Matthew Amans, MD, MScDepartment of Radiology and Biomedical Imaging University of California, San Francisco San Francisco, California Associate Professor of Clinical Radiology Weill Cor
Trang 1MediaCenter.thieme.com
plus e-content online
Trang 2Case-Based Brain Imaging Second Edition
Trang 3Case-Based Brain Imaging Second Edition
A John Tsiouris, MD
Associate Professor of Clinical Radiology Weill Cornell Medical College
NewYork-Presbyterian Hospital New York, New York
Pina C Sanelli, MD, MPH
Associate Professor of Radiology and Public Health Weill Cornell Medical College
NewYork-Presbyterian Hospital New York, New York
Joseph P Comunale, MD
Associate Professor of Clinical Radiology Weill Cornell Medical College
NewYork-Presbyterian Hospital New York, New York
Thieme New York • Stuttgart
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Library of Congress Cataloging-in-Publication Data
Case-based brain imaging / edited by A John Tsiouris, Pina C Sanelli, Joseph P Comunale — 2nd ed
[DNLM: 1 Brain Diseases—diagnosis—Atlases 2 Brain Diseases—diagnosis—Case Reports
3 Diagnostic Imaging—Atlases 4 Diagnostic Imaging—Case Reports WL 17]
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Trang 5To our patients, who are an infinite source of challenging cases that motivate us to continuously
improve our knowledge and skills.
I dedicate this book to my father, Dr John A Tsiouris, for the many sacrifices he made throughout his life
so my brother and I could succeed
Apostolos John Tsiouris, MD
I dedicate this book to my loving and supportive husband, George, and to our three children, Isabella,
Sophia, and Nicholas, who are truly our pride and joy
Pina C Sanelli, MD, MPH
I dedicate this book to my parents, for their unconditional support and encouragement, and to my
colleagues, residents, and fellows, who continue to motivate me to be the best I can be
Joseph P Comunale, MD
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Trang 7Foreword by Robert D Zimmerman, MD, FACR xi
Preface xiii
Acknowledgments .xiv
Contributors xv
Abbreviations xvi
Section I Neoplasms IA Supratentorial Case 1 Low-grade Astrocytoma (WHO Grade II) 3
Case 2 Anaplastic Astrocytoma (WHO Grade III) 7
Case 3 Glioblastoma Multiforme (WHO Grade IV) 12
Case 4 Oligodendroglioma (WHO Grade II or III) 16
Case 5 Central Neurocytoma (WHO Grade II) 21
Case 6 Ganglioglioma (WHO Grade I–III) 27
Case 7 Gliomatosis Cerebri (WHO Grade IV) 32
Case 8 Metastatic Breast Cancer 36
Case 9 Dural Metastasis from Stage IV Breast Cancer 42
Case 10 Lymphomatous Meningitis 47
Case 11 Primary CNS Lymphoma 51
Case 12 Dysembryoplastic Neuroepithelial Tumor (WHO Grade I) 57
Case 13 Ependymoblastoma (WHO Grade IV) 60
Case 14 Pineocytoma (WHO Grade I) 65
Case 15 Pineoblastoma (WHO Grade IV) 68
Case 16 Pineal Region Germinoma 72
Case 17 Pituitary Microadenoma (WHO Grade I) 77
Case 18 Pituitary Macroadenoma 82
Case 19 Rathke Cleft Cyst 87
Case 20 Craniopharyngioma (WHO Grade I) 90
Case 21 Meningioma (WHO Grade I) 94
Case 22 Subependymoma of Fourth Ventricle (WHO Grade I) 99
Case 23 Choroid Plexus Papilloma (WHO Grade I) 103
Case 24 Arachnoid Cyst 107
Case 25 Dermoid Cyst 111
Case 26 Mature Pineal Teratoma 115
Case 27 Colloid Cyst 119
Case 28 Neurenteric Cyst 123
Case 29 Lipoma 127
Case 30 Psammomatoid Ossifying Fibroma 130
Contents
Trang 8IB Infratentorial
Case 31 Juvenile Pilocytic Astrocytoma (WHO Grade I) 137
Case 32 Tectal Glioma (WHO Grade I or II) 141
Case 33 Brainstem Glioma 145
Case 34 Medulloblastoma (WHO Grade IV) 151
Case 35 Ependymoma (WHO Grade II or III) 155
Case 36 Vestibular Schwannoma (WHO Grade I) 161
Case 37 Epidermoid Cyst 166
Section II Inflammatory Diseases IIA Infectious Case 38 Herpes Simplex Virus Type I 173
Case 39 Bacterial Meningitis 177
Case 40 Acute Cerebellitis 184
Case 41 Brain Abscess 188
Case 42 Subdural Empyema 194
Case 43 Neurocysticercosis 199
Case 44 Tuberculosis Meningitis 203
Case 45 Fungal (Aspergillosis) Abscess 207
Case 46 HIV Encephalitis 211
Case 47 Progressive Multifocal Leukoencephalopathy 215
Case 48 CNS Toxoplasmosis 220
Case 49 Cryptococcal Meningitis 224
IIB Non-Infectious Case 50 Systemic Lupus Erythematosus 231
Case 51 Langerhans Cell Histiocytosis 237
Case 52 Mesial Temporal Sclerosis 242
Case 53 Neurosarcoidosis 246
Case 54 Lymphocytic Hypophysitis 251
Case 55 Intracranial Hypotension 255
Section III Cerebrovascular Diseases Case 56 Aneurysmal Subarachnoid Hemorrhage 261
Case 57 Giant Aneurysm 267
Case 58 Mycotic Aneurysm 272
Case 59 Perimesencephalic Nonaneurysmal Subarachnoid Hemorrhage 277
Case 60 Middle Cerebral Artery Embolus and Acute Infarction 281
Case 61 Watershed Injury 287
Case 62 Basilar Artery Thrombosis 292
Case 63 Arterial Dissection 297
Case 64 Hypertensive Hemorrhage 301
Case 65 Global Anoxic Brain Injury 306
Case 66 Cavernous Malformation 312
Case 67 Arteriovenous Malformation 316
Case 68 Developmental Venous Anomaly 322
Case 69 Carotid Cavernous Fistula 326
Case 70 Dural Arteriovenous Fistula 331
Case 71 Primary Angiitis of the CNS 336 viii CONTENTS
Trang 9Case 72 Fibromuscular Dysplasia 342
Case 73 Periventricular Leukomalacia 347
Case 74 Neonatal Hypoxic-Ischemic Encephalopathy 352
Case 75 Moyamoya Disease 358
Case 76 Vein of Galen Aneurysmal Malformation 364
Case 77 Sickle Cell Disease 371
Case 78 Transverse Venous Sinus Thrombosis 377
Case 79 Superficial Siderosis 382
Case 80 Vasospasm 387
Case 81 Primary Cerebral Amyloid Angiopathy 391
Case 82 Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarctions and Leukoencephalopathy 396
Case 83 Isolated Cortical Vein Thrombosis 401
Case 84 Ataxia-Telangiectasia 405
Section IV Neurodegenerative/White Matter Diseases/Metabolic Case 85 Multiple Sclerosis 411
Case 86 Tumefactive Multiple Sclerosis 416
Case 87 Acute Disseminated Encephalomyelitis 421
Case 88 Osmotic Demyelination Syndrome 425
Case 89 Reversible Postictal Cerebral Edema 428
Case 90 Carbon Monoxide Poisoning 431
Case 91 Metachromatic Leukodystrophy 434
Case 92 X-Linked Adrenoleukodystrophy 437
Case 93 Krabbe Disease 440
Case 94 Pelizaeus-Merzbacher Disease 443
Case 95 Metronidazole-induced Encephalopathy 446
Case 96 Amyotrophic Lateral Sclerosis 449
Case 97 Creutzfeldt-Jakob Disease 453
Case 98 Pantothenate Kinase-associated Neurodegeneration 456
Case 99 Multiple System Atrophy–Cerebellar Type 459
Case 100 Alzheimer Dementia Complex 462
Case 101 Multi-Infarct Dementia 466
Case 102 Wernicke Encephalopathy 469
Case 103 Parry-Romberg Syndrome 473
Section V Trauma Case 104 Traumatic Subarachnoid Hemorrhage 479
Case 105 Epidural Hematoma 484
Case 106 Subdural Hematoma 488
Case 107 Diffuse Axonal Injury (DAI) 492
Case 108 Traumatic Parenchymal Hemorrhagic Contusion 497
Case 109 Nonaccidental Trauma 501
Case 110 Subfalcine and Uncal Herniation 505
Case 111 Leptomeningeal Cyst Associated with a Skull Fracture 510
Section VI Congenital/Developmental Malformations and Syndromes VIA Supratentorial Case 112 Agenesis of the Corpus Callosum 517
Case 113 Alobar Holoprosencephaly 522
Trang 10x CONTENTS
Case 114 Hydranencephaly 527
Case 115 Septo-Optic Dysplasia 530
Case 116 Frontoparietal Encephalomeningocele 533
Case 117 Hamartoma of the Tuber Cinereum 538
Case 118 Benign Enlargement of the Subarachnoid Spaces of Infancy 541
Case 119 Porencephalic Cyst 544
Case 120 Sturge-Weber Syndrome 548
Case 121 Neurocutaneous Melanosis 553
VIB Infratentorial Case 122 Chiari I Malformation 559
Case 123 Chiari II Malformation 564
Case 124 Chiari III Malformation 569
Case 125 Dandy-Walker Spectrum 571
Case 126 Dysplastic Cerebellar Gangliocytoma 576
Case 127 Rhombencephalosynapsis 580
VIC Malformations of Cortical Development Case 128 Hemimegalencephaly 587
Case 129 Subependymal Nodular Heterotopia 591
Case 130 Band Heterotopia 595
Case 131 Classic (Type I) Lissencephaly 600
Case 132 Polymicrogyria 605
Case 133 Schizencephaly 609
Case 134 Focal Cortical Dysplasia 613
VID Phakomatoses Case 135 Neurofibromatosis Type I 619
Case 136 Neurofibromatosis Type II 625
Case 137 Tuberous Sclerosis 629
Case 138 Von Hippel-Lindau Disease (Hemangioblastoma) 634
Section VII Cranial Nerves Case 139 Olfactory Neuroblastoma 641
Case 140 Optic Neuritis 644
Case 141 Optic Nerve Glioma 646
Case 142 Optic Nerve Sheath Meningioma 649
Case 143 Pseudotumor of the Cavernous Sinus (Tolosa-Hunt Syndrome) 651
Case 144 Vascular Compression 654
Case 145 Trigeminal Nerve Schwannoma 656
Case 146 Cavernous Sinus Thrombosis 658
Case 147 Bell’s Palsy 661
Case 148 Hemangioma of the Facial Nerve Canal 663
Case 149 Perineural Spread of Parotid Adenoid Cystic Carcinoma 665
Case 150 Meningioma of Jugular Foramen 667
Case 151 Lateral Medullary Acute Infarction 670
Case 152 Glomus Jugulare Tumor 673
Index 675
Trang 11The second edition of the popular Teaching Atlas of Brain Imaging by Drs Fischbein, Dillon and Barkovich has finally been produced after a hiatus of 12 years, now renamed Case-Based Brain
Imaging The wait was clearly worth it!
The editors of this second edition, Drs Tsiouris, Comunale, and Sanelli, are all my colleagues at NewYork-Presbyterian, Weill Cornell Medical College They are outstanding clinicians and teachers who have used their combined experience and expertise to carefully choose 152 first-rate CT and MRI cases that illustrate the key imaging features of the full spectrum of brain disease in an easy-to-access format The result is a book that is both comprehensive and concise Each chapter starts with
an unknown case In many of the chapters, additional companion images and cases are provided to enhance the reader’s knowledge of the topic and demonstrate variations of the profiled disease The key imaging, pathologic, and pathophysiologic findings for each disease are clearly outlined for each case I especially appreciate the Pearls and Pitfalls sections at the end of each case that summarize wise tips for the reader
Since the first edition, there have been major advances in the CT and MR imaging techniques utilized in neuroradiology Numerous cases in this text include imaging techniques such as CT angi-ography, MR angiography, CT and MR perfusion, and MR spectroscopy that are now commonly used
in practice for the diagnosis and surveillance of CNS disease The all-new images are spectacular, having been obtained on state-of-the-art CT and high field MR scanners The discussions are clear and concise, and the references have all been updated and the cases presented in a clean and unclut-tered layout
This book is meant to provide trainees and practicing radiologists, neurologists, and geons with an opportunity to learn quickly about entities they encounter in their daily clinical prac-tice, and it succeeds in this mission admirably If you see it in practice, it is included in this book
neurosur-It also includes numerous rare zebra cases that can cause diagnostic dilemmas Lastly, this excellent text provides the reader with the opportunity to test their skills in the interpretation of unknown cases For me this is the guilty pleasure of this book Let’s face it, radiologists love visual puzzles
The enduring popularity of case-of-the-day presentations, unknown case sessions, and film panels
at our national meetings speaks to this love This book offers each of us the opportunity to test our knowledge on representative cases and, in the process, gain significant information about a variety
of entities
I believe this book will be enormously useful to the reader interested in the imaging of CNS diseases I congratulate my colleagues on their innumerable hours of work on the production of this outstanding case-based review I hope you enjoy reading it as much as I did
Robert D Zimmerman, MD, FACR
Professor of Radiology and Vice Chair for Education
Weill Cornell Medical College
New York, New York
Foreword
Trang 12Since the first edition of the Teaching Atlas of Brain Imaging by Drs Fischbein, Dillon, and Barkovich
published over 10 years ago, imaging of the brain has undergone tremendous changes with marked improvements in both spatial and contrast resolution New computed tomography (CT) scanners are equipped with more detectors to provide faster acquisition of images with improved resolution and decreased movement artifacts These advantages have not only further developed anatomic and functional imaging techniques but have also allowed the translation of CT angiography and perfusion
in clinical practice CT angiography has all but replaced catheter digital subtraction angiography as the initial imaging modality for the diagnosis of most cerebrovascular diseases Magnetic resonance (MR) has also drastically improved, with an appreciable increase in image resolution related to newer software, faster gradients, and receiver coil improvements as well as higher magnet field imaging
New MR techniques such as perfusion, spectroscopy, and diffusion tensor imaging have matured and are now being implemented in the diagnosis and preoperative planning in the clinical setting
The first edition was a very well-organized and immensely useful teaching atlas and review for the radiology resident and neuroradiology fellow It contained clear examples of the most commonly encountered pathologies in brain imaging as well as outstanding examples of the “zebras” in neuro-radiology As was the case with the first edition, we believe that the updated images and informa-tion in this book will be immensely beneficial to all radiology residents, practicing radiologists, and neuroradiologists Neurologists and neurosurgeons in training and practice will also benefit from this text, because imaging has become an indispensable part of their practice for the diagnosis and treatment of CNS diseases
This book is composed of seven sections covering the entire spectrum of brain diseases The sections are organized by pathology and cover brain neoplasms; infectious and inflammatory dis-eases; cerebrovascular diseases; neurodegenerative, white matter, and metabolic diseases; traumatic brain injury; congenital, developmental malformations and syndromes; and the cranial nerves In the preparation of this second edition, we maintained the format of the first edition, but included all new updated images and references The outline format with key bulleted facts allows for a quick review
of the presented pathologies Novel and emerging imaging techniques are included when pertinent
to aiding in diagnosis As in the prior edition, each case includes important pearls and pitfalls for diagnosis of the pathologies presented
It is our sincere hope and expectation that this book will be a valuable tool for the sis of brain diseases for the resident, fellow, and attending physician in radiology, neurology, and neurosurgery
diagno-Preface
Trang 13The three editors would like to wholeheartedly thank all the contributing authors, who were inately composed of an industrious group of our residents and fellows at the NewYork-Presbyterian Hospital–Weill Cornell Medical College Without all their hard work and dedication, this book would not have been remotely possible In particular, Drs Andrew Schweitzer, Janice Jeon, Sahil Sood, Ajay Gupta, and Rachel Gold contributed a large number of cases.
predom-Acknowledgments
Trang 14Matthew Amans, MD, MSc
Department of Radiology and Biomedical Imaging
University of California, San Francisco
San Francisco, California
Associate Professor of Clinical Radiology
Weill Cornell Medical College
NewYork-Presbyterian Hospital
New York, New York
Rachel Gold, DO
North Shore University Hospital
New York, New York
Edward D Greenberg, MD
Interventional Neuroradiologist
Fairfax Radiological Consultants, PC
Inova Fairfax Hospital
New York, New York
Jan Christopher Mazura, MD
Department of Radiology and Biomedical ImagingUniversity of California, San Francisco
San Francisco, California
Sarah Sarvis Milla, MD
Department of RadiologyNYU Langone Medical CenterNew York, New York
Daniel G Rosenbaum, MD
Department of RadiologyWeill Cornell Medical CollegeNewYork-Presbyterian HospitalNew York, New York
Pina C Sanelli, MD, MPH
Associate Professor of Radiology and Public HealthWeill Cornell Medical College
NewYork-Presbyterian HospitalNew York, New York
Andrew Damien Schweitzer, MD
Department of RadiologyWeill Cornell Medical CollegeNewYork-Presbyterian HospitalNew York, New York
Jennifer Shih, MD
Department of RadiologyWeill Cornell Medical CollegeNewYork-Presbyterian HospitalNew York, New York
Sahil Sood, MD
NeuroradiologistValley Radiology Medical Associates, Inc
Los Gatos, California
A John Tsiouris, MD
Associate Professor of Clinical RadiologyWeill Cornell Medical College
NewYork-Presbyterian HospitalNew York, New York
Contributors
Trang 15ADC: apparent diffusion coefficientCECT: contrast-enhanced CTDSA: digital subtraction angiography/angiogramDTI: diffusion tensor imaging
DWI: diffusion-weighted imagingEPI: echo-planar imaging
GRE: gradient recall echoNCCT: noncontrast CTMRS: magnetic resonance spectroscopyPWI: perfusion-weighted imagingSPGR: spoiled gradient recall echoSWI: susceptibility-weighted imagingT1W: T1-weighted
T1W FLAIR: T1-weighted fluid-attenuated inversion recoveryT2W: T2-weighted
T2W FLAIR: T2-weighted fluid-attenuated inversion recoveryTOF: Time-of-flight
Trang 16Section I
Neoplasms
A Supratentorial
Trang 17Fig 1.1 (A, B) Axial T2W fluid-attenuated inversion recovery
(FLAIR) and T1W postcontrast images demonstrate a cumscribed nonenhancing homogeneously T1 hypointense and T2 hyperintense mass within the medial left frontal lobe There is involvement of both the white matter and overlying cortex with local mass effect and effacement of adjacent sulci There is no surrounding vasogenic edema A serpentine flow void within the lesion is most consistent with a vessel Incidental note is made of
well-cir-a nonspecific T2 hyperintense white mwell-cir-atter focus posterior to the mass that is most likely unrelated (C) Coronal T1W postcontrast
spoiled gradient recalled echo (SPGR) image also demonstrates
no significant enhancement within this mass There is mass fect upon the corpus callosum and the left lateral ventricle
ef-Diagnosis
“Low-grade” astrocytoma (WHO grade II)
Differential Diagnosis
• ing edema, cystic change, hemorrhage, or calcifications, but generally indistinguishable on imaging)
Trang 18Grade III anaplastic astrocytoma (typically more infiltrative, more likely to be associated with surround-4 CASE-BASED BRAIN IMAGING
Astrocytomas are primary brain tumors of astrocytic origin Most primary brain tumors in adults arise
supratentorially; ,50% of these are gliomas and ,90% of gliomas are astrocytomas Ten to 15% of
as-trocytomas are “low grade.” These lesions are most commonly located in the frontal or temporal lobes
They most often occur between the ages of 20 and 45 and have a slight male predilection
Trang 19I NEOPLASMS–SUPRATENTORIAL 5
Fig 1.2 Grade II oligoastrocytoma with mild
inter-val growth at 3 years (A–C) Axial T2W FLAIR, T2W,
and GRE images demonstrate a homogeneous circumscribed T2 hyperintense lesion that involves cortex and subcortical white matter within the pos-terior right frontal lobe There is no surrounding vaso-genic edema and minimal mass effect upon adjacent
well-confirms absence of internal calcifications or rhage This lesion is hypointense and nonenhancing on the (D) sagittal T1W postcontrast image After 3 years, the
hemor-(E, F) sagittal postcontrast T1W and axial T2W FLAIR
images reveal stable MR signal characteristics, but mild interval growth Note that the tumor extends to involve more of the right precentral gyrus cortex and has slight-
B
D A
C
Trang 206 CASE-BASED BRAIN IMAGING
predominately involves white matter but often extends to cortex or deep gray matter structures These
lesions may grow slowly over time (Fig 1.2A-F).
Computed Tomography
• Ill-defined low density mass on noncontrast scan
• Little or no contrast enhancement, avid enhancement should raise suspicion for higher grade
neoplasm or infectious etiology
•
A low-grade astrocytoma may be mistaken for infarction, so consider a follow-up scan Acute infarc-tions evolve over a short period of time, whereas low-grade tumors remain stable Alternatively, diffusion-weighted imaging is useful to differentiate acute infarction from tumor
Trang 21Fig 2.1 The (A) axial T2W image demonstrates a
well-demarcated intra-axial mass that is tense compared with brain parenchyma, centered in the left lateral temporal lobe No surrounding edema
hyperin-is noted (B, C) Axial and coronal T1W postcontrast
images demonstrate that the mass is hypointense
to brain parenchyma with no appreciable internal enhancement Note the mild mass effect associated with this lesion, with subtle partial effacement of the left sylvian fissure as compared with the right side
Trang 228 CASE-BASED BRAIN IMAGING
• Glioblastoma multiforme (GBM) (typically enhances, with regions of necrosis, hemorrhage, and
Trang 23I NEOPLASMS–SUPRATENTORIAL 9
• Little or no surrounding edema
• Cystic degeneration and calcification are rare
• Dynamic susceptibility T2* MR perfusion maps show an increased regional cerebral blood volume (rCBV) relative to low-grade astrocytomas
– Stereotactic radiosurgery– Chemotherapy
Fig 2.2 Anaplastic astrocytoma (A) Axial T2W image
demonstrates a well-circumscribed hyperintense lesion centered in the left temporal lobe with internal regions of
cystic change (arrow) Note the relatively well- circumscribed
margins of the mass with minimal adjacent T2 signal mality (B, C) Axial and coronal T1W postcontrast images
demonstrate patchy regions of enhancement ( arrows), a
less common imaging finding associated with these tumors
C
Trang 2410 CASE-BASED BRAIN IMAGING
Fig 2.3 (A, B) Anaplastic astrocytoma within the
right temporal lobe and insula (C) A multivoxel three-
dimensional MR spectroscopy was performed of the tumor to assess for tumor grade and biopsy planning
(D, E) Overlay Cho/NAA and Cho/Cr color ratio maps were
generated to assess for the optimal biopsy site, with the central region demonstrating the highest Cho/NAA and
Cho/Cr ratios targeted intraoperatively (arrows).
Trang 25Thurnher MM World Health Organization classification of tumours of the central nervous system Cancer Imaging 2009;9 Spec No A:S1–3
Young RJ, Knopp EA Brain MRI: tumor evaluation J Magn Reson Imaging 2006;24(4):709–724 Review
Trang 26Fig 3.1 (A, B) Axial T1W pre- and postcontrast images
demonstrate a T1 hypointense mass with irregular, thick
peripheral enhancement (C) Axial T2W image
demon-strates that the mass is peripherally solid and
hyper-intense, containing a central region of fluid intensity
suggestive of necrosis and/or cystic change (D) Axial
GRE demonstrates internal foci of susceptibility effect consistent with hemorrhagic products and/or calcium
(E) DWI reveals that the solid component of the mass
demonstrates hyperintensity representing restricted diffusion (confirmed on ADC maps) most consistent with a hypercellular lesion
B A
Trang 27• Primary central nervous system (CNS) lymphoma (classically a periventricular enhancing mass, can also cross corpus callosum and in certain cases demonstrates central necrosis)
• Anaplastic astrocytoma (may have less necrosis and may contain significant nonenhancing components, but can be indistinguishable)
• Tumefactive demyelination (often incomplete ring of enhancement, patients younger, history of multiple sclerosis [MS])
Discussion Background
Primary malignancies of the CNS account for 1.5% of all malignant disease, and primary malignant gliomas represent 45 to 50% of all intracranial tumors In adults, the majority of gliomas are supraten-torial; in childhood, 70 to 80% are infratentorial
GBM is the most common primary supratentorial neoplasm in an adult; most of these patients are
45 to 55 years of age, and there is a 3:2 male predominance
Clinical Findings
Findings vary with tumor size and location; focal neurologic deficits and seizures are common as are symptoms related to an elevation of intracranial pressure (headache, altered mental status)
• Irregular, heterogeneous, vascular neoplasm; often seen as a reddish-gray rind of tissue around a necrotic core
Microscopic
• Marked neovascularity, increased mitoses, cellular pleomorphism, necrosis, and pseudopalisading are observed
• Lower grade gliomas (WHO grades II, III) have less mitotic activity and pleomorphism and lack necrosis and pseudopalisading
Trang 2814 CASE-BASED BRAIN IMAGING
• MR spectroscopy (MRS)
– Elevated choline, lipid/lactate peaks– Decreased NAA and myoinositol levels
Fig 3.2 GBM T1W postcontrast image demonstrates a large,
heterogeneously enhancing left frontal lobe mass that effaces the frontal horns of the lateral ventricles and causes significant leftward midline shift Note that the enhancement is thick and irregular, with
a central nonenhancing region that reflects necrotic tumor
Fig 3.3 GBM A large infiltrative heterogeneously T2
hyperintense mass is present on the (A) T2 FLAIR image
(B) Coronal postcontrast T1W image demonstrates the
typical heterogeneous enhancement and transcallosal extension, sometimes referred to as a “butterfly glioma”
given its morphology
Trang 29• cytoma to suggest dedifferentiation to GBM
Observe for the development of increasing enhancement or heterogeneity in a grade II or III astro-PITFALLS
• Extent of enhancement or adjacent T2 abnormality signal abnormality often understate the true extent of infiltrating tumor
• During treatment, radiation necrosis can appear identical to recurrent GBM, and may require the use of positron emission tomography (PET)/CT, MR spectroscopy, or MR perfusion to aid in differentiation
Suggested Readings
Henson JW, Gaviani P, Gonzalez RG MRI in treatment of adult gliomas Lancet Oncol 2005;6(3):167–175 Law M, Young RJ, Babb JS, et al Gliomas: predicting time to progression or survival with cerebral blood volume measurements
at dynamic susceptibility-weighted contrast enhanced perfusion MR imaging Radiology 2008;247(2):490–498 Madison MT, Hall WA, Latchaw RE, Loes DJ Radiologic diagnosis, staging, and follow up of adult central nervous system primary malignant glioma Radiol Clin North Am 1994;32:183–196
Fig 3.4 Transcallosal extension of GBM Postcontrast T1W
image demonstrates a right parieto-occipital peripherally hancing mass with extension across the splenium of the corpus callosum Again, the nonenhancing central component likely reflects necrosis or cystic change
Trang 30Fig 4.1 (A) Axial NCCT reveals a heterogeneous
right frontal lobe mass with curvilinear internal calcifications, central hypoattenuation consis-tent with cystic change, and subtle expansion of the right frontal lobe cortex and white matter
(B) The corresponding axial T2W image
demon-strates T2 prolongation involving the right frontal lobe cortex and subcortical white matter There is central T2 hyperintensity that is most consistent with cystic formation as well as foci of internal T2 hypointensity corresponding to the calcifica-tions seen on CT Surrounding vasogenic edema
is minimal to absent given the size of this mass
The extent of calcification is better appreciated
on the (C) axial T2* GRE sequence where
suscep-tibility effect directly corresponds to the internal calcifications
A
C
B
Trang 31• toma (PXA) (typically present at a younger age, often cortical location, usually temporal lobe, less infiltrative, classically mural nodule with a cyst)
Ganglioglioma, dysembryoplastic neuroepithelial tumor (DNET), and pleomorphic xanthoastrocy-• Thrombosed and calcified vascular malformation (should not usually cause significant mass effect unless hemorrhage is present, look for noncalcified large flow voids and prominent draining veins)
Fig 4.1 (continued) (D) An axial T1W image shows
background T1 hyperintensity, which corresponds to eralization/calcification (E, F) Axial and coronal T1W post-
min-contrast images reveal enhancement within the posterior and left anterior aspects of this mass There is leftward displacement of the falx as well as the callosomarginal and pericallosal branches of the anterior cerebral arteries
D
F
E
Trang 3218 CASE-BASED BRAIN IMAGING
Trang 33I NEOPLASMS–SUPRATENTORIAL 19
Magnetic Resonance
• Typically frontal lobe involving both gray and white matter
• Usually hypointense on T1W image, however, areas of mineralization/calcification can be T1 hyperintense
Fig 4.2 Classic oligodendroglioma with cystic change
and calcification (A, B) Axial T2W FLAIR demonstrate
a heterogeneously T2 hyperintense mass that involves the left frontal cortex and subcortical white matter
Large focal areas of intralesional fluid suppression on the (A) T2W FLAIR correspond to cystic degeneration
Smaller areas of stippled hypointensity on the (B) T2W
FLAIR correlating to susceptibility effect on the T2* GRE
(arrows, C) represent calcifications There is mass
ef-fect upon the frontal horns of the bilateral ventricles as well as expansion of the left cingulum, with associated rightward subfalcine herniation Note the paucity of va-sogenic edema despite the tumor’s large size
A
C
B
Trang 3420 CASE-BASED BRAIN IMAGING
Trang 35Case 5
Clinical Presentation
A 27-year-old man presents with increasing headache and visual changes
Radiologic Findings
Fig 5.1 (A) Axial T2W image demonstrates a large
heterogeneous mass with multiple small internal cysts located near the foramen of Monro in the frontal horn of the left lateral ventricle Anteriorly, the mass
is inseparable from the septum pellucidum; orly, the mass displaces the septum pellucidum to the right and results in hydrocephalus due to obstruction
posteri-at the level of the foramen of Monro (B) Axial DWI
demonstrates slight hyperintensity within the mass (but ADC map, not shown, demonstrated no restricted diffusion) (C) Axial GRE image demonstrates punc-
tate regions of internal susceptibility, consistent with
mineralization (continued on page 22)
A
C
B
Trang 3622 CASE-BASED BRAIN IMAGING
Fig 5.1 (continued) (D) Sagittal T1W image shows
that the solid portions of the mass are isointense
to white matter (E) Axial and (F) coronal
postcon-trast T1W images demonstrate mild heterogeneous enhancement
D
F
E
Trang 37typically located in the lateral ventricle, and is often attached to the septum pellucidum (Fig 5.1A)
It is rare, accounting for 0.5% of primary brain tumors, and usually affects young adults (the average age of presentation is 29 years)
Fig 5.2 Nonenhancing central
neurocy-toma (A) Post-contrast axial T2W FLAIR,
(B) axial T1W image, and (C) sagittal T1W
image demonstrate a mass in the left lateral ventricle that is T2 hyperintense, T1 isoin-tense to gray matter, nonenhancing, and containing an internal T1 hyperintense focus
(arrow) compatible with a traversing vein
This case demonstrates that while central neurocytomas typically enhance, enhance-ment does not always occur
Trang 3824 CASE-BASED BRAIN IMAGING
Fig 5.3 Hemorrhagic central neurocytoma (A) Axial
noncontrast CT image of a patient who presented
to the emergency room with acute-onset headache
demonstrates acute hemorrhage into the right
lat-eral ventricle, with additional intraventricular lower
attenuation possibly representing older blood
prod-ucts or mass (B) Axial T2W, (C) DWI, (D) GRE, and
(E) precontrast T1W images demonstrate a
heteroge-neous predominantly T1-hypointense mass centered
in the right lateral ventricular atrium containing nal susceptibility effect, consistent with a hemorrhagic mass as seen on CT (F) Postcontrast axial T1W image
inter-demonstrates minor enhancement and a traversing
Trang 39I NEOPLASMS–SUPRATENTORIAL 25
Imaging Findings Computed Tomography
Fig 5.4 Same patient in Fig 5.3 with follow-up MR
was performed one year later (A) Axial T2W, (B) T2W
FLAIR, (C) gradient recall echo, (D) precontrast T1W,
and (E) postcontrast T1W images demonstrate
sig-nificantly decreased internal gradient susceptibility,
compatible with partial resolution of the blood ucts, and persistence of the mass in the atrium of the right lateral ventricle (F) The MR spectroscopy
prod-Cho:NAA map demonstrates focally elevated prod-Cho:NAA ratios within the mass, consistent with neoplasia
A,B
D,E
C
F
Trang 4026 CASE-BASED BRAIN IMAGING