): 1591–1607 Moosikasuwan JB, Miller TT, Dines DM. Imaging of the painful shoulder in throwing athletes. Clin Sports Med 2006; 25(3):433–443 Ouellette H, Kassarjian A, Tétreault P, Palmer W. Imaging of the overhead throwing athlete. Semin Musculoskelet Radiol 2005; 9(4):316–333 Robinson G, Ho Y, Finlay K, Friedman L, Harish S. Normal anatomy and common labral lesions at MR arthrography of the shoulder. Clin Radiol 2006; 61(10):805–821 Rudez J, Zanetti M. Normal anatomy, variants and pitfalls on shoulder MRI. Eur J Radiol 2008; 68(1):25–35 Sahin G, Demirtaş M An overview of MR arthrography with emphasis on the current technique and applicational hints and tips. Eur J Radiol 2006; 58(3):416–430 Sanders TG, Tirman PF, Linares R, Feller JF, Richardson R. The glenolabral articular disruption lesion: MR arthrography with arthroscopic correlation. AJR Am J Roentgenol 1999; 172(1):171–175 Tuite MJ, Petersen BD, Wise SM, Fine JP, Kaplan LD, Orwin JF. Shoulder MR arthrography of the posterior labrocapsular complex in overhead throwers with pathologic internal impingement and internal rotation deficit. Skeletal Radiol 2007;36(6):495–502 Vanderbeck J, Fenlin J. Shoulder: what the orthopaedic doctor needs to know. Semin Musculoskelet Radiol 2007; 11(1): 57–65 Waldt S, Burkart A, Imhoff AB, Bruegel M, Rummeny EJ, Woertler K. Anterior shoulder instability: accuracy of MR arthrography in the classification of anteroinferior labroligamentous injuries. Radiology 2005; 237(2):578–583 Wischer TK, Bredella MA, Genant HK, Stoller DW, Bost FW, Tirman PF. Perthes lesion (a variant of the Bankart lesion): MR imaging and MR arthrographic findings with surgical correlation. AJR Am J Roentgenol 2002; 178(1):233–237 Woertler K, Waldt S. MR imaging in sports-related glenohumeral instability. Eur Radiol 2006; 16(12):2622–2636
Elbow, Hand, and Wrist Juan de Dios Berná, Ana Canga, and Luis Cerezal
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Case 7.1 Slac Wrist
A 34-year-old male manual worker presented with chronic wrist pain that had increased over the last 6 months. He had a history of a fall on an outstretched hand more than 10 years ago. An MRI performed without prior radiographic study showed a complete rupture of the scapholunate interosseous ligament, the dorsal intercalated segment instability (DISI) pattern of wrist instability, extensive radioscaphoid chondral denudation, and marked bone remodeling of the distal radius. Additionally, a type 2 lunate of Viegas (presence of a facet joint between the hamate and lunate), with advanced chondromalacia in the proximal pole of the hamate bone, and a small central rupture of the triangular fibrocartilage (Palmer class 1A lesion) were observed. Scaphoid resection and carpal arthrodesis resulted in complete pain relief and good functional result.
Fig. 7.1.1
>10˚
Fig. 7.1.2
Fig. 7.1.3
Fig. 7.1.4
137 Elbow, Hand, and Wrist Scapholunate advanced collapse (SLAC) of the wrist refers to a specific pattern of osteoarthritis and subluxation secondary to scaphoid or scapholunate ligament injury with collapse on the radial side of the wrist. SLAC of the wrist is the most common pattern of degenerative arthritis in the wrist. It is more common in men than in women and typically affects manual workers in their dominant wrist. SLAC wrist pattern is the result of many radial-sided wrist entities. The most frequent cause of SLAC is untreated chronic scapholunate dissociation. Scaphoid nonunion advanced collapse (SNAC) is another common cause. Other etiologies include Preiser’s disease (idiopathic avascular necrosis of the scaphoid), midcarpal instability, intraarticular fractures involving the radioscaphoid or capitate-lunate joints, Kienböck disease, capitolunate degeneration, and inflammatory arthritis, such as seen in the crystalline deposition disorders of gout and calcium pyrophosphate dihydrate deposition disease (CPPD). SLAC degeneration follows a specific pattern, starting with narrowing of the radioscaphoid joint at the radial styloid aspect (stage 1A), which on radiographs appears as a sharp elongation of the radial styloid. As the disease progresses, the entire scaphoid fossa is involved (stage 1B). Complete collapse of the radioscaphoid joint changes the normal loadbearing ability of the midcarpal capitolunate joint. Shear stress destroys cartilage in the capitolunate joint and produces joint narrowing and sclerotic changes (stage 2). Characteristically, the radiolunate joint is preserved at all stages of SLAC wrist. Long-standing and untreated SLAC wrist might lead to chronic wrist pain, deterioration of range of motion, and decreased grip strength. Direct palpation of the scapholunate joint or radiocarpal joint generally elicits pain. Pain with resistance against active finger extension, while the wrist is held in passive flexion, is common. The scaphoid shift test also elicits pain. Differential clinical diagnoses of SLAC wrist arthritis include essentially any condition that causes dorsal radial wrist pain, including scaphoid fractures, de Quervain tenosynovitis, scapholunate dissociation, Kienböck disease, distal radial fracture, Preiser’s disease, and scaphotrapezoid-trapezial joint arthritis. Asymptomatic and mild symptomatic SLAC can often be managed with conservative treatment. When the condition becomes more symptomatic, surgery is recommended. In stage 1 SLAC, where the capitolunate joint is spared, proximal row carpectomy preserves partial wrist motion. In stage 2 SLAC, total wrist fusion often is more effective at relieving wrist pain.
Comments
Axial fat-suppressed T2-weighted MRI (Fig. 7.1.1) shows a complete rupture of the scapholunate ligament, involving both dorsal (open arrow) and volar (solid arrow) components. Sagittal T1-weighted MRI (Fig. 7.1.2) shows an increase in the capitolunate angle with lunate dorsiflexion (dorsal intercalated segment instability – DISI deformity). Coronal fat-suppressed T1- and T2-weighted MRI (Figs. 7.1.3 and 7.1.4) reveal chronic rupture of the scapholunate ligament (open arrow) with osseous misalignment and diffuse degenerative changes in the radioscaphoid joint and capitolunate joint (stage 2 SLAC), with chondral denudation, subchondral sclerosis, and marked focal remodeling of the distal radius scaphoid fossa. Note the existence of a type 2 lunate of Viegas and degenerative changes in the hamatolunate joint (hamatolunate impaction syndrome) (solid arrow).
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Case 7.2 Scaphoid Avascular Necrosis
Fig. 7.2.1
Fig. 7.2.3
A 32-year-old man with a history of a fall on his right wrist while playing soccer 5 years before, diagnosed with “wrist sprain” without radiographs, presented with pain and swelling in the anatomical snuff box and restriction of mobility by pain after a recent minor injury acquired while practicing karate. Radiographs showed scaphoid nonunion with a sclerotic proximal fragment; gadolinium-enhanced MRI showed nonenhancement of the proximal pole related to necrosis of the proximal fragment. At surgery, the complete absence of bleeding points confirmed necrosis of the proximal fragment, so vascularized bone grafting was performed. Two years after surgery, the patient remains free of pain and has the full range of motion in his wrist.
Fig. 7.2.2
Fig. 7.2.4
139 Elbow, Hand, and Wrist The scaphoid is the most commonly fractured bone of the carpus. Scaphoid fracture usually results from a fall on a dorsiflexed hand in young active individuals. Wrist disability is a relatively common problem after scaphoid fractures because of the frequency of complications such as delayed union, nonunion, avascular necrosis, deformity or carpal instability, and secondary osteoarthritis. The significant number of scaphoid fracture complications can be attributed to the peculiar vascular anatomy of this bone, with precarious blood supply, especially to the proximal pole, which makes it vulnerable to posttraumatic ischemia and avascular necrosis. The scaphoid bone receives its blood supply mainly from the radial artery, with the dorsal and volar branches entering through the distal portion of the bone. The presence of avascular necrosis of the proximal fragment is the main prognostic factor for outcome after the surgical treatment of scaphoid nonunion. Unfortunately, avascular necrosis has been difficult to diagnose accurately. Physical examination reveals tenderness in the “anatomic snuffbox,” decreased range of motion, swelling, and pain with dorsiflexion. Sclerotic changes in the proximal fragment on conventional radiographs and CT scans correlate poorly with vascular state. Bone scintigraphy is sensitive and can reveal early avascular necrosis, but has a low specificity because areas of minor damage or synovitis may give a positive result; furthermore, the spatial resolution of bone scintigrams is low. Gross inspection of the bone surface during surgery and the presence of punctate bleeding points are usually the most important tests for surgeons assessing the vascular state of the proximal pole in scaphoid nonunion. Signal intensity on conventional MRI is frequently patchy and variable on T1- and T2-weighted sequences in both necrotic and viable bone. Unenhanced MRI does not allow the degree of ischemia or viability of the proximal fragment to be reliably determined. Gadolinium-enhanced MRI is useful to accurately assess the vascular status of the proximal pole in scaphoid nonunions: gadolinium enhancement represents viable bone and the absence of enhancement indicates necrosis. The treatment of scaphoid nonunion with viable proximal pole is bone grafting and internal fixation. Vascularized bone grafting is the recommended therapeutic option in cases of scaphoid nonunion with avascular necrosis in the absence of periscaphoid arthritic changes or established carpal collapse. In long-standing scaphoid nonunion with advanced degenerative changes of the wrist, a salvage procedure is indicated, usually proximal row carpectomy or total wrist fusion.
Comments
Anteroposterior plain-film radiograph (Fig. 7.2.1) shows nonunion of the proximal third of the scaphoid with a sclerotic proximal fragment (open arrow). Coronal fat-suppressed T1and T2-weighted images (Figs. 7.2.2 and 7.2.3) show a proximal fragment that is hypointense on T1-weighted images and hyperintense on T2-weighted images. Oblique sagittal fat-suppressed T1-weighted image (long axis of the scaphoid) after administration of intravenous gadolinium (Fig. 7.2.4) shows the absence of enhancement the proximal fragment (solid arrow), indicating complete necrosis.
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Case 7.3 Intraosseous Ganglia of the Lunate (“PseudoKienböck” Disease) Comments
A 35-year-old woman presented with an 18-month history of right wrist pain and a radiolucent lesion of the lunate on plain-film radiographs. On presentation, tenderness was detected on the dorsal side of the lunate with pain at extreme degrees of motion and without focal swelling. A previous MRI study had misdiagnosed Kienbock’s disease. A new MRI study showed an intraosseous ganglion in the lunate bone with cortical rupture and extension into the scapholunate joint and diffuse lunate bone edema. The lesion was successfully treated surgically with curettage and bone grafting. Three years after surgery, the patient is asymptomatic and the radiographic appearance of the lunate has returned to normal.
Cyst-like lesions in the carpal bones are generally asymptomatic and are often detected incidentally on plain-film radiographs after injuries to the wrist and hand. Intraosseous ganglia are benign cystic lesions located in the subchondral bone adjacent to a joint. They
Fig. 7.3.1
Fig. 7.3.2
Fig. 7.3.3
Fig. 7.3.4
141 Elbow, Hand, and Wrist are often multiloculated lesions filled with fibrous tissue and show mucoid changes. The scaphoid and lunate are most commonly involved. The nature of intraosseous ganglia is still unclear. It is generally believed that there are two types: the primary or idiopathic intraosseous lesion and the secondary lesion caused by the cortical penetration of a previously existing soft-tissue ganglion. The primary type is more frequent. In most cases, cortical defects are demonstrated at surgery. Clinically, intraosseous ganglion always presents as wrist pain. On plain-film radiographs, it appears as a well-defined osteolytic lesion with a surrounding sclerotic area. Bone scintigraphy can differentiate cysts with increased osteoblastic activity from inactive unchanging cysts that should be followed radiographically. CT scans are extremely helpful in locating the cortical defect of the cyst. In most cases of lunate cortical erosions, the defect is located in the lateral (scapholunate) articular surface of the bone. MRI helps delineate the tissues surrounding the bony lesion. The differential diagnosis of painful lytic lesions of the lunate includes enchondroma, chondroblastoma, osteoblastoma, fibrous dysplasia, giant cell tumor, osteoid osteoma, chondromyxoid fibroma, unicameral bone cyst, Kienböck’s disease, rheumatoid arthritis, osteoarthritis, and intraosseous ganglion. Signal change in the lunate bone is often misdiagnosed as Kienböck’s disease. This occurs with particular frequency in ulnar impaction syndrome and intraosseous ganglion of the lunate. In ulnar impaction syndrome, chondromalacia, sclerosis, cysts, and subchondral edema occur on the radial side of the lunate. The distribution of radiographic changes within the lunate bone is the key to distinguishing these conditions from Kienböck’s disease. Intraosseous ganglia appear on plain-film radiographs as an area of hyperlucency, which is frequently radial-sided in communication with the scapholunate joint space. Intraosseous ganglia have low-signal intensity on T1-weighted MRI and high-signal intensity on T2-weighted images, similar to the signal intensity of water. Sharper margins on radiographs and a lack of changes in MRI signal intensity in the triquetral bone or ulnar head help in the diagnosis. The signal intensity pattern in Kienböck’s disease may mimic ulnar impaction syndrome; however, Kienböck’s disease lesions are more diffuse or involve the radial side of the lunate bone compared to involvement of only the ulnar aspect in ulnar impaction syndrome. Furthermore, the triquetral bone and the ulnar head are not affected in Kienböck’s disease. Indications for surgery on intraosseous ganglia include progression of the cyst and continued pain. Most symptomatic intraosseous ganglia can be treated successfully with curettage and bone grafting. Recurrence has been reported, but is unusual.
Anteroposterior plain-film radiograph of the right wrist (Fig. 7.3.1) showing a well-defined cystic lesion in the radial side of the lunate bone with a peripheral sclerotic ring (open arrow). CT (Fig. 7.3.2) shows the cystic lesion of the lunate and fracture of the lunate radial cortex (solid arrow). Fat-suppressed T1- and T2-weighted images (Figs. 7.3.3 and 7.3.4) show a well-defined cystic lesion with cortical breakage and diffuse edema in the lunate bone (arrowheads).
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Case 7.4 Glomus Tumor in the Thumb
Fig. 7.4.1
Fig. 7.4.2
Fig. 7.4.3
Fig. 7.4.4
143 Elbow, Hand, and Wrist A 51-year-old male presented with a 2-year history of pain in the nail bed of his right thumb, which was exacerbated by local pressure and cold. Physical examination revealed a blue focus of discoloration beneath the nail and deformity of the nail plate. Plain-film radiographs of the thumb showed subtle dorsal bone erosion in the distal phalanx. Ultrasound revealed a 5-mm solid hypoechoic nodule beneath the nail, with marked vasculature within the tumor at color Doppler. Thumb MRI demonstrated a well-circumscribed oval nodule that was hypointense on T1-weighted images and enhanced after intravenous administration of contrast material. On T2-weighted images, the tumor was homogeneously hyperintense with a thin hypointense rim. The tumor was surgically excised and the diagnosis of a glomus tumor was established histologically.
Glomus tumors in the fingers are rare benign tumors that arise from the neuromyoarterial glomus, which is an end-organ apparatus with arteriovenous anastomoses (without a capillary bed), located either beneath the nail or over the palmar aspect of the fingertip. The mean age at presentation ranges from 30 to 50 years, and there is a three-to-one female predominance. Clinically, glomus tumors present as a classic triad of paroxysmal pain, hypersensitivity to cold, and point tenderness. Ultrasound can usually visualize the subungual tumor, showing a hypoechoic nodule that appears hypervascular at color Doppler due to the high-velocity flow of intratumor shunt vessels. MRI shows a nodule that is hypo/isointense on T1-weighted images and hyperintense on T2-weighted images, with marked contrast enhancement. When the tumor measures less than 2 mm, both ultrasound and MRI are usually negative. The differential diagnosis includes benign and malignant subungual tumors, such as chondroma and metastasis from lung cancer. The treatment is surgical removal. To avoid nail deformity, it is better to use a periungual approach for tumors in the peripheral region and a transungual approach followed by meticulous repair of the nail bed for tumors in the central region. Recurrent tumors are common. Ultrasound seems less efficient than MRI for differentiating residual tumor tissue from postoperative scar.
Comments
Photograph of the thumb (Fig. 7.4.1) shows a focal deformity of the nail plate (open arrow). Axial and sagittal fat-suppressed T2-weighted images (Figs. 7.4.2 and 7.4.3) show an oval, well-circumscribed, homogeneously hyperintense nodule with a thin hypointense rim (solid arrows) beneath the right thumb nail. Photograph of the thumb after nail avulsion (Fig. 7.4.4) shows the typical macroscopic appearance of the glomus tumor (arrowhead).
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Case 7.5 Carpal Boss
Fig. 7.5.1 Fig. 7.5.2
Fig. 7.5.3
Fig. 7.5.4
145 Elbow, Hand, and Wrist A 24-year-old male presented with a 1-month history of a painful, hard, nonmobile bump at the base of the third metacarpal on the dorsum of his right hand. Palmar flexion of the wrist increased pain and showed the bump more clearly. The patient reported a minor trauma while playing basketball. Lateral plain–film radiographs of the wrist showed an accessory ossicle: os styloideum. MRI revealed bone marrow edema in the accessory ossicle and in the adjacent metacarpal. In light of the absence of clinical improvement, the patient was treated with simple resection of the os styloideum.
Carpal boss could be defined as a bony prominence on the dorsal aspect of the second or third carpometacarpal joint; it may represent degenerative osteophyte formation and/or an accessory ossification center (os styloideum), which is frequently fused to the metacarpal. Its relationship with incomplete dorsal osseous coalition and the absense of the normal dorsal ligament in the carpometacarpal joint has recently been reported. Carpal boss is more common in women (2:1) and in the right hand; its incidence peaks between the third and fourth decades. Although generally asymptomatic, it can occasionally cause pain and limitation of hand motion because of trauma, degenerative changes, or slippage of the extensor carpi radialis longus and brevis tendons. Lateral plain–film radiographs of the wrist with 30° of both supination and ulnar deviation (“carpal boss view”) are usually sufficient to show the bony prominence, so MRI generally is not required to make a specific diagnosis. Nevertheless, MRI provides complementary information, showing bone marrow edema, osteoarthritic changes, joint effusion, and anomalies of extensor tendons. The symptoms have also been attributed to the formation of a small ganglion or inflamed bursa that may develop over the abnormal bone, making the differential diagnosis between carpal boss and dorsal wrist ganglion more challenging. Surgical removal is indicated when conservative treatment does not relieve symptoms. A wedge-shaped carpometacarpal joint resection is usually performed. Care must be taken to remove less than 35% of the joint to prevent carpometacarpal instability.
Comments
Lateral plain-film radiograph of the wrist (“carpal boss view”) (Fig. 7.5.1) shows a small accessory ossicle (os styloideum) over the base of the third metacarpal (open arrow). Sagittal T1-weighted (Fig. 7.5.2), fat-suppressed T2-weighted (Fig. 7.5.3), and axial fatsuppressed T2-weighted (Fig. 7.5.4) images show bone marrow edema in the os styloideum and in the adjacent metacarpal bone (solid arrows).
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Case 7.6 De Quervain Tenosynovitis
Fig. 7.6.2
Fig. 7.6.1
Fig. 7.6.3
Fig. 7.6.4
147 Elbow, Hand, and Wrist A 47-year-old right-handed woman presented with a 6-month history of pain over the radial styloid of her right wrist that was exacerbated by grasping heavy objects. She had no history of trauma. Physical examination indicated tenderness and swelling in the first extensor compartment. Pain increased with thumb and wrist motion, and the Finkelstein test was positive. Ultrasound and MRI confirmed the diagnosis of de Quervain tenosynovitis, and multiple accessory tendons in the first extensor compartment were observed. The patient underwent surgical decompression.
De Quervain disease is a typical example of overuse tenosynovitis of the wrist. This condition usually affects patients who perform repetitive movements of the thumb such as typists and piano players. Low-grade chronic microtrauma at the level of the radial styloid can lead to localized thickening of the extensor retinaculum and subsequent impingement of the extensor pollicis brevis (EPB) and abductor pollicis longus (APL) tendons within the narrow osteofibrous tunnel of the first extensor compartment (stenosing tenovaginitis), which usually entails tendon sheath inflammation (tenosynovitis). The mean age at presentation ranges from 35 to 55 years, and there is a female predominance (8:1). A useful diagnostic maneuver is the Finkelstein test: the patient holds his or her thumb inside the clenched fist while the examiner tilts the wrist in an ulnar direction to stretch the tendons of the first extensor compartment (the test is positive if pain or tenderness is present over the radial styloid). Plain-film radiographs may show focal cortical erosion, sclerosis, or periosteal bone apposition of the radial styloid, and the differential diagnosis should be made with rhizarthrosis and scaphoid fracture. Ultrasound can usually confirm the diagnosis of de Quervain’s tenosynovitis; the ultrasound findings include thickening of the EPB and APL tendons with thickening of the synovial sheath, which usually appears hypervascular at color Doppler due to inflammatory hyperemia. In addition, a thickened and hypoechoic extensor retinaculum is usually observed. In acute phases, a hypoechoic sheath effusion can be demonstrated caudal to the distal edge of the retinaculum. MRI shows enlargement of the EPB and APL tendons and peritendinous edema. There may be high-signal fluid within the tendon sheath on T2-weighted images, and contrast enhancement of the synovial sheath is usually observed. Two main anatomic variants may be encountered in the first compartment: a septum between the EPB and APL and accessory tendons. The intertendinous septum is a vertically oriented band that divides the first compartment into two distinct spaces. It appears hypoechoic on ultrasound and hypointense on both T1- and T2-weighted MRI sequences. Accessory tendons are usually associated with the APL. Axial images (both ultrasound and MRI) give a better view of the retinaculum, intertendinous septum, and accessory tendons. Injection of corticosteroids into the tendon sheath cures this disease in most patients, but surgical release of the first extensor compartment is occasionally required.
Comments
Axial sonogram (Fig. 7.6.1) and longitudinal color Doppler sonogram (Fig. 7.6.2) show a thickened tendon with synovial hypertrophy (hypervascular pattern) and effusion in the tendon sheath (open arrows), just caudal to the distal edge of the extensor retinaculum (which appears hypoechoic and thickened) (solid arrow). Axial T2- and coronal T1-weighted images (Figs. 7.6.3 and 7.6.4) show first extensor compartment tendinosis and surrounding tenosynovitis (arrowheads).
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Case 7.7 Distal Biceps Tendon Rupture
Fig. 7.7.2 Fig. 7.7.1
Fig. 7.7.3
Fig. 7.7.4
149 Elbow, Hand, and Wrist A 24-year-old male manual laborer presented with a sudden painful left elbow after attempting to lift a heavy object. He reported hearing and feeling a pop directly in front of the elbow. Pain, swelling, bruising, and a palpable defect with a proximal lump in the anterior aspect of the arm were perceived on physical examination of the elbow. Complete distal biceps tendon avulsion was confirmed by ultrasound and MRI. The tendon was reattached to the radial tuberosity using a single anterior incision and suture anchors.
Distal biceps tendon rupture is an uncommon injury, representing less than 5% of all biceps ruptures. Conversely, it is the most commonly (completely) torn tendon of the elbow. The distal biceps tendon is approximately 7 cm long and it curves laterally and deeply before inserting into the medial aspect of the radial tuberosity. An aponeurotic expansion (bicipital aponeurosis, also known as lacertus fibrosus) connects the biceps tendon to the medial deep fascia overlying the flexor muscles, covering the median nerve and brachial artery. Rupture usually occurs in the dominant extremity of 40–60-year-old males during heavy weightlifting or vigorous eccentric contraction against resistance with a flexed forearm. The tendon typically tears from the radial tuberosity. A complete tear of the tendon with proximally retracted muscle (“Popeye” sign) is a straightforward clinical diagnosis, but in cases of an intact lacertus fibrosus and consequent absence of significant muscle retraction, the clinical differential diagnosis with partial tears and bicipitoradial bursitis is difficult. In such cases, ultrasound and/or MRI play a key role. Ultrasound is performed with the elbow extended and the patient’s forearm in maximal supination to bring the radial tendon insertion into view; dynamic imaging (with slight supinationpronation or flexion-extension) is especially useful for differentiating complete from partial tears. Traditionally, optimal MRI of the distal biceps tendon is performed in the axial plane with the patient’s arm extended; longitudinal views are difficult to obtain because of the oblique course of the tendon. The FABS (Flexed elbow, ABducted shoulder, forearm Supinated) view with the patient in superman position creates tension in the tendon and minimizes its obliquity and rotation, resulting in a “true” longitudinal view of the tendon. The treatment of choice for complete rupture is early surgical repair. Several different techniques to secure the distal end of the biceps tendon back to the radial tuberosity have been described; the two most common techniques are a two-incision technique using a bone tunnel and single-incision technique with suture anchors or endobutton.
Comments
Longitudinal gray-scale sonogram through the anterior elbow (Fig. 7.7.1) shows hypoechoic fluid filling the distal bed of the retracted distal biceps tendon and surrounding its myotendinous junction (open arrows). Sagittal T2-weighted image (Fig. 7.7.2) shows complete distal biceps tendon avulsion, which appears thickened and retracted (solid arrow). Axial T1-weighted image (Fig. 7.7.3) and fat-suppressed T2-weighted image (Fig. 7.7.4) show fluid surrounding the myotendinous junction (arrowheads) that crosses medially over the median nerve and brachial artery (indicating lacertus fibrosus rupture).
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Case 7.8 Posterior Dislocation of the Elbow
Fig. 7.8.2
Fig. 7.8.1
Fig. 7.8.3
Fig. 7.8.4
151 Elbow, Hand, and Wrist A 32-year-old male manual laborer presented with a shortened left forearm held in flexion. A prominent mass (olecranon) was noted behind the elbow. He reported falling from a 2-meter height onto his outstretched left hand. Plain-film radiographs confirmed the diagnosis of posterior dislocation. After manipulative reduction, plain-film radiographs showed good alignment of bones and no fractures. MRI showed humeral avulsion of both medial and lateral ligament complexes, disruption of anterior and posterior joint capsule, and bone contusion involving the capitellum. The ligaments were reattached surgically and the patient underwent physical therapy.
Elbow dislocation is the most common joint dislocation in children and is second only to shoulder dislocation in adults. The most common type is posterior elbow dislocation (both ulna and radius) and the mechanism of injury is typically a fall onto an outstretched hand. Elbow dislocations can be divided into two categories: simple (without fracture) or complex (with fracture). The ipsilateral upper extremity should be examined for other injuries as well, particularly shoulder and wrist fractures and disruption of the distal radioulnar joint. It is important to note that the ulnar nerve, median nerve, and brachial artery can be compromised. Anteroposterior and lateral plain-film radiographs of the elbow should be obtained to both confirm the diagnosis and detect fractures. After closed reduction, CT is very useful to evaluate intraarticular fractures (i.e., radial head, capitellum, coronoid process), which is important for deciding the appropriate management of the injury. MRI is indicated to assess bone marrow, capsuloligamentous, and soft-tissue injuries. The medial collateral ligament and lateral collateral ligament are responsible for the ligamentous stability of the elbow. These ligaments are well seen on coronal images. The medial (or ulnar) complex consists of three bands: anterior, posterior, and transverse; the anterior band provides most of the resistance to valgus stress. The lateral complex has four bands: the radial collateral ligament, the annular ligament, the accessory collateral ligament, and the ulnar collateral ligament, which courses posteromedially behind the radial neck to insert in the proximal ulna and its oblique orientation allows for lateral and posterior stabilization of the elbow. During elbow instability, capsuloligamentous injury progresses from lateral to medial (stages 1–3), and the elbow might dislocate completely while the anterior band of the medial collateral ligament remains intact (stage 3A), although both medial and lateral complexes are usually avulsed (stage 3B). There is also a variable degree of injury to the common flexor and extensor musculature.
Comments
Lateral plain-film radiograph of the left elbow (Fig. 7.8.1) shows posterior dislocation of the ulna and radius in relation to the distal humerus (open arrow). Coronal T2-weighted gradient-echo images (Figs. 7.8.2 and 7.8.3) show diffuse edema (bone contusion) in the posterior capitellum and complete avulsion of both the medial and lateral collateral ligaments (solid arrows). Sagittal T2-weighted gradient-echo image (Fig. 7.8.4) shows disruption of the anterior and posterior joint capsule (arrowheads).
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Case 7.9 Occult Fracture of the Radial Head
Fig. 7.9.1
Fig. 7.9.3
Fig. 7.9.2
Fig. 7.9.4
153 Elbow, Hand, and Wrist A 32-year-old man with a history of a motorcycle accident 2 months earlier presented with persistent of elbow pain and severe functional impairment. Plain-film radiographs showed no pathological findings. MRI showed an occult fracture of the radial head. CT study was performed to better define the three-dimensional anatomy of the articular fracture and plan the therapeutic approach. The joint was immobilized with a cast and the patient made a complete functional recovery after physical therapy.
The elbow fractures most commonly seen involve the head of the radius (60%), followed by fractures of the distal humerus (30%) and of the coronoid process (5%). Plain-film radiographs usually reveal the abnormality. In some cases, however, particularly if a radial head or coronoid process fracture is nondisplaced or minimally displaced, it may not be apparent on routine examination. In the management of fractures of the elbow, especially of the head of the radius and the capitellum, the correct diagnosis is fundamental not only to decide whether or not to operate, but also to determine the type of surgical procedure that may be indicated. Radiographically occult or equivocal fractures of the elbow may be assessed with MRI. MRI is useful for detecting and characterizing radial head fractures; it is also helpful in ruling out associated collateral ligament injury that may contribute to instability. The integrity of the medial collateral ligament is especially important if excision of the radial head is being considered. When there is ligamentous disruption and instability, displaced fractures of the radial head are best treated with internal fixation. On MRI, radial head fractures are indicated by linear decreased signal intensity within the radial head surrounded by edema. Coronal T1-weighted SE MRI shows the intraarticular fracture with cortical disruption (arrowhead) and mild compression of the radial surface.
Comments
Coronal fat-suppressed T1- and T2-weighted MRI (Figs. 7.9.1 and 7.9.2) show a nondisplaced fracture (open arrows) of the radial head surrounded by bone marrow edema. Coronal and axial CT images (Figs. 7.9.3 and 7.9.4) reveal an intraarticular fracture with cortical disruption (solid arrows) and mild compression of the radial surface.
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Case 7.10 Pigmented Villonodular Synovitis of the Elbow
Fig. 7.10.1
Fig. 7.10.2
Fig. 7.10.3
Fig. 7.10.4
155 Elbow, Hand, and Wrist A 31-year-old man presented with a 6-month history of occasional pain and stiffness in his right elbow. He had no history of trauma. On physical examination, no local heat or tenderness was observed, but discrete swelling and limited range of movement was noted. Plainfilm radiographs were normal. MRI did not show any obvious abnormality, but small effusion and heterogeneous contrast enhancement of the synovium were observed. MR arthrography showed hypertrophied synovium in both the anterior and posterior recesses of the elbow joint with inner hypointense foci on gradient-echo images. The patient underwent a complete arthroscopic synovectomy, and the diagnosis of diffuse pigmented villonodular synovitis (PVNS) was confirmed histologically.
PVNS is a rare benign disorder of an uncertain nature that can affect any synovial joint, bursa, or tendon sheath (also known as giant cell tumor of tendon sheath). Although PVNS was initially considered an inflammatory reactive process, recent observations have shown that this disease may actually be a benign neoplastic process with specific genetic alterations. Most patients range from young to middle-aged adults, and there is a slight male predominance. PVNS almost always involves only one articulation and has a predilection for the lower extremities, particularly the knee. It results in synovial hypertrophy with diffuse hemosiderin deposits within the joint, which virtually never calcifies. The usual clinical presentation includes progressive swelling, stiffness, and locking of the joint. Plain-film radiographs may show a dense effusion and, in tight joints, extrinsic pressure bone erosions. MRI shows synovial thickening and enhancement after intravenous administration of contrast material. Hemosiderin is a magnetic material, its deposit on proliferative synovial tissue results in a spotty low-signal or extensive low-signal area on T1-weighted and T2-weighted images, best visualized on gradient-echo images. Fat-suppressed sequences obscure these deposits. Therefore, foci of low-signal intensity lining and within hypertrophied synovium on gradient-echo images are pathognomonic of PVNS, and the differential diagnosis with noncalcified synovial chondromatosis and rheumatoid pannus is easier to make. PVNS has two presentations in joints: diffuse and focal. If focal, simple surgical excision is appropriate. If diffuse, it is associated with a high risk of local recurrence, so complete synovectomy is indicated. Adjuvant treatment modalities such as medication (imatinib), radiotherapy, or radiosynoviorthesis are sometimes used after synovectomy.
Comments
Sagittal and axial fat-suppressed MR arthrography images (Figs. 7.10.1 and 7.10.2) show filling defects in both the anterior and posterior recesses of the elbow joint due to hypertrophied synovium (open arrows), which contains foci of low-signal intensity that are better depicted on sagittal T2-weighted gradient-echo images (Fig. 7.10.3) (solid arrows). Arthroscopic image (Figs. 7.10.4) shows a lobulated red and brown mass (arrowheads).
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Further Reading Books Atlas de disección anatomoquirúrgica del codo. Llusa M, Forcada P, Ballesteros JR, Carrera A (2009). Elsevier, Amsterdam Green’s Operative Hand Surgery. Green D, Hotchkiss R, Pederson W, Wolfe S (2005). Churchill Livingstone, Philadelphia Imaging of the Musculoskeletal System. Pope T, Morrison B, Bloem H, Beltran J, Wilson D (2007). Elsevier, Amsterdam MRI of Upper Extremity: Shoulder, Elbow, Wrist, and Hand. Steinbach L, Chung CB (2009). Lippincott Williams & Wilkins, Philadelphia Muñeca-Mano Diagnóstico por la imagen. Enfasis en la RM. Recondo JA (2007). Osatek. Vitoria.
Web-Links http://www.eatonhand.com/ http://emedicine.medscape.com/radiology#musculoskeletal http://www.mskcases.com/ http://www.uhrad.com/ http://www.orthopaedicweblinks.com/Teaching_Resources/ index.html
Articles Al-Qattan MM, Al-Namla A, Al-Thunayan A, Al-Subhi F, El-Shayeb AF. Magnetic resonance imaging in the diagnosis of glomus tumors of the hand. J Hand Surg [Br] 2005; 30:535–540 Alemohammad AM, Nakamura K, El-Sheneway M, Viegas SF. Incidence of carpal boss and osseous coalition: an anatomic study. J Hand Surg [Am] 2009; 34:1–6 Bain GI, Turner PC, Ashwood N. Arthroscopically assisted treatment of intraosseous ganglions of the lunate. Tech Hand Up Extrem Surg 2008; 12:202–207 Bennett DC, Hauck RM. Intraosseous ganglion of the lunate. Ann Plast Surg 2002; 48:439–442 Cerezal L, Abascal F, Canga A, Garcia-Valtuille R, Bustamante M, del Pinal F. Usefulness of gadolinium-enhanced MR imaging in the evaluation of the vascularity of scaphoid nonunions. AJR Am J Roentgenol 2000; 174:141–149 Cerezal L, Abascal F, Garcia-Valtuille R, Del Pinal F. Wrist MR arthrography: how, why, when. Radiol Clin North Am 2005; 43:709–731
Cheng XG, You YH, Liu W, Zhao T, Qu H. MRI features of pigmented villonodular synovitis (PVNS). Clin Rheumatol 2004; 23:31–34 Chew ML, Giuffre BM. Disorders of the distal biceps brachii tendon. Radiographics 2005; 25:1227–1237 Cunningham PM. MR imaging of trauma: elbow and wrist. Semin Musculoskelet Radiol 2006; 10:284–292 Dailiana ZH, Zachos V, Varitimidis S, Papanagiotou P, Karantanas A, Malizos KN. Scaphoid nonunions treated with vascularized bone grafts: MRI assessment. Eur J Radiol 2004; 50:217–224 Diop AN, Ba-Diop S, Sane JC et al. [Role of US in the management of de Quervain’s tenosynovitis: review of 22 cases]. J Radiol 2008; 89:1081–1084 Drape JL. Imaging of tumors of the nail unit. Clin Podiatr Med Surg 2004; 21:493–511 Duckworth AD, Ring D, Kulijdian A, McKee MD. Unstable elbow dislocations. J Shoulder Elbow Surg 2008; 17:281–286 Giuffre BM, Moss MJ. Optimal positioning for MRI of the distal biceps brachii tendon: flexed abducted supinated view. AJR Am J Roentgenol 2004; 182:944–946 Glajchen N, Schweitzer M. MRI features in de Quervain’s tenosynovitis of the wrist. Skeletal Radiol 1996; 25:63–65 Ilyas AM, Ast M, Schaffer AA, Thoder J. De quervain tenosynovitis of the wrist. J Am Acad Orthop Surg 2007; 15:757–764 Kaplan LJ, Potter HG. MR imaging of ligament injuries to the elbow. Radiol Clin North Am 2006; 44:583–594 Murphey MD, Rhee JH, Lewis RB, Fanburg-Smith JC, Flemming DJ, Walker EA. Pigmented villonodular synovitis: radiologicpathologic correlation. Radiographics 2008; 28:1493–1518 O’Dwyer H, O’Sullivan P, Fitzgerald D, Lee MJ, McGrath F, Logan PM. The fat pad sign following elbow trauma in adults: its usefulness and reliability in suspecting occult fracture. J Comput Assist Tomogr 2004; 28:562–565 Oka Y, Umeda K, Ikeda M. Cyst-like lesions of the lunate resembling Kienbock’s disease: a case report. J Hand Surg [Am] 2001; 26:130–134 Park MJ, Namdari S, Weiss AP. The carpal boss: review of diagnosis and treatment. J Hand Surg [Am] 2008; 33:446–449 Waitayawinyu T, McCallister WV, Katolik LI, Schlenker JD, Trumble TE. Outcome after vascularized bone grafting of scaphoid nonunions with avascular necrosis. J Hand Surg [Am] 2009; 34:387–394 Waitayawinyu T, Pfaeffle HJ, McCallister WV, Nemechek NM, Trumble TE. Management of scaphoid nonunions. Orthop Clin North Am 2007; 38:237–249 Watson HK, Ballet FL. The SLAC wrist: scapholunate advanced collapse pattern of degenerative arthritis. J Hand Surg [Am] 1984; 9:358–365 Weiss KE, Rodner CM. Osteoarthritis of the wrist. J Hand Surg [Am] 2007;32:725–746
Hip and Pelvis Ara Kassarjian, José Martel-Villagrán, and Ángel Bueno-Horcajadas
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Case 8.1 Postpartum Sacral Fracture
Fig. 8.1.1
Fig. 8.1.3
Fig. 8.1.2
159 Hip and Pelvis A 35-year-old woman presented with right-sided sciatica one week after an uncomplicated vaginal delivery.
There is a wide variety of causes of postpartum pelvic pain, some of which are mechanical in nature. Peripartum sacral fractures, although relatively uncommon, are a recognized cause of postpartum low-back, sacral, or pelvic pain. The exact cause of these fractures is not clear. Pregnancy-related metabolic bone disease, such as osteoporosis, might be a contributing factor. However, it is not entirely clear whether these fractures are fatigue or insufficiency fractures. Clinicians should remember to include sacral fractures within the possible etiologies of postpartum low back and pelvic pain. As demonstrated in this case, MRI can be useful in diagnosing osseous, ligamentous, or muscular etiologies of such pain. Postpartum sacral fractures are typically not visible on radiographs. However, MRI clearly shows the classic appearance of a fracture, which may be unilateral, as in this case, or bilateral. On T1-weighted imaging, a hypointense vertical linear line is seen along the lateral margin of the sacrum. A similar line is often also visible on T2-weighted imaging. In addition, the typical bone marrow edema pattern is seen adjacent to the line, resulting in diffuse low signal adjacent to the fracture line on T1-weighted images and high signal on T2-weighted images.
Comments
Coronal T1-weighted MRI (Fig. 8.1.1) shows a low signal intensity fracture line (open arrow) paralleling the sacroiliac joint with adjacent low signal marrow edema (solid arrow). Coronal T2-weighted MRI (Fig. 8.1.2) shows a low-signal intensity fracture line (open arrow) paralleling the sacroiliac joint with adjacent high signal marrow edema (solid arrow). Oblique fat-suppressed T2-weighted images (Fig. 8.1.3) clearly demonstrate the fracture line with extensive associated bone marrow edema (open arrows).
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Case 8.2 Acute Avulsion Fracture of the Ischial Apophysis
Fig. 8.2.1
Fig. 8.2.2
Fig. 8.2.3
Fig. 8.2.4
161 Hip and Pelvis A 13-year-old girl presented initially with fever and right gluteal pain. She had recurring pain following exercise and while sitting, since an injury to her right pelvic region 1 year earlier. Fifteen days before admission, she had a new injury in the same region. The pain persisted to the point that the night before admission she had acute pain in the right gluteal region requiring analgesics every 3 hours.
Physical examination showed right hip pain on internal rotation and right gluteal tenderness on palpation. Her laboratory tests were all within normal limits. Apophyseal avulsion fractures of the pelvis are common among skeletally immature patients. One of the most common fractures involves the apophysis of the ischial tuberosity, where the hamstrings insert. Ischial apophyseal avulsions are common in children participating in sports that require rapid and forceful hamstring contraction such as sprinting, soccer, and even cheerleading. The injury typically results in acute pain in the gluteal region with loss of strength of the ipsilateral hamstrings and either inability to walk or an antalgic gait. On radiographs, ischial apophyseal avulsions typically appear as a small curved fragment of bone separated from the ischial tuberosity. Occasionally, the separation may be subtle and only noticeable as a mild widening of the physis when compared to the contralateral normal side. At MRI, acute apophyseal avulsions are typically seen as periosteal stripping, hemorrhage, edema, and a fluid-filled cleft between the apophysis and the ischial tuberosity. Significant edema of surrounding soft tissues may be present. In severe cases, significant displacement of the fragment and resultant laxity of the hamstring tendons can give them a wavy appearance. The apophysis itself may be difficult to see depending on the amount of hemorrhage as well as the degree of mineralization of the fragment. In subacute to chronic cases, the MRI appearance can be confusing and may even mimic a neoplastic process. Thus, it is imperative to know the common sites of avulsion injuries in the pelvis to avoid misdiagnosis and subsequent unwarranted biopsies.
Comments
Plain-film radiograph (Fig. 8.2.1) shows a curvilinear bone fragment (open arrow) adjacent to the lateral margin of the right ischial tuberosity (arrow), which is somewhat flattened and irregular compared to the contralateral side. Coronal T1-weighted MRI (Fig. 8.2.2) shows enlargement and ill-definition of the proximal hamstring tendons (open arrow) with some loss of the adjacent fat planes. A thin hypointense curvilinear structure (arrow) represents the avulsed mineralized apophysis. Coronal STIR image (Fig. 8.2.3) shows a hyperintense cleft (open arrow) between the osseous fragment and the ischial tuberosity. The avulsed hamstring tendons (arrow) are expanded, ill-defined, and surrounded by hyperintense edema and hemorrhage. Axial STIR image (Fig. 8.2.4) again shows a hyperintense cleft (open arrow) between the osseous fragment and the ischial tuberosity. The avulsed hamstring tendons (arrow) are expanded and show edema and hemorrhage between the tendon fibers. The sciatic nerve (arrowhead) is surrounded by hemorrhage and edema.
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Case 8.3 Transient Osteoporosis of the Hip
Fig. 8.3.2
Fig. 8.3.1
Fig. 8.3.3
Fig. 8.3.4
163 Hip and Pelvis A 38-year-old man with a 15-day history of progressive mechanical left hip pain presented with increasingly intense pain radiating from the left lumbar region to the left ankle. His pain was so intense that he was unable to walk. On physical examination, he had no spinal or paraspinal tenderness or tenderness over the sacroiliac joints. He had tenderness over the left inguinal region. He had the full range of motion of his left hip, although movements were painful. Neuromuscular exam showed loss of sensation over the lateral thigh but was otherwise normal.
Transient osteoporosis of the hip is a self-limiting syndrome of unknown etiology. Although this idiopathic entity was first described in pregnant women, it is currently seen more commonly in males in their third to fourth decades. Apart from a possible elevation in the erythrocyte sedimentation rate, laboratory findings are typically normal. Initially, plain-film radiographs may be normal whereas bone scintigraphy shows homogeneous increased uptake in the affected femoral head and neck. Subsequent radiographs typically show unilateral demineralization of the femoral head and neck. At MRI, there is a bone marrow edema pattern involving the femoral head and neck, characterized by loss of signal intensity on T1-weighted sequences and high signal intensity on fluid-sensitive sequences (T2, STIR). Associated effusions are common. The pattern of edema must be differentiated from the two other common causes of femoral head and neck edema: osteonecrosis and fractures. One discriminating feature of transient osteoporosis (also called transient bone marrow edema) is the absence of a hypointense line in the femoral head or neck. Following gadolinium administration, homogeneous diffuse enhancement of the marrow in the edematous areas (without unenhanced areas) differentiates this entity from osteonecrosis. Although other diseases, such as neoplasms, can result in marrow edema, they are typically accompanied by other features that help differentiate them from transient osteoporosis. It may be difficult to differentiate transient osteoporosis from infection based, solely on imaging findings. Although transient osteoporosis of the hip is typically a self-limiting disease, the clinical course may be somewhat protracted, with resolution requiring 6–10 months.
Comments
Coronal T1-weighted MRI (Fig. 8.3.1) demonstrates decreased signal in the femoral head and neck (arrow). There is no linear component to the signal abnormality. Axial T1-weighted MRI (Fig. 8.3.2) demonstrates decreased signal in the femoral head (open arrow). There is no linear component to the signal abnormality. Fullness and low signal along the anterior capsule (arrow) represents an effusion. Coronal STIR image (Fig. 8.3.3) shows increased marrow signal in the femoral head and neck (open arrow), consistent with edema. A small effusion is present (arrow). Axial STIR image (Fig. 8.3.4) shows increased marrow signal in the femoral head (open arrow), consistent with edema. A small effusion is present (arrow).
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Case 8.4 Osteolysis Associated with Total Hip Arthroplasty
Fig. 8.4.2
Fig. 8.4.1
Fig. 8.4.3
Fig. 8.4.4
165 Hip and Pelvis A 65-year-old man presented with a 1-month history of atraumatic inguinal and greater trochanteric pain 18 months after total hip replacement for hip fracture. His pain was greater than in the immediate postoperative period and worse in the mornings and when starting to walk. At physical examination, he had nearly full range of hip motion, although painful, and tenderness over the greater trochanter. Loosening of the prosthesis was seen, but the patient declined surgery. Three years later, he developed progressive coxalgia and lumbalgia. He now walks with crutches and has painful limitations of hip flexion, abduction, and adduction but no trochanteric pain.
Although initially called “cement disease,” periprosthetic osteolysis can be seen with both cemented and noncemented prostheses. Although motion in and of itself can cause radiographic lucencies, the lucencies of osteolysis are typically more focal, can be larger, and are more lobular with endosteal scalloping. There may be associated osseous expansion. With larger lesions, the findings may mimic a neoplastic process. Periprosthetic lucencies may be related to loosening, foreign body granulomatous reaction, or infection; however, these entities are not mutually exclusive. For instance, it is not uncommon for loosening to be present in cases of extensive foreign body granulomatous reaction. In fact, some theorize that the granulomatous reaction is actually related to loosening. CT has proven more sensitive than plain-film radiographs to osteolysis associated with prostheses. Serial radiographs do, however, play an important role in the follow-up of hip prostheses, since subtle areas of osteolysis may only be apparent on comparison with prior radiographs.
Comments
Initial postoperative frontal radiograph of the left hip (Fig. 8.4.1) shows a noncemented total hip prosthesis. There is no evidence of hardware-related complications. Frontal radiograph of the left hip 1 year after total hip replacement (Fig. 8.4.2) shows new radiolucencies greater than 2 mm along the superior margin of the acetabular component (open arrow) and along the proximal lateral margin of the femoral component (solid arrow). These findings are suspicious for loosening. Radiograph 2 years after hip replacement (Fig. 8.4.3) demonstrates marked progression of the radiolucencies, particularly along the acetabular component (open arrow). The acetabular component has moved into a more horizontal orientation and is causing remodeling and sclerosis along the medial wall of the acetabulum (arrowhead). More small linear lucencies are also more prominent along the proximal femoral stem (solid arrows). Radiograph 4 years after hip replacement (Fig. 8.4.4) shows extensive acetabular osteolysis with marked protrusio acetabuli and cranial migration of the acetabular component (open arrow). Only a very thin portion of the medial acetabular wall remains intact (solid arrow). Areas of osteolysis along the proximal femoral stem are seen both along its medial (open arrowhead) and lateral aspects. There may be insipient ankylosis between the superior margin of the greater trochanter and the adjacent ilium (closed arrowhead).
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Case 8.5 Osteomalacia with Looser Zones
Fig. 8.5.1
Fig. 8.5.3
Fig. 8.5.2
Fig. 8.5.4
167 Hip and Pelvis A 42-year-old man presented with left knee pain. MRI showed a nondisplaced fracture along the inferior pole of the patella, despite the absence of a history of trauma. Three months later, he had right ankle pain, clinically diagnosed as a sprain. Since the pain did not resolve, MRI was performed and showed a distal fibular fracture. Seven months later, he had right inguinal pain, right ulnar pain, and left hand pain. MRI showed bilateral femoral neck stress fractures, right ulnar fracture, and left third metacarpal fracture. Given the multiple atraumatic fractures, the possibility of myeloma was investigated, even though there was no evidence for myeloma. Further laboratory tests showed a mildly elevated parathyroid hormone level, normal vitamin D levels, and evidence of decreased renal tubular absorption of phosphates. The clinical diagnosis was hypophosphatemic osteomalacia.
Osteomalacia refers to an abnormality of bone due to inadequate or delayed osteoid mineralization. This affects mature cortical and cancellous (spongy) bone. X-linked inherited renal tubular deficiency or phosphate absorption is the most common cause of hypophosphatemic osteomalacia. Adult skeletal manifestations of X-linked hypophosphatemic osteomalacia include diffuse sclerosis, well-defined osteophytes, and Looser zones or Milkman’s pseudofractures. Looser zones are radiolucencies that typically run perpendicular to the cortex of bone and appear similar to fatigue or other insufficiency fractures. In long bones, they may be seen on the convex (tensile) side of the bone. These lucencies represent unmineralized osteoid and can be painful. Given the abnormal bone, these may progress to complete fractures. As these are areas of abnormal bone, these fractures can be considered insufficiency fractures because they occur under normal loading. Treatment for osteomalacia can be monitored by assessing the response/regression of these Looser zones.
Comments
Frontal radiograph of the pelvis (Fig. 8.5.1) shows bilateral inferomedial femoral neck lucencies (open arrows), consistent with insufficiency fractures. Coronal T1-weighted MRI of the pelvis (Fig. 8.5.2) shows hypointense lines on both femoral necks involving the marrow and extending to the cortex (open arrows). Coronal STIR image (Fig. 8.5.3) of the pelvis shows bilateral femoral neck marrow edema (open arrows) and bilateral periosteal and soft-tissue edema (solid arrows). Axial STIR image (Fig. 8.5.4) shows bilateral femoral neck marrow edema (open arrows) due to the bilateral femoral neck insufficiency fractures. Coronal STIR image of the pelvis shows bilateral femoral neck marrow edema (open arrows) and bilateral periosteal and soft-tissue edema (solid arrows).
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Case 8.6 Femoroacetabular Impingement (Predominantly Cam Type)
Fig. 8.6.1
Fig. 8.6.2
Fig. 8.6.3
Fig. 8.6.4
169 Hip and Pelvis A 23-year-old athlete presented with worsening of chronic right hip pain over the past year. He had no history of acute hip injury. Physical examination revealed pain on flexion and internal rotation and a slightly decreased range of motion compared to the left hip.
Femoroacetabular impingement (FAI) is a well-recognized cause of hip pain in athletes of all ages. In essence, FAI implies abnormal contact between the femur and the acetabulum. In cam-type FAI, which appears more frequently in young athletic males, the dominant abnormality is a loss of the normal offset or concavity along the anterosuperior head-neck junction with a relatively normal acetabulum. There are many methods of quantifying the head-neck morphological abnormalities, including measuring the alpha angle, degree of epiphyseal extension, and head-neck offset. In cam-type FAI, damage to the anterosuperior cartilage of the acetabulum occurs initially and is then followed by damage to the anterosuperior acetabular labrum. The triad of an increased alpha angle, anterosuperior cartilage lesions, and anterosuperior labral lesions as seen on MR arthrography is typical of cam-type FAI. In pincer-type FAI, which is more common in middle-aged women, the predominant abnormality involves the acetabulum. Some causes of pincer-type FAI include acetabular retroversion (focal or diffuse), acetabular overcoverage, and coxa profunda. In pincer-type FAI, initially there is damage to the anterosuperior labrum with cartilage damage appearing afterwards. There is also a possible contrecoup lesion, which appears as cartilage damage and bony changes along the posteroinferior acetabular rim and femoral head. Although FAI has classically been divided into cam and pincer types, most patients have a mixed type of FAI with one form predominating. There is some evidence that femoral neck synovial herniation pits or fibrocystic change may be associated with FAI, although it is not clear whether these lesions are more common with cam-type FAI, pincer-type FAI, or occur in equal frequency in the two types. Fibrocystic change or edema along the femoral neck warrants close attention to the subtle changes of FAI. Treatment of FAI involves restoring the normal osseous anatomy and treating associated lesions of the cartilage and labrum. For the femoral contour, osteochondroplasty is often performed to restore the normal concavity of the anterosuperior femoral head-neck junction. Acetabular overcoverage can be treated with acetabular rim trimming or, in severe cases, acetabular reorientation using a periacetabular osteotomy. Labral lesions are repaired if possible and cartilage lesions are typically debrided, although cartilage repair techniques such as microfracture may be attempted.
Comments
Oblique fat-suppressed T1-weighted MR arthrogram (Fig. 8.6.1) demonstrates a subtle loss of the normal concavity/offset along the anterior head-neck junction (open arrow). Coronal fat-suppressed T1-weighted MR arthrogram (Fig. 8.6.2) demonstrates subtle epiphyseal extension along the superolateral head-neck junction (open arrow). Sagittal fat-suppressed T1-weighted MR arthrogram (Fig. 8.6.3) demonstrates an anterosuperior labral tear (open arrow). Axial fat-suppressed T2-weighted image from another patient (Fig. 8.6.4) shows subtle marrow edema along the anterior head-neck junction (open arrow).
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Case 8.7 Pubalgia Due to Common Adductor Tendon Microavulsion
Fig. 8.7.2 Fig. 8.7.1
Fig. 8.7.3
Fig. 8.7.4
171 Hip and Pelvis A 17-year-old male soccer player presented with left groin pain of subacute onset. Physical examination demonstrated tenderness near the symphysis pubis but focal localization of pain was difficult. There was no significant weakness or loss of range of motion, although there was some tenderness on active adduction of the left hip.
Pubalgia is a nonspecific term used to describe groin pain or pain near the symphysis pubis. In athletes, particularly those involved in sports that require rapid acceleration, deceleration, and changes of direction, groin pain can be extremely debilitating and cause a significant decrease in performance. It is often difficult to determine the cause of pain based on clinical examination. MRI elegantly demonstrates the complex anatomy of the symphysis pubis. One major cause of athletic pubalgia is injury to the rectus abdominus-adductor complex and/or to the symphysis pubis. Due to the intimate relationship between the distal rectus abdominus tendon, the symphysis pubis, and the common adductor tendons, injuries of these structures are interrelated. Injuries to these structures can be subtle and easily missed on MRI. Therefore, close attention to imaging technique and meticulous analysis of the images is needed to accurately diagnose these injuries. It is important to differentiate osteitis pubis and adductor tendon or rectus abdominus tendon injury from muscle strains, as the treatment for these entities differs. Tendon tears that do not respond to conservative therapy may require surgical repair; however, osteitis pubis is much more likely to require surgical repair. In recalcitrant cases, osteitis pubis may occasionally be treated with internal stabilization of the symphysis. Muscle strains are treated conservatively.
Comments
Coronal STIR image (Fig. 8.7.1) shows focal high signal along the left inferior aspect of the symphysis pubis, consistent with focal partial adductor tendon avulsion (open arrow). This unilateral extension of high signal is referred to as the secondary cleft sign. Coronal STIR image (Fig. 8.7.2) just posterior to image 1 shows posterior extension of the partial adductor tendon avulsion (open arrow). Axial fat-suppressed T2-weighted image (Fig. 8.7.3) shows focal partial adductor tendon avulsion along the anteroinferior margin of the symphysis pubis (open arrow). Axial fat-suppressed T2-weighted image (Fig. 8.7.4) shows a myotendinous strain of the adductors on the right (open arrow) in a different patient.
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Case 8.8 Osteopoikilosis
Fig. 8.8.1
Fig. 8.8.2
Fig. 8.8.3
Fig. 8.8.4
173 Hip and Pelvis A 21-year-old woman with a history of juvenile chronic arthritis was being followed for positive antinuclear antibodies, thalassemia minor, and iron-deficiency anemia, but had no evidence of associated systemic disease. Abdominal ultrasonography performed to investigate her anemia showed splenomegaly, so CT examination of the abdomen and pelvis was ordered.
Osteopoikilosis is a benign hereditary condition characterized by multiple sclerotic bone lesions composed of compact lamellar bone. Typically, these are small, bilateral, and concentrated around articulations. However, these sclerotic bone lesions can occur anywhere and be of any size. Ovoid lesions in long bones are typically oriented along the long axis of the bone. The lesions are asymptomatic but can resemble osteoblastic metastases. However, unlike osteoblastic metastases, these lesions do not take up radionuclide on bone scintigraphy.
Comments
Frontal radiograph of the pelvis (Fig. 8.8.1) shows increased bone density with multiple small rounded sclerotic lesions (arrows) and more coalescent areas of sclerosis in the posterior ilium near the sacroiliac joints (open arrows). Bone scintigraphy (Fig. 8.8.2) shows no evidence of abnormal radionuclide uptake in areas of sclerotic bone lesions. Axial CT at S2–S3 (Fig. 8.8.3) shows diffuse increased bone density in the iliac bones (open arrows) adjacent to the sacroiliac joints. Multiple small rounded sclerotic bone lesions are seen in both iliac bones and the sacrum (solid arrows). Axial CT scan (Fig. 8.8.4) just inferior to Fig. 8.8.3 shows similar findings with areas of more confluent sclerosis (open arrow) and multiple small rounded sclerotic nodules (solid arrows).
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Case 8.9 Rapidly Destructive Osteoarthritis
Fig. 8.9.2
Fig. 8.9.1
Fig. 8.9.3
Fig. 8.9.4
175 Hip and Pelvis A 78-year-old woman presented with a 10-month history of progressive mechanical pain in the left inguinal region with radiation to the left leg. Physical examination was difficult due to rigidity from Parkinson’s disease. She had 80 degrees of flexion and essentially no internal or external rotation. Laboratory results were normal.
Rapidly destructive osteoarthritis of the hip (Postel’s osteoarthritis) is an uncommon form of osteoarthritis of the hip characterized by severe rapid cartilage loss and bone remodeling/loss over the course of weeks to months. This entity is typically seen in older women and is most commonly a painful unilateral process. The clinical picture can resemble that of a septic joint, and joint aspiration may sometimes be required to rule out infection. However, laboratory parameters typically show no evidence of an infectious process, such as an elevated white blood count or erythrocyte sedimentation rate. In rapidly destructive osteoarthritis, cartilage is lost much faster than in typical osteoarthritis: radiographs show 2 mm or more of joint space lost per year compared to less than 0.8 mm per year in conventional osteoarthritis. Moreover, unlike typical osteoarthritis, rapidly destructive osteoarthritis shows marked bone loss in the acetabulum and femoral head without any significant osteophyte formation. Although neuropathic joints may manifest similar radiographic features, a neuropathic joint is typically painless whereas rapidly destructive osteoarthritis is a painful condition.
Comments
Frontal radiograph of the hip (Fig. 8.9.1) shows moderate degenerative changes with superior joint space loss (open arrow) as well as mild sclerosis and buttressing of the medial aspect of the femoral neck (solid arrow). Frontal radiograph of the pelvis (Fig. 8.9.2) taken 8 months after Fig. 8.9.1 shows obliteration of the superior joint space and ill-definition of the cortex of the acetabular roof with small erosions (open arrow). There is superior subluxation of the femur with flattening and sclerosis of the femoral head (solid arrow) and mild widening of the femoral neck (arrowhead). Coronal STIR MRI of the pelvis (Fig. 8.9.3) on the same date as Fig. 8.9.2 shows deformity and increased signal in the acetabular roof and femoral head (open arrow) with small subchondral cysts in the acetabulum. There is marrow edema in the femoral neck and proximal femoral diaphysis (solid arrow) and edema in the iliacus muscle (open arrowhead). A joint effusion is also present (solid arrowhead). Frontal radiograph of the left hip (Fig. 8.9.4) 15 months after Fig. 8.9.1 shows complete destruction of the femoral head and acetabular roof and superior dislocation of the femur.
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Case 8.10 Osteonecrosis
Fig. 8.10.1
Fig. 8.10.2
Fig. 8.10.3
Fig. 8.10.4
177 Hip and Pelvis A 41-year-old man on chronic steroid therapy presented with right hip pain and functional joint disability.
Avascular necrosis of the femoral head appears in a wide spectrum of clinical conditions: corticoid steroid therapy, alcohol abuse, Gaucher disease, lupus, coagulopathies, hyperlipidemia, organ transplantation, and thyroid disorders; it may also be idiopathic. Osteonecrosis may be caused by emboli or increased bone marrow pressure, with subsequent decreased blood flow, anoxia, and eventual death of trabecular bone. Avascular necrosis is bilateral in 40% of hips; therefore, it is essential to image both hips. In the early stages of osteonecrosis, it is difficult to reach the diagnosis on plain-film radiographs. MRI is the most sensitive method to detect early femoral head osteonecrosis; it also provides information about articular cartilage, marrow conversion, joint fluid, and associated insufficiency fractures. On MRI, ischemic necrosis shows abnormal areas of low signal intensity with different patterns: homogeneous or inhomogeneous areas, a marginal line of low signal intensity with higher signal intensity centrally, subchondral fractures, and cortical collapse. The Ficat grading system classifies the radiographic findings as: grade 0, no pain and no radiological findings; grade I, pain, negative plain films and positive MRI and bone scintigraphy; grade II, positive plain films (sclerosis-lucency), without subchondral fracture on MRI; grade III, crescent sign on plain films and subchondral collapse on MRI; and IV, joint space narrowing and osteoarthritis. Early diagnosis and treatment of the femoral head osteonecrosis improves the prognosis, often preventing significant disability.
Introduction
Positive findings on plain-film radiograph (open arrow) indicate at least stage II osteonecrosis (Fig. 8.10.1). MRI is the most specific and sensitive technique to evaluate osteonecrosis. Oblique coronal T1-weighted MRI of the right hip shows a mixed signal intensity subchondral lesion (arrow) involving approximately 45% of the femoral head (Fig. 8.10.2). Oblique sagittal STIR MRI reveals an area of low signal intensity with a marginal hypointense line (open arrowhead). High signal intensity edema is seen under the cartilage (arrowhead) and also bordering the marginal low signal intensity line; no subchondral fracture is present (Fig. 8.10.3). Oblique coronal T2-weighted GRE MRI demonstrates stage II osteonecrosis and a small hip joint effusion (Fig. 8.10.4).
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Further Reading Books Bone and Joint Imaging. 3rd ed. Resnick D, Kransdorf M (2006). Elsevier, Saunders, Amsterdam, Philadelphia Diagnosis of Bone and Joint Disorders. 4th ed. Resnick D (ed) (2002). Saunders, Philadelphia, PA Imaging of the Musculoskeletal System. Pope T, Bloem J, Beltran J, Morrison W, Wilson D (2008). Saunders, Elservier, Philadelphia, Amsterdam Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. 3rd ed. Stoller DW (2007). Lippincott Williams & Wilkins, Philadelphia Musculoskeletal Imaging: The Requisites. 2nd ed. Manaster BJ, Disler DG, May DA (2002). Elsevier, Amsterdam
Web-Links http://www.wheelessonline.com/ http://www.rad.washington.edu/academics/academic-sections/ msk/teaching-materials/online-musculoskeletal-radiologybook/ http://emedicine.medscape.com/article/398669-overview http://emedicine.medscape.com/article/386808-overview http://www.orthosupersite.com/view.asp?rID=25278#ans
Articles Benli T, Akalin S, Boysan E, Mumcu EF, Kis M, Turkoglu D. Epidemiological, clinical and radiological aspects of osteopoikilosis. J Bone Joint Surg Br 1992; 74-B:504–506 Bloem JL. Transient osteoporosis of the hip: MR imaging. Radiology 1988; 167(3):753–755 Brittenden J, Robinson P. Imaging of pelvic injuries in athletes. Br J Radiol 2005; 78(929):457–468 Guerra JJ, Steinberg ME. Current concepts review: distinguishing transient osteoporosis from avascular necrosis of the hip. J Bone Joint Surg [Am] 1995;77:616 Gupta KB, Duryea J, Weissman BN. Radiographic evaluation of osteoarthritis. Radiol Clin N Am 2004; 42:11–41 Hardy DC, Murphy WA, Siegel BA, Reid IR, Whyte MP. X-linked hypophosphatemia in adults: prevalence of skeletal radiographic and scintigraphic features. Radiology 1989; 171:403 Ito H, Matsuno T, Minami A. Relationship between bone marrow edema and development of symptoms in patients with osteonecrosis of the femoral head. AJR Am J Roentgenol 2006; 186(6):1761–1770 Jacobson JA, Kalume-Brigido M. Case 97: X-linked hypophosphatemic osteomalacia with insufficiency fracture. Radiology 2006; 240(2):607–610
Karataş M, Başaran C, Ozgül E, Tarhan C, Ağildere AM. Postpartum sacral stress fracture: an unusual case of lowback and buttock pain. Am J Phys Med Rehabil 2008; 87(5): 418–422 Kassarjian A, Belzile E. Femoroacetabular impingement: presentation, diagnosis, and management. Semin Musculoskelet Radiol 2008; 12(2):136–145 Kassarjian A, Yoon LS, Belzile E, Connolly SA, Millis MB, Palmer WE. Triad of MR arthrographic findings in patients with femoroacetabular impingement (cam type). Radiology 2005; 236(2):588–592 Keogh CF, Munk PL, Gee R, Chan LP, Marchinkow LO. Imaging of the painful hip arthroplasty. AJR Am J Roentgenol 2003; 180:115–120 Korompilias AV, Karantanas AH, Lykissas MG, Beris AE. Transient Osteoporosis. J Am Acad Ortho Surg 2008; 16(8): 480–489 Lagier R, Mbakop A, Bigler A. Osteopoikilosis: a radiological and pathological study. Skeletal Radiol 1984; 1(1):161–168 Lin JT, Lutz GE. Postpartum sacral fracture presenting as lumbar radiculopathy: a case report. Arch Phys Med Rehabil 2004; 85(8):1358–1361 Major NM, Helms CA. Sacral stress fractures in long-distance runners. Am J Roentgenol 2000; 174:727–729 Nelson EN, Kassarjian A, Palmer WE. MR imaging of sportsrelated groin pain. Magn Reson Imaging Clin N Am 2005; 13(4):727–742 Rosenberg ZS, Shankman S, Steiner GC, Kastenbaum DK, Norman A, Lazansky MG. Rapid destructive osteoarthritis: clinical, radiographic, and pathologic features. Radiology 1992; 182(1):213–216 Stevens MA, El-Khoury GY, Kathol MH, Brandser EA, Chow S. Imaging features of avulsion injuries. Radiographics 1999; 19(3):655–672 Vande Berg BC, Malghem JJ, Lecouvet FE et al. Idiopathic bone marrow edema lesions of the femoral head: predictive value of MR imaging findings. Radiology 1999; 212(2):527–535 Watanabe W, Itoi E, Yamada S. Early MRI findings of rapidly destructive coxarthrosis. Skeletal Radiol 2002; 31(1):35–38 Wootton JR, Cross MJ, Holt KWG. Avulsion of the ischial apophysis. J Bone Joint Surg [Br] 1990; 72:625–627 Wurdinger S, Humbsch K, Reichenbach JR, Peiker G, Seewald HJ, Kaiser WA. MRI of the pelvic ring joints postpartum: normal and pathological findings. J Magn Reson Imaging 2002; 15(3): 324–329 Zajick DC, Zoga AC, Omar IM, Meyers WC. Spectrum of MRI findings in clinical athletic pubalgia. Semin Musculoskelet Radiol 2008; 12(1):3–12 (review) Zoga AC, Kavanagh EC, Omar IM, Morrison WB, Koulouris G, Lopez H, Chaabra A, Domesek J, Meyers WC. Athletic pubalgia and the “sports hernia”: MR imaging findings. Radiology 2008; 247(3):797–807
Knee Joan C. Vilanova, Sandra Baleato, and Joaquim Barceló
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Case 9.1
A 74-year-old woman presented with a 6-month history of pain and swelling in her right knee.
Lipoma Arborescens
Fig. 9.1.1
Fig. 9.1.2
Fig. 9.1.3
Fig. 9.1.4
181 Knee Lipoma arborescens is a rare benign intraarticular lesion characterized by the replacement of subsynovial tissue by mature fat cells giving rise to a villous proliferation. It usually involves the suprapatellar pouch of the knee, although it has also been reported in other locations, including the shoulder, subdeltoid bursa, hip, elbow, hand, and ankle. Bilateral involvement of the knees, wrists, ankles, and hips, as well as multiple joint involvement has also been observed. Clinically, the most common finding is a slow increase in painless swelling, accompanied by intermittent joint effusion. Most affected patients are in the fifth to seventh decades of life. Lipoma arborescens can be similar to other proliferations of the synovial membrane, but its characteristic feature is the macroscopic hypertrophic lipomatous synovial tissue. The term arborescens, from the Latin word arbor meaning tree, defines the characteristic morphology of this lipomatous villous synovial proliferation that resembles a tree. Magnetic resonance images (MRI) of lipoma arborescens correspond to and correlate with the fatty proliferation of the synovial lesion, which makes it possible to reach a specific diagnosis. MRI characterizes soft-tissues better than other imaging techniques and also enables fat suppression (STIR sequences). For these reasons, the histological appearance of lipoma arborescens within the synovial tissue can be perfectly correlated on MRI. Lipoma arborescens must be differentiated from other synovial lesions. The differential diagnosis should include other diffuse pathology of the synovium: villonodular pigmented synovitis, synovial chondromatosis, synovial hemangioma, and rheumatoid arthritis. Villonodular pigmented synovitis typically shows a diffuse low signal associated to hemosiderin. Synovial chondromatosis shows an intermediate-low signal on T1- and T2-weighted images related to the cartilaginous nature of the lesion. An association between lipoma arborescens and osteochondromatosis has been suggested, as there is a differentiation of the synovial tissue in both pathologies: to adipocytes in lipoma arborescens and to osteochondral tissue in osteochondromatosis. The differential diagnosis should also be done with synovial hemangiomas, which show intermediate signal intensity on T1- and T2-weighted images with areas of low-signal intensity due to phleboliths or fluid void within a linear punctate lesion of high-signal intensity, corresponding to fibrous fatty septa between the vascular channels. Chronic rheumatoid arthritis shows intermediate-low signal on T1- and T2-weighted images, associated with the formation of fibrous pannus. Although it has been suggested that lipoma arborescens might be associated with osteoarthritis, rheumatoid arthritis, or trauma, its exact etiology remains unknown.
Comments
Parasagittal T1-weighted image (Fig. 9.1.1) of the suprapatellar pouch of the knee shows the villous lipomatous proliferation of the synovium from a lipoma arborescens (open arrows). A midsagittal T1-weighted image (Fig. 9.1.2) from the same series shows an ossified body (arrow) from synovial osteochondromatosis as a coincidence in the same patient: an association between the two pathologies has been suggested. Coronal STIR sequence (Fig. 9.1.3) demonstrates the low-signal intensity of the lipoma arborescens similar to fat (open arrowhead). Axial T2-weighted image (Fig. 9.1.4) shows the diffuse villous proliferation of the synovium from the suprapatellar pouch (arrowhead).
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A 57-year-old woman presented with intermittent pain and swelling of the knee.
Case 9.2 Pigmented Villonodular Synovitis Comments
Pigmented villonodular synovitis (PVNS) is a rare disease characterized by idiopathic proliferation of synovial tissue in the joint, tendon sheath, and bursa of unknown cause. It may occur in two forms: diffuse or localized. Localized forms appear as a single intraarticular nodule, clinically mimicking a loose body or a torn meniscus. Diffuse forms present clinically as chronic
Fig. 9.2.1
Fig. 9.2.2
Fig. 9.2.3
Fig. 9.2.4
183 Knee monoarthritis. PVNS usually affects patients in the second and third decades of life, with no sex predominance. PVNS is a locally aggressive lesion that may invade and destroy surrounding soft-tissue and bone, resulting in functional deterioration of the joint and extremity. The most common location is the knee, followed by the hip, shoulder, and other joints. Spinal PVNS, frequently involving the posterior elements, is a rare condition. The clinical findings depend on the location and extent of the disease. In the diffuse form, mild pain and limitation of range of motion are the main symptoms. These symptoms are commonly related to joint effusions that occur in episodes: the patient may have completely symptom-free periods between exacerbations. In superficial joints, the swelling and local warmth due to effusion are easily noted. Hemarthrosis is a common finding in diffuse PVNS. Plain-film radiographs may be normal or may reveal nonspecific changes, depending on the severity of the disease. Calcification is rarely seen on plain-film radiographs. Bony changes, including marginal erosion and cysts, occur in one third of the diffuse lesions, particularly in a chronic setting with preservation of joint spaces. The MRI features of PVNS are highly suggestive but not pathognomonic. In addition to its role in diagnosing PVNS, MRI provides detailed information regarding the extent of the disease. MRI is the method of choice since the hemosiderin deposition leads to signal loss on both the T1- and T2-weighted images, particularly on gradient-echo sequences. PVNS manifests on MRI as a stalked mass growing from the synovium with heterogeneous signal intensity in all the imaging sequences manifesting as a combination of low-signal intensity areas (created by the paramagnetic effects of hemosiderin deposits and fibrous tissue) and high-signal intensity areas (representing congested synovium and fat content). Joint effusion is shown as low-intermediate signal on T1-weighted sequences and high signal on T2-weighted sequences. Bone erosions are well demonstrated on MRI, appearing as cortical discontinuity caused by low and high-signal tissue on both T1- and T2-weighted images. Gadolinium enhancement depends on the amount of inflammation and vascularity; PVNS lesions demonstrate intense gadolinium enhancement, which may be useful to differentiate the synovium from nonenhancing fluid and to help define the extent of the lesion. The differential diagnosis includes hemophilic arthropathy, rheumatoid arthritis, amyloid arthropathy, arborescens lipoma, and synovial osteochondromatosis. PVNS is treated with complete synovectomy, which can be done using arthroscopic or open techniques. Incomplete synovectomy is associated with a high incidence of recurrence. Postoperative radiotherapy using low to moderate doses may be beneficial if there is residual tumor or recurrence.
Sagittal T1-weighted FSE image (Fig. 9.2.1) shows lobulated low-signal intensity soft tissue in the suprapatellar pouch and in the popliteal fossa with extracapsular extension. MRI shows bony changes: a high-signal hemorrhagic cyst (open arrow) in the tibial attachment and a complex cyst in the tibial plateau (arrow). On the corresponding sagittal T2-weighted FSE image (Fig. 9.2.2), the synovial proliferation shows low-signal intensity due to hemosiderin deposits. The complex and hemorrhagic bone cysts are well depicted. The most useful sequence to demonstrate the presence of hemosiderin is the T2-weighted gradientecho sequence (Figs. 9.2.3 and 9.2.4) due to the susceptibility artifact from the blood.
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Case 9.3 Spontaneous Osteonecrosis of the Knee
Fig. 9.3.1
Fig. 9.3.2
Fig. 9.3.3
Fig. 9.3.4
185 Knee A 58-year-old woman presented with sudden onset of medial knee pain with no prior trauma.
Idiopathic or spontaneous osteonecrosis of the knee (SONK) is a distinct form of epiphyseal osteonecrosis; its clinical, histologic, and imaging features completely separate SONK from avascular necrosis of the knee. Although the pathogenesis of SONK remains controversial, a mechanical or microtraumatic origin has progressively emerged as the most likely underlying mechanism of SONK. SONK is more common in middle-aged to elderly people and in females. No association with metabolic disorders or therapeutic agents has been found. However, a significant association with meniscal lesions (especially radial tear or prior meniscal resection) has been reported. SONK is usually unilateral and has a strong predilection for the medial femoral condyle (90% of cases). Clinically, patients present severe knee pain of sudden onset in the absence of significant trauma. SONK can be classified into four stages based on symptoms and radiologic criteria. In general, stages I and II, the early stages, are potentially reversible or show no progression, whereas stages III and IV are end stages in the course of the disease and are associated with irreversible destruction of subchondral bone and articular cartilage that requires some form of reconstructive surgery. The most prominent MRI characteristics of SONK are the poorly delimited bone marrow edema pattern and the lack of a peripheral rim as seen in avascular necrosis. Bone marrow edema is not specific to SONK and may also be observed in transient epiphyseal conditions (transient osteoporosis, trauma, infection, transient bone marrow edema, algodystrophy). SONK is seen on MRI as a focal or diffuse hypointense signal abnormality on T1-weighted images; it predominantly involves the weight-bearing, subarticular portion of the medial femoral condyle. On T2-weighted sequences, the signal pattern is usually varied. The insufficiency fracture can be seen as a linear, dark signal focus along the subarticular bone on both T1- and T2-weighted images. Marrow edema and subsequent necrosis replace the normal fat signal of the marrow and appear hypointense on T1-weighted sequences and hyperintense on T2-weighted sequences. Although, the clinical picture of SONK seems similar to several other disorders, certain distinct features, including its typical location, clinical symptoms, relative lack of loose bodies, and late onset of cartilaginous erosion, help distinguish it from other disorders and facilitate the differential diagnosis.
Comments
Sagittal T1-weighted FSE image (Fig. 9.3.1) shows a subchondral low-signal intensity in the medial femoral condyle. The corresponding sagittal T2-weighted GE image (Fig. 9.3.2) shows the focal subchondral area with a low-signal intensity rim due to sclerosis and high-signal due to necrosis. Coronal fat-suppressed proton density-weighted FSE image (Fig. 9.3.3) shows the necrotic lesion with edema surrounding the lesion. Axial fat-suppressed proton density-weighted FSE image (Fig. 9.3.4) depicts the necrotic area.
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Case 9.4 Discoid Meniscus
Fig. 9.4.1
Fig. 9.4.2
Fig. 9.4.3
Fig. 9.4.4
187 Knee A 31-year-old woman was referred for knee pain. At physical examination, she had the full range of motion. Plain-film radiographs of the knee were normal.
Many types of meniscal anomalies have been reported: discoid meniscus, meniscal ossicles, and the meniscal flounce. Discoid meniscus is the most common of these. Discoid lateral meniscus (DLM) is an uncommon normal variant seen in 1–6% of patients undergoing arthroscopic studies. Its congenital or acquired origin remains a question of debate. It is associated with pain, snapping, locking, and instability of the knee but can be entirely asymptomatic. The three types of DLM are complete, incomplete, and the Wrisberg variant. Discoid medial meniscus is much less common, with a reported incidence of 0.12–0.6%. MRI can easily diagnose these entities. On MRI, a discoid meniscus is identified on three or more contiguous 5-mm-thick sagittal images or a meniscal body greater than 15 mm wide or extending into the intercondylar notch is seen on coronal images. The classic configuration is a diffusely thick wafer or slab meniscus with continuity between the anterior and posterior horns. On sagittal MRI, the typical bow-tie configuration of the normal meniscus is not identified. DLM is more susceptible than a normal meniscus to mechanical forces. As a result, individuals with DLM have a higher incidence of meniscal tear and cystic degeneration. In arthroscopic series, meniscal tears in patients with DLM are found in approximately 38–88% of patients. A symptomatic discoid meniscus usually leads to diffusely high-signal that may extend to the joint surface. The treatment of a discoid meniscus depends on its type and whether it is associated with a tear. The complete and incomplete types have a firm, normal posterior tibial attachment and are stable. If a discoid meniscus is discovered with no evidence of a tear, then its presence should be considered incidental and it should be left intact. If a tear is associated with a complete or incomplete discoid meniscus, then partial meniscectomy should be performed. In contrast, the Wrisberg variant has no capsular attachments and the traditional treatment has been total meniscectomy; however, some investigators have recommended partial meniscectomy with repair.
Comments
Consecutive coronal proton density-weighted images (Figs. 9.4.1 and 9.4.2) demonstrate the abnormal width of the lateral meniscus. There is a rupture of the medial meniscus (open arrow). Contiguous sagittal T2-weighted GE MRI (Figs. 9.4.3 and 9.4.4) through the lateral compartment of the knee reveal a lateral discoid meniscus, extending into the intercondylar notch.
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Case 9.5 Osgood-Schlatter Disease
Fig. 9.5.1
Fig. 9.5.3
Fig. 9.5.2
189 Knee A 14-year-old boy presented with tenderness around the right tibial tuberosity.
Osgood–Schlatter disease (OS) is a typical sport-related complaint that occurs in active adolescents. This lesion frequently affects boys between 10 and 15 years of age and is bilateral in about 25–50% of cases. Many theories have been advanced to explain the etiology of the disease; these include trauma, avascular necrosis, infection, and endocrine abnormalities, among others. The most widely accepted explanation is Odgen’s theory that OS is due to an avulsion of the secondary ossification center. OS results from repeated tensile extension forces applied by the quadriceps on the tubercle via the patellar tendon resulting in avulsion of segments of anterior cartilage and/or anterior bone. At physical examination, swelling and prominence of the tibial tubercle are accompanied by extreme local tenderness. The diagnosis of OS is almost always established clinically. Imaging, including radiographs, MRI, and skeletal scintigraphy are mainly useful for excluding other pathology. Findings on plain-film radiographs in OS disease include soft-tissue swelling anterior to the tibial tubercle, blurring of the margins of the patellar tendon and inhomogeneity of the infrapatellar fat pad. The tibial tubercle may be irregularly ossified and fragmented, although in the absence of symptoms, this appearance can appropriately be considered a normal variant. MRI shows enlargement and increased T2-weighted signal intensity of the tendon at its insertion on the tibial tubercle, in the surrounding soft tissues, and in adjacent bone marrow. Skeletal scintigraphy may show asymmetrically increased tracer uptake in or around the patellar tendon. Treatment includes suspension of sporting activity and a variety of conservative therapies: infrapatellar strap, ice, massage, and local injection of steroids or lidocaine. OS is often self-limiting and most patients respond to conservative treatment. Surgery can be an alternative treatment in cases where symptoms persist.
Comments
Sagittal T1-weighted MRI (Fig. 9.5.1) reveals an ossicle of the tendon associated with a defect in the anterior cortex of the tibial tubercle (open arrow). The corresponding sagittal T2-weighted GRE image (Fig. 9.5.2) demonstrates the marrow fat-containing fragment (arrow). Axial T1-weighted MRI (Fig. 9.5.3) of the knee at the level of the patellar tendon insertion on the tibial tubercle shows the ossification (open arrowhead).
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Case 9.6 Chondromalacia
Fig. 9.6.2 Fig. 9.6.1
Fig. 9.6.3
191 Knee A 29-year-old woman presented with a 1-month history of anterior knee pain. MRI was performed after findings on plain-film radiographs were normal.
Chondromalacia of the patellae is pathologic softening of the patellar cartilage. It is one of the most common causes of knee pain in adolescents and young adults. Multiple causes have been reported; trauma and mechanical tracking abnormalities are the most common. Identifying and staging cartilaginous lesions are therefore crucial to establish the correct treatment and halt the progression of the degenerative process. MRI can show signal and morphologic changes in the cartilage and can detect cartilage surface fraying, fissuring, and varying degrees of cartilage thinning. The two most easily implemented techniques for articular cartilage evaluation are the fat-suppressed threedimensional spoiled gradient-echo technique (3D GRE), which produces T1-weighted images and a fast spin-echo technique, which produces T2-weighted images. New MRI methods to evaluate physiological parameters in cartilage include: T2 mapping of articular cartilage, based on the water content of the tissue; sodium imaging, which can depict regions of glycosaminoglycan depletion; and diffusion-weighted imaging and diffusion tensor imaging, which provide information about the architecture and matrix of the cartilage. Cartilage is considered abnormal when focal areas of altered signal are present, as well as irregularities, defects, or swelling of the articular surface and areas of edema or sclerosis of subchondral bone. Several classifications of patellar chondromalacia have been proposed. The International Cartilage Repair Society (ICRS) classification defines five grades: Grade 0: Normal. Homogeneous signal intensity without superficial irregularities. Grade 1: Nearly Normal. Superficial lesions, soft indentation and/or superficial fissures and cracks. Grade II: Abnormal. Lesions extending down to <50% of cartilage depth. Grade III: Severely abnormal. Cartilage defects extending down >50% of cartilage depth as well as down to the calcified layer and down to but not through the subchondral bone. Grade IV: Severely abnormal. Defects include the subchondral plate and also the adjacent cancellous bone. Different surgical procedures are currently available: bone marrow stimulation, osteochondral autografts, autologous chondrocyte transplantation (ACT), and matrixassisted ACT. The main advantage of bone marrow stimulating techniques is their minimally invasive approach. Osteochondral autografting (mosaicplasty) affects the subchondral plate and shows fibrous tissue between the single hyaline plugs, basically leading to a mixed repair tissue. To perform autologous chondrocyte transplantation, a small sample of cartilage is taken in an arthroscopic biopsy and cultivated. The propagated cells are injected beneath a periosteal graft and the defect is closed with watertight sutures.
Comments
Axial T2-weighted FSE images (Figs. 9.6.1 and 9.6.2) reveal increased signal intensity within the cartilage perpendicular to the surface and extending through the cortex (open arrows), making this grade III chondromalacia without subchondral edema. Sagittal T1-weighted FSE image (Fig. 9.6.3) reveals mild subchondral sclerosis (open arrowhead).
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Case 9.7 Meniscal Tear Comments
A 46-year-old woman presented with pain 5 days after acute injury to the knee.
The meniscus is made up of fibrocartilage and provides shock absorption and lubrication. Its circumferential fibers are organized as parallel bundles and serve to resist hoop stresses. Its radially oriented fibers serve to resist shear stress. The periphery of the meniscus (red zone arthroscopically) has greater vascularity and greater healing potential than the avascular portion (white zone). The menisci are wedge-shaped, semilunar (C-shaped) structures with a concave superior surface and a flat inferior surface, allowing maximal congruency between the femur and tibia. Typically, the medial meniscus is larger than the lateral meniscus and has a greater radius of curvature.
Fig. 9.7.2
Fig. 9.7.1
Fig. 9.7.3
193 Knee The normal meniscus has low-signal on all MRI sequences. On sagittal slices, both menisci have a “bow-tie” configuration on the most peripheral sections. The more central slices demonstrate separate anterior and posterior horns with a triangular configuration showing sharp margins. On coronal slices, the anterior and posterior horns span across the tibial plateau, whereas the body has a triangular configuration, reflecting the C-shaped configuration. There are two major criteria routinely applied for the diagnosis of meniscal tear: abnormal signal intensity and abnormal morphology. Increased signal within the meniscus is considered to be a tear when it unequivocally extends to the articular surface. If the abnormal signal intensity comes into contact with the articular surface on a single slice in a single plane, the sensitivity for a meniscal tear is 55% medially and 30% laterally. A three-level grading system characterizes meniscal signal intensity. In grade 1, irregular increased intrameniscal signal does not extend to the articular surface; this is believed to reflect early degenerative findings. In grade 2, the signal is linear and may connect to the capsular margin; these features are believed to reflect more severe degenerative findings. In grade 3, a linear or complex signal extends to the articular surface on more than one slice; this is unequivocally a tear. Meniscal tears are classified as horizontal, vertical (longitudinal, radial, or oblique), or complex. A horizontal tear is parallel to the tibial plateau and separates the meniscus into upper and lower parts. A longitudinal vertical tear is perpendicular to the tibial plateau and propagates parallel to the main (circumferential) axis of the meniscus. A radial vertical tear propagates perpendicular to the main axis. An oblique or parrot-beak vertical tear propagates obliquely to the main axis of the meniscus. A complex tear comprises two or more tear configurations. The second major criterion for meniscal tear is morphology. Meniscal shape is important and subtle findings of amputation may be the only sign of a tear. A bucket-handle tear is a specific type of displaced meniscus that results when the inner meniscal segments of a longitudinal or oblique tear is displaced, most commonly into the intercondylar notch. MRI is also useful and accurate for predicting whether meniscal tears can be repaired. The configuration, location, and size of meniscal tears are important in determining the type of treatment. Four alternatives exist for treatment of meniscal tears: no meniscal surgery, meniscal repair, partial meniscectomy, and complete meniscectomy. Longitudinal and oblique configurations are usually reparable, whereas horizontal, radial, and complex configurations are usually not reparable and require partial meniscectomy. The report of an MRI examination of the meniscus should describe its location (anterior horn, body, posterior horn), plane, shape, completeness, length, and the number of tears. The tear should be described as horizontal, vertical, complex, displaced flap, bucket-handle, or meniscocapsular separation.
Sagittal T2-weighted GRE image (Fig. 9.7.1) shows a horizontal tear of the posterior horn of the medial meniscus extending to the inferior articular surface (open arrow). Coronal fat-saturated proton density-weighted image (Fig. 9.7.2) demonstrates the rupture of the medial meniscus (open arrow). The consecutive image (Fig. 9.7.3) shows inflammatory edema from the medial condyle.
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Case 9.8 Osteochondritis Dissecans
Fig. 9.8.1
Fig. 9.8.2
Fig. 9.8.3
Fig. 9.8.4
195 Knee A 16-year-old athlete presented with a history of vague knee pain over several months that limited his physical training.
There are two main types of OCD: the adult form, which occurs after the physis closes, and the juvenile form, which occurs in patients with an open epiphyseal plate. Although adult osteochondritis dissecans may arise de novo, it is usually the result of an incompletely healed and previously asymptomatic lesion from juvenile osteochondritis dissecans. Adult osteochondritis dissecans usually presents between the ages of 17 and 36 years, but it can be seen at any adult age. The separation of OCD of the knee into juvenile and adult forms is clinically relevant, as the two pathologic conditions have distinctly different clinical courses. OCD of the knee most commonly involves, in order of decreasing frequency, the medial femoral condyle, the lateral femoral condyle, the femoral trochlea, and the patella. Juvenile osteochondritis dissecans occurs in adolescent athletes, more frequently in boys; the average age of the patients at the time of the diagnosis ranges from 11.3 to 13.4 years. About a third of all cases of juvenile OCD are bilateral. The lateral aspect of the medial femoral condyle is the most commonly affected location in the knee. A focal area of subchondral bone and articular cartilage becomes avascular and may detach to form a loose body. The mechanism of this injury is uncertain although both repetitive microtrauma and a single acute trauma event have been implicated. Findings on plain-film radiographs may initially be normal. MRI demonstrates subchondral edema. In later stages, radiographs may show a lucent crescent-shaped defect in the subchondral area with or without loose bodies. MRI can be used for precise staging and postoperative follow-up after chondral transplantation. Stability is the single most important prognostic factor for determining the likelihood of an OCD lesion to heal with conservative therapy. T2-weighted MRI is able to demonstrate the grade of the lesion and the degree of stability as well as to visualize the cartilage; thus, it plays an important role in treatment planning. Fluid between the fragment and adjacent bone indicates disruption of the overlying cartilage and a likelihood that the fragment will separate and become a loose body within the joint. Based on the MRI findings, joints with OCD can be classified into the following stages: Stage I: Thickening of articular cartilage and low signal changes (stable). Stage II: Articular cartilage breached, low-signal rim behind the fragment indicating fibrous attachment (stable). Stage III: Articular cartilage breached, high-signal changes behind the fragment and underlying subchondral bone (unstable). Stage IV: Loose body (unstable). Stages I and II are stable lesions, while stages III and IV describe unstable lesions in which not only is the cartilage breached, but synovial fluid exists between the fragment and underlying bone.
Comments
Sagittal T1-weighted image (Fig. 9.8.1) shows classic osteochondritis with low-signal of the fragment. Corresponding T2-weighted GRE image (Fig. 9.8.2) demonstrates hyperintensity between the lesion (open arrow) and the adjacent bone, representing an unstable lesion. Coronal fat-suppressed proton density-weighted FSE image (Fig. 9.8.3) depicts high signal of the necrotic fragment from the nonweight-bearing lateral aspect of the medial condyle. Axial fat-suppressed proton density-weighted FSE image (Fig. 9.8.4) displays the eccentric lesion.
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Case 9.9 Mucoid Degeneration of the Anterior Cruciate Ligament with Ganglion Bone Cyst
Fig. 9.9.1 Fig. 9.9.2
Fig. 9.9.3
197 Knee A 48-year-old man presented with a 2-year history of increasing pain on motion and difficulty extending the left knee. At physical examination, no swelling, ballottement of the patella, or instability was seen. The range of motion was limited. Plain-film radiographs showed slight degenerative change in the medial side of the knee.
Mucoid degeneration of the anterior cruciate ligament (ACL) is a rare cause of knee dysfunction. Mucoid degeneration of the ACL and ganglia represent different manifestations of the same pathologic condition. Bergin et al. found 76% patients had discrete intraligamentous ganglia, 24% had features consistent with ACL mucoid degeneration only, and 35% had MRI features of both entities. The mean age of patients with ACL mucoid degeneration was 43 years (range 22–66 years). The clinical presentation of mucoid degeneration of the ACL is variable; most cases are discovered incidentally in asymptomatic patients. In some cases, symptoms are varied but nonspecific, including knee pain, locking, clicking or popping sensations, and decreased range of motion. Ganglia anterior to the ACL tend to limit knee extension and posterior cruciate ligament ganglia limit knee flexion. The pathogenesis of cruciate ganglion cysts remains unclear. Two theories have been postulated: the first attributes the presence of a ganglion to mucinous degeneration of the connective tissue, and the second attributes it to herniation of synovial tissue through a defect in the joint capsule of the tendon sheath, similar to those occurring in the wrist. MRI is recognized as the gold standard in characterizing cystic knee lesions and is the only imaging method that can depict mucoid degeneration of the ACL. MRI findings for mucoid degeneration of the ACL are similar to those for intraligamentous ganglion of the ACL. The characteristic MRI features of intraligamentous ganglion include sharply demarcated, homogenous, hyperintense signal intensity on T2-weighted and proton density-weighted images. MRI in mucoid degeneration demonstrates normal orientation of the ligament, thickened and ill-defined ACL fibers, and increased intraligamentous signal intensity on T2-weighted and proton density-weighted images. Mucoid degeneration of the ACL was described as a potential pitfall for the diagnosis of a ligament tear. ACL ganglion cysts commonly occur in association with MRI features of mucoid degeneration and these entities are typically not associated with ligament insufficiency. Intraosseous ganglia at the femoral and tibial attachments have a high association with these entities.
Comments
Sagittal T2-weighted FSE image (Fig. 9.9.1) shows an ill-defined enlarged ligament with increased signal intensity in the normal orientation and two intraosseous cysts at the tibial insertion. Coronal STIR image (Fig. 9.9.2) shows a ganglion cyst in the tibia. Coronal T2-weighted FSE image (Fig. 9.9.3) reveals an intraosseous cyst at the femoral insertion of the ACL.
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Case 9.10 Acute Meniscal and Ligament Tears of the Knee
Fig. 9.10.1
Fig. 9.10.2
Fig. 9.10.3
Fig. 9.10.4
199 Knee A 15-year-old boy presented with pain in his left knee 6 weeks after an acute traumatic injury. Complex injuries of the knee are common after accidents or sports-related injuries.
MRI is the preferred imaging technique to assess joint injuries. These lesions occur as a result of multiple forces (varus, valgus, rotation, and hyperextension) applied to the joint. Depending on the mechanism of injury, different patterns can be recognized. The normal ACL is a straight, taut structure that runs parallel to the roof of the intercondylar notch. ACL tears occur more frequently (70%) in the middle aspect of the ligament. Sagittal T2-weighted images are recommended to depict the ACL. Different signs reveal ACL injuries. Primary signs involve the absence of the normal dark band of the ACL. Secondary signs are bone-related injuries due to the indirect mechanism of the traumatic event (microfracture of the posterolateral aspect of the tibial plateau and lateral femoral condyle) and soft-tissue signs secondary to the anterior translation of the tibia. These indirect signs have a low sensitivity but a high specificity. The posterior cruciate ligament (PCL) appears as a low-signal structure in the intercondylar notch, gently curving between the posterior aspect of the proximal tibia and the distal femur. Most PCL tears are incomplete and intrasubstance and are best seen on sagittal images. Isolated PCL injuries make up only 30% of cases. The medial collateral ligament (MCL) originates on the medial aspect of the distal femur and inserts on the medial aspect of the proximal tibia. MRI shows the MCL as a thin dark band. MCL injuries are revealed on fluid-sensitive coronal sequences and their treatment with either immobilization or surgery depends on the presence or absence of meniscal tear or ACL injuries. The menisci are fibrocartilaginous structures attached to the superior aspect of the tibial plateau. MRI is the best imaging modality for the evaluation of meniscal trauma. The normal meniscus is devoid of signal on all sequences, but linear images are seen within the menisci when they are torn. Medial meniscus tears are associated with MCL rupture in nearly 70% of cases. Meniscal tears are described as horizontal, vertical, radial, and longitudinal. A different type of meniscal tear is the bucket-handle tear (BHT), which tends to involve the medial meniscus. BHT is a longitudinal vertical tear with unstable displaced inner fragment that can usually be found in the intercondylar notch. The presence of the displaced fragment within the intercondylar notch is known as the “double PCL” sign and can be seen on sagittal images.
Comments
Coronal fat-suppressed T2-weighted FSE MRI (Figs. 9.10.1 and 9.10.2) reveals increased signal in the distal insertion of the MCL (open arrow) and a BHT of the medial meniscus with a fragment displaced into the notch (arrow). Edema on the lateral condyle of the femur is an indirect sign of ACL rupture (Fig. 9.10.1). Sagittal T2-weighted FSE (Fig. 9.10.3) and GRE (Fig. 9.10.4) MRI through the intercondylar notch shows the absence of the ACL (open arrowhead) without clearly identifiable fibers. The PCL shows increased signal with surface disruption on its proximal insertion (arrowhead). A small joint effusion is present.
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Further Reading Books Diagnosis of Bone and Joint Disordes. Vol 1–5. Resnik D, Niwayama G (2002). Saunders, Philadelphia Fundamentals of Skeletal Radiology. Helms CA (2005). WB Saunders, Philadelphia Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. Stoller DW (2006). Lippincott Williams & Wilkins, Philadelphia Musculoskeletal Imaging: The Requisites (Requisites in Radiology). Manaster BJ, May DA, Disler DG (2006). Mosby-Yearbook, St Louis Musculoskeletal MRI. Kaplan P, Helms CA, Dussault R, Anderson M (2001). WB Saunders, Philadelphia
Web-Links http://www.rad.washington.edu/mskbook Approaches To Differential Diagnosis In Musculoskeletal Imaging by Michael L. Richardson, M.D http://chorus.rad.mcw.edu/index/6.html Chorus: collaborative hypertext of radiology>musculoskeletal system http://www.med-ed.virginia.edu/courses/rad/ext/ Introduction to radiology > skeletal trauma radiology https://www.skeletalrad.org/Default.aspx American Society of Skeletal Radiology http://www.indy rad.iupui.edu/public/ddaven/main.htm Skeletal Radiology Tutorial. Department of Radiology. Indiana University Medical Center
Articles Anders RK, Crim JR. Osteochondral injuries. Semin Ultrasound CT MR 2001; 22(4): 352–370 (review) Bejia I, Younes M, Moussa A, Said M, Touzi M, Bergaoui N. Lipoma arborescens affecting multiple joints. Skeletal Radiol 2005; 34(9):536–538 Endo Y, Schweitzer ME, Bordalo-Rodrigues M, Rokito AS, Babb JS. MRI quantitative morphologic analysis of patellofemoral region: lack of correlation with chondromalacia patellae at surgery. AJR Am J Roentgenol. 2007; 189(5):1165–1168 Fox MG. MR imaging of the meniscus: review, current trends, and clinical implications. Radiol Clin North Am 2007; 45(6): 1033–1053 Garner HW, Ortiguera CJ, Nakhleh RE. Pigmented villonodular synovitis. Radiographics. 2008; 28(5):1519–1523 Gil HC, Levine SM, Zoga AC. MRI findings in the subchondral bone marrow: a discussion of conditions including transient osteoporosis, transient bone marrow edema syndrome, SONK, and shifting bone marrow edema of the knee. Semin Muscu loskelet Radiol 2006; 10(3):177–186 (review)
Hirano A, Fukubayashi T, Ishii T, Ochiai N. Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease. Skeletal Radiol 2002; 31(6):334–342 Hofmann S, Kramer J, Vakil-Adli A, Aigner N, Breitenseher M. Painful bone marrow edema of the knee: differential diagnosis and therapeutic concepts. Orthop Clin North Am 2004; 35(3): 321–333 Jee WH, McCauley TR, Kim JM et al. Meniscal tear configurations: categorization with MR imaging. AJR Am J Roentgenol 2003; 180(1):93–97 Kijowski R, Blankenbaker DG, Shinki K, Fine JP, Graf BK, De Smet AA. Juvenile versus adult osteochondritis dissecans of the knee: appropriate MR imaging criteria for instability. Radiology 2008; 248(2):571–578 Kocher MS, Tucker R, Ganley TJ, Flynn JM. Management of osteochondritis dissecans of the knee: current concepts review. Am J Sports Med 2006; 34(7):1181–1191 (review) Lang P, Noorbakhsh F, Yoshioka H. MR imaging of articular cartilage: current state and recent developments. Radiol Clin North Am 2005; 43(4):629–639 (review) Lee YG, Shim JC, Choi YS, Kim JG, Lee GJ, Kim HK. Magnetic resonance imaging findings of surgically proven medial meniscus root tear: tear configuration and associated knee abnormalities. J Comput Assist Tomogr 2008; 32(3):452–457 LLopis E, Padrón M. Anterior knee pain. Eur J Radiol 2007; 62(1):27–43 Luhmann SJ, Schootman M, Gordon JE, Wright RW. Magnetic resonance imaging of the knee in children and adolescents. Its role in clinical decision making. J Bone Joint Surg Am 2005; 87(3):497–502 McCauley TR. MR imaging of chondral and osteochondral injuries of the knee. Radiol Clin N Am 2002; 40(5):1095–1107 Murphey MD, Rhee JH, Lewis RB, Fanburg-Smith JC, Flemming DJ, Walker EA. Pigmented villonodular synovitis: radiologicpathologic correlation. Radiographics. 2008; 28(5):1493–1518 Oei EH, Ginai AZ, Hunink MG. MRI for traumatic knee injury: a review. Semin Ultrasound CT MR 2007; 28(2):141–157 Raissaki M, Apostolaki E, Karantanas AH. Imaging of sports injuries in children and adolescents. Eur J Radiol 2007; 62(1): 86–96 Rohren EM, Kosarek FJ, Helms CA. Discoid lateral meniscus and the frequency of meniscal tears. Skeletal Radiol 2001; 30(6): 316–320 Samoto N, Kozuma M, Tokuhisa T, Kobayashi K. Diagnosis of the “large medial meniscus” of the knee on MR imaging. Magn Reson Imaging 2006; 24(9):1157–1165 Vilanova JC, Barceló J, Villalón M, Aldomà J, Delgado E, Zapater I. MR imaging of lipoma arborescens and the associated lesions. Skeletal Radiol 2003; 32(9):504–509 Wall E, Von Stein D. Juvenile osteochondritis dissecans. Orthop Clin North Am 2003; 34(3):341–353 (review) Yates PJ, Calder JD, Stranks GJ, Conn KS, Peppercorn D, Thomas NP. Early MRI diagnosis and nonsurgical management of spontaneous osteonecrosis of the knee. Knee 2007; 14(2): 112–116
Ankle and Foot Xavier Tomas and Ana Isabel Garcia
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A 63-year-old woman presented with a 3-month history of left ankle pain. She recalled a traumatic ankle sprain 6 months before. Plainfilm radiographs and MRI were obtained.
Case 10.1 Osteochondral Talar Lesion Introduction
The name “osteochondral lesion” mainly describes a posttraumatic lesion involving an area of hyaline cartilage at an articular surface and its underlying subchondral bone. This process can precipitate to loss of continuity at the talar articular surface, with decreased range of ankle motion and eventually osteoarthritis. Findings at plain-film radiography can be normal in the earliest stage (Stage I of the Berndt and Harty classification), when no detached fragment is present. Many patients report a previous ankle sprain with normal radiographs and atypically prolonged pain.
Fig. 10.1.1
Fig. 10.1.2
Fig. 10.1.4
Fig. 10.1.3
Fig. 10.1.5
203 Ankle and Foot MRI is the gold standard for diagnosing and staging osteochondral lesions. A subtle poorly delimited subchondral focus that is hypointense on T1-weighted and hyperintense on T2-weighted images reveals focal marrow edema due to subchondral trabecular compression without detachment (Stage I). A well-delimited, nondisplaced subchondral lesion that is hypointense on T1-weighted and hyperintense on T2-weighted sequences, surrounded by an incomplete ring (Stage II) or fluid cysts (Stage IIA on Anderson et al.’s classification) that are hyperintense on T2-weighted sequences, suggests a partially detached osteochondral fragment. A well-delimited, nondisplaced subchondral lesion that is hypointense on T1-weighted and hyperintense on T2-weighted sequences, surrounded by a complete ring of fluid that is hyperintense on T2-weighted sequences, suggests a partially detached osteochondral fragment that is not displaced from its talar dome bed (Stage III). If the subchondral lesion is completely detached and displaced (loose body), a Stage IV osteochondral lesion is diagnosed. It is critical to report whether the osteochondral lesion is stable or unstable, as unstable lesions may require surgical repair. If unenhanced MRI cannot establish this difference, postcontrast images can give additional information such as congruity of the chondral articular surface or vascular continuity of the lesion with the donor site (viability). Indirect MR arthrography of the ankle can be useful to improve lesion enhancement. In cases where it is difficult to evaluate whether the subchondral fragment is detached from the talar dome, direct MR arthrography of the ankle can determine whether the contrast material completely undercuts the osteochondral fragment from the donor site. Furthermore, direct MR arthrography of the ankle can clearly depict focal articular cartilage defects and intra-articular loose bodies. CT cannot depict bone marrow edema; thus, it cannot detect early osteochondral lesions. For this reason, CT should be used as an additional technique for visualizing subchondral detachment (Stages II–III) and bony fragmentation, which are pathognomonic of a Stage IV lesion. The differential diagnosis must be done with talar fracture (linear morphology of the fracture line), avascular necrosis (bone infarct with sclerotic margins due to talar neck fracture or predisposing entities such sickle-cell anemia or steroid treatment), and transient osteoporosis (homogeneous, reversible edema without a focal subchondral lesion). If both sides of the ankle joint are affected, arthritis (posttraumatic, crystal-deposition, septic, etc.) should also be considered.
Axial proton density-weighted MRI (Fig. 10.1.1) shows a well-delimited, heterogeneous osteochondral lesion in the medial talar dome (arrow). Pre- and postcontrast sagittal fat-suppressed T1-weighted MRI (Figs. 10.1.2 and 10.1.3) show intense osteochondral contrast uptake (arrow), suggesting a stable lesion with preserved vascular continuity with the parent bone (Stage II). In another patient, sagittal fat-suppressed T2-weighted MRI (Fig. 10.1.4) shows a subtle hyperintense osteochondral area (arrow) without signs of detachment; a stage I osteochondral lesion due to subchondral trabecular compression was diagnosed. In another patient, a sagittal reformatted MDCT image (Fig. 10.1.5) confirms a subchondral talar dome lesion with osteochondral fragmentation at the articular surface (arrow); a stage IV osteochondral lesion was diagnosed and confirmed at surgery.
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A 21-year-old woman presented with right foot deformity and ecchymosis after a fall from a height of 6 m.
Case 10.2 Calcaneal Fracture Introduction
The calcaneus has four articulating surfaces: three that articulate superiorly with the talus and one that articulates anteroinferiorly with the cuboid. Of the three superior, the anterior is supported by the calcaneal beak and the middle is
Fig. 10.2.1
Fig. 10.2.2
Fig. 10.2.3
Fig. 10.2.4
205 Ankle and Foot supported by the sustentaculum tali. Both the anterior and middle facets are separated from the posterior facet by a groove, the calcaneal sulcus. The canal formed between this sulcus and the talus is the sinus tarsi. The calcaneus is the most commonly fractured tarsal bone and accounts for about 2% of all fractures. Calcaneal fractures have characteristic appearances based on the mechanism of injury and are divided into two major groups: intra-articular and extra-articular. Most calcaneal fractures (70–75%) are intra-articular and result from axial loading that produces shear and compression fracture lines. Sanders’ system is the most used for classifying intra-articular fractures. Extra-articular fractures account for about 25–30% of calcaneal fractures and include all fractures that do not involve the posterior facet. Thus, the first step in staging these fractures is to rule out posterior facet involvement to determine whether the fracture is intra- or extra-articular. Plain-film radiographs of the ankle and foot are among the most frequently requested imaging tests in the emergency room. The American College of Radiologists (ACR) has established some guidelines for obtaining ankle radiographs in patients with the following clinical findings: (1) inability to bear weight immediately after the injury, or (2) point tenderness over the medial malleolus, or on the posterior edge or inferior tip of the lateral malleolus or talus or calcaneus, or (3) inability to ambulate for four steps in the emergency room. Bone scintigraphy is a highly sensitive imaging procedure for diagnosing hidden or stress fractures of the ankle and foot, but this technique has poor spatial resolution and specificity compared to CT or MRI. The ACR recommends MDCT for patients with high energy polytrauma and in those with complex foot and ankle fractures. The complexity of this anatomic area makes the use of cross-sectional imaging very useful in the detection and accurate description of each of these fractures. For instance, it is essential to evaluate the integrity of joint surfaces and the presence of loose intra-articular fragments; furthermore, reconstructed 3-D images can aid in planning surgery. MRI is considered the best imaging tool for evaluating ankle lesions, because it can show extra-articular and noncomminuted intra-articular fractures as well as associated softtissue lesions (tendon tears, ligament sprains, etc.).
Lateral plain-film radiograph of the left calcaneus (Fig. 10.2.1) shows calcaneal fracture lines with an abnormal calcaneal or Böhler’s angle (5°; normal 20–40°) and Gissane’s critical angle (75°; normal 120–145°). Both diminished pathologic angles confirm calcaneal posterior facet collapse. Axial MDCT image (Fig. 10.2.2) shows a severe comminuted intra-articular fracture of the calcaneus (Type IV on the Sanders Classification). Sagittal MDCT reformatted image (Fig. 10.2.3) clearly shows a central joint depression pattern; the posterior facet of the subtalar joint (arrow) is affected. This sign classifies this fracture as “intra-articular.” Coronal MDCT reformatted image (Fig. 10.2.4) of the calcaneus depicts two shear fracture lines (arrows) that separate the sustentacular (S), middle (M), and tuberosity (T) fragments (“double split”), with widening of the calcaneus.
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Case 10.3 Complete Achilles Tendon Tear
Introduction
A 45-year-old man presented with abrupt onset of pain over the posterior aspect of the leg, difficulty in walking, and inability to tiptoe on the injured side. Thompson’s test, carried out by squeezing the calf, was positive. Ultrasound and MRI were requested to confirm or rule out a full-thickness Achilles tendon tear and to evaluate the gap and the plantaris tendon to decide on the most appropriate treatment.
The Achilles tendon is the most commonly injured ankle tendon. Achilles tendon tears tend to occur 2–6 cm superior to the calcaneal insertion, which corresponds
Fig. 10.3.1 Fig. 10.3.2
Fig. 10.3.3
207 Ankle and Foot to a zone of relative avascularity; moreover, the particular disposition of the fibers in this zone results in an area of increased internal stress on tendon contraction. Achilles tendon rupture is most common in patients between the ages of 30 and 50 years, and it often occurs in tendons with previous degeneration. Partial ruptures usually occur in well-trained athletes secondary to trauma, often lateral in location with longitudinal or transverse splits. In contrast, complete ruptures tend to occur in middle-aged and poorly conditioned men. Partial tears without a tendinous gap can mimic chronic Achilles tendinosis, which presents heterogeneity, thickening, or waviness of the tendon on MRI and ultrasonography. The clinical history may differentiate the two pathologies; MRI can help to distinguish between them because partial tears are often associated with subcutaneous edema or hemorrhage within Kager´s fat pad and intratendinous hemorrhage with high signal intensity on T1-weighted images. However, this distinction may not be of great clinical importance since both partialthickness tears and tendinosis are usually initially treated by conservative measures. It is important to determine whether there is a large tendinous gap in partial tears or a complete discontinuity in the Achilles tendon, because these conditions are often treated by casting the ankle in the equinus position or by surgical repair. Clinical examination in complete tears is sometimes equivocal because the flexor, peroneal, and plantaris tendons also contribute to plantar flexion and can compensate for an injured Achilles tendon, and imaging can help in the diagnosis. Ultrasonography has proven accurate in differentiating partial-thickness tears or tendinosis from full-thickness tears of the Achilles tendon: an undetectable tendon at the site of injury, tendon retraction, and posterior acoustic shadowing at the ends of the torn tendon are characteristics of full-thickness tears. MRI is better for differentiating acute and chronic ruptures, showing edema and bleeding (intermediate signal intensity on T1- and high signal intensity on T2-weighted images) in cases of acute ruptures and scar or fat in chronic ruptures. Sagittal and axial T1-weighted and fat-suppressed proton density-weighted or STIR images are required. MRI is also better for evaluating a torn plantaris tendon, which may mimic an Achilles tendon tear or an intact plantaris tendon in a complete Achilles tendon tear simulating a large partial tear. Assessment of the status of the plantaris tendon is also important for planning surgical repair of the Achilles using the plantaris as an anatomical reference. Imaging techniques should assess the site of the tear, its extent, and the degree of retraction and fraying of the tendon edges. Some large partial ruptures or complete ruptures with a tendinous gap of 3 cm or less may be repaired with an end-to-end anastomosis. Complete ruptures with a tendinous gap greater than three require a flap graft.
Sagittal T1-weighted SE MRI (Fig. 10.3.1) shows a complete Achilles tendon rupture with a gap less than 3 cm (open arrow). Note the fat herniation into the tendon defect (arrow). Sagittal fat-saturated T2-weighted FSE MRI (Fig. 10.3.2) shows the edema and hemorrhage in the gap and in the adjacent soft-tissues (open arrow heads). In the axial proton density-weighted FSE MR image (Fig. 10.3.3), the plantaris tendon is intact and is displaced posteriorly into the defect created by the tear (arrowhead); this finding can be mistaken for residual intact fibers of the Achilles tendon.
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Case 10.4 Lateral Collateral Ligament Sprain
Fig. 10.4.1
Two men, one 38-years-old and the other 30-years-old, fell during a sporting activity. At admission, the first patient presented significant pain, swelling, and tenderness over the lateral aspect of the ankle joint; the second patient presented only lateral ankle pain. A lateral collateral ligament sprain was suspected in both, and findings on plain-film radiographs obtained to rule out associated bone fracture were normal. Due to the significant swelling, the first patient underwent MRI at admission to evaluate the ligaments involved and to exclude other associated lesions. The second patient underwent MRI 1 year later for chronic lateral ankle pain.
Fig. 10.4.2
Fig. 10.4.4
Fig. 10.4.3
Fig. 10.4.5
209 Ankle and Foot The lateral collateral ligament is one of the most frequently injured ligaments in ankle sprains; it is commonly due to inversion with internal rotation of the foot combined with ankle plantar flexion. This ligament comprises the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL), corresponding to the inferior group of the lateral stabilizing ligaments of the ankle joint below the syndesmotic ligaments. The weak ATFL is the most commonly torn ankle ligament, and it is usually injured alone (approximately 70% of all ankle ligament ruptures). With more severe inversion stress, the rest of the ligaments rupture in the following order: after the ATFL, the CFL can be involved (a combined rupture in 20–40% of cases), followed by the stronger PTFL, whose rupture is uncommon except in severe ankle trauma with dislocation. Imaging evaluation of the injured ankle often begins with anteroposterior plain-film radiography, which, like CT, can detect bony impairment, i.e., fractures, avulsion fractures at the insertion, and bone diastases. Stress radiographs are of questionable value: pain, edema, and muscle spasm hinder image acquisition, and differences in radiographic technique and in the amount of force applied to the joint make reliable interpretation difficult. Although sonography is rarely used in this context and requires a confident examiner, it can be used to examine the soft-tissue structures around the ankle joint, including the ligaments and associated peroneal tendon tears. MRI clearly demonstrates the torn ligament, especially on axial images, as a discontinuous or enlarged ligament with adjacent edema or hemorrhage in the acute phase, evenly involving the capsular structure. In chronic tears, MRI shows a discontinuous ligament or often an intact but irregular ligament with thickening, thinning, or detachment. MRI is also indicated for evaluating associated features like syndesmotic injuries, bone contusion, osteochondral fractures, and tendon tears. Most acute ankle sprains have a good prognosis, and conservative treatment is commonly proposed. However, in severe ruptures in which the ligament fails to heal after conservative treatment or in competitive athletes, surgical repair may be the treatment of choice. Some patients can develop chronic ankle pain due to instability, anterior impingement syndrome, or sinus tarsi syndrome. MRI can demonstrate synovitis and fibrosis in the anterolateral gutter in patients with impingement syndrome, and obliteration of sinus tarsi fat in those with sinus tarsi syndrome.
Introduction
First patient at admission: Axial proton density-weighted (Fig. 10.4.1) and axial fat-suppressed T2-weighted (Fig. 10.4.2) FSE MR images of the ankle joint. The ATFL cannot be seen in the anterior aspect of the talofibular joint (open arrows); this corresponds to a complete tear. A hematoma is seen in the adjacent soft-tissues (arrows). Axial proton densityweighted FSE MR image at a lower level (Fig. 10.4.3) shows a signal change in the CFL, consistent with sprain (open arrow head). Second patient with chronic pain 1 year after the sprain: Axial proton density-weighted (Fig. 10.4.4) and axial T2-weighted (Fig. 10.4.5) FSE MR images showed a soft-tissue lesion in the anterior aspect of the talofibular joint (arrow heads), causing impingement syndrome.
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Case 10.5 Syndesmotic Ankle Sprain
Fig. 10.5.1
Fig. 10.5.2
Fig. 10.5.3
Fig. 10.5.4
211 Ankle and Foot After being injured in a match, a 27-year-old male soccer player presented with severe ankle pain that increased with external rotation. Plain-film radiographs of the ankle performed in the emergency room ruled out a fracture. MRI was requested to evaluate the condition.
Ankle sprains are among the most common athletic injuries and represent a significant source of persistent pain and disability. Despite the high incidence of ankle sprains in athletes, syndesmotic injuries have historically been misdiagnosed. The four syndesmotic ligaments are the anterior (AITFL) and posterior (PITFL) inferior tibiofibular ligaments, the transverse inferior tibiofibular ligament, and the interosseous ligament, which is a thickening of the distal portion of interosseous membrane. A common variant (Basset or Duke Ligament) can be found, forming the distal fascicle of the AITFL. Syndesmotic sprain can occur alone or in conjunction with ankle fractures or other ligamentous injuries. The AITFL is the most frequently injured ligament. Syndesmotic sprains account for 18% of all ankle sprains in professional soccer players, and they take substantially longer to heal than the more common isolated collateral ligament injuries. When clear tibiofibular diastasis is absent, the acute injury calls for conservative management. Anteroposterior and mortise weight-bearing plain-film radiographs of syndesmotic sprain can show syndesmotic clear space due to tibiofibular diastasis (normal <6 mm) if the syndesmotic sprain is complete, and they can rule out associated ankle fractures. However, because most syndesmotic sprains are incomplete, findings on plain-film radiographs are often normal. CT should be used as a complementary technique to rule out fractures; joint surfaces and loose bone fragments must be carefully evaluated. MRI is the technique of choice. MRI findings are best seen on axial images, where high signal intensity on T2-weighted images due to fluid within the tibiofibular space is considered an important secondary sign of acute syndesmotic tear. Contour irregularity or frank discontinuity of ligaments and tibiofibular space diastasis can be found. Chronic syndesmotic injury manifests as a thickened hypointense AITFL or as an ossification of the interosseous membrane. The differential diagnosis of syndesmotic sprain should include lateral ankle instability (collateral ligament tear), fibular fracture, compartment syndrome, and posterior impingement.
Comments
Axial proton density-weighted FSE MRI (Fig. 10.5.1) shows syndesmotic ligament (AITFL) disruption (arrow). The PITFL is preserved (arrowhead). Axial fat-suppressed T2-weighted FSE (Fig. 10.5.2) at the same level as in Fig. 10.5.1 shows hyperintense fluid and discontinuity of the AITFL (arrow) as well as a posterior tibial bone bruise (arrowhead). Axial proton density-weighted FSE (Fig. 10.5.3) and axial fat-suppressed T2-weighted FSE MRI (Fig. 10.5.4), both obtained caudal to Figs. 10.5.1 and 10.5.2, show an anterior tibiofibular fascicle of the lateral ligament complex preserving its disposition (arrow).
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Case 10.6 Plantar Fasciitis
Fig. 10.6.1
Fig. 10.6.2
Fig. 10.6.3
Fig. 10.6.4
213 Ankle and Foot A 50-year-old male surgeon presented progressive heel pain in his right foot that increased after playing squash.
Most abnormalities of the plantar fascia are found near the calcaneal insertion and usually involve the medial bundle. Plantar fasciitis is the most common cause of heel pain; it can be found in young athletes (exceptionally, an acute plantar fascia rupture can be seen in this group) as well as in overweight patients. It is commonly associated with long periods of weight bearing or sudden changes in weight bearing or activity. The main clinical symptom is pain that begins with the first steps in the morning, decreasing after that and then increasing again after long weight bearing. US is useful in diagnosing plantar fasciitis; it is less expensive than MRI and its reported sensitivity and specificity are 80 and 89%, respectively, compared with MRI. The thickness of normal fascia measures 3–4 mm; in plantar fasciitis, the plantar fascia appears hypoechoic and measures greater than 5 mm at the calcaneal insertion. Furthermore, US-guided percutaneous treatment is effective in the management of plantar fasciitis, and US can objectively measure the response to treatment. MRI may show thickening (greater than 5 mm) and heterogeneous signal of the plantar fascia, with T2 hyperintensity, surrounding soft-tissue edema, calcaneal enthesophytosis (“bone spur”), and subcortical calcaneal edema. The differential diagnosis of plantar fasciitis must include plantar fibromatosis, which is generally located more distally and presents single or multiple nodules, and other entities that can affect the plantar heel, such as systemic enthesopathic processes like seronegative arthritides or sarcoidosis, calcaneal stress fracture (related to the posterior calcaneal area rather than the plantar area), and tarsal tunnel syndrome (plantar muscles affected with diffuse edema in the acute phase or atrophy in the chronic phase).
Introduction
Sagittal STIR MRI (Fig. 10.6.1) shows a subtle thickening of the lateral cord of proximal plantar fascia (arrow) with a high signal area of edema in the adjacent subcutaneous fat. Sagittal STIR MRI (Fig. 10.6.2) depicts greater thickening of the medial cord of the proximal plantar fascia (arrow). Coronal T2*-weighted MRI (Fig. 10.6.3) shows heterogeneous signal and thickening of the plantar fascia (arrow). Sagittal STIR MRI (Fig. 10.6.4) in another patient with plantar fasciitis shows a thickened proximal area of plantar fascia (arrow) without marked edema in adjacent subcutaneous fat. In the chronic stage of plantar fasciitis, plantar thickness may increase and soft-tissue edema may decrease.
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Case 10.7 Plantar Fibromatosis
Fig. 10.7.1
Fig. 10.7.3
Fig. 10.7.2
Fig. 10.7.4
215 Ankle and Foot A 55-year-old woman complained of mild plantar pain and a subcutaneous nodule in her left foot. Her orthopaedist confirmed a soft-tissue nodule along the medial plantar surface measuring nearly 1 cm and fixed to plantar aponeurosis. MRI was requested to characterize nodule type and extension. Histological study after surgical excision showed the nodule was surrounded by plantar aponeurosis; microscopically, it was composed of a nodular mixture of fibroblasts and collagen fibbers without malignant transformation.
Plantar fibromatosis (Ledderhose’s disease) is a type of superficial fibromatosis characterized by nodular thickening (single or multiple) arising from the plantar fascia of the foot, often in nonweight-bearing lesions. In some patients, it can be associated to Dupuytren’s contracture. Clinical symptoms include a solid, fixed subcutaneous nodule, which can be softly painful. US is an excellent technique to diagnose plantar fibromatosis: it shows a hypoechoic, heterogeneous nodule arising from the anterior part of the plantar fascia. MRI is highly accurate in detecting soft-tissue tumors. Plantar fibromatosis is seen as a nodule growing along the long axis of the plantar fascia; it has heterogeneous signal intensity equal to or less than that of skeletal muscle on both T1- and T2-weighted spin-echo MRI, although it may be slightly hyperintense if the cellular component is increased. About 50% of these nodules present significant solid contrast enhancement. The differential diagnosis of plantar fibromatosis should first include plantar fasciitis, which is located close to the calcaneus, without nodules. Plantar fibromatosis should also be distinguished from other soft-tissue tumors that can affect the plantar area: ganglion cyst (hypointense on T1-weighted and hyperintense on T2-weighted images), lipoma (hyperintense on T1-weighted images; fat signal that ceases on fat-suppressed T2-weighted or STIR images), neurogenic tumors (arising from nerves, generally painful), giant cell tumor of tendon sheath (hypointense foci on T2-weighted images due to hemosiderin), synovial sarcoma (heterogeneous mass arising and growing along tendon sheaths; bone destruction may be present), and finally soft-tissue chondroma, a very rare tumor (coarse calcifications within the tumor on plain films, MRI signal voids).
Introduction
Sagittal T1-weighted MRI (Fig. 10.7.1) shows a single isointense nodule (arrow) through the long axis of the plantar fascia (anterior part of the medial cord) extending to the plantar subcutaneous tissue. Sagittal T2*-weighted MRI (Fig. 10.7.2) at same plane as in Fig. 10.7.1 shows intermediate signal without hypointense foci (arrow). Coronal fat suppressed T1-weighted MRI (Fig. 10.7.3) depicts an isointense plantar nodule (arrow) arising from the medial margin of the medial cord of the plantar fascia. A skin marker was attached to localize the lesion. Coronal postcontrast FS T1-weighted MRI (Fig. 10.7.4) at the same level as in Fig. 10.7.3 reveals intense nodular enhancement (arrow), with subtle hypointense linear areas due to plantar fibers inside the nodule.
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Case 10.8 Tarsal Tunnel Syndrome
Fig. 10.8.1 Fig. 10.8.2
Fig. 10.8.3
Fig. 10.8.4
217 Ankle and Foot A 68-year-old woman presented with an 8-week history of nocturnal paresthesias and pain in the plantar aspect of her right foot that worsened with activity. Physical examination showed tenderness to palpation and positive percussion of the tibial nerve over the tarsal tunnel (Tinel’s sign). MRI was requested to evaluate tarsal tunnel syndrome.
Tarsal tunnel syndrome refers to neuropathy due to entrapment or compression of the posterior tibial nerve or one of its branches located in the fibrous-osseous tunnel beneath the flexor retinaculum and caudal to the tibial malleolus. This tunnel contains other anatomic structures, including the tibialis posterior, flexor digitorum longus, and flexor hallucis longus tendons. The syndrome can arise from trauma or occupation of the space by varicosities, ganglia, or anomalous muscles (flexor digitorum accessorius longus), but up to 50% of cases are idiopathic. Plain-film radiographs should rule out talocalcaneal coalition and fractures of the sustentaculum tali or medial tubercle. CT should be used as a complementary technique to visualize hidden bone fractures. Ultrasonography can be extremely useful for identifying space-occupying lesions in tarsal tunnel syndrome. MRI is considered the technique of choice because it is highly sensitive in detecting lesions such as varicosities, ganglia, lipomas, neurogenic tumors, thickened flexor retinaculum as well as talar coalition, exostosis, or fracture. Furthermore, MRI can detect abnormal signal in denervated muscle (hyperintense edema on T2-weighted images in the acute stage or hyperintense fatty atrophy on T1-weighted images in chronic stages), which could be a key finding to diagnose tunnel tarsal syndrome. The differential diagnosis of tunnel tarsal syndrome must include local pathology, such as tarsal coalition, calcaneal stress fracture, tibialis posterior tenosynovitis, plantar fasciitis, diabetic foot neuroarthropathy, osteoarthritis, as well as distant pathology such as L5 or S1 radiculopathy.
Introduction
Coronal T1-weighted MRI (Figs. 10.8.1 and 10.8.2) shows severe fatty atrophy of denervated abductor hallucis muscle (arrow) and osteoarthritic sustentacular and subtalar changes with a beak-shaped bony process (arrowhead) occupying the space of the medial plantar nerve, the larger of the two terminal divisions of the tibial nerve. Other nearby plantar muscles, such as the quadratus plantae, flexor digitorum brevis, and abductor digiti quinti, are preserved. Axial FS T2-weighted FSE MRI (Fig. 10.8.3.) shows no hyperintensity in the abductor hallucis muscle (arrow) due to edema; an acute phase of compression neuropathy can be excluded. Other etiologies of tunnel tarsal syndrome, such as varicosities, or different etiologies of local pain, such as stress fractures, can be ruled out. Coronal T1-weighted MRI in a normal patient without tunnel tarsal syndrome (Fig. 10.8.4) shows the absence of compression neuropathy of the medial plantar nerve and the normal morphology of the abductor hallucis muscle (arrow).
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Case 10.9 Diabetic Foot
Fig. 10.9.2 Fig. 10.9.1
Fig. 10.9.3
Fig. 10.9.4
219 Ankle and Foot A 34-year-old woman diagnosed several years earlier with type II diabetes mellitus complicated with chronic renal failure presented with a 2-week history of foot disturbances. Physical examination found foot deformity and skin erythema. Electromyography revealed severe mixed neuropathy. \Plain-film radiography of the foot showed osteopenia and several bone erosions. Bone scintigraphy, CT, and MRI were requested to evaluate diabetic foot pathology.
Diabetic foot is a frequent complication in both type I and type II diabetes mellitus. In patients with diabetic foot disorders, it is crucial to differentiate between neuropathic arthropathy (Charcot’s joint), which usually occurs in patients with long-standing diabetes, and osteomyelitis, which is frequently associated with foot ulcers with deep tracks and soft-tissue abscesses. Plain-film radiographs of neuropathic arthropathy can show osteopenia, forefoot osteolysis, fractures, and fragmentation. Bone scintigraphy is highly sensitive in diagnosing osteomyelitis in the diabetic foot. In a recent study, 99mTc-HMPAO leukocyte scintigraphy combined with a 99mTc-MDP bone scintigraphy scan showed a sensitivity of 92.6% and a specificity of 97.6%; moreover, neuroarthropathy did not affect the accuracy of the scintigraphic techniques. The high spatial resolution of this test is very helpful to differentiate bone infection from soft-tissue infection, especially in cases of neuroarthropathy. CT should be used as a complementary technique to visualize bony destruction, gas bubbles in the bone, or bony sequestration. Reconstructed 3-D images can aid in planning surgery. Currently, MRI is the best imaging technique because it is highly sensitive in detecting both soft-tissue lesions (skin ulcers and tracts, cellulitis, and abscesses) and bone lesions (hypointense replacement of bone marrow on T1-weighted images). MRI can also stage diabetic foot lesions accurately. Postcontrast images can provide additional information (rim abscess enhancement, diffuse cellulitis enhancement), but coexistent renal failure in those patients must be kept in mind. The differential diagnosis of diabetic foot neuroarthropathy must include diabetic foot osteomyelitis, osteoarthritis, talus or navicular osteonecrosis, and crystal deposition arthritis.
Introduction
Plain-film radiographs of both feet (Fig. 10.9.1) show extensive erosions and bone destruction in the tarsometatarsal and intermetatarsal joints, periosteal reaction in metatarsal bones, and soft-tissue edema in the right foot (arrow). Leukocyte bone marrow scintigraphy with a 99mTc-HMPAO scan (Fig. 10.9.2) does not show increased uptake within the bones right foot and thus rules out osteomyelitis. Only a subtle focus of uptake due to a skin ulcer is noted (arrow). CT (Fig. 10.9.3) confirms extensive bone destruction with fragmentation in the tarsal area (arrow). Sagittal T1-weighted MRI (Fig. 10.9.4) shows diffuse low signal intensity affecting the talus, cuboids, and metatarsals with bone erosions and periosteal reaction in the proximal fifth MTT.
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Case 10.10 Intermetatarsal Bursitis and Morton’s Neuroma
Fig. 10.10.1
Fig. 10.10.3
A 56-year-old man presented with right forefoot disturbances of several weeks’ evolution; his plantar foot pain increased with activity. Physical examination found pain and tenderness in the spaces between the first and third metatarsal heads when compression was applied. Plain-film radiographs of the foot showed no pathological findings. MRI was requested to evaluate forefoot pathology.
Fig. 10.10.2
Fig. 10.10.4
221 Ankle and Foot Intermetatarsal or Morton’s neuromas and intermetatarsal bursitis are two common causes of forefoot pain. Mechanically induced chronic microtrauma due to excessive weight-bearing stress on the forefoot predisposes to these pathologies. The intermetatarsal bursa can grow around the intermetatarsal nerve, making manifestations of bursitis and Morton’s neuroma indistinguishable. Morton’s neuroma is not a true tumor; its represents perineural fibrosis, which occurs mainly in the second or third intermetatarsal spaces, in the third common digital branch of medial plantar nerve, and rarely in the first or fourth. A transition from intermetatarsal bursitis (acute stage) to fibrosis (chronic stage), with both entities often coexisting at presentation, has been adduced. Histological examination shows endoneural edema in early stages and perineural, epineural, and endoneural fibrosis in late stages. On US, intermetatarsal bursitis is seen as a compressible, well-defined anechoic or hypoechoic collection of variable size surrounding metatarsal heads; in contrast, Morton’s neuroma shows a noncompressible nodular morphology, which varies from hypo- to hyperechoic, with a diameter greater than 3 mm in dorsoplantar thickness. MRI is the technique of choice for evaluating the forefoot because it is highly sensitive in the detection of both soft-tissue lesions (bursitis, neuromas, tumors) and bone lesions (metatarsal fractures, Freiberg’s disease). Intermetatarsal bursitis appears as a well-defined collection that is hypointense on T1-weighted images and hyperintense on T2-weighted images; contrast-uptake is limited to the peripheral area (“ring-like enhancement”). Small fluid collections with a transverse diameter of 3 mm or less in the first three intermetatarsal bursas may be physiologic. Fibrotic changes in Morton’s neuroma can lead to hypointense to isointense T1-weighted signal and isointense to hyperintense signal on FS T2-weighted and STIR sequences; contrast uptake varies depending on the maturity of the lesion and associated inflammation. The differential diagnosis of intermetatarsal bursitis and Morton’s neuroma should include other causes of forefoot pain such as metatarsal fracture (metatarsal bone marrow edema and cortical-periosteal reaction), osteochondrosis of the second metatarsal head (also known as Freiberg’s disease, with flattening and edema), and soft-tissue tumors (neurogenic, synovial sarcoma..; mainly hyperintense on T2-weighted images with intense contrast uptake).
Introduction
Coronal T1-weighted MRI (Fig. 10.10.1) shows an isointense single nodule (arrow) in the third intermetatarsal space, and another larger isointense mass in the first intermetatarsal space (arrowhead) extending to the plantar subcutaneous tissue. Coronal T2-weighted MRI (Fig. 10.10.2) shows hypointense signal in the third intermetatarsal space nodule (arrow), suggesting a fibrous composition, and a markedly hyperintense signal in the well-demarcated mass in the first intermetatarsal space (arrowhead), suggesting a fluid component. Axial FS T1-weighted MRI (Fig. 10.10.3) and axial postcontrast FS T1-weighted MRI (Fig. 10.10.4) at the same level as in Fig. 10.10.3 reveal subtle nodular enhancement (arrow) of the third intermetatarsal lesion (Morton’s neuroma) and intense ring-enhancement due to intermetatarsal bursitis (arrowhead) of the first intermetatarsal space.
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Further Reading Books Diagnostic Imaging: Orthopaedics. Stoller DW, Tirman PFJ, Miriam A, Bredella M (2004). Elsevier, Philadelphia, PA. ISBN 0-7216-2920-2 Imaging of the Musculoskeletal System. 2-volume set. Thomas Pope, MD, Hans Bloem, MD, Javier Beltran, MD, William Morrison, MD, David Wilson, MD (2008). Saunders, Elsevier, Philadelphia, Amsterdam. ISBN 978-1-4160-2963-2 Problem Solving in Musculoskeletal Imaging. William BM, Timothy GS (2008). Mosby, Elsevier, London, Philadelphia, PA. ISBN 978-0-323-04034-1
Web-Links http://www.acr.org/. American College of Radiology http://www.rsna.org/. RSNA Society http://www.yottalook.com/. Medical Imaging Search Engine http://www.i-fab.org/. International Foot and Ankle Biomechanics http://www.arrs.org/. ARRS Society
Articles Anderson IF, Crichton KJ, Grattan-Smith T, Cooper RA, Brazier D. Osteochondral fractures of the dome of the talus. J Bone Joint Surg Am. 1989; 71(8):1143–1152 Ashman CJ, Klecker RJ, Yu JS. Forefoot pain involving the metatarsal region: differential diagnosis with MR imaging. Radiographics 2001; 21(6):1425–1440 Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 1959; 41-A:988– 1020 (no abstract available) Bowers CA, Mendicino RW, Catanzariti AR, Kernick ET. The flexor digitorum accessorius longus-a cadaveric study. J Foot Ankle Surg 2009; 48(2):111–115. Epub 2009 Jan 9 Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med 1991; 19(3):294–298 Campbell SE, Warner M. MR imaging of ankle inversion injuries. Magn Reson Imaging Clin N Am 2008; 16(1):1–18 Coughlin MJ. Common causes of pain in the forefoot in adults. J Bone Joint Surg Br 2000; 82(6):781–790 Dalinka MK, Alazraki NP, Daffner RH, DeSmet AA, El-Khoury GY, Kneeland JB, Manaster BJ, Morrison WB, Pavlov H, Rubin DA, Steinbach LS, Weissman BN, Haralson RH III. Expert Panel on Musculoskeletal Imaging. Suspected ankle fractures. [online publication]. Reston (VA): American College of Radiology (ACR); 2005; 4
Daftary A, Haims AH, Baumgaertner MR. Fractures of the calcaneus: a review with emphasis on CT. Radiographics 2005; 25(5):1215–1226 (review) Hartgerink P, Fessell DP, Jacobson JA, van Holsbeeck MT. Fullversus partial-thickness Achilles tendon tears: sonographic accuracy and characterization in 26 cases with surgical correlation. Radiology 2001; 220(2):406–412 Hilary U. Foot and ankle imaging. Radiol Clin North Am 2008; 46(6):957–1130 Kane D, Greaney T, Shanahan M, Duffy G, Bresnihan B, Gibney R, FitzGerald O. The role of ultrasonography in the diagnosis and management of idiopathic plantar fasciitis.Rheumatology (Oxford) 2001; 40(9):1002–1008 Kreitner KF, Ferber A, Grebe P, Runkel M, Berger S, Thelen M. Injuries of the lateral collateral ligaments of the ankle: assessment with MR imaging. Eur Radiol 1999; 9:519–524 Loredo R, Sanders TG. Imaging of osteochondral injuries. Clin Sports Med. 2001; 20(2):249–278 (review) Masciocchi C, Catalucci A, Barile A. Ankle impingement syndromes. Eur J Radiol. 1998; 27(suppl 1):S70–S73 Morrison WB, Schweitzer ME, Wapner KL, Lackman RD. Plantar fibromatosis: a benign aggressive neoplasm with a characteristic appearance on MR images. Radiology 1994; 193(3): 841–845 Nagaoka M, Matsuzaki H. Ultrasonography in tarsal tunnel syndrome. J Ultrasound Med 2005; 24(8):1035–1040 Poirier JY, Garin E, Derrien C, Devillers A, Moisan A, Bourguet P, Maugendre D. Diagnosis of osteomyelitis in the diabetic foot with a 99mTc-HMPAO leucocyte scintigraphy combined with a 99mTc-MDP bone scintigraphy. Diabetes Metab 2002; 28(6 pt 1):485–490 Quinn SF, Murray WT, Clark RA, Cochran CF. Achilles tendon: MR imaging at 1.5 T. Radiology 1987; 164(3):767–770 Robbin MR, Murphey MD, Temple HT, Kransdorf MJ, Choi JJ. Imaging of musculoskeletal fibromatosis. Radiographics 2001; 21(3):585–600 (review) Russell JM, Peterson JJ, Bancroft LW. MR imaging of the diabetic foot. Magn Reson Imaging Clin N Am 2008; 16(1):59–70, vi Sabir N, Demirlenk S, Yagci B, Karabulut N, Cubukcu S. Clinical utility of sonography in diagnosing plantar fasciitis. J Ultra sound Med 2005; 24(8):1041–1048 Sanders R, Fortin P, DiPasquale T, Walling A. Operative treatment in 120 displaced intraarticular calcaneal fractures. Results using a prognostic computed tomography scan classification. Clin Orthop Relat Res 1993; 290:87–95 Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA 2005; 293(2):217–228 (review) Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med 2007; 35(7):1197–1207. Epub 2007 May 22 (review) Zanetti M, Strehle JK, Zollinger H, Hodler J. Morton neuroma and fluid in the intermetatarsal bursae on MR images of 70 asymptomatic volunteers. J Radiol 1997; 203(2):516–520 Zehava SR. Update on the ankle and foot. MRI Clin North Am 2001; 9(3):413–671
