MRI Brain: Atlas and Text [1 ed.] 9352500229, 9789352500222

Table of contents :
Cover
Contents
1. MRI Basics: Physics
• MR W orking in a Nutshell 3
• A dvantages of MRI 5
• Disadvantages of MRI (Compared to CT Scan) 5 • Multipl
2. N ormal Cross-sectional MR Anatomy of Brain 8
• Axial Image Planes: Parallel to Skull Base 9
• Axial Image L evel A1 10
• Axial Image L evel A2 11
• Axial Image L evel A3 12
• Axial Image L evel A4 13
• Axial Image L evel A5 14
• Axial Image L evel A6 15
• Axial Image L evel A7 16
• C oronal Section: Parallel to Coronal Suture 17 • C oronal
• C oronal Image L evel C2 19
• C oronal Image L evel C3 20
• C oronal Image L evel C4 21
• Midline Sagittal Image: Parallel to Sagittal Suture 22 • Gro
3. MRI of Signals and Sequences
• Glossary of T erms 26
• Examples f or Basic MR Signal Intensity Nomenclature 28
• Note on Sequences 28
• Examples of C ommon MR Sequences and their U se 30
• Diffusion Weighted Imaging: A n Important Tool for Diagnosing Stro
4. P rinciples of Intracranial Space Occupying L esions ( ICSOL )/Tumor Di
• Determine W hether the L esion is Intra-axial v ersus
• P a tient’s A ge and Sex 41
• MRI Signal Intensity 41
• T1W Bright L esions 41
• Classic L ocation 42
• T ype and Degree of C ontrast Enhancement 43 • T h
5. MRI Atlas of Cases
• C ase 1: Cerebral Pilocytic Astrocytoma 45
• C ase 2: Left Falx Meningioma 49
• C ase 3: Cerebellopontine Angle Meningioma 52
• C ase 4: Recurrent Central Neurocytoma 57
• C ase 5: Brainstem Glioma 59
• C ase 6: Cerebellar Pilocytic Astrocytoma 61
• C ase 7: Right Falx Meningioma 64
• C ase 8: Atypical Meningioma 66
• C ase 9: Multiple Meningiomas 69
C ases (1–30): Tumors
• C ase 10: Hemangiopericytoma 72
• C ase 11: Craniopharyngioma 75
• C ase 12: Left Glioblastoma Multiforme 78
• C ase 13: Right Glioblastoma Multiforme 81
• C ase 14: Optic Groove Meningioma 83
• C ase 15: CP Angle Epidermoid 85
• C ase 16: Dysembryoplastic Neuroepithelial Tumor 88
• C ase 17: Planum Sphenoidale Meningioma 90
• C ase 18: Posterior Cranial Fossa Meningioma 93
• C ase 19: Low Grade Glioma 96
• C ase 20: Pituitary Secreting Macroadenoma 99
• C ase 21: Jugular Foramen Schwannoma 103
• C ase 22: Cerebellar Hemangioblastoma 105
• C ase 23: Central Nervous System Lymphoma 108
• C ase 24: Pituitary Microadenoma 111
• C ase 25: Infratentorial Ependymoma in Adult 114
• C ase 26: Classical Acoustic Schawannoma 116
• C ase 27: Juxtatentorial Meningioma 119
• C ase 28: Convexity Meningioma 121
• C ase 29: Benign Glioma 123
• C ase 30: Craniopharyngioma in Adult 125
C ases (31–49): Congenital Lesions
• C ase 31: Schizencephaly: Closed Lip Type 128
• C ase 32: Schizencephaly: Open Lip Type 130
• C ase 33: Dysgenesis of Corpus Callosum and Associated Lipoma 132
• C ase 34: Lipoma of Corpus Callosum 135
• C ase 35: Type 1 Chiari Malformation 137
• C ase 36: T ype 1 Chiari Malformation with Syrinx 1 139
• C ase 36A: T ype 1 Chiari Malformation with Syrinx 2 141
• C ase 37: Classic Arachnoid Cyst 143
• C ase 38: Arachnoid Cyst: Posterior Cranial Fossa 146
• C ase 39: Craniovertebral Junction Anomaly: Basilar Invagination Fossa
• C ase 40: Classic Colloid Cyst 152
• C ase 41: Rathke’s Cyst 154
• C ase 42: Cerebellopontine Angle: Epidermoid 156
• C ase 43: Intraventricular Epidermoid 159
• C ase 44: P artial Dysgenesis of Corpus
C allosum with Interhemispheric Cyst 162
• C ase 45: Joubert Syndrome 164
• C ase 46: Quadrigeminal Plate Arachnoid Cyst with Obstructive Hydroceph
• C ase 47: Dandy-Walker Variant 169
• C ase 48: Posterior Cranial Fossa Giant Cyst 171
• C ase 49: Quadrigeminal Plate L arge Arachnoid Cyst 173
C ases (50–67): Vascular
• C ase 50: Cavernoma Left Frontal Lobe 176
• C ase 51: A cute Right Middle Cerebral Artery T erritory Ischemic Infa
• C ase 52: Giant Aneurysm of Basilar Artery Trunk 182
• C ase 53: Right Subacute Subdural Hematoma 184
• C ase 54: L ateral Medullary Syndrome ( W allenberg’s Syndrome) 187
• C ase 55: Venous Infarct: Left Temporal Lobe 189
• C ase 56: Acute Right Thalamic Ischemic Infarct 191
• C ase 57: Giant Aneurysm Supraclinoid Segment of Internal Carotid Arte
• C ase 58: Left Transverse Sinus Thrombosis 196
• C ase 59: Right Cerebellar Ischemic Infarct 198
• C ase 60: Anterior Cerebral Artery Aneurysm with Subarachnoid Hemorrhag
• C ase 61: Vein of Galen Malformation 203
• C ase 62: Cavernoma with Recent Bleed 205
• C ase 63: Right Posterior Watershed Infarct 207
• C ase 64: Vertebrobasilar Insufficiency 209
• C ase 65: Cerebral Venous Thrombosis 211
• C ase 66: P osterior Reversible Ischemic Encephalopathy 213
• C ase 67: Intraventricular Hemorrhage 216
C ases (68–78): Infectons/Infestations 219
• C ase 68: Solitary Tuberculoma 219
• C ase 69: Multiple Tuberculomata 222
• C ase 70: Tuberculous Cerebral Abscess 224
• C ase 71: T uberculosis of the Optic Nerve Sheath 227
• C ase 72: Bacterial Meningoencephalitis 229
• C ase 73: Toxoplasmosis 232
• C ase 74: Opportunistic Brain Infection in Immunocompromised Patient
• C ase 75: Neurocysticercosis 237
• C ase 76: Acute Disseminated Encephalomyelitis 239
• C ase 77: Viral Encephalitis 242
• C ase 78: Rhino-Orbito-Cerebral Zygomycosis 245
C ases (79–100): Miscellaneous
• C ase 79: Wilson’s Disease 248
• C ase 80: Tuberous Sclerosis 250
• C ase 81: Central Pontine Myelinolysis 253
• C ase 82: Neurosarcoidosis 256
• C ase 83: Idiopathic Intracranial Hypertension ( IICHT )/Pseudotumor C
• C ase 84: Obstructive Hydrocephalus: Aqueductal Stenosis 261
• C ase 85: T r aumatic Atlantoaxial Joint Subluxation 263
• C ase 86: Central Pontine Myelinolysis 2 265
• C ase 87: Mesial Temporal Sclerosis 267
• C ase 88: Tolosa-Hunt Syndrome 270
• C ase 89: Fahr’s Disease 272
• C ase 90: Normal Pressure Hydrocephalus 274
• C ase 91: Adrenoleukodystrophy 277
• C ase 92: Ectopic Neurohypophysis 279
• C ase 93: Diffuse Axonal Injury 282
• C ase 94: Devic Disease 284
• C ase 95: Leigh’s Disease 287
• C ase 96: Huntington’s Chorea 289
• C ase 97: Empty Sella Syndrome and A queductal Stenosis 292
• C ase 98: Neuroglial Cyst 295
• C ase 99: Neurofibromatosis Type 1 297
• C ase 100: Neurofibromatosis Type 2 300
Index
Introduction
MRI Basics: Physics
MR WORKING IN A NUTSHELL
H o w it all Works in a Nutshell?
H o w are Images Obtained?
ADVANTAGES OF MRI
DISADVANTAGES OF MRI (COMPARED TO CT SCAN)
MULTIPLANAR CAPABILITY IN MR
Normal Cross-sectional MR Anatomy of Brain
A XIAL IMAGE PLANES: PARALLEL TO SKULL BASE
C ORONAL SECTION: PARALLEL TO CORONAL SUTURE
MIDLINE SAGITTAL IMAGE: PARALLEL T O SAGITTAL SUTURE
GROSS BRAIN ANATOMY AS SEEN IN MR IMAGES (FIGURES 2 TO 6)
C H A P T E R
MRI of Signals and Sequences
GLOSSARY OF TERMS
NOTE ON SEQUENCES
EXAMPLES FOR BASIC MR SIGNAL INTENSITY NOMENCLATURE
EXAMPLES OF COMMON MR SEQUENCES AND THEIR USE
T1W Axial
T2W Axial
T1W Axial with Gadolinium Contrast Agent
D WI Axial
FLUID ATTENUATION INVERSION RECOVERY (FLAIR)
C oronal Image
MR Angiography ( MRA )
R OLE OF MRI CONTRAST AGENT
P r econtrast Image
DIFFUSION WEIGHTED IMAGING: AN IMPORTANT T OOL FOR DIAGNOSING STROKE
P rinciples of DWI
P ostcontrast Image
P rinciples of Intracranial Space Occupying Lesions ( ICSOL )/T umor Diagnosis by MRI
L OOK FOR CLASSIC LOCATION/MORPHOLGY/SIGN
DETERMINE WHETHER THE LESION IS INTRA-AXIAL VERSUS EXTRA-AXIAL
P A TIENT’S AGE AND SEX
MRI SIGNAL INTENSITY
T 1 W BRIGHT LESIONS
CLASSIC LOCATION
TYPE AND DEGREE OF CONTRAST ENHANCEMENT
THE EXTENSION AND/OR SPREAD OF THE TUMOR
C H A P T E R
MRI Atlas of Cases
CASES ( 1 – 3 0 ) : TUMORS
CASE 1: CEREBRAL PILOCYTIC ASTROCYTOMA
CASE 2: LEFT FALX MENINGIOMA
CASE 3: CEREBELLOPONTINE (CP) ANGLE MENINGIOMA
CASE 4: RECURRENT CENTRAL NEUROCYTOMA
CASE 5: BRAINSTEM GLIOMA
CASE 6: CEREBELLAR PILOCYTIC ASTROCYTOMA
CASE 7: RIGHT FALX MENINGIOMA
CASE 8: ATYPICAL MENINGIOMA
CASE 9: MULTIPLE MENINGIOMAS
CASE 10: HEMANGIOPERICYTOMA
CASE 11: CRANIOPHARYNGIOMA
CASE 12: LEFT GLIOBLASTOMA MULTIFORME
CASE 13: RIGHT GLIOBLASTOMA MULTIFORME
CASE 14: OPTIC GROOVE MENINGIOMA
CASE 15: CP ANGLE EPIDERMOID
CASE 16: DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOR
CASE 17: PLANUM SPHENOIDALE MENINGIOMA
CASE 18: POSTERIOR CRANIAL FOSSA MENINGIOMA
CASE 19: LOW GRADE GLIOMA
CASE 20: PITUITARY SECRETING MACROADENOMA
CASE 21: JUGULAR FORAMEN SCHWANNOMA
CASE 22: CEREBELLAR HEMANGIOBLASTOMA
CASE 23: CENTRAL NERVOUS SYSTEM LYMPHOMA
CASE 24: PITUITARY MICROADENOMA
CASE 25: INFRATENTORIAL EPENDYMOMA IN ADULT
CASE 26: CLASSICAL ACOUSTIC SCHAWANNOMA
CASE 27: JUXTATENTORIAL MENINGIOMA
CASE 28: CONVEXITY MENINGIOMA
CASE 29: BENIGN GLIOMA
CASE 30: CRANIOPHARYNGIOMA IN ADULT
CASES (31–49): CONGENITAL LESIONS
CASE 31: SCHIZENCEPHALY: CLOSED LIP TYPE
CASE 32: SCHIZENCEPHALY: OPEN LIP TYPE
CASE 33: DYSGENESIS OF CORPUS CALLOSUM AND ASSOCIATED LIPOMA
CASE 34: LIPOMA OF CORPUS CALLOSUM
CASE 35: TYPE 1 CHIARI MALFORMATION
CASE 36: TYPE 1 CHIARI MALFORMATION WITH SYRINX 1
CASE 36A: TYPE 1 CHIARI MALFORMATION WITH SYRINX 2
CASE 37: CLASSIC ARACHNOID CYST
CASE 38: ARACHNOID CYST: POSTERIOR CRANIAL FOSSA
CASE 39: CRANIOVERTEBRAL JUNCTION ANOMALY: B ASILAR INVAGINATION FOSSA
CASE 40: CLASSIC COLLOID CYST
CASE 41: RATHKE’S CYST
CASE 42: CEREBELLOPONTINE ANGLE: EPIDERMOID
CASE 43: INTRAVENTRICULAR EPIDERMOID
CASE 44: PARTIAL DYSGENESIS OF CORPUS CALLOSUM WITH INTERHEMISPHERIC CYST
CASE 45: JOUBERT SYNDROME
CASE 46: QUADRIGEMINAL PLATE ARACHNOID CYST WITH OBSTRUCTIVE HYDROCEPHALUS
CASE 47: DANDY-WALKER VARIANT
CASE 48: POSTERIOR CRANIAL FOSSA GIANT CYST
CASE 49: QUADRIGEMINAL PLATE LARGE ARACHNOID CYST
CASES (50–67): VASCULAR
CASE 50: CAVERNOMA LEFT FRONTAL LOBE
CASE 51: ACUTE RIGHT MIDDLE CEREBRAL ARTERY TERRITORY ISCHEMIC INFARCT
CASE 52: GIANT ANEURYSM OF BASILAR ARTERY TRUNK
CASE 53: RIGHT SUBACUTE SUBDURAL HEMATOMA
CASE 54: LATERAL MEDULLARY SYNDROME (WALLENBERG’S SYNDROME)
CASE 55: VENOUS INFARCT: LEFT TEMPORAL LOBE
CASE 56: ACUTE RIGHT THALAMIC ISCHEMIC INFARCT
CASE 57: GIANT ANEURYSM SUPRACLINOID SEGMENT OF INTERNAL CAROTID ARTERY
CASE 58: LEFT TRANSVERSE SINUS THROMBOSIS
CASE 59: RIGHT CEREBELLAR ISCHEMIC INFARCT
CASE 60: ANTERIOR CEREBRAL ARTERY ANEURYSM WITH SUBARACHNOID HEMORRHAGE
CASE 61: VEIN OF GALEN MALFORMATION
CASE 62: CAVERNOMA WITH RECENT BLEED
CASE 63: RIGHT POSTERIOR WATERSHED INFARCT
CASE 64: VERTEBROBASILAR INSUFFICIENCY
CASE 65: CEREBRAL VENOUS THROMBOSIS
CASE 66: POSTERIOR REVERSIBLE ISCHEMIC ENCEPHALOPATHY
CASE 67: INTRAVENTRICULAR HEMORRHAGE
CASES (68–78): INFECTIONS/ INFESTATIONS
CASE 68: SOLITARY TUBERCULOMA
CASE 69: MULTIPLE TUBERCULOMATA
CASE 70: TUBERCULOUS CEREBRAL ABSCESS
CASE 71: TUBERCULOSIS OF THE OPTIC NERVE SHEATH
CASE 72: BACTERIAL MENINGOENCEPHALITIS
CASE 73: TOXOPLASMOSIS
CASE 74: OPPORTUNISTIC BRAIN INFECTION IN IMMUNOCOMPROMISED PATIENT
CASE 75: NEUROCYSTICERCOSIS
CASE 76: ACUTE DISSEMINATED ENCEPHALOMYELITIS
CASE 77: VIRAL ENCEPHALITIS
CASE 78: RHINO-ORBITO-CEREBRAL ZYGOMYCOSIS
CASES (79–100): MISCELLANEOUS
CASE 79: WILSON’S DISEASE
CASE 80: TUBEROUS SCLEROSIS
CASE 81: CENTRAL PONTINE MYELINOLYSIS
CASE 82: NEUROSARCOIDOSIS
CASE 83: IDIOPATHIC INTRACRANIAL HYPERTENSION (IICHT)/PSEUDOTUMOR CEREBRI
CASE 84: OBSTRUCTIVE HYDROCEPHALUS: A QUEDUCTAL STENOSIS
CASE 85: TRAUMATIC A TLANTOAXIAL JOINT SUBLUXATION
CASE 86: CENTRAL PONTINE MYELINOLYSIS 2
CASE 87: MESIAL TEMPORAL SCLEROSIS
CASE 88: TOLOSA-HUNT SYNDROME
CASE 89: FAHR’S DISEASE
CASE 90: NORMAL PRESSURE HYDROCEPHALUS
CASE 91: ADRENOLEUKODYSTROPHY
CASE 92: ECTOPIC NEUROHYPOPHYSIS
CASE 93: DIFFUSE AXONAL INJURY
CASE 94: DEVIC DISEASE
CASE 95: LEIGH’S DISEASE
CASE 96: HUNTINGTON’S CHOREA
CASE 97: EMPTY SELLA SYNDROME AND A QUEDUCTAL STENOSIS
CASE 98: NEUROGLIAL CYST
CASE 99: NEUROFIBROMATOSIS TYPE 1
CASE 100: NEUROFIBROMATOSIS TYPE 2
Index

Citation preview

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MRI BRAIN

ATLAS AND TEXT

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MRI BRAIN

ATLAS AND TEXT

G Balachandran MD DNB DMRD FICR

Associate Professor of Radiology Sri Manakula Vinayagar Medical College and Hospital Puducherry, India

Foreword PC Rajaram

The Health Sciences Publisher New Delhi | London | Philadelphia | Panama

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Jaypee Brothers Medical Publishers (P) Ltd. Headquarters Jaypee Brothers Medical Publishers (P) Ltd. 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 E-mail: [email protected] Overseas Offices J.P. Medical Ltd. Jaypee-Highlights Medical Publishers Inc. Jaypee Medical Inc. 83, Victoria Street, London City of Knowledge, Bld. 237, Clayton The Bourse SW1H 0HW (UK) Panama City, Panama 111, South Independence Mall East Phone: +44-20 3170 8910 Phone: +1 507-301-0496 Suite 835, Philadelphia, PA 19106, USA Fax: +44(0) 20 3008 6180 Fax: +1 507-301-0499 Phone: +1 267-519-9789 E-mail: [email protected] E-mail: [email protected] E-mail: [email protected] Jaypee Brothers Medical Publishers (P) Ltd. 17/1-B, Babar Road, Block-B, Shaymali Mohammadpur, Dhaka-1207 Bangladesh Mobile: +08801912003485 E-mail: [email protected]

Jaypee Brothers Medical Publishers (P) Ltd. Bhotahity, Kathmandu, Nepal Phone: +977-9741283608 E-mail: [email protected]

Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2016, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. Inquiries for bulk sales may be solicited at: [email protected]

MRI Brain: Atlas and Text First Edition: 2016 ISBN: 978-93-5250-022-2 Printed at

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Dedicated to All the patients and their relatives, but for whom, we could not have learnt neuroradiology

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Foreword I have great pleasure in writing this foreword. MRI Brain: Atlas and Text book is a collection of neuroradiology cases that have been meticulously collected, followed and worked up till the final diagnosis was established. The book is written by one of my old students. Dr G Balachandran has already written 3 books on radiology, which have been well-received by students. The book maintains the unique features found in all of his books—that is line diagrams for images to facilitate easy appreciation of image findings. The book fairly covers a wide spectrum of neuroradiology cases which we come across in our daily practice. Apart from images and line diagrams, there is a brief interpretation of images, description of the case findings and relevant references for further reading. Useful tables are also included. I recommend the book to all radiology postgraduates and neuroradiologists.

PC Rajaram MD DMR FICR PhD

Director Barnard Institute of Radiology and Oncology Madras Medical College Chennai, Tamil Nadu, India

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Preface There are several books available on brain MRI. Unfortunately, they are either very costly or voluminous for a general medical practitioner to buy and read. Moreover, he may not have enough time during his medical practice. When a general medical practitioner refers MRI-brain for his patient, he should be able to obtain maximum information from this study, especially regarding his patient’s illness, so that he can treat his patient appropriately. For this, the general practitioner should have some basic knowledge about MRI interpretation. It is not possible to cover the entire spectrum of brain MRI and for this purpose, there are several excellent textbooks. What a general practitioner wants, is a good grasp of basic MRI-brain and interpretation of common brain diseases which he is likely to encounter in his daily practice. I have collected case studies of brain MRI from patients who are referred to our institution. All the cases are proved at surgery or by biopsy. This collection of brain MRI cases is presented as an atlas for the benefit of a general practitioner. I hope and trust that this MRI atlas of common brain diseases will prove to be very handy for interpreting MRI brain diseases, which the general practitioner comes across in his day-to-day practice.

G Balachandran

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Acknowledgments I thank all, my postgraduate students, colleagues, hospital staff, radiographers, operation theater staff and others, who were instrumental in making this mammoth book.

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Contents 1. MRI Basics: Physics •  MR Working in a Nutshell  3 •  Advantages of MRI  5 •  Disadvantages of MRI (Compared to CT Scan)  5 •  Multiplanar Capability in MR  6 2.

1

Normal Cross-sectional MR Anatomy of Brain 8 •  Axial Image Planes: Parallel to Skull Base  9 •  Axial Image Level A1  10 •  Axial Image Level A2  11 •  Axial Image Level A3  12 •  Axial Image Level A4  13 •  Axial Image Level A5  14 •  Axial Image Level A6  15 •  Axial Image Level A7  16 •  Coronal Section: Parallel to Coronal Suture  17 •  Coronal Image Level C1  18 •  Coronal Image Level C2  19 •  Coronal Image Level C3  20 •  Coronal Image Level C4  21 •  Midline Sagittal Image: Parallel to Sagittal Suture  22 •  Gross Brain Anatomy as seen in MR Images  23

3. MRI of Signals and Sequences •  Glossary of Terms  26 • Examples for Basic MR Signal Intensity Nomenclature  28

26

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•  Note on Sequences  28 •  Examples of Common MR Sequences and their Use  30 •  Fluid Attenuation Inversion Recovery (FLAIR)  34 •  Role of MRI Contrast Agent  36 • Diffusion Weighted Imaging: An Important Tool for Diagnosing Stroke  37

4. Principles of Intracranial Space Occupying Lesions (ICSOL)/Tumor Diagnosis by MRI 39 •  Look for Classic Location/Morpholgy/Sign  39 • Determine Whether the Lesion is Intra-axial versus Extra-axial  40 •  Patient’s Age and Sex  41 •  MRI Signal Intensity  41 •  T1W Bright Lesions  41 •  Classic Location  42 •  Type and Degree of Contrast Enhancement  43 •  The Extension and/or Spread of the Tumor  43 5. MRI Atlas of Cases Cases (1–30): Tumors

45 45

•  Case 1: Cerebral Pilocytic Astrocytoma  45 •  Case 2: Left Falx Meningioma  49 •  Case 3: Cerebellopontine Angle Meningioma  52 •  Case 4: Recurrent Central Neurocytoma  57 •  Case 5: Brainstem Glioma  59 •  Case 6: Cerebellar Pilocytic Astrocytoma  61 •  Case 7: Right Falx Meningioma  64 •  Case 8: Atypical Meningioma  66 •  Case 9: Multiple Meningiomas  69

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Contents xv

•  Case 10: Hemangiopericytoma  72 •  Case 11: Craniopharyngioma  75 •  Case 12: Left Glioblastoma Multiforme  78 •  Case 13: Right Glioblastoma Multiforme  81 •  Case 14: Optic Groove Meningioma  83 •  Case 15: CP Angle Epidermoid  85 •  Case 16: Dysembryoplastic Neuroepithelial Tumor  88 •  Case 17: Planum Sphenoidale Meningioma  90 •  Case 18: Posterior Cranial Fossa Meningioma  93 •  Case 19: Low Grade Glioma  96 •  Case 20: Pituitary Secreting Macroadenoma  99 •  Case 21: Jugular Foramen Schwannoma  103 •  Case 22: Cerebellar Hemangioblastoma  105 •  Case 23: Central Nervous System Lymphoma  108 •  Case 24: Pituitary Microadenoma  111 •  Case 25: Infratentorial Ependymoma in Adult  114 •  Case 26: Classical Acoustic Schawannoma  116 •  Case 27: Juxtatentorial Meningioma  119 •  Case 28: Convexity Meningioma  121 •  Case 29: Benign Glioma  123 •  Case 30: Craniopharyngioma in Adult  125 Cases (31–49): Congenital Lesions

128

•  Case 31: Schizencephaly: Closed Lip Type  128 •  Case 32: Schizencephaly: Open Lip Type  130 •  Case 33: Dysgenesis of Corpus Callosum and Associated Lipoma  132 •  Case 34: Lipoma of Corpus Callosum  135 •  Case 35: Type 1 Chiari Malformation  137 •  Case 36: Type 1 Chiari Malformation with Syrinx 1  139

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•  Case 36A: Type 1 Chiari Malformation with Syrinx 2  141 •  Case 37: Classic Arachnoid Cyst  143 •  Case 38: Arachnoid Cyst: Posterior Cranial Fossa  146 •  Case 39: Craniovertebral Junction Anomaly: Basilar Invagination Fossa  149 •  Case 40: Classic Colloid Cyst  152 •  Case 41: Rathke’s Cyst  154 •  Case 42: Cerebellopontine Angle: Epidermoid  156 •  Case 43: Intraventricular Epidermoid  159 •  Case 44: Partial Dysgenesis of Corpus Callosum with Interhemispheric Cyst  162 •  Case 45: Joubert Syndrome  164 •  Case 46: Quadrigeminal Plate Arachnoid Cyst with Obstructive Hydrocephalus  167 •  Case 47: Dandy-Walker Variant  169 •  Case 48: Posterior Cranial Fossa Giant Cyst  171 •  Case 49: Quadrigeminal Plate Large Arachnoid Cyst  173 Cases (50–67): Vascular

176

•  Case 50: Cavernoma Left Frontal Lobe  176 •  Case 51: Acute Right Middle Cerebral Artery Territory Ischemic Infarct  179 •  Case 52: Giant Aneurysm of Basilar Artery Trunk  182 •  Case 53: Right Subacute Subdural Hematoma  184 •  Case 54: Lateral Medullary Syndrome (Wallenberg’s Syndrome)  187 •  Case 55: Venous Infarct: Left Temporal Lobe  189 •  Case 56: Acute Right Thalamic Ischemic Infarct  191 •  Case 57: Giant Aneurysm Supraclinoid Segment of Internal Carotid Artery  194

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Contents xvii

•  Case 58: Left Transverse Sinus Thrombosis  196 •  Case 59: Right Cerebellar Ischemic Infarct  198 •  Case 60: Anterior Cerebral Artery Aneurysm with Subarachnoid Hemorrhage  201 •  Case 61: Vein of Galen Malformation  203 •  Case 62: Cavernoma with Recent Bleed  205 •  Case 63: Right Posterior Watershed Infarct  207 •  Case 64: Vertebrobasilar Insufficiency  209 •  Case 65: Cerebral Venous Thrombosis  211 •  Case 66: Posterior Reversible Ischemic Encephalopathy 213 •  Case 67: Intraventricular Hemorrhage  216 Cases (68–78): Infectons/Infestations

219

•  Case 68: Solitary Tuberculoma  219 •  Case 69: Multiple Tuberculomata  222 •  Case 70: Tuberculous Cerebral Abscess  224 •  Case 71: Tuberculosis of the Optic Nerve Sheath  227 •  Case 72: Bacterial Meningoencephalitis  229 •  Case 73: Toxoplasmosis  232 •  Case 74: Opportunistic Brain Infection in Immunocompromised Patient  234 •  Case 75: Neurocysticercosis  237 •  Case 76: Acute Disseminated Encephalomyelitis  239 •  Case 77: Viral Encephalitis  242 •  Case 78: Rhino-Orbito-Cerebral Zygomycosis  245 Cases (79–100): Miscellaneous

248

•  Case 79: Wilson’s Disease  248 •  Case 80: Tuberous Sclerosis  250

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xviii MRI Brain: Atlas and Text

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•  Case 81: Central Pontine Myelinolysis  253 •  Case 82: Neurosarcoidosis  256 •  Case 83: Idiopathic Intracranial Hypertension (IICHT)/Pseudotumor Cerebri  259 •  Case 84: Obstructive Hydrocephalus: Aqueductal Stenosis 261 •  Case 85: Traumatic Atlantoaxial Joint Subluxation  263 •  Case 86: Central Pontine Myelinolysis 2  265 •  Case 87: Mesial Temporal Sclerosis  267 •  Case 88: Tolosa-Hunt Syndrome  270 •  Case 89: Fahr’s Disease  272 •  Case 90: Normal Pressure Hydrocephalus  274 •  Case 91: Adrenoleukodystrophy  277 •  Case 92: Ectopic Neurohypophysis  279 •  Case 93: Diffuse Axonal Injury  282 •  Case 94: Devic Disease  284 •  Case 95: Leigh’s Disease  287 •  Case 96: Huntington’s Chorea  289 •  Case 97: Empty Sella Syndrome and Aqueductal Stenosis  292 •  Case 98: Neuroglial Cyst  295 •  Case 99: Neurofibromatosis Type 1  297 •  Case 100: Neurofibromatosis Type 2  300

Index 303

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Introduction The 100 brain cases, which were referred for MRI to our hospital were carefully studied. The final diagnosis was confirmed either from a neurosurgeon or a neuropathologist. The case material are arranged in a systematic manner so that the reader can easily navigate the case material. The initial chapters are devoted to basics of MRI-principles, pulse sequences, normal brain anatomy, interpretations, etc. Each case study in this atlas, has a unique way of presentation. The images are followed by their interpretations and descriptions highlighting important features of the disease. Tables and signs are also given as and where possible. Each case material has reference for further reading. The language chosen is simple and easy to follow so that even a budding medical doctor can understand and interpret. The purpose of the book is to make the general practitioner to get them acquainted with common brain diseases in their MRI study, to get an idea of various manifestations, to feel ease when ordering MRI brain and interpreting those images, to cross-check their findings with the official report.

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CHAPTER

1

MRI Basics: Physics The following text gives a brief introduction to the basic and fundamental physics of MR imaging. The unnecessary physics and technical jargon have been deliberately avoided. Magnetic Resonance Imaging (MRI) is an imaging modality based on an interaction between transmitted radiofrequency (RF) waves and hydrogen nuclei in human body under the influence of a strong magnetic field. The simple single steps of an MR examination can be described:  The patient is placed in a magnet (MRI scanner).  A radiowave is sent in.  The radiowave is turned off.  The patient’s body emits a signal.  The signal is received and used for reconstruction of the image.  Normally, protons in hydrogen atoms (which are abundant in our body) are moving in a random fashion. Each proton in hydrogen nuclei behave like tiny magnets, always spinning on their axes. The protons behaving like little magnets align themselves when placed in an external magnetic field (magnetic), but still keep spinning. They are aligned in two ways—either parallel or antiparallel to the external magnetic field depending upon their energy states. The magnetic forces of net aligned protons add up their forces in the direction of the external magnetic field. At equilibrium, net magnetization is parallel to the main axis of the external magnetic field. This is called longitudinal magnetization.

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2 MRI Brain: Atlas and Text

  A radiofrequency (RF) pulse is now sent into disturb these protons. The spinning protons are disturbed and they wobble a toy spinning ‘top’. When the RF pulse and the protons have same frequency, the protons pick up some energy from the radiowave, by a phenomenon called resonance. Thus, RF pulse tips longitudinal magnetization into the transverse plane, creating “transverse magnetization”. Some of the protons pick up energy, and go from a lower to a higher energy level. The radiofrequency pulse exchanges energy with the protons, and change their energy state.  When the RF pulse is switched off, the protons begin to lose their excess energy by a process known as relaxation which are determined by two time constants, T1 and T2 which are different and independent processes. The electrical signal given by the relaxing protons is received by an antenna and is used for generating images.  The number of free hydrogen nuclei determines the exchange of energy, thereby the relaxation time constants (T1 and T2) and contribute to the final signal. The bound hydrogen nuclei have less signal (e.g. cortical bone), while free hydrogen nuclei have more signal (e.g. fat). Different tissues have different T1 and T2 relaxation times under the same magnetic field. The differences in the relaxation times of different tissues are the key to the excellent contrast among them on the MR image created. T1-weighted images (T1W) are used for tissue discrimination, while T2-weighted images (T2W) are very sensitive to the presence of increased water and to differences in susceptibility between tissues.  T1 or T1 (T-one) (Spin-lattice, thermal, or longitudinal) relaxation time is measured in milliseconds. T1 reflects the characteristic time constant for spins to align themselves with the external magnetic field. T1 weighted (T1W) sequence are designed to distinguish tissues with differing T1 relaxation times. T1W image is one whose contrast is mainly determined by T1 relaxation time. Tissues with a short T1 time (e.g. fat) appear bright, while tissues with a long T1 time (e.g. water) appear dark in T1W images.

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MRI Basics: Physics 3

MR WORKING IN A NUTSHELL

Figure 1:  Hydrogen atom to magnetic resonance imaging

Figure 2:  Overview of MR instrumentation

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4 MRI Brain: Atlas and Text

 T2 (T-two) (Spin-spin or transverse): Relaxation time reflects the characteristic time constant for loss of phase coherence among spins, caused by interactions between the spins, resulting in loss of transverse magnetization and MR signal. T2 weighted (T2W) sequence are designed to distinguish tissues with differing T2 relaxation times. T2W image whose contrast depends primarily on T2 relaxation time. Tissues with short T2 time (e.g. water) appear bright, while tissues with long T2 time (e.g. fat) appear dark in T2W images.

How it all Works in a Nutshell? The basic components of an MRI scanner include the main magnet, gradients, and coils. The patient lies on the table along the direction of the magnetic field. All of the protons within the patient’s body align with this main magnetic field. The protons are then excited by a radiofrequency (RF) pulse which elevates the hydrogen atoms to an excited state. These hydrogen atoms then relax to their normal resting state. However, the time that it takes for each hydrogen atom to relax depends on their local tissue environment. Hydrogen atoms in water relax at different rates than hydrogen in soft tissue. It is this difference in relaxation times that enables us to generate an MR image.

How are Images Obtained? Magnetic resonance imaging (MRI) uses magnetic fields and radiofrequency (RF) waves to create images. It is most often tuned to create images by manipulating protons (hydrogen atoms, high in concentration in water and fat within the body). Differences in proton density and the molecular structure surrounding them leads to protons giving off different RF signal characteristics which results in tissue contrast in the MR image.

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MRI Basics: Physics 5

ADVANTAGES OF MRI  Non-ionizing, for they do not use X-ray as medium for imaging.  Multiplanar imaging is automatically possible, for images in sagittal, coronal and transverse planes are generated simultaneously.  Superior contrast in tissue give exquisite anatomical details.  Certain tissue diagnosis is possible, e.g. lipoma, edema, age of hemorrhage, etc.  MR myelogram is created without injection of any contrast medium.  In tumor imaging, it gives exact anatomical details regarding the tumor limits, edema limits, vascularity, etc.

DISADVANTAGES OF MRI (COMPARED TO CT SCAN) Pertaining to lumbar imaging:  It has low sensitivity for calcium, therefore cannot diagnose calcification clearly.  It has low sensitivity for acute hemorrhage.  Scan time is prolonged.  Contraindications prevent certain patients from entering the MRI system. Patients with metallic implants such as cochlear implant, steel sutures, pacemakers, etc. are not allowed inside the MR scanner.  Patients with claustrophobia cannot tolerate the study and some young children may need anesthesia.  Intravenous contrast agents may be needed.

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6 MRI Brain: Atlas and Text

MULTIPLANAR CAPABILITY IN MR

Figure 3:  Sagittal image

Figure 4:  Axial image

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MRI Basics: Physics 7

Figure 5:  Coronal image

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CHAPTER

2

Normal Cross-sectional MR Anatomy of Brain In both CT and MRI scans, the axial sections of the brain are taken from base to vault (Fig. 1). The section are taken parallel to the skull-base line. Similarly, coronal sections are taken parallel to the coronal plane and parasagittal section are taken parallel to the mid-sagittal plane. In order to show important anatomical features, T1W-MR images are taken. Each of the following page contains four-square boxes. The arrangement in each box is shown here. Actual Brain Image

Annotated Corresponding Image

Line Diagram of Above Image

Important Anatomical Landmarks

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Normal Cross-sectional MR Anatomy of Brain 9

AXIAL IMAGE PLANES: PARALLEL TO SKULL BASE

Figure 1:  Axial brain sections, both in CT and MRI studies, are taken from base (Level A1) to vault (Level A7).

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10 MRI Brain: Atlas and Text

AXIAL IMAGE LEVEL A1

•  4th ventricle is a midline structure and is just posterior to the medulla. •  Note the olivary nucleus. •  The corticospinal tract forms a pyramid in anterior aspect of medulla •  There are two cerebellar emispeheres which form main part of posterior cranial fossa.

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Normal Cross-sectional MR Anatomy of Brain 11

AXIAL IMAGE LEVEL A2

•  Note the temporal lobes projected within both the middle cranial fossae. •  The belly of the pons forms a prominent outline anteriorly.   The IV ventricle is immediately posterior to the pons. •  The vermis, a midline structure, connecting two halves of the cerebellar hemispheres. Note the IV ventricle between the vermis and pons. •  Note the flocculus in the lateral aspect of the cerebellar hemispheres. •  Note the CN-VIII in the cerebello angle (CP angle)

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12 MRI Brain: Atlas and Text

AXIAL IMAGE LEVEL A3

•  The CN-II optic nerve seen extending from the orbital apex, anteriorly in the anterior cranial fossa. •  Note the temporal lobes projected within both the middle cranial fossae •  The CN-V is seen extending from anterolateral aspect of the pons. •  The vermis, a midline structure, connecting two halves of the cerebellar hemispheres. Note the IV ventricle between the vermis and pons •  The transverse venous sinus lies posterior to the cerebellar hemispheres.

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Normal Cross-sectional MR Anatomy of Brain 13

AXIAL IMAGE LEVEL A4

•  Note the cross-section of midbrain. •  The cerebral peduncles anteriorly and the red nuclei are seen behind it. •  Note the position of cerebral aqueduct and the inferior collicili below it. •  The superior part of cerebellum is seen in midline. •  Note frontal, temporal and occipital lobes of the cerebrum. Insular cortex separates frontal from temporal lobe. •  Note the hippocapmus of the temporal lobe.

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14 MRI Brain: Atlas and Text

AXIAL IMAGE LEVEL A5

•  The III ventricle is slit like is in midline, sandwiched between two thalami. •  The thalami and lentiform nuclei (globus pallides and putamen) are separated by posterior limb of internal capsule. •  Note the anterior limb of internal capsule separating caudate nuclei from the lentiform nuclei. •  Note the position of pulvinar nuclei of thalami and superior colliculi of the midbrain.

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Normal Cross-sectional MR Anatomy of Brain 15

AXIAL IMAGE LEVEL A6

•  Note the rostrum anteriorly and splenium of corpus callosum posteriorly placed. •  Both in front and behind the corpus callosum note the cingulated gyri •  The III V is in midline between two thalami and anterior nuclei of thalami. •  Note the putamen and insular cortex on either side.

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16 MRI Brain: Atlas and Text

AXIAL IMAGE LEVEL A7

•  Note the central sulcus (Rolandic fissure), separating pre- and postcentral gyri. •  The rolandic fissure separates frontal lobe from parietal lobe. •  Note the centrum semiovale. •  Note the cerebral white matter, cortical sulci and gyri, almost symmetrical.

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CORONAL SECTION: PARALLEL TO CORONAL SUTURE

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18 MRI Brain: Atlas and Text

CORONAL IMAGE LEVEL C1

•  The body of corpus callosum is anterior to the frontal horns. •  The corpus callosum is a mdline structure. •  The septum pellucidum separates both the frontal horns of the lateral ventricles. •  Immediately lateral to the frontal horns lie the head of the caudate nuclei. •  The head of caudate nuclei is separated from the putamen by the anterior limb of the internal capsule. •  The optic chiasma is in midline. •  The sylvian fissure separates the frontal lobe from the temporal lobes.

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Normal Cross-sectional MR Anatomy of Brain 19

CORONAL IMAGE LEVEL C2

•  Note the medially located globus pallidus and laterally placed putamen. •  Note the superior,middle and inferior lobe gyri in frontal and temporal lobes. •  The insular cortex is separating frontal from temporal cortex. •  Note the amygdale in the medial temporal cortex. •  The two optic tracts are seen in the lower part of the images.

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20 MRI Brain: Atlas and Text

CORONAL IMAGE LEVEL C3

•  Note the two globus pallidus—major and minor, well seen. •  The two rounded mammillary bodies are seen just below lower end of the III V. •  The two hippocampi are seen just medial to the tail of the temporal horn of the lateral ventricle.

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Normal Cross-sectional MR Anatomy of Brain 21

CORONAL IMAGE LEVEL C4

•  Note the position of temporal cerebral peduncles and pons body. •  The III V is in midline sandwiched between two thalami. •  Note the different parts of medial temporal lobe •  The two fornices are superior to the III V.

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22 MRI Brain: Atlas and Text

MIDLINE SAGITTAL IMAGE: PARALLEL TO SAGITTAL SUTURE

•  This is a midline sagittal view. •  Note the aqueduct of Sylvius in midline. •  It runs in midline, separating the quadrigeminal plate of midbrain from rest of midbrain. •  The different parts of corpus callosum-rostrum, body and splenium—from front to back are best seen.

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Normal Cross-sectional MR Anatomy of Brain 23

GROSS BRAIN ANATOMY AS SEEN IN MR IMAGES (FIGURES 2 TO 6)

Figure 2:  T1W mid-sagittal shows frontal, parietal, occipital lobes, corpus callosum tentorium forming roof of posterior fossa

Figure 3:  T1W para-sagittal shows frontal, parietal, occipital and temporal lobes, Sylvian fissure separating temporal lobe from rest of brain

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24 MRI Brain: Atlas and Text

Figure 4:  T1W axial shows caudate nucleus putamen, globus pallidus thalamus on either side of midline III V. Internal capsule between caudate nucleus and lentiform nucleus

Figure 5: T1W mid-sagittal shows hypothalamus optic chiasma infundibulum pituitary gland—posterior (Bright signal) and anterior (light white)

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Normal Cross-sectional MR Anatomy of Brain 25

A

B

C

D

Figures 6A to D:  Coronal sections: (A) T2W; (B) T1W; (C) Line Diagram; (D) T1W with gadolinium contrast. Abbreviations: (1) Optic chiasma; (2) Internal carotid artery (cavernous part); (3) Infundibulum (Pituitary stalk); (4) Pituitary gland; (5) Cavernous linus. (Right and left side)

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CHAPTER

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MRI of Signals and Sequences GLOSSARY OF TERMS  CP angle: cerebello-pontine angle.  Diffusion-weighted Imaging (DWI): Imaging techniques designed to measured MRI signal by the amount of diffusion (random thermal motion) of water molecules in the selected voxels.  Flair: Fluid attenuated inversion recovery, a special sequence.  Gadolinium: Lanthanide (Gd) element that is paramagnetic in its trivalent state. It has been used as the active component of most contrast agents in MR imaging because of its effect of strongly decreasing the T1 relaxation times of the tissues to which it has access. Although toxic by itself, it can be given safely in a chelated form such as Gd-DTPA, which still retains much of its strong effect on relaxation times. Gadolinium diethylene triamine penta-acetic acid complex, a gadolinium chelate; only contrast agent, used in MRI studies. Hyperintense (more intense): If an abnormality is bright (white) on MR, we describe it as hyperintense. Hypointense (less intense): If an abnormality is dark on MR, we describe it as hypointense. Isointense (the same intensity): If an abnormality is the same intensity to a reference structure, we describe it as isointense.

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MRI of Signals and Sequences 27

 MRI: Magnetic resonance Imaging.  MRA: Magnetic resonance angiography.  T1 or T1 (T-one): Spin-lattice or longitudinal relaxation time; the characteristic time constant for spins to tend to align themselves with the external magnetic field. Starting from zero magnetization in the z-direction, the z-magnetization will grow to 63% of its final maximum value in a time T1.  T1-Weighted (T1W): A T1W image created typically by using short repetition (TR) and echotime (TE). The tissue contrast and brightness are predominately determined by T1 signals. Imaging within T1-weighted images tissue with a short T1 is bright while tissue with a long T1is dark.  T2 or T2 (T-two): Spin-spin or transverse relaxation time; the characteristic time constant for loss of phase coherence among spins oriented at an angle to the static magnetic field, due to interactions between the spins, with resulting loss of transverse magnetization and MR signal. Starting from a nonzero value of the magnetization in the xy-plane, the xy-magnetization will decay so that it loses 63% of its initial values in a time T2, if relaxation is characterized by a simple single exponential decay.  T2-Weighted (T2W): Often used to indicate an image where most of the contrast between tissues or tissue states is due to differences in tissue T2 T2 Wan image created typically by using longer TE and TR times whose contrast and brightness are predominately determined by T2 signals. In T2-weighted images tissue with a short T2 is dark, while tissue with along T2 is bright.  Proton Density (PD): Pulse sequences with short TE and long TR, i.e. the images are either T1- nor T2-weighted. T1W and T2W sequences are the basic sequences used in all MRI studies. Other sequences are derivatives of these basic sequences.

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28 MRI Brain: Atlas and Text

EXAMPLES FOR BASIC MR SIGNAL INTENSITY NOMENCLATURE

Figure 1:  An axial T2 MRI image through the suprasellar cistern Notice that the gray matter is brighter than the white matter, the cerebral spinal fluid in the suprasellar cistern (SC) and quadrigeminal plate cistern (QC) is very bright, and the globes are bright. These help us identify this as a T2 image.   There is a suprasellar epidermoid mass (outlined by arrows) which is has hyperintense T2 signal.  Some areas of the mass in fact share signal characteristics that are similar to CSF and therefore can be described as isointense with respect to CSF.

NOTE ON SEQUENCES MRI is the imaging technique that has most benefitted from technological innovation. The many advances have led to improvements in quality and acquisition speed. 

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MRI of Signals and Sequences 29

Figure 2:  An axial T1 MRI image of the brain through the same level as above Notice how the lesion is dark on T1, or hypointense. How to tell that this is a T1-weighted image? Notice that the gray matter is darker than the white matter and the CSF and globes are dark. No enhancing vessels or dura mater are seen, telling us that this image is a non-contrast T1 image.

Each sequence is a subtle combination of radiofrequency pulses and gradients. Whatever the type of sequence, the aims are to favor the signal of a particular tissue (contrast), as quickly as possible (speed), while limiting the artifacts and without altering the signal to noise ratio. Examples of commonly used sequences are shown in the following table. Each sequence is shown with an example of an images, usefulness and appearances of various tissues in each sequence.

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30 MRI Brain: Atlas and Text

EXAMPLES OF COMMON MR SEQUENCES AND THEIR USE T1W Axial

Figure 3:  T1 weighted axial MRI

     

Useful for evaluating anatomical details CSF—black/dark Fat (scalp)—bright white Brain white matter—white Brain gray matter—gray Blood vessels—dark.

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MRI of Signals and Sequences 31

T2W Axial

Figure 4:  T2 weighted axial MRI

    

Useful for evaluating pathology—edema CSF-bright white Fat (scalp)—gray Brain white matter—gray Brain gray matter—light white.

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32 MRI Brain: Atlas and Text

T1W Axial with Gadolinium Contrast Agent

Figure 5:  T1 weighted axial with gadolinium contrast agent

 Useful for evaluating blood brain barrier (BBB) in the setting of a pathology  CSF—black/dark  Fat (scalp)—bright white  Brain white matter—white  Brain gray matter—gray  Blood vessels—bright white.

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MRI of Signals and Sequences 33

DWI Axial

Figure 6:  Diffusion weighted imaging axial

     

Useful for—stroke imaging, abscess Cellular tumors CSF—dark White matter—gray Gray matter: Lighter than white matter Fuzzier image than FLAIR.

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34 MRI Brain: Atlas and Text

FLUID ATTENUATION INVERSION RECOVERY (FLAIR) Coronal Image

Figure 7:  Coronal image

   

Useful to differntiate normal from abnormal fluid collection CSF: Dark White matter: Gray Gray matter: Lighter than white matter.

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MRI of Signals and Sequences 35

MR Angiography (MRA)

Figure 9:  Magnetic resonance angiography

 It can be performed without the use of contrast or with contrast (gadolinium).  In non-contrast MRA, bright signal is generated by forward blood flow within a vessel but not the vessel itself.  Important disadvantages are very expensive, over-estimates size, stenosis.

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36 MRI Brain: Atlas and Text

ROLE OF MRI CONTRAST AGENT Precontrast Image

Figure 10:  Precontrast image

Notice how the schwannoma within the left internal auditory canal gets brighter after contrast. Although contrast is not always necessary, in many situations, it can be very helpful. Some typical indications for using contrast include neoplasm, infection, inflammation, and vascular disease. More specifically, contrast is used to evaluate for areas of bloodbrain barrier breakdown. If there is a breakdown of the blood brain barrier, contrast is able to penetrate the central nervous system (CNS) and may be taken up by various pathologic processes such as tumors, infection and demyelinating disease. To assess whether a lesion enhances after contrast administration, for different types of enhancement indicate a particular pathology. In neuroimaging we use gadobenate dimeglumine, based on element gadolinium (Gd). Nephrogenic systemic fibrosis (NSF) is a rare but serious complication of gadolinium use.

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MRI of Signals and Sequences 37

Postcontrast Image

Figure 11:  Postcontrast imaging

DIFFUSION WEIGHTED IMAGING: AN IMPORTANT TOOL FOR DIAGNOSING STROKE Principles of DWI DWI detects when water (hydrogen protons) are unable to diffuse freely.  Normally, cells are packed loosely enough that the water surrounding them can move or diffuse rather easily.  With cytotoxic edema in ischemia the cells swell secondary to failure of the Na/K pump and the space between the cells becomes very narrow. Subsequently, the water that normally surrounds the cells cannot diffuse as easily and becomes “restricted.” DWI is very sensitive at detecting this change, becoming bright/positive within minutes of acute ischemia. When there is a tumor, inflammation, or other process that breaks down the capillary endothelium water leaks out of the vessels and there is

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38 MRI Brain: Atlas and Text

A

B Figures 12A and B:  Principles of diffusion weighted imaging

an increasing amount of water surrounding the brain cells. This is called vasogenic edema. In this case the water can actually diffuse more easily than usual because of the larger gaps between cells. DWI will not be positive in this circumstance.

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Principles of Intracranial Space Occupying Lesions (ICSOL)/ Tumor Diagnosis by MRI LOOK FOR CLASSIC LOCATION/MORPHOLGY/SIGN Some images, especially on MRI, are almost pathognomonic or are so typical in a certain clinical context that they can quickly be used to make or exclude a diagnosis. Some examples are: A colloid cyst of the third ventricle; a dermoid cyst and an epidermoid cyst in CP angle; a lipoma near corpus callosum; a hamartoma of the tuber cinereum in a patient with gelastic seizures; a dysplastic gangliocytoma of the cerebellum; a cystic hemangioblastoma of the cerebellum with a strongly enhancing mural nodule in a patient with a known von Hippel-Lindau disease; the giant cell astrocytoma in a patient with tuberous sclerosis presenting as an enhancing mass in the foramen of Monro in a patient with subependymal calcifications; many meningiomas with a broad implantation on the dura and with homogeneous enhancement and a dural tail; vestibular schwannomas extending within a funnel-shaped widened internal auditory canal and ice-cone sign. Nonetheless, one has to bear in mind that for all these lesions atypical forms also exists.

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40 MRI Brain: Atlas and Text

DETERMINE WHETHER THE LESION IS INTRA-AXIAL VERSUS EXTRA-AXIAL This is crucial finding. An intra-axial lesion is one which is involving the brain primarily and is within the pia mater, e.g. primary brain tumor. An extra-axial lesion is one which is outside brain substance and is outside piamater, e.g. meningioma. Once this distinguishing is made, then the differential diagnosis becomes less and easier. Extra-axial lesions cause white matter buckling, expand the ipsilateral subarachnoid space, and can be surrounded by a cerebrospinal fluid (CSF) cleft or halo. Intra-axial lesions expand the cortex of the brain, do not widen subarachnoid spaces, and have a specific way of spreading into the brain. Radiologically, identifiable anatomical clues that a tumor is extra-axial in location include the following:  Widening of ipsilateral subarachnoid space  CSF cleft between mass and brain parenchyma  Deviation of pial vessels between mass and brain tissue  Buckling of white matter  Bony changes (e.g. hyperostosis in meningioma). The essential distinction that a neuroradiologist must make is whether a lesion is intra-axial (intraparenchymal) or extra-axial (outside the brain substance; i.e. meningeal, dural, epidural, or intraventricular). This distinction has been made easier by the multiplanar capabilities of magnetic resonance (MR) imaging, e.g. the quintessential and most common extra-axial mass is the meningioma, a readily treatable and diagnosable lesion. The meningioma is not only extra-axial, but also intradural. Extra-axial intradural lesions buckle the white matter, expand the ipsilateral subarachnoid space, and sometimes cause reactive bony changes. On MR scans, one can visualize the dural margin and determine that the lesion is extra-axial. The prototypical extra-dural (epidural) extra-axial mass, a bone metastasis, displaces the dura inward (is superficial to the dural coverings) but otherwise may have the same contour as an intradural extra-axial mass. We can classify a lesion as intra-axial, if: (1) it expands the cortex of the brain;

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Principles of ICSOL/Tumor Diagnosis by MRI 41

(2) there is no expansion of the subarachnoid space; (3) the lesion spreads across well-defined boundaries; and (4) the hypointense dura and pial blood vessels are peripheral to the mass

PATIENT’S AGE AND SEX Specific tumors occur in children under age 2, e.g. choroid plexus papilloma, anaplastic astrocytoma, and teratoma. In the first decade of childhood, medulloblastoma, ependymoma of the fourth ventricle, brainstem glioma, craniopharyngeoma, and hypothalamic glioma are found. Glioblastoma, meningioma, oligo-dendroglioma, pituitary adenoma, Schwannoma, and metastases are almost exclusively seen in adults. Meningiomas are mostly found in females in the fifth decade.

MRI SIGNAL INTENSITY The signal intensities of normal structures and of pathological findings on conventional T1 and T2-weighted MR images depend on many factors and therefore have to be carefully studied. The amount of water, the proton density, the chemical structure and or/binding, the presence or absence of blood flow or CSF, calcification, fat, blood degradation products, melanin, etc. are all factors influencing the signal characteristics. Most tumoral lesions appear bright on T2-weighted images and dark on T1-weighted images. In lesions with a cystic appearance, one can only state very confidently that the lesion is truly a cyst, if it is exactly isointense to CSF on all routine sequences and if its signal is totally attenuated on fluid-attenuated inversion recovery (FLAIR) images.

T1W BRIGHT LESIONS A bright appearance on T1-weighted images and a dark appearance on T2-weighted images can be due to the presence of fat, such as in lipoma, dermoid cysts, or teratoma; melanin, such as in melanoma and metastasis of melanoma; mucin, in

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42 MRI Brain: Atlas and Text

metastasis of mucinous adenocarcinoma of the gastrointestinal tract, such as sigmoid carcinoma; colloid material in a colloid cyst of III ventricle and Rathke cleft cyst; and even calcification in oligodendroglioma. A bright aspect on both T1 and T2-weighted images can be due to cholesterine in cholesterol granuloma or the cystic component of craniopharyngioma, high protein content in tumoral cysts or the presence of methemoglobin in hemorrhagic neoplasms. Flow voids point to hypervascular tumors such as hemangioblastoma or some hypervascular metastases. Calcification can appear as dark dots within a tumor, but some totally calcified meningiomas can be totally dark.

CLASSIC LOCATION The location of the tumor can suggest certain diagnoses. Glioblastoma is almost exclusively seen in the supratentorial araea, while a cystic pylocytic astrocytoma in childhood and hemangioblastomas in adults are preferentially infratentorial. A cerebellar mass in a patient over age 50 is likely to be a metastasis. A cortical lesion is likely to be a pleomorphic xanthoastrocytoma, ganglioglioma, or dysembroblastic neuroepithelial tumor (DNET), a corticomedullary lesion is most likely to be a metastasis or oligodendroglioma; and a deep periventricular lesion could be an astrocytoma, ependymoma or lymphoma, the latter more specifically, if multiple. Primary glial tumors arise deep in the white matter, away from the cortex. Some tumors have a predilection for the suprasellar area. Besides the classical hypothalamic glioma, craniopharyngioma can occur. In the pineal region, pineocytoma, and pineoblastoma have to be differentiated from germinoma and even from tectal glioma. In patients with temporal lobe epilepsy, cystic lesions with an enhancing mural nodule in the uncus of the temporal lobe frequently correspond to ganglioglioma. Intraventricular tumors have a very specific differential diagnosis, varying even according to which specific ventricle the lesion is located in age of patient, etc.

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Principles of ICSOL/Tumor Diagnosis by MRI 43

Once established as intra-axial or extra-axial, the specific location of the mass becomes equally important in imaging analysis since certain histological types of intracranial tumor tend to occur with higher frequency in specific locations. Thus, accurate compartmentalization of the mass will limit the differential diagnosis to a relevant few types of tumors and help direct further imaging evaluation and treatment.

TYPE AND DEGREE OF CONTRAST ENHANCEMENT A major factor of interest is the type and degree of contrast enhancement. In most meningiomas and acoustic Schwannomas, enhancement is homogeneous, except for some intratumoral cystic areas, calcifications, or flow voids. Homogeneous enhancement can also be seen in nodular metastases at the corticomedullary junction, periventricular lymphoma, germinoma and other pineal gland tumors, pilocytic astrocytoma in the brainstem and the suprasellar area and in the solid part of cystic or fluid-secreting pilocytic astrocytomas or hemangioblastoma. The enhancement of oligodendroglioma tends to be patchier. High-grade primary tumors, exemplified by glioblastoma multiforme, are very anarchic, multilocular, thickwalled ring-enhancing masses. The rings have a shaggy inner margin with a thick and irregular wall. Bridging septa may cross the necrotic cavities and nodular formations can be present on the septa. Another typical pattern of enhancement is the ring-enhancing lesion. It is typically seen in metastasis but also in glioblastoma and even in non-tumoral lesions such as abscess, multiple sclerosis, chronic hematoma, and a variety of infectious and inflammatory lesions.

THE EXTENSION AND/OR SPREAD OF THE TUMOR Another point to consider in the differential diagnosis is tumor extension and/or spread. Diffusely infiltrating astrocytomas spread along white matter tracts and as such do not respect the

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44 MRI Brain: Atlas and Text

boundaries of the cerebral lobes. Glioblastoma of the corpus callosum shows a typical butterfly extension to the fontal or occipital lobes. Ependymomas of the fourth ventricle in children tend to extend not only through the foramen of Magendie to the cisterna magna, but also through the lateral foramina of Lushka to the cerebellopontine angle. Oligodendroglioma typically shows a cortical extension. Primitive neuroectodermal tumors (PNETs) such as medulloblastomas and pineoblastoma tend to seed very quickly via the cerebrospinal fluid to the subarachnoid space, with formation of multiple tumoral nodules on the surface of the brain and spinal cord. Germinoma of the pineal gland very specifically spreads to the hypophyseal infundibulum; this location can even be the sole manifestation of the disease.

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CHAPTER

5

MRI Atlas of Cases CASES (1–30): TUMORS CASE 1: CEREBRAL PILOCYTIC ASTROCYTOMA

A

B

Figures 1A and B:  (A) T1W axial: A well-defined hypointense, large lesion (dotted black arrows) in left parieto-occipital region. No mass effect or midline shift is seen; (B) T2W axial: A well-defined intra-axial mass in the left parieto-occipital region, with a large cystic component measuring 5.6 × 3.9 cm, and a peripheral solid component measuring 1.6 × 2.6 cm. There is no evidence of edema. The signal intensity of the cystic component was higher than that of the CSF (thick arrows)

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46 MRI Brain: Atlas and Text

C

D

Figures 1C and D: (C) FLAIR axial: The lesion shows hyperintensity (thick arrows) indicating abnormal fluid collection and not CSF; (D) T1W axial with Gd: The cystic component shows mild peripheral ring enhancement, while the solid component shows heterogeneous enhancement. There is no significant sign of hydrocephalus. The posterior part of the body of left lateral ventricle is displaced

DISCUSSION Pilocytic astrocytomas (PA) usually arise in the cerebellum, brainstem, hypothalamic region, or optic pathways, but they may occur in any area where astrocytes are present. Less common locations include the cerebral hemispheres, cerebral ventricles, velum interpositum, and spinal cord. Pilocytic astrocytomas (PA) may be found throughout the brainstem and frequently extends in an exophytic fashion from its dorsal surface. In adults, the tumor more frequently occurs in the cerebral hemisphere. In pediatric group, the most common site of occurrence of pilocytic astrocytoma is the cerebellum. These tumors are usually discrete, indolent lesions associated with

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MRI Atlas of Cases 47

cyst formation. The cysts may be unilocular or multilocular, with an associated tumor nodule. Cross-sectional imaging often demonstrates a classic appearance: a cystic mass with an enhancing mural nodule. Less common appearances are quite nonspecific. At MR, pilocytic astrocytoma is typically a sharply demarcated lobular mass, although lesions of the diencephalon can show significant infiltrative extension on MR, a feature that often cannot be fully appreciated on CT. More than two-thirds of cases show macroscopic cyst formation. On MR, the solid part of the lesion can be either isointense to brain parenchyma or markedly hyperintense on T2-weighted images. Most lesions have an obvious cystic component. The degree of surrounding vasogenic edema is usually small. When it does occur, the area of edema is smaller in size than the diameter of the tumor. Postcontrast imaging features are similar to those reported with CT. The mural nodules of pilcytic cerebellar astrocytomas may enhance intensely and uniformly or inhomogeneously. The remainder of the cyst wall may enhance completely, partially, or not at all. Most patients are presented in the first 2 decades of life. The cerebellum, optic nerve and chiasm, and hypothalamic region are the most common locations, but the tumor can also be found in the cerebral hemisphere and rarely ventricles, and spinal cord. Most of the lesions occur in or near the midline. In adults, the tumor more frequently occurs in the cerebral hemisphere. Four predominant imaging patterns of pilocytic astrocytoma have been described: (1) Mass with a non-enhancing cyst and an intensely enhancing mural nodule (21% of cases); (2) Mass with an enhancing cyst wall and an intensely enhancing mural nodule (46%); (3) Necrotic mass with a central non-enhancing zone (16%); and (4) Predominantly solid mass with minimal to no cyst like component (17%). Surrounding vasogenic edema is rarely present, and this feature provides a valuable clue to the correct diagnosis.

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48 MRI Brain: Atlas and Text

BIBLIOGRAPHY 1. Atlas Scott W. Magnetic Resonance Imaging of the Brain and Spine, 3rd edn. Lippincott Williams & Wilkins.  Philadelphia, PA, 2002. 2. Osborne AG. Diagnostic Neuroradiology. Mosby-Year Book, Inc. St. Louis, MO. 1994.

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CASE 2: LEFT FALX MENINGIOMA

A

B

C

D

Figures 1A to D:  (A) T1W axial: A well-defined, isointense signal intensity, soild extra-axial mass, 3.2 × 4.0 cm. Close to the midline in left frontal region (dotted arrows); (B) T2W axial: A well-defined, heterogeneous signal intensity, soild extra-axial mass, 3.2 × 4.0 cm. Close to the midline in left frontal region. The lesion had broad implantation base on falx. There was a hyperintense ring around the lesion and mild dema. (thick black arrow); (C) T1W coronal with Gd: Homogeneous enhancement with well-defined dural tail. The superior sagittal sinus was separated (arrow); (D) T1W axial with Gd: Homogeneous enhancement with well-defined dural tail. The superior sagittal sinus was separate (arrow)

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50 MRI Brain: Atlas and Text

DISCUSSION Meningiomas are the most common non-glial brain tumors with an incidence of 2–3 per 100,000. The highest incidence is in women 40–60 years old. Since only 10% of meningiomas cause symptoms, many are discovered incidentally on imaging studies or at autopsy. They are slow-growing, extra-axial tumors that are usually benign and arise from the meningothelial cells of the arachnoid. Most meningiomas are homogeneous masses with sharply defined margins, although calcifications (whorled, sandlike deposits known as psammoma bodies) are seen in 15–20% of cases. They can be found along the external surface of the brain or in the ventricles. The most common location for a meningioma is along the superior sagittal sinus, but one can also arise along the sphenoidal ridge, olfactory groove, falx cerebri, or tentorium. Meningiomas usually present as solitary masses, and multiple tumors would raise the suspicion of neurofibromatosis type 2. Progesterone, estrogen, and androgen receptors exist on a subset of meningiomas and could be a potential target for treatment. The radiographic assessment of a meningioma is best done with MRI. These tumors are typically isointense to gray matter on T1-weighted MRI and often hypointense on T2-weighted MRI. Meningiomas can occasionally be appreciated on plain skull films by the visualization of bone erosion, calcification, or hyperostosis, or enlarged middle meningeal artery groove. Clinically, meningiomas produce variable symptoms based on their location in the brain. Cerebral convexity meningiomas may first be noticed by symptoms from the mass effect, they induce: headache, confusion, papilledema, or focal seizures. In contrast, parasagittal or falx meningiomas may result in a progressive spastic weakness or loss of sensation on the side of the body opposite to the tumor.

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MRI Atlas of Cases 51

BIBLIOGRAPHY 1. Abeloff. Clinical Oncology, 2nd edn, Churchill Livingstone, Inc. 2000. pp.1166-69. 2. Cotran, Ramzi S. Robbin’s Pathologic Basis of Disease, 6th edn, WB Saunders Company, 1999. pp. 1350-1. 3. Juhl. Paul and Juhl’s Essentials of Radiologic Imaging, 7th edn, Lippincott, Williams, Wilkins, 1998. pp. 388-90.

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CASE 3: CEREBELLOPONTINE (CP) ANGLE MENINGIOMA

A

B

C D Figures 1A to D:  (A) T1W axial: A broad based, hypointense, 3.9 × 3.5 × 3.0 cm, extra-axial solid mass (black dotted arrow) in the left cerbellopontine angle. Note the midline fourth ventricle (arrow) compressed and displaced; (B) T2W axial: A broad based, hyperintense, extra-axial solid mass in the left cerbellopontine angle. Note the midline fourth ventricle (thin arrow) compressed and displaced to right side. Note pressure effect on the pons (thick arrow); (C) T1W axial with Gd: Homogeneous dense enhancement of the entire mass (white dotted arrow) The mass shows an enhancing dural tail (arrowhead); (D) T1W coronal with Gd: Homogeneous dense enhancement of the entire mass (black dotted arrow). The mass shows an enhancing dural tail (arrowheads). The auditory canal and VIII cranial nerve was normal

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MRI Atlas of Cases 53

DISCUSSION The cerebellopontine (CP) angle is bound anterolaterally by the posterior aspect of the petrous temporal bone and posteromedially by the cerebellum and pons. It contains important vascular structures and cranial nerves, and is subject to a certain gamut of lesions, notably tumors with interesting radiological manifestations. Radiological investigation of these lesions has seen significant improvement in recent decades. Magnetic resonance is the imaging modality of choice for lesions of the CP angle and internal auditory canal. Lesions of the CP angles usually are divided into those native to the angle (vestibular Schwannoma, meningioma, epidermoid, arachnoid cyst, metastases, lipoma, etc.) and those extending to the angle from adjacent structures (gliomas, ependymomas, choroid plexus papillomas, vascular malformations). Vestibular Schwannomas are by far the most important lesion of the CP angle. The CP angle is a site for certain tumors—eight cranial nerve Schwannomas, meningiomas, inclusion dermoid; metastasis; epidermoid; ependymoma; vestibulocochlear (acoustic) Schwannoma accounts for well over half of all the abnormalities encountered in this region. Meningiomas are the most common, non-glial, primitive intracranial tumors; their prevalence among operated tumors is around 13–19%. They may occur at any age but have a peak incidence around 45 years of age; 60% occur in females. The most frequent sites for infratentorial meningiomas are: the petrous bone, clivus, foramen magnum, tentorium; extremely rare is an intraventricular meningioma of the fourth ventricle. On MRI, meningiomas tend to be isointense to cortex and hypointense to white matter in T1-weighted images; in T2weighted images meningiomas are again isointense to slightly or markedly hyperintense. Enhancement with gadolinium (Gd) is usually very marked and homogeneous. MRI has the advantage over CT of being able to provide images in different planes; coronal images are very useful in demonstrating critical areas

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54 MRI Brain: Atlas and Text

such as the middle fossa or the upper convexity; MRI shows much better than CT the relationship of the tumor with vascular structures, the carotid siphon, venous sinuses, their compression or obstruction and all topographical relationships useful for surgical planning. The meningioma is the second most common mass lesion of the cerebellopontine angle, with 13–18% of all neoplastic lesions in this location being meningioma. Less than 5% of all intracranial meningiomas occur in the cerebellopontine angle. The acoustic Schwannoma, from which meningiomas must be distinguished, is by far the most common tumor in this region. Meningiomas, however, tend to be larger, more hemispheric in shape rather than spherical, and more homogeneously enhancing. Meningiomas may be associated with hyperostosis. Broad, dural based, with a dural tail, unilobar mass. They do not have a propensity to involve the internal auditory canal (which is a fairly constant feature of Schwannomas). The visualization of the normal seventh and eighth nerve bundles favors the diagnosis of a meningioma. Table 1:  Common cerebellopontine angle: Lesions Pathology

Example

1. Congenital

•  Epidermoid cyst •  Arachnoid cyst •  Lipoma •  Neurofibromatosis type 2

2. Inflammatory

Sarcoidosis

3. Vascular

•  Aneurysm (vertebrobasilar, PICA, AICA) •  Arteriovenous malformation

4. Benign tumor

•  Acoustic Schwannoma •  Meningioma •  Facial nerve Schwannoma

5. Malignant tumor

•  Metastasis, systemic or subarachnoid spread •  Brainstem glioma, pedunculated •  Ependymoma

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MRI Atlas of Cases 55 Table 2:  MRI: Differential diagnosis of common CPA lesions Lesion

MRI findings

1. Lipoma

TlW high signal CPA mass (parallels subcutaneous and marrow fat intensity); Fat suppression protocol like “STIR” lesion “disappears”

2.  White epidermoid cyst

Rare imaging presentation of more common lesion; high T1 signal probably secondary to high-protein content of internal fluid; restriction (high signal) on diffusion; insinuates adjacent CSF spaces and structures

3. Aneurysm

Ovoid CPA mass with calcified rim (CT) and complex layered signal (MR) •  MR signal complex with high signal areas from methemoglobin in aneurysm lumen or wall •  Does not enter lAC. MRA diagnostic

4.  Epidermoid cyst

T1W Isointense or slightly hyperintense to CSF signal; lack of any attenuation or “incomplete attenuation” on FLAIR; high signal on diffusion (DWI) scans makes diagnosis certain

5.  Arachnoid cyst

Pushes broadly on adjacent structures, does not insinuate: •   T1 and T2 FLAIR signal follows CSF signal; Fully attenuates on FLAIR sequence (low signal) •  Shows no restriction on diffusion weighted imaging (low signal)

6.  Acoustic Schwannoma

TlWI Intermediate signal most common, T1W + Gd. Avidly enhancing cylindrical (lAC) or “ice-cream on cone” (CPA-lAC) mass centered on porus acusticus, widened Internal Auditory Canal (IAC)

7. Meningioma

•  C  ECT: Calcified dural-based mass eccentric to porus acusticus •  T 1 C+ MR: Broad dural-base with associated dural “tails” Avoid contrast enhancement. Normal IAC

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56 MRI Brain: Atlas and Text

BIBLIOGRAPHY 1. Lalwani AK, et al. Preoperative differentiation between meningioma of the cerebellopontine angle and acoustic neuroma using MRI. Otolaryngol Head Neck Surg. 1993;109:88-95. 2. Schmalbrock P, et al. Assessment of internal auditory canal tumors: a comparison of contrast-enhanced T1-weighted and steady-state T2-weighted gradient-echo MR imaging. AJNR. 1999;20:1207-13.

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CASE 4: RECURRENT CENTRAL NEUROCYTOMA

A

B

C

D

Figures 1A to D:  (A) T2W axial: A well-defined heterogenous intraventricular mass with small cysts within the mass, with obstruction at foramen of Monro (dotted black arrow); (B) T1W axial: The septum pellucidum (white dotted arrow) is displaced and the mass is seen arising from the left side. The left lateral ventricle is more dilated than the right side (thick black arrow); (C) FLAIR axial: The septum pellucidum is displaced and the mass is seen arising from the left side; (D) T2W coronal: Better the intraventricular location of the tumor

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58 MRI Brain: Atlas and Text

DISCUSSION Central neurocytomas are rare intraventricular neoplasms of the central nervous system, compromising 0.25–0.5% of brain tumors. The diagnosis and management of these tumors remains controversial since most clinical series are small. Typically, patients with central neurocytomas have a favorable prognosis, but in some cases the clinical course is more aggressive. Although histological features of anaplasia do not predict biologic behavior, proliferation markers including MIB-1 might be more useful in predicting relapse. Radiologically, the typical appearance of a central neurocytoma as reported in the literature is that of a well-circumscribed mass confined to the anterior portion of the lateral ventricles. Punctate or coarse calcifications and multiple small cysts within the tumor are often observed. Mild-to-moderate contrast enhancement is common. Intraventricular oligodendroglioma or ependymoma may be indistinguishable from central neurocytoma without ultrastructural and immunohistochemical studies. Imaging of central neurocytoma is usually characteristic. Most of them occur as an exophytic, well circumscribed, globular mass that protrudes into the ventricles. Radiological differential diagnosis includes the intraventricular tumors of the lateral ventricles, such as ependymoma, giant cell astrocytoma, pilocytic astrocytoma and neurocytoma.

BIBLIOGRAPHY 1. Goergen SK, Gonzales MF, McLean CA. Intraventricular neurocytoma: radiologic features and review of the literature. Radiology. 1992;182:787-92. 2. Smoker WRK, Townsend JJ, Reichman MV. Neurocytoma accompanied by intraventricular hemorrhage: case report and literature review. AJNR. 1991;12:765-70.

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CASE 5: BRAINSTEM GLIOMA

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B

C

D

Figures 1A to D: (A) T2W axial: Hyperintensity in diffusely enlarged brainstem (dotted black arrows). The IV is displaced posteriorly; (B) T1W axial: Hyporintensity in diffusely enlarged brainstem. The fourth ventricle is displaced posteriorly; (C) T1W sagittal:  The full extent of the tumor; (D) T1W axial with Gd: Contrast agent does not show any enhancement

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60 MRI Brain: Atlas and Text

DISCUSSION Brainstem gliomas constitute about 15% of all pediatric CNS tumors with peak incidence between 3 and 10 years of age. These are highly aggressive tumors commonly presenting with symptoms of double vision, weakness, unsteady gait, difficulty in swallowing, headache, dysarthria, nausea, and vomiting. There is an increased incidence of brainstem gliomas in patients with neurofibromatosis type 1. MRI multiplanar images assist in the establishment of the tumor diagnosis, identification of tumor epicenter, and prediction of its biological behavior. Diffuse neoplasms tend to smoothly enlarge the affected area without focal areas of exophytic tumor. They are generally poorly marginated and involve more than 50% of the brainstem in the axial plane at the level of maximal involvement. Minimal or no contrast enhancement is seen after gadolinium, although enhancement is commonly seen after radiation therapy. Focal tumors are generally well marginated and involve less than 50% of brainstem in the axial plane. Focal neoplasms often enhance and have a better prognosis in general than diffuse neoplasms. Diffuse gliomas are unfortunately the most common brainstem lesions, and they have the worst prognosis among the brainstem gliomas.

BIBLIOGRAPHY 1. Hueftle MG, Han JS, Kaufman B, Benson JE. MR imaging of brainstem gliomas. J Comput Assist Tomogr. 1985;9(2):263-7. 2. Smith RR. Brainstem tumors. Semin Roentgenol. 1990;25(3):249-62.

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CASE 6: CEREBELLAR PILOCYTIC ASTROCYTOMA

A

B

C

D

Figures 1A to D: (A) T1W sagittal:  A large well-defined hypointense lesion (dotted black arrow), inside the cerebellum, compressing the IV ventricle and displacing the brainstem; (B) T1W axial:  A midline, large well-defined hypointense lesion, arising from the vermis of the (dotted black arrow) cerebellum, compressing the IV ventricle and displacing the brainstem; (C) T1W axial with Gd:  Ring enhancement of the cystic wall (thick arrow); (D) T2W axial:  Midline, large well-defined isointense lesion, arising from the vermis of the cerebellum (dotted black arrow) compressing the IV ventricle and displacing the brainstem. There is minimal edema around the mass

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62 MRI Brain: Atlas and Text

DISCUSSION Most patients are presented in the first 2 decades of life. The cerebellum, optic nerve and chiasm, and hypothalamic region are the most common locations, but the tumor can also be found in the cerebral hemisphere and rarely ventricles, and spinal cord. Most of the lesions occur in or near the midline. In adults, the tumor more frequently occurs in the cerebral hemisphere. Clinical presentation of patients with a pilocytic astrocytoma varies with its site of origin. Headaches, vomiting, gait disturbance, blurred vision, diplopia, and neck pain are common symptoms in patients with a cerebellar pilocytic astrocytoma. Clinical signs usually include hydrocephalus, papilledema, truncal ataxia, appendicular dysmetria, head tilt, VI nerve palsy, and nystagmus. Pilocytic astrocytoma carries one of the highest survival rates of any brain tumor. At MR imaging, pilocytic astrocytoma is typically isointense to hypointense relative to normal brain with T1-weighted pulse sequences and hyperintense compared with normal brain with T2-weighted pulse sequences. As expected for a tumor of low biologic activity, the degree of surrounding vasogenic edema is diminished in comparison with that seen in high-grade (WHO grade III and IV) glial neoplasms. When it does occur, the area of edema is smaller in size than the diameter of the tumor. Postcontrast imaging features are similar to those reported with CT. Because of its superiority to CT in assessing the posterior fossa and the usefulness of multiplanar imaging, MR imaging is regarded as the imaging study of choice for evaluation of pilocytic astrocytomas. The well-demarcated appearance of virtually all (96%) pilocytic astrocytomas is misleading, as most (64%) show infiltration into the surrounding brain parenchyma at histologic examination.

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MRI Atlas of Cases 63

BIBLIOGRAPHY 1. Felix R, Schorner W, Laniado M, et al. Brain tumors: MR imaging with gadolinium-DTPA. Radiology. 1985;156:681-8. 2. Fulham MJ, Melisi JW, Nishimiya J, Dwyer AJ, Di Chiro G. Neuroimaging of juvenile pilocytic astrocytomas: an enigma. Radiology. 1993;189:221-25.

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CASE 7: RIGHT FALX MENINGIOMA

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B

Figures 1A and B: (A) T1W axial:  A well-defined, hypointense, soild extraaxial mass, 3.2 × 4.0 cm, close to the midline in right frontal region (dotted black arrow). The lesion had broad implantation base on falx cerebri; (B) T1W axial with Gd: homogeneous enhancement with well-defined dural tail. The superior sagittal sinus was separate (thick arrow)

DISCUSSION Meningomas are solid, well-marginated benign lesions originating from the meninges. These tumors account for approximately 20% of adult brain tumors. They occur predominantly in middle-aged patients with a female preponderance. The most common sites of origin include the bilateral convexities, parasagittal regions, parafalcine, sphenoid wing, olfactory groove, and suprasellar region. They uncommonly arise infratentorially (approximately 10%). Most meningomas are homogeneously solid tumors, but there may be on occasion foci of necrosis as well as scarring, cystic degeneration, or calcification. They are generally characterized by isointensity to relative hypointensity on T1-weighted images and slightly increased signal intensity in T2-weighted images. There is relatively little associated vasogenic edema in relationship to the

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MRI Atlas of Cases 65

size of the lesion, likely secondary to its slow-growing nature. PostGadolinium-enhanced MR images demonstrate homogeneously intense enhancement. In addition, the enhancing dural tail may also be identified. Although meningiomas are histologically benign, they may invade surrounding structures including the dura and contiguous bony structures. Meningiomas may produce a hyperostotic reaction. This is a nonspecific finding which may also be produced by metastatic carcinoma. On rare occasions, the meningioma may completely penetrate the calvarium to invade the scalp. Meningiomas are the most common, non-glial, primitive intracranial tumors; their prevalence among operated tumors is around 13–19. The most common locations are: falx and parasagittal (25%), convexity (20%), sphenoid (20%) olfactory groove (10%) suprasellar (10%), posterior fossa (10%), middle fossa (3%) and intraventricular (2%). They uncommonly arise infratentorially (approximately 10%). The most frequent sites for infratentorial meningiomas are: the petrous bone, clivus, foramen magnum, tentorium; extremely rare is an intraventricular meningioma of the fourth ventricle. Meningiomas are readily diagnosed by MR imaging, and most are asymptomatic.

BIBLIOGRAPHY 1. German C Castillo. Imaging in Brain Meningioma, emedicine. medscape. 2. Metwally MYM. Textbook of Neuroimaging: a CD-ROM publication. Metwally, MYM (Ed). WEB-CD agency for electronic publication, version 10.3a July 2009.

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CASE 8: ATYPICAL MENINGIOMA

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B

C

D

Figures 1A to D: (A) T2W axial:  A large isointense mass, expanding the calvarium in the right frontal region and show convex extension of the tumor, both intracranially and extracranially (dotted black arrows); (B) T1W axial:  A large isointense mass, expanding the calvarium in the right frontal region. Such local extension of a meningeal tumor is a atypical feature (black arrows); (C) T2W coronal:  A large isointense mass, expanding the calvarium in the right frontal region. Black lines within the mass indicate flow voids in this vascular tumor. The tumor encroached the right orbit, causing proptosis (arrowheads); (D) T1W axial with contrast study:  Homogeneous dense enhancement with the characteristic dural tail in both anterior and posterior borders prominent bone involvement with marked thickening of the calvaria, as well as extracranial soft-tissue extension (black arrows)

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MRI Atlas of Cases 67

DISCUSSION The most common locations are falx and parasagittal (25%), convexity (20%), sphenoid (20%) olfactory groove (10%) suprasellar (10%), posterior fossa (10%), middle fossa (3%) and intraventricular (2%). The typical features of meningiomas include a unilobar extra-axial mass with sharply circumscribed margins and inward displacement of the cortical gray matter. On precontrast studies, meningiomas are characteristically hypointense to isointense with T1-weighted pulse sequences and isointense to hyperintense with T2-weighted pulse sequences. On MR images obtained with gadolinium, the mass homogeneously enhances with the characteristic dural tail. Feature

Typical

Atypical

– Location

Intracranial only, near the large dural sinuses and skull base where they most commonly occur.

Extracranial extension

–  Typical sites

Cerebral convexity, parasagittal, sphenoid wing, CP angle

Any site

– Age

5-6 decade

Younger

– Sex

Female

Any

–  Signal intensity

Hypo to isotense

Hyper-iso

–  Contrast study

Dense homogeneous

Heterogeneous

–  Calvarial changes

Common

Uncommon

–  Dural tail

Seen in 60% cases

Uncommon

 Atypical site: Sites include the orbit (optic nerve sheath), the paranasal sinus, the choroid plexus (intraventricular), and the diploic space of the calvaria such as (entirely intraosseous)  Atypical imaging features such as large meningeal cysts, hemorrhage marked edema and various metaplastic changes (including fatty transformation)

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68 MRI Brain: Atlas and Text

 Atypical contrast enhancement such as ring enhancement or heterogeneous enhancement  Both intracranial and extracranial extension of meningioma is atypical. Meningiomas are readily diagnosed by MR imaging, and most are asymptomatic atypical meningiomas account for 7.2% of all meningiomas, whereas malignant meningiomas are rare and constitute approximately 2.4%. Malignant and atypical meningiomas are more prone to recurrence and aggressive growth, which increases patient morbidity and mortality. Meningiomas may occasionally have an atypical appearance and atypical enhancement pattern secondary to necrosis, scarring, previous hemorrhage, or fat deposition.

BIBLIOGRAPHY 1. Buetow MP, et al. Typical, atypical, and misleading features in meningioma. Radiographics. 1991;11(6):1087-106.

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CASE 9: MULTIPLE MENINGIOMAS

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B

C

D

Figures 1A to D: (A) T2W axial:  Extra-axial, multiple, round, well-defined hyperintense lesions in right side of calvarium; (B) T1W right parasagittal with Gd:  Multiple, large, contrast-enhancing lesions close to calvarium in parietal region. One lesion is close to tentorium; (C) T2W coronal: Extraaxial, multiple, round, well-defined hyperintense lesions in right side of calvarium, one in intraventricular region; (D) T1W LT parasagittal with Gd: Multiple, large, contrast-enhancing lesions close to calvarium in frontal region

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70 MRI Brain: Atlas and Text

Note: This is 57-year-old female patient. She had nine meningiomas—three in falx cerebri, five in parasagittal and one in intraventricular locations. All were in supratentorial compartment. Largest measured 39 mm and smallest 9 mm. Only five showed dural tail. The patient had no evidence of neurofibromatosis.

DISCUSSION The term multiple meningioma is used to describe the simultaneous or sequential appearance of 2 or more independently situated meningiomas, not necessarily of the same pathologic subtype. However, the current concept is that these tumors are due to inherent multicentricity of the dural foci, possibly influenced by hormonal factors. Multiple spinal meningiomas are rarer than multiple cranial meningiomas. Multiple meningiomas occurring in different neuraxial compartments are distinctly rare. They may occur at any age but have a peak incidence around 45 years of age; 60% occur more commonly in females. Although multiple meningiomas are associated with neurofibromatosis type 2 (central neurofibromatosis), the majonity of patients do not have other characteristic features such as multiple schwannomas. Only 1% are multiple, usually in associated with neurofibromatosis. Multifocal recurrence of aggressive meningiomas may be encountered after resection of an initially solitary lesion.   Though there are various criteria for the diagnosis of NF2, all require either a family history of NF2 or presence of a vestibular schwannoma. Our patient did not have either. Families with multiple meningiomas have been reported, without chromosome 22q deletions. Meningomas are solid, well-marginated benign lesions originating from the meninges. On MRI, meningiomas tend to be isointense to cortex and hypointense to white matter in T1-weighted images; in T2-weighted images meningiomas are again isointense to slightly or markedly hyperintense. Enhancement with gadolinium (Gd) is usually very marked and homogeneous. In addition, enhancing dural tail may also be

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identified. Most meningomas are homogeneously solid tumors, but there may be on occasion foci of necrosis as well as scarring, cystic degeneration, or calcification. There is relatively little associated vasogenic edema in relationship to the size of the lesion, likely secondary to its slow-growing nature. Induction of meningiomas has been reported after both high and low doses of radiation. The latency period in such cases may be as long as 20 years, correlating inversely with radiation dose and directly with patient age at the time of exposure. Radiation-induced meningiomas are typically rapidly growing and aggressive tumors with frequent multiplicity.

BIBLIOGRAPHY 1. Young-Cho Koh, Heon Yoo, et al. Multiple meningiomas of different pathological features: case report. Journal of Clinical Neuroscience. 2001;84:40-4. 2. Zee CS, Chin T, Segall HD, et al. Magnetic resonance imaging of meningiomas. Semin Ultrasound CT MR. 1992;13:154-69.

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CASE 10: HEMANGIOPERICYTOMA

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Figures 1A to D: (A) T2W axial:  A well-defined extra-axial hyperintense mass in left frontoparietal region (black dotted arrow); (B) T1W sagittal: A well-defined extra-axial isointense mass in left frontoparietal region (black dotted arrow); (C) T1W axial:  A well-defined extra-axial isointense mass in left frontoparietal region (black dotted arrow); (D) T1W axial with contrast Gd:  Faint enhancement

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DISCUSSION Hemangiopericytoma of the meninges is an aggressive, highly vascular neoplasm that is commonly grouped with angioblastic or malignant meningiomas. However, hemangiopericytoma of the meninges is a distinct nosologic entity arising from the vascular pericytes rather than from meningothelial cells; thus, it is not a true meningioma at all. Hemangiopericytomas represent less than 1% of all central nervous system tumors. Surgically, hemangiopericytomas are described as well-emarcated masses attached to the dura, and are associated with profuse bleeding on resection. These are aggressive lesions that tend to occur at an earlier age than other meningeal tumors, recur with high frequency, and metastasize extracranially, predominantly to bone, lung, liver, kidney, pancreas, and adrenals. Intracranial hemangiopericytomas are dural-based hypervascular masses similar to meningiomas; however, histologically, they are not meningiomas, and they often have different CT and MR imaging features. Intracranial hemangiopericytomas are rare, extra-axial, multilobulated masses that typically occur in patients in their fourth and fifth decades. Although meningiomas are frequently associated with dural invasion and with development of abnormal vessels, hemangiopericytomas are more aggressive, tend to recur even after gross total resection, and occasionally have extracranial metastases. Unlike meningiomas, which frequently show hyperostosis of adjacent bone and may have intratumoral calcifications on unenhanced CT scans, hemangiopericytomas show bone erosion and lack calcifications and hyperostosis. These tumors generally recur more frequently and earlier than meningiomas, and they have a greater propensity to develop distant metastases. The following features are suggestive (but not pathognomonic) of a meningeal hemangiopericytoma: a multilobulated contour, a narrow dural base or mushroom’shape, large intratumoral vascular

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signal voids on MR images, multiple irregular feeding vessels on angiograms, and bone erosion rather than hyperostosis. Prominent penitumoral edema and increased signal on T2-weighted MR images are more common in the syncytial and the angioblastic meningiomas (a category that includes hemangiopericytoma) than in other types. Young male are affected. No calcification even at histology.

BIBLIOGRAPHY 1. Chiechi MV, Smirniotopoulos JG, Mena H. Intracranial hemangiopericytomas: MR and CT features. AJNR. 1996;17:1365-71. 2. Servo A, Jaaskelainen J, Wahlsrom T, Haltia M. Diagnosis of intracranial hemangiopericytomas with angiography and CTscanning. Neuroradiology. 1985;27:38-43.

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CASE 11: CRANIOPHARYNGIOMA

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Figures 1A to D:  (A) T1W coronal: A large, midline, suprasellar mass (dotted black arrow); (B) T1W sagittal: An intrasellar mass with a large suprasellar component, displacing the midbrain, thalamus (thick arrow); (C and D) T2W coronal:  A large hyperintense suprasellar mass (dotted black arrows)

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DISCUSSION A craniopharyngioma is an epithelially derived hormonally inactive lesion that arises from squamous epithelia rests along the involuted hypophyseal from the remnants of Rathke’s duct.1,2 Craniopharyngioma are lobulated, well-delineated cystic masses generally located in the sella turcica, suprasellar cistern and the third ventricle,2,3 but can be anywhere along the craniopharyngeal duct.4 They vary in size from a few millimeters to several centimeters, but the epicenter is the suprasellar cistern. Three to five percent of intracranial brain tumors are craniopharyngioma and account for 6–9% of intracranial tumors in the 8–12-year-old age group. There is also a type of craniopharyngioma that affects adults ages 40–60 called a papillary craniopharyngioma, but it is much less common.3 Symptoms of a craniopharyngioma are related to the increase in intracranial pressure due to the tumor. They include headache, nausea, vomiting, hormonal imbalances, and visual disturbance.3 Most hormone imbalances (75%) are lack of growth hormone. Forty percent of patients show a discrepancy of luteinizing hormone. Twenty-five percent of patients show a corticotropin or thyroid stimulating hormone deficiency. This is important to diagnose because these patients require perioperative replacement corticosteroids during surgery. The visual disturbance is related to an impingement of the tumor on the optic pathway at the level of the chiasm or optic tracts.1 CT imaging is used to identify a craniopharyngioma and MR imaging is used to determine the location and extent of the tumor.1 In a CT, an adamantinomatous craniopharyngioma will show the characteristic calcification as hyperdense areas. A wpapillary craniopharyngioma will not calcify.4 The cystic regions of the tumor will show as either hypodense or isodense to cerebral spinal fluid depending on the cholesterol content of the cyst.1 The nodular regions and the rims will enhance after contrast. On MRI, the tumor will appear heterogeneous. It is hypointense on T1-weighted and hyperintense on T2-weighted. The increased signal is due to protein and blood components in cystic solution.2

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Treatment of craniopharyngioma is controversial. There have been assertive attempts at total resection, with only moderate results. Limited resection, which carefully avoids damage to adjacent structures, followed by radiotherapy has similar cure rates as total resection but less morbidity.4 For recurrent lesions, surgery is recommended but rather difficult since craniopharyngiomas tend to be well-encapsulated and adherent and possibly invasive into surrounding tissues, such as the hypothalamus (superior), optic chiasm (anterior), pituitary gland (inferior), and elements of the circle of Willis (peripherally).1 Surgery also has a higher mortality rate (30%). Lesions removed by surgery often recur within 5 years of the surgery.3

REFERENCES 1. Zimmerman RA, Bilaniuk LT, Savino PJ. Visual pathways. In: Head and Neck Imaging, 4th edn. Peter M Som, Hugh D (Eds). Curtain. St. Louis: Mosby. 2003.pp.751-2. 2. Osborn AG. Diagnostic Neuroradiology. St. Louis: Mosby, 1994. 3. Lum C, Kucharczyk W, Montanera WJ, Becker, LE. Sella turcica and parasellar region. In: Scott W Atlas (Ed). Magnetic Resonance Imaging of the Brain and Spine, 3rd edn. Atlas. Philadelphia: Lippincott Williams and Wilkins. 2002.pp.1313-8. 4. Sanders WP, Chundi VV. Extra-axial tumors including pituitary and parasellar. In: William W Orrison Jr (Ed). Neuroimaging. Philadelphia: WB Saunders Co. 2002.pp.696-700.

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CASE 12: LEFT GLIOBLASTOMA MULTIFORME

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Figures 1A to D:  (A) T1W axial:  A 54 × 50 mm sized, heterogeneous, hypointense mass in the white matter of the left temporal lobe, extending into the parietal and occipital lobes. There is effacement of the left lateral ventricle (temporal horn and body) and a midline shift to the right, minimal edema; (B) T2 W axial:  Images, the mass is much brighter than the surrounding tissue. The mass appears larger than on T1 because the surrounding edema is also high intensity on T2; (C) T1W axial with gadolinium (Gd):  With contrast medium, there is a thick, irregular ring enhancement; (D) T1W parasagittal with Gd: Irregular thick ring enhancement with marked central necrosis

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DISCUSSION Gliomas are the most common primary tumors of the central nervous system in adults. About 40–50% of primary central nervous system tumors are gliomas. Approximately, 50% of these are glioblastoma multiforme and 7% are astrocytomas. Astrocytic tumors can be divided into grades I–IV, with grade I being the most benign and grade IV being the most malignant. Glioblastoma multiforme refers to a malignant neoplasm with abundant glial pleomorphism. Occurring most commonly in the 5th–7th decades, glioblastoma multiforme usually develops in the cerebral hemispheres (more often in the frontal lobes than the temporal lobes or basal ganglia) but almost never in the cerebellum. It grows as an irregular mass in the white matter and infiltrates the surrounding parenchyma by coursing along white matter tracts, frequently involving the corpus callosum and crossing the midline to produce the characteristic ‘butterfly’ appearance. Conventional MR images are sometimes not adequate to differentiate cystic glioblastomas from brain abscesses. Generally, brain abscesses with their dense and viscous structure exhibit high signal intensity and their apparent diffusion coefficient (ADC) value is low, while cystic brain tumors display low signal intensity on diffusion-weighted images with high ADC values. Brain tumors which contain infected or hemorrhagic material can show similar diffusion-weighted MRI signal properties as abscesses. Differential diagnosis includes glioblastoma multiforme, anaplastic astrocytoma, metastatic tumor, and lymphoma, tuberculoma, or abscess. Metastasis should be considered but is less likely given that the patient is young and has no history of a primary tumor. Metastatic foci are smaller, more peripherally located and often associated with relatively more edema than would be expected for their size. Lymphomas may demonstrate low signals on T2 images (due to high nuclei to cytoplasma ratio) and tend to enhance homogeneously without necrosis. Brain abscess should also be mentioned but it is typically identifiable as a thin, regular rim of enhancement around a central cavity.

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BIBLIOGRAPHY 1. Dahlen R, et al. Supratentorial brain tumors. In: Taveras JM, Ferrucci JT (Eds). Radiology Diagnosis Imaging Intervention. Philadelphia, Lippincott. Vol. 3,1994. 2. Forbes G, et al. Syllabus: Special course in neuroradiology. RSNA. 1994. 3. Hakyemez B, Erdogan C, Yildirim N, Parlak M. Glioblastoma multiforme with atypical diffusion-weighted MR findings. Br J Radiol. 2005;78(935):989-92.

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CASE 13: RIGHT GLIOBLASTOMA MULTIFORME

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Figures 1A to C:  (A) T1W axial: A large ill-defined, hypointense mass in right frontoparietal region. There is mass effect, right lateral ventricle is partly effaced, with mild midline shift; (B) T2W axial: Heterogeneous mass with edema all around. There are cystic areas in the middle of the mass; (C) T1W axial with gadolinium (Gd): The mass shows irregular, incomplete, peripheral contrast enhancement

DISCUSSION Glioblastoma multiforme is the most common and most malignant primary intracranial tumor. It is a type of astrocytoma. Necrosis is the hallmark. Hemorrhage, edema and mass effect are common. Histologic appearance is highly variable. Usually, located in deep cerebral white matter, especially frontal and temporal lobes. They commonly cross the corpus callosum. Worst

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prognosis. Central nervous system (CNS) extension is common including satellite lesions, ependymal and pial extension and subarachnoid and cerebrospinal fluid (CSF) seeding. Imaging features: It can be highly vascular calcification is uncommon, and when present is thought to be related to a pre-existing low grade astrocytoma. MRI T1-weighted images demonstrate a heterogeneous signal mass with central necrosis and marked heterogeneous enhancement. Prominent flow voids and hemorrhage are often present. Occasionally, infiltrating glioblastoma multiformes (GBMs) may have minimal or no enhancement T2-weighted images demonstrate marked hyperintensity representing edema and tumor extension. Neoplastic cells can be found far beyond demonstrable T2 signal abnormalities and enhancing areas. Lesions may be multifocal (microscopic connections to satellite lesions) or multicentric (isolated, separate lesions with no connection). GBMs commonly spread along white matter tracts (corpus callosum, commissures, and capsules) and may seed the CSF resulting in drop metastases to the spine.

BIBLIOGRAPHY 1. Atlas SW. Adult supratentorial tumors. Semin Roentgenol. 1990; 25:130-54. 2. Osborn AG. Diagnostic Neuroradiology. 1994.pp.541-50.

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CASE 14: OPTIC GROOVE MENINGIOMA

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Figures 1A and B:  (A) T2W axial:  A well-defined heterogeneous mass epicentered at left orbital apex, encroaching the orbit, displacing the optic nerve and causing left eye proptosis; (B) T1W axial:  Dense contrast enhancement. The mass medially extends to cavernous sinus, sphenoid sinus

DISCUSSION Meningiomas arise from arachnoid cap cells, and they usually are attached to the dura. These tumors may arise from any location where meninges exist (e.g. nasal cavity, paranasal sinuses, middle ear, mediastinum). The term optic nerve sheath meningioma (ONSM) does not indicate a definite site of origin. ONSM may be either primary or secondary. Primary ONSMs arise from the cap cells of the arachnoid surrounding the intraorbital or, less frequently, the intracanalicular optic nerve. Secondary ONSMs are extensions of intracranial meningioma into the orbit. Secondary ONSMs are much more common than primary ONSMs.

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Like intracranial meningiomas, ONSMs are contrastenhancing lesions. The classic imaging “tram-tracking” sign can be easily visualized and consists of the thickened optic nerve sheath containing the lesion surrounding the nonenhancing, radiolucent optic nerve.1,2 This thickened optic nerve can appear as a calcified nerve sheath on CT images. On coronal views, the tumor demonstrates a doughnut shape, with the dense nerve sheath tumor encircling the optic nerve. Homogeneous, intense enhancement of dural-based masses is characteristic of intracranial meningiomas. Although intracranial tumors as a whole show a higher prevalence in males than in females, meningiomas have a 2:1 female-to-male ratio.3

REFERENCES 1. Lindblom B, Truwit CL, Hoyt WF. Optic nerve sheath meningioma: Definition of intraorbital, intracanalicular, and intracranial components with magnetic resonance imaging. Ophthalmol. 1992;99(4):560-6. 2. Yock DH. Magnetic Resonance Imaging of CNS Disease, 2nd edn. St. Louis, MO: Mosby, 2002. 3. Baser ME, Friedman JM, Wallace AJ, Ramsden RT, Joe H, Evans DJR. Evaluation of clinical diagnostic criteria for neurofibromatosis 2. Neurology. 2002:59(11):1759-65.

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CASE 15: CP ANGLE EPIDERMOID

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Figures 1A to D:  (A) T1W axial:  A hypointense, cystic mass with internal septations. Mass effect on IV ventricle; (B) T1W axial with gadolinium (Gd): Rim enhancement and faint central deputation enhancement; (C) T2W axial:  A hyperintense, cystic mass with internal septations. Mass effect on IV ventricle; (D) T2W coronal:  A hyperintense, cystic mass with internal septations. Mass effect on IV ventricle

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DISCUSSION Epidermoid cysts arise from the inclusion of ectodermal epithelial tissue during neural tube closure in the first week of embryogenesis. They contain desquamated stratified keratinized epithelium. They are the third most common mass lesion to occur within the cerebellopontine angle (CPA) region behind vestibular Schwannomas and meningiomas, accounting for approximately 5% of all CPA masses. Epidermoid cysts have fluid like signal characteristics on spin-echo T1- and T2-weighted sequences; therefore, they appear similar to cerebrospinal fluid (CSF) within the CPA cistern and similar to CSF-containing arachnoid cysts on these sequences. Typical epidermoid cysts do not enhance, and therefore, administration of IV gadolinium does not reliably enable them to be visualized against the background of CSF on T1-weighted images. Although diffusionweighted imaging (DWI) can show clear elevation of signal within an epidermoid cyst and this may be crucial in the postoperative state to confirm the presence of residual tumor, DWI has relatively poor resolution compared with conventional anatomic MRI sequences and cannot depict the margins of the tumor relative to important cisternal structures such as intracranial vessels and cranial nerves. Epidermoid cysts most often show mixed isoto high signal intensity on fluid-attenuated inversion recovery (FLAIR) imaging that differentiates them from arachnoid cysts, which show complete signal suppression due to their CSF content. However, CSF pulsation artifact within the adjacent posterior fossa cisterns may obscure the margins of epidermoid cysts. On MR cisternography, a heavily T2-weighted 3D sequence that depicts cisternal structures in fine detail, epidermoid cysts appear hypointense to CSF with lobulated margins. This allows their precise anatomic relationship to other cisternal structures such as vessels and nerves to be clearly depicted for surgical planning.

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BIBLIOGRAPHY 1. Bonneville F, Sarrazin JL, Marsot-Dupuch K, et al. Unusual lesions of the cerebellopontine angle: a segmental approach. Radiographics. 2001;21:419-38. 2. Tampieri D, Melanson D, Ethier R. MR imaging of epidermoid, cysts. Am J Neuroradiol. 1989;10:351-6.

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CASE 16: DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOR

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Figures 1A to D:  (A) T1W axial image:  An intra-axial hypointense subcortical lesion in the right posterior temporal region; (B) FLAIR axial sequences:  A well-defined, triangular shaped, 4.6 × 2.8 cm hyperintense lesion with typical central bubbly appearance due to small, multiple, cystic lesions divided by thin septa; (C) T2W axial sequences: A welldefined, triangular shaped, 4.6 × 2.8 cm hyperintense lesion with typical central bubbly appearance due to small, multiple, cystic lesions divided by thin septa. There was no mass effect, edema or calcification; (D) T1W axial with contrast:  No contrast  enhancement

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DISCUSSION Daumas-Duport et al. defined   the clinical radiologic criteria of dysembryoplastic neuroepithelial tumor (DNET) as follows: (1) partial seizures, with or without secondary generalization, beginning before the age of 20 years, (2) no neurologic deficit or stable congenital deficit, (3) cortical location of the lesion as best demonstrated by MR imaging, and (4) neither mass effect nor peritumoral edema findings at imaging.1 Diffuse astrocytomas and World Health Organization (WHO) grade-II oligodendrogliomas may in some cases share this neuroradiologic aspect. It is of the utmost importance to distinguish DNETs from gliomas, because DNETs can be cured by surgery alone. This is of particular interest in children because of the highly deleterious effect of adjuvant therapies. The typical neuroimaging findings are often discovered in the work-up of focal epileptic seizures in young patients.2 The other differential diagnosis includes– ganglioglioma, pleomorphic xanthoastrocytoma.

REFERENCES 1. Carla Fernandez, Girard N, Paz PA, Bouvier-Labit C. The usefulness of MR imaging in the diagnosis of dysembryoplastic neuroepithelial tumor in children: A study of 14 cases. Am J Neuroradiol. 2003;24:829-34. 2. Raz E, Tirur R, Kapilamoorthy, Gupta AK, Fiorelli M. Dysembryoplastic neuroepithelial tumor. Radiology. 2012;265: 1317-20.

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CASE 17: PLANUM SPHENOIDALE MENINGIOMA

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Figures 1A to D: (A) T1W sagittal: An isointense mass in suprasellar region, extending anteriorly to sphenoidal wing (dotted black arrow); (B) T1W axial: An isointense mass in suprasellar region, extending anteriorly to sphenoidal wing (dotted black arrow); (C) T1W sagittal with contrast gadolinium (Gd): Homogeneous dense enhancement, with evidence of a dural tail (thick arrow); (D) T1W with axial with contrast (Gd): Homogeneous dense enhancement (arrowhead)

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MRI Atlas of Cases 91

DISCUSSION Meningiomas are the most common nonglial primary tumors of the central nervous system and the most common extra-axial neoplasms, accounting for approximately 15% of all intracranial tumors. They are usually benign neoplasms, with characteristic pathologic and imaging features. They occur predominantly in middle-aged patients with a female preponderance. Meningiomas are solid, well-marginated benign lesions originating from the meninges. The most common sites of origin include the both cerebral convexities, parasagittal regions, parafalcine, sphenoid wing, olfactory groove, and suprasellar region. They uncommonly arise infratentorially (approximately 10%). Most meningiomas are homogeneously solid tumors, but there may be on occasion foci of necrosis as well as scarring, cystic degeneration, or calcification. The magnetic resonance imaging characteristics of meningioma are generally characterized by isointensity to relative hypointensity on T1-weighted images to the contiguous gray matter. T2-weighted images generally demonstrate slightly increased signal intensity in relationship to the contiguous gray matter. There is relatively little associated vasogenic edema in relationship to the size of the lesion, likely secondary to its slow-growing nature. Postgadolinium enhanced MR images demonstrate homogeneously intense enhancement. In addition, the enhancing dural tail may also be identified.

Dural Tail This sign represents thickening and enhancement of the dura mater in continuity with a mass, which on MR images, gives the appearance of a tail arising from the mass. The dural tail is thought to represent reactive change; however, it may also be due to tumor invasion. Three criteria need to be met for a ‘positive’ dural tail sign—the tail should be seen on two successive images through the tumor, it should taper

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away from the tumor, and it must enhance more than the tumor. This sign has been traditionally considered as highly specific for meningioma. However, it is seen only in 60% of meningiomas. Although meningiomas are histologically benign, they may invade surrounding structures including the dura and contiguous bony structures. Meningiomas may produce a hyperostotic reaction. This is a nonspecific finding which may also be produced by metastatic carcinoma. On rare occasions, the meningioma may completely penetrate the calvarium to invade the scalp. Meningiomas may occasionally have an atypical appearance and atypical enhancement pattern secondary to necrosis, scarring, previous hemorrhage, or fat deposition.

BIBLIOGRAPHY 1. German C Castillo. Meningioma Brain: eMedicine, 2007. 2. Preoperative evaluation of a sphenoid ridge meningioma. www.medcyclopaedia.com.

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CASE 18: POSTERIOR CRANIAL FOSSA MENINGIOMA

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Figures 1A to D:  (A) T1W axial:  A large extra-axial mass from right side posterior part of calvarium. The IV ventricle is displaced and obstructed (dotted black arrows); (B) FLAIR-axial: The mass to be hyperintense (thick arrows); (C) T1W axial with gladelinium (Gd): Homogeneous dense enhancement (arrowheads) with the classical dural tail on either side of the lesion (thin arrow); (D) T1W sagittal with Gd: The enhancing mass abutting the tentorium, compressing the brainstem and causing hydrocephalus. The torcula and straight sinuses were free

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94 MRI Brain: Atlas and Text

DISCUSSION Posterior fossa sites account for approximately 10% of meningiomas. Meningiomas arise from the posterior surface of the petrous temporal bone in the cerebellopontine angle (40%), the tentorial leaf and the free margin (30%), the clivus (10%), and the foramen magnum (8%), which are the most common infratentorial locations. Meningiomas of the posterior cranial fossa are difficult to diagnose but, when detected, are often amenable to surgical removal. The posterior fossa meningiomas arise in the following sites: Class I, cerebellar convexity; Class II, tentorium cerebelli; Class III, posterior surface of the petrous portion of the temporal bone (meningiomas of the cerebellopontine angle); Class IV, clivus; Class V, foramen magnum. MRI of the brain demonstrates a large left sided extraaxial posterior fossa mass. It is isointense to the cerebellum on T1- weighted images, and hyperintense on T2. Following contrast administration it vividly and homogeneously enhances. There is no evidence of calcification or hemorrhage, however, it does modestly restrict on diffusion-weighted images (DWI).  Enhance MR scans are useful in detecting small meningiomas that are isointense with adjacent cortex on all pulse sequences. Postcontrast studies can also delineate the precise extent of en plaque lesions. This “en plaque” morphology may be seen alone or in association with spherical components. The superficial location, homogeneous pattern and intense contrast enhancement of the tumor remain characteristic. Sixty percent of meningiomas have a collar of thickened, enhancing tissue that surrounds their dural attachment, called dural tail. In some cases, such thickening correlates with either “en plaque” extension of tumor or the presence of meningiomatous islands surrounding the main lesion. In other cases, dural enhancement near the base of a meningioma represents reactive thickening dura without tumor involvement.

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The dural tail sign is highly suggestive but not specific for meningioma. Other lesions such as Schwannoma, glioblastoma multiforme, and metastases occasionally are associated with a dural tail. Distinguishing an atypical meningioma from a hemangiopericytoma is difficult on imaging. When a large mass such as this invades bone, giving both as a differential is prudent. 

BIBLIOGRAPHY 1. Atlas SW. Magnetic Resonance Imaging of the Brain and Spine, 2nd edn. Lippincott-Raven Publishers. Philadelphia, PA, 1996. 2. Osborne AG. Diagnostic Neuroradiology, 1st edn. Mosby-Year Book, Inc. St. Louis, MO, 1994.

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CASE 19: LOW GRADE GLIOMA

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Figures 1A to D:  (A) T2W axial:  A mass with increased signal intensity (dotted black arrow) compared with normal brain. There is evidence of midline shift; (B) T1W axial:  A mass with decreased signal intensity (thick arrow) compared with normal brain. There is evidence of midline shift; (C) FLAIR-axial:  A mass with increased signal intensity (arrowhead) compared with normal brain. There is evidence of midline shift; (D) T1W axial with Gd: Faint enhancement (dotted black arrow) compared with normal brain. There is evidence of midline shift

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MRI Atlas of Cases 97

DISCUSSION Supratentorial low-grade glioma is a heterogeneous group of brain tumors, accounting for roughly 10–15% of all adult primary intracranial tumor. Low-grade gliomas are uncommon primary brain tumors classified as histologic grades I or II in the World Health Organization (WHO) classification. The most common variants are pilocytic and low-grade astrocytomas, oligodendrogliomas, and mixed oligoastrocytomas located in the cerebral hemispheres. Prognostic factors that predict progression-free and overall survival include young age, pilocytic histology, good Karnofsky performance status, gross total resection, lack of enhancement on imaging. Low-grade astrocytomas are primary tumors (rather than extra-axial or metastatic tumors) of the brain. Astrocytomas are one type of glioma, a tumor that forms from neoplastic transformation of the so-called supporting cells of the brain, the glia or neuroglia. Gliomas arise from the glial cell lineage from which astrocytes, oligodendrocytes, and ependymal cells originate. The corresponding tumors are astrocytomas, oligodendrogliomas, and ependymomas. Grading of a glioma is based on the histopathologic evaluation of surgical specimens. On MRI, low-grade gliomas show decreased signal relative to surrounding brain on T1 sequences. Low-grade (WHO grade II) gliomas, including astrocytoma, oligodendroglioma, and mixed glioma (oligoastrocytoma), account for 10–20% of primary brain tumors inadults. Although such tumors are more indolent than high-grade gliomas, there is considerable variability in their clinical behavior. They are capable of malignant transformation and, ultimately, are almost universally fatal. Pathologically, these tumors are diffuse and infiltrative but lack such an a plastic features as necrosis, endothelial proliferation, and mitotic activity.

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BIBLIOGRAPHY 1. Khalida L, Caroneb M, Dumrongpisutikula N, Imaging characteristics of oligodendrogliomas that predict grade. Am J Neuroradial. 2012;33:852-7. 2. Law M, Yang S, Wang H, et al. Glioma grading: sensitivity, specificity, and predictive values of perfusion MR imaging and proton MR spectroscopic imaging compared with conventional MR imaging. Am J Neuroradiol. 2003;24:1989-98.

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CASE 20: PITUITARY SECRETING MACROADENOMA

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Figures 1A to D:  (A) T1W sagittal: A large isointense intrasellar mass (dotted black arrow) with suprasellar extension (thick arrow). Note the expanded sella turcica. The bright neurohypophyseal signal is displaced posteriorly; (B) T1W coronal:  A large isointense intrasellar mass with suprasellar extension (thick arrow), giving it a typical figure of eight (8) appearance. Note the optic chiasma splaying. There is also a parasellar extension into the right cavernous sinus (thin arrow); (C) T1W sagittal with Gd:  Homogeneous contrast enhancement (dotted black arrow); (D) T1W coronal with Gd: Right internal carotid artery encasement (thin arrow)

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Note: In the clinical setting of amenorrhea and raised prolactin levels, a diagnosis of hyperprolactinemia was done.

DISCUSSION Pituitary masses make-up approximately 10% of all intracranial neoplasms and nearly half of all sellar and juxtasellar masses. Macroadenomas are found twice as often as microadenomas in imaging studies. These masses are more often found in adults, with less than 10% of pituitary neoplasms occurring in children. They occur four to five more often in females than males. Most pituitary adenomas are clinically silent. Three-fourths of all symptomatic cases are due to excessive hormonal secretion. The remaining one-quarter of cases show symptoms of tumoral mass effect including headache, cranial nerve palsy, and cerebrospinal fluid rhinorrhea. Larger tumors may result in displacement of the optic chiasm and visual field defects. Hemorrhage, headache, vomiting, ophthalmoplegia, or visual loss may occur. Pituitary neoplasms are classified according to (a) size and hormonal activity. Microadenomas are masses 10 mm. (b) Types of hormone secreted, e.g. prolactin, growth hormone, etc. The most common secretory macroadenoma is the prolactinoma. Prolactin-producing hypophyseal adenoma (prolactinoma) is the most common functional pituitary adenoma. Its prevalence peaks in women between 20 and 30 years of age. Hyperprolactinemia can be a cause of infertility and is associated with diminished gonadotropin secretion, secondary amenorrhea, and galactorrhea. When a patient is suspected to have hyperprolactinemia not associated with drugs, MR imaging is the foremost and only imaging technique that can depict a pituitary adenoma. Most pituitary adenomas are benign and slow growing. Patients with macroadenomas typically present due to mass

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effect symptoms rather than hormonal excess. The adenoma may extend superiorly and stretch or compress the optic chiasm, compress the infundibulum, or extend laterally into the cavernous sinus. An expanding macroadenoma may also erode the sella turcica. A central constriction or “waist” where the mass narrows to pass through the diaphragma sella produces a “figure 8” sign. Invasion into the cavernous sinus is a poor prognostic sign, as it indicates tumor aggressiveness and predicts a more difficult surgical resection. Tumor may block drainage of interstitial fluid through Virchow-Robin spaces to the subarachnoid space. Distention of Virchow-Robin spaces may result to fluid retention that appears as edematous change along the optic tract. Gadolinium enhanced imaging provides useful presurgical information as to location and size of the adenoma. Recurrence rates after resection are 16% after 8 years and 35% after 20 years. Postsurgical findings may be obscured for 3–4 months due to swelling and inflammation. Bromocriptine therapy is useful in treatment of hyperprolactinemia associated with pituitary microadenoma. Reduction in tumor size can be expected within one week of therapy. MR imaging is useful in monitoring responsiveness to therapy or development of hemorrhage, cyst, or necrosis. It is important to exclude cavernous sinus invasion, as this is a poor prognostic sign. Invasion may be excluded if the normal pituitary gland appears compressed between the tumor and cavernous sinus. If invasion occurs, the tumor appears encase in the internal carotid artery. Uncomplicated macroadenoma is isodense to the pituitary gland on CT and isointense to gray matter on MR images. Macroadenomas are more variable in appearance on NECT and MR images due to necrosis, hemorrhage, or cyst. Complicated cases will appear heterogeneous and demonstrate patches of intense enhancement. Cavernous invasion is possible with superior bulging of the masses through the diaphragm sellae into the supersellar cistern. Sagittal and coronal T1WI may reveal upward growth of tumor and compression of the optic chiasm. Degree of compression is correlated to severity of visual impairment. Edematous changes may appear as high-signal

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along the optic tract on coronal and axial T2-weighted images. These are not present in all cases and are not correlated with visual defects. Pituitary macroadenoma has to be differentiated from meningioma, aneurysm, craniopharyngioma, astrocytoma, etc. With appropriate clinical settings and imaging findings these can be differentiated.

BIBLIOGRAPHY 1. Arita K, Uozumi T, Yano T, et al. MRI visualization of complete bilateral optic nerve involvement by pituitary adenoma: a case report. Neuroradiology. 1993;35:549-50. 2. Ikeda H, Yoshimoto T. Visual disturbances in patients with pituitary adenoma. Acta Neurological Scandinavica. 1995;92:157-60. 3. Saeki Naokatsu, Uchin Yoshio, Murai Hisayuki, et al. MR imaging study of edema-like change along the optic tract in patients with pituitary region tumors. AJNR. 2003;24:336-42.

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CASE 21: JUGULAR FORAMEN SCHWANNOMA

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Figures 1A and B:  (A) T1W axial: Tumor with low signal intensity within the enlarged left jugular foramen. The tumor is well-demarcated with smooth borders. There is cystic component towards the posterior cranial fossa; (B) T1W axial with Gd: The main portion of the tumor is located within the jugular foramen and below the skull base

DISCUSSION Patients often present with symptoms consistent with eighth cranial nerve injury or cerebellar or brainstem compression. Symptoms relating to injury of the ninth or 10th to 12th cranial nerves are less common. Although the clinical presentation of a Schwannoma of the jugular foramen may suggest the presence of a vestibular Schwannoma, appropriate imaging techniques and interpretation should permit correct differentiation of tumor origin. Jugular foramen Schwannoma is a very rare tumor and only very few cases have been reported in the literature. Usually, it is misdiagnosed often as acoustic neuroma and the diagnosis is rarely made peroperatively. It has significant neurological morbidity and mortality jugular foramen tumors are rare skull

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base lesions that present diagnostic and complex management problems. Cranial nerve sheath tumors constitute 5% to 10% of all intracranial neoplasms. They most commonly arise from the vestibular portion of the eighth cranial nerve. A very large vestibular Schwannoma may cause ninth cranial nerve palsy. Schwannomas of the jugular foramen, usually with origin from the ninth nerve, are rare, but the presenting symptoms may be similar to those of a vestibular Schwannoma owing to mass effect by tumor growth in the posterior cranial fossa low T1 signal, high T2 signal, and marked (or moderate) contrast enhancement.

DIFFERENTIAL DIAGNOSIS 1. Meningiomas usually have a lower T2 signal and higher precontrast CT attenuation than do Schwannomas. In addition, they may show calcification and hyperostosis; growth within the jugular foramen and/or below the skull base is unusual. 2. Glomus jugulare. This is a highly vascular tumor, with intense contrast enhancement and, typically, multiple small flow voids (salt and pepper appearance on MR images). The Schwannomas do not show internal flow voids. In contrast to Schwannomas of the jugular foramen, glomus jugulare tumors have enlarged the jugular foramen, produce irregular erosion of the margin of the jugular foramen, with decalcification or destruction of the surrounding bone.

BIBLIOGRAPHY 1. Caldemeyer KS, Mathews VP, Azzarelli B, Smith RR. The jugular foramen: a review of anatomy, masses, and imaging characteristics. Radiographics. 1997;17:1123-39. 2. Eldevik P, Gabrielsen T, Jacobsen E. Imaging findings in schwannomas of the jugular foramen. AJNR. 2000;21:1139-44. 3. Grossman RI, Yousem DM. Neuroradiology: The Requisites. St Louis: Mosby; 1994.pp.68-70.

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CASE 22: CEREBELLAR HEMANGIOBLASTOMA

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C Figures 1A to C:  (A) T1W axial: A large intracerebellar heterogeneous mass (dotted black arrows) displacing the IV ventricle anteriorly (thick arrow); (B) T2W axial: The mass to be hyperintense (dotted black arrows) with many signal voids areas; (C) T1W axial with Gd: Dense enhancement of the intra-axial mass (thin arrows)

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DISCUSSION Hemangioblastoma is a pathologically benign lesion of the central nervous system. This rare tumor is most commonly seen in the cerebellum, however, hemangioblastomas involving the spinal cord have been reported. Other locations, including the supratentorial compartment, optic nerve and peripheral nerves, are extremely rare. The disease is relatively rare in children, and is seen more commonly in adult males between the third and fifth decades. Most cases of hemangioblastomas are sporadic, however, an association between Von Hippel-Lindau (VHL) disease is seen in about 25% of cases. Hence, in patients with hemangioblastomas, abdominal imaging in addition to a complete neural axis imaging is recommended by some to evaluate for additional lesions that may be associated with VHL syndrome. The clinical presentation depends on the location. Intracranial lesions typically present with a long history of minor neurological symptoms, followed by an acute exacerbation that may necessitate emergent surgical intervention. Diagnosis by imaging modality has improved with the introduction of magnetic resonance imaging (MRI). MRI is superior to CT in the diagnosis of posterior fossa hemangioblastoma. This is due to the presence of beam hardening artifacts in the posterior fossa on CT. The imaging findings mirror the gross features of the tumor. Hemangioblastomas are highly vascular tumors with two principal components, i.e. capillaries and stromal cells. The tumor typically consists of an intramural solid nodule with a cystic component (about 60% of all tumors), purely solid tumors are also seen, however, purely cystic tumors are very rare. On T1-weighted images the solid component presents as an isointense intramural nodule. On T2-weighted images, the lesion is isointense. There is usually uniform enhancement of the solid component on postcontrast images.

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Surgery is the preferred treatment modality for the tumor. Surgery may be preceded by Gamma Knife Stereotactic Surgery or endovascular embolization to shrink the tumor or reduce its vascularity.

BIBLIOGRAPHY 1. Georg AE, Lunsford LD, Kondziolka D, Flickinger JC, Maitz A. Hemangioblastoma of the posterior fossa. The role of multimodality treatment. Arq Neuropsiquiatr. 1997;55(2):278-86. 2. Sano T, Horiguchi H. Von Hippel-Lindau disease. Microsc Res Tech. 2003;60:159-64. 3. Sharma RR, Cast IP, O’Brien C. Supratentorial hemangioblastoma not associated with Von Hippel-Lindau complex or polycythemia: case report and review of the literature. Br J Neurosurg. 1995;9(1):81-4.

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CASE 23: CENTRAL NERVOUS SYSTEM LYMPHOMA

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C Figures 1A to C:  (A) T2W axial: A heterogeneous mass involving left side basal ganglia, thalamus, with evidence of midline shift, mass effect. There is mild edema around the mass; (B) FLAIR axial: A heterogeneous mass involving left side basal ganglia, thalamus, with evidence of midline shift, mass effect. There is mild edema around the mass; (C) T1W axial with Gd: Dense enhancement of the solid components

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DISCUSSION The most common location is supratentorial compartment, especially involving frontal and parietal lobes. The lesions are clustered around the ventricles, Gray-white matter junction and often involve corpus callosum. Sometimes they about and extend along the ependymal surface. In T1W images appear heterogeneous from hemorrhage, necros and in T2W images appear homogeneous isointense/hypointense. They show strong homogeneous enhancement. The incidence increases in immunocompromised persons. Differential diagnoses includes toxoplasmosis, glioblastoma multiforme (GBM). Abscess, progressive multifocal leukoencephalopathy (PML), non-Hodgkin lymphoma (NHL).

Glioblastoma Multiforme  Butterfly glioma involving corpus callosum—hemorrhage common.  Enhancement typically heterogeneous—necrosis with ring enhancement in 95%.

Abscess  T2 hypointense rim, diffusion restriction typical—peripheral enhancement with central necrosis.  Enhancement often thinner on ventricular side; MRS: Elevated amino acids in cystic cavity (low TE).

Progressive Multifocal Leukoencephalopathy  White matter T2 hyperintensity, involves subcortical; U-fibers.  May involve corpus callosum typically nonenhancing.

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BIBLIOGRAPHY 1. Koeller KK, et al. Primary central nervous system lymphoma: radiologic-pathologic correlation. Radiographies. 1997;17(6):1497526. 2. Stadnik TW, et al. Diffusion-weighted MR imaging of intracerebral masses: Comparison with conventional MR imaging and histologic findings. AJNR. 2001;22:969-76.

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CASE 24: PITUITARY MICROADENOMA

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Figures 1A to D: (A) T1W coronal: Precontrast image shows a small isointense lesion in pituitary gland; (B) Dynamic imaging:  T1W coronal early phase shows uniform enhancement of rest of pituitary gland, while the microadenoma remains unenhanced (dotted black arrow); (C) T1W sagittal with Gd: Uniform enhancement of rest of pituitary gland, while the microadenoma remains unenhanced; (D) T1W coronal with Gd: Uniform enhancement of rest of pituitary gland, while the microadenoma remains unenhanced

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DISCUSSION Pituitary neoplasms are classified according to size and hormonal activity. Microadenomas are masses 10 mm. Although pituitary microadenomas are much more common than macroadenomas on pathologic examinations, macroadenomas are twice as frequent on imaging studies. Macroadenomas are the single most common suprasellar mass (1/3 to 1/2 of lesions). Intrapituitary lesion that enhances less rapidly than surrounding normal gland. Two-thirds of microadenomas appear hypodense and one-third show early enhancement on CT. Circumscribed, well-demarcated mass surrounded by crescentic rim of compressed anterior pituitary. Most appear hypointense on T1-weighted images and approximately one-half are hyperintense on T2 images. Gadolinium contrast improves sensitivity and specificity for microadenoma as much as 10%. Following IV gadolinium contrast injection in a dynamic MR study, the gland shows early enhancement and the microadenoma stays as a nonenhancing area. Later the gland clears and the microadenoma enhances. Enhanced scans show 70–90% seen as relatively hypointense, more slowly enhancing than normal pituitary. Some: 10–30% can be seen only on dynamic contrast-enhanced scans. Prolactin-secreting = 30-400/0 of symptomatic adenomas. Most microadenomas have lower signal intensity than the normal pituitary gland on T1-weighted images. A convex outline of the pituitary gland or deviation of the pituitary stalk can also be detected. Dynamic study with intravenous bolus injection of contrast medium is the preferred technique for assessing microadenomas, as it allows excellent delineation between the tumor and the normal pituitary gland. In the dynamic study, the normal pituitary gland and stalk show strong enhancement in the early phase of dynamic imaging, whereas microadenomas show relatively weak enhancement.

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BIBLIOGRAPHY 1. Bartynski WS, et al. Dynamic and conventional spin-echo MR of pituitary microlesions. AJNR. 1997;18:965-72. 2. Osborn A. Diagnostic Neuroradiology. St Louis: CV Mosby, 1994. 3. Rand T, et al. Evaluation of pituitary micro-adenomas with dynamic MR imaging. Eur J RadioI. 2002;41:131-5.

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CASE 25: INFRATENTORIAL EPENDYMOMA IN ADULT

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Figures 1A to D:  (A) T2W axial: A 2.5 × 2.9 cm Midline, hyperintense mass arising from fourth ventricle; (B) T2W coronal: Heterogeneous contrast enhancement of the mass; (C) T1W axial with Gd:  The mass also showed extension through exit foramina of Luschka and Magendie which are classical presentation of ependymoma; (D) T1W sagittal with Gd:  The anterior extension of the mass is compressing the brainstem with evidence of obstructive hydrocephalus

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Note: This 48-year-old male was referred for evaluation of symptoms of intracranial hypertension.

DISCUSSION An ependymoma is a glioma derived from differentiated ependymal cells. They therefore occur in a peri/intraventricular location intracranially. They may also arise anywhere along the course of spinal ependyma. Intracranially 60% are infratentorial, and of these the vast majority occur in the fourth ventricle. Typically they present in children less than five. A smaller number appear in 30–40 year-old. The tumors are slow growing and lobulated. They tend to fill the ventricle and can extend out the exiting foramina of Luschka and Magendie. About onehalf will present with calcifications. Often they will be cystic when supratentorial. These tend to be isodense on CT, iso/ hypointense on T1, and iso/hyperintense on T2. Enhancement is heterogeneous and moderate. On precontrast and postcontrast MRI, tumors often appear heterogeneous secondary to necrosis, hemorrhage, and calcification. Prognosis is moderate as many will die from recurrence or progression.

BIBLIOGRAPHY 1. Osborn AG, et al. Diagnostic Imaging Brain, 1st edn. Amirsys Publishers. 2004. 2. Spoto GP, et al. Intracranial ependymoma and subependymoma: MR manifestations. A[NRAm] Neuroradiol. 1990;11:83-91.

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CASE 26: CLASSICAL ACOUSTIC SCHAWANNOMA

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Figures 1A to D:  (A) T1W axial:  An isointense round mass arising from the widened left internal acoustic meatus; (B) T1W axial with Gd: Dense contrast enhancement with the typical ice-cone appearance; (C) T2W coronal:  A hyperintense heterogeneous mass in left cerebellopontine angle; (D) T2W axial:  A 2 × 1.8 cm hyperintense heterogeneous mass in left cerebellopontine angle, widening the cistern

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Note: This is a case of 62 years old female with unilateral hearing loss.

DISCUSSION Acoustic neuromas are intracranial, extra-axial tumors that arise from the Schwann cell sheath investing either the vestibular or cochlear nerve. It is the second most common intracranial extra-axial neoplasm in adults. Acoustic neuromas account for approximately 80% of tumors found within the cerebellopontine angle. The remaining 20% are principally meningiomas. In rare cases, a facial nerve neuroma, vascular tumor, lipoma, or metastatic lesion is found within the cerebellopontine angle. The presence of a homogeneous, small or intermediate-sized tumor in the cerebellopontine angle-cistern, with a tumor component in the internal auditory canal that enhances homogeneously or slightly in homogeneously or: avidly enhancing cylindrical or ice-cream on cone after contrast administration strongly suggests the diagnosis of acoustic Schwannoma. The visualization of the normal seventh and eighth nerve bundles favors the diagnosis of a meningioma. Larger acoustic Schwannomas tend to be more heterogeneous in morphology and signal intensity, owing to the presence of intratumoral cysts, areas of different cellular histology (Antoni type A or type B tissue), calcifications, or regions of hemorrhage. This significant heterogeneity on MR images is more characteristic of acoustic Schwannoma than of meningioma. Other signs are important in the differential diagnosis: a tumor centered at the meatus of the internal auditory canal and/or with an “acute angle” with the petrous bone is more likely to be an acoustic schwannoma, whereas a broad-based, obtuse-angled tumor in contact with the tentonium or with a dural tail sign is more likely to be a meningioma. The dural tail sign is highly suggestive of meningioma, but it is not specific and has recently been described in a case of acoustic Schwannoma.

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The mass will look ovoid to cylindrical. If the lesion is small, it will be intracanalicular, looking like an ovoid to cylindrical mass. A large mass will have a canal component plus a CPA cistern extension. This lesion will look like an ice-cream on cone. The 100% of these lesions enhance strongly. The differential diagnosis for a CPA mass on imaging will be the following: Epidermoid cyst, arachnoid cyst, meningioma, facial nerve Schwannoma, metastasis and lymphoma or an aneurysm.

BIBLIOGRAPHY 1. Osborn AG, et al. Diagnostic Imaging Brain, 1st edn. Amirsys Publishers. 2004. 2. Sperfeld AD. et al. Occurrence and characterization of peripheral nerve involvement in neurofibromatosis type 2. Brain. 2002;125 (Pt 5):996-1004.

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CASE 27: JUXTATENTORIAL MENINGIOMA

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Figures 1A to D:  (A) T2W axial:  A well-defined, midline, oval-shaped, posterior fossa, isointense mass measuring 4.4 × 3.6 × 3.8 cm; (B) T1W sagittal: A mass which has a broad tentorial attachment, juxtaposed around the tentorial incisura, with supratentorial extension measuring 3.6 × 1.9 × 1.6 cm. Note the obstruction at aqueduct of sylvius; (C) T1W sagittal with Gd:  A homogeneous contrast enhancement with dural tail. Note mild compression of the brain stem; (D) T1W coronal with Gd: The contrast enhancement showing a figure-of-eight appearance of this transtentorial meningioma

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Note: This is a 49-year-male referred for evaluation of acute obstructive hydrocephalus which was shunted successfully. Such an uncommon location has not been reported previously to the best of our knowledge.

DISCUSSION Meningiomas account for approximately 20% of all intracranial tumors, with a peak incidence at 45 years, and a 2 : 1 female predominance. Common sites, in descending order of frequency are, convexity adjacent to superior sagittal sinus, sphenoid ridge, cavernous sinus, tentorium, planum sphenoidale, clivus, cerebellopontine angle, optic nerve sheath. In one series, 8.1% of meningiomas arose in the posterior fossa and just oven onethird of posterior fossa meningiomas arose from the tentonium. Although these tumors are relatively rare and are notorious for their ability to escape recognition, clinically, they are benign lesions. Most juxtatentorial lesions may be localized accurately on contrast-enhanced axial section scans by use of the opacified tentorial bands. Lesions that lie lateral edge of the diverging bands are supratentorial. Lesions that lie medial to the V-shaped tentorial bands are infratentorial and/or incisural. Flattening of the tentorial border of a lesion helps to identify its location. Use of the tentorial bands identifies transincisural extension of meningioma reliably, but does distinguish well between true transtentorial growth of meningioma and marked upward bulging of the tentorium from purely infratentorial meningioma.

BIBLIOGRAPHY 1. Buetow MP, Buetow PC, Smirniotopoulos JG. Typical, atypical, and misleading features in meningioma. RadioGraphics. 1991;11: 1087-106. 2. Naidich TP, Leeds NE, Kricheff II. The tentorium in axial section II: lesion localization. Radiology. 1977;123:639-48.

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CASE 28: CONVEXITY MENINGIOMA

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Figures 1A to D: (A) T1W axial:  A large isointense round mass, measuring 8.9 × 6.7 cm in the right cerebral convexity. Note the midline shift and mass effect on the right lateral ventricle. Note the absence of edema; (B) T2W axial: Multiple signal voids indicating increased vascularity. There are focal areas of necrosis in the medial part of the mass; (C) T2W coronal:  Multiple signal voids indicating increased vascularity. Note the broad base of attachment to the calvarium; (D) T1W sagittal with Gd:  Dense contrast enhancement. No perceptible dural tail was seen

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Note: A 27-year-old female, an uncommon age. Patient refused further evaluation for detecting associated neurofibromatosis.

DISCUSSION Meningiomas are the most common nonglial primary tumors of the central nervous system and the most common extra-axial neoplasms. They are usually benign neoplasms, with characteristic pathologic and imaging features. However, there are several important histologic variants of meningioma, and even a histologically typical meningioma can have unusual or misleading radiologic features that may not be suggestive of meningioma. The typical meningioma is a homogeneous, hemispheric, markedly enhancing extra-axial mass located over the cerebral convexity, in the parasagittal region, or arising from the sphenoid wing. Meningiomas may originate in unexpected locations such as the orbit, paranasal sinus, or ventricles or be entirely intraosseous (within the calvaria). Unusual imaging features such as large meningeal cysts, ring enhancement, and various metaplastic changes (including fatty transformation) can be particularly misleading. Because complete surgical resection is the definitive treatment for meningiomas, the single most important feature regarding therapy is tumor location, as it substantially affects surgical accessibility. Meningiomas originate from special meningothelial cells of the arachnoid membrane or the arachnoid granulations. Most meningiomas are spherical masses, with broad implantation on the underlying dura mater. Meningiomas are not invasive, with evidence of a well-delineated interface between the tumor and the brain. Meningiomas are typically highly vascularized. Convexity meningiomas (25%) arising from the dura that overlies the cerebral hemispheres. The falx meningioma or parasagittal meningiomas (25%), arising from the falx cerebri.

BIBLIOGRAPHY 1. Osborn AG, et al. Diagnostic Imaging Brain, 1st edn. Amirsys Publishers. 2004. 2. Takeguchi T, et al. The dural tail of intracranial meningiomas on fluidattenuated inversion-recovery images. Neuroradiol. 2004;146:130-5.

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CASE 29: BENIGN GLIOMA

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Figures 1A to D:  (A) T1W axial:  A well-defined hypointense lesion in right parietal region; (B) T2W axial:  Increased signal intensity. The lesion measured 32 × 26 mm, with well-defined borders, no edema, no mass effect, and no calcification; (C) DWI:  Increased signal intensity indicating water movement restriction within the lesion; (D) T1W axial with Gd: No contrast enhancement

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Note: A 42-years-old female was referred for evaluation of seizures.

DISCUSSION Low-grade astrocytomas are primary tumors (rather than extra-axial or metastatic tumors) of the brain. Astrocytomas are one type of glioma, a tumor that forms from neoplastic transformation of the so-called supporting cells of the brain, the glia or neuroglia. Gliomas arise from the glial cell lineage from which astrocytes, oligodendrocytes, and ependymal cells originate. The corresponding tumors are astrocytomas, oligodendrogliomas, and ependymomas. Grading of a glioma is based on the histopathologic evaluation of surgical specimens. Several classification schemes have been proposed. Vast majority of gliomas in adults are supratentorial, while in children they are infratentorial. The peak age incidence is between 20–50 years. Both CT scan and MRI can aid in the diagnosis of low-grade glioma. Typical CT findings of a low-grade glioma show lower attenuation than the surrounding brain. A mild-mass effect may be noted. Obstructive hydrocephalus can be confirmed. Low-grade gliomas also may show evidence of calcification. If a contrast CT scan is obtained, the tumor usually does not enhance. On MRI, low-grade gliomas show decreased signal relative to surrounding brain on T1 sequences. On T2 sequences, higher signal reflects both the tumor and surrounding edema. Pilocytic astrocytomas often are associated with a cyst, which may be particularly prominent on T2-weighted sequences.

BIBLIOGRAPHY 1. George Jallo, Ethan A Benardete. Low-grade Astrocytoma. e-Medicine, Jan 10, 2007. 2. Recht LD, Bernstein M. Low-grade gliomas. Neurol Clin. 1995; 13(4):847-59.

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CASE 30: CRANIOPHARYNGIOMA IN ADULT

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Figures 1A to D:  (A) T1W axial: A well-defined, hyperintense suprasellar mass; (B) T2W axial:  A hypointense suprasellar mass measuring 36 × 29 mm; (C) T1W sagittal: A hyperintense suprasellar mass with evidence of hydrocephalus; (D) T2W coronal: A hypointense suprasellar mass with evidence of hydrocephalus

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Note: A 63-year-old male was referred for evaluation of chronic headache. His MR images showed a well-defined, midline TI, with evidence of obstructive hydrocephalus. The lesion was hypointense in T2W, FLAIR, DWI sequences. There was no contrast enhancement. His CT scan (not shown) showed dense calcific focus in superior aspect of the mass. The other differential considered were dermoid, epidermoid, and Rathke’s cyst.

DISCUSSION Craniopharyngioma is a histologically benign, extra-axial, slow-growing tumor that predominantly involves the sella and suprasellar space. Despite its histologic appearance, craniopharyngiomas occasionally behave like malignant tumors. Craniopharyngiomas are dysodontogenic epithelial tumors derived from the Rathke’s cleft, which is the embryonal precursor to the adenohypophysis. The craniopharyngeal duct is the embryonal structure along which the eventual adenohypophysis and infundibulum migrate. Tumors can occur anywhere along the course of this duct from the pharynx to the sella turcica and third ventricle, which partially explains the location of the tumor (see Anatomy). The trigger for tumor growth is not clear. Three distinct subtypes have been distinguished on the basis of histologic appearance: adamantinomatous, papillary, and mixed. Regarding adamantinomatous tumor (pediatric type), the classic and most common appearance is that of a cystic tumor, usually with a solid component. The classic appearance of the papillary variant (adult type) is different from that of the other. A bimodal age distribution is seen, with the first peak occurring in childhood and early adolescence, predominately at age 5–10 years. The second peak (for papillary types) occurs at age 40–60 years. Craniopharyngiomas are classified into 3 groups: sellar, prechiasmatic, and retrochiasmatic. The adamantinous craniopharyngioma is a mixed solid-cystic or mainly cystic lobulated suprasellar or intrasellar/suprasellar tumor occurring in children and adults, typically with large nonenhancing hyperintense cysts on T1-weighted images. The squamous-

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papillary craniopharyngioma is a predominantly solid or mixed solid-cystic suprasellar tumor occurring in adults, appearing as a hypointense cyst on noncontrast T1-weighted images. Calcifications and recurrent tumors are more often observed in adamantinous tumors but can be seen in squamous-papillary tumors as well. Statistically significant parameters useful for differentiating the two tumor subtypes are the encasement of vessels, the lobulated shape, and the presence of hyperintense cysts in adamantinous tumors, and the round shape, the presence of hypointense cysts, and the predominantly solid appearance in squamous-papillary tumors.

BIBLIOGRAPHY 1. Sartoretti-Schefer S, Wichmann W, Aguzzi A, Valavanis A. MR differentiation of adamantinous and squamous-papillary craniopharyngiomas. Am J Neuroradiol. 1997; 18:77-87.

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CASES (31–49): CONGENITAL LESIONS CASE 31: SCHIZENCEPHALY: CLOSED LIP TYPE

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C Figures 1A to C: (A) T2W axial: Right side cortical hyperintensity (dotted black arrow) and a nipple like extension of right side (black arrow) ventricle indicating closed lip schizencephaly; (B) T2W axial:  At a lower level shows right side cortical hyperintensity and a nipple like extension of right side ventricle indicating closed lip schizencephaly; (C) T1W axial: Right side cortical hypor intensity and a nipple like extension of right side ventricle indicating closed lip schizencephaly

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MRI Atlas of Cases 129

DISCUSSION Schizencephaly is a congenital brain malformation characterized by clefts extending from pial surface of cerebral mantle to ventricle. In MRI, a cleft is seen coursing from the ventricular ependyma to the pial surface of the brain. The inner surface of the cleft is pia-lined and communicates with the ependyma of the ventricle. There is deformity of ventricle at site of closed-lip Schiz points to cleft. The septum pellucidum absent, partially deficient, or present. Regarding the gray matter there is Infolding of gray matter along transmantle clefts, gray matter may be nodular, pachy or polygyric or heterotopic type. Schizencephaly is a neuronal migrational disorder with clefts between ventricles and subarachnoid space and, therefore no gliosis. The lips of the cleft may be apposed (closed-lipped, Type I) or gaping (open-lipped, Type II). The closed-lipped variety may be missed if the clefts are tightly apposed, but a dimple at the ventricle-cleft interface should suggest the diagnosis. The clefts are usually seen in the supratentorial space (near the sylvian fissure) coursing to the lateral ventricles and occurs most commonly in the frontal (44%), frontoparietal (30%), and occipital (19%) lobes. Bilateral involvement (35–67%) is associated with seizures, worse developmental delay, and developmental dysphasia. Motor dysfunction.

BIBLIOGRAPHY 1. Hayashi N, et al. Morphological features and associated anomalies of schizencephaly in the clinical population: Detailed analyis of MR images. Neuroradiology. 2002;44(5):418-27.

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CASE 32: SCHIZENCEPHALY: OPEN LIP TYPE

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Figures 1A to D: (A) T2W axial:  A large cleft (dotted black arrow) in left cerebral cortex. The cleft is lined by ependymal cells. Note also the absent septum pellucidum; (B) T1W axial:  A large cleft in left cerebral cortex. The cleft is lined by ependymal cells. Note also the absent septum pellucidum; (C) FLAIR axial:  A large cleft in left cerebral cortex. The cleft is lined by ependymal cells. Note also the absent septum pellucidum; (D) T2W coronal:  A large cleft in left cerebral cortex. The cleft is lined by ependymal cells. Note also the absent septum pellucidum (thick arrow)

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MRI Atlas of Cases 131

DISCUSSION Schizencephaly is a neuronal migrational disorder with clefts between ventricles and subarachnoid space and therefore no gliosis. The lips of the cleft may be apposed (closed-lipped, Type I) or gaping (open-lipped, Type II). If it is unilateral, clinical presentation may be seizures or motor deficit ‘congenital’ hemiparesis. If it is bilateral clinical presentation may be hemi or quadriparesis, microcephaly or hydrocephalus, spasticity, severe developmental delays, mental retardation (MR) is the differential point in this lesion and distinguishes it from encephalomalacic abnormalities (porencephaly), which are usually lined by white matter. The inner surface of the cleft is pia-lined and communicates with the ependyma of the ventricle, which differentiates the lesion from an enlarged Sylvian fissure seen in premature infants.

BIBILOGRAPHY 1. Hayashi N, et al. Morphological features and associated anomalies of schizencephaly in the clinical population: Detailed analyis of MR images. Neuroradiol. 2002;44(5):418-427. 2. Osborn AG, et al. Diagnostic Imaging Brain, 1st edn. Amirsys Publishers. 2004.

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CASE 33: DYSGENESIS OF CORPUS CALLOSUM AND ASSOCIATED LIPOMA

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Figures 1A to D: (A) T1W axial:  Parallel lateral ventricles, dilated posterior part of the lateral ventricles (dotted black arrow) (colpocephaly), linear hyperintense, midline foci with intraventricular extension; (B) T1W axial:  Flower shaped midline hyperintense (arrow) mass, dilated posterior part of the ventricles (colpocephaly) with intraventricular extension; (C) T1W sagittal: Flower shaped midline hyperintense foci. Note the absence of corpus callosum (arrow). (D) T1W coronal: Flower shaped midline hyperintense mass. Note the displaced anterior cerebral artery branches (arrowhead)

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MRI Atlas of Cases 133

DISCUSSION Intracranial lipomas are very rare tumors. They may constitute 0.1% of all intracranial tumors. The pathogenesis of corpus callosum lipoma is controversial. Lipomas are variously considered to be derivative of embryological meninx primitive, or hyperplasia of leptomeningeal fat cells. Corpus callosum lipoma can be an isolated anomaly or associated with other anomalies such as agenesis of corpus callosum, Chiari II, interhemispheric cyst, or migrational anomalies. The most common location of intracranial lipoma is the corpus callosum. Other common locations are quadrigeminal cistern, cerebellopontine angle cistern, and choroid plexus region. Agenesis of the corpus callosum is one of the more common congenital abnormalities (occurring in 0.7% of all births). Patients with this anomaly often present with refractile seizures or mental retardation. If the splenium is absent, colpocephaly, dilation of the occipital horns of the lateral ventricles caused by a decrease in the posterior white matter mass, is seen. With complete agenesis, a high-riding, posteriorly oriented, dilated third ventricle; parallel and widely spaced orientation of the lateral ventricles; and impression on the medial aspect of the lateral ventricles because of probst bundles are seen. The MR is superior to computed tomography (CT) as it can diagnose associated structural anomalies also. Sagittal MR image depicts the corpus callosum in great anatomical detail. MR shows hyperintense mass on T1 and T2-weighted images. No enhancement is seen in postcontrast images.

FINDINGS IN AGENESIS OF CORPUS CALLOSUM  Colpocephaly  High-riding enlarged third ventricle  Incomplete development of hippocampal formation  Interhemispheric cyst or lipoma  Medial impingement of Probst bundle on ventricles  Missing some parts of corpus callosum

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134 MRI Brain: Atlas and Text

 No cingulate sulcus with radially oriented fissures (eversion of cingulate gyrus) into the high-riding third ventricle  Pointed, crescent-shaped frontal horns  Septum pellucidum absent or widely separated.

BIBLIOGRAPHY 1. Georgy BA, Hesselink JR, Jernigan TL. MR imaging of the corpus callosum. AJR. 1993;160(5):949-55. 2. Rubio G, Garcia Guijo C, Mallada JJ. MR and CT diagnosis of intracranial lipoma. AJR. 1991;157(4):887-8.

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CASE 34: LIPOMA OF CORPUS CALLOSUM

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Figures 1A to D: (A and B) T1W sagittal: Normally formed corpus callosum. There is a curvilinear, comma shaped hyperintense foci (dotted black arrow) in the splenium of the corpus callosum, in midline. Normal corpus callosum; (C and D) T1W axial:  Normally formed corpus callosum and ventricular size. There is a linear hyperintense midline focus in the splenium of the corpus callosum, normal ventricles

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136 MRI Brain: Atlas and Text

DISCUSSION Brain lipomas are not hamartomas or true neoplasms. They are congenital malformations representing persistence and maldifferentiation of the meninx primitiva (a mesenchymal neural crest derivative which forms part of the dura, arachnoid, subarachnoid cisterns, and the pia). Greater than 50% are associated with other specific brain malformations. The incidence is rare representing only 1–5% of brain tumors. There are 2 main subtypes: 1. Tubulonodular: Large, bulky, round or cylindrical mass with high incidence of corpus callosum dysgenesis, frontal lobe anomalies and cephaloceles. 2. Curvilinear: Thin lesions which curve around the splenium. 80–95% of the time the lipomas are midline. 50% are dorsal and pericallosal. Other locations include the quadrigeminal, ambient, suprasellar and cerebellopontine cisterns. A lipoma can be associated with agenesis or dysgenesis of the corpus callosum.

DIFFERENTIAL DIAGNOSIS OF HYPERINTENSE FOCI IN T1W-IMAGES  Fat, lipoma  Old hemorrhage  Contrast agent, gadolinium (Gd)  High protein content  Melanin  Cholesterol.

BIBLIOGRAPHY 1. Gaskin CM, et al. Lipomas, lipoma variants, and well-differentiated liposarcomas (atypical lipomas). AJR. 2004;182:733-9. 2. Ickowitz V, et al. Prenatal diagnosis and postnatal follow-up of peri callosal lipoma: Report of seven new cases. AJNR. 2001;22:767-72.

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CASE 35: TYPE 1 CHIARI MALFORMATION

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Figures 1A and B: (A) T1W sagittal:  Cerebellar tonsillar herniation (dotted black arrow), up to C2 level well below the foramen magnum. Note also the kinking of the medullary-cervical cord junction. Note the typical peg shaped appearance of the herniated tonsil; (B) T2W sagittal: Cerebellar tonsillar herniation, up to C2 level well below the foramen magnum. Note also the kinking of the medullary-cervical cord junction (thick arrow). Note the typical peg shaped appearance of the herniated tonsil

DISCUSSION This is the mildest of the hindbrain malformations and is characterized by displacement of deformed cerebellar tonsils more than 5 mm caudally through the foramen magnum. The brainstem and 4th ventricle retain a relatively normal position although the 4th ventricle may be small and slightly distorted. The Chiari Type I is characterized by caudal (inferior) protrusion of ‘peg-shaped’ cerebellar tonsils below foramen magnum. In MRI T1W sagittal image shows pointed, triangular-shaped (peg-like) cerebellar tonsils more than 5 mm below foramen magnum, with surrounding CSF in foramen magnum effacement. There is also short clivus, apparent descent 4th ventricle, medulla. The T2W sagittal image may shows cervical cord syringomyelia.

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138 MRI Brain: Atlas and Text

Sometimes tonsillar impaction in FM without caudal herniation can also be symptomatic. There may be absent cisterna magna, posteriorly angled odontoid with compressed brainstem, short posterior arch C1. Low tonsils with normal rounded shape are usually asymptomatic. Staging, grading or classification criteria: I = asymptomatic: 14–50%, treatment controversial II = brainstem compression III = hydrosyringomyelia Associated with: Syringohydromyelia (20–30%), hydrocephalus (25–44%), malformation of skull base + cervical spine: basilar impression (25%), craniovertebral fusion (occipitalization of C1 10%, incomplete ossification of C1-ring 5%), Klippel-Feil anomaly (10%), platybasia—benign cerebellar ectopia 5 mm clinical symptoms likely. Chiari I. Other finding seen include:  10% congenital tonsilar ectopia, present as adults  12 mm always symptomatic  Syrinx—seen in 50%, 90% if symptomatic  Hydromyelia—fluid distention of central canal  Syringomyelia—cerebrospinal (CSF) dissected into paracentral cavity  Skull base anomalies—25%, platybasia, basilar invagination  Atlanto-occipital fusion, fused cervical vertebrae (Klippel-Feil).

BIBLIOGRAPHY 1. Greenlee JD, et al. Chiari 1 malformation in the very young child: The spectrum of presentations and experience in 31 children under age 6 years. Pediatrics. 2002;110(6):1212-9.

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CASE 36: TYPE 1 CHIARI MALFORMATION WITH SYRINX 1

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Figures 1A and B: (A) T2W sagittal: Cerebellar tonsillar herniation, well below the foramen magnum. There is a hyperintense linear foci (dotted black arrow) in the middle of the cervical cord, suggesting a syringomyelia. Note the typical peg-shaped appearance of the herniated tonsil; (B) T1W sagittal: Cerebellar tonsillar herniation, well below the foramen magnum. There is a hypointense linear foci (thick arrow) in the middle of the cervical cord, suggesting a syringomyelia

DISCUSSION In its pure form, a Chiari I malformation shows tonsils down to the C1–C2 region but with normal brainstem location. The incidence of cervical syringohydromyelia in these flagrant cases has been reported to be between 20% and 73% and the incidence of syringomyelia in symptomatic patients with Chiari I malformations and tonsillar herniation greater than 5 mm is reported to be 53% in the surgical literature. No hydrocephalus is present, and the fourth ventricle is normal in location. There is an association with Klippel-Feil syndrome (C2–C3 fusion), short clivus, odontoid or C1 abnormalities, compression of CSF spaces posterior and lateral to the cerebellum, and reduced height of the supraocciput.

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140 MRI Brain: Atlas and Text

BIBLIOGRAPHY 1. Loder RT, et al. Sagittal profiles of the spine in scoliosis associated with an Arnold-Chiari malformation (type 1) with or without syringomyelia. J Pediatr Orthop. 2002;22(4):483-91.

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CASE 36A: TYPE 1 CHIARI MALFORMATION WITH SYRINX 2

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Figures 1A to D:  (A) T2W sagittal: Cerebellar tonsillar herniation through foramen magnum, syringomyelia of cervicothoracic cord, mild cerebellar atrophy, tectal beaking; (B) T1W coronal: Cerebellar tonsillar herniation through foramen magnum; (C) T2W sagittal-zoomed: Cerebellar tonsillar herniation through foramen magnum, syringomyelia of cervicothoracic cord, mild cerebellar atrophy, tectal beaking; (D) T2W axial: A large syrinx occupying central 2/3rds of cervical cord

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142 MRI Brain: Atlas and Text

DISCUSSION Dr Hans Chiari first described three hindbrain disorders associated with hydrocephalus in 1891. They have neither an anatomical nor embryological correlation with each other, but they all involve the cerebellum and spinal cord and are thought to belong to the group of abnormalities that result from failure of normal dorsal induction. These include neural tube defects, cephaloceles, and spinal dysraphic abnormalities. Symptoms range from headache, sensory changes, vertigo, limb weakness, ataxia and imbalance to hearing loss. Only those with a type I Chiari malformation may be born grossly normal. The abnormalities are best shown on midline sagittal T1-weighted magnetic resonance imaging (MRI), but suspicious features on routine axial computed tomographic brain scans (an abnormal IVth ventricle, a ‘full’ foramen magnum, and absent cisterna magna) should be recognized and followed up with MRI.

BIBLIOGRAPHY 1. Donald M Hadley. The chiari malformations. J Neurol Neurosurg Psych. 2002;72:ii38-ii40.

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CASE 37: CLASSIC ARACHNOID CYST

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Figures 1A to D:  (A) T1W axial:  A well-defined hypointense area (dotted black arrow) in the right side of the middle cranial fossa. Note the signal intensity is similar to that of adjacent CSF in insular cistern; (B) T2W axial: A well-defined hyperintense area (thick arrow) in the right side of the middle cranial fossa. Note the signal intensity is similar to that of adjacent CSF in insular cistern; (C) FLAIR axial:  A well-defined hypointense (dotted white arrow) area in the right side of the middle cranial fossa. Note the signal intensity is similar to that of adjacent CSF in insular cistern. There is no suppression of signal intensity; (D) DWI axial: A well-defined hyperintense (arrowhead) area in the right side of the middle cranial fossa. Note the signal intensity is similar to that of adjacent CSF in insular cistern

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144 MRI Brain: Atlas and Text

DISCUSSION Arachnoid cysts are benign, congenital, intra-arachnoidal spaceoccupying lesions that are filled with clear cerebrospinal fluid (CSF). They usually do not communicate with the ventricular system. The cysts tend to be unilocular, smoothly marginated expansile lesions that are moulded by the surrounding structures. They are common, representing 1% of all intracranial masses. Most arachnoid cysts are supratentorial. About 50–60% are found in the middle cranial fossa, anterior to the temporal lobes. Other locations include the suprasellar cistern and posterior fossa (10%), where they occur most commonly in the cerebellopontine angle cistern. Less common locations are within the interhemispheric fissure; over the cerebral convexity; or in the choroidal fissure, cisterna magna, quadrigeminal cistern, and the vermian fissures. The most difficult lesion to distinguish from the arachnoid cyst is an epidermoid cyst. Epidermoid cysts can appear nearly identical to CSF on CT scans. On MR images, epidermoid cysts appear arachnoid cysts typically suppress completely on fluidattenuated inversion recovery (FLAIR) images and do not restrict on diffusion-weighted images. Arachnoid cysts displace adjacent arteries and cranial nerves rather than engulf them, as epidermoid cysts often do.

ESSENTIAL DIAGNOSTIC FEATURES OF CLASSIC ARACHNOID CYST 1. Sharply demarcated extra-axial cystic mass. 2. These displace adjacent brain parenchyma-mass effect. 3. Adjacent skull bone may show scalloping, indicating long duration of mass. 4. The classic arachnoid cyst has no identifiable internal architecture and does not enhance.

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MRI Atlas of Cases 145

5. The classic arachnoid cyst typically has the same signal intensity as CSF at all sequences. T1W, T2W, PD, FLAIR, DWI, ADC. 6. The typical site is middle cranial fossa.

BIBLIOGRAPHY 1. Flodmark O. Neuroradiology of selected disorders of the meninges, calvarium and venous sinuses. AJNR. 199213:483-91. 2. Weiner SN, et al. MR imaging of intracranial arachnoid cysts. JCAT. 1987;11:236-41.

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CASE 38: ARACHNOID CYST: POSTERIOR CRANIAL FOSSA

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Figures 1A to D: (A) T2W axial: A well-defined cystic lesion, with hyperintense signal, in right side of the cerebellum (dotted black arrow). The fourth ventricle is deformed and displaced (thick arrow); (B) T1W axial: A well-defined cystic lesion, with hypointense signal, in right side of the cerebellum (dotted black arrow). The fourth ventricle is deformed and displaced (thick arrow); (C) FLAIR axial: A well-defined cystic lesion, with hypointense signal, in right side of the cerebellum (dotted black arrow). The fourth ventricle is deformed and displaced (thick arrow). The signal drop out is similar to that of CSF elsewhere; (D) DWI axial: High signal intensity (arrowhead), because there is restriction of water movement. The signal increase is similar to that of CSF elsewhere

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MRI Atlas of Cases 147

DISCUSSION Cystic or cyst-like malformations of the posterior fossa represent a spectrum of disorders, including the Dandy-Walker malformation, vermian-cerebellar hypoplasia, mega cisterna magna, and arachnoid cyst. Differentiation of these lesions may be difficult with routine cross-sectional imaging; however, an accurate diagnosis is essential for proper treatment planning and genetic counseling. Dandy-Walker malformation is easily diagnosed on the basis of the classic triad: complete or partial agenesis of the vermis, cystic dilatation of the fourth ventricle, and enlarged posterior fossa. Vermian-cerebellar hypoplasia is a general classification that describes congenital malformations with a normal-sized posterior fossa, varying degrees of vermian and cerebellar hypoplasia, and a prominent retrocerebellar cerebrospinal fluid space that communicates freely with a normal or dilated fourth ventricle. Mega cisterna magna can be asymmetric and can manifest apparent mass effect, simulating the appearance of an arachnoid cyst; therefore, ventriculography or cisternography may be needed to demonstrate communication of the cystic mass with the subarachnoid space. A careful review of the embryologic development is essential in understanding these malformations and in making a more accurate radiologic diagnosis.

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148 MRI Brain: Atlas and Text

DIFFERENTIAL DIAGNOSIS OF COMMON CYSTIC LESIONS IN POSTERIOR CRANIAL FOSSA Features

Arachnoid cyst

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Isointense to CSF on all sequences

Vein location

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Mass effect Bone remodeling

Positive Present

Sulci

Flattened

Intrathecal contrast DWI Ca**/Fat

Delayed opacification Dark (–/–)

Hyperintense on FLAIR, slightly hyperintense to CSF on T1 Nondisplaced; epidermoids envelop vascular structures Positive Intradural epidermoids slowly remodel bone; intradiploic epidermoids have beveled edges Grows into sulcul space Outlines mass Bright (±/±)

Widened CSF spaces as a result of atrophy* Isointense to CSF on all sequences

Coursing through CSF

Negative Absent

Enlarged Immediate opacification Dark (–/–)

BIBLIOGRAPHY 1. Kollias SS, Ball WS, Prenger Jr EC. Cystic malformations of the posterior fossa: differential diagnosis clarified through embryologic analysis, RadioGraphics. 1993;13:1211-31.

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CASE 39: CRANIOVERTEBRAL JUNCTION ANOMALY: BASILAR INVAGINATION FOSSA

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Figures 1A and B:  (A) T1W sagittal: The cervical vertebrae (dotted black arrow) has invaginated into the foramen magnum. Note the enlarged clivus kinking of the cervicomedullary junction; (B) T1W sagittal with Gd: Cervical vertebrae has invaginated into the foramen magnum. Note the enlarged clivus (thick arrow) kinking of the cervicomedullary junction (thin arrow)

DISCUSSION Basilar invagination is a craniocervical junction  abnormality where the tip of the odontoid process projects above the foramen magnum. It  may be  congenital or acquired (also termed basilar impression) and is often associated with platybasia. There  is  stenosis of the foramen magnum and compression of the medulla oblongata resulting in neurological symptoms, obstructive hydrocephalus, syringomyelia. Both of these terms basilar invagination and basilar impression are often used interchangeably because in both cases there is

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150 MRI Brain: Atlas and Text

upwards migration of the upper cervical spine, but precisely, basilar impression is defined as upward displacement of vertebral elements into the normal foramen magnum with normal bone, while basilar invagination is a similar displacement due to softening of bones at the base of the skull. Thus, different terms are used according to whether bone is normal or not. Basilar invagination is abnormally high position of vertebral column prolapsing into skull base. Basilar invagination refers to upward protrusion of the odontoid process into the infratentorial space. Two lines must be drawn: (1) McGregor’s line, extending from the posterior margin of the hard palate to the undersurface of the occiput, and (2) Chamberlain’s line, from the hard palate to the opisthion (the midportion of the posterior margin of the foramen magnum). If the dens extends more than 5 mm (or half its height) above these lines, basilar invagination is present. There are two types: A. Primary—congenital bone defect in occipitocervical junction.  Occipitocervical bone defect – Atlanto-occipital assimilation (“Occipitalization “). – Atlantoaxial dislocation. – Stenosis or deformity of the foramen magnum. – Incomplete fusion of the posterior arch of the atlas. – Fusion of cervical vertebrae or syndrome Klippel-Feil. – Basiocciput hypoplasia. B. Secondary—Known as basilar impression  Generalized as in osteopenia. Osteomalacia, Paget disease and hyperparathyroidism.  Osteogenesis imperfecta, cretinism, achondroplasia, osteopetrosis, mucopolysaccharidoses.  Localized as in local bone destruction. Tumor or infection. Trauma

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MRI Atlas of Cases 151

Some Useful Anatomic Landmarks in Skull Lateral Image

Thick black arrow line is McGregor line

BIBLIOGRAPHY 1. Goel A, Bhatjiwale M, Desai K. Basilar invagination: a study based on 190 surgically treated patients. J Neurosurg. 1998;88(6):962-8. 2. Samimi SS, Lesley WS. Craniocervical CT and MR imaging of Schwartz-Jampel syndrome. Am J Neuroradiol. 2003;24(8):1694-6.

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CASE 40: CLASSIC COLLOID CYST

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Figures 1A and B: (A) T1W axial: A well-defined, round, midline, hyperintense (dotted black arrow) mass at the level of the foramen of Monro; (B) T2W axial: A well-defined, round, midline, isointense (thick arrow) mass at the level of the foramen of Monro

DISCUSSION It is a benign lesion, buy in a dangerous location. Colloid cysts are benign mucin-containing cysts and account for 0.5–1% of primary brain tumors and 15–20% of intraventricular masses, without any sex predilection. More than 99% are found wedged in the foramen of Monro. The cysts are typically attached to the anterosuperior portion of the third ventricular roof. The pillars of the fornix straddle the cyst. The posterior aspect of the frontal horns is often splayed laterally. Rarely, cysts are found at other sites, including the lateral ventricles, cerebellar parenchyma, and various extra-axial locations. Even relatively small colloid cysts may produce sudden acute hydrocephalus. Occasionally brain herniation with rapid clinical deterioration and even death ensue. The best diagnostic clue to a colloid cyst is its location at the foramen of Monro. The classic colloid cyst appears as a

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MRI Atlas of Cases 153

well-delineated hyperattenuated mass on nonenhanced CT scans. Attenuation correlates inversely with hydration state. On T1weighted MR images, two-thirds of colloid cysts are hyperintense. The majority are isointense to brain on T2-weighted images. The imaging appearance of a colloid cyst is almost pathognomonic. Occasionally, the colloid cyst may have a variable appearance due to intracystic cholesterol and protein components. The most common ‘lesion’ mistaken for a colloid cyst is cerebrospinal fluid (CSF) flow artifact (MR pseudocyst) caused by pulsatile turbulent CSF flow around the foramen of Monro. Occasionally, a neurocysticercosis cyst may occur at the foramen of Monro. Neoplasms such as subependymoma or choroid plexus papilloma that may occur.

BIBLIGRAPHY 1. Armao D, Castillo M, Chen H, Kwock L. Colloid cyst of the third ventricle: Imaging–pathologic correlation. Am J Neuroradiol. 2000;21:1470-7. 2. Socin HV, Born J, Wallemacq C, Betea D, Legros JJ, Beckers A. Familial colloid cyst of the third ventricle: neuroendocrinological follow-up and review of the literature. Clin Neurol Neurosurg. 2002;104:367-70.

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CASE 41: RATHKE’S CYST

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C Figures 1A to C: (A) T1W sagittal: A triangular hyperintense (dotted black arrow) midline suprasellar mass with intrasellar extension; (B) T1W axial: A triangular hyperintense midline (thick arrow) suprasellar mass; (C) T1W sagittal with Gd: A triangular hyperintense midline suprasellar mass with intrasellar extension

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MRI Atlas of Cases 155

DISCUSSION Rathke cleft cysts are embryologic remnants of Rathke’s pouch, the neuroectoderm that ascends from the oral cavity to the sellar region to form the pituitary anterior lobe and pars intermedia. Thus, they are non-neoplastic cyst arising from remnants of embryonic Rathke cleft. They are smoothly lobulated, welldelineated nonenhancing, noncalcified intra/suprasellar cyst with intracystic nodule content varies from clear cerebrospinal fluid (CSF) like fluid to thick mucoid material. Sometimes an uncommon but pathognomonic “posterior ledge sign” may be seen. Upward extension through diaphragma sellae with ledge of tissue overlying posterior. Rathke’s cleft cysts often may be difficult to differentiate from other intrasellar or suprasellar masses on radiologic studies. Because cyst fluid of Rathke’s cleft cysts shows variable intensities on MR images, the specific diagnosis is often difficult when based on MR signal intensity values alone. The presence of an intracystic nodule with characteristic signal intensities on MR images may be indicative of the diagnosis of Rathke’s cleft cyst. Rathke’s cleft cysts are often difficult to distinguish from cystic craniopharyngiomas or cystic pituitary adenomas on radiologic studies. In T1W images, signal varies with cyst content (serous vs mucoid) (hypo or hyperintense). Intracystic, yellow waxy solid nodules have recently been reported in Rathke cysts containing cholesterol or mucinous proteins probably accounting for the bright signal on T1WI in some cysts. The differential diagnosis is a craniopharyngioma or hemorrhagic pituitary gland; the presence of calcification, soft-tissue mass, or areas of enhancement would lead one away from Rathke cleft cyst as the diagnosis.

BIBLIGRAPHY 1. Kucharczyk W, Peck WW, Kelly WM, Norman D, Newton TH. Rathke cleft cysts: CT, MR imaging, and pathologic features. Radiology. 1987;165:491-5. 2. Sumida M, Uozumi T, Mukada K, Arita K, Kurisu K, Eguchi K. Rathke cleft cysts: correlation of enhanced MR and surgical findings. Am J Neuroradiol. 1994;15:525-32.

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CASE 42: CEREBELLOPONTINE ANGLE: EPIDERMOID

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Figures 1A to D: (A) FLAIR axial: A hyperintense focus (dotted black arrow) in right cerebellopontine (CP) angle, the arrowhead points to the mucocele in the sphenoid sinus; (B) T1W coronal with Gd (thick arrow): Contrast enhancing mass in the CP angle; (C) T1W axial: A well-defined 1.2 × 1.8 cm markedly hyperintense, lobulated, capsulated mass in the right CP angle. The VIII cranial is partly attached. The lesion is compressing the brainstem; (D) T2W axial (arrowhead): The lesion is slightly hyperintense to CSF

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MRI Atlas of Cases 157

DISCUSSION Epidermoids are inclusion cyst arise from ectodermal inclusions (normal epithelial cells) into the neural tube around the 5–6 weeks of gestation. They represent 0.2–1.8% of all primary intracranial tumors. The most common location for epidermoid cysts is the cerebellopontine angle cistern (40–50%), where they are the third most common tumor (after acoustic schwannoma and meningioma). Other sites of predilection is the paramidline locations, are the petrous apex, parasellar region and chiasmal region. They typically present as an extra-axial mass with undulating borders. Most epidermoid cysts are isointense or slightly hyperintense to cerebrospinal fluid (CSF) on both T1- and T2-weighted MR images. They do not suppress completely on Fluid-attenuated inversion recovery (FLAIR) images and restrict (show high signal intensity) on diffusion-weighted images. Most epidermoid cysts do not enhance, although some minimal rim enhancement occurs in approximately 25% of cases. Compared with the classic epidermoid cyst, white epidermoids show reversed signal intensity on MR images, with high signal intensity on T1- and low signal intensity on T2-weighted images. Rare “white epidermoids” have high protein content. They insinuate within the cistern encasing adjacent nerves and vessels. The major differential consideration for the epidermoid cyst is an arachnoid cyst. Arachnoid cysts are isointense to CSF at all sequences, including FLAIR. They displace rather than invade structures as in the epidermoid. Finally, arachnoid cysts do not show water restriction on diffusion-weighted images. In T1 and T2W, the tumor’s signal intensity approximates that of the CSF. In PDW, the lesions are hyperintense to CSF. In diffusion weighted imaging (DWI), the lesions are strongly hyperintense comparing to CSF and brain tissue. In FLAIR sequences, the lesions exhibit mixed (predominantly high) signal intensities.

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158 MRI Brain: Atlas and Text

On T1W postcontrast and T2W images, the lesion is just visible because of slight mass effect with signal approximating that of CSF. FLAIR and constructive interference in steady state (CISS) sequences show the lesion as heterogeneous hyperintense and hypointense respectively. Diffusion W and corresponding ADC map show restriction relative to CSF with signal on ADC maps similar to brain parenchyma.

BIBLIOGRAPHY 1. Kallmes DF, et al. Typical and atypical MR imaging features of intracranial epidermoid tumors. AJR. 1997;169:883-7. 2. Ochi M, et al. Unusual CT and MR appearance of an epidermoid tumor of the cerebellopontine angle. AJNR. 1998;19:1113-5.

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CASE 43: INTRAVENTRICULAR EPIDERMOID

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Figures 1A to D:  (A) T1W axial: An isointense midline intraventricular mass (dotted black arrow) with areas of hyperintensity, involving both the lateral ventricles. The mass is predominantly in the frontal horns; (B) FLAIR axial: Irregular, expansile, intraventricular mass (arrow); (C) T1W sagittal: There is no significant edema, mass effect, midline shift of brain parenchyma. There are no evidence of calcification and hemorrhages (arrowhead); (D) DWI axial (arrow): The intraventricular mass is well seen. The anterior part of the lateral ventricles are grossly dilated

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160 MRI Brain: Atlas and Text

DISCUSSION Epidermoids represent 0.2–1% of all intracranial masses. They arise from inclusion of epithelial remnants trapped during 3–5 weeks of fetal life (remember that choroid plexus are also formed from invagination of ectodermal tissues). Intraventricular epidermoids are more common in 4th ventricle followed by lateral ventricles. More common in middle age; very rare in children. If ruptured, aseptic meningitis occurs. Long T1 and T2 are due to keratin in solid crystalline state. Epidermoids have restricted AIDS dementia complex (ADC) and complex fluid-attenuated inversion recovery (FLAIR) signal, unlike arachnoid cysts. Intraventricular epidermoids are slow growing, and presentation is nonspecific in the form of deteriorating mental functions. Generally, seen in the fifth decade, but they have also been observed in the pediatric age group. MRI usually show a heterogeneous lesion, often having a connection to the midline through the choroidal fissure. Epidermoid tumors represent 0.2–1% of all primary intracranial tumors. Intracranial epidermoid tumors are histologically benign, slow-growing, congenital neoplasms of the central nervous system. The lesions are of developmental etiology, due to migration of epiblast inclusion at the time of formation of the cerebral vesicle. They usually present in adults and are the most common in the cerebellopontine angle or suprasellar region protruding in the subarahnoid space. Epidermoids occurring within the lateral ventricles are very rare.

Differential Diagnosis The differential diagnosis are central intraventricular menigioma, central neurocytoma, and subependymal giant cell astrocytoma.

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MRI Atlas of Cases 161

BIBLIOGRAPHY 1. Bhatoe HS, Mukherji JD, Dutta V. Epidermoid tumour of the lateral ventricle. Acta Neurochirurgica. 2006;148(3):339-42. 2. Franko A, Holjar-Erliæ I, Miletiæ D. Lateral ventricle epidermoid, Radiol Oncol. 2008;42(2):66-8. 3. Meng L, Yuguang L, Shugan Z, et al. Intraventricular Epidermoids. J Clin Neurosci. 2006;13:428-30.

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CASE 44: PARTIAL DYSGENESIS OF CORPUS CALLOSUM WITH INTERHEMISPHERIC CYST

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Figures 1A to D:  (A) T2W axial: Colpocephaly, dilated 3rd ventricle, and normal 4th ventricle; (B) T2W axial: There is a right side interhemispherical cyst (dotted black arrow) measuring 8.9 × 3.8 cm communicating with dilated 3rd ventricle (thick arrow); (C) FLAIR axial: Colpocephaly, (thin arrow) dilated 3rd ventricle, and normal 4th ventricle; (D) T1W sagittal: Posterior body and splenium of corpus callosum were absent (thick black arrow). Both frontal lobes showed relatively smooth cortex. There was radial arrangement of medial hemispheric sulci

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MRI Atlas of Cases 163

DISCUSSION The association of both interhemispheric cysts and DandyWalker malformation with agenesis of corpus callosum (ACC) is well recognized. Barkovich’s classification scheme is on the basis of ventricular, cystic, and gross morphologic abnormalities, with the aim of associating types of cysts that may share elements of common origin and, possibly, prognosis. The various subtypes of cysts were classified with the assumption that the presence of a specific type of underlying cyst, ventricular defect, diencephalic malformation, or genetic anomaly produces malformations, deformations, or disruptions because of mass effect that may have similar imaging appearance. It is important to note that Barkovich designed their classification system to rely on postnatal, not prenatal, imaging techniques and not to include pathologic or histologic diagnosis. The Barkovich classification divides cases of interhemispheric cysts associated with adenoid cystic carcinoma (ACC) into type 1 cysts, which are diverticula of the lateral or third ventricles, and type 2 cysts, which are loculated and do not appear to communicate with the ventricular system. The origin of the interhemispheric cyst in ACC is controversial. Neurenteric, arachnoid, and ependymal cysts have all been suggested as possible causes.

BIBLIOGRAPHY 1. Manjunathay C, Kishor VH, Patil PH, et al. CT and MR appearance of interhemispheric cyst with agenesis of corpus callosum—a case report. Ind J Radiol Imag. 2006;16:4:715-7. 2. Stroustrup Smith A, Levine D. Appearance of an interhemispheric cyst associated with agenesis of the corpus callosum. Am J Neuroradiol. 2004;25(6):1037-40.

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CASE 45: JOUBERT SYNDROME

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Figures 1A to D:  (A) T2W sagittal:  Horizontally placed superior cerebellar peduncle (arrowhead) and large fourth ventricle; (B) T1W axial: Deep interpeduncular fossa with Molar tooth appearance between (dotted black arrow); (C) T1W axial: Bat wing appearance of fourth ventricle (between the thick arrows); (D) T2W axial:  Bat wing appearance of fourth ventricle (between the thick arrows)

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MRI Atlas of Cases 165

Note: A 12-year-old girl presented with ataxic movements and delay in speech.

DISCUSSION Joubert syndrome is characterized early with neonatal hyperapnea or apnea, occulomotor disturbance, dysmorphic features, global developmental delay and neuropathological abnormalities of cerebellum and brainstem. A link between CHARGE syndrome (coloboma of eye, heart defects, atresia of choana, retarded growth and development, genital hypoplasia and ear abnormalities or deafness) and Joubert syndrome has been reported. MRI of brain show nonvisualization of cerebellar vermis at the normal anatomic location suggesting agenesis of cerebellar vermis, opposition of the cerebellar hemispheres is seen. Superior cerebellar peduncles are horizontally placed along with deep interpeduncular fossa causing the typical “molar tooth” appearance. Fourth ventricle show a typical “bat wing” appearance. The imaging feature of the molar tooth is characteristic. Other characteristic findings include the ‘bat wing’ shaped superior fourth ventricle on axial images. There is thinned isthmus on sagittal images. Coronal images show agenesis/hypoplasia of vermis with a cleft in the midline. The characteristic appearance of the midbrain, with the enlarged superior cerebellar peduncles and the absence of their decussation, gives the ‘molar tooth’ appearance. Characteristic pathological findings of cerebellar vermian hypoplasia with midline cleft is seen. The most striking feature is the absence of the cerebellar vermis thought to be important for control of balance, regulation of muscle tone and saccadic (rapid) eye movements, although it should be noted that many lesions of the cerebellum could have this effect. The dentate nuclei, the major source of cerebellar output to the cerebral cortex, are fragmented into islands.

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166 MRI Brain: Atlas and Text

Malformation of various pontine and medullary structures, including the basis pontis, reticular formation, inferior olivary, dorsal column and solitary tract nuclei, have been reported, which may explain the respiratory defects in Joubert syndrome.

BIBLIOGRAPHY 1. Barkovich A. Pediatric Neuroimaging. Philadelphia: Lipincott Williams & Wilkins; 2005.pp.392-4. 2. Quisling RG, Barkovich AJ, Maria BL. Magnetic resonance imaging features and classification of CNS malformations in Joubert syndrome. J Child Neurol. 1999;14:628-35. 3. Romano S, Boddaert N, Desguerre I, et al. Molar tooth sign and superior vermian dysplasia: a radiological, clinical and genetic study. Neuropediatrics. 2006;37:42-5.

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CASE 46: QUADRIGEMINAL PLATE ARACHNOID CYST WITH OBSTRUCTIVE HYDROCEPHALUS

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Figures 1A to D: (A) T2W axial:  Grossly dilated both lateral ventricles (dotted black arrow) and third ventricle (thick black arrow); (B) T1W axial:  Grossly dilated both lateral ventricles (dotted black arrows) and third ventricle (thick black arrow); (C) FLAIR axial:  Grossly dilated both lateral ventricles (dotted black arrow) and third ventricle (thick black arrow); (D) T1W sagittal:  Grossly dilated lateral ventricles (dotted black arrow) and third ventricle (thick black arrow). The arrowhead shows small fourth ventricle

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168 MRI Brain: Atlas and Text

DISCUSSION Arachnoid cyst: A congenital anomaly of the arachnoid membrane that leads to CSF sequestration or focal impairment of CSF circulation. They are situated entirely within diverticular outpouchings of the subaracnoid space, in the arachnoid membrane. On MR using FLAIR and diffusion weighted imaging, arachnoid cysts are isointense to CSF. Location and size vary considerably. Rupture of an arachnoid cyst may cause a subdural hygroma or intercranial hemorrhage.

Differential Diagnosis 1. Epidermoid cyst: A true cyst lined by squamous epithelium. On MR using FLAIR the cyst may appear identical to an arachoid cyst, however it will differ on DWI. There is decreased with epidermoids so they will appear brighter than CSF, compared with an arachnoid cyst which follows the signal of CSF since there is no restricted diffusion. 2. Dermoid inclusion cyst: A rare ectodermal inclusion cyst with cheesy or greasy contents. Similar to epidermoid cysts, they are lined by squamous epithelium, but dermoid cysts have a more developed underlying stroma and may house dermal appendages (hair follicles and adnexae). MRI will show signal hyperintensity on T1 and variability on T2. 3. Teratoma (well-differentiated): A tumor of tissues inconsistent to the site of origin with derivatives from all three germ layers. May have both solid and cystic components and contain calcifications.

BIBLIOGRAPHY 1. Juhl. Paul and Juhl’s Essentials of Radiogic Imaging, 7th edn. Lippincott Williams and Wilkins. 1998. pp. 406-7. 2. Koch CA, Pacak K. Intracranial arachnoid cysts. Journal of Clinical Endocrinology and Metabolism. 2000;85(3). 3. Quadrigeminal cyst—MyPACS.net,www.mypacs.net/cases/ -1497063.htm

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CASE 47: DANDY-WALKER VARIANT

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Figures A to C: (A) T1W sagittal:  Grossly dilated lateral ventricle, third ventricle (dotted black arrow) fourth ventricle and cyst in posterior cranial fossa; (B) T1W axial: Cyst in a normal sized posterior cranial fossa cisterna magna (thick black arrow) seen; (C) T2W axial: Cyst in posterior cranial fossa, vermian hypoplasia (arrowhead) seen. Normal occipital bone

Note: This is a 7-year-old girl referred for evaluation of hydrocephalus

DISCUSSION D’Agostino and Hart et al. defined the characteristic triad of Dandy-Walker malformation as consisting of (1) complete or partial agenesis of the vermis, (2) cystic dilatation of the fourth ventricle, and (3) an enlarged posterior fossa with

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170 MRI Brain: Atlas and Text

upward displacement of lateral sinuses, tentorium, and torcular herophili. This triad is typically found in association with supratentorial hydrocephalus, which should be considered a complication rather than part of the malformation complex. Classically, posterior fossa cystic malformations have been divided into Dandy-Walker malformation, Dandy-Walker variant, mega cisterna magna, and posterior fossa arachnoid cyst. Precisely differentiating the malformations may not be possible using imaging studies. Dandy-Walker malformation, variant, and mega cisterna magna are currently believed to represent a continuum of developmental anomalies on a spectrum that has been termed the Dandy-Walker complex. Retrocerebellar arachnoid cysts of developmental origin are uncommon but clinically important. True retrocerebellar arachnoid cysts displace the fourth ventricle and cerebellum anteriorly and show significant mass effect and thinned occipital squma. Because there are different surgical therapy approaches for posterior fossa arachnoid cyst and Dandy-Walker malformation, it is essential to differentiate between the two entities. Mega cisterna magna consists of an enlarged posterior fossa secondary to an enlarged cisterna magna, with a normal cerebellar vermis, fourth ventricle and normal occipital squma.

BIBLIOGRAPHY 1. Pascual-Castroviejo I, et al. Dandy-Walker malformation: analysis of 38 cases. Childs Nerv Syst. 1991;7(2):88-97.

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CASE 48: POSTERIOR CRANIAL FOSSA GIANT CYST

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Figures 1A to D: (A) T2W axial:  A large cyst in retrocerebellar area displacing the cerebellum anteriorly, scalloping the occipital bone. There are septations within the giant cyst; (B) T1W axial: The cyst is typically hypointense; (C) FLAIR axial:  The cyst is hypointense similar to CSF; (D) T1W sagittal:  A large cyst in retrocerebellar area, displacing the cerebellum vanteriorly, scalloping the occipital bone is better seen

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172 MRI Brain: Atlas and Text

DISCUSSION This is intra-arachnoid CSF-filled sac that does not communicate with ventricular system. The classical MR finding are sharply demarcated round/ovoid extra-axial cyst that follows CSF attenuation/signal. This is an atypical location for these types of cysts. Arachnoid cysts displace but do not engulf vessels, cranial nerve. They show scalloping of the occipital inner table, indicating long-term pathology. They often are asymptomatic and found incidentally. FLAIR sequences differentiates other such pathologies in posterior cranial fossa.

BIBLIOGRAPHY 1. Barkovich AJ, et al. Revised classification of posterior fossa cysts and cyst-like malformations based on the results of multiplanar MR imaging. AJR. 198;153:1289-300.

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CASE 49: QUADRIGEMINAL PLATE LARGE ARACHNOID CYST

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Figures 1A to D: (A) T2W axial:  A well-defined cystic lesion 4.9 × 4.3 × 5.2 cm located infratentorially in the region of quadrigeminal plate; (B) T1W axial:  The cyst was located to the left of midline, displacing the left thalamus, left atrium of left lateral ventricle. The lesion showed signal intensity similar to CSF in all pulse sequences; (C) FLAIR axial: Signal suppression similar to CSF in arachnoid cyst; (D) DWI axial:  Signal similar to CSF in arachnoid cyst

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174 MRI Brain: Atlas and Text

DISCUSSION The quadrigeminal plate cistern is the fluid-filled space located cephalad to the fourth ventricle. The plate is comprised of the superior and inferior colliculi, while the cistern is the space immediately posterior to them. It is bounded by the quadrigeminal plate, the splenium of the corpus callosum, the cerebellar vermis, and the tentorial margin. Compression of this space may result in increased intracranial pressure and hydrocephalus by aqueductal stenosis. The differential diagnosis for quadrigeminal plate cysts includes but is not limited to: arachnoid cyst—a congenital anomaly of the arachnoid membrane that leads to CSF sequestration or focal impairment of CSF circulation. They are situated entirely within diverticular outpouchings of the subaracnoid space, in the arachnoid membrane. On MR using FLAIR and DWI, arachnoid cysts are isointense to CSF. Location and size vary considerably. CT will show hypodense structure distorting nearby structure with the same density as CSF. Rupture of an arachnoid cyst may cause a subdural hygroma or intercranial haemorrhage. The best diagnostic clue is a sharply demarcated extra-axial cyst that can displace or deform adjacent brain. Scalloping of the adjacent calvarium is often seen. The classic arachnoid cyst has no identifiable internal architecture and does not enhance. The cyst typically has the same signal intensity as CSF at all sequences. Occasionally, however, hemorrhage, high protein content, or lack of flow within the cyst may complicate the MR appearance arachnoid cysts have an increased prevalence of coexisting subdural hematomas, especially when they occur in the middle cranial fossa. The most difficult lesion to distinguish from the arachnoid cyst is an epidermoid cyst. Epidermoid cysts can appear nearly identical to CSF on CT scans. On MR images, epidermoid cysts appear isointense to CSF, although close inspection often shows they are not precisely identical in signal intensity to CSF. Arachnoid cysts typically suppress completely on FLAIR images and do not restrict on diffusion-weighted images. Occasionally an arachnoid

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MRI Atlas of Cases 175

cyst can be slightly hyperintense on images obtained with a long repetition time and a short echo time. Arachnoid cysts displace adjacent arteries and cranial nerves rather than engulf them, as epidermoid cysts often do. Dermoid inclusion cyst is a rare ectodermal inclusion cyst with cheesy or greasy contents. Similar to epidermoid cysts, they are lined by squamous epithelium, but dermoid cysts have a more developed underlying stroma and may house dermal appendages (hair follicles and adnexae). On CT, it will appear as a well circumscribed, rounded mass whose contents have negative attenuation values and may demonstrate hair. MRI will show signal hyperintensity on T1 and variability on T2. Teratoma (well-differentiated) is a tumor of tissues inconsistent to the site of origin with derivatives from all three germ layers. May have both solid and cystic components and contain calcifications. CT and MR imaging is variable.

BIBLIOGRAPHY 1. Choi SK, Starshak RJ, Meyer GA, Kovnar EH, Sty JR . Arachnoid cyst of the quadrigeminal plate cistern: report of two cases. Am J Neuroradiol. 1986;7(4):725-8.

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CASES (50–67): VASCULAR CASE 50: CAVERNOMA LEFT FRONTAL LOBE

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Figures 1A to D: (A) T1W axial:  A hyperintense ring with a centrally placed heterogeneous signal mass with popcorn-like shape (dotted black arrow) in the left frontal region; (B) T1W sagittal:  A hyperintense ring with a centrally placed heterogeneous signal mass with popcorn-like shape (dotted black arrow) in the left frontal region; (C) T2W axial:  At a higher level shows a hypointense ring with a heterogeneous signal central mass. (dotted black arrow), with mild edema all around the mass (thick arrow); (D) T2W axial:  A hypointense ring with a heterogeneous signal central mass (dotted black arrow), with mild edema all around the mass

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MRI Atlas of Cases 177

DISCUSSION Cavernous angiomas (cavernomas) belong to a group of intracranial vascular malformations that are developmental malformations of the vascular bed. Cavernous angiomas are considered to be congenital vascular hamartomas composed of closely apposed endothelial-lined sinusoidal collections with slow blood flow and little to no neural tissue. The lesions can occur on a familial basis. As a cause of hemorrhage, cavernous angiomas are far less common than hypertension; nevertheless, as a cause of hemorrhage, they must be excluded, especially in young patients. Cavernous angiomas represent approximately 1% of intracranial vascular lesions and 15% of cerebrovascular malformations. Cavernous angiomas can occur at any age, but they are most likely to occur in patients from 20–40 years. Intracranial vascular malformations are grouped into four types: 1. Capillary malformations 2. Cavernous malformations 3. Venous malformations 4. Arteriovenous shunting malformations. The types of vascular malformations are defined on the basis of their gross and histopathologic characteristics. Grossly, cavernous angiomas are typically discrete multilobulated lesions that contain hemorrhage in various stages of their evolution. Cavernous angiomas are considered to be congenital vascular hamartomas composed of closely approximated endotheliallined sinusoidal collections without significant amounts of interspersed neural tissue. The lack of intervening neural tissue is the only histopathologic characteristic that differentiates these lesions from capillary telangiectases. Patients may be asymptomatic, although they often present with headaches, seizures, or small parenchymal hemorrhages. The 40–50% of patients present with seizures, 20% with focal neurologic deficits, and 10–25% with hemorrhage. Cavernous angiomas can be found in any part of the brain, as they can occur at any location along the

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178 MRI Brain: Atlas and Text

vascular bed. Frontal and temporal lobes are the most common sites of occurrence, and 80–90% of the lesions are supratentorial. The deep cerebral white matter, corticomedullary junction, and basal ganglia are common supratentorial sites; whereas the pons and cerebellar hemispheres are common posterior fossa sites. Cavernous angiomas will contain calcium approximately 40–60% of the time with little or no mass effect unless there has been a recent hemorrhage MRI findings of parenchymal cavernous angiomas demonstrate typical, popcorn-like, smoothly circumscribed, well-delineated complex lesions. The core is formed by multiple foci of mixed signal intensities, which represents hemorrhage in various stages of evolution. Common findings on T1WI imaging are “popcorn ball” appearance of mixed hyperintense and hypointense blood-containing “locules.”

Differential Diagnosis: “Popcorn Ball” Appearance Lesion  Arteriovenous malformation  Hemorrhagic neoplasm  Calcified neoplasm ( i.e. oligodendroglioma)

BIBLIOGRAPHY 1. Chaloupka JC, Huddle DC. Classification of vascular malformations of the central nervous system. Neuroimaging Clin N Am. 1998;8(2):295321. 2. Jacobsen JC, Naul LG. Brain, Cavernous Angiomas. (Article Last Updated: Jul 28, 2005) eMedicine: www.emedicine.com/radio/ topic95.htm. 3. Osborne AG. Intracranial vascular malformations. In: Diagnostic Neuroradiology. Mosby-Year Book. 1994;284:311-4.

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CASE 51: ACUTE RIGHT MIDDLE CEREBRAL ARTERY TERRITORY ISCHEMIC INFARCT

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Figures 1A to D: (A) T2W axial:  A hyperintense focus (thick black arrows) in right middle cerebral artery (MCA) territory. There is a white dot (dotted black arrow) indicating old lacunar infarct; (B) FLAIR axial image:  A welldefined hyperintense area in the right MCA territory indicating acute ischemic infarct. The black dot (dotted black arrow) shows an old lacular infarct. Note the sparing of the water-shed zones (arrowheads); (C) DWI (Diffusion-weighted) axial image: Water restriction (thin arrows), in the same area as above, (hyperintensity), indicating acute infarct; (D) ADC (apparent diffusion coefficient) axial image: The opposite signals, i.e. hypointensity in the same area (dotted black arrows), confirming the acute ischemic infarct

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180 MRI Brain: Atlas and Text

Note: High signal in the lacunar infarct, indicating chronic ischemic infarct. Table 1:  MR signal intensity—acute vs chronic infarct (From above case)

Infarct

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Right MCA infarct

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Decreased

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Decreased

Increased

DISCUSSION The goal of imaging is to diagnose the precise type of stroke (hemorrhagic or ischemic) so that appropriate management can be promptly implemented. Diagnostic imaging of acute stroke should reliably help to: (1) exclude intracranial hemorrhage; (2) differentiate between irreversibly affected brain tissue (dead brain) and reversibly impaired tissue (tissue at risk) that might benefit from early treatment; and (3) identify stenosis or occlusion of major extra- and intracranial arteries. On conventional magnetic resonance imaging (MRI) sequences, regions of increased signal intensity are seen on proton density (PD), T2, and FLAIR magnetic resonance images a few hours after the onset of stroke symptoms. T1 images show hypointensity, i.e. decreased signal intensity. Approximately 80% of infarction will be detected on MRI within 24 hours. Diffusion-weighted MRI (DWI) is a technique sensitive to the restriction of Brownian motion of extracellular water due to the imbalance caused by cytotoxic edema. Acute ischemic lesions are characterized by a high signal on DWI and a low apparent diffusion coefficient (ADC) value due to the shift of water from the extracellular to the intracellular compartment. Restricted diffusion in acute ischemic lesions is attributed to: accumulation of intracellular water; cytotoxic edema; disruption of high-energy metabolism; and loss of ion homeostasis. DWI is nearly always positive 1 hour after the clinical onset of symptoms.

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MRI Atlas of Cases 181

About 15% of MCA infarction is initially hemorrhage, i.e. secondary hemorrhage is also not uncommon in MCA infarcts, usually after 1–3 days or after thrombolytic therapy.

BIBLIOGRAPHY 1. Burdette J, Ricci PE, Petitti N, Elster AD. Cerebral infarction: time course of signal intensity changes on diffusion-weighted MR images. Am J Roentgenol. 1998;171:791-5. 2. Lansberg MG, Thijs VN, O’Brien MW, et al. Evolution of apparent diffusion coefficient, diffusion-weighted, and T2-weighted signal intensity of acute stroke. Am J Neuroradiol. 2001;22:637-44. 3. Thurnher MM, Castillo M. Imaging in acute stroke. Eur Radiol. 2005;15:408-15.

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CASE 52: GIANT ANEURYSM OF BASILAR ARTERY TRUNK

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Figures 1A to D: (A) T1W sagittal:  An oval mass (dotted black arrows) in prepontine cistern, displacing the brainstem posteriorly; (B) T1WGd enhanced sagittal: Oval enhancing mass (dotted black arrows) in prepontine cistern, displacing the brainstem; (C) MR angiography in axial plane:  Giant aneurysm (black arrow); (D) MR angiography in sagittal plane:  Giant aneurysm (thick arrow)

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MRI Atlas of Cases 183

DISCUSSION Basilar trunk aneurysms are rare, fusiform in shape, and mainly present by compression or atherothrombosis of the brainstem. Intracranial saccular aneurysm are, true aneurysm as they are arterial outpouching that lacks internal elastic lamina, muscular layers.

Location The 90–95% arise from circle of Willis:  90% in anterior circulation (IC-PCoA, ACoA most common sites)  10% posterior (basilar artery bifurcation, PICA most common sites). Usual sizes:  Small (2–3 mm) to giant (> 2.5 cm).  In TlW-patent aneurysm signal varies, 50% have “flow void”  50% iso/heterogeneous signal: Partially/completely thrombosed aneurysm. Signal depends on age(s) of clot, common = mixed signal, laminated thrombus. In T2W typically hypointense, may be laminated with very hypointense rim. In FLAIR—acute subarachnoid hemorrhage show high signal in adjacent sulci, cisterns, if aneurysm ruptures.

BIBLIOGRAPHY 1. Christopher Buckle, Meheroz H. Rabadi, Bilateral pontine infarction secondary to basilar trunk saccular aneurysm: Arch Neurol. 2006;63(10):1498-9. 2. Killu AM, images in clinical medicine: giant basilar-artery aneurysm. Lanzino G. N Engl J Med. 2012;367(19):8.

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CASE 53: RIGHT SUBACUTE SUBDURAL HEMATOMA

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Figures 1A to D: (A) Axial T2WI:  A hyperintense extra-axial collection in right side (dotted black arrows) compressing adjacent brain parenchyma consistent with subacute blood (methemoglobin). There is evidence of midline shift, mass effect (the right side ventricle is effaced). Note also the contre-coup effect, in the form of scalp subacute hematoma on the opposite left side. (arrowhead). There is also a large area of hemorrhagic contusion in the right frontal lobe (thick arrow); (B) Axial T2WI at a higher level: A hyperintense extra-axial collection in right side (dotted black arrows). The typical crescenteric shape of subdural collection is shown; (C) T2W axial:  At a lower level shows right subdural collection with mass effect; and midline shift; (D) T2W axial: The medial border of the subdural collection is typically serrated (thick arrows) unlike an epidural collection

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MRI Atlas of Cases 185

DISCUSSION A subacute (± 3 days–3 weeks old) subdural hemorrhagic collection in subdural space appears typically as a crescentshaped, hyperintense, extra-axial collection that spreads diffusely over affected hemisphere with a serrated medial border. The MR signal intensity vary with age and organization of hemorrhage. It is due to traumatic stretching and tearing of bridging cortical veins as they cross subdural space to drain into the adjacent dural venous sinuses. Trauma may be minor, particularly in elderly. The differential diagnosis includes. Other subdural collections like effusion, empyema, hygroma, etc. The SDHs are categorized into acute, subacute, and chronic forms. Clinically, SDHs are seen in 10–20% of all head trauma. The 10–30% of chronic SDHs rebleed, as cortical veins are stretched by the SDH itself in addition to the formation of friable vascular neomembranes.

Epidural Hemorrhage vs Subdural Hemorrhage Finding

Epidural hemorrhage (EDH)

Subdural hemorrhage (SDH)

Shape Size Cause Medial border Crossing Fracture Presentation

Lentiform Confined to origin Arterial rupture Sharp Dural attachments Always present Acute

Crescenteric Spread along entire hemisphere Veins rupture Serrated Sutures Not always Chronic

SUBDURAL HEMORRHAGE Finding

Acute

Sub-acute

Chronic

Time Signal intensity Contrast study

6 hrs–3 days Hypointense -

CSF/blood level

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3 days–3 weeks Hyperintense Enhancing membrane -

More than 3 weeks Hypointense Enhancing membrane seen

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186 MRI Brain: Atlas and Text

BIBLIOGRAPHY 1. Osborn AG, Blaser S, Salzman K. Diagnostic Imaging: Brain. WB Saunders Company. 2004;i:2:10-21. 2. Osborn AG. Diagnostic Neuroradiology. Mosby. 1994.pp.205-11.

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CASE 54: LATERAL MEDULLARY SYNDROME (WALLENBERG’S SYNDROME)

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Figures 1A to D: (A) T1W axial:  A well-defined hypointense lesion (dotted black arrow) in the left lateral medulla; (B) T2W axial: A well defined hyperintense lesion (dotted black arrow) in the left lateral medulla; (C) FLAIR axial:  A well-defined hyperintense lesion (dotted arrow) in the left lateral medulla; (D) DWI axial: Water restriction-hyperintense signal (thick arrow) indicating acute ischemic infarct

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188 MRI Brain: Atlas and Text

DISCUSSION Lateral medullary syndrome (also called Wallenberg’s syndrome and posterior inferior cerebellar artery syndrome) is a disease in which the patient has a constellation of neurologic symptoms due to injury to the lateral part of the medulla in the brain, resulting in tissue ischemia and necrosis. It is the clinical manifestation resulting from occlusion of the posterior inferior cerebellar artery (PICA) or one of its branches or of the vertebral artery, in which the lateral part of the medulla oblongata infarcts, resulting in a typical pattern. The most commonly affected artery is the vertebral artery, followed by the PICA, superior middle and inferior medullary arteries. This syndrome is characterized by sensory deficits affecting the trunk and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side with the infarct. Specifically, there is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face. This crossed finding is diagnostic for the syndrome.

BIBLIOGRAPHY 1. Cormier PJ, Long ER, Russell EJ. MR imaging of posterior fossa infarctions: vascular territories and clinical correlates. Radiographics. 1992;12:1079-96. 2. Sacco RL, Freddo L, Bello JA, et al. Wallenberg’s lateral medullary syndrome: clinical-magnetic resonance imaging correlations. Arch Neurol. 1993;50:609-14.

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CASE 55: VENOUS INFARCT: LEFT TEMPORAL LOBE

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Figures 1A to D:  (A) T1W axial: There is subtle hyperintensity in left temporal lobe (dotted black arrows), vein of Labbe involvement; (B) T2W axial: There is a wedge shaped hyperintensity due to hemorrhage + edema (thick arrows); (C) MR venography in axial:  Filling defect due to thrombosis (arrowhead); (D) MR venography in sagittal:  Filling defect due to thrombosis (arrowhead)

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190 MRI Brain: Atlas and Text

DISCUSSION Venous thrombosis has a nonspecific presentation and therefore it is important to recognize subtle imaging findings and indirect signs that may indicate the presence of thrombosis. Although these findings are often present on initial scans, they are frequently detected only in retrospect. Clinically patients with venous thrombosis often present with seizures, which is not a symptom in patients with an arterial infarction. On a routine nonenhanced MR think of the possibility of venous thrombosis when:  Direct signs of a thrombus  Infarction in a nonarterial location, especially if it is bilateral and hemorrhagic  Cortical or peripheral lobar hemorrhage  Cortical edema. Venous infarcts are often bilateral, in/close midline, hemorrhagic and in a nonarterial territory, atypical location. The most frequently thrombosed venous structure is the superior sagittal sinus. Infarction is seen in 75% of cases. The abnormalities are parasagittal and frequently bilateral. Hemorrhage is seen in 60% of the cases. Direct signs

Indirect signs/venous infarct

Clinical

1. Dense clot sign 2. Cord sign 3. Empty delta sign 4. Loss of normal flow void

Venous infarct, if it is bilateral, bithalamic, parasagittal; Temporal lobe infarct, cortical edema/hemorrhage Peripheral lobar hemorrhage

Seizures Headache Loss of consciousness

BIBLIOGRAPHY 1. Provenzale JM, Joseph GJ, Barboriak DP. Dural sinus thrombosis: findings on CT and MR imaging and diagnostic pitfalls. AJR. 1998;170:777-83. 2. Zimmerman RD, Ernst RJ. Neuroimaging of cerebral venous thrombosis. Neuroimaging Clin North Am. 1992;2:463-85.

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CASE 56: ACUTE RIGHT THALAMIC ISCHEMIC INFARCT

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Figures 1A to D:  (A) T1W axial: A well-defined hyperintense lesion in right side thalamus (dotted black arrow); (B) T2W axial: A well-defined hypointense lesion in right side thalamus (thick black arrow); (C) DW axial: Hyperintenese signal in the same area indicating water restriction due to cytotoxic edema secondary to ischemic infarct; (D) T1W sagittal: A well-defined hyperintense lesion in the thalamus (thin arrow)

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192 MRI Brain: Atlas and Text

DISCUSSION The thalamus receives blood supply from four sources. 1. Tuberothalamic or polar artery from posterior communicating artery (PCOM) 2. Paramedian from (basilar communicating artery) 3. Inferolateral or lateral geniculate from–posterior cerebral artery (PCA) 4. Posterior choroidal from PCA. Thalamic infarcts may present with acute onset of dementia, more commonly seen with bilateral thalamic infarcts but which can also occur with unilateral infarction. Our patient presented with hemiplegia. Thalamic infarcts are classified into anterior, paramedian, inferolateral, and posterior territories as per the arterial supply respectively. There are three clinical syndromes associated with lateral thalamic infarction: 1. Hemisensory loss, hemiataxia, and involuntary movements 2. Pure sensory stroke 3. Sensori-motor stroke. Variations of vascular supply of the thalamus and of extent of collateralization are frequent, thus making the attribution of individual vascular occlusion patterns to a constellation of clinical deficiency symptoms and infarcts demonstrated by neuroimaging rather difficult as this original and interesting case seems to confirm. Our case represents an anteromedian type of unilateral thalamic infarct. The size of the lesion is beyond that for a lacunar infarct. There is lack of perilesional edema and mass effect on adjacent structures. Magnetic resonance (MR) spectroscopy usually shows elevated lactate and reduced choline, creatine, and N-acetylaspartate (NAA) within the infarct.

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MRI Atlas of Cases 193

Differential Diagnosis Tuberculoma; glioma; lymphoma.

BIBLIOGRAPHY 1. Carrera E, Michel P, Bogousslavsky J. Anteromedian central, and posterolateral infarcts of the thalamus: three variant types. Stroke. 2004;35:2826-31. 2. Boiten J, Lodder J. Ataxic hemiparesis following thalamic infarction. Stroke. 1990;21:339-40.

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CASE 57: GIANT ANEURYSM SUPRACLINOID SEGMENT OF INTERNAL CAROTID ARTERY

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Figures 1A to D: (A) T2W coronal: A well-defined signal void lesion (dotted black arrows) in suprasellar region. Note the normal signal voids in cavernous part of both internal carotid artery (ICA); (B) T1W axial with Gd: Dense contrast enhancement of the lesion (thick arrows); (C) T1W axial with Gd: Dense contrast enhancement of the lesion (dotted white arrow). Note the left A1 vessel is arching around the mass; (D) T1W coronal with Gd: Dense contrast enhancement of the lesion (thin arrows). The giant aneurysm is arising from the terminal bifurcation site of right internal carotid artery (ICA) supraclinoid part

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MRI Atlas of Cases 195

DISCUSSION Most intracranial aneurysms are saccular (or so called berry) aneurysms and occur at predictable sites around the circle of Willis. However, unusual types of aneurysms are occasionally encountered, including dissecting, fusiform, serpentine, blood blister type, traumatic, mycotic (or infectious), atheromatous and giant aneurysms, all of which may manifest with hemorrhage, thromboembolic events, or mass effect. Approximately 85% of intracranial aneurysms are located around the anterior communicating artery (30–35%), the posterior communicating artery (30–35%), the middle cerebral artery bifurcation (20%), the basilar artery (5%), the internal carotid artery (ICA) terminus or posterior wall, the superior cerebellar artery (SCA), or the posterior inferior cerebellar artery (PICA). Aneurysm size is traditionally reported as being small (50 mm). The most serious presentation of intracranial aneurysms is subarachnoid hemorrhage (SAH). Despite improvements in diagnostic and therapeutic techniques, the mortality rate for SAH is relatively unchanged at approximately 50%. MR angiography (MRA) has been used as a technique to detect aneurysms in patients (usually in the nonacute setting) with clinical features suspicious for the presence of an aneurysm or a family history of aneurysms. Three-dimensional time-of-flight (TOF) MRA is the most widely accepted technique because it provides good spatial resolution, is relatively insensitive to signal loss caused by turbulent flow, and can be performed within a time span that allows anatomic MRI during the same imaging session. The spatial resolution of MRA at 1.5 T is on the order of 1 mm. With 3 T scanners, spatial resolution may reach 0.6 mm.

BIBLIOGRAPHY 1. Mawad ME, Klucznik RP. Giant serpentine aneurysms: radiographic features and endovascular treatment. AJNR. 1995;16:1053-60. 2. Ronkainen A, Puranen MI, Hernesniemi JA, et al. Intracranial aneurysms: MR angiographic screening in 400 asymptomatic individuals with increased familial risk. Radiology. 1995;195:35-40.

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CASE 58: LEFT TRANSVERSE SINUS THROMBOSIS

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Figures 1A to D:  (A) T1W axial: Hyperintense focus in the left temporal subcortical region (dotted black arrows); (B) T2W axial: Hyperintense area in the left temporal lobe (arrowheads); (C) T1W axial: Hyperintense area in the left temporal cortical region; (D) MRV coronal oblique: Nonvisualization of left transverse sinus and multiple collaterals (thick arrows)

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MRI Atlas of Cases 197

DISCUSSION Dural venous sinus thrombosis, seen in a number of conditions, including dehydration, hypercoagulable states, infection, tumor invasion, and in conjunction with oral contraception, may be a cause of neurologic deterioration. Acute dural sinus thrombosis leads to distinct stages of parenchymal changes, the severity of which depends on the degree of venous congestion, which, in turn,is closely related to intradural sinus pressure. As intradural sinus pressure increases, progression from mild parenchymal change to severe cerebral edema and/or hematoma may occur if thrombolysis is delayed. The sites of parenchymal changes usually reflect thrombosis in the adjacent dural sinus. For example, bilateral frontal, parietal, and occipital lobe edema or hemorrhage usually corresponds to superior sagittal sinus thrombosis. However, the site of parenchymal change does not always reflect the site of thrombosis. Also, posterior fossa dural sinus thrombosis may cause supratentorial changes as well as edema or hemorrhage of the cerebellum and brainstem.

BIBLIOGRAPHY 1. James M Provenzale, Peter G Kranz. Dural sinus thrombosis: sources of error in image interpretation. American Journal of Roentgenology. 2011;196:23-31. 2. Vijay RK. The cord sign. Radiology. 2006;240:299-300.

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CASE 59: RIGHT CEREBELLAR ISCHEMIC INFARCT

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Figures 1A to D:  (A) T1W axial: A well-defined hypointense area (dotted black arrows) in the right cerebellar hemisphere; (B) T2W axial: A welldefined hyperintense area (thick black arrows) in the right cerebellar hemisphere; (C) DWI: Hyperintensity in the above area, indicating acute ischemic infarct; (D) T2W coronal: Infarct in right inferior cerebellar hemisphere infarct

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MRI Atlas of Cases 199

DISCUSSION Infarction of the cerebellum is a relatively uncommon subtype of ischemic stroke, which may involve any of the three arteries supplying the cerebellum: 1. Superior cerebellar artery (SCA) 2. Anterior-inferior cerebellar artery (AICA) 3. Posterior-inferior cerebellar artery (PICA) Cerebellar infarcts account of approximately 1.5–2.3% of all cerebral infarction.1,2 Many of the symptoms of cerebellar infarction are nonspecific, such as nausea, vomiting, dizziness, unsteadiness and headache, and the clinical diagnosis relies on focused neurological examination and a reasonable index of suspicion. Examination findings include incoordination, ataxia and horizontal nystagmus. Patients may also present with altered conscious state or coma. The posterior-inferior cerebellar artery (PICA) territory includes all of the posterior-inferior cerebellum, the ipsilateral cerebellar tonsil, and the ipsilateral inferior vermis. The PICA also frequently supplies the posterolateral medulla and infarction in this location results in the lateral medullary syndrome or the socalled Wallenberg’s syndrome. The clinical manifestations and structures affected in Wallenberg’s syndrome include:  Ipsilaterally: Preganglionic Horner syndrome (descending reticulospinal tracts to cord sympathetics)  Ataxia (cerebellum, inferior peduncle): Facial pain, numbness, impaired sensation (CN V nucleus, spinal tract)  Dysphagia, hoarseness, diminished gag reflex (CN’s IX and X)  Diminished taste (CN IX nucleus and solitary tract)  Vertigo, nausea, vomiting (vestibular nuclei and connections)  Nystagmus, diplopia, oscillopsia (restiform body, inferior and medial vestibular nuclei)  Hiccups  Contralaterally  Numbness, decreased pain and temperature in trunk and extremities (spinothalamic tract). The variability in vascular supply of the cerebellum and medulla is reflected by PICA

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200 MRI Brain: Atlas and Text

infarcts. Sometimes a PICA infarct produces the classic Wallenberg’ syndrome described above while others may spare the medulla. Single PICA branch occlusions can affect a very small area. PICA Infarctions. Infarction in the distribution of the PICA typically encompasses the posteroinferior surface of the cerebellar hemisphere and ipsilateral vermis. The lateral medulla may or may not be involved with PICA infarctions. The extent of a PICA territory infarction and the amount of deep white matter involvement depend on the variability of the PICA distribution and on the reciprocal and balanced supply of this region by the AICA and the SCA.

MRI IN ISCHEMIC STROKE STAGE

T1W

T2W

DWI

ADC

•  Hyperacute (0–6 hours) •  Acute (6 hours–4 days) •  Subacute (4–14 days) •  Chronic (> 2 weeks)

Isointense

Isointense

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Low

Low intensity

High intensity

Bright

Low

Low intensity

High intensity

Normal

Low intensity

High intensity

High intensity High intensity

High

Abbreviations: ADC, Apparent diffusion coefficient; DWI, Diffusion-weighted imaging; T1WI, T1-weighted imaging; T2WI, T2-weighted imaging.

REFERENCES 1. Cormier PJ, Long ER, Russell EJ. MR imaging of posterior fossa infarctions: vascular territories and clinical correlates: Radiographics. 1992;12:1079-96. 2. Tohgi H, Takahashi S, Chiba K, et al. Cerebellar infarction. Clinical and Neuroimaging Analysis in 293 patients. The Tohoku Cerebellar Infarction Study Group. Stroke. 1993;24(11):1697-701.

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CASE 60: ANTERIOR CEREBRAL ARTERY ANEURYSM WITH SUBARACHNOID HEMORRHAGE

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Figures 1A to D:  (A) T1W sagittal: Hyperintense foci in frontal sulci (dotted black arrow); (B) T1W axial: Hyperintense foci in anterior interhemispheric fissure (dotted black arrow); (C) DWI: Hyperintense foci in anterior interhemispheric fissure and frontal cortex (dotted black arrow); (D) MRA axial plane: An aneurysm in the anterior cerebral artery (thick black arrow)

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202 MRI Brain: Atlas and Text

DISCUSSION The MRI can provide additional details about the regional anatomy and the size, shape, and content of an aneurysm. Most intracranial aneurysms appear as an area of flow void larger than the healthy vessels in that region. Their interior usually enhances significantly after the intravenous administration of contrast agent. Most giant aneurysms have calcifications and an intraluminal clot, but their residual lumen may be depicted as a region of flow void. The thrombosed areas may have variable signal intensity, which represents blood products at different stages. MRIs may also depict small amounts of parenchymal blood surrounding the aneurysms; this finding indicates which of the multiple aneurysms have bled. MRA is useful in detecting intracranial aneurysms in both symptomatic patients and asymptomatic patients. The prevalence of intracranial aneurysms is estimated at about 2% of adults; the majority (85%) of intracranial aneurysms are in the anterior circulation, commonly in the circle of Willis. The 30% of cerebral aneurysms are in the anterior communicating artery. Most aneurysms do not rupture and the incidence of subarachnoid hemorrhage due to rupture is roughly 1 case per 10,000 people annually. Aneurysms smaller than 7 mm have a very low risk of rupture; aneurysms that cause symptoms and/or are over 10 mm have a higher likelihood of rupture, and may require surgical management.

BIBLIOGRAPHY 1. Federico C Vinas, James G Smirniotopoulos, et al. Brain Aneurysm Imaging, emedicine.medscape.com/article/337027. 2. Riku P, Kivisaaria, Oili Salonena, Antti Servoa, et al. MR Imaging after aneurysmal subarachnoid hemorrhage and surgery: a long-term follow-up study. AJNR. 2001;22:1143-8.

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CASE 61: VEIN OF GALEN MALFORMATION

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Figures 1A to D: (A) Axial T2W MRI: A VGM in a 5-year-old female child. The dilated median prosencephalic vein of Markowski (dotted black arrow); (B) Sagittal TlWI MR:  A classic VGM. The MPV (dotted black arrow) drains via the falcine sinus (thick arrow). The straight sinus is absent (arrowhead); (C) Multiple collaterals: Draining into the dilated median prosencephalic vein, suggesting choroidal type of VGM; (D) MRA axial:  View dilated arterial feeders and draining veins to the—Pseudocaput medusae

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204 MRI Brain: Atlas and Text

Note: Our case is female child aged 5 years and our’s a choroidal type of VGM.

DISCUSSION The VGM is misnomer; malformation actually involves the median prosencephalic vein (MPV) of Markowski. It is an arteriovenous fistula (AVF) involving aneurysmal dilatation of the MPV. There are dilated arteries feeding into large midline venous pouch (MPV) in neonate/infant located at the quadrigeminal plate cistern is the most common characteristic finding. MR show multiple arterial feeders and flow voids. Flow void or mixed intensity are due to fast or turbulent flow. In T1W-MPV, hyperintense foci within pouch may represent a thrombus and hyperintense foci within brain: Calcification. MRA (angiography) delineates arterial feeders and MRV (venography) draining veins of MPV. Clinically, the child presents with heart failure or hydrocephalus. Age: Neonatal > infant presentation most common; rare adult presentation. Gender: M:F = 2:1.

Grading Criteria Choroidal or mural classification based on angioarchitecture of VGM:  Choroidal: Multiple feeders from pericallosal, choroidal, and thalamo-perforating arteries. : Few feeders from uni- or bilateral collicular or posterior  choroidal arteries.

BIBLIOGRAPHY 1. Jones B, et al. Vein of Galen aneurysmal malformation: diagnosis and treatment of 13 children with extended clinical follow-up. AJNR. 2002;23:1717-24. 2. Osborn A. Diagnostic Imaging: Brain. Amirsys Publishers, 2004.

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CASE 62: CAVERNOMA WITH RECENT BLEED

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Figures 1A to D: (A) T1W axial: A well-defined hyperintense focus (dotted black arrow) in left temporal lobe; (B) T2W axial: Hyperintense focus (dotted black arrow) with a rim of hypointensity, suggesting recent bleed; (C) DWI:  Hyperintense focus (thick arrow) with a rim of hypointensity, suggesting recent bleed; (D) MRV:  The oval lesion in line of vein, near left transverse sinus (dotted black arrow)

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206 MRI Brain: Atlas and Text

DISCUSSION Cerebral cavernous hemangioma  (also known as cavernous malformations or simply cavernomas) are a common cerebral vascular malformation  usually with characteristic appearances on MRI. Histologically, cavernous malformations are composed of a mulberry-like cluster of dilated thin-walled capillaries, with surrounding hemosiderin. Unlike arteriovenous malformations (AVMs), there is no normal brain between the interstices of these lesions. Cerebral cavernomas tend to be supratentorial   but can be found anywhere including the brainstem. They are usually solitary, MRI is the modality of choice demonstrating a characteristic ‘popcorn’ or ‘berry’ appearance with a rim of signal loss due to hemosiderin, which demonstrates prominent blooming on susceptibility weighted sequences. T1 and T2 signal is varied internally depending on the age of the blood produces and small fluid levels may be evident. If a recent bleed has occurred, then surrounding edema may be present. The lesions generally do not enhance, although enhancement is possible. The differential is that of other causes of cerebral microhemorrhages including:  Cerebral amyloid angiopathy: Usually numerous small foci  Chronic hypertensive encephalopathy: More common in the basal ganglia  Diffuse axonal injury (DAI)  Cerebral vasculitis  Radiation vasculopathy  Hemorrhagic metastases.

BIBLIOGRAPHY 1. Blitstein MK, Tung GA. MRI of cerebral microhemorrhages. AJR. 2007;189(3):720-5. 2. Vogler R, Castillo M. Dural cavernous angioma: MR features. AJNR. 1995;16(4):773-5.

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CASE 63: RIGHT POSTERIOR WATERSHED INFARCT

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Figures 1A and B: (A) T2W axial:  Hyperintense focus in right posterior watershed zone (dotted black arrows); (B) T1W axial:  Hypointense focus in right posterior watershed zone (thick black arrows)

DICSUSSION Cerebral infarcts in border zones are defined as ischemic lesions in an area between two neighboring vascular territories. These territories can be further classified in two broad categories as: (a) External (cortical) or (b) Internal (subcortical) border zones. Border zone infarcts constitute approximately 10% of all cerebral infarcts. Carotid stenosis or occlusion may occur without marked distal embolization, producing ‘watershed’ or border-zone infarction. Vascular watersheds are the distal arterial territories often at borders between two vascular distributions. Major border zones are found between the anterior and middle cerebral arteries and the middle and posterior cerebral arteries. Reduction in flow affects these zones to the greatest extent because they are farthest from the heart. Borderzone infarcts occur in the posterior parietal region (MCA/PCA border zone), the frontal lobes (ACA/ MCA border zone), and the basal ganglia. These infarcts are often

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208 MRI Brain: Atlas and Text

small and may be confused with lacunar infarcts. The key to diagnosis is the presence of multiple infarcts or wedge-shaped infarcts at the interface between different vascular territories and evidence of carotid occlusion or slow flow. Unilateral posterior external border zone infarcts have been related to cerebral emboli either of cardiac origin or from the common carotid artery, whereas bilateral infarcts are more likely to be caused by underlying hemodynamic impairment (vascular stenosis) Internal (subcortical) border zone infarcts, which typically appear in a linear rosary-like pattern in the centrum semiovale, are caused mainly by hemodynamic compromise. External (cortical) border zone infarcts are believed to be caused by embolism, sometimes with associated hypoperfusion. External border zone infarcts usually follow a benign clinical course, whereas internal border zone infarcts are associated with higher morbidity and a higher risk for future stroke.

TYPES OF WATERSHED INFARCTS Type of infarcts

Location

Border zone

External/cortical

•  Frontal lobe •  Occipital lobe •  Paramedian white matter

•  Between ACA and MCA •  Between PCA and MCA •  Between ACA and MCA

Internal/Subcortical

•  Between LS and MCA •  Between HA and ACA •  Between ACHA and MCA

BIBLIOGRAPHY 1. Hendrikse J, Petersen ET, van Laar PJ, Golay X. Cerebral border zones between distal end branches of intracranial arteries: MR imaging. Radiology. 2008;246(2):572-80. 2. Mangla R, Kolar B, Almast J, Ekholm SE. Border zone infarcts: pathophysiologic and imaging characteristics. RadioGraphics. 2011;31:1201-14.

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CASE 64: VERTEBROBASILAR INSUFFICIENCY

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Figures 1A to D: (A) T2W axial:  Hyperintense focus in right cerebellar lobe; (B) T2W axial:  Hyperintense focus in pons; (C) T2W coronal: Hyperintense focus in pons, more on left side; (D) MRA:  Marked stenosis of basilar artery, small right vertebral artery

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210 MRI Brain: Atlas and Text

DISCUSSION The clinical findings are also correlated with the findings on MR imaging and MR angiography. The most extensive brain lesions are seen in patients with severe basilar and/or combined vertebrobasilar disease. One-half of these, patients show nonspecific-scattered foci of T2 lengthening, similar to the findings found in patients with noncritical stenosis. MR imaging invariably demonstrated more lesions than are clinically suspected. Even though the brain lesions tended to be more extensive in patients with severe vascular disease, the amount of brain tissue damage was not an adequate parameter to document the degree of vascular narrowing. The degree of vascular narrowing is useful in therapy planning MR angiography is a useful complementary examination when lesions in the basilar and distal vertebral vascular territories are diagnosed on MR imaging. MR angiography can differentiate critical from noncritical stenosis and can thus play a key role in the therapeutic decision-making process.

BIBLIOGRAPHY 1. Seynaeve P, Hasso AN, Thompson JR, Hinshaw DB. Basilar and distal vertebral artery occlusive disease: correlation of MR imaging and MR angiography. Jr J Belge Radiol. 1996;79(2):61-7. 2. Wentz K, Rother J, Schwartz A, et al. Intracranial vertebrobasilar system: MR angiography. Radiology. 1994;190:105-10.

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CASE 65: CEREBRAL VENOUS THROMBOSIS

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Figures 1A to D: (A) T2W axial:  Ill-defined hyperintense foci in right temporo-occipital region; (B) T2W axial: Ill-defined hyperintense foci in right fronto-parietal region; (C) T1W axial: Increased signal intensity in right sigmoid sinus in right transverse sinus (cord sign); (D) T1W axial: Increased signal intensity in right sigmoid sinus (cord sign)

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212 MRI Brain: Atlas and Text

Notes: Non-enhanced MR imaging revealed subacutehemorrhagic infarcts involving right side of brain not confined to any particular arterial territory. The right venous sinus-transverse, sigmoid sinus showed slow flow due to thrombosis.

DISCUSSION The hemorrhagic infarct in this patient was not typical of an MCA territory ischemic arterial infarct. Moreover, the patient did not have any neurological deficit. The cause of such a venous infarct was found to be due to a thrombosis in superior sagittal sinus, as revealed by MRV.

BIBLIOGRAPHY 1. Chang R. Isolated cortical venous thrombosis presenting as Subarachnoid. Hemorrhage. 2004;25/10/1676; www.ajnr.org. 2. IC Duncan. Imaging of cerebral isolated cortical vein thrombosis. 2005;184/4/1317, www.ajronline.org. 3. Mahesh R Patel. Brain, venous sinus thrombosis; e-Medicine. Oct 16, 2008.

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CASE 66: POSTERIOR REVERSIBLE ISCHEMIC ENCEPHALOPATHY

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Figures 1A to D: (A) T2W axial:  Hyperintense foci involving both parietooccipital lobes, but asymmetrically; (B) T1W axial: Hyporintense foci involving both parieto-occipital lobes, but asymmetrically; (C) FLAIR axial: Hyperintense foci involving both parieto-occipital lobes, but asymmetrically; (D) FLAIR axial:  Hyperintense foci involving right frontal and both parietal lobes

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214 MRI Brain: Atlas and Text

Note: A 23-year-old female in postpartum. There was also involvement of both cerebellar hemispheres, left side of brainstem. There was evidence of water restriction in DW images. MR venography was normal.

DISCUSSION Posterior reversible encephalopathy syndrome (PRES) describes a usually reversible neurologic syndrome with a variety of presenting symptoms ranging from headache, altered mental status, seizures, and vision loss to loss of consciousness. The term describes a potentially reversible imaging appearance and symptomatology that is shared by a diverse array of causes including hypertension, eclampsia and pre-eclampsia, immunosuppressive medications such as cyclosporine, various antineoplastic agents, severe hypercalcemia, thrombocytopenic syndromes, Henoch-Schönlein purpura, hemolytic uremic syndrome, amyloid angiopathy, systemic lupus erythematosus, and various causes of renal failure. The typical imaging findings of PRES are most apparent as hyperintensity on FLAIR images in the parieto-occipital and posterior frontal cortical and subcortical white matter; less commonly, the brainstem, basal ganglia, and cerebellum are involved. Atypical imaging appearances include contrast enhancement, hemorrhage, and restricted diffusion on MRI. Diffusion-weighted imaging is particularly useful in distinguishing the reversible vasogenic edema from the cytotoxic edema of complete infarction. The calcarine and paramedian occipital-lobe structures are usually spared, a fact that distinguishes reversible posterior leukoencephalopathy from bilateral infarction of the posterior-cerebral-artery territory. PRES cases are classified as either mild, moderate, or severe on the basis of the extent of hyperintensity on FLAIR imaging and the presence of mass effect. The risk of both ischemic infarction, which accounts for 60% of all strokes, and intracranial hemorrhage is high in the peripartum period and

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MRI Atlas of Cases 215

puerperium, but not during the 9-month course of pregnancy itself. Thrombotic infarcts result from hypercoagulable states and thrombosis on top of existing atherosclerotic plaques. Embolic infarcts can result from dissections due to prolonged difficult labor, cardiac valvular disease, and the rare dilated peripartum cardiomyopathy. In those conditions, infarctions typically occur in the major arterial distributions. Watershed infarcts can result from dissections and significant obstetric hemorrhage. Acute fluctuations of blood pressure can result in variable degrees of vasospasm and vasodilatation. This impairment of the cerebral autoregulation eventually leads to disruption of the bloodbrain barrier in the posterior circulation. The predilection for the posterior circulation and watershed zones is believed to be related to its sparse vasomotor sympathetic innervation.

BIBLIOGRAPHY 1. Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996;334:494-500. 2. McKinney AM, Short J, Truwit CL, McKinney ZJ, Kozak OS, SantaCruz KS, Teksam M. Posterior reversible encephalopathy syndrome: incidence of atypical regions of involvement and imaging findings. AJR. 2007;189:904-12.

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CASE 67: INTRAVENTRICULAR HEMORRHAGE

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Figures 1A to D: (A) T1W axial:  Hyperintense focus in left frontal and occipital horns. Note CSF/blood fluid level in right occipital horn; (B) T1W axial at a higher level: Hyperintense focus in left frontal and occipital horns; (C) FLAIR axial:  Hyperintense focus in left frontal and occipital horns. Note CSF/blood fluid level in right occipital horn; (D) FLAIR axial:  Hyperintense focus in left frontal and occipital horns. Note CSF/blood fluid level in right occipital horn. Note the periventricular extension of blood

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MRI Atlas of Cases 217

Note: A 65-year-old male patient was referred for MRI examination  for disorientation.

DISCUSSION Intraventricular hemorrhage (IVH) merely denotes the present of blood within the ventricular system of the brain, and is responsible for significant morbidity due to the development of obstructive hydrocephalus in many of these patients. It can be divided into primary (i.e. the dominant finding is that of blood in the ventricles, with little, if any parenchymal blood) or secondary (where a large extraventricular component is present [e.g. parenchymal or subarachnoid] with secondary extension into the ventricles). Primary intraventricular hemorrhage is far less common than secondary.  In adults, secondary intraventricular hemorrhage is usually the result of an intracerebral hemorrhage (typically basal ganglia hypertensive hemorrhage) or subarachnoid hemorrhage with ventricular reflux.

Causes of Primary Intraventricular Hemorrhage in Adults  Intraventricular tumors – Ependymoma – Choroid plexus/intraventricular metastases – Adjacent parenchymal tumors (e.g. GBM) Vascular malformations: – Aneurysm (e.g. PICA aneurysms have a tendency to fill the 4th ventricle, with little basal cistern blood) – Arteriovenous malformations (AVM) – Subependymal cavernous malformations

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218 MRI Brain: Atlas and Text

Secondary Causes of Intraventricular Hemorrhage Intracerebral hemorrhage: – Hypertensive hemorrhage, hemorrhage (common) – Lobar hemorrhage. Subarachnoid hemorrhage.

especially

basal

ganglia

MRI MRI is more sensitive than CT to detect very small amounts of blood, especially in the posterior fossa, where CT is limited by artifact.  Both FLAIR and more recently susceptibility weighted imaging (SWI) (especially at 3T) appear to be more sensitive to even small amounts of blood. Especially, the latter will demonstrate tiny amounts of blood pooling in the occipital horns, and resulting in susceptibility induced signal drop out. On FLAIR, the signal intensity will vary depending on the timing of the scan. Within 48 hours, blood will appear as hyperintense to the attenuated adjacent CSF. Later the signal is more variable and can be difficult to distinguish from flow-related artefact (particularly in the third and fourth ventricles), unless other sequences are also used.

BIBLIOGRAPHY 1. Bakshi R, Kamran S, Kinkel PR, et al. Fluid-attenuated inversionrecovery MR imaging in acute and subacute cerebral intraventricular hemorrhage. AJNR. 1999;20(4):629-36. 2. Sohn CH, Baik SK, Lee HJ, et al. MR imaging of hyperacute subarachnoid and intraventricular hemorrhage at 3T: a preliminary report of gradient echo T2*-weighted sequences. AJNR. 2005;26(3):662-5.

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CASES (68–78): INFECTIONS/ INFESTATIONS CASE 68: SOLITARY TUBERCULOMA

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Figures 1A to D:  (A) T1W axial:  An ill-defined isointense lesion (dotted arrow) in left frontal region, with edema effacing the sulci and gyri (thick arrow); (B) T2W axial:  A isointense mass (dotted black arrow) with marked edema around it (thick arrow); (C) T1W axial with Gd: Homogeneous enhancement (thin arrow) of the lesion in left frontal pole; (D) T1W sagittal with Gd: Homogeneous enhancement of the lesion in left frontal pole (thin arrow)

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DISCUSSION Tuberculomas are a common form of central nervous system (CNS) tuberculosis presenting as intracranial space-occupying lesions. They usually present with seizures, focal neurological deficits, and/or raised intracranial pressure. They vary in size, from smaller lesions of about a centimeter to larger lesions confused with mass lesions. MR imaging characterizes these lesions and is valuable in making the diagnosis. Hypointensity on T2-weighted images is considered to be a strong indicator in the appropriate clinical setting which helps in the diagnosis. However, signal intensity varies with the stage of tuberculoma. In the noncaseous stage, the granuloma is hypointense in T1W and hyperintense in T2W sequences, with homogeneous enhancement. Whereas, the solid caseating tuberculoma is isointense in T1W and hypointense in T2W sequences, with ring enhancement. T2 shortening is ascribed to a combination of factors—caseation, macrophages and their byproducts (free radicals), fibrosis/gliosis, and inflammatory infiltrate. The hypointensity or isointensity on T2-weighted images may reflect restricted mobile protons within high protein contents in organized caseation, cellular and collagenous layers, the presence of heterogeneously distributed free radicals produced by macrophages during active phagocytosis, and/or highly immobile saturated fatty acids. The conglomerate or coalescent ring enhancement correlated histologically with both the layers of inner collagenous fibers and outer inflammatory cellular infiltrates. In addition, the characteristic location of the lesion in the basal cisterns and along the middle cerebral artery distribution in the Sylvian fissures aid in further characterizing the lesions as possibly tuberculomas.

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BIBLIOGRAPHY 1. Brismar J, Hugosson C, Larsson SG, Lundstedt C, Nyman R. Imaging of tuberculosis III. Tuberculosis as a mimicker of brain tumour. Acta Radiol. 1996;37(4):496-505. 2. Gupta RK, Prakash M, Mishra AM, Husain M, Prasad KN, Husain N. Role of diffusion weighted imaging in differentiation of intracranial tuberculoma and tuberculous abscess from cysticercus granulomas-a report of more than 100 lesions. Eur J Radiol. 2005;55(3):384-92. 3. Kim TK, Chang KH, Kim CJ, Goo JM, Kook MC, Han MH. Intracranial tuberculoma: comparison of MR with pathologic findings. Am J Neuroradiol. 1995;16(9):1903-8.

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CASE 69: MULTIPLE TUBERCULOMATA

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Figures 1A to D:  (A) T1W axial:  Ill defined hypointense area completely effacing the basal cistern is seen; (B) T1W axial with contrast agent Gd:  Conglomeration of multiple ring enhancing lesions in basal cistern; (C) T1W coronal with Gd:  Multiple ring enhancing lesions in posterior cranial fossa; (D) T1W sagittal with Gd:  Multiple ring enhancing lesions in posterior cranial fossa

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MRI Atlas of Cases 223

Notes: This patient presented with acute obstructive hydrocephalus for which ventriculoperitoneal (VP) shunting was done immediately. Hence, the ventricles are decompressed in the above images.

DISCUSSION Intracranial tuberculomas originate as a conglomerate of small tubercles that join to form a mature tuberculoma composed of a central caseation necrosis surrounded by a zone of fibroblasts, epithelioid cells, Langhans giant cells, and lymphocytes. In the early stage of tuberculoma formation, there is a predominate inflammatory reaction with an abundance of giant cells and a capsule poor in collagenous tissue. Later, the capsule becomes richer in collagen, and the surrounding inflammatory reaction may disappear. The central portion of the lesion is transformed into caseous material by a necrotic process the outer enhancing portion of the tuberculoma histologically consisted of layers of inner collagenous fibers and outer inflammatory cellular infiltrates; the former usually correlated with a rim of slight hyperintensity and the latter correlated with complete or partial rim of slight hypointensity on T1-weighted images. On T2-weighted images, both layers showed heterogeneous isointensity or hypointensity no separable from each other. Central caseation necrosis of the tuberculoma was seen mostly as isointense or hypointense on all pulse sequences, particularly on T2-weighted images. The signal intensity and ring-enhancing pattern of the lesion may play an important role in differentiating an intracranial tuberculoma from other ring-enhancing lesions in the brain.

BIBLIOGRAPHY 1. Chang KH, Han MH, Roh JK, et al. Gd-DTPA enhanced MR imaging in intracrnaial tuberculosis. Neuroradiology. 1990;32:19-25. 2. Gupta RK, Pandey R, Khan EM, Mittal P, Gujral RB, Chhabra DK. Intracranial tuberculomas: MRI signal intensity correlation with histopathology and localised proton spectroscopy. Magn Reson Imaging. 1993;11(3):443-9.

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CASE 70: TUBERCULOUS CEREBRAL ABSCESS

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Figures 1A to D: (A) T1W axial image:  An isointense round lesion in deep left frontoparietal region. There is diffuse hypointensity around the lesion; (B) T2W axial:  A well-defined abscess in deep left frontoparietal region. The lesion had  a hypointense center, indicating caseous necrosis, with an thick walled capsule. There was marked edema extending from brain inferior surface to the cortical surface in left side. There was mass effect and midline shift; (C) DWI images:  Mild water restriction; (D) T1W axial with Gd:  A well-defined, thickwalled, irregular ring enhancing lesion

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MRI Atlas of Cases 225

DISCUSSION Cerebral tuberculosis or tuberculosis of the brain manifests predominantly as tuberculous meningitis followed by tuberculoma, tuberculous abscess, and other concomitant forms such as cerebral miliary tuberculosis, tuberculous encephalopathy, tuberculous encephalitis, and tuberculous arteritis. Different forms of cerebral tuberculosis are mainly caused by Mycobacterium tuberculosis and also by nontuberculous mycobacteria such as M. avium-intracellulare in human immunodeficiency virusinfected persons. Cerebral tuberculosis is diagnosed based on clinical features, cerebrospinal fluid studies combined with radiological images. Early diagnosis, prompt institution of antitubercular treatment, and the clinical stage at which the patient presents are important and deciding factors for final outcome. The MRI features of tuberculoma depend on whether the lesion is noncaseating/caseating, with solid center or liquid center, and appear as isotense on gray matter with a slight hypertense rim on T1-weghted images. Noncaseating lesions are hypertense on T2weighted images with nodular enhancement, whereas caseating tuberculomas vary from isointense to hypotense on T2-weighted images with ring enhancement.

Tuberculoma versus Tubercular Abscess Tuberculoma by definition is a parenchymal infection in which granulomas are found, whereas a tuberculous (TB) abscess contains pus but is devoid of granulomas and caseation. In either case, there may be ring enhancement. Tuberculomas usually have decreased T2 signal, whereas the TB abscess is bright on T2 and has a hypointense wall. Both tuberculoma and TB abscess can be surrounded by T2 bright edema in the adjacent brain. There is some evidence that diffusion-weighted imaging (DWI) and ADC are normal in tuberculomas whereas restriction of water movement is seen in TB abscesses. MRS has shown that there are differences between bacterial and mycobacterial

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brain abscesses. Although both can show elevations in lipid and lactate, mycobacterial infections show a conspicuous absence of the other bacterial metabolites. Tuberculomas may also show an elevated lipid peak related to case.

BIBLIOGRAPHY 1. Farrar DJ, Flanigan TP, Gordon NM, Gold RL, Rich JD. Tuberculous brain abscess in a patient with HIV infection: case report and review. Am J Med. 1997;102:297-301. 2. Gupta RK, Vatsala DK, Husain N, et al. Differentiation of tuberculous from pyogenic brain abscesses with in vivo proton MR spectroscopy and magnetization transfer. MR Imaging AJNR. 2001;22:1503-9.

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CASE 71: TUBERCULOSIS OF THE OPTIC NERVE SHEATH

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Figures 1A to D: (A) T1W axial:  Thickening of the right optic nerve sheath extending from the optic chiasma. Note the asymmetric temporal horns; (B) T1W axial with Gd: Marked focal enhancement of the right optic nerve sheath and adjoining optic chiasma; (C) T1W sagittal: Thickening of the right optic nerve sheath extending from the optic chiasma; (D) T1W sagittal with Gd:  Marked focal enhancement of the right optic nerve sheath and adjoining optic chiasma

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Note: This patient was on (ATT) antituberculous regimen for meningitis. He presented with visual disturbances and that was thought to be drug induced. (e.g. ethambutol). Our images confirmed that the patients’ visual symptoms were due to tuberculous optic nerve/chiasma involvement and not drug induced.

DISCUSSION Optic perineuritis (OPN) also termed perioptic neuritis, is an uncommon inflammatory disorder involving the optic nerve. Even though it is an uncommon extrapulmonary manifestation of TB infection, it is important to recognize it because a 12% incidence has been reported. In most cases, diagnosis requires both corroborative evidence, such as a positive skin test, raised ESR, positive CXR for TB, and exclusion of other causes, etc. This case is unique as OPN is a rare association of TB and is also an interesting case due to association of orbital apex syndrome and OPN due to TB without any systemic evidence of TB that is also a rare presentation. Therefore, OPN should be considered in cases of atypical presentation of optic neuritis. ATT drugs especially ethmabutol, INH can damage bilateral optic nerves or retinas and cause acute or insidious bilateral visual loss.

BIBLIOGRAPHY 1. Ali Raghibi, Wan Hazabbah Wan Hitam, Raja Azmi Mohd Noor. Zunaina embong optic perineuritis secondary to tuberculosis: A rare case presentation. Asian Pacific Journal of Tropical Biomedicine. 10.1016/S2221-1691. 2. Hughes EH, Petrushkin H, Sibtain NA, Stanford MR, Plant GT, Graham EM. Tuberculous orbital apex syndromes. Br J Ophthalmol. 2008;92(11):1511-7.

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CASE 72: BACTERIAL MENINGOENCEPHALITIS

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Figures 1A to D: (A) T2W axial images:  Ill-defined hyperintense signal in right temporoparietal region (dotted black arrow). There is evidence of mild mass effect. Note dilated left temporal horn (thin arrow); (B) TIW axial images: Ill-defined hypointense signal in right temporoparietal region (dotted black arrow). There is evidence of mild mass effect. Note dilated left temporal horn (thin arrow); (C) T1W axial with contrast Gd:  At a higher level shows increased vascularity (thick arrow). There is mass effect on the body of right lateral ventricle; (D) T1W coronal with contrast Gd: Increased vascularity in right sylvian fissure (thick arrow) focal gyral enhancement. The vessels were prominent, with perivascular zone prominence, gyri were swollen. Note the mass effect on the right frontal horn

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Note: MRV was normal. DWI showed increased signal intensity.

DISCUSSION Focal intracerebral lesions in acute clinical setting in children always pose a diagnostic problem. In our case, there was evidence of focal meningoencephalitis in the form of gyral enhancement, meningeal enhancement. Clinical improvement was noticed after antituberculous treatment was started. Tuberculous meningitis may manifest in two forms: 1. Leptomeningitis (menignoecephalitis): most common 2. Pachymeningitis. In leptomeningitis, thick tuberculous exudate forms within the subarachnoid space at the base of brain, most pronounced in the interpeduncular fossa, anterior to the pons  and  around the cerebellum. It may also extend into the sylvian fissures, but uncommonly over the surfaces of the cerebral hemispheres. Eventually mass-like regions of caseous necrosis can form within this exudate. Complications include an arteritis which may result in ischemic infarcts. This is seen in approximately a third of cases, and is more common in children. Obstructive hydrocephalus is common. The differential diagnosis will also depend on the particular manifestation. For tuberculous leptomenigitis consider:  Pyogenic meningitis  Leptomeningeal carcinomatosis. For tuberculous pachymeningitis consider:  Neurosarcoidosis  En plaque meningioma  Lymphoma/leukemic infiltration  Erdheim-Chester disease. Viral encephalitis, cortical vein thrombus. Herpes is typically confined to the temporal lobe. MRV did not reveal any filling defect.

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BIBLIOGRAPHY 1. Gupta RK, Gupta S, Singh D, et al. MR imaging and angiography in tuberculous meningitis. Neuroradiology. 1994;36(2):87-92. 2. Gupta RK, Lufkin RB. MR Imaging and Spectroscopy of Central Nervous System Infection. Springer US. 2001:ISBN:0306465515. 3. Koelfen W, Freund M, Guckel F, et al. MRI of encephalitis in children: Comparison of CT and MRI in the acute stage with long-term followup. Neuroradiol. 1996;38:73-9.

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CASE 73: TOXOPLASMOSIS

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Figures 1A and B: (A) T1W axial:  A well-defined isointense round lesion in right side of midbrain (dotted black arrow); (B) T1W axial with Gd: Ring enhancement of the right side midbrain lesion (thick arrow)

Note: This patient presented with Weber’s syndrome (III CN palsy + contralateral hemiplegia). Patient was a known case of HIV.

DISCUSSION Toxoplasmosis is the most common cause of brain abscesses, and B-cell lymphoma is the most common cause of brain neoplasm in an immunocompromised patient. However, toxoplasmosis occurs 2–3 times more frequently than lymphoma in AIDS patients in many geographic areas. Toxoplasmosis is caused by opportunistic infection with the obligate intracellular protozoan Toxoplasma gondii; the incidence ranges between 13.4% and 33% of patients with central nervous system (CNS) complications of AIDS. Primary CNS lymphoma in AIDS is nearly always of high-grade B-cell type, and cells contain the Epstein-Barr virus. Therefore, it has been hypothesized that CNS lymphoma in AIDS may arise from Epstein-Barr virus–infected B-cells. Primary brain lymphoma accounts for 2–10% of brain lesions in patients with

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MRI Atlas of Cases 233

AIDS differentiation of cerebral toxoplasmosis and lymphoma in AIDS patients can be a challenging clinical problem. The two diseases occasionally have been documented to coexist, which further complicates diagnosis. Either disease can present as a single brain mass lesion or as multifocal lesions, with similar neurologic symptoms and signs depending on the location(s) and size of the destructive lesion(s). Toxoplasmosis lesions are most commonly located in the cerebral hemispheric white matter and subcortical gray matter, such as thalamus and basal ganglia. MR demonstrates multiple discrete high-signal foci on T2-weighted images that are mostly heterogeneous, with well-circumscribed margins, and are hyperintense on postcontrast MR edema and hemorrhages commonly are associated with these lesions. MR spectroscopy in a toxoplasmosis lesion, lactate and lipids are markedly elevated, whereas all other normal brain metabolites are virtually absent, which is consistent with the anaerobic acellular environment of an abscess. In contrast, lymphoproliferative lesions show mild-to-moderate increase in lactate and lipids, with preservation of some normal metabolites, but markedly elevated choline, probably because of the increased cellularity.

BIBLIOGRAPHY 1. Berry M, Mukhopadhyay S, Suri S, Chaudhury V. Diagnostic Radiology: Neuroradiology Including Head and Neck Imaging. Jaypee Brothers Medical Publishers (P) Ltd. ISBN: 9788180616365. 2. Lee GT, Antelo F, Anton A. Mlikotic cerebral toxoplasmosis. RadioGraphics. 2009;29:1200-5. 3. Ramsey RG, Gean AD. Neuroimaging of AIDS. Central nervous system toxoplasmosis. Neuroimaging Clin N Am. 1997;7(2):171-86.

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CASE 74: OPPORTUNISTIC BRAIN INFECTION IN IMMUNOCOMPROMISED PATIENT

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Figures 1A to D: (A) T2W axial:  A 3.5 × 2.8 cm hyperintense mass in left basal ganglia, thalamic region. There was marked edema involving left frontal, parietal temporal, basal ganglia, left side midbrain and left cerebellar hemisphere. There was also midline shift and mass effect; (B) T1W axial:  The lesion is hypointense; (C) T1W axial with Gd: Revealed more lesions. The lesions showed confluence of ring lesions in left basal ganglia region; (D) T1W sagittal with Gd: Revealed more lesions. The lesions showed confluence of ring lesions in left basal ganglia region

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MRI Atlas of Cases 235

DISCUSSION Toxoplasmosis. Approximately 70% of cerebral toxoplasmosis lesions are multifocal. Neurologic presentations include subacute headaches, fever, seizures, focal neurologic signs, and progressive dementia. Serology for toxoplasma frequently is positive, but specificity is low; only one-third of cases show a rise in the titer of IgG antibody, and only 50% show intrathecal production of antibody to Toxoplasma gondii. Equally disappointing are the recent studies in polymerase chain reaction for T. gondii in plasma and cerebrospinal fluid, which show low sensitivity and occasional false-positive results. Subsequent clinical response to antitoxoplasma therapy is been the main criterion for diagnosis. Toxoplasmosis lesions are most commonly located in the cerebral hemispheric white matter and subcortical gray matter, such as thalamus and basal ganglia. MR demonstrates multiple discrete high-signal foci on T2-weighted images that are mostly heterogeneous, with well-circumscribed margins, and are hyperintense on postcontrast MR edema and hemorrhages commonly are associated with these lesions.

DIFFERNTIAL DIAGNOSIS  Lymphoma. Between 19% and 71% of primary brain lymphomas present as solitary lesions on neuroimaging studies. Typical clinical presentation consists of progressive neurologic deterioration with encephalopathy, focal signs, and seizures leading to death within 3 months. Cerebrospinal fluid cytology rarely is diagnostic, and brain biopsy generally is required for diagnosis. In the non-AIDS population, primary brain lymphoma shows a solid pattern of contrast enhancement on CT and MR, and subependymal spread of lymphoma encasing the ventricles is highly characteristic when present. The solid hypercellular peripheries of lymphoma lesions are much wider than the inflammatory zones around toxoplasmosis lesions. These lesions on average are larger

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and fewer than toxoplasma lesions. However, in the setting of AIDS, lymphoma often is multicentric and can grow rapidly, more than doubling in size within two weeks. Central areas of necrosis may result from thrombosis and deterioration of the vessels in the oldest parts the lesions. Therefore, on MR, lymphoma is hypointense on T1-weighted images, isointense to hyperintense on T2-weighted images, and often ring enhancing.  In addition to lymphoma, differential diagnoses of focal brain lesions in AIDS include progressive multifocal leukoencephalopathy, cryptococcoma, tuberculoma, syphilitic gumma, bacterial abscesses, lymphomatoid granulomatosis and focal encephalitic lesions of cytomegalovirus combined lesions of lymphoma with toxoplasmosis, or with progressive multifocal leukoencephalopathy, cytomegalovirus, or Candida have been reported in AIDS. There is preliminary evidence that MR spectroscopy is helpful in differentiating toxoplasmosis from lymphoma. Some investigators have found high fludeoxyglucose F18 uptake correlated with a malignant process. However, MR spectroscopy is noninvasive and without radiation, and may become more readily available than positron emission tomography, because it can be performed on clinical MR.

BIBLIOGRAPHY 1. Chang L, Cornford ME, Chiang FL, et al. Radiologic-pathologic correlation. Cerebral toxoplasmosis and lymphoma in AIDS. Am J Neuroradiol. 1995;16(8):1653-63. 2. Gupta RK, Lufkin RB. MR Imaging and Spectroscopy of Central Nervous System Infection. Springer US. 2001:ISBN:0306465515.

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CASE 75: NEUROCYSTICERCOSIS

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Figures 1A to D: (A) T1W axial: With contrast agent shows two “ring with a dot appearance” (dotted black arrows), suggestive of colloidal vesicular stage of neurocysticercosis; (B) T1W axial: With contrast agent shows a “ring with a dot appearance” (dotted black arrow), suggestive of colloidal vesicular stage of neurocysticercosis; (C) T1W coronal with contrast agent: Two “ring with a dot appearance” (dotted black arrows), suggestive of colloidal vesicular stage of neurocysticercosis; (D) T1W sagittal with contrast agent:  Two “ring with a dot appearance” (dotted black arrows), suggestive of colloidal veicular stage of neurocysticercosis

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DISCUSSION Neurocysticercosis is a common neurologic disease caused by the encysted larva of the tapeworm Taenia solium. It can affect any organ, but the most common sites of involvement are the central nervous system (subarachnoid space, ventricles, or spinal cord), eye, and muscle. Neurocysticercosis has been classified into active and nonactive forms on the basis of clinical presentation, results of (cerebrospinal fluid) analysis (i.e, hypoglycorrhachia, eosinophils in sediment, and cysticercus-specific immunoglobin G antibody level), and imaging findings. The active forms include arachnoiditis with or without ventricular obstruction and vasculitis with or without infarction. On the basis of radiologic findings, neurocysticercosis is divided into five stages: noncystic, vesicular, colloidal vesicular, granular nodular, and calcified nodular. It is important to detect as many NCC lesions as possible because the number of lesions remains a main issue when treatment options are discussed. For instance, massive infections of the central nervous system are a potential contraindication to antiparasitic treatment. Considering this specific topic, we found that the last T1-gadolinium images demonstrated significantly more lesions than did all other sequences. This finding could be explained by an improvement in the detection of lesions in the degenerative phase (vesicular colloidal, granular nodular and, in some cases, calcified nodular), which are prone to present enhancement related to an active inflammatory reaction elicited by the parasite in these stages.

BIBLIOGRAPHY 1. LT Lucatoa, MS Guedesa, JR Satoc, et al. The role of conventional MR imaging sequences in the evaluation of neurocysticercosis. AJNR. 2007;28:1501-4. 2. Zee CS, Go JL, Kim PE, et al. Imaging of neurocysticercosis. Neuroimaging Clin N Am. 2000;10:391-407.

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CASE 76: ACUTE DISSEMINATED ENCEPHALOMYELITIS

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Figures 1A to D:  (A) T2W axial:  Diffuse hyperintensity in pons (dotted black arrow); (B) T2W axial:  Diffuse hyperintensity in pons (dotted black arrow), giant panda sign; (C) T1W sagittal:  Focal areas of hypointensity (thick arrow) in enlarged upper cervical cord; (D) T1W sagittal: Focal areas of hyperintensity (thick arrow) in enlarged lower cervical cord

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240 MRI Brain: Atlas and Text

Diffusion weighted imaging (DWI) also showed hyperintense foci involving mid pons, upper pons. The lesions were bilateral and fairly symmetrical. The fluid attenuation inversion recovery (FLAIR) image showed marked hyperintensity in these areas simulating a ‘smiling face’ sign. There were periventricular, bilateral symmetrical hyperintensities, involving the white matter. The T1W images showed hypointensities in the above mentioned areas. The spinal cord showed diffuse cord enlargement with segmental hyperintensities in cervical and thoracic spinal cord. The was no contrast enhancement.

DISCUSSION Acute disseminated encephalomyelitis (ADEM) and multiple sclerosis (MS) are both inflammatory demyelinating diseases of the central nervous system (CNS). Whereas ADEM is usually a monophasic illness, MS is by definition a multiphasic disease, which frequently results in step wise or steadily progressive deterioration in neurological function. For this reason differentiation of ADEM from MS in a patient with a single clinical episode attributable to CNS demyelination is of prognostic importance. Certain clinical features may help to differentiate the two conditions. ADEM often produces a widespread CNS disturbance with coma or drowsiness, seizures, and multifocal neurological signs implicating the brain, spinal cord and optic nerves. In contrast, MS usually presents as a monosymptomatic syndrome such as optic neuritis or a subacute myelopathy. ADEM may also present in this way although with some differences. Thus, optic neuritis in ADEM is usually simultaneously bilateral whereas in MS it is more often unilateral; myelopathy in MS is frequently partial but in ADEM it is often complete and associated with areflexia. Nevertheless, no clinical feature is exclusive to one or other disorder. The distinction of MS from ADEM on a single scan in these patients might be facilitated if there were reliable means of determining the age of lesions. In MS, lesions would be of a

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MRI Atlas of Cases 241

varying age; in most patients with ADEM, they would all be the same age. Studies in MS using gadolinium-DTPA enhanced MRI show a mixture of enhancing and nonenhancing lesions and there is evidence that enhancement (which indicates an abnormal blood-brain barrier) is a consistent feature of new and active lesions. Given that ADEM is usually a monophasic disease, it might be expected that all lesions would enhance in the acute phase, while none would do so in the chronic phase. Gadolinium-DTPA enhanced MRI may therefore prove useful in distinguishing monophasic and multiphasic disease, but a study of enhancement in ADEM has yet to be performed certain patterns of MRI abnormality in ADEM which would be unusual in MS. In particular, there was a pattern in some cases of extensive and relatively symmetric abnormalities in the cerebral and cerebellar white matter, and in one case in the basal ganglia, a rare finding in MS. Serial MRI offers help in differentiating monophasic from multiphasic disease.

BIBLIOGRAPHY 1. Kesselring J, Miller DH, Robb SA, et al. Acute disseminated encephalomyelitis. MRI findings and the distinction from multiple sclerosis. Brain. 1990;11:291-302. 2. Singh S, Alexander M, Korah IP. Acute disseminated encephalomyelitis: MR imaging features. Am J Roentgenol. 1999;173:1101-7.

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CASE 77: VIRAL ENCEPHALITIS

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Figures 1A to D: (A) T2W axial: Diffuse hyperintensity (dotted black arrow) in right high frontoparietal region; (B) T1W axial: Diffuse hyperintensity (dotted black arrow) in right high frontoparietal region; (C) T2W axial: Diffuse hyperintensity (dotted black arrow) in right temporal region. The insular and cingulate gyri were also involved. The cortical gyri were swollen, with mild mass effect; (D) T2W coronal: Diffuse hyperintensity with swollen gyri in right side (dotted black arrow). Note the mass effect on the right lateral ventricle (thick arrow)

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MRI Atlas of Cases 243

DISCUSSION Encephalitis refers to parenchymal inflammation caused by a variety of pathogens, most commonly viruses. Some agents have a predilection for particular areas of the brain; for example, herpes simplex Type I favors the limbic system, cytomegalovirus favors the periventricular white matter, and Listeria monocytogenes favor the brainstem and cerebellum. Other agents may affect multifocal areas of cortex. MR imaging usually shows abnormal hypertensity on T2- and fluid attenuation inversion recovery (FLAIR)-weighted images in the gray matter, white matter, and/or deep gray nuclei; diffusion restriction is commonly seen. Viral encephalitis is one of the most common cause of fatal encephalitis. Patients will usually present with altered consciousness, mentation, focal CN deficits, seizures, and other neurologic deficits, along with fever. T2-weighted MRI will usually reveal a unilateral increase in signal intensity in the temporal region, with cingulate and insulate gyri often involved. In fact, this combination of findings, cingulate and temporal region edema, is the discriminatory factor which makes this appearance classic for herpes simplex virus encephalitis. The involvement of two different vascular territories, the anterior cerebral artery (ACA) supplying the cingulate gyrus, and the middle cerebral artery (MCA) supplying the frontotemporal region, makes a vascular etiology less likely, leaving an inflammatory etiology to be the most likely cause. Isolated hyperintensity of the substantia nigra on T2-weighted images in patients with St Louis Encephalitis. The thalamic lesions were characteristically bilateral and were hemorragic in Japanese encephalitis. Changes on MRI included abnormalities of the brainstem, basal ganglia and spinal cord. Bilateral lentiform nucleus involvement, especially the putamen is seen in Cruztfield Jacob’ encephalitis. T2-weighted MRI reveals hyperintensity corresponding to edematous changes in the temporal lobes inferior frontal lobes, and insula, with a predilection for the medial temporal lobes. Foci of hemorrhage occasionally can be observed on MRI. MRI is preferred for imaging and follow-up studies of viral encephalitis.

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Typically, temporal lobe T2 hyperintensity spares the basal ganglia in HSV infection. Although this appearance was previously believed pathognomonic for herpes involvement, similar findings can be observed in progressive multifocal leukoencephalopathy and primary CNS lymphoma. Patchy parenchymal or gyral enhancement can be observed. Reports of restricted diffusion in herpes encephalitis exist with corresponding T2 hyperintensity reflecting edema. Reports suggest diffusion-weighted imaging may be more sensitive in the detection of HSV involvement than conventional MRI sequences and may mimic an infarct with involvement of the cortical regions of the temporal lobe.

BIBLIOGRAPHY 1. Handiquea SK, Dasb RR, Barmanb K. Temporal lobe involvement in Japanese encephalitis: Problems in differential diagnosis. AJNR. 2006;27:1027-31. 2. Tsuchiya K, Katase S, Yoshino A, Hachiya J. Diffusion-weighted MR imaging of encephalitis. Am J Roentgenol. 1999;173:1097-9.

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CASE 78: RHINO-ORBITO-CEREBRAL ZYGOMYCOSIS

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Figures 1A to D:  (A) T2W axial:  Left eye proptosis (thin arrow), increased signal in the retrobulbar orbital fat, and left ethmoidal sinusitis (dotted black arrow). Further T2W axial show loss of normal signal void from left internal carotid artery and focal increased signal intensity in left temporal lobe; (B) T2W axial: Mucosal thickening in ethmoidal, maxillary and sphenoidal sinuses. There is increased signal intensity in left temporal lobe (thick arrow); (C) T1W axial with Gd: Fat suppressed shows thickening of left side cavernous sinus (thick arrow) biopsy of nasal/sinus mucosa revealed mucormycosis; (D) T1W axial with Gd: Marked mucosal thickening in maxillary sinus (dotted black arrows) and faint enhancement in left temporal lobe lesion and leptomeningeal enhancement

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DISCUSSION Fungal sinusitis is an important clinical problem with diverse manifestations. It should be considered in all immunocompromised patients, patients with poorly controlled diabetes and in all patients with chronic sinusitis. It is the most lethal form of fungal sinusitis, with a reported mortality of 50–80%. Up to 80% of invasive fungal infections in this group are caused by fungi belonging to the order zygomycetes, such as Rhizopus, Rhizomucor, Absidia, and Mucor, and infection by these organisms is sometimes termed zygomycosis. It is caused by one of the members of the mucoraceal family, including Absidia, Mucor, and Rhizopus. After inhalation into the nasal cavity and paranasal sinuses, the fungi infect the immunosuppressed or diabetic host by causing a necrotizing vasculitis of the nose and sinuses, and rapidly extend into the orbits, deep face, and cranial cavity. This results from perivascular, perineural, or direct soft-tissue invasion by the fungi, causing a suppurative arteritis, vascular thrombosis, and infarction of surrounding tissues. In the appropriate clinical context invasive fungal sinusitis is defined by the presence of fungal hyphae within the mucosa, submucosa, bone, or blood vessels of the paranasal sinuses. Invasive fungal sinusitis is subdivided into acute invasive fungal sinusitis, chronic invasive fungal sinusitis, and chronic granulomatous invasive fungal sinusitis. Conversely, noninvasive fungal sinusitis is defined by the absence of hyphae within the mucosal and other tissues of the paranasal sinuses. Noninvasive fungal sinusitis is subdivided into allergic fungal sinusitis and fungus ball. These five subtypes are distinct entities with different clinical and radiologic features, the imaging findings of rhinocerebral mucormycosis on CT and MR imaging are diagnostic. These include soft-tissue opacification of sinuses with hyperdense material, nodular mucosal thickening, and an absence of fluid levels in the maxillary, ethmoid, frontal, and sphenoid sinuses, in decreasing order of incidence. Sinus contents have a variety of MR signal characteristics, including T2 hyperintensity or marked hypointensity on all sequences,

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possibly secondary to the presence of iron and manganese in the fungal elements. Soft-tissue infiltration of the deep face and obliteration of the normal fat planes in the infratemporal fossa, pterygopalatine fossa, pterygomaxillary fissure, and periantral fat are often present. Typically, proptosis occurs because of enhancing soft-tissue masses crowding the orbital apex and the cavernous sinuses. Thickening and lateral displacement of the medial rectus muscle are characteristic of orbital invasion from disease in the ethmoid sinuses. Lack of enhancement of the superior ophthalmic vein or ophthalmic and internal carotid arteries may be seen and is related to vasculitis and thrombosis. Intracranial findings include infarcts related to vascular thrombosis, mycotic emboli, and frontal lobe abscesses. CT is better to assess for bone changes, MR imaging is superior in evaluating intracranial and intraorbital extension of the disease.

BIBLIOGRAPHY 1. Aribandi M, McCoy VA, Bazan C 3rd. Imaging features of invasive and noninvasive fungal sinusitis: a review. Radiographics. 2007; 27(5):1283-96. 2. Chan LL, Singh S, Jones D, Diaz EM Jr, Ginsberg LE. Imaging of mucormycosis skull base osteomyelitis. Am J Neuroradiol. 2000;21(5):828-31.

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CASES (79–100): MISCELLANEOUS CASE 79: WILSON’S DISEASE

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Figures 1A to D:  (A) T1W FLAIR: Bilateral, symmetrical hyperintensities involving of basal ganglia, (dotted black arrows) thalami (thick arrows); (B) T2W axial: Bilateral, symmetrical hyperintensities involving of midbrain (dotted black arrow); (C) T1W axial: Bilateral, symmetrical hyperintensities involving of both sides of pons (thick arrow) and tegmentum, near the aqueduct of Sylvius; (D) T2W coronal: Bilateral, symmetrical hyperintensities involving of basal ganglia, thalami (thick arrow)

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DISCUSSION Wilson’s disease is an autosomal recessive disorder involving copper metabolism. Copper accumulates in the tissues of patients primarily in the liver and later in the brain. In Wilson’s disease, ceruloplasmin, the serum transport protein for copper, is deficient. Copper is accumulated in the liver, and after hepatic binding sites are saturated. In the brain, there is a predilection for the extrapyramidal system, leading to disorders of movement. The earliest symptoms of Wilson’s disease are dysarthria and difficulty with the hands, but personality and psychiatric problems develop later, together with neurologic abnormalities that can be grouped into four common clinical types: Parkinsonian, pseudosclerotic (tremor, dysarthria, and ataxia), dystonic, and choreic. Neurologic symptoms of Wilson’s disease are usually caused by cerebral copper accumulation sufficient to destroy nerve cells. Proton density- and T2-weighted and FLAIR images reveal symmetrical high-signal intensity in the putamina and in the heads of the caudate nuclei, with an impression of some swelling of these nuclei. The globus pallidus appeared uninvolved. The brain lesions are usually bilateral and often symmetrical, involving the putamen, caudate nucleus, globus pallidus, claustrum, thalamus, cortical/subcortical regions, mesencephalon, pons, vermis, and dentate nucleus.

BIBLIOGRAPHY 1. King AD, Walshe JM, Kendall BE, Chinn RJ, Paley MN, Wilkinson ID, et al. Cranial MR imaging in Wilson’s disease. AJR. 1996;167(6):1579-84. 2. Sener RN. Diffusion MR imaging changes associated with Wilson disease. AJNR. 2003;24(5):965-7.

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CASE 80: TUBEROUS SCLEROSIS

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Figures 1A to D: (A) T1W axial: Multiple isointense subependymal nodules (dotted black arrows) on both lateral ventricles bodies; (B) T1W axial images with contrast: Multiple isointense subependymal nodules on either side of foramen of Monro. One large nodule in left side shows contrast enhancement (thick arrow); (C) T1W sagittal with contrast: One large nodule, at foramen of Monro, measuring 10 × 6 mm, showing contrast enhancement (thick arrow); (D) T2-weighted coronal: Multiple cortical tubers in both cerebral hemispheres, the largest measuring 8 mm (arrowhead)

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DISCUSSION Tuberous sclerosis was first described by von Recklinghausen. But Bourneville provided a detailed report of the neurologic symptoms and gross cerebral pathologic features of tuberous sclerosis. Tuberous sclerosis is now recognized as the second most frequently occurring neurocutaneous syndrome after neurofibromatosis type 1 and is characterized by dysplasias and neoplasias of organs derived from all three embryonic germ layers. The clinical diagnosis of this disease in the past typically depended on the identification of the characteristic cutaneous manifestations of tuberous sclerosis and the classic triad of seizures, mental retardation, and facial angiofibromas. The four major intracranial manifestations of tuberous sclerosis are subependymal nodules, subependymal giant cell astrocytomas, cortical tubers, and white matter abnormalities. Numerous white matter abnormalities have been identified by using cross-sectional imaging. These include wedgeshaped, tumefactive, and linear or curvilinear (i.e. radial band) lesions in the cerebral hemispheres and multiple linear bands extending from a conglomerate focus near the fourth ventricle into the cerebellar hemisphere. White matter abnormalities are commonly seen at CT, but they are generally more numerous and conspicuous at MR imaging. Magnetization transfer and fluidattenuated inversion-recovery images are particularly sensitive to these abnormalities; consequently, MR imaging findings may be dominated by white matter changes in some patients with tuberous sclerosis. Visualization of radial bands, which appear to be specific to tuberous sclerosis, may be helpful in distinguishing this disease from other possible entities such as demyelinating or dysmyelinating processes, infection, tumor, or ischemic change. This neurocutaneous syndrome which produces various types of benign tumors involving various organs, such as rhabdomyomas in the heart, angiomyolipomas in the kidneys, and astrocytomas in the brain. The most frequent neurological signs of tuberous sclerosis are epilepsy and mental retardation, which respectively affect about 80% and 60% of the patients. Astrocytomas are

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present only in 5–10% of the cases. Although these tumors are histologically benign and homogeneous in nature, consisting of subependymal giant cell astrocytomas, they have a potentially severe prognosis as they represent the major cause of death in tuberous sclerosis. When they grow, this results in the obstruction of CSF flow because they are localized near the foramen of Monro, on one or both sides.

BIBLIOGRAPHY 1. Bernauer TA. The radial bands sign. Radiology. 1999;212:761-2. 2. Nabbout R, Santos M, Rolland Y, Delalande O, Dulac O, Chiron C. Early diagnosis of subependymal giant cell astrocytoma in children with tuberous sclerosis. J Neurol Neurosurg Psychiatry. 1999;66: 370-5.

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CASE 81: CENTRAL PONTINE MYELINOLYSIS

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Figures 1A to D:  (A) T2W axial: A well-defined central hyperintense lesion (dotted black arrow); (B) T1W sagittal: Symmetrical central pontine hyperintense signals (black arrow); (C) T1W axial: Symmetrical central pontine hyperintense signals (black arrow); (D) FLAIR axial: Marked hyperintensity in central pons (dotted black arrow)

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DISCUSSION Central pontine myelinolysis (CPM), first described in 1959 by Adams et al, is characterized by regions of demyelination throughout the brain but that are most prominent in the pons. The original patients studied were all chronic alcoholics, but subsequently, the condition has been found in children and in other patients with electrolyte abnormalities, most notably hyponatremia that had been corrected rapidly. The symptoms of CPM include spastic quadriparesis, pseudobulbar palsy, and acute changes in mental status leading to altered levels of consciousness, coma, or death. This condition originally was thought to be uniformly fatal, but theme have been recent reports of survival accompanied by varying degrees of residual neurologic deficits are prolonged T1 and T2 relaxation within the central pons, with sparing of the pontine tegmentum and ventrolateral pons. Typically, the clinical symptoms are spastic paraparesis or quadriparesis with pseudobulbar palsies including extraocular muscle weakness, dysarthria, and dysphagia—worsen rapidly 3–5 days after correction of an electrolyte imbalance. Ultimately, a state of pseudocoma (locked-in syndrome) occurs, and death may follow within 3–5 weeks. The typical histopathologic features include symmetric demyelination of the base of the pons, spreading centrifugally from the median naphe. There is relative sparing of the ventrolateral longitudinal fibers, neurons, axis cylinders, and blood vessels. Central pontine myelinolysis (CPM) occurs in the setting of rapidly corrected hyponatremia, especially in chronically debilitated patients. Central pontine myelinolysis (CPM) is an osmolar disturbance resulting in demyelination that is initially difficult to detect with convention CT and MR imaging. Conventional imaging findings (MR and CT) typically lag clinical manifestations, limiting the utility of imaging in early diagnosis of CPM. Because myelinolytic lesions are not demonstrated within the first 2 weeks by using conventional MR imaging pulse sequences, later imaging has been advocated to confirm the diagnosis. Furthermore, the diagnosis of CPM is not ruled out in the setting of normal imaging. CT is even less sensitive than MR imaging for

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detection of early changes of CPM. MR imaging findings of CPM include symmetric signal intensity abnormality in the central pons at T2-weighted and FLAIR imaging. This may progress to classic hyperintense trident-shaped central pontine abnormality, with sparing of the ventrolateral pons and corticospinal tracts. There is associated decreased T1-signal intensity without enhancement or mass effect. The distribution of the imaging findings mirrors the demyelination pathophysiology. In DWI, restricted diffusion is the first imaging manifestation of CPM, occurring within 24 hours of clinical onset of tetraplegia and before detection of abnormalities on conventional MR images including T1-weighted spin-echo, T2-weighted spin-echo, and FLAIR images.

BIBLIOGRAPHY 1. Miller GM, Baker HL Jr, Okazaki H, Whisnant JP. Central pontine myelinolysis and its imitators: MR findings. Radiology. 1988;168: 795-802. 2. Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. Am J Neuroradiol. 2004;25:210-3.

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CASE 82: NEUROSARCOIDOSIS

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Figures 1A to D:  (A) T1W axial: An ill-defined hypointense lesion along the basal meninges, close to the left side cavernous sinus. (thick black arrow); (B) T1W axial with Gd: Marked thickening and enhancement of the pachymeninges (dotted black arrow); (C) T1W coronal with Gd: Marked thickening and enhancement of the pachymeninges, especially along the tentorium and calvarium. (dotted black arrows); (D) T1W sagittal with Gd: Marked thickening and enhancement of the pachymeninges, especially along the tentorium and calvarium (thick black arrow). Note the dural tail (arrowhead)

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DISCUSSION Sarcoidosis is a multisystem granulomatous disease of unknown etiology, usually presenting with hilar adenopathy and pulmonary infiltration. This typical presentation is seen in about 90% of cases. Sarcoidosis can also present systemically, involving the skin, eye, lymph nodes, bones, and central nervous system. Central nervous system involvement has been found in 5 to 16% of sarcoidosis cases at autopsy, however, neurologic symptoms occur in about 3 to 9% of cases. In those patients presenting with isolated neurologic symptoms, the most common manifestations appears to be optic or facial nerve disease. Histopathologically, the CNS involvement is believed to be primarily leptomeningeal with inflammatory exudates extending from the subarachnoid space along the Virchow-Robin spaces into the brain parenchyma. The Virchow-Robin spaces are relatively large at the base of the brain, which may correlate with the involvement of the basal leptomeninges, including the hypothalamus, pituitary, third ventricle, optic and other cranial nerves. Radiologically, the granulomatous lesions are usually isointense relative to gray matter on T1-weighted images, and isointense to hyperintense on T2-weighted images and enhance homogeneously. The pachymeninges consist of the dura and arachnoid. Although normal dura enhances, it should appear thin and patchy. The differential diagnosis for abnormal pachymeningeal enhancement includes the following:  Postoperative status  Intracranial hypotension  Granulomatous disease (sarcoidosis and Wegener’s granulomatosis)  Infection (fungal, tuberculous, and syphilis)  Primary neoplasm (meningioma, reactive)  Metastatic disease (breast carcinoma, prostate carcinoma, and lymphoma)

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Intracranial hypotension results in very thick pachymeninges. Enhancement is attributable to vasocongestive effects. The leptomeninges are typically uninvolved. Granulomatous and infectious conditions classically occur along the basilar pachymeninges, as in our case. Biopsy confirmed the sarcoidosis. Meningiomas enhance avidly and sometimes display a dural tail. Reactive pachymeningeal enhancement and thickening can occur more than 1 cm away from an underlying intra-axial neoplasm as a result of vasocongestion and edema. Metastases to the pachymeninges are often associated with leptomeningeal enhancement as well. BIBLIOGRAPHY 1. Bode MK, Tikkakoski T, Tuisku S, Kronqvist E, Tuominen H. Isolated neurosarcoidosis: MR findings and pathologic correlation. Acta Radiologica. 2001; 42(6):563-7. 2. Osborn AG. Diagnostic Neuroradiology. Mosby, 1994. 3. Smirniotopoulos JG, Murphy FM, Rushing EJ, Rees JH, Schroeder JW. Patterns of contrast enhancement in the brain and meninges. Radiographics. 2007;27(2):525-51.

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CASE 83: IDIOPATHIC INTRACRANIAL HYPERTENSION (IICHT)/PSEUDOTUMOR CEREBRI

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Figures 1A to D: (A) T2W axial:  Tortuosity of the optic nerve (dotted black arrow); (B) T2W sagittal:  Flattening of the posterior globe (thick arrow) and enlarged optic nerve sheath (dotted black arrow); (C) T2W axial:  Tortuosity of the optic nerve (short thick arrow) and empty sella (long thick arrow); (D) MRV in coronal plane:  Bilateral transverse sinus stenosis (arrowheads)

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DISCUSSION Pseudotumor cerebri is a clinical entity of uncertain etiology characterized by intracranial hypertension. The syndrome classically manifests with headaches and visual changes in women with obesity. Traditionally, imaging ruled out secondary causes of elevated CSF pressure but now may reveal findings frequently seen in patients with PTC including the following: flattening of the globe, an empty sella, an enlarged optic nerve sheath, protrusion and enhancement of the optic nerve head, and increased tortuosity of the optic nerve. The absence of a clear identifiable etiology for a clinical syndrome characterized by elevated ICP exists in nearly 90% of cases, and this ambiguity inevitably has led to the replacement of the misnomer benign intracranial hypertension with IIH in light of the incidence of vision loss resulting from this condition. The empty sella sign is associated with the longstanding effects of increased ICP and is thought to result from a downward herniation of an arachnocele through the diaphragma sella. Transverse sinus narrowing can be seen best on MR venography and is thought to represent the effect of increased ICP. This particular imaging finding is more frequently noticed on MR venography studies. Globe flattening may be explained by the direct correlation between elevated ICP and IOP via the transmission of elevated CSF pressure through the subarachnoid space, extending through the Optic nerve sheath to the posterior globe. Protrusion of the right optic nerve head and horizontal tortuosity of the optic nerve are seen.

BIBLIOGRAPHY 1. Degnana AJ, Levya LM. Pseudotumor cerebri: brief review of clinical syndrome and imaging findings. AJNR. 2011;32:1986-93. 2. Suzuki H, Takanashi J, Kobayashi K, et al. MR imaging of idiopathic intracranial hypertension. AJNR. 2001;22:196-9.

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CASE 84: OBSTRUCTIVE HYDROCEPHALUS: AQUEDUCTAL STENOSIS

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Figures 1A and B:  (A) T1W sagittal: Dilated lateral ventricle (dotted black arrow) and stenosed aqueductal of sylvius (thick arrow); (B) T1W axial: Slit like fourth ventricle (arrowhead)

DISCUSSION Congenital hydrocephalus occurs in 1 fetus out of every thousand, with 20% of these caused by aqueductal stenosis. The condition of aqueductal stenosis may be congenital, including X-linked and autosomal recessive inheritance, or acquired through an intrauterine infection or intraventricular hemorrhage. The MR imaging modality is most often utilized to diagnose aqueductal stenosis due to its high contrast resolution, multiplanar capabilities, and sensitivity to flow. On conventional spin-echo images, a cerebrospinal fluid (CSF) flow void can be evaluated in the aqueduct. A flow void is caused by flow speed variations of the CSF related to the cardiac cycle. The degree of CSF flow void

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on T2-weighted images is more frequent in children between 1 and 6 years of age compared to adults, and least frequent in neonates. In the case of an aqueductal stenosis, the CSF flow void is either pronounced or absent. A pronounced flow void occurs when the aqueduct is more narrow than normal but not completely obstructed. In this case, the same amount of CSF has to pass through a narrower channel and, therefore, has increased velocity. In the case of complete obstruction of the aqueduct, the CSF flow void is absent. In some cases of aqueductal stenosis, the characteristic CSF flow voids are not present.

BIBLIOGRAPHY 1. Atlas S, et al. Aqueductal stenosis: Evaluation with gradient-Echo rapid MR imaging. Radiology. 1988;169:449-53. 2. Parkkola R, et al. Cerebrospinal fluid flow in children with normal and dilated ventricles studied by MR imaging. Acta Radiologica. 2001;42:33-8.

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CASE 85: TRAUMATIC ATLANTOAXIAL JOINT SUBLUXATION

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Figures 1A to D: (A) T2W sagittal: Displaced fracture of tip of dens (3); Other structures shown are 1. Anterior arch of atlas (C1), 2. Posterior arch of atlas, 4. Body of Dens (C2); (B) T1W sagittal: Kinking and compression of cervical cord at C2 level (Dotted black arrow); (C) T2W sagittal: It showed fracture of the tip of dens, displacement of the fractured segment along with anterior arch of atlas. There was a type II dens fibrous tissue separating them from rest of the body of dens. All fratured ends were smooth with well-defined cortex; (D) T1W sagittal: Zoomed area of dens tip fracture. The atlantodens distance was >6 mm. The dens-basion distance was 1. There was wide separation of arches of atlas, interspinous distance between C1 and C2

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DISCUSSION Stability of the atlantoaxial joint is predominantly maintained by the cruciate ligament and the alar ligaments. The cruciate ligament is formed by the superior and inferior longitudinal bands and the transverse ligament. The transverse ligament of the atlas attach posterior to the synovial cavity that surrounds the dens, providing posterior and lateral stability to the joint. The paired alar ligaments attach the anterolateral dens to the skullbase for additional support. The atlantoaxial distance is normally maintained in flexion and extension. Disruption of the transverse ligaments leads to atlantoaxial subluxation, which is defined as an increase in the distance between the posterior aspect of the C1 arch and the dens to greater than 2.5 mm in adults. In children the upper limit of the atlantoaxial distance is 5 mm. Without the posterior support of the transverse ligament the dens is displaced posteriorly, which is most pronounced on flexion views. The most common cause of transverse ligament laxity is rheumatoid arthritis. Other causes include traumatic rupture of the transverse ligament and Down’s syndrome. Atlantoaxial subluxation can be complicated by narrowing of the spinal canal and cord compression. This is not only due to posterior displacement of the dens but by pannus formation around the dens which can only be seen on MRI. Atlantoaxial instability (AAI) is characterized by excessive movement at the junction between the atlas (C1) and axis (C2) as a result of either a bony or ligamentous abnormality. Neurologic symptoms occur when the spinal cord is involved.

BIBLIOGRAPHY 1. Dorothy I Bulas, Charles R Fitz, Dennis L Johnson. Traumatic atlantooccipital dislocation. Radiology. 1993;188:155-8. 2. Hung SC, Wu HM, Guo WY. Revisiting anterior atlantoaxial subluxation with overlooked information on MR images. Am J Neuroradiol. 2009. 3. Philip F, Benedetti Linda M, Fahr Lawrence, R Kuhns. MR imaging findings in spinal ligamentous injury. AJR. 2000;175:661-5.

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CASE 86: CENTRAL PONTINE MYELINOLYSIS 2

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Figures 1A and B:  (A) T2W axial: Hyperintense foci seen in entire pons belly (dotted black arrow); (B) T1W axial: Hypointense foci seen in entire pons belly (thick arrow)

DISCUSSION Central pntine myelinolysis (CPM) is a demyelinating disease primarily of the pons, but also occasionally associated with extrapontine demyelinating lesions in the region of the thalami, basal ganglia, white matter of the cerebellum and in the deep layers of the cerebral cortex. The most common underlying condition is chronic alcoholism and associated hepatic cirrhosis. Other underlying conditions include correction of hyponatremia, liver transplantation and severe burns. Although the etiology and pathogenesis of the disease are still uncertain, it is thought to be due to sudden changes in serum sodium levels which have been found to cause patches of demyelination in animal studies. The variety of clinical presentation causes a clinical diagnosis to be difficult. In recent years, neuroradiological modalities, in particular MRI, have been utilized to further support a diagnosis of CPM. The radiological findings, however, do not closely correlate with the

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clinical picture and can lag behind for weeks. The classic lesion of CPM is described as a symmetrical butterfly-shaped patch of demyelination within the dorsal pons. Chronic lesions of CPM are composed of intense fibrillary gliosis with astrocyte proliferation. MRI is the preferred imaging modality especially for early diagnosis. Initially, abnormalities are typically not seen on T1weighted images, but lesions in the central pons may appear hyperintense on T2-weighted and fluid-attenuation inversion recovery (FLAIR) images, presumably due to the presence of endothelial injury-induced microhemorrhages. Occasionally, these lesions can appear symmetrical and hypointense on T1weighted images. Contrast enhancement of the lesions may be present during the first four weeks after the onset of symptoms. These early abnormalities are thought to be due to central pontine edema, which is reversible, while later abnormalities due to demyelination are irreversible.

BIBLIOGRAPHY 1. Martin PF, et al. Central pontine myelinolysis: clinical and MRI correlates. Postgrad Med J. 1995;71:430-42. 2. Yuh W, et al. Temporal changes of MR findings in central pontine myelinolysis. AJNR. 1995;16:975-7.

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CASE 87: MESIAL TEMPORAL SCLEROSIS

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Figures 1A to D:  (A) T2W axial: Hippocampal atrophy and dilated temporal horn in right side (dotted black arrow); (B) T1W axial: Hippocampal atrophy and dilated temporal horn in right side (dotted black arrow); (C) T1W right parasagittal: Temporal opercular atrophy (arrowhead); (D) T2W thin coronal: Altered signal and size asymmetry within the hippocampal formations (thick arrow) and dilatation of temporal horn. Other finding are—atrophy of the fornix and mammillary body in right side

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DISCUSSION Clinical discussion: Hippocampal pathology is the most common cause of intractable temporal lobe epilepsy Mesial temporal sclerosis is characterized by hippocampal sclerosis, gliosis, and cell loss. Internal morphological structure of the hippocampus is disturbed and replaced with gliotic tissue. Hippocampal sclerosis occurs in 65% of epilepsy patients in autopsy studies. Patients present with memory dysfunction and history of febrile seizure. electroencephalography (EEG) will reveal localized anterior temporal lobe abnormality. Neuroimaging discussion: CT is less sensitive than MRI in detection of hippocampal pathology. Hippocampal assessment in MRI is best performed using two planes, one plane through the body of the hippocampus and the other plane at a right angle to this. The coronal view is most sensitive in detecting volume reduction and T2 signal change while the axial plane can better assess posterior extent of hippocampal abnormality. Hippocampal atrophy is hypointense on T1WI and hyperintense on T2WI. T1WI gives better anatomic detail as to the precise location of abnormality. Note that high signal on T2WI may also represent small tumor, increased cerebrospinal fluid (CSF) space, trauma, or flow artifact (Jackson). It may be difficult to diagnose bilateral abnormality because of the size and shape variability of hippocampal structure. Gradient echo technique (SPGR) is more sensitive than spin echo technique because smaller slice thickness allows for improved gray white matter differentiation. Volume study may reveal atrophic, triangularlyshaped hippocampus instead of oval shape. Temporal horn of the lateral ventricle is often enlarged on the side of the atrophic hippocampus. Volume reductions in ipsilateral structures such as the amygdala, mammillary body and fornix may be present. The PET imaging is another useful modality in detection of epileptogenic region in the temporal lobe. During interictal periods, FDG hypometabolism is evident at the focus. This hypometabolism may extend beyond the focus but has not been correlated quantitatively with degree of cell loss. PET offers

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greater spatial resolution than single-photon emission computed tomography (SPECT), and is, therefore, the modality of choice in functional imaging.

BIBLIOGRAPHY 1. Bronen RA, Chang F, Charles JT, et al. Imaging finding in hippocampal sclerosis: correlations with pathology. AJNR. 1991;12:933-40. 2. Jackson GD, Barkovic SF, Duncan JS, Connelly A. Optimizing the diagnosis of hippocampal sclerosis using MR imaging. AJNR. 1993;14:753-62.

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CASE 88: TOLOSA-HUNT SYNDROME

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Figures 1A to D: (A) Axial T1W: Inflammatory thickening of the left side cavernous sinus (dotted black arrow); (B) Axial T2-W: Inflammatory thickening of the left side cavernous sinus (dotted black arrow); (C) Coronal T1-W with Gd: Widening of the cavernous sinus in left side. The granulation tissue is partially encasing the left internal carotid artery shows fullness and enhancement of the left cavernous sinus (thick arrow); (D) Coronal T1-W with Gd: Widening of the cavernous sinus in left side (thick arrow).

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DISCUSSION Tolosa–Hunt syndrome is an idiopathic inflammatory condition of the cavernous sinus which typically presents with pain in the V1 distribution from involvement of the fifth nerve, as well as paresis of the extraocular muscles secondary to involvement of cranial nerves three, four and six in the cavernous sinus. There may also be a Horner’s syndrome secondary to involvement of the sympathetic fibers in the cavernous sinus. The imaging findings are nonspecific, and other entities, such as lymphoma or meningioma involving the cavernous sinus need to be carefully considered. Our patient fulfills all the criteria for Tolosa-Hunt syndrome, namely, recurrent painful ophthalmoplegia, optic nerve involvement, and dramatic response to high-dose steroid therapy with rapid clearing of pain and improvement of vision. Tolosa-Hunt syndrome is one of the facial pain syndromes caused by an idiopathic granulomatous disease involving the cavernous sinus and/or superior orbital fissure which is usually unilateral and presents with an intense ophthalmoplegia and sensory loss over the forehead, while sparing the pupil. The symptoms are secondary to some combination of involvement of cranial nerves III, IV, VI and the ophthalmic division of V. The inflammation is often responsive to corticosteroids and, therefore, it is important to distinguish this entity from lesions such as meningioma, Schwannoma and metastatic disease which might be treated surgically. Magnetic resonance imaging is probably the most valuable technique for diagnosis and continuing followup of these lesions, which may progress as in this case.

BIBLIOGRAPHY 1. Goadsby PJ, Lance JW. Clinicopathological correlation in a case of painful ophthalmoplegia: Tolosa-Hunt syndrome. J Neurol Neurosurg Psychiatry. 1989;52:1290-3. 2. Kwan ESK, Wolpert SM, Hedges TR III, Laucella M. Tolosa-Hunt syndrome revisited: not necessarily a diagnosis of exclusion. Am J Neuroradiol. 1987;8:1067-107. 3. Odabasi Z, Gokcil Z, Atilla S, Pabuscu Y, Vural O, Yardim M. The value of MRI in a case of Tolosa-Hunt syndrome. Clin Neurol Neurosurg. 1997;99(2):151-4.

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CASE 89: FAHR’S DISEASE

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Figures 1A and B:  (A) T1W axial: Bilateral symmetrical, hyperintense foci in basal ganglia, thalamus (dotted black arrows); (B) T2W axial: Hypointense foci in region of dentate nuclei of cerebellum (thick arrows)

DISCUSSION Fahr’s syndrome (Disease) or familial idiopathic basal ganglia calcification is characterized by bilateral basal ganglia calcification particularly the globus pallidus but also the caudate, dentate, and cerebral white matter. The calcium deposits occur in the extracellular and extravascular space often surrounding the capillaries. It is not clear whether the calcification in Fahr’s disease is a metastatic deposition, secondary to local disruption of blood brain barrier, or is due to disorder of neuronal calcium metabolism. Typically the age at onset of clinical symptoms is 30–60 years. There is neither a cure for Fahr’s disease, nor a standard course of treatment. The prognosis is variable and hard to predict.

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DIFFERENTIAL DIAGNOSIS  Normal symmetric basal ganglia calcifications in the elderly.  Pathologic basal ganglia calcifications from endocrine causes or Fahr’s syndrome.  Postinflammatory causes, such as TB, toxoplasmosis, cysticercosis, congenital HIV.

BIBLIOGRAPHY 1. Avrahami E, et al. MRI and CT correlation of the brain in patients with idiopathic intracranial calcification. J Neurol. 1994;241:381-4. 2. Geschwind DH, et al. Identification of a locus on chromosome 14q for idiopathic basal ganglia calcification (Fahr’s disease). Am J Hum Genet. 1999;65:764-72.

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CASE 90: NORMAL PRESSURE HYDROCEPHALUS

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Figures 1A and B:  (A) T1W axial near vault: Symmetrical dilatation of bodies of both the lateral ventricles (dotted black arrows); (B) T1W sagittal: Dilatation of all the ventricles, thinning of body of corpus callosum (thick arrow)

Notes: His MRI studies showed bilateral symmetrical ventricular dilatation involving lateral ventricles, 3rd ventricles with relative sparing of 4th ventricle. There was no evidence of senile atrophic changes. There was no abnormally decreased signal intensity of the structures of the medial temporal lobes; therefore there is no dilatation of the parahippocampal fissures or atrophy of the structures of the medial temporal lobe, including the hippocampus. The corpus callosum was uniformly thinned out. There was no evidence of periventricular signal changes. The cause for hydrocephalus was probably due to normal pressure hydrocephalus.

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MRI Atlas of Cases 275

DISCUSSION Normal pressure hydrocephalus (NPH) is characterized by gait disturbance, mental deterioration, apraxia and urinary incontinence in patients with an enlarged ventricular system and normal cerebrospinal fluid (CSF) pressure. An important pathophysiological feature of NPH is dysfunctional CSF dynamics with reduced absorption through the arachnoid villi, compensatory CSF flow into the periventricular white matter, and transcapillary CSF resorption. The periventricular tissue is characterized pathologically by disruption of the ependyma, edema, neuronal degeneration, and gliosis. CSF studies in patients with NPH have shown neuronal degeneration and no major demyelination. Symptom severity also has been related to CSF levels of neurofilament protein, a marker of neuronal degeneration. A dilated ventricular system is a prerequisite for the diagnosis of NPH. On MR images, marked aqueductal CSF flow (the flow void sign) has been described in NPH, correlating with a favorable outcome after shunt surgery. While this “aqueductal flow void phenomenon” can be observed in healthy individuals, it is most pronounced in patients with chronic, communicating NPH; is less evident in patients with acute, communicating hydrocephalus; and is least evident in patients with atrophy. Ventricular compliance is known to be essentially normal in atrophy; mildly decreased in acute, communicating hydrocephalus; and severely decreased in NPH. The degree of aqueductal signal loss is believed to reflect the velocity of the pulsatile CSF motion, which in turn depends on the relative ventricular compliance and surface area. The diagnosis of NPH was based on the presence of the following: 1) gait disturbance; 2) mental deterioration, urinary incontinence, or both; 3) enlarged ventricles at MR imaging with an Evan’s index (maximal width of frontal horns/maximal width of inner skull) >0.30; 4) lumbar CSF pressure caudate heads) > globi pallidi (GP). The sites of involvement are brainstem substantia nigra/subthalamic nuclei, pons, medulla thalami, dentate nuclei. Diffuse supratentorial white matter T2 hyperintensity may accompany the deep gray matter findings. These areas do not enhance. The telltale laboratory finding is metabolic acidosis with increased lactate levels; the lactate may be detectable with proton or phosphorus magnetic resonance spectroscopy (MRS) examination. The disease is thought to be due to a deficiency in the enzymes associated with pyruvate breakdown; its accumulation leads to lactic acid build-up.

BIBLIOGRAPHY 1. Medina L, et al. MR findings in patients with subacute necrotizing encephalomyelopathy (Leigh syndrome): correlation with biochemical defect. AJR. 1990;154(6):1269-74. 2. Rossi A, et al. Leigh syndrome with COX deficiency and SURFl gene mutations: MR imaging findings. AJNR. 2003;24(6):1188-91.

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CASE 96: HUNTINGTON’S CHOREA

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Figures 1A to D:  (A) T2W axial: Bilateral caudate nuclei (CN) atrophy; (B) T1W axial: Bilateral caudate nuclei atrophy; (C) FLAIR axial: Bilateral caudate nuclei (CN) atrophy; (D) T2W coronal: Bilateral caudate nuclei (CN) atrophy with changes in the frontal horns (Squaring)

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Notes: A 37-year-old female was referred for evaluation of chorea. Huntington gene was positive with three repeats, consistent with Huntington chorea.

DISCUSSION Huntington chorea refers to the  movement disorder seen in Huntington  disease (HD). Unintentional choreoathetoid movements, which demonstrate abrupt random timing and distribution. There is associated memory impairment, with onset at 40–50 years of age. HD is  an autosomal dominant disorder, caused by a mutation in the huntingtin gene on the short arm of chromosome 4. MRI shows there is rounding and dilation of the frontal horns of the lateral ventricles, secondary to caudate/ frontal lobe atrophy. Hypometabolism/hypoperfusion are seen in affected areas on positron emission tomography (PET) and single-photon emission computerized tomography (SPECT) caudate nucleus atrophy is measured on axial images at level of 3rd ventricle. Intercaudate distance (CC) between most medial aspects of CN. CC compared with distance between most lateral aspects of frontal horns (FH) and distance between inner tables (IT) of skull at level of CC • FH/CC ratio • 1CC/IT ratio (bicaudate ratio): is the Most specific and sensitive measure for HD.

DIFFERENTIAL DIAGNOSIS Leigh disease:  Subacute necrotizing encephalomyelopathy – Changes in putamen, CN, and tegmentum – Nonenhancing hypodensities (infarcts) on CT – Tl hypo-, T2 hyperintensities (infarcts) – No atrophy of CN and putamina – Focal involvement of white matter, thalamus, brainstem and cerebellum

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MRI Atlas of Cases 291

Wilson disease:  Rigidity, tremor, dystonia, gait difficulty, dysarthria  CT: Low densities in basal ganglia (BG), cerebellar nuclei, brainstem, and white matter  T2WI: Symmetrical signal hyperintensity in CN, putamen, midbrain, and pons (gliosis and edema) – Asymmetrical hypointensity in frontal white matter – Characteristic irregular areas of hypointensity in CN and putamen  Atrophy of CN and brainstem on CT, MR. Hallervorden-Spatz disease:  Involuntary movements (choreoathetosis), spasticity  Progressive dementia in young adults  Characteristic iron deposition in globus pallidus (GP), red nuclei, substantia nigra (SN) – Diffuse hypointensity in these structures on T2WI – Eye of the tiger sign: Central spot of high signal in medial GP on T2WI  Globus pallidus (GP) atrophy, ± cortical, CN atrophy carbon monoxide poisoning  Bilateral CT hypodensity, T2 hyperintensity in GP.

BIBLIOGRAPHY 1. Grossman RI, Yousem DM. Neuroradiology: The Requisites. Mosby Inc. 2003. ISBN:032300508X. 2. Ho VB, et al. Juvenile Huntington disease: CT and MR features. Am J Neuroradiol. 1995;16:1405-12.

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CASE 97: EMPTY SELLA SYNDROME AND AQUEDUCTAL STENOSIS

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Figures 1A to D: (A) T1W sagittal: Grossly dilated lateral ventricles, aqueductal stenosis, CSF like fluid collection in ballooned sella and thin corpus callosum; (B) T2W axial: CSF collection in sella turcica, small fourth ventricle; (C) T1W axial:  CSF collection in sella turcica, small fourth ventricle; (D) Grossly, symmetrically, dilated bodies of lateral ventricles and periventricular capping due to interstitial edema

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MRI Atlas of Cases 293

Note: A 35-year-old female was referred for evaluation of chronic headache.

DISCUSSION Empty sella syndrome is one in which CSF is easily noted in the empty or partially empty sella due to a patulous diaphragma sellae and extension of the suprasellar arachnoid space inferiorly. This may be seen with aging and in women with pseudotumor cerebri (idiopathic intracranial hypertension) empty sella. In primary type, sella is expanded; the residual pituitary tissue is displaced to the floor of the sella turcica. Secondary causes of partially empty sella include pituitary infarction, surgery, and radiation therapy. Aqueductal stenosis (AS) is the most common cause of congenital  obstructive hydrocephalus, but can also be seen in adults as an acquired abnormality. Aqueductal stenosis can be divided into congenital and acquired, with different etiologies and thus different demographics.   Congenital – Aqueductal webs or diaphragms – Gliosis  Acquired – Extrinsic compression - Tectal plate glioma - Pineal tumor - Posterior fossa tumor - Cerebral vascular malformation – Intrinsic - Infection: meningitis/ventriculitis - Subarachnoid hemorrhage (SAH).

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294 MRI Brain: Atlas and Text

The clinical presentation depends on the severity and age of presentation. Better delineates the extent of obstructive hydrocephalus, with enlargement (often marked) of the lateral and third ventricles. The aqueduct may show funnelling superiorly. The fourth ventricle is not dilated. In cases of secondary obstruction, the underlying abnormality may also be evident. An MRI CSF flow study is helpful.

BIBLIOGRAPHY 1. Levitsky DB, Mack LA, Nyberg DA, et al. Fetal aqueductal stenosis diagnosed sonographically: how grave is the prognosis? Am J Roentgenol. 1995;164(3):725-30. 2. Stoquart-el Sankari S, Lehmann P, Gondry-jouet C, et-al. Phasecontrast MR imaging support for the diagnosis of aqueductal stenosis. Am J Neuroradiol. 2009;30(1):209-14.

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CASE 98: NEUROGLIAL CYST

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Figures 1A to D: (A) T2W axial:  A well-defined hyperintense cystic lesion 1.8 × 1.3 cm in left frontal lobe. There was hypointense peripheral gliotic changes; (B) T1W axial: Hypointensity in the cystic area; (C) FLAIR axial:  Markedly hypointense surrounded by hyperintense ring; (D) DWI:  A well-defined hyperintense cystic lesion 1.8 × 1.3 cm in left frontal lobe. There was hypointense peripheral gliotic changes

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296 MRI Brain: Atlas and Text

Notes: A 33-year-old male was referred for evaluation of seizures. The lesion was intra-axial and showed signal changes similar to CSF in all pulse sequences.

DISCUSSION A neuroglial cyst  (or glioependymal cyst) is a rare  benign epithelial-lined lesion that can potentially occur anywhere in the neuraxis. It represents less than 1% of intracranial cysts. They are glial cells lined, fluid filled cavity, located within the white matter. They can be intra or extra parenchymal with the former being more common. The frontal lobe is thought to be the most typical location. Neuroglial cysts usually follow CSFs signal, hence they are hypointense on T1 and hyperintense on T2. They do not enhance with gadolinium. They are usually suppressed on T2 FLAIR sequences.

DIFFERENTIAL DIAGNOSIS General imaging differential considerations include:  Porencephalic cyst  Arachnoid cyst: Especially for extra parenchymal neuroglial cysts  Ependymal cyst  Epidermoid cyst.

BIBLIOGRAPHY 1. Epelman M, Daneman A, Blaser SI, et al. Differential diagnosis of intracranial cystic lesions at head US: correlation with CT and MR imaging. Radiographics. 2006;26(1):173-96. 2. Osborn AG, Preece MT. Intracranial cysts: radiologic-pathologic correlation and imaging approach. Radiology. 2006;239(3):650-64. 3. Patel A, Ablett M: Neuroglial Cyst, EURORAD case files, 10.1594/ EURORAD/CASE.7682.

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CASE 99: NEUROFIBROMATOSIS TYPE 1

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Figures 1A to D: (A) T2W axial:  Marked plexiform thickening of the lateral side of face and scalp. The plexiform lesion was extending into right orbit, giving rise to proptosis; (B) T1W axial:  The sheet like mass was extending into cavernous sinus as far as the Meckel’s cave. Because of the sphenoid wing hypoplasia the temporal lobe was seen herniating into right orbit; (C) T1W axial with Gd contrast: The plexiform mass showed contrast enhancement. He also had hyperintense focus in right basal ganglias; (D) Plain X-ray skull:  The classic empty orbit sign due to sphenoid wing hypoplasia

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298 MRI Brain: Atlas and Text

Note: A 17-year-old boy was referred for evaluation of unilateral proptosis. He had 4 of the 7 diagnostic criteria for neurofibromatosis-type 1. His ophthalmic examination revealed hamartomas suggestive of Lisch nodules. There was family history of cutaneous neurofibromatosis. Plain X-ray of the skull revealed right side sphenoid wing hypoplasia making the orbit look empty.

DISCUSSION Neurofibromatosis-type 1(NF1) is an inherited phakomatosis with multisystem manifestations. This autosomal dominant condition is one of the most common genetic diseases of the central nervous system, affecting 1:3,000–5,000 of the population. The abnormal gene locus is on the long arm of chromosome 17. There are a number of diagnostic criteria which need to be fulfilled to make the diagnosis. The diagnosis of NF1 requires two or more of the following: 6 or more café-au-lait spots over 5 mm in maximum diameter; 2 or more neurofibromas, or one plexiform neurofibroma; axillary or inguinal freckling; optic gliomas; 2 or more pigmented hamartomas of the iris (Lisch nodules); osseous lesions such as sphenoid dysplasia or thinning of the cortex of a long bone; 1st degree relative with NF1. Clinically, the features include the underlying tumor or enlargement of the soft tissue secondary to plexiform lesions. In addition, epilepsy, mental retardation and precocious puberty, this latter due to hypothalamic involvement, are also features. The most important features from the imaging point of view include gliomas of the optic pathway, kyphoscoliosis, vascular dysplasias, nerve sheath tumors, macrocephaly and sphenoid wing dysplasia. Bony dysplasia of the sphenoid wing is a well-recognized complication of NF1 and this may be associated with herniation of the temporal lobe into the orbits. There is also an increased incidence of plexiform neurofibromas around the orbit and periorbital regions.

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MRI Atlas of Cases 299

Neurofibromas in general and in particular, plexiform neurofibromas are common associations of NFM type 1. Craniofacial plexiform neurofibromas are particularly typical and often involve the orbit producing impaired movement and exophthalmos. They are locally aggressive tumors formed of chords of Schwann cells, collagen, cellular matrix and neurons. On MRI, lesions are mainly low signal on T1 sequences when compared with the brain, with high signal on T2 and variable contrast enhancement.

BIBLIOGRAPHY 1. Jacquemina C, Bosleyb TM, Svedberg H. Orbit deformities in craniofacial neurofibromatosis type 1. AJNR. 2003;24:1678-82. 2. Reed D, Robertson WD, Rootman J, Douglas G. Plexiform neurofibromatosis of the orbit: CT evaluation. Am J Neuroradiol. 1986;7:259-63.

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CASE 100: NEUROFIBROMATOSIS TYPE 2

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Figures 1A and B: (A) T1W axial with Gd:  Bilateral enhancing lesions in internal auditory canals (arrowheads). The lesion in the left shows typical ice-cone appearance; (B) T2W sagittal:  Intramedullary lesion at C3 level and extradural lesion at T4 level

DISCUSSION This case of neurofibromatosis type 2 (NF2) showed the classical ”MISME” syndrome, viz. Multiple Intracranial Schwannomas, Meningiomas, and Ependymomas. This is a hereditary syndrome causing multiple cranial nerve schwannomas, meningiomas, and spinal tumors. It is an autosomal dominant and all NF2 families have chromosome 22q12 abnormalities. The diagnostic criteria are bilateral vestibular Schwannomas; or 1st degree relative with NF2 and 1 vestibular Schwannoma; or 1st degree relative with NF2 and 2 of the following:  Neurofibroma  Meningioma  Glioma  Schwannoma  Posterior subcapsular lenticular opacity.

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MRI Atlas of Cases 301

BIBLIOGRAPHY 1. Aoki S, et al. Neurofibromatosis types 1 and 2: cranial MR findings. Radiology. 1989;172(2):527-34. 2. Pont MS, et al. Lesions of skin and brain: modern imaging of the neurocutaneous syndromes. Am J Roentgenol. 1992;158(6):1193-203.

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Index.indd 303

Index Page numbers followed by f refer to figure and t refer to table

A Abscess 109 Acoustic schwannoma 54, 55, 117 Adenoid cystic carcinoma 163 Adrenoleukodystrophy 277 AIDS dementia complex 160 Aneurysm 54, 55, 217 Apparent diffusion coefficient 79, 180 Aqueductal stenosis 261, 292, 293 Aqueductal webs or diaphragms 293 Arachnoid cyst 54, 55, 146, 148, 168, 296 Arteriovenous fistula 204 Arteriovenous malformation 54, 206, 217 Artery basilar communicating 192 posterior communicating 192 tuberothalamic or polar 192 Atlantoaxial instability 264 Atresia of choana 165 Axonal injury, diffuse 206, 282

B Bacterial meningoencephalitis 229 Barkovich’s classification 163 Basal cistern blood 217

Basal ganglia 108f, 206 hemorrhage 218 Basilar invagination 150 Blood brain barrier 32 Brain anatomy of 8 temporal lobe rest of 23f tuberculosis of 225 Brainstem glioma 54, 59 Breast carcinoma 257

C Capillary malformations 177 Carotid artery, internal 25, 195 Caudate nucleus putamen 24f Cavernous sinus 25, 271 Cavernous malformations 177, 206 Central hyperintense lesion 253f Central nervous system 82, 220, 232, 240 lymphoma 108 Central pontine myelinolysis 2, 253, 254, 265 Cerebellar artery anterior-inferior 199 posterior-inferior 188, 195, 199 superior 195 Cerebellar atrophy 141f Cerebellar hemangioblastoma 105

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Cerebellar ischemic infarct 198 Cerebellar lobe 209f Cerebellar pilocytic astrocytoma 61 Cerebellar tonsillar herniation 137f, 139f Cerebellopontine angle 26, 53, 86 meningioma 52, 54t, 156 Cerebellum 61f, 199 Cerebral amyloid angiopathy 206 Cerebral artery anterior 243 middle 243 posterior 192 territory ischemic infarct 179 Cerebral cavernous hemangioma 206 Cerebral infarcts 207 Cerebral pilocytic astrocytoma 45 Cerebral tuberculosis 225 Cerebral vascular malformation 293 Cerebral vasculitis 206 Cerebral venous thrombosis 211 Cerebrospinal fluid 40, 82, 86, 144, 153, 155, 157, 261, 268, 275 Cervical vertebrae 149f Chamberlain’s line 150 Charge syndrome 165 Chiari malformation 137 Cholesterol 136 Choroid plexus/intraventricular metastases 217 Colloid cyst 152 Coloboma of eye 165 Colpocephaly 133, 162f

Congenital lesions 128 Convexity meningioma 121 Corpus callosum 133, 135f, 292f agenesis of 133, 163 parts of 133 tentorium 23f Cortical hyperintensity 128f Cranial fossa giant cyst, posterior 171 meningioma, posterior 93 middle 143f posterior 146 Craniopharyngioma 75 in adult 125 Craniovertebral junction anomaly 149 Cystic lesion 295f in posterior cranial fossa 148 Cystic mass with internal septations 85f Cystic or cyst-like malformations of posterior fossa 147

D Dandy-Walker malformation 147, 170 Dermoid inclusion cyst 168 Devic disease 284, 285 Diffusion-weighted images 26, 86, 94, 225 Dural tail sign 91 Dural venous sinus thrombosis 197 Dysembryoplastic neuroepithelial tumor 88 Dysgenesis of corpus callosum 132

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Index 305

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Ectopic neurohypophysis 279 En plaque meningioma 230 Encephalitis 243 Encephalomyelitis 239 Encephalomyelopathy 290 Endovascular embolization 107 Ependymal cyst 296 Ependymoma 54, 217 Epidermoid cyst 54, 55, 86, 168, 296 Epidural hemorrhage vs subdural hemorrhage 185 Epithelioid cells, zone of 223 Epstein-Barr virus 232 infected B-cells 232 Erdheim-Chester disease 230 Eye proptosis 245f

Gadolinium 26 Ganglioglioma 42 Giant aneurysm of basilar artery trunk 182 supraclinoid segment of internal carotid artery 194 Giant panda sign 239f Glioblastoma multiforme 81, 82, 95, 109 Gliomas 97, 193, 300 benign 123 low grade 96 Gliosis 293 Globus pallidus thalamus 24f Granulomatous disease 257

F Facial nerve schwannoma 54 Fahr’s syndrome 272 Falx meningioma 49, 64 Fat, lipoma 136 Fatty acids 277 Fibroblasts, zone of 223 Foramen magnum 149f Foramen of Monro 152 Foramen schwannoma, jugular 103 Foramen, left jugular 103f Fossa tumor 293 Frontal sulci 201f Fungal infection 257

H Hemorrhage 218 causes of intraventricular 218 old 136 Hallervorden-Spatz disease 291 Heart defects 165 Hemangiopericytoma 72 Hemorrhagic metastases 206 Hippocampal formation, development of 133 Huntington’s chorea 289, 290 Huntington’s disease 290 Hydrocephalus, normal pressure 274 Hydrogen atom to magnetic resonance imaging 3f Hydromyelia 138

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Hypertensive encephalopathy, chronic 206 Hypothalamus optic chiasma 24f

I Idiopathic intracranial hypertension 259 Ill-defined hypointense lesion 222f in right temporo-occipital region 211f, 229f Ill-defined isointense lesion 219f Infarct, acute vs chronic 180t Interhemispheric cyst or lipoma 133 Intracerebellar heterogeneous mass 105f Intracerebral hemorrhage 218 Intracranial hypotension 257 of posterior pituitary 279f Intraventricular hemorrhage 216, 217 Intraventricular tumors 217 Ischemic encephalopathy, posterior reversible 213 Ischemic stroke 200 Isointense subependymal nodules, multiple 250f

J Jacob’ encephalitis 243 Joubert syndrome 164 Jugular foramen schwannoma 103 Juxtatentorial meningioma 119

L Langhans giant cells 223 zone of 223 Leigh’s disease 287 Leptomeningeal carcinomatosis 230 Leptomeningitis 230 Leukoencephalopathy, progressive multifocal 109 Lipoma 54, 55 of corpus callosum 135 Lobar hemorrhage 218 Lymphocytes, zone of 223 Lymphoma 193, 257 Lymphoma/leukemic infiltration 230

M Malignant tumor 54 McGregor’s line 150 Medullary syndrome, lateral 187 Medullary-cervical cord junction 137f Menignoecephalitis 230 Meningioma 54, 55, 64, 91, 257, 300 atypical 66 multiple 69 of posterior cranial fossa 94 Meningitis 293 Mental retardation 131 Mesial temporal sclerosis 267 Metastases 95 Metastatic disease 257 Methemoglobin 184f

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Index 307

N Neoplasm 257 Nephrogenic systemic fibrosis 36 Neurocysticercosis 237 colloidal vesicular stage of 237f Neurocytoma, recurrent central 57 Neuroepithelial tumor dysembryoblastic 42 dysembryoplastic 89 Neurofibroma 300 Neurofibromatosis type 1 297 type 2 54, 300 Neuroglial cyst 295 Neuromyelitis optica 285 Neurosarcoidosis 230, 256 Non-Hodgkin lymphoma 109 Nuclei of cerebellum 272f

O Obstructive hydrocephalus 261 Optic chiasma 25 Optic groove meningioma 83 Optic nerve right 227f sheath, tuberculosis of 227 tortuosity of 259f Optic perineuritis 228

Pilocytic astrocytomas 46, 62 Pineal tumor 293 Pituitary gland 25 infundibulum 24f Pituitary microadenoma 111 Pituitary neoplasms 112 Pituitary secreting macroadenoma 99 Pituitary stalk 25 Planum sphenoidale meningioma 90 Pleomorphic xanthoastrocytoma 42 Pons belly 265f Pons, diffuse hyperintensity in 239f Porencephalic cyst 296 Probst bundle on ventricles 133 Prosencephalic vein, median 204 Prostate carcinoma 257 Proton density 27 Pseudotumor cerebri 259, 260 Pyogenic meningitis 230

Q Quadrigeminal plate arachnoid cyst, 173 with obstructive hydrocephalus 167

P

R

Pachymeningitis 230 Parenchymal neuroglial cysts 296 Parenchymal tumors 217 Parieto-occipital lobes 213f Parieto-occipital region 45f

Radiation vasculopathy 206 Radiofrequency pulse 2 Rathke’s cleft cyst 154, 155 Rhino-orbito-cerebral zygomycosis 245

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S Sarcoidosis 54, 257 granulomatosis 257 Sella syndrome, empty 292 Skull 151 Smiling face’ sign 240 Solitary tuberculoma 219 Spinal meningiomas, multiple 70 Subarachnoid hemorrhage 218, 293 Subcapsular lenticular opacity, posterior 300 Subdural hematoma, right subacute 184 Subdural hemorrhage 185 Subependymal cavernous malformations 217 Suprasellar cistern 28f Suprasellar mass 125f Syphilis 257 Syringohydromyelia 138 Syringomyelia 138 of cervicothoracic cord 141f Syrinx 138

T Taenia solium 238 Tectal plate glioma 293 Temporal lobe 189, 205 Teratoma 168 Thalamic ischemic infarct, acute right 191 Tolosa-Hunt syndrome 270, 271 Toxoplasma gondii 235 Toxoplasmosis 232

Transverse sinus thrombosis 196 Traumatic atlantoaxial joint subluxation 263 Tuberculoma 193, 225 Tuberculoma vs tubercular abscess 225 Tuberculomata, multiple 222 Tuberculous abscess 225 cerebral 224 Tuberculous leptomeningitis 230 Tuberculous pachymeningitis 230 Tuberculous, infection 257 Tuberous sclerosis 250, 251 Tubulonodular lipoma 136 Tumor 45 benign 54

V Vein of Galen malformation 203 Venous infarct 189 Venous malformations 177 Ventriculitis 293 Vertebrobasilar insufficiency 209 Viral encephalitis 242 Virchow-Robin spaces 101, 257

W Wallenberg’s syndrome 187, 188 Watershed infarct, right posterior 207 Watershed infarct, types of 208 Weber’s syndrome 232 Wegener’s granulomatosis 257 White epidermoid cyst 55 Wilson’s disease 248, 291

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