ExDDx Brain & Spine PDF

ii
Anne G. Osborn, MD, FACR Kevin R. Moore, MD

Distinguished Professor of Radiology Pediatric Radiologist and euroradiologist
William H. and Patricia W. Child Primary Children's Medical Center
Presidential Endowed Chair in Radiology Department of Medical Imaging
University of Utah School of Medicine Salt Lake City, Utah
Salt Lake City, Utah
Lubdha M. Shah, MD
Jeffrey S. Ross, MD Assistant Professor of Radiology
Neuroradiology University of Utah School of Medicine
Barrow eurologicallnstitute Salt Lake City, Utah
St. Joseph's Hospital
Phoenix, Arizona
Miral D. Jhaveri, MD
Assistant Professor
Karen L. Salzman, MD Department of Diagnostic Radiology & Nuclear Medicine
Associate Professor of Radiology Rush University Medical Center
Division of Neuroradiology Chicago, Illinois
University of Utah School of Medicine
Bronwyn E. Hamilton, MD
Assistant Professor of Radiology
Julia Crim, MD Oregon Health & Science University
Chief of Musculoskeletal Radiology Portland, Oregon
Professor of Radiology
Susan I. Blaser, MD, FRCPC
Staff euroradiologist
The Hospital for Sick Children
Bryson Borg, MD Associate Professor, Neuroradiology
Chief of Neuroradiology, MagnetIC Resonance Imaging University of Toronto
Keesler Medical Center Ontario, Canada
Keesler Air Force Base,Mississippi
Gregory L. Katzman, MD, MBA

Professor and Chairman, Radiology
University of Texas Medical Branch
lohn Sealy Distinguished Endowed Chair of Radiology
Galveston, Texas
AMIRSYS
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ISBN: 978-1-9318-8402-0
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Library of Congress Cataloging-in-Publication Data
Expertddx. Brain and spine / [edited by] Anne G. Osborn, Jeffrey S. Ross, Karen L. Salzman. -- 1st ed.
p.;cm.
includes bibliographical references and index.
ISBN 978-1-931884-02-0
1. Brain--Diseases--Diagnosis--Atlases. 2. Spine--Diseases--Diagnosis--Atlases.3. Diagnosis, Differential. I. Osborn, Anne G., 1943-
II. Ross, Jeffrey S. Oeffrey Stuart) III. Salzman, Karen L. IV. Title: Bra.in and spine.
[DNLM: 1. Brain Diseases--diagnosis--Handbooks. 2. Diagnosis, Differential--Handbooks. 3. Diagnostic Imaging--Handbooks. 4.
Spinal Diseases--diagnosis--Handbooks. WL 39 E96 2009]
RC386.S.E97 2009
616.807S--dc22
200804133S
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To our (amilies and loved ones IVhose L1llSlinting support dllring the grlleling proce.5So( creating a bmlld-
neIV kind o( book IVas essential (evm crt/cia I) La ollr success. T/Janks and big /Jllgs!
v
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CONTRIBUTING
AUTHORS
Yoshimi Anzai, MD, MPH
Professor, Department of Radiology
University of Washington Medical Center
Seattle, Washington
Nancy J. Fischbein, MD
Associate Professor of Radiology and, by courtesy,
Otolaryngology-Head and Neck Surgery
Stanford University Medical Center
Stanford, California
Gary M. Nesbit, MD
Professor of Radiology, Neurology, Neurosurgery,
and the Dotter Interventionallnstitute
Oregon Health & Science University
Portland, Oregon
Sheri Harder, MD
Assistant Professor of Radiology
Lorna Linda University Medical Center
Lorna Linda, California
James D. Eastwood, MD
Associate Professor of Radiology
Duke University Medical Center
Durham, North Carolina
H. Ric Harnsberger, MD
Professor of Radiology
R.C. Willey Chair in Neuroradiology
Troy Hutchins, MD
Visiting Instructor
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viii
x
EXPERf(D D
BRAIN AND SPINE
Once the appropriate technical protocols have been delineated, the best quality images obtained,
and the cases queued up on PACS, the diagnostic responsibility reaches the radiology reading room. The
radiologist must do more than simply "lay words on" but reach a real conclusion. If we cannot reach a
definitive diagnosis, we must offer a reasonable differential diagnosis. A list that's too long is useless; a list
that's too short may be misleading. To be useful, a differential must be more than a rote recitation from
some dusty book or a mnemonic from a lecture way back when. Instead, we must take into account key
imaging findings and relevant clinical information.
With these considerations in mind, we at Amirsys designed our Expert Differential Diagnoses series-
EXPERTddx for short. Leading experts in every subspecialty of radiology identified the top differential
diagnoses in their respective fields, encompassing specific anatomic locations, generic imaging findings,
modality-specific findings, and clinically based indications. Our experts gathered multiple images, both
typical and variant, for each EXPERTddx. Each features at least eight beautiful images that illustrate the
possible diagnoses, accompanied by captions that highlight the pertinent imaging findings. Hundreds
more are available in the eBook feature that accompanies every book. In classic Amirsys fashion, each
EXPERTddx includes bulleted text that distills the available information to the essentials. You'll find
helpful clues for diagnoses, ranked by prevalence as Common, Less Common, and Rare but Important.
Our EXPERTddx series is designed to help radiologists reach reliable-indeed, expert-conclusions.

Whether you are a practicing radiologist or a resident/fellow in training, we think the EXPERTddx series
will quickly become your practical "go-to" reference.
Anne G. Osborn, MD
Executive Vice President and Editor-in-Chief, Amirsys Inc.
Paula J. Woodward, MD
Executive Vice President and Medical Director, Amirsys Inc.
ix
PREFACE
Expert Differential Diagnosis: Brain and Spine is comprised of over 250 expert differential diagnoses that
cover a broad spectrum of central nervous system diseases focused on the brain and spine. As with all
books in the EXPERTddx series, each topic is grouped according to anatomic location, generic imaging
finding(s), modality-specific finding(s), or clinically based finding(s). A number of modules actually reflect
more than one category. For example, "Suprasellar Masses, Pediatric" is both an anatomic location and
a clinical (age-specific) finding while "Tllsointense Suprasellar Mass" is both a modality-specific and
anatomically driven differential diagnosis.
Some EXPERTddxs have two or in a few cases even three modalilty-specific findings paired with an
anatomic location (e.g., "Tl/T2 Isointense Parenchymal Lesions"). Obviously, the possible combinations
of findings, locations, and clinical indications could generate a nearly infinite list of expert differential
diagnoses. Too few EXPERTddxs are too superficial to be helpful. Too many becomes overwhelming. Our
expert panel has created what we think is a very useful list of EXPERTddxs in the brain and spine (head
and neck, the third "leg" of neuroradiology, will follow in 6 months). We know we have inevitably left
some EXPERTddxs off the list. Equally inevitable, we also know we may have left an entity or two or three
off an individual EXPERTddx that could have/should have been included. So we invite you, our readers,
to send us your comments and suggestions. One of the great advantages of having an eBook companion
included as part of your purchase is that updates, revisions, and additions will be added throughout the
book's life. Have a suggestion or comment? Want to request a new EXPERTddx? Email me at aosborn@
amirsys.com and we will consider your suggestions. You just might find your idea showing up within a
few weeks' time! Have a cool case or a better illustration? Send it along! Because we have created the
whole new EXPERTddx series with you, our busy practicing colleagues in mind, we really do welcome your
input!
Finally, we have written Expert Differential Diagnosis: Brain and Spine so that it will be useful to both
general radiologists as well as neuroradiologists and our colleagues in allied clinical specialties such as
neurology and neurosurgery. We have included broad, overview ("general") EXPERTddxs as well as highly
detailed, more in-depth modules that contain rare diagnoses only a subspecialist might need. Regardless
of your level of specialization, we hope you will enjoy using our book and find it helpful in your daily
practice. If it improves diagnostic accuracy and thus enhances patient care, we will have achieved our goal
in publishing the Expert Differential Diagnosis series.
Anne G. Osborn, MD, FACR

Distinguished Professor of Radiology
William H. and Patricia W. Child
Presidential Endowed Chair in Radiology
xi
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ACKNOWLEDGMENTS
Text Editing
Douglas Grant Jackson
Ashley R. Renlund, MA
Kellie J. Heap
Image Editing
Jeffrey J. Marmorstone
Mitch D. Curinga
Medical Text Editing

llenry J. Baskin, Jr., MD
Art Direction and Design

Lane R. Bennion, MS
Richard Coombs, MS
Production Lead
Melissa A. Iloopes
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SECTIONS
PART I
Skull and Brain
Scalp, Skull
Meninges
Ventricles, Periventricular Regions
Extra-Axial Spaces and Subarachnoid Cisterns
Brain Parenchyma, General
Supratentorial Brain Parenchyma
Infratentorial Brain Parenchyma
Sella/Juxtasellar, Pineal Region
Arteries
Veins, Venous Sinuses
PART II
Spine
Trans-Spatial
Craniovertebral Junction
Vertebral Body - Posterior Elements
Intervertebral Disc - Endplate
Extradural
Intradural-Extramedullary
Intramed u lIary
xv
SECTION 2
PART I Meninges
Skull and Brain
Anatomically Based Differentials
SECTION 1 Dural Calcification(s) 1·2·2
Scalp, Skull
Dural-based Mass, Solitary 1·2·4
Anatomically Based Differentials Dural-based Masses, Multiple 1·2·8
Miral D. [haveri, MD
Skull Normal Variants 1·1-2
Miral D. Jhaveri, MD Falx Lesions 1·2·12
Scalp Mass 1·1·4
Generic Imaging Patterns
Generic Imaging Patterns Thick Dura/Arachnoid, Generalized 1·2·14
Yoshimi Anzai, MD, MPH & Judy Tan, MD
"Hair on End" 1·1·6
Miral D. Jhaveri, MD Pial Enhancement 1·2·16
Yoshimi Anzai, MD, MPH & Judy Tan, MD
Thick Skull, Generalized 1·1·8
Miral D. Jhaveri, MD Dural Tail Sign 1·2·20
Miral D. /haveri, MD
Thick Skull, Localized 1·1·12
Thin Skull, Generalized

1·1·14 SECTION 3
Thin Skull, Localized 1-1-16 Ventricles, Periventricular
Miral D. /haveri, MD Regions
Lytic Skull Lesion, Solitary 1·1·18
Multiple Lucent Skull Lesions 1·1·22

Miral D. Jhaveri, MD Ventricles, Normal Variants 1·3·2
Sclerotic Skull Lesion, Solitary 1·1·26 Susan I. Blaser, MD, FRCPC
Miral D./haveri, MD Choroid Plexus Lesions 1·3·6
Sclerotic Skull Lesions, Multiple 1·1·30 Karen L. Salzman, MD
Miral D./haveri, MD Ependymal/Subependymal Lesions 1·3-8
Clinically Based Differentials Lateral Ventricle Mass 1-3·12

Karen L. Salzman, MD
Macrocephaly 1·1-32
Thick Septum Pellucidum 1-3·16
Microcephaly 1·1·38
Foramen of Monro Mass 1·3-18
Third Ventricle Mass, General 1·3·22

Third Ventricle Mass, Body/Posterior 1-3·26

Cerebral Aqueduct/Periaqueductal Lesion 1·3·28

XVI
Fourth Ventricle Mass 1-3-32 Generic Imaging Patterns
Korell L. Salzillo II, MD
Enhancing Cranial Nerve(s) 1-4-46
Alllle G. Osbam, MO, FACR
CSF-like Extra-Axial Fluid Collection 1-4-50
"Bubbly-Appearing" Intraventricular Mass 1-3-36 Yasl1imi Alllai, MO, MPH & Jllrly TOI7,MO
/Jramvy" E. HOllliltall, MD
CSF-like Extra-Axial Mass 1-4-52
Ependymal Enhancement 1-3-40 Yasllimi Alllai, MO, MPI-j & Jlldy TOI7,MO
Bromvyn E. Hamilton, MD
Sulcal/Cisternal Enhancement 1-4-54
Large Ventricles 1-3-44 Sl1eri L. /larrler, MO
Bramvy" E. HOllliltall, MO
Fat in Sulci/Cisterns/Ventricles 1-4-58
Small Ventricles 1-3-48 Yasllillli Allzai, MD, MPH & Jllrly Tall, MD
Bronwy" E. HamiltoIJ, MD
Asymmetric Lateral Ventricles 1-3-50 Modality-Specific Imaging Findings

/JroIlWYII E. Homiltall, MO
Irregular Lateral Ventricles 1-3-54 Extra-Axial Flow Voids 1-4-60
Bromvyn E. Hamilton, MD JOllies O. Eastwaad, MO
Periventricular Enhancing Lesions 1-3-58 T1 Hyperintense CSF 1-4-62

Brollwy" E. Hamilton, MD Branwy" E. Hamilton, MD
FLAIR Hyperintense CSF 1-4-64
/JromvYII E. HOllliltal7, MD
Modality-Specific Imaging Findings
T2 Hypointense Extra-Axial Lesions 1-4-68
Intraventricular Calcification(s) 1-3-62 Bronwyn E. Hamilton, MD
Hyperdense CSF 1-4-72
Periventricular Calcification 1-3-66 Bronwyn E. Harniltofl, MD
5115011
J. Blaser, MO, FRCPC
Hyperdense Extra-Axial Mass(es) 1-4-74
Periventricular T2/FLAI R Hyperintense Lesions 1-3-72 Miral o. JllOveri, MO
Tray /llItellil7s, MO & Korell L. Salzillo 11,MO
Hypodense Extra-Axial Mass(es) 1-4-76
Brollwyn E. Hamilton, 1\1D
SECTION 4
Extra-Axial Spaces and SECTION 5
Subarachnoid Cisterns Brain Parenchyma, General
Anatomically Based Differentials Generic Imaging Patterns

Cistern, Subarachnoid Space Normal Variants 1-4-2 Multiple Enhancing Lesions, General 1-5-2
KorCll L. Salzillo 11,MD Karen L. Salzman, MD
Epidural Mass, Brain 1-4-4 Ring-Enhancing Lesion, Solitary 1-5-6
SI1CriL. Harrier, M 0 Yasllillli Allzoi, MO, MPH & Jlldy Tall, MO
Enlarged Sulci, Generalized 1-4-8 Ring-Enhancing Lesion, Multiple 1-5-12

Alllle G. Osba/"ll, MO, FACR Yasl1imi Al7l0i, MO, MPH & Jllrly Tall, MO
Effaced Sulci, Generalized 1-4-12 Solitary Cystic Parenchymal Mass, General 1-5-16
Alllle G. Osbom, MD, FACR AlIl7e G. Osbam, MO, FACR
Effaced Sulci, Focal 1-4-16 CSF-like Parenchymal Lesion(s) 1-5-22

Alllle G. Osbom, MO, FAC/I Al7l7e G. Osbam, MO, FACR & James o. Eostwaorl, MO
Interhemispheric Fissure Cysts 1-4-20 Cyst with Nodule 1-5-28

Alllle G. Osbam, MD, FACR Troy lIutchins, MD & Karen L. Salzman, MD
CPA Mass, Adult 1-4-24 Fat-like Lesion(s), General 1-5-32
H. /lie Homsberger, MO Sireri L. Harrier, MO
Cystic CPA Mass 1-4-28

H. Rie Homsberger, MD Modality-Specific Imaging Findings
Prepontine Cistern Mass 1-4-32 Solitary Parenchymal Calcification 1-5-34
Gregary L. Kotzmal7, MO, MBA
Alllle G. Osbom, MO, FACR
Cisterna Magna Mass 1-4-38 Multiple Parenchymal Calcifications 1-5-40
Gregary L. Kotlmol7, MO, M/JA
Al7l1e G. Osbom, MO, FACR
Foramen Magnum Mass 1-4-42 Solitary J-1yperdense Parenchymal Lesion 1-5-44
Al7l7e G. Osbam, MO, FACR
Multiple Hyperdense Parenchymal Lesions 1-5-50
Arme G. Osbom, MO, FACR
XVII
Solitary Hypodense Parenchymal Lesion 1-5-56 Thin Corpus Callosum 1-6-40
Anne G. Osborn, MD, FACR Susan T. Blaser, MD, FRCPC
Multiple Hypodense Parenchymal Lesions 1-5-60 Abnormal Shape/Configuration of Corpus 1-6-46
Karen L. Salzman, MD Callosum
Susan T. Blaser, MD, FRCPC
Multiple Brain Hyperintensities (T2/FLAlR), 1-5-64
Common Corpus Callosum Holes 1-6-52
Gary M. Nesbit, MD Karen L. Salzman, MD
Multiple Brain Hyperintensities (T2/FLAlR), Less 1-5-70 Corpus Callosum Lesion without Mass Effect 1-6-54
Common Karen L. Salzman, MD
Gary M. Nesbit, MD
Corpus Callosum Mass 1-6-56
Multiple Brain Hyperintensities (T2/FLAIR), Rare 1-5-76 Karen L. Salzman, MD
but Important Corpus Callosum Splenium Lesion 1-6-58
Gary M. Nesbit, MD Karen L. Salzman, MD
Multiple Hypointense Foci on T2 1-5-80 Basal Ganglia Calcification 1-6-62
Nancy f. Fischbein, MD Karen L. Salzman, MD
Multiple Hypointense Foci on GRE/SWI 1-5-82 Tl Hyperintense Basal Ganglia 1-6-66
Nancy f. Fischbein, MD Karen L. Salzman, MD
Tl/T2 Hyperintense Parenchymal Lesions 1-5-86 T2 Hyperintense Basal Ganglia 1-6-70
Anne G. Osborn, MD, FACR Karen L. Salzman, MD
Tl Hypointense, T2 Hyperintense Parenchymal 1-5-90 Enlarged Perivascular Spaces 1-6-74
Lesions Karen L. Salzman, MD
Perivascular Space Enhancing Lesions 1-6-76
TlfT2 Isointense Parenchymal Lesions 1-5-94 Karen L. Salzman, MD
Bilateral Basal Ganglia Lesions 1-6-80
Restricted Diffusion 1-5-98 Nancy f. Fischbein, MD
Putamen Lesion(s) 1-6-84
Tl Hyperintense Parenchymal Lesion(s) 1-5-102 Karen L. Salzman, MD
Globus Pallidus Lesion(s) 1-6-86
Clinically Based Differentials Unilateral Thalamic Lesion 1-6-90
Brain Tumor in Newborn/Infant 1-5-106
Susan T. Blaser, MD, FRCPC Bithalamic Lesions 1-6-92
Nancy f. Fischbein, MD
Brain Tumor in Child> 1 Year 1-5-112
Susan T. Blaser, MD, FRCPC "Pulvinar Sign" 1-6-96
Epilepsy, General 1-5-118
Bronwyn E. Hamilton, MD Tectal (Quadrigeminal Plate) Lesion 1-6-98
Midbrain Lesion 1-6-100

SECTION 6 Nancy f. Fischbein, MD

SECTION 7
Anatomically Based Differentials Infratentorial Brain Parenchyma
Asymmetric Cerebral Hemispheres 1-6-2
Thick Cortex 1-6-8
Susan T. Blaser, MD, FRCPC Large Brainstem 1-7-2
Thin Cortex 1-6-14
Susan T. Blaser, MD, FRCPC Small Brainstem 1-7-4
Focal Cortical Mass 1-6-20
fames D. Eastwood, MD Pontine Lesion 1-7-6
Nancy f. Fischbein, MD
Cortical Hyperintensity T2/FLAIR 1-6-24
Karen L. Salzman, MD Medulla Lesion 1-7-10
1-6-28 Nancy f. Fischbein, MD
Cortical Enhancement
Karen L. Salzman, MD Infratentorial Midline Cyst 1-7-14
Solitary White Matter Lesion 1-6-30
Gary M. Nesbit, MD Cerebellar Atrophy 1-7-18
Confluent White Matter Lesions 1-6-34
Gary M. Nesbit, MD Cerebellar Mass 1-7-22
XVlll
Vermis Mass 1-7-28
Gregory L. Katzmall, MD, MBA
Low erebellar Tonsils 1-7-32 Hyperdense Suprasellar Mass 1-8-52
Gregory L. Katzmall, MD, MBA AlIl1e G. Osbom, MD, FACR
Tl Isointense Suprasellar Mass 1-8-54

Alllle G. Osborn, MD, FACR
1'1 Hyperintense Suprasellar Mass 1-8-56
"Cystic-Appearing" Posterior Fossa Lesion 1-7-34 Alllle G. Osborn, MD, FACR
SlIsall I. Blaser, MD, FRCPC
T1 Hypointense Suprasellar Lesion 1-8-58
AlIl1e G. Osborn, MD, FAC/I
Clinically Based Differentials
Posterior Fossa eoplasm, Adult 1-7-40 SECTION 9
Al1l1e G. Osborn, MD, FACR
Posterior Fossa Neoplasm, Pediatric 1-7-44 Arteries

SlIsal1l. Blaser, MD, FRCPC

SECTION 8 Abnormalities of Arterial Shape/Configuration 1-9-2
Am.e G. Osborn, MD, FACR
Sella/Juxtasellar, Pineal Region 1-9-6
Fusiform Arterial Enlargement
Siler; L. Harder, MD
Pineal Region Mass, General 1-8-2 Modality-Specific Imaging Findings
Gregory L. Katzmal1, MD, MBA
Ilyperattenuating ("Dense") Artery 1-9-8
Pineal Gland Mass
Karel1 L. Salzman, MD
1-8-6 Slier; L. Harder, M °
Vascular Calcification(s) 1-9-10
Quadrigeminal istern Mass 1-8-8 Gregory L. Katzlllal1, MD, MBA
Gregory L. Katzmall, MD, MBA
Pineal + Suprasellar Lesions 1-8-10

Karen L. Salzmall, MD SECTION 10
Sella/Pituitary Normal Variants 1-8-12 Veins, Venous Sinuses
SeliarIJuxtaseliar Calcification 1-8-14

Al1l1e G. Osborn, MD, FACR Anatomically Based Differentials
Enlarged Pituitary Gland 1-8-18 Dural Sinus Lesion, General 1-10-2
Al1l1e G. Osbom, MD, FACR Bro"wy" E. Hamillol1, MD & AlIl1e G. Osbom, MD, FAC/I
lntrasellar Lesion 1-8-20 Enlarged Cortical Veins 1-10-8

Alllle G. Osborn, MD, FACR jmlles D. Eastwood, MD
Cystic Intrasellar Mass 1-8-22 Enlarged Deep (Medullary/Ependymal) Veins 1-10-10

Alllle G. Osborn, MD, FACR james D. Eastwood, MD
Suprasellar Mass, General 1-8-24 Unilateral Cavernous Sinus Mass 1-10-14

Amle G. Osborn, MD, FACR Alllle G. Osbom, MD, FACR
Suprasellar Masses, Pediatric 1-8-30 Bilateral Cavernous Sinus Lesions 1-10-18

SlIsall I. Blaser, MD, FlICPC A.me G. Osbom, MD, FACR
Suprasellar Cystic Mass 1-8-36 Meckel Cave Lesion 1-10-22

Al1l1e G. Osborn, MD, FACR A.lIle G. Osbom, MD, FACR
Calcified Suprasellar Mass 1-8-40

Al1l1e G. Osborn, MD, FACR Modality-Specific Imaging Findings
Enhancing Suprasellar Mass 1-8-42
Hyperdense Dural Sinus 1-10-26
A.lIle G. Osbom, MD, FACR
Absent/Thin Infundibular Stalk 1-8-44
Thick Infundibular Stalk 1-8-46
A.me G. Osborn, MD, FACR
Hypothalamus Lesion 1-8-48
XIX
SECTION 2
PART II Craniovertebral Junction
Spine
SECTION 1 Cranio-Cervical junction Acute Injury 11-2-2
Julia Grim, MD
Trans-Spatial
CVj Abnormality, General 11-2-4
Julia Grim, MD
Anatomically Based Differentials CVj Soft Tissue Abnormality 11-2-8
Jeffrey S. Ross, MD
Cervical, Chronic Post-Traumatic Abnormality 11-1-2
Julia Grim, MD
Cervical, Lower, Post-Traumatic Bony 11-1-4 Generic Imaging Patterns
Abnormality CI-C2 Instability 11-2-12
Julia Grim, MD
Julia Grim, MD
Thoracic Bony Trauma 11-1-6 Odontoid Deformity 11-2-14
Julia Grim, MD
Julia Grim, MD
Lumbar Bony Trauma 11-1-8
Julia Grim, MD
SECTION 3
Generic Imaging Patterns Vertebral Body - Posterior
Scoliosis 11-1-10 Elements
Julia Grim, MD
Kyphosis 11-1-12
Julia Grim, MD Anatomically Based Differentials
Kyphoscoliosis, Child 11-1-14 Congenital Vertebral Anomalies 11-3-2
Julia Grim, MD Julia Grim, MD
Platyspondyly, Diffuse 11-1-16 Cervical Bony Fusion 11-3-4
Julia Grim, MD Julia Grim, MD
Sacral Mass, Adult 11-1-18
Lubdha M. Shah, MD
Sacrococcygeal Mass, Pediatric 11-1-22
Kevin R. Moore, MD Flattened Vertebral Body, Solitary 11-3-6
Julia Grim, MD
Sacral Deformity 11-1-26
Bryson Borg, MD Flattened Vertebral Body, Multiple 11-3-8
Julia Grim, MD
Dysmorphic Vertebral Body 11-3-10
Clinically Based Differentials Julia Grim,MD
Acute Back Pain/Radiculopathy, Post-Operative 11-1-30 Enlarged Vertebral Body/Posterior Element 11-3-12
Kevin R. Moore, MD Lubdha M. Shah, MD
Chronic Back PainJRadiculopathy, 11-1-36 Enlarged Neural Foramen 11-3-16
Post-Operative Bryson Borg, M0
Kevin R. Moore, MD
Vertebral Body ScallopingJWidened Canal 11-3-18
Acute Upper Extremity PainJWeakness 11-1-42 Bryson Borg, MD
Kevin R. Moore, MD
Spondylolisthesis 11-3-20
Lower Extremity Pain 11-1-48 Jeffrey S. Ross, MD
Bryson Borg, MD
Bony Lesion, Aggressive 11-3-24
Back Pain, Adult 11-1-52 Lubdha M. Shah, MD
Bryson Borg, MD
Fracture, Vertebral Body 11-3-28
Back Pain, Pediatric 11-1-56 Julia Grim, MD
Kevin R. Moore, MD
Facet Abnormality, Non-traumatic 11-3-32
Lubdha M. Shah, MD
Fracture, Posterior Element 11-3-34

Julia Grim, MD
Pedicle Abnormality 11-3-36

Bryson Borg, MD
xx
Modality-Specific Imaging Findings Extradural Lesion, Solid Enhancement 11-5-16
Kevin R. Moore, MD
Enlarged Vertebral Body, Soap Bubble Expansion 11-3-38
Lllbd/IO M. SIlO/I, MD
Vertebral Body Sclerosis, Focal 11-3-42
Bryso/l Borg, MD Soft Tissue Calcification, Paraspinal 11-5-20
/11/;0 Cr;m, MD
Vertebral Body Sclerosis, Diffuse 11-3-44
Bryso/l Borg, MD Extradural, Normal Marrow Signal 11-5-22
Kev;/I R. Moore, MD
Vertebral Body Thickened Bony Trabeculae 11-3-46
Lllbd/IO M. Shah, MD Extradural, Abnormal Marrow Signal 11-5-26
Kev;n R. Moore, MD
Vertebral Body, Tl Hyperintense Signal, Diffuse 11-3-48
Kevin R. Moore, MD Extradural Lesion, T1 Hyperintense 11-5-30
Bryson Borg, M 0
Vertebral Body, TJ Hyperintense Signal, Focal 11-3-50
Kevin R. Moore, MD Extradural Lesion, T1 Hypointense 11-5-32
Bryso/l Borg, MD
Vertebral Body, Tl Hypointense Signal, Diffuse 11-3-52
Kevin R. Moore, MD Extradural Lesion, T2 Hyperintense, T1 11-5-36
Vertebral Body, Tl Hypointense Signal, Focal 11-3-56 Isointense
Bryson Borg, M 0
Bryso/l Borg, MD
Extradural Lesion, T2 Hypointense, Tl 11-5-40
I-Iypointense
SECTION 4 Bryson Borg, MD

Lumbar Soft Tissue Mass, Pediatric 11-5-42
Generic Imaging Patterns Kev;" R. Moore, MD
Disc Contour Abnormality 11-4-2
Jeffrey S. //055, M 0
Intervertebral Disc/Endplate Irregularity 11-4-6 SECTION 6
Jeffrey S. Ross, MD Intrad ural- Extramed uIlary
Vertebral Endplate Contour Abnormality 11-4-10
/Illia Crilll, MD
Modality-Specific Imaging Findings Cauda Equina Enhancement, Diffuse 11-6-2
Jeffrey S. Ross, MD
Intervertebral Disc, Tl Hypointense 11-4-12
Jeffrey S. Ross, M 0
Subarachnoid Space Narrowing 11-6-6
Blyso/l Borg, MD
Intervertebral Disc, T2 Hyperintense 11-4-14
Intradural/Extramedullary, Leptomeningeal 11-6-8
Enhancement
Vertebral Endplate Signal Abnormality 11-4-16 Kevin R. Moore, MD

SECTION 5 Intradural/Extramedullary Lesion, No 11-6-12
Extradural Enhancement
Kev;n R. Moore, MD
Intradural/Extramedullary Lesion, Solid 11-6-14
Anatomically Based Differentials Enhancement
Epidural Mass, Spine 11-5-2 Kevin R. Moore, MD
Bryso/l Borg, MD Intradural Lesion, Serpentine 11-6-18
11-5-8 Jeffrey S. Ross, MD
Ventral/Lateral Paraspinal Mass
Jeffrey S. Ross, M 0 Intradural/Extramedullary Lesion, Multiple 11-6-20
Bryson Borg, M 0

Paraspinal Muscle Abnormality 11-5-10
Jeffrey S. Ross, MD Intradural/Extramedullary Lesion, 11-6-22
Extradural Lesions, Multiple 11-5-12 Ring/Peripheral Enhancement
Bryso/l Borg, MD Kev;n R. Moore, MD
Extradural Lesion, No Enhancement 11-5-14 Intradural/Extramedullary Lesion, T1 11-6-26

/11/;0 Cr;m, MD Hyperi n tense
Jeffrey S. Ross, MD
XXI
Intradural/Extramedullary Lesion, T1 11-6-28 Clinically Based Differentials
Hypointense
/effrey S. Ross, MD Myelopathy 11-7-48
Kevin R. Moore, MD
Intradural/Extramedullary Lesion, Tl Hypo, T2 11-6-32
Hypo
/effrey S. Ross, MD
Intradural/Extramedullary Lesion, T2 Hyper, Tl 11-6-34
Iso
/effrey S. Ross, M D

Cauda Equina Syndrome 11-6-36
Bryson Borg, MD
SECTION 7
Intramedullary
Intramedullary Mass 11-7-2
Bryson Borg, MD
Conus Abnormality 11-7-6
Bryson Borg, MD

Cord, Small/Atrophic 11-7-10
Bryson Borg, MD
Intramedullary Lesions, Multiple 11-7-12
Lubdha M. Shah, MD
Intramedullary Lesion, Solid Enhancement 11-7-14

Lubdha M. Shah, MD
Intramedullary Lesion, No Enhancement 11-7-18
Lubdha M. Shah, MD
Intramedullary Lesion, Diffuse/Ill-defined 11-7-20

Enhancement
Jeffrey S. Ross, MD
Intramedullary Lesion, Ring/Peripheral 11-7-24
Enhancement
Lubdha M. Shah, MD

Intramedullary Lesion, Tl Hypointense, T2 11-7-26
Hypointense
Lubdha M. Shah, MD
Intramedullary Lesion, T1 Hypointense 11-7-28
Lubdha M. Shah, MD
Intramedullary Lesion, T2 Hyperintense, Tl 11-7-30
Isointense
LlIbdha M. Shah, MD
Intramedullary Lesion, T1 Hyperintense 11-7-34

Lubdha M. Shah, MD
Cord Lesion, T2 Hyperintense, Ventral 11-7-38
Lubdha M. Shah, MD
Cord Lesion, T2 Hyperintense, Dorsal 11-7-40
Lubdha M. Shah, MD
Cord Lesion, T2 Hyperintense, Central 11-7-44
Lubdha M. Shah, MD
XXII
xxv
PART I
Skull and Brain
Scalp, Skull
Meninges
Extra-Axial Spaces and Subarachnoid Cisterns
Sella/Juxtasellar, Pineal Region
Arteries
SECTION 1
Scalp, Skull
Skull Normal Variants 1-1-2
Scalp Mass 1-1-4

"Hair on End" 1-1-6
Thick Skull, Generalized 1-1-8
Thick Skull, Localized 1-1-12
Thin Skull, Generalized 1-1-14
Thin Skull, Localized 1-1-16
Lytic Skull Lesion, Solitary 1-1-18
Multiple Lucent Skull Lesions 1-1-22
Sclerotic Skull Lesion, Solitary 1-1-26
Sclerotic Skull Lesions, Multiple 1-1-30

Macrocephaly 1-1-32
Microcephaly 1-1-38
SKULLNORMAL VARIANTS
0..
co
o DIFFERENTIAL DIAGNOSIS o Vascular Grooves
(f)
• Usually inner table
C Common
• Caused by meningeal arteries, veins
•..
I'll
co
• Skull Normal Variants
• Outer table produced by superficial
o Arachnoid Granulations, Calvarium
'tl
c temporal artery branches
o Vascular Grooves
I'll
o Venous Lakes
o Venous Lakes
• Round or oval configuration
o Emissary Veins
• Diploic venous channel can usually be
o Parietal Thinning
traced into venous lakes
o Asymmetric Marrow, Petrous Apex
o Emissary Veins
o Asymmetric Foramina Ougular, Oval e)
• Connect meningeal veins/dural venous
o Aerated Clinoids
sinuses with pericranial (scalp) veins
o Accessory Sutures (e.g., Mendosal)
• Chiefly in frontal, parietal bones
• Hyperostosis Frontalis Interna o Parietal Thinning
Less Common • Elongated oval-shaped thinness
• Prominent Convolutional Markings • Upper part of parietal bone involved
o Asymmetric Marrow, Petrous Apex
Rare but Important
• Wormian Bones • Non-pneumatized marrow hyperintense
on TlWI
• Opposite side pneumatized
ESSENTIAL INFORMATION • Hyperostosis Frontalis Interna
o Predominately inner table overgrowth
Key Differential Diagnosis Issues
o Usually bilateral, symmetrical
• Important to recognize normal anatomic
o Frontal; usually stops at coronal suture
variations
o ± Orbital roofs, parietal bones
o These are "leave me alone" lesions
o Should not be mistaken for real disease Helpful Clues for Less Common Diagnoses
(e.g., metastases) • Prominent Convolutional Markings
o Brain pulsations - inner table depressions
Helpful Clues for Common Diagnoses
o Children> > adults
o Arachnoid Granulations, Calvarium Helpful Clues for Rare Diagnoses
• Sharply demarcated defect in inner table • Wormian Bones
• Adjacent to/within dural venous sinuses o Lamboid suture> fontanelles
• CSF density/intensity o Variable size, number (2-3 normal)
Arachnoid Granulations, Calvarium Emissary Veins
I
1 Axial NEeT shows a sharply marginated osseous defect
due to an arachnoid granulation invaginatjng through
Axial bone CT shows linear defects in the calvarium
caused by prominent emissary veins 81. Also note a
the inner table of the right occipital bone 81. prominent venous lake ~.
2
SKULL NORMAL VARIANTS en
"
r::
Parietal Thinning Asymmetric Marrow, Petrous Apex

(Left) Axial bone CT shows
classic bilateral parietal
thinning 8t a normal
variation. (Right) Axial bone
CT shows a typical example
of asymmetric aeration of the
pelrous apex. There;s
normal {ally marrow
the left petrous apex =
with an aerated right pelrous
within
apex 81.
Aerated C1inoids
asymmetric jugular foramina,
with the left 81 larger than
the right =:l. More
commonly the right is larger
than the left. (Right) Coronal
bone CT shows bilateral
aerated clinoids 81.
Hyperostosis Frontalis Interna Wormian Bones

hypertrophic bone {ormation
along the inner table of
frontal bones 8t consistent
with benign hyperostosis
frontalis interna. (Right)
Bone CT shows a
diamond-shaped wormian
bone in the region of the
anterior fontanelle ~.
I
1
3
SCALP MASS
a.
ro
u DIFFERENTIAL DIAGNOSIS • Enhancing mass + skull changes: Metastasis,
(f) squamous/basal cell carcinoma
Common
CD
..
c:
C'Cl
• Subgaleal Hematoma
• Foreign Body
• Subgaleal Hematoma
"'C
c: o Not confined by cranial sutures
ro • Lipoma
• Sebaceous Cyst o Traumatic, post-surgical
• Metastases, Skull • Lipoma

o Well-defined fat density/signal intensity
less Common • Sebaceous Cyst
• Dermoid Cyst o Often fluid density/intensity
• Epidermal Inclusion Cyst • Metastases, Skull
• Basal Cell Carcinoma o Destructive skull lesion with associated
• Squamous Cell Carcinoma scalp mass
• Edema/Anasarca
• Hemangioma Helpful Clues for less Common Diagnoses
• Venolymphatic Malformations • Dermoid Cyst
• Neurofibromatosis Type 1 o Midline, frontotemporal> parietal
o Fat density, signal
• Lymphoma
• Langerhans Cell Histiocytosis • Epidermal Inclusion Cyst
o Location similar to dermoid cyst
Rare but Important o Fluid density, signal
• Sinus Pericranii • Venolymphatic Malformations
• Atretic Cephalocele o Multiseptate cystic masses ± intracystic
• Sarcoma (Kaposi, etc.) hemorrhage/fluid levels
o ± Phleboliths (signal voids)
ESSENTIAL INFORMATION • Neurofibromatosis Type 1
o Plexiform neurofibroma unencapsulated,
Key Differential Diagnosis Issues infiltrating
• Density of mass on NECT helpful • Langerhans Cell Histiocytosis
o Hyperdense: Acute subgaleal hematoma o "Punched-out" skull lesion without reactive
o Fat density: Lipoma, dermoid cyst sclerosis
o Fluid density: Sebaceous cyst, epidermal o ± Enhancing soft tissue mass
inclusion cyst
Subgaleal Hematoma Lipoma
I
1 Axial NECT shows a posl-lraumauc acute hyperdense
subgaleal hematoma not confined by sutures ~ as well
Axial NECT shows a homogeneous fat density lipoma
(;8 in the frontal scalp.
as an epidural hematoma =.
4
SCALP MASS ,.-
(Jl
c:
Cl
::l
Co
..,
OJ
Sebaceous Cyst Metastases, Skull Cl
(Left) Axial NECT shows a ::l

well-defined fluid density (Jl
()
sebaceous cyst [;g in the 0>
subcutaneous fat of the "0
occipital scalp. (Right) Axial (Jl
T1 C+ MR shows a
""c:
destructive metastasis &:I
centered in diploic space
that destroys both inner &
oUler tables and extends
both medially into epidural
space & laterally into
subgaleal space.
Dermoid Cyst Basal Cell Carcinoma

(Left) Axial NECT shows a
lesion =
well-circumscribed,
within the
subcutaneous
oval
tissues near
the right orbit with density
similar to that of the
subcutaneous rat, typical or a
dermoid cyst. (Right)
Coronal CECT shows an
enhancing soft tissue mass
~ with superficial ulceration
P.:;. On excisional biopsy,
this proved to be a basal cell
carcinoma. The underlying
calvarium was not involved.
Neurofibromatosis Type 1 Langerhans Cell Histiocytosis

(Left) Axial T2WI FS MR in
patient with
neurofibromatosis type 7 and
a scalp mass shows the
infiltrating "whorlsl! of tumor
= that are typical of
plexiform neurofibroma.
(RighI) Axial CECT shows a
lytic skulliesioll ~ in a child
with an associated large
enhancing scalp mass a
typical of Langerhans cell
histiocytosis.
I
1
5
OJ "HAIR ON END"
-'"
(f)
0-
ro DIFFERENTIAL DIAGNOSIS • Expanded diploic space
()
(f) o Thalassemia
c: Common • Most severe in thalassemia major
nl
•... • Anemias o Sickle Cell Disease
llJ
o Thalassemia • 5% of radiographs show "hair on end"
"0
c: o Sickle Cell Disease
nl • Hemangioma, Skull
o Hereditary Spherocytosis o Sharply marginated expansile skull lesion
• Hemangioma, Skull o Spiculated "hair on end" (sunburst) or
• Metastases, Skull "honeycomb" pattern
Less Common • Metastases, Skull
• Neuroblastoma, Metastatic o Localized or diffuse
• Iron Deficiency Anemia o Dural/scalp involvement common
• Cyanotic Congenital Heart Disease o Often known primary malignancy
Rare but Important Helpful Clues for Less Common Diagnoses

• Leukemia • Neuroblastomar Metastatic
o Skull/orbit ± sutural widening
• Osteopetrosis
• Granulocyte Colony-Stimulating Factor • Iron Deficiency Anemia
(G-CSF) Treatment o Severe, chronic
o Mostly nutritionally deprived children
• Cyanotic Congenital Heart Disease
ESSENTIAL INFORMATION o Marrow expansion in uncorrected complex
Key Differential Diagnosis Issues CHD can mimic thalassemia
• "Hair" Helpful Clues for Rare Diagnoses
o Expanded diploe + spiculated periostitis • Leukemia
o Accentuated trabeculae between o Almost always with sub- or epidural tumor
inner/outer tables • Osteopetrosis
• "On end" o Expanded marrow space ~ spiculated
o Trabeculae oriented perpendicular to periosteal reaction
inner, outer tables o Pattern similar to severe anemias
Helpful Clues for Common Diagnoses • Granulocyte Colony-Stimulating Factor
• Anemias (G-CSF) Treatment
o General etiology o Long-term treatment in severe congenital
• Red marrow hyperplasia neutropenia
Thalassemia Thalassemia
I
1 Lateral radiograph shows typical appearance of
thalassemia with dense striations in a widened diploic
Axial bone CT shows lypical "hair on endM appearance
of the skull secondary to marked thickening of the
space, giving the "hair on end" appearanceEB diploic marrow space EB Thalassemia major is the
most common cause of this imaging finding.
6
"HAIR ON END" (J)
"
c:
III
::::l
Co
Sickle Cell Disease

..•
OJ
Sickle Cell Disease III
(Left) Lateral scout ::::l

radiograph from CT shows (j)
Cl
marked diploic thickening OJ
= with "hair on end" "0
appearance in a patient with (j)
A
sickle cell disease. (Right) c:
5agiltal T1 WI MR shows
marked diploic thickening
~ with "hair on end"
appearance = in severe
sickle cell anemia.
Hemangioma, Skull Neuroblastoma, Metastatic

(Left) Anteroposterior
radiograph demonstrates a
well-demarcated lesion
within the left frontal bone
&J with spiculated or
honeycomb appearance
from intra diploic trabecular
thickening. (Right) Coronal
T1 C+ MR shows classic
"hair on end" pa£lern,
typical for metastalic
neuroblastoma =:I.
Neuroblastoma, Metastatic leukemia

radiograph shows periosteal
new bone projecting from
both inner &J and outer =:I
table of the skull with
bidirectional spiculation in
metastatic neuroblastoma.
(Right) Axial CCCT shows a
spiculated appearance of the
outer and inner calvarium
~ due to extensive marrow
involvement in leukemia.
Note large enhancing masses
along the dura =:I and in the
scalp~".
I
1
7
THICK SKULL, GENERALIZED
-'(fJ'"
0-
ro DIFFERENTIAL DIAGNOSIS • Phenytoin (Dilantin) Use, Chronic
u
(fJ o Look for combination of thick skull +
c: Common cerebellar atrophy = probable chronic
co • Skull Normal Variants Dilantin therapy
"-
III
o Diffusely Thick Skull, ormal o Up to 34% among patients with seizure
"0
c: o Hyperostosis Frontalis Interna disorder + anticonvulsant therapy
co
• Phenytoin (Dilantin) Use, Chronic • Shunted Hydrocephalus
• Shunted Hydrocephalus o Chronic shunted hydrocephalus often
• Metastases (Diffuse Sclerotic) associated with diffuse calvarial thickening
• Paget Disease o Look for thick skull + shunt + chronic
Less Common collapsed ventricles
• Microcephaly • Metastases (Diffuse Sclerotic)
• Fibrous Dysplasia o Fat-suppressed Tl C+ scans helpful in
• Hyperparathyroidism detecting calvarial, subtle dural metastases
o Common with prostate & breast metastasis
• Acromegaly
• Subdural Hematoma, Chronic (Calcified) o Look for associated focal/diffuse
• Anemias dura-arachnoid involvement

o Iron Deficiency Anemia • Paget Disease
o Sickle Cell Disease o Initial osteolytic change of skull in
o Thalassemia osteoporosis circumscripta
• Extramedullary Hematopoiesis o Late osteosclerotic phase
• Osteoblastic areas crossing sutures
Rare but Important • Marked thickening of the diploic space
• Sclerosing Bone Dysplasias • "Tam-o'-shanter" skull
o Osteopetrosis
• Focal areas of sclerosis in expanded
o Pycnodysostosis diploic space: "Cotton wool" appearance
o Melorheostosis
(of skull)
• Fluorosis o Platybasia with basilar invagination
Helpful Clues for Less Common Diagnoses
ESSENTIAL INFORMATION • Microcephaly
Key Differential Diagnosis Issues o Skull overgrowth occurs secondary to
• Diffuse diploic space expansion small brain

with/without adjacent cortical thickening o Small brain causes = developmental
• Most common cause by far of "thick skull" = anomalies or a result of very early insult
normal variant! • Fibrous Dysplasia
o Can involve any aspect of skull
Helpful Clues for Common Diagnoses o Can be focal or extensive
• Skull Normal Variants o Medullary expansion with ground-glass
o Most common cause
appearance is classic
o Females normally have significantly
o Four disease patterns
thicker parietal/occipital bones than males • Monostotic (70-80%)
o Hyperostosis frontalis interna
• Polyostotic (20-30%)
• Usually bilateral, symmetrical • Craniofacial (can be isolated; up to 50%
• Spares areas occupied by superior sagittal of polyostotic)
sinus, cortical venous channels • Cherubism (mandible, maxilla)
• Often ends at coronal sutures • Hyperparathyroidism
• May extend to parietal bones, orbital o Granular appearance of skull with multiple
roofs areas of normal bone interspaced between
• Females> 3S years old • "Salt & pepper" or "pepper pot skull"
I • 0 clinical significance
• Etiology unknown
appearance
o Loss of distinction of inner & outer table
1
8
THICK SKUll, GENERALIZED ,.-c:
CJl
o Loss of lamina dura Helpful Clues for Rare Diagnoses

o Brown tumors
• Sclerosing Bone Dysplasias
o Chronic renal disease: Secondary
o Osteopetrosis
hyperparathyroidism • Marked sclerosis and deposition of
o t Serum calcium, t parathyroid hormone, ~ osteopetrotic bone
serum phosphorus • Neurologic deficits: Blindness,
• Acromegaly conductive hearing loss, facial nerve
o Calvarial hyperostosis (esp. inner table)
palsy due to foraminal encroachment
o Prognathism (elongation of mandible)
o Skeletal series diagnostic for diffusely
o Sellar enlargement, erosion dense bones
o Enlarged paranasal sinuses (mainly
• Fluorosis
frontal): 75% o Skull shows minimal changes in fluorosis
o t Growth hormone & IGF-l
o Bones at the base show marked thickening
• Subdural Hematoma, Chronic (Calcified) o Occipital protuberance very prominent,
o Chronic calcified subdural hematoma
falx calcification
along inner table simulates thick skull o Skeletal survey helpful
o Look for subtle cleavage between calcified
membranes and the inner table Other Essential Information
• Anemias • Appearance of thick skull caused by
o Chronic anemias: Hemolytic or iron o Thick cortex (e.g., hyperostosis frontalis)
deficiency o Expanded diploic space (e.g., metastases,
o "Hair on end" skull with beta thalassemia anemia)
o Thick skull due to diploic space o Adjacent tissue (e.g., old calcified subdural
enlargement hematoma)
o Parietal bones most commonly affected,
relative sparing of the occipital squamae SELECTED REFERENCES
• Extramedullary Hematopoiesis 1. Chow KM et al: Cerebral alrophy and skull thickening due
o ECT: Smooth homogeneous hyperdense to chronic phenytoin lherapy. CMAJ. 176(3):321·3.2007
masses mimicking subdural hematoma 2. She R et al: Hyperostosis frontalis interna: case report and
review of literature. Ann Clin Lab Sci. 34(2):206-8, 2004
o Osseous findings of underlying disease
3. Hollar MA: The hair-on-end sign. Radiology. 221(2):347-8,
• Thalassemia: "Hair on end" skull 2001
• Osteopetrosis: Dense bone obliterating 4. Ita K et al: Accentualed temporal line on the frontal skull
radiograph: a sign of hyperparathyroidism. Radiology.
medullary space 192(2):497-S02, 1994
Diffusely Thick Skull, Normal Hyperostosis Frontalis Interna
I
Axial bone CT demonSlrales a diffusely lhick skull.
which is commonly seen as a normal variation. changes of benign hyperoslosis inlerna =.
Axial bone CT shows diffuse skulllhickening with classic
1
predominantly bifronlal in this pauent.
9
THICK SKUll, GENERALIZED
Shunted Hydrocephalus
(Left) Sagillal TI WI MR
demonslrales dirruse skull
lhickening ~ secondary 10
chronic Oilanlin therapy.
NOlice also cerebellar
alrophy (Right) Laleral
radiograph shows diffuse
skulllhickening in a patient
wilh chronically shunted
hydrocephalus. The shunt
lube ~ is also seen.
Metastases (Diffuse Sclerotic) Paget Disease

(Leh) Axial bone CT shows a
diffuse thick skull wilh focal
sclerotic regions in a
patient with prostate
melaSlasis. (Right) Axial
T I WI MR shows lhe lypical
MR appearance of diffuse,
extensive skull Paget disease
wilh diffuse calvarial diploic
thickening and
heterogeneous marrow ~.
(Left) Axial bone CT in an

extremely retarded 5 , year
old shows diffuse skull
thickening secondary to
small brain. (Right) Axial
bone CT shows a Ihick skull
due 10POlyoslOtiC (ibrous
dysplasia. NOle lhe
characteristic ground·glass
appearance or the diploic
space l:ll.
I
1
10
THICK SKULL, GENERALIZED en
~
c:
III
:J
C-
..,
O:!
Hyperparathyroidism Subdural Hematoma, Chronic (Calcified) III
(Left) Axial bone CT shows :J
thick skull with mild sclerosis Ul
()
and a granular appearance Q)
of the diploe, as well as loss -0

of distinction of inner & Duler Ul
table, in a patient with
chronic renal failure and
'"c:
secondary
hyperparathyroidism. (Right)
Axial T2WI MR demonstrates
chronic, calcified, bifrontal
subdural hematomas EE
resulting in skull thickening.
Sickle Cell Disease Thalassemia

fLeft) Coronal T2WI MR
shows diffuse bone
thickening with marked
diploic widening E±l of both
calvarium & skull base.
(Right) Coronal bone CT
shows diffuse diploic
thickening with "hair on
end" = appearance caused
by blood-forming bone
marrow hyperplasia. The
underlying brain is normal.
Osteopetrosis
(Left) Coronal T1 WI MR
shows diffuse skull
thickening and a dural-based
mass = in extramedullary
hematopoiesis. (Right) Axial
bone CT shows dirruse
sclerosis and thickening
involving the skull base and
facial bones in a patient with
osteopetrosis.
I
1
11
THICK SKULL, LOCALIZED
n.
('(l
()
DIFFERENTIAL DIAGNOSIS • Sclerotic: Dural-based mass, adjacent
(j) calvarium thickened, ± dural tail
c: Common • lntradiploic: lntradiploic mass thickens,
III
•... • Hyperostosis Frontalis lnterna expands calvaria ± cortical
a:l • Meningioma
1J d estru ction/thicken ing
c: • Metastasis (Osteoblastic)
III • "En plaque": Nodular dural thickening +
= Less Common associated extensive hyperostosis
• Fibrous Dysplasia (juxta-orbital most common site)
• Paget Disease • Metastasis (Osteoblastic)
• Dyke-Davidoff-Masson o Common with prostate, breast metastasis
• Cephalhematoma (Calcified) o Look for associated focal/diffuse
• Chronic Subdural Hematoma ( alcified) dura-arachnoid involvement
• Osteomyelitis (Chronic) Helpful Clues for Less Common Diagnoses
Rare but Important • Fibrous Dysplasia
• Osteosarcoma o Young patient
• Osteochondroma o Medullary expansion ("ground-glass")
• Frontometaphyseal Dysplasia • Paget Disease
• Osteopetrosis o Late osteosclerotic phase
• Osteopathia Striata o Focal areas of sclerosis in expanded diploic
space ("cotton wool" appearance)
• Dyke-Davidoff-Masson
ESSENTIAL INFORMATION o Cerebral atrophy + ipsilateral
Key Differential Diagnosis Issues compensatory osseous hypertrophy &
• Focal cortex t ± diploic expansion hyperpneumatization of paranasal sinuses
• Look for associated dural lesion • Cephalhematoma (Calcified)
o Birth trauma, subperiosteal hemorrhage
Helpful Clues for Common Diagnoses o Early: Thin calcified shell, late sequelae:
• Hyperostosis Frontalis Intema Incorporation of the calcified rim into the
o Middle-aged, older women
outer table of the skull
o Bilateral, symmetrical (bifrontal) • Chronic Subdural Hematoma (Calcified)
o Overgrowth mostly inner table
o Chronic calcified SDH along inner table
o Ends at coronal suture
simulates thick skull
• Meningioma o Looks like "double" skull on MR
o Three patterns
Hyperostosis Frontalis Interna Meningioma
I
1 Sagittal T 1 WI MR shows a typical example 01 local skull
thickening lrom benign hyperostosis =.
Note that the
Sagittal T1WI MR shows an intradiploie meningioma 81
with a massively thickened calvarium ~
thickening stops at coronal suture =.
12
THICK SKULL, LOCALIZED
III
::l
C-
...
D)
III
Fibrous Dysplasia
:::l
(Left) Axial CECT shows
localized hypemslOsis B>'
with associated enhancing
dural-based soft tissue ~ in
pmstate metastasis. (Right) (JJ
Axial bone CT shows
well-de(ined focal calvarial
'"c
appearance
characteristic
=-
thickening with gmund-g/ass
for fibrous
dysplasia.
Paget Disease Dyke-Davidoff-Masson

both lytic and blastic Paget
disease as evidenced by
focal lysis =with sclemtic
diploic expansion and
thickened cortices EB.
(Right) Axial bone CT shows
left fmntal calvarial
thickening
pneumatization
=with over
of the frontal
sinus E1 in
Dyke-Davidoff-Masson.
Cephalhematoma (Calcified) Chronic Subdural Hematoma (Calcified)

localized skull thickening
due to a calcified
cephalhemalOma SlI. (Right)
Axial T2WI MR shows an
unusual appearance
resembling a "double skull".
Outer dark lines Ei:I are outer
table, while the middle dark
line ~ represents inner
table; the intervening area is
marrow. Note additional
crescentic area deep £0 inner
table demarcated by an
unusual third black line =.
This represents an old
calcified
hematoma.
chronic subdural
I
1
;;:J THIN SKUll, GENERALIZED
.::£
(f)
a.
ro DIFFERENTIAL DIAGNOSIS • Obstructive Hydrocephalus
u
(f) o Etiology can be intra- or extraventricular
c: Common o Unless shunted -+ skull gradually thinned
ro
•... • Normal Infant Skull • Aqueductal Stenosis
CD
"0
• Obstructive Hydrocephalus o Lateral, 3rd ventricles t, 4th normal
c: • Aqueductal Stenosis
'" Helpful Clues for Less Common Diagnoses
;;:J
.::£
Less Common • Lacunar Skull
(f)
• Lacunar Skull o Membranous bone dysplasia -+ thin bone
• Hyperparathyroidism • Thinned calvarium is developmental,
• Hypophosphatasia NOT caused by hydrocephalus
Rare but Important • Resolves spontaneously by age 6 months
• Rickets although minor residua may persist into
• Osteogenesis Imperfecta adulthood
• Cleidocranial Dysplasia o Associations
• Primordial Dwarfism • Chiari 2, myelomeningocele ±

encephalocele
• Hyperparathyroidism
ESSENTIAL INFORMATION o Osteopenia + cortical thinning
Key Differential Diagnosis Issues o "Salt and pepper" calvarium
• Gradual calvarial thinning: Chronic t ICP o t Parathyroid hormone

(e.g., aqueductal stenosis) • Hypophosphatasia
• Demineralization: Hyperparathyroidism o Serum alkaline phosphatase ~
• Poor ossification o Decreased ossification of skull, vertebrae
o Hypophosphatasia, rickets • Skull may be "boneless"
o Osteogenesis imperfecta • Short tubular bones poorly/irregularly
ossified with "frayed" metaphyses
Helpful Clues for Common Diagnoses (similar to rickets)
• Normal Infant Skull
o Newborn: Vault thin, comprised of Helpful Clues for Rare Diagnoses
membranous bone • Osteogenesis Imperfecta
o Parietal bones thin, often barely visible o Osteoporosis + osseous fragility
o Frontal, occipital bones more ossified o Multiple fractures
o Severe underossification common in o Thin cortex, ~ ossification BOS
premature infants o Multiple wormian bones
Normal Infant Skull
I
1 Axial bone CT shows normal generalized thin calvarial
bones in a newborn E!:I with mildly overfapping sutures.
Axial NECT shows massively dilated ventricles in
chronically obstructed hydrocephalus associated with
diffuse thinning of calvarium E:I.
14
THIN SKULL, GENERALIZED
III
::l
Co
OJ
..,
Lacunar Skull Lacunar Skull III
::l
(Left) Late,al ,adiograph in a
patient with Chiari 2 en
n
malformation shows the III
typical appearance of -0
"lacunar" skullEz, also en

known as Luckenshadel.
(Right) Axial bone CT in the
'"
c
same patient shows a

characteristic "lacunar" skull
in Chiari 2 malformation.
Hyperparathyroidism Hypophosphatasia
radiograph in a 13 year old
with parathyroid adenoma
shows demineralization and
generalized thinning of the
skull =. Note the subtle
"saIL and pepper"
appearance of the calvarium
~ (Right) Lateral
radiograph shows the
thin skull =
hypomineralized, markedly
with infantile
of a newborn
hypophosphatasia.
Cleidocranial Dysplasia
radiograph of a skull shows a
classic "boneless" skull in
osteogenesis imperfecta.
Ossification of only the facial
bones and two small regions
of the cranium It] is present.
(Right) Bone CT with 30
shaded surface display
shows generalized calvarial
thinning with multiple
wormian bones in and
around lambdoid suture.
I
1
15
:J THIN SKULL, LOCALIZED
-'(j)"
a.
ro DIFFERENTIAL DIAGNOSIS o Pressure erosion of adjacent calvarium
<.)
(j) 050-65% middle fossa; 5-10% convexity
c: Common • Mega Cisterna Magna
III
•.... • Skull Normal Variants o Enlarged cisterna magna & intact vermis,
al o Parietal Thinning
"t:l normal cerebellar hemispheres
c: o Squamous Temporal, Occipital Bones
III o Scalloped occipital squamae
:J • Arachnoid Cyst
-'C/)" • Mega Cisterna Magna
• Slow Growing Neoplasm
Less Common o Any cortically based slow growing
• Slow Growing Neoplasm neoplasm can cause inner table scalloping
o Oligodendroglioma o Oligodendroglioma
o D ET • Partially Ca++ cortical/subcortical mass
o Ganglioglioma o DNET
o Diffuse Astrocytoma, Low Grade • Young patient, chronic epilepsy
• Paget Disease • "Bubbly" cortical mass
• Scalp Lesions o Ganglioglioma
o Dermoid Cyst • Partially cystic enhancing mass
o Epidermoid Cyst (child/young adult)
o Neurofibroma o Diffuse Astrocytoma, Low Grade
Rare but Important • White matter> cortex, nonenhancing
• Meningioma • Paget Disease
• Linear Scleroderma (Coup de Sabre) o "Osteoporosis/osteolysis circumscripta"
o Early destructive phase
• Well-defined lysis; frontal> occipital
ESSENTIAL INFORMATION • Both inner, outer tables involved (inner
Key Differential Diagnosis Issues usually more)
• Evaluate underlying brain, overlying scalp! • Scalp Lesions
o Pressure erosion of outer table
Helpful Clues for Common Diagnoses o Dermoid, epidermoid cysts; neurofibroma
o Parietal, squamous thinning Helpful Clues for Rare Diagnoses
o Inner table intact; diploe, outer table thin • Meningioma
• Arachnoid Cyst o Can erode, invade, destroy calvarium
o Well-delineated CSF-like extra-axial mass
Parietal Thinning Arachnoid Cyst
I
1 Axial bone CT shows classic symmetric biparietal
thinning II] Lhai is striking but normal.
Axial NECT shows a typical arachnoid cyst with
localized thinning of the adjacent calvarium =:iI.
16
THIN SKULL, LOCALIZED ,..
CJl
c:
III
::l
a.
III
..,
III
(Left) Sagittal T I WI MR
::l
shows a mega cisterna (Jl
()
magna associated with mild Q)
thinning of the adjacent "0

occipital bone lID. Vermis
and fourth ventricle are
,..
(Jl
c
normal. (Right) Axial T/ C+
MR shows a nonenhancing
low signal intensity
oligodendroglioma in the left
frontal region = associated
with subtle thinning 01 the
left frontal bone 81 as
compared to the right.
(Left) Axial T2WI MR shows

a very classical appearance
of a well-delineated
cortically based "bubbly"
mass, a ONET8I. Note
focal cortical thinning ~.
(Righi) Axial T2WI MR
shows a lobulated cortically
based ganglioglioma -7
causing localized thinning of
the skull 81.
(Left) Lateral radiograph

shows osteoporosis
circumscripta, a specific
appearance in early Pagel
disease of the skull 81.
(Right) Coronal J 1 C+ MR
shows an atypical
meningioma with solid and
cystic components invading
the SSS81 with associated
focal thinning of the
calvarium c::£
I
1
17
LYTIC SKULL LESION, SOLITARY
c.
C1l DIFFERENTIAL DIAGNOSIS • Surgical Defects, Calvarial
U
CfJ o Check history!
t: Common o Burr holes, surgical defects
•...
'" • Skull Normal Variants well-marginated
III
"lJ
• Surgical Defects, Calvarial • Metastasis
t: o Burr Holes o Destructive, permeative
'" o CSF Shunts and Complications o Enhancing mass centered in diploe
• Metastasis o ± Associated dural/scalp soft tissue
Less Common o Often known primary malignancy
• Epidermoid Cyst • Breast, lung, prostate most common
• Langerhans Cell Histiocytosis Helpful Clues for Less Common Diagnoses
• Plasmacytoma • Epidermoid Cyst
• Paget Disease o Involves both inner, outer tables
• Hemangioma o Well-defined
• Dermoid Cyst o Lacks central trabeculae
• Fibrous Dysplasia o Dense sclerotic margins
• Leptomeningeal Cyst o Typically round or lobulated
• Osteomyelitis o Restricts (hyperintense) on DWI
Rare but Important • Langerhans Cell Histiocytosis
• Cephalocele o "Eosinophilic granuloma"
• Tuberculosis o Well-defined lytic lesion
• Neurosarcoidosis o "Beveled" edge (inner table involved>
• Sinus Pericranii outer)
• Aneurysmal Bone Cyst o No marginal sclerosis
• Aggressive Fibromatosis o ± Adjacent soft tissue mass
0<5 years
o "Hole within hole", "button sequestrum"
ESSENTIAL INFORMATION on ECT
Key Differential Diagnosis Issues • Plasmacytoma
• Margins of lytic lesion helpful o Lytic lesion with scalloped, poorly
o Surgical defects: Well-marginated marginated, non-sclerotic margins
o Metastasis, osteomyelitis: Permeative o Often large at presentation
o Epidermoid: Dense sclerotic o Biconvex expansion of involved bone
o Histiocytosis: "Beveled" edge • Paget Disease
o Lytic phase: Well-defined lucent defect
Helpful Clues for Common Diagnoses o "Osteoporosis circumscripta"
• Skull Normal Variants o Frontal> occipital
o Vascular grooves
o Inner & outer tables both involved; inner
• Inner table: Meningeal arteries, veins usually more
• Outer table: Superficial temporal artery o Cortical thickening, coarse trabeculation -
o Venous channels
hypointense Tl/T2WI
• Thin-walled veins, venous "lakes" • Hemangioma
• Connect meningeal veins/dural venous o Lytic diploic space lesion
sinuses with pericranial veins o Well-circumscribed
• Diploic venous channel can usually be o "Spoke wheel" or "reticulated" pattern
traced into venous lakes o Strong enhancement
o Pacchionian (arachnoid) granulations
• Dermoid Cyst
• Within/adjacent to dural venous sinus o Well-circumscribed unilocular cyst
• Round/oval filling defect in venous sinus containing fat
I • Large lesions remodel inner table
• CSF density/signal intensity
o Expands diploe
1
18
(J)
LYTIC SKULL LESION, SOLITARY
"
c:
o Commonly near the anterior fontanelle, • Neurosarcoidosis

glabella, nasion, vertex, subocciput o Isolated area of bone translucency
• Leptomeningeal Cyst • Well-demarcated margins
o "Growing fracture" on radiography/NECT o Uncommon presentation
o Late complication of skull fracture with o Look for associated
dural laceration • Pituitary/infundibulum, dural-based
o Smoothly marginated skull defect masses (f)
o Hyperintense on T2WI • Hilar adenopathy (CXR) "

c
• Osteomyelitis • Sinus Pericranii

o Usually complication of trauma, sinusitis, o Vascular scalp mass communicates with
mastoiditis dural venous sinus via transcalvarial vein
o Frontal> temporal bone o Transcalvarial vein courses through
o Mixed lytic/proliferative lesion well-defined bone defect
o Moth-eaten/permeative medullary & o Common frontal (40%)
cortical destruction o Midline or paramedian
o "Pott puffy tumor" = frontal soft tissue o Superior sagittal sinus most commonly
swelling involved
o Often associated: Epidural abscess! • Aggressive Fibromatosis
o Benign fibrous tumor of infancy
Helpful Clues for Rare Diagnoses
o Solitary/multiple benign myofibroblastic
• Cephalocele tumors
o Herniation of brain, meninges, CSF,or a
• Subcutaneous tissue, muscle, bone,
combination of all three
occasionally viscera
o Dural laceration + dehiscent skull defect
• Neck lesions may extend intracranially
o Can be congenital or acquired (surgery,
o Well-defined lytic lesion with/without
trauma)
sclerotic rim
• Congenital: Parietal, occipital; young
o Can mimic any malignant or aggressive
patient
infection!
• Acquired: Basifrontal, history of
o May need biopsy
trauma/su rgery
• "Atretic cephalocele" should be in
differential diagnosis of any midline
subscalp mass in child, especially parietal
region
Skull Normal Variants Burr Holes
I
Sagittal NECT - 3D VRT display of normal inner calvarial
vault shows vascular groove for middle meningeal artery
Coronal 3D NEG shows a burr hole .-7, shunt tubing
Ell in this patient with history of myelomeningocele and
1
& veins arachnoid granulations a norma/thinning Chiari 2 malformation. Premature closure of the right
of squamous temporal bone!CB corona/suture is a/50 present
19
=~
OJ LYTIC SKULL LESIONr SOLITARY
(/)
0-
ro
()
(/)
C Metastasis Epidermoid Cyst

III
•... (Lefl) Axial bone CT shows a
llJ Iylic skull lesion with
1J
C irregular margins in a lung
III carcinoma metastasis t:2S.
(Right) Laleral radiograph of
skull shows an epidermoid
cyst presenting as a
well-defined lytic lesion with
dense sclerotic margins 81.
Langerhans Cell Histiocytosis

(Left) Axial NECT shows an
epidermoid cyst presenting
as a well-defined lytic lesion
with dense sclerotic margins
SI. (RighI) Axial NECT
shows a large destructive
lesion with associated soft
tissue mass in a patient with
Langerhans cell histiocytosis
SI.
Plasmacytoma Paget Disease

(Left) Axial bone CT shows a
typical appearance of
plasmacytoma involving the
petrous apex, inner ear, and
clivus =:I. (RighI) Axial bone
CT shows bOlh lytic and
blastic Paget disease as
evidenced by focal lysis =:I
within a background of
diffuse sclerotic diploic
expansion and thickened
cortices
I
1
20
LYTIC SKULL LESION, SOLITARY ,..<:
en
III
:J
0-
Hemangioma
...
m
Dermoid Cyst III
(Left) Axial bone CT shows a :J

sharply marginated expansile en
()
hemangioma with a Q)
reticulated intra diploic
trabecular thickening SII. "en
(Right) Coronal bone CT
shows a fat density lytic
'"
<:
lesion involving the

sphenoid, consistent with a
dermoid cyst
Fibrous Dysplasia
variant case of mixed lucent
= and sclerotic SII
("Pagetoid") fibrous
dysplasia affecting the left
frontal bone. (Right) Axial
bone CT shows a defect in
the skull with herniation of
dura in a posHraumalic
leptomeningeal cyst =.
Osteomyelitis Sinus Pericranii

permeative pallern of
destruction in (rontal
osteomyelitis E.J with an
associated scalp swelling =.
(Right) Coronal T1 C+ rs
MR shows a subcutaneous
enhancing mass =
communicaling with a
lranscalvarial vein ~
through a well-delineated,
corticated skull defect SII.
I
1
21
:> MULTIPLE LUCENT SKUll LESIONS
.0£
(f)
Q.
cu DIFFERENTIAL DIAGNOSIS • Common in frontal and parietal bones
U
(f) • Very thin walls
c: Common • Communicate with meningeal veins and
•..
III
al
• Skull Normal Variants dural sinuses
o Venous Lakes o Arachnoid Granulations
"'C
c: o Emissary Veins, Transcranial • Punched out defects inner table
III
o Arachnoid Granulations subjacent to dural venous sinuses
:>
-"
(f)
o Prominent Convolutional Markings • CSF density/intensity
o Parietal Foramina o Prominent Convolutional Markings
• Treatment-Related • Related to pulsation of brain
o Burr Holes • Inner table, frequent in children
o Surgical Defects, Calvarial • Become prominent in craniosynostosis,
• Metastases, Skull chronic raised intracranial pressure
• Osteoporosis o Parietal Foramina
• Myeloma • Two symmetric openings on each side of
Less Common sagittal suture in the upper edge of
• Langerhans Cell Histiocytosis parietal bones
• Hyperparathyroidism • Usually very small, permit passage of
• Lymphoma, Metastatic, Intracranial emissary veins
• Hemangioma • Treatment-Related
o Burr holes, shunt-related, surgical defects
• Leukemia
o Sharply marginated
• Osteomyelitis, Skull
• Osteoradionecrosis • Metastases, Skull
o Permeative skull destruction ± scalp/dural
• Chiari 2 (Lacunar Skull)
soft tissue
Rare but Important o Often known primary malignancy
• Neurosarcoid o Commonly lung, breast, renal, thyroid
• Neurofibromatosis Type 1 (Lambdoid • Osteoporosis
Defects) o Older age group
• Syphilis, Acquired o Spotty demineralization appearing as
lucent lesions
ESSENTIAL INFORMATION • Myeloma
o Multiple, well-circumscribed, lytic,
Key Differential Diagnosis Issues punched out, round lesions
• As with solitary lucent skull lesion, margins o Skeletal survey helpful
helpful
o Sharply demarcated: Treatment-related,
myeloma • Langerhans Cell Histiocytosis
o Sharply marginated lytic defect with
o Permeative: Metastasis, osteomyelitis
o Beveled: Histiocytosis
bevelled margins
o Associated soft tissue mass
o Inner table involvement: Convolutional
o Large lesions: Geographic destruction
markings, arachnoid granulations
o Brain: Thick enhancing infundibulum,
Helpful Clues for Common Diagnoses absent posterior pituitary bright spot
• Skull Normal Variants o 2-5 years: Multifocal disease
o Venous Lakes • Hyperparathyroidism
• Diploic venous can usually be traced to o Mottling of the cranial vault due to
area of lucency trabecular bone resorption
• Slightly ragged configuration, poorly o Alternating areas of lucency and sclerosis:
defined margin "Salt and pepper" skull
I o Emissary Veins, Transcranial
• Extremely variable positions
o Brown tumors: Multiple well-defined lytic
lesions
1
22
MULTIPLE LUCENT SKULL LESIONS en
c"
:
III
o t Parathyroid hormone o Involves both inner, outer tables :l
a.
• Hemangioma o Squamous portions of temporal/occipital m
...•
o Sharply marginated expansile lesion bones, parietal bones III
o Diploic space, honeycomb, or sunburst :l

Helpful Clues for Rare Diagnoses en
appearance pattern ()
• Neurosarcoid III
o 1/3 have thin sclerotic rim -0
o Uncommon
o Multiple uncommon (f)
o Well-circumscribed lytic lesion
• Leukemia o Involves inner, outer tables of calvarium
"
c:
o Osteopenia with multiple lytic lesions
o Sharp, non-sclerotic margins
o Sutural diastasis: Produced by t
• Neurofibromatosis Type 1 (Lambdoid
intracranial pressure
Defects)
o Tubular and flat bones more commonly
o Lambdoid suture defect
involved
o Associated sphenoid wing dysplasia
o Skeletal survey may be helpful
o Plexiform neurofibromas of scalp, orbit
• Osteomyelitis, Skull common
o Permeative destruction ± scalp/epidural
• Syphilis, Acquired
soft tissue o Lytic areas with demineralization/sclerosis
o Usually occurs as a complication of trauma
of the outer table, diploe
or sinusitis o Inner table less involved
o Brain abscess is most common
o Irregular worm-eaten osseous destruction
complication
o Associated presence of mucocutaneous
• Osteoradionecrosis findings or generalized lymphadenopathy
o Mixed region of lysis and sclerosis
o Radiates outward from epicenter of
radiation portal SELECTED REFERENCES
• Chiari 2 (Lacunar Skull) 1. Connor SE et al: Imaging of the petrous apex: a pictorial
o Caused by inherited mesenchymal defect, review. Br J Radiol. 81(965):427-35, 2008
2. Porto Let al: Central nervous system imaging in childhood
not hydrocephalus/increased intracranial leukaemia. Eur J Cancer. 2004
pressure 3. Smith JK et al: Imaging manifestations of neurosarcoidosis.
o Not same as prominent convolutional AJR Am J Roentgenol. 182(2):289-9S, 2004
4. Hasegawa M et al: Multicentric infantile myofibromatosis
marklngs (normal variant) in the cranium: case report. Neurosurgery. 36(6): 1200-3,
o Present at birth, largely resolves by 6 1995
5. Zimmerman RD et al: Cranial CT findings in patients with
months meningomyelocele. AJR Am J Roentgenol. 1979
o Minor changes may persist into adulthood
Venous lakes Emissary Veins, Transcranial
I
Axial bone CT shows multiple linear lucent areas ~
due to prominent emissary veins. Note a fromal venous
Axial bone CT shows small lucent foci in diploic space
I:l:l. All could be traced traversing skull on multiple
1
lake E:I with small venous tributaries It]. sections. findings are typical for emissary veins seen
"endon".
23
= MULTIPLE LUCENT SKULL LESIONS
Cl.
co
u
(f)
c: Arachnoid Granulations
•..
III
(Left) Coronal bone CT
al shows a large arachnoid
"0
c: granulation of the central
III skull base~. CECT scan
:l (not shown) demonstrated
CSF within the lucent defect.
en
"" (Right) Lateral radiograph in
a 6 year old shows
prominent convolutional
markings ~ Note that the
sella ~ is normal, without
enlargement or erosion to
suggest increased intracranial
pressure.
Parietal Foramina Burr Holes

radiograph shows large
symmetric lytic areas in the
parietal bones, consistent
with a large parietal foramina
~ (Right) Coronal oblique
30 NECT shows a burr hole
~ with shunt tubing ~
Surgical Defects, Calvarial

(Left) Axial CECT in a patient
with pterional approach
anterior tempora/lobectomy
shows surgical defects in
squamous temporal bone
~. Remote cerebellar
hemorrhage ~ occurred as
a complication of the
procedure. (Right) Axial
bone CT shows multiple
areas of permeative
destruction -7 in the
calvarium of a patient with
breast carcinoma metastasis.
I
1
24
MULTIPLE LUCENT SKULL LESIONS
III
::l
Cl.
.,
OJ
Osteoporosis Myeloma III
::l
ill-defined areas of Ul
demineralization = in
()
OJ
-0
osteoporosis. Lesions do not
destroy bone; entire diploic Ul
space appears moderately
deossified. (Right) Axial bone
"
c
CT shows multiple punched

out defects ~ in the
calvarium in a patient with
multiple myeloma.
Langerhans Cell Histiocytosis Hyperparathyroidism

bilateral mastoid destructive
lesions in a patient with
Langerhans cell histiocytosis
~. (Right) Lateral
radiograph shows a pattern
of trabecular resorption of
mixed lytic Ii8 and dense
areas ~ that has been
termed "salt and pepper" in
hyperparathyroidism.
Chiari 2 (Lacunar Skull)

(Left) Axial T t C+ MR shows
multiple enhancing lesions
E:I in a patient with multiple
calvarial hemangiomas.
(Right) Lateral radiograph
shows the typical
appearance of "/acunar"
skull a/50 known as
Luckenschadel, involving
inner & outer tables of
squamous bones and due to
mesenchymal defects, not
hydrocephalus.
I
1
25
:J SClEROTIC SKUll LESION, SOLITARY
.><:
(f)
0-
ro DIFFERENTIAL DIAGNOSIS • Sclerotic, cystic, or mixed bone changes
u
(f) also seen
c: Common • Can show variable enhancement,
ro
•... • Metastasis sometimes striking
co • Osteoma
"0 • Meningioma-Associated Hyperostosis
c: • Fibrous Dysplasia o More common with en plaque
ro
=
:J
• Meningioma-Associated Hyperostosis meningioma than globular form
.><:
(f) • Paget Disease o En plaque meningioma
less Common • Adjacent bony hyperostosis often
• Osteomyelitis, Skull (Chronic) disproportionately greater than
• Calcified Cephalohematoma underlying tumor
o Cause of hyperostosis is controversial
Rare but Important • Reactive or tumoral infiltration
• Calvarium Fracture (Chronic, Depressed) • Paget Disease
• Meningioma (Intraosseous) o Older patient (vs. younger with fibrous
• Hemangioma dysplasia)
• Craniostenosis o Late sclerotic phase
• Widening of diploic space + coarsened
ESSENTIAL INFORMATION trabeculae
• Inner table, diploic space more involved
Key Differential Diagnosis Issues than outer table
• Outer/inner table: Osteoma • Round or oval area of sclerosis (usually
• Diploic space (DS) ± outer/inner table: within prior areas of "osteoporosis
Sclerotic metastasis circumscripta")
• DS expansion + outer> inner table: FD • Diffuse> > solitary involvement
• DS expansion + inner> outer table: Paget
disease Helpful Clues for less Common Diagnoses
• Osteomyelitis, Skull (Chronic)
Helpful Clues for Common Diagnoses o Rare in calvarium
• Metastasis • Classic imaging finding = "button
o Most common tumors with intrinsically
sequestrum"
sclerotic metastases • Dense island of dead bone within
• Prostate well-defined lytic area
• Breast • Also seen in numerous other entities
• Lymphoma • Common: Eosinophilic granuloma,
o Any lytic metastasis can become sclerotic
healing burr hole
after treatment • Less common/rare: Tuberculous osteitis,
o Use contrast-enhanced MR to assess radiation-induced bone necrosis,
intracranial involvement metastasis, Paget disease
• Osteoma o More common in skull base
o Well-circumscribed, dense, hyperostotic • Spread of infection from paranasal
o Location sinuses, mastoid, petrous apex air cells
• Paranasal sinuses (frontal most common) • Ill-defined area of mixed osteosclerosis,
• Calvarium lysis
• Facial bones, mandible o ± Epidural/subdural empyema, brain
o Outer table> inner table
abscess
• Fibrous Dysplasia o Consider contrast-enhanced MR to assess
o 70% of all FD cases are monostotic
extent
o Expansile, widened diploic space
• Calcified Cephalohematoma
o Imaging patterns relate to relative content
o Usually associated with birth trauma
I of fibrous vs. osseous tissue
• Classic: "Ground-glass" appearance
• Acute subperiosteal hemorrhage
1
26
SClEROTIC SKULL LESION, SOLITARY ,.-
Ul
C
III
• Healing stage may result in rim • Can mimic metastasis :J
0-
calcification • Hemangioma ...
CD
o Late sequelae o Osseous hemangiomas of calvarium III
:J
• Calcified rim incorporated into outer account for 0.2% of bone neoplasms
(J)
table o Benign vascular anomalies of bone (")
W
• Outer table eventually becomes sclerotic, o Expand diploic space, outer> inner table "0
thickened o Most are lytic, some sclerotic (rim) with ,.-

Ul
"sunburst" appearance c
o Highly vascular
• Calvarium Fracture (Chronic, Depressed)
o Rare
• Variable histology
• Can be venous, cavernous, or capillary
• Most depressed skull fractures are
type
elevated, repaired
o ± Intracranial extension
o May have associated cephalocele with
o ± Dural "tail sign"
bony reaction (lysis> sclerosis)
o Can mimic meningioma
• Meningioma (Intra osseous)
o Primary calvarial meningiomas rare • Craniostenosis
o Premature suture fusion
• 1-2% of all meningiomas
o One of most common craniofacial
• Sometimes termed "ectopic" or
"extradural" meningioma anomalies
o Can be syndromic (over ISO associated) or
• Best term = primary extradural
nonsyndromic
meningioma
o Classification
• Usually isolated (nonsyndromic)
o Sagittal suture most commonly affected
• Purely extracalvarial (type 1)
o Dense suture "bone bridge" or "beaking"
• Purely calvarial (type 2)
• Calvarial with extracalvarial extension
(type 3) SELECTED REFERENCES
o Typical presentation 1. Ilukki J et al: Single suture craniosynostosis: diagnosis and
• Middle-aged, older patient imaging. Front Oral BioI. 12:79-90,2008
2. Agrawal Vet al: lntraosseous intracranial meningioma.
• Slow growing scalp swelling ± pain AJNR Am J Neuroradiol. 28(2):314-5, 2007
o Focal skull mass 3. Tokgoz N et al: Primary intraosseous meningioma: CT and
• Diploic space enlarges MRI appearance. AJNR Am J Neuroradiol. 26(8):2053-6,
2005
• Mixed lysis, sclerosis; lysis often
predominates
Metastasis
I
Axial bone CT shows a sclerotic metastasis from prostate
carcinoma HJ that involves the diploic space as well as
Axial bone CT shows a solitary sclerotic metastasis E>
from breast carcinoma. This could also possibly have
1
the inner table. been a lytic metaSlasis that has been treated and
become scleroUc.
27
SClEROTIC SKULL LESIONr SOLITARY
a.
OJ
U
(fJ
C Osteoma Osteoma
1tI
~ (Left) Axial bone CT shows a
co classic large osteoma arising
"C
C from the outer table of the
1tI occipital bone 81. (RighI)
Axial bone CT shows an
osteoma ~ arising from the
inner table of the frontal
bone. Osteomas arise more
commonly from the outer
rather than the inner table.
Fibrous Dysplasia
(Lefl) Axial bone CT shows a
wel/-defined focal calvarial
thickening with ground-glass
appearance characteristic for
fibrous dysplasia =. (RighI)
Axial NECT shows an
example of cystic fibrous
dysplasia of the superior
orbital rim. Note lucent
cavity c;. surrounded by
thick sclerotic rind l~ and
the lucent rim 8
Meningioma-Associated Hyperostosis Paget Disease

(Lefl) Axial bone CT shows
focal hyperostosis associated
with an en plaque
meningioma 81. (RighI)
Axial bone CT shows mostly
late-stage thickening,
sclerosis of temporal bone
with a few scattered lytic
areas=.
I
1
28
SCLEROTIC SKULL LESION, SOLITARY
III
:J
0-
ro
.,
Osteomyelitis, Skull (Chronic) Osteomyelitis, Skull (Chronic) III
(Left) Axial bone CT shows :J

classic" bullon sequestrum" (JJ
o
as a residual of chronic Cl
calvarial osteomyelitis. Note -0
peripheral dense bony (JJ

sclerosis 1m surrounding c
""
dense "sequestrum" E'J of
dead bone within
well-defined lucenl area.
(Right) Axial bone CT in a
patienl with a long history of
ear infections shows typical
appearance of chronic otitis
media wilh malleus 1::1 and
incus 81 surrounded by
inflammatory debris. Note
overlying calvarial sclerosis,
thickening ffi
Calcified Cephalohematoma Meningioma (Intraosseous)

calcified cephalohematoma
E'J with calcified rim
incorporated into outer table
of skull. (Rigl1t) Axial bone
CT shows thick left frontal
bone with lobulated
hyperostosis 1::1 extending
from outer lable. SoFt tissue
mass overlies hyperostosis
81. MR (not shown)
demonstrated hyperostosis
infiltrating, expanding diploic
space. Primary inlraosseous
meningiomas originate
within diploic space, may
extend both intra- and
eXlracranially.
Hemangioma
focaf expansile calvarial mass
with well-delineated sclerotic
margins d>, (Right) Axial
NECT shows scferosis and
fusion of metopic suture =
thaI caused a "keel-shaped"
forehead (trigonocephaly) in
this 7 month old infant.
I
1
29
SCLEROTIC SKUll lESIONS, MULTIPLE
DIFFERENTIAL DIAGNOSIS o Frontal, sphenoid, maxillary, ethmoid

bones more commonly involved
c: Common o Widened diploic spaces with outer table>
nl
"-
• Metastases, Skull inner table involvement
lD
"0 less Common o Ground-glass or sclerotic appearance
c: • Paget Disease
nl • Fibrous Dysplasia
o Late osteosclerotic phase
• Paget Disease
o Blastic lesions, often crossing sutures
Rare but Important o "Tam-o'-shanter" skull: t t Diploic space,
• Hyperparathyroidism ("Brown Tumor") particularly inner table
• Osteoma o "Cotton wool" skull: Focal areas of sclerosis
• Osteopoikilosis within previous areas of osteoporosis
• MeJorheostosis circumscripta
• Osteopathia Striata
• Hyperparathyroidism ("Brown Tumor")
ESSENTIAL INFORMATION o Trabecular bone resorption in cranial vault
Key Differential Diagnosis Issues o Alternating areas of lucency and sclerosis:
• Osteoblastic metastasis, especially from "Salt and pepper" appearance

o Brown tumors: Can become ossified during
prostate, by far the most common cause
reparative process
Helpful Clues for Common Diagnoses • Osteoma
• Metastases, Skull o In Gardner syndrome, multiple osteomas
o Osteoblastic or treated • Round dense lesions of outer table (less
• Most common = prostate carcinoma common in inner table)
• Any lytic metastasis following favorable o Colonic polyposis + soft tissue tumors
response to treatment (especially desmoid)
o Other malignancies with sclerotic • Osteopoikilosis
metastases include breast, colon, o Sclerosing bone dysplasia
melanoma, bladder, soft tissue sarcoma • Multiple radiopaque round, oval, or
Helpful Clues for less Common Diagnoses lanceolate spots of t radiodensity
• Fibrous Dysplasia o Predilection for epiphysis/metaphysis in
o 20-30% polyostotic long and short tubular bones
o Skull involvement rare
Metastases, Skull Metastases, Skull
I
1 Axial bone CT shows multiple sclerotic metastases
from prostate carcinoma.
= mixed lytic, sclerotic calvarial metastases =
Axial bone CT in a patient with lung carcinoma shows
with
adjacent ossific foc; E!2 from destroyed bone ;n
adjacent dural soft tissue masses.
30
SCLEROTIC SKULL LESIONS, MULTIPLE
III
:J
Co
..,
OJ
Fibrous Dysplasia III

:J
mulliple lesions of classic (j)
()
polyostolic fibrous dysplasia OJ
-0
H2 with expansion and
ground-glass matrix. (Right)
Axial bone CT shows mixed
sclerotic, lucent process
af(ecting sphenoid bone, leFt
maxilla. Maxillary sinus
lumen is obliterated PlIiJ; leFt
pterygomaxillary Fissure~ is
narrowed.
Paget Disease Paget Disease

shows a classic appearance
of Pagel disease, with
changes consistent with
osteoporosis circumscripla
H2 and a "COllon wool"
appearance due to multiple
sclerotic lesions (Right)
Axial bone CT shows diFFuse
calvaria/thickening with
multiple sclerotic areas 11:.'I in
a background of osteolysis in
a palient with Paget disease.
Osteoma
(LeFt) Coronal bone CT
shows generalized skull
thickening secondary to
chronic renal insufficiency
and secondary
hyperparathyroidism. Note
the Focal areas of
osteosclerosis 8:1. (Right)
Anteroposterior radiograph
shows large osteomas =::l.
I-Iere, they are part of
Gardner syndrome. This
patient a/so has a long
history of polyposis of the
colon.
I
1
31
MACROCEPHALY
n.
ro DIFFERENTIAL DIAGNOSIS • Aqueductal Stenosis
u
CI) o Look for associated hemosiderin, vascular
c: Common anomalies
III
•... • Benign Familial Macrocrania • Arachnoid Cyst
a:l • Hydrocephalus and Obstructed CSF Spaces
"'0 o Steady-state acquisition sequence to
c: o Intraventricular Hemorrhage identify cyst wall
III
o Aqueductal Stenosis • Enlarged Subarachnoid Spaces
::::J
-"
en o Arachnoid Cyst o Look for traversing veins
o Enlarged Subarachnoid Spaces o Natural history: Resolution by 12-18
o Villous Hypertrophy of the Choroid Plexus months
o Subdural Hematoma, Chronic • Villous Hypertrophy of the Choroid
Less Common Plexus
• Dandy-Walker Continuum o Likely on a spectrum, including choroid
• Neoplasm plexus papilloma

o Glioblastoma Multiforme o Bilateral choroid plexus lesions typical
o Teratoma • Subdural Hematoma, Chronic
• Neurocutaneous Disorders o MR identifies hemorrhagic components
o Neurofibromatosis Type 1 Helpful Clues for Less Common Diagnoses
o Tuberous Sclerosis Complex • Dandy-Walker Continuum
• Hemimegalencephaly o Classic Dandy-Walker & Blake pouch cyst:
• Megalencephaly Syndromes Vermian angulation, large bony posterior
Rare but Important fossa
• Hydranencephaly o Classic Dandy-Walker
• Inborn Errors of Metabolism • Incompletely lobulated vermis, deficient
o Glutaric Aciduria Type 1 fastigial recess/primary fissure
o MLCI o Blake pouch cyst
o Mucopolysaccharidosis • Intact vermis, fastigial recess, and
o Alexander Disease primary fissure
o Canavan Disease • Neoplasm
• Achondroplasia o Large, bulky neonatal tumors
• Fibrous Dysplasia o Glioblastoma Multiforme

• Enhancement, necrosis, hemorrhage
o Teratoma
ESSENTIAL INFORMATION • Fat, calcium, enhancing soft tissue
Key Differential Diagnosis Issues • Neurofibromatosis Type 1
• Macrocephaly = head circumference> 2 o Look for foci of abnormal signal intensity
standard deviations above mean for (FASI), optic nerve gliomas, cafe-au-lait
age-matched controls spots
• Macrocephaly = macrocrania o Macrocrania predominantly derived from
• Megalencephaly = subtype of macrocrania bulky white matter
• Imaging infants/children with macrocephaly • Tuberous Sclerosis Complex
o Hydrocephalus or white matter o Cutaneous markers (ash-leaf spots) may be
abnormality found? Use contrast! occult in 1st year of life
• Glutaric aciduria type 1 = child abuse mimic o Look for Ca++ subependymal nodules,
radial Iines
Helpful Clues for Common Diagnoses • Hemimegalencephaly
• Benign Familial Macrocrania o Look for cutaneous markers & stigmata of
o Family history important
overgrowth syndromes
• Intraventricular Hemorrhage • Hypomelanosis of Ito
I o Hemosiderin not always apparent on
follow-up images
• Proteus syndrome
• Linear sebaceous nevus syndrome
1
32
MACROCEPHALY en
;J;
c:
III
• Megalencephaly Syndromes • Canavan Disease ::l
C.
o Clues in name o MRS key: t t NAA
..•
OJ
• Megalencephaly, polymicrogyria • Achondroplasia III
::l
syndrome o Small skull base
(J)
• Megalencephaly with dilated • Jugular foramina coarctation: CSF n
D>
Virchow-Robin spaces drainage impaired "0
• Cerebral gigantism (Soto syndrome) • Foramen magnum coarctation: (J)

A
• Macrocrania-cutis marmorata CervicomedulJary compression c:
telangiectatica congenita • Fibrous Dysplasia
o Focal or diffuse (leontiasis ossea) may t
head circumference
• Hydranencephaly
o Classic radiograph/CT: Ground-glass
o Distinguish from maximal hydrocephalus
o MR (T2): Black velvet appearance
o MR shows cortex, falx
• Glutaric Aciduria Type 1
o Bilateral temporal lobe hypoplasia & large SELECTED REFERENCES
sylvian fissures 1. Colombani M et al: A new case of megalencephaly and
o Resembles bilateral middle cranial fossa perisylvian polymicrogyria with post-axial polydactyly and
hydrocephalus: MPPH syndrome. fur J Med Genet.
arachnoid cysts 49(6):466-71,2006
o Crisis: Caudate, putamen, globus paIlidus 2. Groeschel Set al: Magnetic resonance imaging and proton
swelling, & t signal magnetic resonance spectroscopy of megalencephaly and
dilated Virchow-Robin spaces. Pediatr Neurol. 34(1):35-40,
• MLCI 2006
o Diffusely t white matter signal 3. D'Ambrosio AL et al: Villous hypertrophy versus c1,oroid
o Temporal pole & frontoparietal cysts plexus papilloma: a case report demonstrating a diagnostic
role for the proliferation index. Pediatr Neurosurg.
o Macrocrania differentiates from CMV 39(2):91-6,2003
(common microcephaly) 4. Medina LS et al: Children with macrocrania: clinical and
imaging predictors of disorders requiring surgery. AJNR Am
• Mucopolysaccharidosis J Neuroradiol. 22(3):564-70, 2001
o Dilated perivascular spaces 5. Wilms G et al: CT and MR in infants with pericerebral
• Alexander Disease collections and macrocephaly: benign enlargement of the
subarachnoid spaces versus subdural collections. AJNR Am
o Enhancement is the key to diagnosis! J Neuroradiol. 14(4):855-60, 1993
o Infant: Frontal swelling & t signal &
enhancement
o Juvenile: Brainstem foci of t signal &
enhancement
Hydrocephalus and Obstructed CSF

Benign Familial Macrocrania Spaces
I
Sagittal T1WI MR shows a normal-appearing corpus
callosum and callosal isthmus E'l gyral pattern, myelin
Anteroposterior radiograph shows massive macrocrania
in a child with untreated hydrocephalus.
1
maturation, and midline slfuclures in this child with
benign familial macrocrania. 33
:::> MACROCEPHALY
-><
(f)
a.
ro
u
(f)
Hydrocephalus and Obstructed CSF
c: Spaces Intraventricular Hemorrhage
l\l
•... (Left) Axial NECT shows
CD massive tri·ventricular
'tl
c: hydrocephalus. The choroid
l\l
=-
plexus dangles in the fluid
and the massa
intermedia ~ is stretched
thin. (Right) Axial T2WI MR
in a 27 week gestational age
(corrected) premature infant
shows an age-appropriate
immature sulcal pattern.
There is a small focus of
ependymal hemosiderin ~
in the right trigone, a small
clot 0:> in the left.
Intraventricular Hemorrhage Aqueductal Stenosis

(Left) Axial T2' CRE MR in
an infant born prematurely
with shunted hydrocephalus
shows evidence of
hemosiderin and volume loss
in left caudothalarnic groove
82. Diffuse hemosiderin
staining 1::1 of the ependyma
follows remote IVI I. (Right)
Sagittal T2WI MR shows
hydrocephalus and a
(unnel-shaped aqueduct of
Sylvius ~ The appearance
is typical, with the proximal
aqueduct splayed and the
distal aqueduct closed.
Arachnoid Cyst Arachnoid Cyst

(Left) Sagittal T2WI MR
shows marked
hydrocephalus and a 3rd
ventricular arachnoid cyst.
The wall of the cyst ~
obstructs the proximal
aqueduct. Note additional
infracerebellar & and
retrocerebellar 1::1 csr
loculations. (Right) Axial
T2WI MR shows an
arachnoid cyst almost
completely filling the left
hemicranium. Note shift of
midline structures and
marked calvarial expansion
'=;. due to the effect of
I long-standing csr pulsation.
1
34
CIl
MACROCEPHALY
""c:
Villous Hypertrophy of the Choroid

Plexus
(Left) Coronal ultrasound
shows prominent
pericerebral subarachnoid
fluid. The subarachnoid
space (between l:ll and l:llJ
measures over 10 mm. Veins
~ traverse the space,
confirming that the fluid is in
the subarachnoid, not
subdural, compartment.
(Right) SagiHal T1 C+ MR
shows marked
hydrocephalus. There was
symmetrical slightly nodular
enlargement of the choroid
plexus BI in this child.
Villous hypertrophy is on a
spectrum with CP papilloma.
Subdural Hematoma, Chronic

(Left) Axial FLAIR MR shows
bilateral subdural collections
BI of differing signal
intensities and therefore
likely different ages.
Collections were nearly
isodense on CT (not shown).
(Right) SagiHal T2WI MR
shows hydrocephalus, patent
aqueduct, CSF flow voids
fastigial crease I?--l<
primary fissure a large
tegmento-vermian angle, &
incomplete vermian
lobulation. This case is in the
continuum between "c1assic
Dandy-Walker" and Blake
pouch cyst.
Glioblastoma Multiforme Teratoma

(Left) Axial T2WI MR in a 6
week old infant with
macrocrania shows a
massive supratentorial low
signal mass m with vascular
flow voids l:ll. There is
obstruction of both foramina
of Monro by this lesion with
resultant hydrocephalus. A
small intraventricular
hemorrhage ~ is present.
(Right) Sagittal T2WI MR in a
newborn shows a complex
calcified midline mass
Fat, soft tissue were seen on
CT. There is a dorsal cyst ~
and anomalous sinus ICB
I
1
35
::J MACROCEPHALY
-'"
en
0-
ro
()
en
c: Neurofibromatosis Type 1 Tuberous Sclerosis Complex
III
•... (Left) Axial T2WI MR shows
III bilateral hyperintensE foci in
"C
c: the globus pallidus and
III visualuaclS 81. Note
hyperintensity, slight
enlargement of pillars of
fornix =. (Right) Sagillal
TlWI MR in a newborn
matter lines =-
shows extensive radial white
typical of
tuberous sclerosis. Prior to
myelin maturation these are
best seen on TI WI
sequences. There are Focal
calcifications S':I in
subependymal nodules.
Megalencephaly Syndromes
(Left) Sagittal TI WI MR in a
child with cerebral gigantism
shows thick corpus callosum
without isthmus ~ Note
overgrown cerebellum with
impaction of herniated
cerebellar tonsils 81 into
foramen magnurn. (Right)
Coronal T2WI MR shows
cerebellum, falx -;>. a tiny
amount of occipital brain
tissue 0:> along the
tentorium. No other
significant supratentorial
structures are seen. Thalami
(not shown) were present.
CSF pulsations led to cranial
vault enlargement.
Glutaric Aciduria Type 1

prominent sylvian fissures
0:>, reflecting temporal lobe
hypoplasia. Note increased
signal intensity in caudate
heads 81, putamina
globus pallidus !::l during
&=-
acute metabolic crisis in this
child. (Right) Sagillal T2 WI
MR shows bulky white
maller with markedly
abnormal signal. Note
temporal lobe ~
frontoparietal cysts E±l near
vertex. Large head
circumference distinguishes
this from CMV
I
1
36
MACROCEPHALY
Dl
::::s
C-
O)
~
Mucopolysaccharidosis Alexander Disease Dl
(Left) Sagillal T7WI MR ::::s
shows dilated perivascular [f)

(")
spaces 1:12. Callosal and OJ
perilrigonal distribution is the -0
most common. (Right) Axial

T2WI MR shows a frontal
predominance of white
maller signal increase.
Additionally, the caudate
heads ~ and putamina ~
are bright
Alexander Disease Canavan Disease

(Left) Coronal T7 C+ MR
shows enhancement of
teardrop-shaped fomiceal
columns Sl chiasm
periventricufar
and =
while matter
1:12. Frontal white mailer ~
is hypointense. This case
illustrates the importance of
contrast administration in
evaluating any unknown
while maller disorder.
(Right) Axial NECT shows
diffuse decreased white
matter allenuation =.
Thalami E!;,J are also low in
signal, as this is not a pure
leukodystrophy. MRS
showed elevated NAA.
Achondroplasia Fibrous Dysplasia

(Lefl) Sagillal T7 WI MR
shows prominent
pericerebral fluid ~ and
typical glabellar indentation
81. The skull base is short,
and the foramen magnum is
narrow 1:12. (RighI) Axial
T7WI MR in a teen with
leontiasis Qssea shows diffuse
calvarial and skull base
thickening by fibrous
dysplasia. There is a typical
ground-glass appearance.
Note severe narrowing of the
left lAC 81 and the orbital
fissures ~ _
I
1
37
:J MICROCEPHALY
~
(j)
Cl.
roo o BUT look for evidence of trauma/fractures
DIFFERENTIAL DIAGNOSIS
(j) on ALL available films
c: Common o Brain imaging
...
t\l • Secondary/Acquired from • Global atrophy or hemiatrophy
aJ o Hypoxic Ischemic Encephalopathy
"0
• Hemosiderin
c: o TORCH Infections • Meningitis
t\l
o Nonaccidental Trauma o Early infancy: Group B strep the most
:J
-'C/)" o Meningitis damaging
o Fetal Alcohol Syndrome • Hypothalamus
Less Common • Chiasm
• Primary/Genetic with • Inferior basal ganglia
o Gyral Simplification • Diffuse cortex, often asymmetric
o Cortical Dysplasia • Fetal Alcohol Syndrome
o Midline Anomaly o Microcephaly
o Cerebellar Hypoplasia • By tape measure or MR volumetrics

o Hypomyelination
• Anomalies may occur, but not specific
o Diffusion tensor imaging (DTI) reported to
Rare but Important show abnormal connectivity
• Microlissencephaly
• Pseudo-TORCH
o Aicardi-Goutieres • Gyral Simplification
o Small, grossly normal brain
• Progeroid Syndromes
o Looks like "small, but perfect brain"
o Cockayne
o Corpus callosum may appear thick, lack
isthmus
ESSENTIAL INFORMATION • Cortical Dysplasia
Key Differential Diagnosis Issues o Any severe, diffuse dysplasia
• Was head circumference ever normal? • Lissencephaly

• Decreased cranio-facial ratio on sagittal view • Pachygyria
helpful, tape measure best • Midline Anomaly
o Holoprosencephaly, agenesis CC
Helpful Clues for Common Diagnoses o Assess corpus callosum presence, size,
• Hypoxic Ischemic Encephalopathy shape
o Patterns helpful, even if no history • Is there an isthmus?
• Profound: Atrophy, gliosis posterior o Holoprosencephaly
putamen, lateral thalami, rolandic cortex • Most severe are the smallest
• Prolonged progressive: Typical watershed • Cerebellar Hypoplasia
encephalomalacia o May be clue to rare disorders
• Mixed: Features of both, ± calcified • Microlissencephaly
thalami • TUBAIA mutations: Lissencephaly PLUS
• TORCH Infections cerebellar hypoplasia
o Agents most frequently causing o Assess degree of deficiency
microcephaly • Fastigial recess, primary fissure
• Cytomegalovirus (CMV) most common • Degree of vermian lobulation
by far • Tegmento-vermian angle (is the inferior
• Rubella (now rare) 4th ventricle open?)
o Look for cortical dysplasia, periventricular
• Hypomyelination
Ca++, hypomyelination (typically o May be a clue to rare disorders
associated with CMV) • Early onset West syndrome with cerebral
• Nonaccidental Trauma hypo myelination and reduced white
I o History is crucial matter
1
38
MICROCEPHALY en
~
c:
Ql
• 3-phosphoglycerate dehydrogenase SELECTED REFERENCES ::l
Co
deficiency
• Progressive encephalopathy, edema,
1. Gul A et al: Novel protein·truncating mutations in the ..•
t1J
Ql
aspm gene in families with autosomal recessive primary
::l
hypsarrhythmia, optic atrophy (PEHO) microcephaly. J Neurogenet. 21(3):153-63, 2007
2. Hassan MJ et al: Previously described sequence variant in (j)
Helpful Clues for Rare Diagnoses CDK5RAP2 gene in a pakistani family with autosomal
(')
III
recessive primary microcephaly. BMC Med Genet. 2007 '0
• Microlissencephaly 3. Kure-Kageyama H et al: A patient with simplified gyral (j)
o "Z-shaped" brainstem pattern followed by progressive brain atrophy. Brain Dev.
o Callosal agenesis 29(6):383-6,2007 "
c:
4. Ornoy A et al: Fetal effects of primary and secondary
o Surface often totally smooth
cytomegalovirus infection in pregnancy. Reprod Toxicol.
o Very small brain 21(4):399-409,2006
• Pseudo-TORCH 5. Tang BL: Molecular genetic determinants of human brain
size. Biochem Biophys Res Commun. 345(3):911-6, 2006
o Aicardi-Goutieres 6. Sztriha L et al: Extreme microcephaly with
• Autosomal recessive, important to agyria-pachygyria, partial agenesis of the corpus callosum,
and pontocerebellar dysplasia. J Child Neurol. 20(2):] 70-2,
diagnose 2005
• Elevated CSF alpha-interferon 7. Abdel-Salam GM et al: Aicardi-Goutieres syndrome: clinical
• Early onset: TREXI mutation and neuroradiological findings of 10 new cases. Acta
Paediatr. 93(7):929-36, 2004
• Late onset: RNASEH2Bmutation 8. de Vries 15 et al: The spectrum of cranial ultrasound and
• Imaging CMV-like magnetic resonance imaging abnormalities in congenital
cytomegalovirus infection. Neuropediatrics. 3S(2): 113-9,
• Ca++ 2004
• Hypomyelination 9. Riley EP et al: Teratogenic effects of alcohol: a decade of
• Atrophy brain imaging. Am J Mod Genet C Semin Med Genet.
127(1):35-4], 2004
• Progeroid Syndromes
o Cockayne
• Cachectic dwarfism with mental
retardation
• Disorder of DNA repair
• Several mutations known
• Lack phenotype-genotype correlation
• Facies & neuroimaging progressive
• Basal ganglia/dentate Ca++
• Demyelination
• Atrophy
I
Coronal fLAIR MR shows cystic encephalomalacia SII
in the border zone distribution in this 3 year old with a
Axial NEeT in a 3 month old infant shows fusion or the
coronal sutures E2 due to severe brain volume loss,
1
history of peripartum prolonged partial asphyxia. shrunken and calcified putamina
following severe mixed HIE.
=and thalami ~
39
MICROCEPHALY
-'='"
(f)
0.
ro
u
(f)
TORCH Infections TORCH Infections

(Left) Axial T2W/ MR shows
diffuse white matter
increased signal,
periventricufar calcificaUons
6R periventricular cysts B
and diffuse franta/lobe
po/ymicrogyria 81 in an
infant with confirmed
cytomegalovirus. (Right)
Sagittal ultrasound shows
perivenlricular calcifications,
seen here as foci of
increased echogenicity =:I.
Note peri ventricular cyst E!ll
in this patient of conFirmed
congenital cytomegalovirus.
Nonaccidental Trauma Nonaccidental Trauma

diffuse right hemispheric
swelling and signal increase,
left mesial frontal edema
and a right pancake subdural
=
hematoma 81. There is shift
of midline structures and
compression of the ipsilateral
lateral ventricle. (Right) Axial
NECT on follow-up in the
same child, whose head
circumference is {ailing
below normal, shows right
hemispheric volume loss and
sulcal widening =:I.
(Left) Axial T2WI MR during

the subacute phase of
recovery following neonatal
group B strep meningitis
shows global volume 1055.
The left hemisphere 81 is
more affected than the right,
although both are involved.
r ocal necrosis of the globus
pallidi =:I and hypothalamus
is present. (Right) Axial T2WI
MR in the chronic stage in
the same infant shows
calvarial thickening 81 and
global, but asymmetric,
volume 105s. Cavitary globus
pallidus =:I changes are now
I seen.
1
40
MICROCEPHALY (J)
c"
:
Ql
::s
Q.
III
..,
Fetal Alcohol Syndrome Fetal Alcohol Syndrome Ql
(Left) Sagiual TI WI MR in a ::s

3 year old with FAS and (j)
(')
microcephaly shows only a Q)
decreased crania-facial ratio. "0
Microcephaly in fetal alcohol (j)
syndrome is easily confirmed
by tape measure, as routine
"
c
anatomic imaging is usually

normal. Volumelrics and OTi
do, however, show
abnormalilies. (Right) Axial
T2WI MR in a 39 week fetus
shows a few cerebral
remnants. Hydranencephaly
in this fetus follows exposure
to alcohol, smoking, and
polydrug abuse.
Gyral Simplification Gyral Simplification

(Left) Sagiual T7WI MR
shows a decreased
crania-facial ratio and lack of
a callosal isthmus S1. The
brainstem and cerebellum
are normal. (Right) Axial
T2WI MR shows a relatively
normal appearing brain.
rlowever, closer perusal
reveals mild trigonocephaly
!:::I and generalized gyral
simplification S1. The myelin
maturation is normal.
(Left) Axial NfeT shows a

thick cortex with thin outer
layer, sparse cell layer, and
thick inner band of gray
matter. Primitive sylvian
fissures and very shallow
sulci are present. (Right)
Axial TlWI MR shows a
similar appearance to the
previous image in another
child
I
1
41
::> MICROCEPHALY
.:£
(fJ
Cl.
Cll
<.l
(fJ
C Midline Anomaly Midline Anomaly

•..
III
(Left) Sagittal T2WI MR in an
al infant with severe
"'C
C microcephaly shows absence
III of the corpus callosum,
cortex crossing the midline
~ fused deep gray
structures and a large
dorsal cyst There is also
a single central incisor ~.
(RighI) Axial T2WI MR again
shows the large dorsal cyst
There is a monovenUicle
gray matter crossing the
=
midline [;> and a primitive
fused hippocampus ~
shows mildly hypoplastic
vermis with prominent
surrounding CSF. The
fasligial recess, primary
fissure, and vermian
lobu/aUon are present
(RighI) Sagittal T2WI MR
shows upward rotation of
severely hypoplastic vermis
in an infant with callosal
agenesis, microcephaly, and
only primitive sulcalion =.
Fastigiaf crease and primary
fissure are seen. Vermian
lobulation is simplified. The
mesencephalon is "angled"
but not "Z4shaped".

shows a very thin corpus
callosum SlI in this
microcephalic infant (RighI)
Axial T2WI MR shows
corresponding severe
hypomyelination.
I
1
42
MICROCEPHALY
OJ
::::l
C.
OJ
....•
Microlissencephaly OJ
(Left) Sagittal T2WI MR ::::l
shows a "Z-shaped" Ul
brainslem and severe <>
OJ
cerebellar hypoplasia. There -0
is open inferior 4th ventricle Ul
microcephaly, callosal
agenesis, and a smooth
'"
c
cortical surface. (Right) Axial

T2WI MR shows a complete
lack of cerebral gyral
formation in the same child.
Aicardi-Goutieres Aicardi-Goutieres
(Left) Axial N[CT in this
infant shows TORClI-like
calcifications within the basal
ganglia. (Right) Axial T2WI
MR shows hypomyelination
and severe atrophy in the
same patient. Calcifications
SI are relatively occult on
MR in this child.

volume loss,
hypomyelination, and hazy
increased signal intensity of
the basal ganglia 8l
representing calcification.
(Right) Coronal T2WI MR
shows volume loss and
hypomyelination in the same
child. These findings became
more apparent with serial
imaging.
I
1
43
SECTION 2
Meninges
Dural Calcification(s) 1-2-2
Dural-based Mass, Solitary 1-2-4
Dural-based Masses, Multiple 1-2-8
Falx Lesions 1-2-12

Thick Dural Arachnoid, Generalized 1-2-14
Pial Enhancement 1-2-16
Dural Tail Sign 1-2-20
CIl
OJ DURAL CALCIFICATlON(S)
Ol
C
C
OJ
::2 DIFFERENTIAL DIAGNOSIS a ot be confused with true falx lipoma on
c TlWI
C1l Common • Meningioma
•....
aJ • Physiologic Calcification, Dura a Calcified (20-25%): Diffuse, focal,
"0
c • Osseous Metaplasia (Falx Contains Fatty sand-like, sunburst, globular, rim
C1l
Marrow) • Subdural Hematoma, Chronic
• Meningioma a Inner membrane calcification (in 0.3-2.7%)
• Subdural Hematoma, Chronic termed "Matrioska head" or "armored
Less Common brain"
• Basal Cell Nevus Syndrome Helpful Clues for Less Common Diagnoses
• Benign Nonmeningothelial Tumors • Basal Cell Nevus Syndrome
• Hyperparathyroidism a Multiple jaw cysts (odontogenic
• Hemodialysis keratocysts in 80-90%), mandible>
• Meningitis maxilla, rib anomalies
Rare but Important a Calcification of falx (eventually 100%),
• Pseudohypoparathyroidism tentorium, peri-clinoid ligaments, dural,
• Familial Tumoral Calcinosis (Hypo- or choroid plexus & basal ganglia
Hyperphosphatemic) • Benign Nonmeningothelial Tumors
a NECT best diagnostic tool
a Osteoma most common: Round dense
ESSENTIAL INFORMATION lesion of the inner or outer table (outer
Key Differential Diagnosis Issues table more common), no enhancement,
• Physiologic calcification of the dura no diploic involvement
a Chondroma, osteochondroma less
common incidental finding on NECT
common
Helpful Clues for Common Diagnoses • Hyperparathyroidism
• Physiologic Calcification, Dura a Dural calcification, osteopenia and
a Common in the middle-age and elderly,
osteosclerosis of skull giving "salt and
falx or tentorium pepper" appearance
• Osseous Metaplasia (Falx Contains Fatty • Hemodialysis
Marrow) a Long term hemodialysis, associated
a Incorrectly labeled "dense calcification" on secondary/tertiary hyperparathyroidism
NECT a Calcifications falx, tentorium common
Osseous Metaplasia (Falx Contains Fatty

Physiologic Calcification, Dura Marrow)
I
2 Axial bone CT shows physiologic calcification of the
falx.
Axial NEeT shows thick calvarium and very prominent,
=.
thick ossification along the falx
2
DURAL CALCIFICATlON(S) en
c:
""
ll.l
~
a.
Osseous Metaplasia (Falx Contains Fatty OJ
....
Marrow) Meningioma III
(LeFt) Sagiltal T1 WI MR ~
shows high signal Irom
fat-containing osseous
metaplasia along the lalx
cerebri Cl:I. (Right) Axial
bone CT shows marked
hyperostosis and
calcification in this
plaque-like meningioma Cl:I
along the lelt inner table 01
the skull.
Subdural Hematoma, Chronic Basal Cell Nevus Syndrome

(Left) Axial bone CT
demonstrates bilateral
chronic subdural collections
with dense calcification
along the inner membranes.
Shunt tubes are noted in the
lateral ventricles. (Right)
Axial NECT demonstrates
extensive dural calcification
primarily involving the (alx
cerebri and tentorium
cere belli 9- in a patient with
basal cell nevus syndrome
and multiple jaw cysts.
(Left) Axial NECT

demonstrates a rare,
lobulated, calcified,
chondroma arising from the
lelt Iron tal dura Cl:I. (Rigl1t)
Axial NECT shows densely
calcilied dura, especially
prominent along the
tentorium =. Faint
calcification in the basal
ganglia SI is seen.
I
2
3
en DURAL-BASED MASS, SOLITARY
Q)
Ol
C
·c
Q)
DIFFERENTIAL DIAGNOSIS o Does not cross sutures unless sutural
:2
c
diastasis/fracture present, can cross falx &
Common tentorium
...
a:l"' • Epidural Hematoma o Trauma history, calvarial fracture in
"0
c • Meningioma 85-95%
"' • Metastases, Meningeal • Meningioma
• Neurosarcoid o Hyperostosis, cortical irregularity,
• Lymphoma, Metastatic, Intracranial calcification, peritumoral edema, trapped
• Empyema CSF clefts common
less Common o Best imaging tool: MR + contrast
• Tuberculosis 095% enhance homogeneously & intensely,
• Meningioma, Atypical and Malignant dural tail often present
• Benign Nonmeningothelial Tumors o MRS: Elevated alanine
• Malignant Nonmeningothelial Tumors • Metastases, Meningeal
• Langerhans Cell Histiocytosis o Multiple> solitary lesions
• Plasmacytoma o Skull often but not always infiltrated
• Neuroblastoma, Metastatic o Often known extracranial primary
• Leukemia neoplasm
• Neurosarcoid
Rare but Important o 5% present as solitary dural-based
• Pseudotumor, Intracranial extra-axial mass
• Hypertrophic Pachymeningitis o Presence of associated leptomeningeal
• Extramedullary Hematopoiesis enhancement additional clue
• Rosai-Dorfman Disease o Abnormal CXR, labs (increase ESR, ACE
• Neurocutaneous Melanosis levels)
(Melanocytoma/Mela noma) • Lymphoma, Metastatic, Intracranial
• Fibro-Osseous Lesion (Calcifying o Localized dural mass mimicking
Pseudo neoplasm) meningioma
o 10-30% of patients with systemic
ESSENTIAL INFORMATION lymphoma may develop secondary CNS
involvement
o Leptomeningeal, parenchymal
involvement more common
• Empyema
o Extra-axial fluid collection with
rim-enhancement & restricted diffusion
o Look for paranasal sinus or mastoid disease
Helpful Clues for less Common Diagnoses
• Tuberculosis
o Giant tuberculoma may mimic
meningioma
o Abnormal CXR, lab values
o Travel history to endemic areas,
immunocompromised
o MRS: Elevated lipid/lactate
• Meningioma, Atypical and Malignant
o Dural-based lesion locally invasive with
areas of necrosis & marked brain edema
o Indistinct tumor margins, may extend into
I brain, skull, scalp
o Biopsy is essential
2
4
DURAL-BASED MASS, SOLITARY
• Benign Nonmeningothelial Tumors (}Homogeneously enhancing extra-axial

(}Lesions of dura, skull, skull base, NECT tumor(s) in patient with known or
best diagnostic tool suspected myeloproliferative disorder
(}Chondroma: Expansile, lobulated, Helpful Clues for Rare Diagnoses
curvilinear matrix calcification, mild • Pseudotumor, Intracranial
enhancement (}Enhancing, infiltrating meningeal mass
(}Osteochondroma: Stalk is contiguous with (}Predilection for meninges of cavernous
the parent bone intramedullary marrow, sinus area or basal meninges
may see calcified matrix in cap atop (}Intracranial involvement in absence of
cortical bone orbital disease is rule (> 90%)
(}Osteoma: Round dense lesion of the inner • Extramedullary Hematopoiesis
or outer table (outer table more common), (}Patients with chronic anemia or marrow
no enhancement, no diploic involvement depletion
• Malignant Nonmeningothelial Tumors (}Multiple> solitary
(}Highly aggressive dural, skull, scalp lesions (}Lobulated, homogeneous
invading locally (}Mimics subdural hematoma on NECT
(}Biopsy is essential (}Strong homogeneous enhancement
• Langerhans Cell Histiocytosis • Rosai-Dorfman Disease
(}Well-defined lytic skull lesion, beveled (}Sinus histiocytosis with massive
edge, associated dural & scalp soft tissue lymphadenopathy
(}Younger age group (}Multiple> solitary
• Plasmacytoma (}Mimics meningiomatosis, sarcoid,
(}Solitary dural mass in patient with extramedullary hematopoiesis
multiple myeloma, mimics meningioma
(}Skeletal survey may help
• Neuroblastoma, Metastatic SELECTED REFERENCES
(}Age < 5, known extracranial disease, 1. Sahin F et al: Dural plasmacytoma mimicking meningioma
calvarial-based mass, often around in a patient with multiple myeloma. J Clin Neurosci.
13(2):259-61, 2006
orbit/sphenoid wings 2. Richiello A et al: Dural metastasis mimicking falx
(}NECT: "Hair-on-end" spiculated periostitis meningioma. Case report.J eurosurg Sci. 47(3):167-71;
discussion 171, 2003
• Leukemia 3. Goldsher 0 et al: Dural "tail" associated with meningiomas
(}May present with or mimic hematoma on Gd-DTPA-enhanced MR images: characteristics,
differential diagnostic value, and possible implications for
treatment. Radiology. 176(2):447-50, 1990
Epidural Hematoma
I
Axial NEeT shows a classic biconvex hyperdense mass
in the left middle cranial fossa typical for epidural
hematoma =. Left (rontal contusions are a/so present
enhancing dural-based mass
pattern ~
=
Coronal T1 C+ M R shows a densely, homogeneously
with faim "sunburst"
Note the U,ill dural tail associated with the
2
8'1. massl!:lD.
5
(f)
Ql DURAL-BASED MASS, SOLITARY
Ol
c
C
Ql
:2
c
C1l
•...
al (Left) Axial T I WI MR shows
"0 a renal cell carcinoma
c
C1l metastasis = involving the
calvarium with associated
scalp and dural-based mass.
(Right) Axial T7 C+ MR
shows a neurosarcoid with
linear and nodular coating of
the medulla, pons, and
midbrain = and focal
dural-based mass along the
tentorium B.
shows a dural-based
enhancing mass in the region
of the cisterna magna = in
a patient with systemic
lymphoma. Note prominent
"dural tails" PJ:!:l. (Right)
Coronal TIWI MR show "en
plaque" focal dural
thickening SiI that can
mimic meningioma. Notice
the faint ependymal
enhancement around the
temporal horn ~ indicating
ependymitis.
(Leh) Coronal T7 C+ MR
shows enhancing mass .=
mushrooming
/I /I inwards
(deforming underlying brain)
as well as outwards into the
scalp PJ:!:l with
displacement/invasion of
superior sagillal sinus ~.
(Right) Axial bone CT
demonstrates a large
expansile hyperde/lSe lesion
with a chondroid matrix =
arising from the left occipital
bone. Ilistologically proven
chondrobfastoma.
I
2
6
DURAL-BASED MASS, SOLITARY (f)
"
C
Neuroblastoma, Metastatic
heterogeneous enhancement s:
CI>
of a primary meningeal :J
sarcoma with a dura/-based :J
mass skull destruction, co
CI>
and scalp infi/tralion 8:11. CJ>
(Rigl1t) Coronal T7 C+ MR
demonstrates an intensely
enhancing diploic
space/scalp metaSlasis
with displacement of the
=
superior sagillal sinus by the
epidural tumor EillI.
leukemia
(Left) Axial CECT
demonstrates
homogeneously enhancing
extra·axial dura/-based
masses in patient with
systemic leukemia. Note
poorly defined margins,
brain infiltration [;>J with
edema. (Rigl1t) Coronal Tl
C+ FS MR shows mass in lefl
cavernous sinus = in a
patient with infiltrating
intracranial pseudolumor.
Dural "taW' P.:tJ along middle
fossa (foor a/50 represents
pseudOlumor.
shows a solitary dural-based
mass = in a patient with
striking spinal extramedullary
hematopoiesis. This was the
only intracranial lesion.
(Right) Axial Tl C+ MR
shows dural-based, strongly
enhancing masses in this
patient with known sinus
histiocytosis with massive
lymphadenopathy.
I
2
7
(/)
Q) DURAL-BASED MASSES, MULTIPLE
Ol
c:::
c:::
Q)
DIFFERENTIAL DIAGNOSIS • ± Foci of old hemorrhage
~
c:::
Common Helpful Clues for Less Common Diagnoses
<0
"- • Meningioma (Multiple Meningiomatosis) • Neurosarcoid
III
"0 o Multifocal, dural-based foci
c::: • Metastases, Meningeal
<0 o Presence of associated leptomeningeal
• Subdural Hematomas, Chronic
enhancement additional clue
Less Common o Other findings
• Neurosarcoid • Abnormal CXR
• Neurofibromatosis Type 2 • Increased erythrocyte sedimentation rate
• Lymphoma, Metastatic, Intracranial (ESR) & serum angiotensin converting
Rare but Important enzyme (ACE)
• Extramedullary Hematopoiesis • Neurofibromatosis Type 2
• Langerhans Cell Histiocytosis o Multiple inherited schwannomas,
• Erdheim-Chester Disease meningiomas, & ependymomas
• Rosai-Dorfman Disease o Best diagnostic clue: Bilateral vestibular
• Epidural Hematoma schwannomas

• Myeloma o Schwannomas on cranial nerves and spinal
• Leukemia nerve roots
• Tuberculosis o Only 10% of patients with multiple
meningiomas have F2
• Lymphoma, Metastatic, Intracranial
ESSENTIAL INFORMATION o Multiple or solitary dural mass mimicking
Key Differential Diagnosis Issues meningioma
• > 95% multiple dural-based masses are either o 10-30% of patients with systemic
meningiomas or metastases lymphoma may develop secondary CNS

involvement
Helpful Clues for Common Diagnoses • Parenchymal> dural involvement
• Meningioma (Multiple Meningiomatosis)
o 1-9% of imaged meningioma cases Helpful Clues for Rare Diagnoses
o Most occur in women • Extramedullary Hematopoiesis
o Can occur in absence of NF2 o Found in patients with chronic anemias or
o MRS: Characteristic alanine peak marrow depletion
• Metastases, Meningeal o Smooth homogeneous dural-based masses
o Skull often but not always infiltrated o Mimics subdural hematoma on NECT
o Multifocal > solitary lesions o Isointense with brain on T1 WI,
o NECT, bone algorithm, for osseous hypointense on T2WI
evaluation o Enhances strongly, homogeneously
o MR C+ if dural, scalp involved o May show osseous findings of underlying
o Often known extracranial primary disease
neoplasm o Confirm with Tc-99m-sulfur colloid scan
• Prostate, breast, neuroblastoma • Langerhans Cell Histiocytosis
• Subdural Hematomas, Chronic o Well-defined lytic skull lesion with
o Remote trauma history "beveled edges"
o NECT o Associated dural & scalp soft tissue masses
• Varying density common

• Fluid-fluid levels o Patients often present with diabetes
• Less common: Calcification of inner insipidus
membranes • Thick, enhancing infundibulum
o MR • Absent posterior pituitary bright spot
I • T1 C+ thick, enhancing,
membranes
dural • Erdheim-Chester
o Non-Langerhans
Disease
type histiocytosis
2
8
DURAL-BASED MASSES, MULTIPLE (/)
"
c:
III
o Affects multiple organs (including long o ± Underlying contusions of brain :l
Co
bones, skin, lung, soft tissue) parenchyma OJ
.,
o Histiocytic infiltration of long bone • Myeloma III
:l
metaphyses o Dural-based masses with lytic skull lesions
• Manifests as sclerotic appearance on o Skeletal survey may be helpful $:
CD
:l
conventional radiographs • Leukemia :l
<0
o Dural mass lesions most common o May present with or mimic hematoma CD
(fl
• Falx cerebri, tentorium, sella/parasellar o Homogeneously enhancing extra-axial
regions tumor(s) in patient with known or
• Biopsy essential for diagnosis suspected myeloproliferative disorder
o May involve brain parenchyma • Tuberculosis
• Rosai-Dorfman Disease o Marked meningeal enhancement, with
o Sinus histiocytosis with massive basilar predominance, parenchymal
lymphadenopathy tuberculomas, pachymeningeal
o Propensity to arise from the base of the involvement with dural thickening,
skull, para sellar region, orbit enhancement (may mimic meningioma)
o May resemble multiple meningiomatosis, o Abnormal CXR & lab values
sarcoid o Travel history to endemic areas,
o CNS Rosai-Dorfman disease has definite immunocompromised
male predominance
o Dural-based, extra-axial enhancing masses
SELECTED REFERENCES
most common finding
1. Sundaram C et al: Isolated Rosai Dorfman disease of the
o May infiltrate brain with striking
central nervous system presenting as dural-based and
perilesional cerebral edema intraparenchymallesions. Clin europathol. 24(3):112-7,
o Biopsy essential for diagnosis 2005
2. Ahn JY et al: Meningeal chloroma (granulocytic sarcoma)
• Epidural Hematoma in acute lymphoblastic leukemia mimicking a falx
o Trauma history meningioma. J Neurooncol. 60(1):31-5, 2002
o < 5% multiple/bilateral 3. BendsZlls M et al: Diagnosing dural metastases: the value of
HI magnetic resonance spectroscopy. Neuroradiology.
o NECT (acute phase) 43(4):285-9,2001
• Hyperdense biconvex extra-axial mass 4. Goyal M el al: Imaging appearance of pachymeningeal
tuberculosis. AJR Am J Roentgenol. 169(5):1421-4, 1997
• 90-95% associated skull fracture 5. Wilson JD et al: Mill features of intracranial sarcoidosis
o Does not cross sutures mimicking meningiomas. Clin Imaging. ]8(3):184-8, 1994
• May if sutural diastasis/fracture present
o Can cross falx & tentorium
Meningioma (Multiple Meningiomatosis) Metastases, Meningeal
I
Axial TI C+ MR shows multiple, lobulaled,
strongly--enhancin{5; dural-based masses characteristic
Coronal TI C + M R shows dural thickening and multiple
dural-based melastasis ~. Notice the infiltraled 2
lor multiple meningiomalosis syndrome. The patienl inhomogeneously hypointense skull 81.
had no evidence for NF2.
9
Vl
Q) DURAL-BASED MASSES, MULTIPLE
Ol
C
C
Q)
~
c:
•..
III
IlJ
Subdural Hematomas, Chronic
"t:l shows a lelt parieta/l:ll and
c:
III a very small right parietal
chronic subdural hematoma
~ Both contain old blood.
Note extensive dural
thickening and enhancement
1:]. (RighI) Axial T7 C+ MR
shows marked enhancement
01 multi(ocal dural-based
neurosarcoid =.
(Lefl) Axial T7 C+ MR shows

extensive meningiomalOsis/
in the posterior fossa
schwannoma
=.
in the left
lAC-CPA SI and a tiny one
at the (undus 01 the right lAC
I:ll. (RighI) Axial T I C+ MR
demonstrates multiple
dural-based enhancing
masses I:';] in the region of
the cisterna magna and lelt
CPA in a patient with
systemic B cell lymphoma.
Extramedullary Hematopoiesis Langerhans Cell Histiocytosis

(Left) Axial T7 C+ MR shows
multiple, enhancing,
dural-based lesions along lalx
cerebr; m. I esions were
very hypointense on T2WI.
(Rig"') Axial CECT shows
multiple, destructive,
osseous, and dura/-based =
masses.
I
2
10
DURAL-BASED MASSES, MULTIPLE CIl
"
c:
Erdheim-Chester Disease Rosai-Dorfman Disease

(Left) Axial T I C+ MR shows
mulliple enhancing foci in
the brain parenchyma =::I
and cavernous sinus/orbital
apex B in a patient with
non-Langerhans histiocytosis.
(Righi) Coronal T1 C+ MR
shows multiple, dural-based,
strongly enhancing masses in
a patient with known sinus
histiocytosis with massive
lymphadenopathy
(Rosai-Dorfman disease).
Epidural Hematoma Myeloma

(Lefl) Axial NECT shows
bilateral epidural hematomas
PJ:i:l. Note rapid bleeding with
ffuid-ffuid levels 2>. Bilateral
epidural hematomas are
uncommon (in contrast to
subdural hematomas).
(Righi) Axial NEeT shows
mulliple deSlruclive skull and
dural-based hyperdense
masses II] in a patient with
known myeloma.

large bilaleral convexity
leukemic dural masses =::I.
The outer and inner
calvarium HI appears
spiculated due to the
extensive marrow
involvement. (Right) Coronal
T1 WI MR shows nodular "en
plaque" dural thickening =::I
along bOlh sides of
tentorium. Notice faint
ependymal enhancement
around the temporal horn
-7 indica ling ependymilis.
I
2
11
(f)
Q) FALX lESIONS
OJ
C
C
Q)
:2 DIFFERENTIAL DIAGNOSIS • Osseous Metaplasia
c o Different from simple "dense dural
III Common calcification" on NECT
•...
III • Physiologic Calcification, Dura o Look for cortex and medullary space (bone
'0
c: • Osseous Metaplasia CT)
III
• Subdural Hematoma, Acute o Most common in anterior/mid-falx
• Meningioma o Mottled hyperintensity (1'1WI) surrounded
• Metastases, Meningeal by hypointense dense cortex (T2WI)
less Common o "Blooms" on GRE
• Neurosarcoid o True falx lipoma rare (look for chemical
• Extra-Axial Empyema shift artifact)
• Subdural Hematoma, Acute
Rare but Important o Can be isolated; may extend along
• Intracranial Hypotension convexities, tentorium
• Hypertrophic Pachymeningitis o Look for signs of nonaccidental trauma
• Erdheim-Chester Disease (shaking) in children with
• Rosai-Dorfman Disease interhemispheric SDH
• Extramedullary Hematopoiesis • Meningioma
• Chondrosarcoma o Common location for meningiomas
• Solitary Fibrous Tumor o Most arise along middle 1/3rd of the
• Hemangiopericytoma superior sagittal sinus (SSS)
• Dural A-V Fistula o May grow into, occlude SSS
o Look for "dural tail" sign
ESSENTIAL INFORMATION • Metastases, Meningeal
o Can mimic meningiomas
• Smooth dural thickening, enhancement Helpful Clues for less Common Diagnoses
usually benign • Neurosarcoid
• "Lumpy-bumpy" not always malignant! o Nodular, "lumpy-bumpy" falx
• Extra-Axial Empyema
Helpful Clues for Common Diagnoses o Frontal sinusitis - empyema ± posterior
• Physiologic Calcification, Dura extension along falx
o Common in the middle-aged/elderly, falx o Rim-enhancement, restricts on DWI
or tentorium
o Dense amorphous Ca++ plaques
Osseous Metaplasia Subdural Hematoma, Acute
I
2 Sagittal T1WI MR shows high signal from fat-containing
osseous metaplasia along the falx cerebri 1:]. Also note
Axial NECT shows acute subdural hemorrhage, with a
farger, parafalcine, interhemispheric component HJ and
chronically thrombosed, superior sagittal and straight a smaller convexity component =.
sjnuse5~.
12
FALX LESIONS
Neurosarcoid
(Left) Coronal TI C+ MR
shows strongly enhancing
mass attached to lalx. (Right)
Axial T1WI MR shows
"lumpy-bumpy"
enhancement along the lalx
and frontal dura in a patient
with neurosarcoid =.
Extramedullary Hematopoiesis
(Left) Axial TI C+ FS MR
shows a classic
multiloculated paralalcine
subdural empyema 1:1'2 with
rim enhancement (Right)
Axial T2WI MR shows
multiple, lobulated,
dural-based masses ~ along
the falx. Lesions are much
more hypoinlenS€ than
typical meningiomas.
Dural A-V Fistula

(Lelt) Lateral angiography in
the early venous phase,
shows a very hypervascular
faJcine mass ~ with
multiple prominent draining
veins The pre-operative
diagnosis was meningioma.
HPC was lound at surgery.
(Right) Lateral angiography
shows a large posterior
meningeal artery ~
prominent parafalcine
vessels occluded SSS
Acutely thrombosed dAvr
mimicked brain tumor on
MR. (Courtesy P Skejo,
MOJ.
I
2
13
'"
Q) THICK DURA/ARACHNOID, GENERALIZED
OJ
C
C
Q)
DIFFERENTIAL DIAGNOSIS o MR sequences reveal blood products (GRE)
:2
C
• Meningitis
III Common o Dura/arachnoid pattern in meningitis less
•...
III • Dural Thickening, Post-Operative common than pia/subarachnoid
"'C
c • Metastases, Meningeal • Intracranial Hypotension
III
• Subdural Hematoma, Chronic o Diffuse dural enhancement typical
• Meningitis o "Slumping midbrain", low tonsils &
• Intracranial Hypotension subdural effusions/hematomas
Less Common Helpful Clues for Less Common Diagnoses
• Neurosarcoid • Neurosarcoid
• Lymphoma, Metastatic, Intracranial o Dural thickening & enhancement
• Hypertrophic Pachymeningitis o Predilection for basal cisterns
• Meningioma • Lymphoma, Metastatic, Intracranial
Rare but Important o Usually diffuse, multifocal with underlying
• Pseudotumor, Intracranial bone involvement

• Extramedullary Hematopoiesis o May selectively affect meninges
• Hypertrophic Pachymeningitis
o Diffuse dural thickening & enhancement
ESSENTIAL INFORMATION o Idiopathic; etiology often undetermined
Key Differential Diagnosis Issues even with biopsy
• Dura is a thick dense fibrocollagenous sheet • Meningioma
that is attached to skull at sutures o Focal or diffuse dural enhancement
• Arachnoid is a thin layer, loosely attached to o May see adjacent bone changes
the dura & contains arachnoid villi o Multiple associated with F2

Helpful Clues for Common Diagnoses Helpful Clues for Rare Diagnoses
• Dural Thickening, Post-Operative • Pseudotumor, Intracranial
o Post-operative dural enhancement may o Enhancing, infiltrative meningeal mass
appear within hours, last months/years o Predilection for cavernous sinus region &
• Metastases, Meningeal basal meninges

o Smooth or nodular enhancement; usually • Extramedullary Hematopoiesis
accompanied by adjacent skull lesions o Homogeneous enhancement in patients
• Subdural Hematoma, Chronic with chronic anemias or marrow depletion
o Smooth dural enhancement
Dural Thickening, Post-Operative Metastases, Meningeal
I
2 Coronal T1 c+ MR shows smoolh durallhickening ~
& enhancement after a left parietal craniotomy.
Axial T1 C+ MR shows diffuse enhancement = related
to metastatic disease. Metastatic disease is typically
Posl-operaUve dural enhancement is usually diffuse 8, nodular 8, associated wilh adjacenl bone changes.
may lasl for years afler the procedure. Disease may be focal or diffuse.
14
THICK DURA/ARACHNOID, GENERALIZED
Subdural Hematoma, Chronic

shows diffuse dural
enhancement =
related to a
chronic subdural hematoma
E2. Hematomas show
I'b/ooming" artifact on CRE
sequences & may become
calcified. (Right) Axial T1 C+
MR shows diffuse dural
enhancement II] in this
meningitis patient
Leptomeningeal
enhancement is much more
common than
pachymeningeal (dural)
enhancement in meningitis.
Meningitis remains a
clinical-laboratory diagnosis.
Neurosarcoid
(Left) Coronal T1 C+ FS MR
shows smooth dural
thickening & enhancement
r=l in this patient with
chronic headaches. Sagittal
images (not shown) revealed
a 'I slumping" midbrain
typical of intracranial
hypotension. (Right) Axial T1
C+ FS MR shows both
smooth dural enhancement
SI & leptomeningeal
enhancement in this
neurosarcoid patient. Dural
disease is common in
neurosarcoid. There is a
basilar predominance of the
meningeal disease.
enhancement
hypertrophic
=
diffuse dural thickening &
classic for
pachymeningitis. Idiopathic
pachymeningitis can mimic
neoplasm or aggressive
infection. The enhancement
may be smooth or nodular.
(Right) Coronal T1 C+ MR
shows multiple extra-axial,
dural-based masses due to
meningiomas ~ in this
patient with type 2
neurofibromatosis. Bilateral
vestibular schwannomas are
also present.
I
2
15
en PIAL ENHANCEMENT
Q)
CJ)
c
c
Q)
:::2; DIFFERENTIAL DIAGNOSIS o Gyriform enhancement in a vascular

C
territory typical
I'll
Common • Associated with wedged-shaped area of
In"- • Meningitis T2/FLAIR hyperintensity
"0
c: • Metastases, Meningeal • Neurosarcoid
I'll
• Cerebral Infarction, Subacute o Pial enhancement often associated with
• Neurosarcoid dural mass(es)
Less Common • Predilection for basal cisterns
• Vasculitis o Parenchymal disease & leptomeningeal
• Glioblastoma Multiforme disease (approximately 1/3 each)
• Sturge-Weber Syndrome o Facial nerve palsy & other cranial
• Moyamoya neuropathies common

o Review CXR to look for bilateral
Rare but Important symmetrical hilar lymphadenopathy
• Wegener Granulomatosis, Brain
• Lyme Disease Helpful Clues for Less Common Diagnoses
• Dural A-V Fistula • Vasculitis
• Meningioangiomatosis o Heterogeneous group of CNS disorders
• eurocutaneous Melanosis characterized by nonatheromatous
inflammation & necrosis of vessel walls
o In addition to pial enhancement, may see
ESSENTIAL INFORMATION T2 hyperintensities, hemorrhage &/or
Key Differential Diagnosis Issues restricted diffusion
• Pia is innermost layer of leptomeninges o DSA/CTA: Alternating stenosis & dilatation
which covers brain & invaginates into sulci primarily 2nd & 3rd order branches
• Enhancement is typically related to • Glioblastoma Multiforme
infectious/inflammatory, vascular or o May cause focal or diffuse pial
neoplastic processes enhancement in addition to primary

• Differentiate infectious & noninfectious enhancing mass
processes to narrow differential • Related to primary extension of tumor or
metastases
Helpful Clues for Common Diagnoses • Sturge-Weber Syndrome
• Meningitis o Enhancement related to pial angiomatosis:
o Typical signs & symptoms of infection:
Unilateral 80%, bilateral 20%
Fever, neck stiffness, increased WBC o Cortical Ca++, atrophy, & enlarged
o Can be divided into pyogenic, ipsilateral choroid plexus
lymphocytic & chronic meningitis o Occipital, parietal & frontal/temporal lobes
o TB, fungal meningitis often basilar & • Moyamoya
confluent o Idiopathic progressive arteriopathy of
o FLAIR MR: Sulcal hyperintensity
childhood
o Normal enhanced brain MR does not o Progressive narrowing of distal ICA &
exclude meningitis (clinical diagnosis) proximal circle of Willis vessels with
• Metastases, Meningeal secondary collateralization
o Nodular or mass-like leptomeningeal
o Cloud-like lenticulostriate &
enhancement typical thalamostriate collaterals on angiography
o Common primary tumors include breast,
o Lenticulostriate collaterals: Enhancing
lung, melanoma & lymphoma "dots" in basal ganglia & "net-like" thin
o Primary tumor often known
vessels in basal cisterns
• Cerebral Infarction, Subacute o FLAIR: "Ivy sign": Slow-flowing engorged
o May see enhancement in late acute or pial vessels, thickened arachnoid
I early subacute infarct o Leptomeningeal enhancement
(contrast-enhanced "ivy sign")
2
16
PIAL ENHANCEMENT
III
Helpful Clues for Rare Diagnoses Neurofibromatosis
o found in 50% of ::l
Co
patients (particularly NF2) ..,
ll::J
• Wegener Granulomatosis, Brain
o Nonneoplastic, aseptic, necrotizing • Neurocutaneous Melanosis III
::l
o Congenital phakomatosis characterized by
vasculitis that preferentially involves upper ~
giant or multiple cutaneous melanocytic C1>
& lower respiratory tracts & kidneys ::l
nevi & benign & malignant CNS melanotic ::J
o Soft tissue mass in nose with septal & «)
lesions C1>
non-septal bone destruction (j)
o Foci of T1 hyperintensity (parenchymal

o May extend into orbits & intracranially,
melanosis) in amygdala or cerebellum
affecting meninges
o Diffuse leptomeningeal enhancement
• Lyme Disease
o Hydrocephalus common
o Multisystem inflammatory disorder may
present as meningitis, encephalitis &/or Alternative Differential Approaches
vasculitis • Infectious/inflammatory lesions: Meningitis,
o Lesions simulate multiple sclerosis in a neurosarcoid, Lyme disease
patient with skin rash & flu-like illness • Vascular lesions: Cerebral infarction,
o T2 hyperintensity in periventricular white vasculitis, Sturge-Weber syndrome,
matter Moyamoya disease, Wegener
o Meningeal enhancement & CN? granulomatosis, dural A-V fistula
enhancement common • Neoplastic lesions: Metastases, glioblastoma
• Dural A-V Fistula multiforme
o Network of tiny vessels in wall of
thrombosed dural venous sinus
SELECTED REFERENCES
o Look for flow voids of collateral vessels
1. Chu we et al: eurocutaneous melanomatosis with a
o Diffuse dural enhancement is rare rapidly deteriorating course. AJ RAm J Neuroradiol.
• Meningioangiomatosis 24(2):287-90,2003
o Rare 2. Byrd SE Cl al: MR imaging of symptomatic neurocutaneous
melanosis in children. Pediatr Radiol. 27(1):39-44, 1997
o Hamartomatous cortical/leptomeningeal 3. Aizpuru RN et al: Meningioangiomatosis: clinical,
malformation radiologic, and histopathologic correlation. Radiology.
179(3):819-21, 1991
o Cortical mass with Ca++ & enhancement
o Can infiltrate parenchyma via perivascular
spaces
o Enhancement pattern: Linear, granular or
gyriform
Metastases, Meningeal
I
Coronal T1 c+ MR shows diffuse leptomeningeal
enhancement It] in this patient with TB meningitis. T8
Axial T1 C+ FS MR shows abnormal enhancement
along the optic nerves ICR left temporal & occipital
2
& fungal meningitides are often basilar & confluent. cerebral sulci It] in a breast cancer patient. Meningeal
melastases may be smooth or nodular.
17
(/)
Q} PIAL ENHANCEMENT
Ol
C
C
Q}
~
C
•..
01
tD (Left) Corona/ TI C+ MR
"'C shows diffuse
c
01 leptomeningeal
carcinomatosis = with
extensive enhancement.
Meningeal metastases can
mimic other meningeal
processes including
meningitis & neurosarcoid.
(Right) Axial TI C+ MR
shows leptomeningeal
occipita/lobe =
enhancement in the left
related to a
subacute posterior cerebral
artery infarct. There was
corresponding T2/FLAIR
hyperintensity in the same
vascular distribution.
Vasculitis
(Left) Axial TI C+ MR shows
finear & nodular
enhancement !!:ill. Pial
enhancement is often
associated with dural
disease. Patients commonly
present with cranial
neuropathies. eNS disease is
present in 5% of
neurosarcoid patients.
shows focal pial =

(Right) Corona/ TI C+ MR
enhancement in this
& dural
vasculitis patient related to

TB meningitis. T2 images
(not shown) show extensive
hyperinlensily in the basal
ganglia.
Glioblastoma Multiforme Sturge-Weber Syndrome

extensive pial enhancement
related to diffuse CSF
seeding of GBM. These
malignant tumors often have
associated ependymal
extension which results in
CSF seeding. (Right) Axial TI
C+ MR shows extensive
bilateral enhancement
related lO pial angiomatosis.
This is typically unilateral
(BO%), & the occipita/lobe
is most commonly involved.
Angiomatosis is a congenital
malformalion in which fetal
cortical veins faillo develop
I normally.
2
18
PIAL ENHANCEMENT CIl
"
c
III
::s
a.
III
.,
III

::s
punctate enhancement =
related to lenticulostriate
collateral vessels in the basal
ganglia & mild diffuse pial
enhancement related to
slow-flOIY in engorged pial
vessels & thick arachnoid.
The collaterals give the
angiographic appearance of
"pufr of smoke", moyamoya
in Japanese. (RighI) Coronal
T1 C+ MR shows pial
enhancement I!:J2 & basal
ganglia enhancement =
due to formation of
collaterals in moyamoya
disease.
shows enhancing CN]
CNS bilaterally within
& =
Meckel cave 811. CN7 was
also involved in this Lyme
disease patient. Imaging
often mimics multiple
sclerosis with perivenlricular
while maller lesions &
enhancement. (Right) Axial
T1 C+ FS MR shows
enhancement in the left
internal auditory canal-=
involving CN 7 related to
Lyme disease. Meningeal
enhancement & involvement
of the facial nerve is
common.
Meningioangiomatosis Neurocutaneous Melanosis

patient with
=
focal serpentine cortical/pial
enhancement in this
meningioangiomalosis. This
lesion is a hamartomatous
malformation. CT showed
calcification of the lesion.
(Right) Axial T1 C+ MR show
the entire surface of the
brain and adjacent
subarachnoid space enhance
intensely related to pial
melanosis. Note
hydrocephalus caused by
csr
reduced absorption of
through the arachnoid villi. I
2
19
<Jl
<I> DURAL TAIL SIGN
OJ
c
C
<I>
~ DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
c • Meningioma
nl Common
a 35-80% of intracranial meningiomas
In"- • Meningioma
"t:l
• Metastases, Meningeal associated with dural tail
c
nl a More common with convexity, falx
Less Common meningiomas
• Neurosarcoid • Less frequently seen in posterior fossa
• Lymphoma, Metastatic, Intracranial • Least common in spine
• Tuberculosis a Usually reactive change rather than direct
Rare but Important neoplastic invasion

• Histiocytosis • Metastases, Meningeal
• Meningioma, Atypical and Malignant a Adjacent skull often but not always
• Erdheim-Chester Disease infil trated

• Leukemia a Often but not always multifocal
• Lymphocytic Hypophysitis a Often known extra cranial primary
• Pituitary Macroadenoma neoplasm: Prostate, breast, neuroblastoma

• Hemangioma, Calvarial a Beware: Breast metastasis can mimic
• Schwan noma meningioma!
• Rosai-Dorfman Disease Helpful Clues for Less Common Diagnoses
• Neurosarcoid
a Occasionally (5%) presents as solitary,
ESSENTIAL INFORMATION
dural-based, extra-axial mass
Key Differential Diagnosis Issues a Presence of associated leptomeningeal
• "Dural taiJ" actually a 3D "collar" around enhancement additional clue
dural-based lesion a Abnormal CXR, lab values (ESR, ACE levels
• Benign reactive dural thickening> elevated)
neoplastic invasion • Lymphoma, Metastatic, Intracranial
• Suggestive of meningioma but not a Localized dural mass mimics meningioma
pathognomonic a Dural tail probably infiltrative tumor
• Look for scalp, skull lesions • Tuberculosis
• Clinical history, laboratory helpful a Basilar leptomeningitis common
• Biopsy may be necessary for confirmation a Dural involvement less common
a Focal dural mass may mimic meningioma
Meningioma Metastases, Meningeal
I
2 Axial TI C+ FS MR shows classic convexity meningioma
=.
with dural tail sign Note that benign (reactive) dural
Coronal T7WI MR shows calvarial metastasis with
associated dural, scalp soft tjssue involvement Notice
thickening is slightly more hyperintense than neoplasm
itself
the dural tail =.
20
DURAL TAIL SIGN
III
::::l
C.
...
OJ
III

::::l
marked enhancement of a s:
CD
multifocal dural-based ::::l
neurosarcoid = with a ::l
(Q
subtle dural tail ~ along the CD
(j)
right posterior petrous
temporal bone. (Right)
Coronal T1 C+ MR shows
basilar meningitis and
tuberculomas in sylvian
fissure 81. Note dural
thickening along right
cavernous sinus =.
leukemia
(Leh) Coronal T1 C+ MR
shows a granulocytic
sarcoma with intense
enhancement &.. Note dural
tail [;> enhances even more
strongly than the tumor.
(Right) SagiLtal T1 C+ FS MR
shows lymphocytic
hypophysitis =:I enhancing
intensely and uniformly,
inseparable from the
pituitary gland. Note a subtfe
"dural tail sign" 81 along
basisphenoid.
Pituitary Macroadenoma
(Leh) SagiLtal T1 C+ MR
shows a classic pituitary
macroadenoma with sellar
erosion and suprasellar
extension =. Notice a thin
dural tail extending inferiorly
along the clivus 81. (Right)
vestibular schwannoma
entering lAC =:I. Note the
dural tail Elll a rare finding
with schwannomas.
I
2
21
SECTION 3
Ventricles, Normal Variants 1-3-2
Choroid Plexus Lesions 1-3-6
Ependymal/Subependymal Lesions 1-3-8
Lateral Ventricle Mass 1-3-12
Thick Septum Pellucidum 1-3-16
Foramen of Monro Mass 1-3-18
Third Ventricle Mass, General 1-3-22
Third Ventricle Mass, Body/Posterior 1-3-26
Cerebral Aqueduct/Periaqueductal Lesion 1-3-28
Fourth Ventricle Mass 1-3-32

"Bubbly-Appearing" Intraventricular Mass 1-3-36
Ependymal Enhancement 1-3-40
Large Ventricles 1-3-44
Small Ventricles 1-3-48
Asymmetric Lateral Ventricles 1-3-50
Irregular Lateral Ventricles 1-3-54
Periventricular Enhancing Lesions 1-3-58

Intraventricular Calcification(s) 1-3-62
Periventricular Calcification 1-3-66
Periventricular T2/FLAIR Hyperintense Lesions 1-3-72
en
c VENTRICLES, NORMAL VARIANTS
o
Ol
QJ
~ • Sagittal, coronal thin-section T2WI
~
ro
:J • High resolution FIESTA
'C
U Common • CSF flow study
C
QJ
• Asymmetric Lateral Ventricles (ALV) • Intraventricular contrast outlines
'C
> • Intraventricular CSF Pulsation Artifact obstruction
QJ
0.. (Flow-Related) • Intravenous contrast (helpful in
en
QJ
• Cavum Septi Pellucidi (CSP) ± Cavum Vergae detecting small lesions)
U
'C
• Coarctation of Anterior Horns • Intraventricular CSF Pulsation Artifact
C Less Common (Flow-Related)
QJ
> • Connatal Cysts o Most common on high field MR
• Germinolytic Cysts • FLAIRsequence most commonly affected
• Look at another sequence or another
Rare but Important
plane (artifact disappears)
• Open Inferior 4th Ventricle (Blake Pouch
• Typically occur in phase-encoding axis
:J Remnant)
• Look for phase artifact propagating
-"en across image
ESSENTIAL INFORMATION • When in doubt, change phase-encoding
direction and repeat sequence
• Cavum Septi Pellucidi (CSP) ± Cavum
• ormal variants are asymptomatic Vergae
• Frequency varies with site o Developing ventricle closes from posterior
o Lateral ventricle variants common
- anterior
o Fourth ventricle less common
• Therefore cavum vergae (CV) does not
o Third ventricle variants (such as thick
occur in isolation
floor) uncommon (rare at imaging) but
• CSP can exist ± CV but not reverse
important for endoscopic third o CSP lacks ependymal lining (term "5th
ventriculostomy ventricle" inaccurate)
• Clinical history key! o CSP leaflets should be parallel
o Headaches
• If septal leaflets are not parallel, consider
o Papilledema
encysted cavum
o History of prior trauma, infection
• Look for signs of obstructive
Helpful Clues for Common Diagnoses hydrocephalus
• Asymmetric Lateral Ventricles (ALV) • Look for evidence of prior trauma with
o Leaflet of septum pellucidum ± "pushed" to epi-GRE or SWI to detect hemorrhagic
smaller ventricle side residua
o ALV + normal hemisphere • Coarctation of Anterior Horns
• Usually normal variant o Normal variant
• Exclude obstruction at foramen of o Exclude subependymal pseudocysts seen
Monro with inborn errors of metabolism, TORCH,
• Cyst or web ischemia
• Tumor (e.g., choroid plexus neoplasm) o Findings helpful in distinguishing coarcted
o ALV+ abnormal hemisphere anterior horns from pathologic
• Larger hemisphere: Hemimegalencephaly subependymal pseudocysts
(ipsilateral ventricle large, often • Peroxisomal biogenesis disorder
deformed) (Zellweger): Cortical dysplasia,
• Smaller hemisphere: Unilateral atrophy hypo myelination, stippled epiphyses,
or porencephaly hypotonia
o ALV = sign of functioning shunt if shunt • Mitochondrial disorders: MRS lactate
in smaller ventricle doublet
I o Helpful techniques in evaluating
ventricles, possible obstruction
3
2
VENTRiClES, NORMAL VARIANTS
III
• TORCH (cytomegalovirus): Look for Helpful Clues for Rare Diagnoses ::J
Co
microcephaly, periventricular
• Open Inferior 4th Ventricle (Blake Pouch CIJ
....•
calcifications Remnant) III
• Hypoxic ischemic insult of newborn: ::J

o Presence of complete vermis, fastigial
History of perinatal distress! recess
Helpful Clues for less Common Diagnoses • Differentiates Blake pouch remnant from
• Connatal Cysts Dandy-Walker cyst
o Considered normal variant o Usually non-obstructive
o May be anterior choroid plexus cysts o FIESTA, CSF flow sequences helpful
• Controversial entity
• Transient finding
SELECTED REFERENCES
• Present at birth
I. Kiroglu Y el al: Cerebral lateral ventricular asymmetry on
• Spherical form CT: how much asymmetry is representing pathology? Surg ;;0
CD
• Can be multiple Radiol Anal. 30(3):249-55, 2008 co
• Lined with epithelium 2. van Baalen A et al: Anterior choroid plexus cysts: o'
::J
distinction from germinolysis by high-resolution (J)
• Partial "double wall" due to ependymal sonography. Pediatr Int. 50(1):57-61, 2008
folding 3. Munoz A et al: Cisternography and ventriculography
• No hemosiderin gadopentate dimeglumine-enhanced MR imaging in
pediatric patients: preliminary report. AJNR Am J
• No septations euroradiol: 28(5):889-94, 2007
• Germinolytic Cysts 4. Robinson AJ et al: The cisterna magna septa: vestigial
remnants of Blake's pOlich and a potentia) new marker for
o Juxtaventricular subependymal normal development of the rhombencephalon. J
pseudocysts Ultrasound Med. 26(1):83-95, 2007
• Result from germinolysis 5. Robinson AJ et al: The fetal cerebellar vermis: assessment
for abnormal development by ultrasonography and
• Lined with germinal/glial cells (not magnetic resonance imaging. Ultrasound Q. 23(3):2) 1-23,
ependymal cells) 2007
• May have hemosiderin 6. Born CM et al: The septum pellucidum and its variants. An
MRI study. Eur Arch Psychiatry Clin Neurosci.
• May have septations 254(5):295-302, 2004
o Probably NOT normal variant 7. Rohde V et al: Virtual MRI endoscopy: detection of
anomalies of the ventricular anatomy and its possible role
• Rarely isolated, look for other signs of as a presurgical planning tool for endoscopic third
CNS pathology ventriculostomy. Acta Neurochir (Wien). 143(11):1085-91,
• Distinguish from connatal cysts 2001
8. Bakshi R et al: Intraventricular CSF pulsation artifact on
fast fluid-attenuated inversion-recovery MR images:
analysis of 100 consecutive normal studies. AJNR Am J
Neuroradiol: 2] (3):503-8,2000
Asymmetric lateral Ventricles (AlV) Asymmetric lateral Ventricles (AlV)
I
Axial TlAIR MR s!lows mild asymmetry
=-
ventricles. Right lateral ventricle is larger
of laleral
bUl both
Coronal T2WI MR s!lows mild bowing of seplalleaflets
p:m across midline without any evidence of interstitial
3
are normal in size. There is neither obstruction nor
perivenuicular edema.
edema. Upper third ventricle, Fornices
sligl1tly displaced across midline.
= are also
3
l/)
c VENTRiClES, NORMAL VARIANTS
a
Ol
Q)
a:::
~
~ Intraventricular CSF Pulsation Artifact Intraventricular CSF Pulsation Artifact
:J
U
(Flow-Related) (Flow-Related)
E
c (Left) Coronal FL4IR MR
Q)
>
'C
shows typical bilateral
Q) anterior horn CSF Ilow
0.. related pulsation artilact I:'JI.
l/) (Right) Coronal T1WI MR in
Q)
u
'C
the same case during the
same examination shows
C absence of any mass or
Q)
> bleed within the
normal-appearing anterior
horns.
Intraventricular CSF Pulsation Artifact Intraventricular CSF Pulsation Artifact

(Flow-Related) (Flow-Related)
(Left) Axial rL4IR MR shows
prominent, inhomogeneous
signal within third ventricle
~ loramen 01 Monro I:'JI.
shows prominent {Jow
artifact= in anleroinferior
third ventricle. Artifact can
mimic colloid cyst but
fornices ~ are normal
(colloid cysts typically in
upper third ventricle,
wedged between pillars 01
lornix).
Cavum Septi Pellucidi (CSP) ± Cavum

Vergae
(Left) Axial FL4IR MR shows
cavum septi pellucidi PJ::l.
The fornices are represented
by tear drop-shaped
thickenings allhe posterior
aspect of the septalleallets
I:'JI. Walls of CSP are parallel.
(Right) Axial rL4/R MR in the
same case as previous
image, shows cavum septi
pellucid; is continuous with
patent cavum vergae. The
septal leaflets are parallel
and unbowed.
I
3
4
VENTRICLES, NORMAL VARIANTS VI
"
c:
Coarctation of Anterior Horns Coarctation of Anterior Horns

(Left) Axial TI WI MR shows
right caudate head <
CD
"stuck" to anterior wall of
~
:::!.
anterior horn of lateral
n
ventricle. Coaptated CO
(coarcted) frontal, occipital
horns are not uncommon '"
variants. (RighI) Axial T2WI
attachment =
MR shows similar ependymal
leading 10
coarctation of right anterior
horn.
;0
CD
<0
o
:::J
'"
Connatal Cysts Con natal Cysts

(Left) Coronal ultrasound
shows a tiny strand =
connecting the walls of the
anterior horn in a premature
infant on day I of life.
shows the same cyst = in
the same patient during the
neonatal period. Note the
gestational age appropriate
incomplete development of
the gyri and sulci in this
premature inFant.
Open Inferior 4th Ventricle (Blake

Germinolytic Cysts Pouch Remnant)
(Lefl) Axial FLAIR MR in
newborn with seizure shows
subependymal cyst 1:7 along
caudothalamic groove. A
distinct fluid-fluid level
within the cyst represents
dependent layering of blood
products. Small hemorrhagic
germinolytic cyst arising from
germinal matrix. (RighI)
incomplete closure of inFerior
aspect of fourth ventricle.
There is an increased angle
~ between the vermis and
brainslem due to presence of
Blake pouch remnant.
I
3
5
<JJ
C CHOROID PLEXUSLESIONS
o
0>
<1l
~
DIFFERENTIAL DIAGNOSIS Helpful Clues for Less Common Diagnoses
Common • Choroid Plexus Papilloma
o Strongly enhancing, lobulated
• Choroid Plexus Cyst
intraventricular mass in child
• Enlarged Choroid Plexus
o Atrium of lateral ventricle 50%, left> right
Less Common • Meningioma
<JJ
<1l • Choroid Plexus Papilloma o Solid, enhancing intraventricular mass
U
.'C" • Meningioma o Origin of intraventricular location related
<1l • Metastasis, Intraventricular to embryological invagination of
> • Ventriculitis/Plexitis
C
arachnoid cells into choroid plexus
III
•....
• Sturge-Weber Syndrome • Metastasis, Intraventricular
CO • Neurofibromatosis Type 2 o Enhancing choroid plexus mass
'C
c
III
Rare but Important • Ventriculitis/Plexitis
• Choroid Plexus Carcinoma o Enhancing ependyma & choroid plexus
• Lipoma o Ventriculomegaly with debris level
• Langerhans Cell Histiocytosis • Sturge-Weber Syndrome
o Enlarged, enhancing "angiomatous"
ipsilateral choroid plexus
ESSENTIAL INFORMATION o May be only finding in first 6 months
Key Differential Diagnosis Issues o Related to abnormal fetal cortical veins
• Most common cause of choroid plexus mass • Neurofibromatosis Type 2
in adults is benign degenerative cyst o Extensive choroid plexus Ca++,
uncommon manifestation
• Choroid Plexus Cyst Helpful Clues for Rare Diagnoses
o Common incidental finding in older • Choroid Plexus Carcinoma
patients (40% prevalence); bilateral o Enhancing intraventricular mass &
o In fetus, consider trisomy 18 or 21 ependymal invasion
• Enlarged Choroid Plexus • Lipoma
o Normal in fetus, may be giant o Extra-axial mass with fat intensity
o May occur after hemispherectomy o 40-50% interhemispheric fissure, may
o May occur with collateral venous drainage extend into choroid plexus
(i.e., AVM,Sturge-Weber) • Langerhans Cell Histiocytosis: Rarely
presents as enhancing choroid plexus masses
Choroid Plexus Cyst Choroid Plexus Cyst
I
3 Axial T1 C+ M R shows choroid
xanthogranulomas 1::1. Common in the elderly, they are
plexus Axial ultrasound shows small choroid plexus cysts I!:11l
within normal prominent echogenic choroid plexus 1::1-
typically located in the lateral ventricle atria, within the The fetus also had a cardiac anomaly, overlapping
choroid plexus glomus. Cyst walls may enhance. fingers, & clubfeet; trisomy 18.
6
CHOROID PLEXUS LESIONS C/I
"
c:
Ql
::J
C.
..•
lJl
Choroid Plexus Papilloma Meningioma Ql

::J
a lobular, enhancing mass
arising from the choroid
plexus glomus =.
"ydrocephalus often
accompanies choroid plexus
tumors &, may be related to
mechanical obstruction or
CSF overproduction.
Frond-like morphology,
internal flow voids & vibrant
enhancement are
characteristic. (Right) Axial
T I C+ MR shows a uniformly ;:0
<ll
enhancing mass in atrium of (Q
left lateral ventricle, the most 0'
::J
common location of an (fl
intraventricular meningioma.
Metastasis, Intraventricular Ventricu Iitis/Plex itis

shows an enhancing choroid
plexus mass with subtle
ependymal involvement 81.
Intraventricular metastases
typically involve the choroid
plexus. Additional lesions are
common with intracranial
metastatic disease. (Right)
Coronal n C+ MR shows
ventriculitis & plexilis, a
complication of this patient's
cerebral abscess &,
meningitis. Note enlarged,
enhancing choroid plexus E1
& intense ventricular wall
enhancement.
Sturge-Weber Syndrome Langerhans Cell Histiocytosis

left cerebral hemiatrophy
with compensatory
thickening of the calvarial
diploic space =.
Serpentine
leptomeningeal-pial
enhancement &, hypertrophy
of the ipsilateral choroid
plexus ~ is typical. (Right)
Axial TI C+ MR shows an
choroid plexus =
enhancing granuloma in the
in this
child with systemic LCH.
Perivascular spread of LCiI is
also seen in the basal ganglia
E1 as subtle enhancement.
I
3
7
rn EPENDYMAl/SUBEPENDYMAllESIONS
c
o
Ol
Q)
a:: DIFFERENTIAL DIAGNOSIS o White matter lesions along lines of
neuronal migration may extend to
Common ependyma
• Normal Variant (Mimic) o Subependymal giant cell astrocytoma
• Tuberous Sclerosis Complex (SGCA) in 5-10%
• Subependymal Giant Cell Astrocytoma • Subependymal Giant Cell Astrocytoma
• Focal Cortical Dysplasia o Enlarging, enhancing intraventricular mass
• Heterotopic Gray Matter in patient with tuberous sclerosis complex
• Developmental Venous Anomaly o Typically at foramen of Monro
• Multiple Sclerosis • Focal Cortical Dysplasia
less Common o Radially oriented white matter bands
• Metastases • Thin linear/wedge-shaped "comet-tail"

o Glioblastoma Multiforme shaped hyperintensities
o Lymphoma, Primary CNS • Extend from ependymal to subcortical
o Germinoma white matter
o Medulloblastoma (PNET-MB) • Best seen on FLAIR> T2WI
o Ependymoma o Associated with overlying cortical
o Choroid Plexus Carcinoma thickening
• Ventriculitis • Mild mass effect common
• Opportunistic Infection, AIDS • Non-enhancing, mildly T2 bright
o Imaging & histologic features similar to
Rare but Important cortical/subcortical tubers of TSC
• Neurosarcoid • Heterotopic Gray Matter
• TORCH, General o Nonenhancing nodules along inner
• Vasculitis ventricle margin
• Langerhans Cell Histiocytosis o Gray matter signal on all sequences
• Alexander Disease o May be associated with seizures or
incidental
ESSENTIAL INFORMATION • Developmental Venous Anomaly
o Enhancing "Medusa head" with enlarged
Key Differential Diagnosis Issues draining vein
• Ependyma is the thin epithelial membrane o May have enlarged subependymal veins
lining the ventricular system of the brain & o Often occurs at angle of ventricle
spinal cord o Focal, unilateral lesion
• Subependymallesions lie beneath the • Multiple Sclerosis
ependyma o Demyelinating process characterized by
• Majority of ependymal/subependymal periventricular lesions
lesions are infectious or neoplastic o Enhancing lesions often extend to involve
Helpful Clues for Common Diagnoses ependyma
• Normal Variant (Mimic) o Incomplete ring suggests demyelination
o Normal "indentations" into ventricles: Helpful Clues for less Common Diagnoses
Caudate heads, thalami, pes hippocampus, • Metastases
facial colliculus o Etiology: CNS > systemic primaries
o Subependymal veins enhance & may
• P ET-MBmost common (pediatrics)
mimic pathology • GBM & anaplastic gliomas (adults)
• Tuberous Sclerosis Complex • Lymphoma/leukemia can seed CSF
o Calcified subependymal nodules classic
o Narrow differential by history & imaging
o Cortical/subcortical tubers at juxtacortical • Ventriculitis
location o Ventriculomegaly with debris levels &
I ependymal enhancement
3
8
EPENDYMALISUBEPENDYMAL LESIONS (Jl
r::
""
o Periventricular T2 hyperintensity • Vasculitis

characteristic o Suggested by linear enhancement along
o Usually due to intraventricular rupture of the course of deep white matter
adjacent brain abscess, meningitis or shunt penetrating vessels
complication o Enhancement may extend to ependyma
• Opportunistic Infection, AIDS o Usually associated with confluent
o Toxoplasmosis & lymphoma may extend surrounding T2 hyperintensity
along ventricular margins o DWI restriction is common
o CMV cause ventriculitis, meningitis or • Langerhans Cell Histiocytosis
ischemia; ventriculitis common o Rare subependymal involvement
o TB may cause ventriculitis o May involve choroid plexus & mimic
Helpful Clues for Rare Diagnoses subependymal disease

• Alexander Disease
• Neurosarcoid
o Predilection for frontal lobes
o Dural & leptomeningeal disease common
o Intense bands of enhancement in
o Ependymal, perivascular space
periventricular/subependymal location
enhancement
o Near complete lack of myelination in
o Pial enhancement with underlying white
infants with large head suggest diagnosis
matter T2 hyperintensity characteristic
o May involve choroid plexus & extend to Alternative Differential Approaches
ventricular margin • Considerations in seizure patients: Tuberous
• TORCH, General sclerosis, heterotopic grey matter or focal
o Congenital infections caused by cortical dysplasia
transplacental transmission of pathogens • Lesions with minimal or no mass effect:
o White matter volume loss & T2 Focal cortical dysplasia, ventriculitis,
hyperintensity common to all TORCH vasculitis, dysmyelinating conditions,
infections TORCH
o Periventricular calcification may be seen in • Mass lesions: Gray matter heterotopia,
CMV or Toxoplasmosis SGCA, metastases, lymphoma
o CMV: Microcephaly, periventricular
pseudocysts & hyperintensities; commonly
associated with migrational disorders
o Toxoplasmosis: Parenchymal &
periventricular calcifications
Normal Variant (Mimic) Tuberous Sclerosis Complex
I
Coronal T2WI MR shows normal hippocampal gray Axial NECT shows mulUple calcified = & non-calcified
3
not be mistaken for heterotopia.
=.
matter which line the temporal horns and should SlI subependymal nodules, characterisUc for tuberous
sclerosis. Subependymaf nodules are present in 98% of
TSCpatients.
9
CI)
c EPENDYMAlISUBEPENDYMAllESIONS
o
Ol
OJ
0::
~
~
.g
'" Subependymal Giant Cell Astrocytoma Focal Cortical Dysplasia
C (left) Axial CECT shows
OJ
>
'C
ventriculomegaly & a mixed
OJ calcified, cystic & solid
D... subependymal giant cell
CI) astrocytoma E2 at the
OJ
U foramen of Monro. SCCAs
'C
are identified in 10-15% of
C patients with TSC. (Right)
OJ
> Coronal FU\IR MR shows a
C characteristic band of high
III signal =::I extending to the
~
CO ependymal surface in
"tl conjunction with focafly
c thickened abnormal
III
appearing cortex ~ in this
patient with focal cortical
dysplasia.
Heterotopic Gray Matter Developmental Venous Anomaly

(left) Axial T2WI MR shows
subependymalnodules of
gray maller = lining inner
margin of lateral ventricles.
Islands of left frontal
dysplastic gray matter are
also seen extending to the
ventricle !:ll. (Right) Axial
T1 C+ FS MR shows classic
"Medusa head" of a
developmental venous
anomaly. Dilated hair-like
medullary veins = converge
on a single "collector vein II
E2 that drains into
subependymal venous
system.
Multiple Sclerosis Glioblastoma Multiforme

(left) Axial FU\IR MR shows
a hyperintense mass-like
lesion in a patient not
previously diagnosed with
MS. Note involvement of the
corpus callosum !:ll &
extension to the ventricular
ependyma E2. (Right)
Coronal T1 C+ MR shows a
mass in the right temporal
lobe biopsy proven
GBM. A 4th ventricular mass
~ with subependymal
enhancement = represents
CSF tumor spread.
I
3
10
EPENDYMAlISUBEPENDYMAL LESIONS en
,.-
c:
ell
::::l
Co
...
to
Choroid Plexus Carcinoma ell
(Lefl) Axial CECT shows ::::l

perivenlricular enhancement
!:::l representing
subependymal spread of
primary CNS lymphoma.
Secondary lymphoma often
causes dural disease. (RighI)
Axial T7 C+ MR shows
massive left lateral ventricle
choroid plexus carcinoma
~ with multiple nodules of
metastatic CSF spread
;:0
Cll
<C
o
::::l
Ul
Ventriculitis Ventriculitis
striking ependymal
enhancement -=
around
moderately enlarged lateral
ventricles. Ventriculitis was
caused by rupture of an
abscess in/a the left lateral
ventricle. Several
parenchymal
are also seen =
enhancing
likely
representing microabscesses.
foci
(RighI) Coronal FLAIR MR

shows perivenlricular
hyperintensity = in CMV
ventriculitis in this AIDS
patient. CMV is a common
cause of ventriculitis in AIDS
patients.
TORCH, General Alexander Disease

bilateral ventricular & basal
ganglia calcification. Note
the primitive appearance of
the sylvian cisterns due (0
bilateral opercular
polymicrogyria Elll!. The
patient had microcephaly
and venlriculomegaly in
CMV infection. (Right) Axial
CECT shows bilateral frontal
deep white matter low
density consistent with
demyelination & symmetric
enhancement of caudate
heads, putamina, & frontal
periventricuJar
E:I.
white matter
I
3
11
en
c LATERALVENTRICLEMASS
.Q
Ol
Ql
cr: DIFFERENTIAL DIAGNOSIS o Intraventricular cysts are often isolated,
~
ro 4th ventricle most common
:J
U
'C
Common o Intraventricular lesions are best seen on
C
Ql
• Choroid Plexus Cyst FLAIR&T1 MR
> • Intraventricular Hemorrhage
'C
Ql Helpful Clues for Less Common Diagnoses
0.. • Neurocysticercosis
en
• Choroid Plexus Papilloma
Ql Less Common o Most common primary intraventricular
U
'C • Choroid Plexus Papilloma neoplasm of childhood
C
Ql • Meningioma o Top CNS neoplasm in children < 1 Y
> • Metastasis, Intraventricular o Lateral ventricle atrium most common site
C
.;;; • Subependymal Giant Cell Astrocytoma o Hydrocephalus very common
....
co (SGCA) o May metastasize throughout CSF
"C
c • Central Neurocytoma • Meningioma
ro
• Subependymoma o 1-2% of meningiomas are intraventricular
:J
• Neurosarcoid o Lateral ventricle atrium most common
-"(/)
• Ependymal Cyst site, left> right
Rare but Important o If seen in a child, consider NF2
• Choroid Plexus Carcinoma o Lobular, strongly enhancing mass
• Ependymoma • Metastasis, Intraventricular

• Cavernous Malformation o Intraventricular metastases much less
• Lymphoma, Primary C S common than parenchyma, skull/dura,
• Astrocytoma subarachnoid disease
• Langerhans Cell Histiocytosis o Usually lateral ventricle related to choroid
• Epidermoid Cyst plexus, ependyma less common
• Teratoma o Primary tumor often known
• Subependymal Giant Cell Astrocytoma
(SGCA)
ESSENTIAL INFORMATION o Enhancing mass at foramen of Monro in
Key Differential Diagnosis Issues tuberous sclerosis (TS) patients
• Lateral ventricle masses differentiated by o Occurs in 15% of TS patients
o Location within lateral ventricle o Often cause ventricular obstruction
o Patient age • Central Neurocytoma
o "Bubbly" mass with enhancement
Helpful Clues for Common Diagnoses o Frontal horn or body of lateral ventricle
• Choroid Plexus Cyst • Typically attached to septum pellucid urn
o Most common intraventricular mass o Ca++ common, 50-70%
o Arise in choroid plexus glomus,
• Subependymoma
degenerative (xanthogranulomas) o T2 hyperintense lobular, nonenhancing
o All ages (usually older patients)
intraventricular mass
o Considered normal variant (40%
o 4th ventricle> lateral> 3rd ventricle
prevalence); usually bilateral o Variable enhancement, often none to mild
o Commonly FLAIR& DWI hyperintense
• Neurosarcoid
o In fetus, consider Trisomy 18 or 21
o Solitary or multifocal enhancing CNS
• Intraventricular Hemorrhage masses with lung disease
o Typically related to trauma
o Dura, leptomeninges, subarachnoid spaces
o Commonly associated with traumatic SAH
most commonly involved
o May be first presentation of AVM
o Ventricular system variably involved,
o May become Ca++ mass in chronic phase
commonly associated with hydrocephalus
• Neurocysticercosis • May involve choroid plexus
I o Ventricle is 3rd most common location,
after subarachnoid spaces & parenchyma
• Ependymal Cyst
o onenhancing thin-walled congenital cyst
3
12
lATERAL VENTRIClE MASS CII
"
c::
o Follows CSF on all sequences o Follows CSF on all sequences except FLAIR
o Lateral ventricle atrium most common site &DWI
Helpful Clues for Rare Diagnoses • Teratoma
o Midline mass containing Ca++, soft tissue,
• Choroid Plexus Carcinoma <
cysts, & fat C1>
o Enhancing intraventricular mass with ;:!.
o Intraventricular location is rare :0.
ependymal invasion n
Alternative Differential Approaches CO
• Ependymoma
o 4th ventricle> > > > lateral ventricle • Lateral ventricle mass: Child '"
o 1/3rd supratentorial, majority o Choroid plexus papilloma> > carcinoma
periventricular white matter o SGCA (young adult)
o Ca++ common (50%); ± cysts, hemorrhage o Ependymoma
• Cavernous Malformation • Lateral ventricle mass: Adult
o Ca++ & hemosiderin rim common o Choroid plexus cyst> > neurocysticercosis ;:0
C1>
o Rarely intraventricular, 2.5-11% of cases o Meningioma (Q
o
• Lymphoma, Primary CNS o Metastasis ::l
o Typically enhancing lesions within basal o Central neurocytoma '"
ganglia, periventricular WM o Subependymoma
o Often involve, cross corpus callosum o Lymphoma
o Frequently abut, extend along ependymal • Lateral ventricle mass: Location
surfaces o Near/adjacent to foramen of Monro:
• Astrocytoma SGCA, subependymoma, central
o Often spreads from corpus callosum into neurocytoma
fornix or septum pellucidum o Body: Central neurocytoma,
o Primary intraventricular is less common subependymoma
o Typically frontal horn or body of lateral o Atrium: Choroid plexus cyst, choroid
ventricle plexus papilloma, metastasis, meningioma,
o Imaging varies with tumor grade ependymal cyst, choroid plexus carcinoma
• Langerhans Cell Histiocytosis o All locations: Neurocysticercosis,
o Rarely presents as enhancing choroid neurosarcoid, lymphoma
plexus masses
• Epidermoid Cyst
o Congenital epithelial inclusion cysts
Choroid Plexus Cyst Intraventricular Hemorrhage
I
Coronal T1 C+ MR shows classic choroid plexus Axial NECT shows traumaUc subarachnoid hemorrhage,
3
xanthogranulomas = in an elderly patient.
Contrast-enhanced scans show cyst walls enhance but
hemorrhagic
hemorrhage (lVH) =. =.
contusion & intravent.ricu/ar
Traumatic IVH is relatively
uncommon & usually reflects severe injury.
contents do not. They are often FlAIR & OWl bright.
13
(/)
c LATERAL VENTRICLE MASS
.Q
OJ
Q)
n::
Neurocysticercosis Choroid Plexus Papilloma

the colloidal vesicular stage
of neurocysticercosis with
intraventricular lesions ~.
(/)
Q)
Often the eccentric scolex
u
·C
may be seen in the vesicular
stage on T2/rLAIR &
C
Q) post-contrast images. (Right)
> Axial CECT shows lobulated,
C enhancing, trigonal mass
III with hydrocephalus. Margins
•...
CO of this choroid plexus
"tl papilloma show
c characteristic frond-like
III
irregularities. Etiology of the
hydrocephalus may be mass
effect or CSF
overproduction.
Metastasis, Intraventricular
(Left) Axial T1 C+ FS MR
shows large meningioma =
in the atrium of left lateral
ventricle. Tumor has
"trapped" occipita/8ll and
temporal horns. IRight) Axial
T1 C+ FS MR shows an
enhancing mass in the frontal
horn of the lateral ventricle
in this patient with metastatic
melanoma. Following
resection of this mass, the
patient developed additional
brain parenchymal
metastatic foci.
Subependymal Giant Cell Astrocytoma

(SGCA) Central Neurocytoma
a classic SCCA I:] in the
foramen of Monro in this
tuberous sclerosis patient.
Moderate hydrocephalus &
corticallUbers ~ are seen.
shows a bubbly mass in the
body of the right lateral
ventricle with heterogeneous
enhancement & enlargement
of the right frontal horn. The
mass is attached to the
septum pellucidum, typical
of central neurocytoma.
I
3
14
LATERAL VENTRiClE MASS Ul
"
c:
Neurosarcoid
a small mass in the left lateral <
C1>
ventricle near the septum :::l
pellucidum. There is no ~
evidence of obstructive Q:
C1>
hydrocephalus. The mass is en
hyperintense to gray matter
& did not enhance following
contrast, typical of
subependymoma. (Right)
intensely enhancing masses
lateral ventricles =
in the choroid plexi of both
&
thickening of infundibulum
;0
C1>
<0
~. eNS involvement is seen o
:::l
in approximately 5% of en
sarcoid patients.
shows an ependymal cyst in
the enlarged atrium of the
left lateral ventricle. Note the
thin cyst wall
choroid plexus
==. & displaced
This was
an incidental finding. The
lateral ventricle atrium is the
most common site. (Right)
ependymoma in the
atrium of the right lateral
ventricle. Note flow voids &J
and extensive perilumoraf
edema [<±. Most
supralenwrial ependymomas
are parenchymal.
Teratoma
subependymal spread
lymphoma. Primary CNS
of =
lymphoma is classically
located in perivenlricular
WM & abuts &/or extends
along ependymal surfaces as
in this case. (Right) Axial
T1WI MR shows
heterogeneous mass with
scallered small hyperintense
foei, consistent with fat ~ &
marked ventricular
dilatation. Presence of fat &
Ca++ indicates teratomatDus
histology rather than choroid
plexus tumor or
ependymoma. I
3
15
CJ)
c THICK SEPTUM PELLUCIDUM
.2
OJ
Q)
0::
Common • Lymphoma, Primary CNS
o Enhancing lesions in basal ganglia or
• Cavum Septi Pellucidi (CSP)
• Astrocytoma periventricular white matter typical
o Often extend along ependymal surfaces
Less Common • Germinoma
CJ)
Q) • Lymphoma, Primary CNS o Ventricular disease related to CSF seeding
u
E • Germinoma o Primary intraventricular germinoma, rare
c
Q) • Metastasis, Intraventricular • Metastasis, Intraventricular
> • eurofibromatosis Type 1
C
o May involve septum pellucidum by
ttl
"- Rare but Important ependymal spread
CO o Gray-white junction lesions most common
"C • Alexander Disease
c • Fused Fornices (Holoprosencephaly) • Neurofibromatosis Type 1
ttl
o Thickening related to presumed
:J
.><: hamartomatous involvement of forniceal
III
ESSENTIAL INFORMATION columns as they pass through septal leaves
Key Differential Diagnosis Issues o Hypothalamic tumors may also infiltrate
• Septum pellucid urn should be 2 mm or less septum pellucidum
• Any neoplasm with propensity for Helpful Clues for Rare Diagnoses
ependymal/subependymal spread may cause • Alexander Disease
thickened septum pellucidum o Diffuse, symmetric bifrontal white matter
Helpful Clues for Common Diagnoses disease in a macrocephalic infant
• Cavum Septi Pellucidi (CSP) o Columns of fornix/septum pellucidum
o Cystic CSF cavity of septum pellucidum may be involved
between frontal horns, normal variant o Enhancing periventricular rim, particularly
o Follows CSF on all sequences around frontal horns in early disease
o May have associated mass effect • Fused Fornices (Holoprosencephaly)
• Astrocytoma o Fused fornices is a specific sign (lobar),
o Often involves septum pellucidum from may mimic thick septum pellucidum
ependymal spread or corpus callosum o Absent septum pellucidum
o Primary tumor of septum pellucid urn rare o Frontal lobe hypoplasia
o Imaging varies with tumor grade
Cavum Septi Pellucidi (CSP)
I
3 Axial T7 WI MR shows the classic appearance of CSP
= with posterior extension into a cavum vergae, seen
Axial T1 C+ MR shows enhancing mass infiltrating
fornices, corpus callosum splenium, and septum
as a CSF-signal collection between the bodies of the
lateral ventricles.
pellucidum
biopsy.
=. Glioblastoma mu/tiforme found at
16
THICK SEPTUM PElLUCIDUM CJl
"
c:
Ql
:J
a.
..•
OJ
Ql
(Left) Coronal T1 c+ MR
:J
shows an enhancing left
insular mass with ependymal
spread of tumor causing
thickening & enhancement
of the septum pellucidum.
(Rig/It) Axial T1 C+ MR "U
shows subependymal spread ...<.
CO
with involvement of the co

septum pellucidum. Primary :J
CNS lymphoma is classically ::!.
()
located in peri ventricular c:
white matter & abuts &/or ...
III
extends along ependymal ;0

surfaces. Involvement of
co
c.c
leptomeninges or dura is o·
:J
more common in secondary en
lymphoma.
(Left) Axial NECT shows

hyperdense ventricular
metastases related 10
germinoma. There is
extensive tumor along the
lateral ventricles & filling the
occipital horns. (Right) Axial
T1 C+ MR shows ependymal
spread of metastatic
melanoma. While primary
malignant brain tumors such
as GBM, germinoma, &
lymphoma commonly spread
along ependyma, this is a
recognized but uncommon
site for tumor deposits from
extracraniaf neoplasms.
pellucidi =
thickening of the septi
in this NFl
patient, presumed to
represent hamartomatous
infiltration. Note also Focal
areas of increased signal
intensity in the globus
pallidus bilaterally. (Right)
fullness & increased
enhancement in the fornices
P.:D as well as abnormal
signal in the {rontal while
mailer, caudate heads, &
anterior putamina, typical of
infantile Alexander disease.
I
3
17
(J)
c: FORAMEN OF MONRO MASS
.Q
Ol
Q)
~ o Pillars of fornix straddle, drape around cyst
o Attached to anterior 3rd ventricular roof
Common o Cysts typically do not enhance, but may
• CSF Flow Artifact have "rim-enhancement" on MR
• Colloid Cyst
(J)
• Neurocysticercosis
Q) Less Common o Cyst with "dot" inside (vesicular stage)
U
.'C" • Neurocysticercosis o Convexity subarachnoid spaces most
Q) • Tuberous Sclerosis Complex (Subependymal common; ventricles least common
> Nodule) o Intraventricular cysts are often isolated
• Subependymal Giant Cell Astrocytoma o Imaging varies with development stage,
(SGCA) host response
• Metastasis, Intraventricular • Tuberous Sclerosis Complex
• Astrocytoma (Fornix, Septum Pellucidum) (Subependymal Nodule)
::1
-"
• Subependymoma o Calcified subependymal nodules 98%
en • Central Neurocytoma o Cortical/subcortical tubers, 70-95%
• Germinoma o White matter lesions along lines of
• Vertebrobasilar Dolichoectasia (VBD) neuronal migration
Rare but Important o If subependymal nodule at foramen of
• Choroid Plexus Papilloma Monro enlarges, likely a SGCA
• Choroid Plexus Cyst • Subependymal Giant Cell Astrocytoma
• Cavernous Malformation (SGCA)
• Ependymal Cyst o Enhancing mass at foramen of Monro in
• Alexander Disease tuberous sclerosis (1'S)patients
o Occurs in 15% of TS patients
o Often cause ventricular obstruction
ESSENTIAL INFORMATION • Metastasis, Intraventricular
Key Differential Diagnosis Issues o Primary tumor often known
• Foramen of Monro connects inferior lateral o Often multiple lesions at gray-white
ventricles with 3rd ventricle junctions
• Majority of foramen of Monro lesions are o Typically involve choroid plexus if
related to flow artifact or a normal variant intraventricular
• Colloid cyst is most common, representing • Astrocytoma (Fornix, Septum pellucidum)
15-20% of intraventricular masses o Often spreads into fornix or septum
• SGCA is most common in a child pellucidum from corpus callosum
• Age is a helpful differentiating feature o Primary tumor involvement less common
o Imaging varies with tumor grade
• Subependymoma
• CSF Flow Artifact o 1'2 hyperintense, lobular, nonenhancing,
o Mu1tiplanar technique confirms artifact
intraventricular mass
o Look for phase artifact
o Intraventricular, inferior 4th ventricle
• Cavum Septi Pellucidi (CSP) typical (60%)
o Cystic CSF cavity of septum pellucidum
• Lateral & 3rd ventricles less common
between frontal horns, normal variant o Lateral ventricle: Attached to septum
o Often associated with a posterior
pellucidum or lateral wall
continuation, cavum vergae o May occur at foramen of Monro
o Follows CSF on all sequences
o Typically no or mild enhancement
o May have associated mass effect
• Central Neurocytoma
• Colloid Cyst o "Bubbly" mass with moderate to strong
I o Hyperdense mass at foramen of Monro on
CT is characteristic
enhancement
3
18
FORAMEN OF MONRO MASS en
"
c:
III
o Lateral ventricle, attached to septum o Ca++ & T2 hypointense hemosiderin rim :J
C.
pellucid urn common
• Germinoma o Rarely intraventricular, 2.5-11% of cases
..•
III
III
:J
o Propensity to hug midline near the 3rd • Ependymal Cyst
ventricle - 80-90% o Nonenhancing thin-walled congenital cyst <
CD
o Pineal region: 50-65%; suprasellar: 25-35% with CSF density/intensity ;l
::>.
Q.
o Primary intraventricular germinoma is o Intraventricular common, typically lateral CD
(fl
rare, typically 3rd ventricle ventricle
o Ventricles often involved by CSF seeding • Alexander Disease
• Vertebrobasilar Dolichoectasia (VBD) o Diffuse, symmetrical bifrontal WM disease
o Long segment irregular fusiform or ovoid in macrocephalic infant
arterial dilatation o Thick enhancing periventricular rim
o Typically occurs in vertebrobasilar system (particularly around frontal horns)
;0
more than carotid o Intense enhancement characteristic of CD
(Q
• Extreme VBD can cause hyperdense early disease O·
:J
foramen of Monro mass o Columns of fornix often involved (fl
o Look for "flow void", phase artifact on MR

Alternative Differential Approaches
o CTA is also diagnostic for this pseudomass
• Foramen of Monro mass: Adult
Helpful Clues for Rare Diagnoses o Pseudomass: CSF flow artifact, VBD, CSP
• Choroid Plexus Papilloma o Colloid cyst
o Enhancing ventricular papillary mass with o Neurocysticercosis
hydrocephalus in a child o Metastasis, intraventricular
o Atrium of lateral ventricle most common o Astrocytoma
location (50%) o Subependymoma
o 3rd ventricle primary is less than 10% o Central neurocytoma
• Choroid Plexus Cyst o Choroid plexus cyst
o Typically bilateral & arise in choroid • Foramen of Monro mass: Child
plexus glomus of adults o Cavum septi pellucidi (CSP)
o Considered part of normal aging o Tuberous sclerosis complex/SGCA
o May rarely occur in foramen of Monro o Germinoma
o Commonly DWI & FLAIRhyperintense o Choroid plexus papilloma
• Cavernous Malformation o Ependymal cyst
o Alexander disease
CSF Flow Artifact Cavum Septi Pellucidi (CSP)
I
3rd venlnde & foramen of Monro =-
Axial TI WI MR shows a flow arUfact in & around the
which mimics a
Coronal T7 c+ MR shows an unusually large cavum
septi pellucidi with mass effect. There is lateral bowing
3
mass. A flow artifact is typically seen on [LAIR images. of the leaves of the septum pellucidum & lateral
Multiplanar technique confirms artifact displacement of the foramen of Monro =. 19
'"
c FORAMEN OF MONRO MASS
.2
Ol
Q)
a:
(Left) Axial T1 WI MR shows

a hyperintense lesion allhe
foramen of Monro. Note
u
'"
Q)
cyst =
draping of fornices over the
classic for colloid
cyst. These are typically
.'C" hyperdense on CT & may
Q) present acutely with
> hydrocephalus. (Right)
C Coronal T1 C+ MR shows a
III farge cystic intraventricular
"-
!Xl mass 1:1 with an enhancing
'0 nodule. Intraventricular cysts
C are not uncommon in
III
neurocyslicercosis, but a
:l lesion of this size is unusual.
-"en Intraventricular cysts are
often isolated.
Tuberous Sclerosis Complex

(Subependymal Nodule)
nodules =
calcified subependymal
at the foramen of
& subcortical tubers =

Monro & low density cortical
typical or tuberous scferosis.

If a subependymal nodule at
the foramen of Monro
enlarges, SCCA is likely.
shows a right foramen of
Monro mass II] in a
tuberous sclerosis patient, (a
SCCA). Note small
enhancing subependymal
nodule in left foramen of
Monro. SCCAs are WHO
grade I tumors.
Astrocytoma (Fornix, Septum

Pellucidum)
shows an enhancing renal
cell carcinoma metastasis It]
at the foramen of Monro
with associated
hydrocephalus which mimics
a SCCA. Typically,
intraventricular metastases
occur in the choroid plexus.
(Right) Axial CECT shows a
heterogeneously enhancing
mass that appears to have
arisen within & thickened the
septum pellucidum. Note
ependymal spread ~ in this
glioblastoma multiforme
patient with CSF seeding.
I
3
20
FORAMEN OF MONRO MASS Ul
"
c:
III
::l
Q.
..•
lJl
III
Central Neurocytoma
::l
an enhancing mass at the <
-ro..•
Cl>
foramen of Monro, attached ::l
10 the septum pellucidum .
o·
Typically these tumors have
(J)
no or mild enhancement &
are asymptomatic. (Right)
Coronal T7 C+ MR shows a
heterogeneous "bubbly"
ventricular mass with bowing
of the septum pellucidum.
Central neurocytomas are
typically located in the
lateral ventricle, atlached to
the septum pellucidum.
"ydrocephalus related to
foramen of Monro
obstruction is common.
Germinoma Vertebrobasilar Dolichoectasia (VBD)

multiple masses related to
synchronous pineal &
suprasellar germinomas.
Enhancing tumor infiltrates
the ependyma of the frontal
horns & anterior columns of
the fornix E:II at the foramen
of Monro. Tumar seeding &
brain invasion are common
findings with CNS
germinoma. (Right) Axial
NECT shows a slightly
hyperdense "mass" at the
foramen of Monro =.The
mass was caused by extreme
fusiform ectasia of the basilar
artery.
Cavernous Malformation Alexander Disease

multiple Jocules with mixed
signal intensity, consistent
with hemorrhages of
different ages in this
cavernous malformation.
shows full forniceal columns
with marked enhancement
~. Enhancement
corresponds 10 foci of
Rosenthal fiber
accumulation. There is also
subtle enhancement around
the frontal horns. Diagnosis
required brain biopsy in the
past Testing for mutations
CFAP are now possible.
in I
3
21
(/)
c THIRD VENTRICLEMASS, GENERAL
.2
en
OJ
0::: DIFFERENTIAL DIAGNOSIS o Posterior part of frontal horns splayed
L
.!l1 laterally around cyst

:J
t.l Common
'C Helpful Clues for Less Common Diagnoses
C • MR Artifacts, Flow-Related
OJ
> • Massa lntermedia, Normal • Genninolna
'C
OJ o CNS germinomas have a propensity to hug
n.. • Colloid Cyst
the midline near 3rd ventricle - 80-90%
U
'"
OJ Less Common o Location: Pineal region - 50-65%;
'C • Germinoma suprasellar - 25-35%; basal ganglia and
C
OJ • Neurocysticercosis thalami - 5-10%
> • Neurosarcoid o Primary intraventricular germinoma
c:
III • Prominent Massa Intermedia, Chiari 2 involving 3rd ventricle is rare
"- • Vertebrobasilar Dolichoectasia (Mimic)
CO o Ventricles usually involved from CSF
-c
c:
III
Rare but Important dissemination
• Choroid Plexus Papilloma • Neurocysticercosis
:J
-"11l • Craniopharyngioma o Convexity subarachnoid spaces most
• Pituitary Macroadenoma common location

• Tuber Cinereum Hamartoma o May involve cisterns> parenchyma>
• Chordoid Glioma ventricles

• Lymphoma, Primary CNS o Intraventricular cysts are often isolated,
• Langerhans Cell Histiocytosis 4th ventricle most common

• Glioma • Neurosarcoid
o Solitary or multifocal C S mass(es) with
lung disease
ESSENTIAL INFORMATION o Location: Dura, leptomeninges,
Key Differential Diagnosis Issues subarachnoid space most common
• Vast majority of 3rd ventricular "masses" are • Often involves basal cisterns, particularly
artifact or normal anatomy optic chiasm, hypothalamus,
• Colloid cyst is only common lesion that is infundibulum, cranial nerves
classically located in 3rd ventricle o Brain parenchyma: Hypothalamus> brain
• These masses often occur in other locations stem> cerebral> cerebellar hemispheres
but may occur primarily in 3rd ventricle o Ventricular system variably involved,
o Germinoma, choroid plexus papilloma, commonly associated with hydrocephalus

craniopharyngioma, macroadenoma, • Prominent Massa Intermedia, Chiari 2
lymphoma, hypothalamic hamartoma o Large massa intermedia, typical of Chiari 2
• Newly described rare tumor, chordoid o Third ventricle may be high-riding if
glioma is primary to 3rd ventricle corpus callosum agenesis present

• Vertebrobasilar Dolichoectasia (Mimic)
Helpful Clues for Common Diagnoses o Long segment irregular fusiform or ovoid
• MR Artifacts, Flow-Related arterial dilatation
o May be differentiated from true mass by o Typically occurs in vertebrobasilar system
associated phase artifact more than carotid circulation
o Multiplanar technique confirms artifact
o Ectatic basilar artery may indent 3rd
• Massa Intermedia, Normal ventricle and/or foramen of Monro
o Normal grey matter connection of medial
o MR (flow artifact) or CTA is diagnostic
thalamus (interthalamic adhesion)
o Absent in up to 20% of human brains Helpful Clues for Rare Diagnoses
o Unclear function • Choroid Plexus Papilloma
• Colloid Cyst o Strongly enhancing, lobulated,
o 99% wedged into foramen of Monro intraventricular mass in child
o Location: Atrium of lateral ventricle (50%),
I o Attached to anterior 3rd ventricular roof
o Pillars of fornix straddle, drape around cyst left> right; 4th ventricle (40%)
o 3rd ventricle primary less than 10%
3
22
THIRD VENTRIClE MASS, GENERAL CIl
""
c:
III
• Craniopharyngioma • Langerhans Cell Histiocytosis ::l
Q.
o Partially cystic/solid, calcified suprasellar o Proliferation of Langerhans cell histiocytes OJ
....•
mass in child forming granulomas in any organ system III
::l
o Location: Suprasellar (75%); suprasellar o Often thick enhancing infundibulum,
and intrasellar (21%); intrasellar (4%) absent posterior pituitary bright spot <
<1l
o Rare ectopic locations: 3rd ventricle, o Rarely presents as enhancing choroid ~

:0.
Q.
nasopharynx, sphenoid sinus plexus masses, nodules of leptomeninges, <1l
C/l
• Pituitary Macroadenoma basal ganglia, cerebellar white matter, and
o Enhancing sellar and suprasellar mass brain parenchyma
o Rarely have ectopic origins outside • Glioma
pituitary fossa o Primary astrocytomas and ependymomas
• 3rd ventricle, sphenoid or cavernous of 3rd ventricle are rare
sinus, pituitary stalk o Imaging depends on tumor type and grade
• Tuber Cinereum Hamartoma Alternative Differential Approaches
o Nonneoplastic congenital collection of
• 3rd ventricle mass: Adult
heterotopic neurons and glia originating o Pseudomass: MR artifacts, flow-related,
from tuber cinereum (3rd ventricle floor) vertebrobasilar dol ichoectasia
o Small (typically - 1 em), round, mass
o Colloid cyst
contiguous with tuber cinereum o Neurocysticercosis
o Sessile or pedunculated round mass,
o Neurosarcoid
similar in density/intensity to gray matter o Pituitary macroadenoma
o T1 C+: Nonenhancing (if enhances, o Chordoid glioma
consider glioma or other tumor) • 3rd ventricle mass: Child
• Chordoid Glioma o Germinoma
o Rare, slow growing, non-invasive glial
o Choroid plexus papilloma
tumor of 3rd ventricle o Craniopharyngioma
o Enhancing mass in anterior 3rd ventricle
o Tuber cinereum hamartoma
contiguous with hypothalamic or o Langerhans cell histiocytosis
suprasellar structures
• Lymphoma, Primary CNS
o Enhancing lesion in basal ganglia or
peri ventricular white matter
o Commonly abuts or extends along
ependymal surface
MR Artifacts, Flow-Related
I
Coronal T1 C+ MR shows a lIow artifact in the 3rd
=.
ventricfe which can mimic a ventricular mass Often
Axial T1WI MR shows the normal massa intermedia
(interlhalamic adhesion) as it connects Ule medial
3
an associated phase artifact is seen. Multiplanar thalami=. This normal anatomic connection may
technique confirms the artifact. occasionally mimic a mass.
23
'"
c THIRD VENTRICLE MASS, GENERAL
.Q
OJ
Q)
a:::
~
~
::J
U
'C Colloid Cyst Germinoma
C (Left) Axial NECT shows a
Q)
>
'C
classic hyperdense colloid
Q) cyst in the anterior 3rd
a.. ventricle, causing mild
hydrocephalus. NOle lhe
'"
Q)
C3 Fornices =.:I are draped and

'C
splayed around lhe mass.
CQ) (Right) Axial T1 C+ MR
> shows an enhancing tumor
c: projecting From lhe pineal
l'Cl region in/a lhe poslerior 3rd
~
ell ventricle. Germinomas are
"C the most common in the
c: pineal region and lypically
l'Cl
involve lhe venlricles by csr
spread.
Neurocysticercosis
neurocysLicercus cyst in Jrd
ventricle ~ causing acute,
severe obstructive
hydrocephalus wilh
lransependymal CSF flow
=.:I. (Right) Coronal T1 C+
MR shows mulliFocal, dural,
parenchymal, & venlricular
masses in a sarcoid patient
Involvement of lareral
ventricles is much more
common than 3rd ventricular
=.:I disease. CNS is involved
in 5-15 % of cases.
Prominent Massa Intermedia, Chiari 2 Vertebrobasilar Dolichoectasia (Mimic)

lypical Features of a Chiari 2
malformation including an
enlarged massa intermedia
!:l:I and colpocephaly. An
enlarged massa intermedia
may occasionally mimic a
3rd ventricular mass. A
high-riding 3rd venlricle may
also be seen if there is
agenesis of corpus callosum.
(Rig"') Axial CECT shows an
enhancing II mass at
II
foramen of Monro m. Initial

diagnosis was colloid CYSI.
MR showed high flow
caused by extreme FusiForm
I ectasia of the basilar artery.
3
24
THIRD VENTRICLE MASS, GENERAL ,..c:
CIl
III
::l
Co
OJ
.,
III
Choroid Plexus Papilloma Craniopharyngioma
::l
(Left) Axial CECT shows an
enhancing lobular mass <
CD
arising from the roof of the ;:.
3rd ventricle with significant :0.
n
associated hydrocephalus in CD
this child. The imaging (J)
appearance is typical, but

the location is unusual for a
choroid plexus papilloma.
(Right) Coronal TfWI MR
shows a homogeneously
hyperintense mass, likely a
reflection of
cholesterol-laden fluid, filling ;u
CD
the 3rd ventricle. These (Q
suprasellar masses rarely o·
::l
occur in the 3rd ventricle. (J)
(Left) Axial Tf C+ MR shows

an invasive macroadenoma
that extends from the sellar
and suprasellar regions into
the 3rd ventricle!:l1. Ectopic
pituitary macroadenomas
may rarely occur;, primarify
in the 3rd ventricle. (Right)
Sagittal Tf WI MR shows a
round mass = contiguous
with the tuber cinereum
within the 3rd ventricle,
isoimense to gray matter. No
enhancement is typical. If
enhancement is seen, must
consider glioma or other
tumors.
Glioma
an enhancing mass in 3rd
ventricle =. This rare tumor
is found only in anterior 3rd
ventricle & is associated with
hydrocephalus &
compression of adjacent
structures. (Right) Axial Tf
C+ MR shows an enhandng
mass in upper 3rd ventricle
=::I in a child, just be/ow
foramen of Monro. Note
associated hydrocephalus.
Astrocytoma diagnosed at
surgery. Initial pre-operative
diagnosis was choroid plexus
papilloma, although no
lobulation was seen. I
3
25
(IJ
c THIRD VENTRICLE MASS, BODY/POSTERIOR
.Q
Cl
Q)
0::: • Neurocysticercosis
~ DIFFERENTIAL DIAGNOSIS
C1l
:::J o Cystic lesion typically slightly
U Common hyperintense to CSF
E
c
Q)
• Pulsatile CSF o ± Discrete eccentric scolex
>
'C
• Dilated Suprapineal Recess o Cisterns> parenchyma> ventricles
Q)
ll.. • Neurocysticercosis
(IJ
Q) Less Common • Germinoma
u
'C • Germinoma o Usually extension from pineal tumor
CQ) • Prominent Massa Intermedia, Chiari 2 o Strong enhancement, ± CSF seeding
> • Choroidal Metastases
c: o Restricted diffusion due to high cellularity
III
~
• Choroid Plexus Papilloma • Prominent Massa Intermedia, Chiari 2
ell o Large mass a intermedia typical of Chiari 2
Rare but Important
"c:
III • Xanthogranuloma • Choroidal Metastases
• Ependymal Cyst o Tl hypo T2 hyperintense; avidly enhance
o Lateral ventricles> 3rd > 4th
ESSENTIAL INFORMATION o Strongly enhancing, lobulated mass
Key Differential Diagnosis Issues o Hydrocephalus, t intracranial pressure 2°
• True primary posterior 3rd ventricle masses to increased CSF production
rare o Lateral ventricle> > 3rd
• Most represent extension from pineal Helpful Clues for Rare Diagnoses
pathology • Xanthogranuloma
Helpful Clues for Common Diagnoses o CT variable
• Pulsatile CSF o MR Tl iso-hyper/T2 hyperintense

o 2° to time-of-flight effects/turbulent flow o Lateral> > 3rd ventricle
o t With thinner slices, longer TE, imaging o Obstruction infrequent (3rd > lateral)
perpendicular to flow • Ependymal Cyst
o Evaluate other planes for real vs. artifact o Nonenhancing thin-walled cyst
• Dilated Suprapineal Recess o CSF density/intensity
o Chronic aqueductal stenosis (any etiology) o Rare in 3rd ventricle
o Third ventricle dilates
o May deform rostral tectum, mimic tectal
glioma
Pulsatile CSF Dilated Suprapineal Recess
I
3 Axial FLAIR MR shows CSF flow anomaly
manifesUng as a hypoinlense "pseudolesion" of the
= Sagillal T2WI MR reveals dilated suprapineal recess -?
from chronic aqueductal stenosis !:l2. Note dilated
posterior 3rd ventricle. Examining other sequences & lateral venfJicJe with upward bowing of corpus callosum
planes confirmed this as flow artifact. ~ flallened fornices f2iJ.
26
THIRD VENTRICLE MASS, BODY/POSTERIOR CJl
c:
""
Neurocysticercosis
(LeFt) Axial T7 C+ MR
demonstrates a classic
neurocyslicercosis cyst =
with an enhancing nodule
representing the scolex 811-
(Right) Sagi!!al T7 C+ MR
shows a robustly enhancing,
predominantly solid tumor
that Fil/sthe posterior 3rd
ventricle, suprapineal recess,
and inferior recesses DJ. The
pineal gland appears
engulFed by the mass and is
probably the source of the ;0
(1)
tumor. <0
o
OJ
Ul
Prominent Massa Intermedia, Chiari 2 Choroidal Metastases

an enormous massa
intermedia ~ that nearly
fills the entire third ventricle.
(Right) Axial T1W/ MR
reveals two lesions which are
isoinlense with gray maller
=:I that are pineal &
suprasellar masses involving
the 3rd ventricle. Biopsy
disclosed embryonal
carcinoma.
Xanthogranuloma
(Left) Axial rU\/R MR shows
a heterogeneous mass =
involving the posterior 3rd
ventricle. Note
ventriculomegalyand
transependymal CSF
resorption E:I from
obstructive hydrocephalus.
(Right) Axial N[CT
demonstrates a close-up
view of a hyperdense mass
in the 3rd ventricle =:I.
I
3
27
en
c
CEREBRAL AQUEDUCT/PERIAQUEDUCTAL LESION
.Q
Ol
OJ
cr: DIFFERENTIAL DIAGNOSIS o Multifocal hypointense T2*/GRE foci
~
~ related to blood product susceptibility
:J
o
·C
Common • Neurocysticercosis
C • Aqueductal Stenosis o Cisterns> parenchyma> ventricles
OJ
>
·C • Tectal Glioma o Basal cistern cysts may be racemose
OJ
0... Less Common (grape-like), causing an aqueduct lesion
en
OJ • Diffuse Axonal Injury (DAI) • Multiple Sclerosis
li o Multiple T2 hyperintensities in
·C • eurocysticercosis
C
OJ • Multiple Sclerosis periventricular white matter (WM) &
> • Enlarged Perivascular Spaces callososeptal interface; 10% infra tentorial
c: o Internuclear ophthalmoplegia (I 0):
• Diffuse Astrocytoma, Low Grade
"'
~
ell • Encephalitis (Miscellaneous) Characteristic clinical finding related to
"0
• Intraventricular Hemorrhage brainstem lesion involving medial
c:
longitudinal fasciculus, present within
"':J • Wilson Disease
periaqueductal region
.:.t. Rare but Important
(J) • Enlarged Perivascular Spaces
• Metastasis, Parenchymal o Benign fluid-filled structures, accompany
• Wernicke Encephalopathy penetrating arteries
• Behc;:et Disease o PVS usually 5 mm or less; may expand
• Gliomatosis Cerebri (GC) o Most common location for expanded
• Leigh Syndrome "giant" PVS is midbrain; may cause
• Alexander Disease hydrocephalus
o Single or multiple well-delineated cysts
ESSENTIAL INFORMATION isointense with CSF; no enhancement
Key Differential Diagnosis Issues o Nonenhancing T2 hyperintense mass;
• Cerebral aqueduct/periaqueductallesions supratentorial 2/3, infra tentorial 1/3
may be separated by lesion type o 50% of brains tern "gliomas" are low grade
o Masses & pseudomasses
astrocytoma
o Infectious/inflammatory processes versus • Occur in pons & medulla of children,
metabolic disorders may involve midbrain
Helpful Clues for Common Diagnoses o Usually no enhancement, if C+ worry
• Aqueductal Stenosis about malignant progression
o Focal reduction in aqueduct size, • Encephalitis (Miscellaneous)
congenital or benign acquired o Location dependent on etiology
o Funnel-shaped aqueduct with "ballooned" o Diffuse brain parenchymal inflammation
lateral & 3rd ventricles & foramen of caused by a variety of pathogens, most
Monro proximal to obstruction commonly viruses
o Normal 4th ventricle & foramina distal o Abnormal T2 hyperintensity of GM ± WM
o All patients with suspected AS should be or deep gray nuclei
scrutinized for an obstructing mass! o Epstein-Barr virus: Symmetric BG, thalami,
• Tectal Glioma cortex, or brainstem
o t T2 signal mass; ± enhancement o Varicella-zoster virus: Brainstem/cortical
o Expands tectum, obstructs aqueduct GM, cranial nerves
o Indolent, most only need CSF diversion o Japanese encephalitis: Bilateral thalami,
brainstem, cerebellum, spinal cord,
cerebral cortex
• Diffuse Axonal Injury (DAI)
o Listeria rhombencephalitis: Brainstem &
o Multifocal punctate hemorrhages at
cerebellum
corticomedullary junction, corpus
I callosum, deep gray matter (GM) & upper
brainstem (dorsolateral midbrain & pons)
3
28
CEREBRALAQUEDUCT/PERIAQUEDUCTAllESION C/l
"
c:
III
o West Nile virus: Brainstem, substantia o T2 hyperintense lesions in brainstem, BG :J
C.
nigra, BG, thalami, anterior horn (cord), &/or deep WM III
..,
cerebellum o Variable enhancement III
:J
o Enteroviral encephalomyelitis: Brainstem, • Gliomatosis Cerebri (GC)
spinal cord, & cerebellum o T2 hyperintense infiltrating mass with <
Ct>
enlargement of involved structures, no or ~
• Intraventricular Hemorrhage ::l.
Cl
o Associated with significant trauma minimal enhancement CD
(J)
o May occur within cerebral aqueduct o Brainstem involvement 10-15%

• Wilson Disease • Leigh Syndrome
o Symmetric T2 hyperintensity or mixed o Lesions predominantly in brainstem, BG
signal in putamen, globus pallidus (GP), (particularly putamen) & cerebral WM
caudate, & thalami o Bilateral, symmetric increased T2 in
o Characteristic "face of the giant panda" putamina & periaqueductal gray matter
::0
sign at midbrain o Edema characteristic of early disease Ct>
<0
Helpful Clues for Rare Diagnoses • AJexander Disease a

:J
o Diffuse, symmetric, bifrontal WM signal (J)
• Metastasis, Parenchymal
abnormality & enhancement
o May involve brainstem; typically multiple
o Obstructive hydrocephalus, especially
lesions
neonatal/infantile subtypes 2° to aqueduct
• Wernicke Encephalopathy
obstruction from periaqueductal disease
o Curable neurologic disease caused by
thiamine deficiency Alternative Differential Approaches
o Triad of neuro-ophthalmologic • Masses: Tectal glioma, NCC, PVS, diffuse
manifestations, ataxia, & global confusion astrocytoma, metastases, GC
o Symmetric increased T2 signal surrounding • Pseudomasses: AS, encephalitis, Behc;:et
aqueduct & 3rd ventricle, floor of 4th • Infectious/Inflammatory: MS, encephalitis,
ventricle & medial thalami Behc;:et
o May affect only periaqueductal grey matter • Metabolic: Wilson disease, Wernicke
• Behc;:etDisease encephalopathy, Leigh syndrome, Alexander
o Multisystem vasculitis of unknown origin, disease
CNS involvement 5-10%
o Classic triad of oral & genital ulcerations
with uveitis
Aqueductal Stenosis Tectal Glioma
I
Sagittal T1WI MR shows large lateral & 3rd ventricles,
with a normal 4th. The "funnel-shaped" stenotic
Sagittal T2WI MR shOl'VSa tecta I plate glioma ~ as a
homogeneous, mildly T2 hyperintense mass. Lesions in
3
aqueduct SI & dilated optic & infundibular recesses of this location often cause obslructive hydrocephalus,
the 3rd ventricle are well seen I!::l. requiring shunting.
29
C/)
c CEREBRAL AQUEDUCT/PERIAQUEDUCTAL LESION
o
en
Ql
0::
Neurocysticercosis
in dorsolateral midbrain
a common location in the
=
(Left) Axial NECT shows OAI
brainstem. This traumatic

C/) axonal Slrelch injury typically
Ql
"0 occurs at corlicomedullary
'C
junctions, along corpus
C callosum, deep gray mailer
Ql
> & upper brainslem. (Right)
Sagillal TI WI MR shows
enlarged lateral ventricles &
a large cystic intravenlricular
mass with a nodule 81. NCC
may cause a periaqueductal
lesion from an
intraventricular lesion or
racemose NCC in lhe basal
cisterns.
Multiple Sclerosis Enlarged Perivascular Spaces

a round hyperintense MS
leg mentum =
plaque in the midbrain
involving the
anterior periaqueduclal gray
maller. A lesion in this
location often causes
internuclear
ophthalmoplegia (lNO), a
clinical finding characteristic
of MS. (Right) Sagillal T IWI
MR shows markedly
enlarged perivascular spaces
resulting in a periaqueductal
lesion. When these spaces
become markedly enlarged,
they most commonly aFFecl
the midbrain.
Diffuse Astrocytoma, low Grade Encephalitis (Miscellaneous)

(LeFt) Sagillal T2WI MR
shows a foca/tegmental
mesencephalic glioma PJ::i:I
involving midbrain 8-
cerebral peduncle. Mass
effect from lUmors in this
location oflen result in
hydrocephalus, requiring
shunting. Brainstem gliomas
typically involve pons.
(Right) Axial fLAIR MR
shows t signal within lhe
midbrain I:] relaled 10 West
Nile encephalitis. Brainstem,
cerebellum, basal ganglia, &
thalamic involvement is
classic For West Nile
I encephalitis.
3
30
CEREBRAL AQUEDUCT/PERIAQUEDUCTAL LESION CJl
"
c:
III
::::l
Co
..•
III
Intraventricular Hemorrhage Wilson Disease III

::::l
subarachnoid & <
Ctl
intraventricular hemorrhage
~
related to a gunshot wound. :::!.
Q.
Note hyperdensity in
cerebral aqueduct ="!. Ctl
en
(RighI) Axial T2WI MR
shows hyperintensity without
mass effect involving the
dorsal pons & midbrain. The
midbrain hyperintensity
illustrates the" face of the
giant panda" sign ~.
Hyperintensity in the
midbrain tegmentum, with
sparing of red nuclei & lateral
portion of the substantia
nigra, is typical.
Gliomatosis Cerebri (GC)

(Left) Axial FUlIR MR shows
acute Wernicke
encephalopathy with
hyperintensity in midbrain
involving periaqueductal
gray. Involved structures
include mamillary bodies,
thalami, cortex, & subcortical
WM. (Right) Axial FUlIR MR
shows hyperintensity in
brainslem & media/temporal
lobes, enlargement with
preservation of underlying
architecture. CC usually
involves hemispheric WM.
Involvement of brainslem is
uncommon, 10-15% or
cases.

symmet,;c signal abnormality
in the periaqueductal gray
="!. Symmetric signal
abnormality of deep gray
structures & brainstem are
characteristic of
mitochondrial disorders.
Leigh syndrome classically
involves putamen, thalami, &
periaqueductal gray. (Right)
Sagittal T1 C+ MR shows
fornix =-
enhancement
Aqueductal
in chiasm,
& aqueductE!:l.
involvement is
common &
in infantile
juvenile Alexander disease &
may cause hydrocephalus. I
3
31
en FOURTH VENTRiClE MASS
c
a
Cl
(!)
a: o Heterogeneous, enhancing mass
• Pllocytic Astrocytoma
Common o Cyst with enhancing mural nodule
• Medulloblastoma (PNET-MB) o Typically cerebellar hemisphere rather
• Ependymoma than intraventricular
• Pilocytic Astrocytoma o 60% are cerebellar; 30% optic
en
(!)
• Brainstem Glioma, Pediatric nerve/chiasm
u
-c Less Common • Brainstem Glioma, Pediatric
C o Intrinsic to brainstem, not 4th ventricle
(!) • Subependymoma
> • Choroid Plexus Papilloma o May be dorsally exophytic, project
c: posteriorly into 4th ventricle
<0 • Neurocysticercosis
en"- • Epidermoid Cyst Helpful Clues for Less Common Diagnoses
"C
c: • Hemangioblastoma • Subependymoma
<0
• Metastasis, Intraventricular o Inferior 4th ventricle, obex (60%)
• Atypical Teratoid-Rhabdoid Tumor (ATRT) o Middle-aged, older adults
Rare but Important o T2 hyperintense lobular mass
• "Trapped" 4th Ventricle o No or mild enhancement is typical
• Ependymal Cyst • Choroid Plexus Papilloma
• Dermoid Cyst o 40% involve 4th ventricle (posterior
• Lipoma medullary velum), CPA, & foramina of

• EncephaJocraniocutaneous Lipomatosis Luschka
• Rosette-Forming Glioneuronal Tumor o 4th ventricle common location in adults
• Central eurocytoma o Lateral ventricle more common in child
o Lobular, vibrantly enhancing mass
ESSENTIAL INFORMATION o Convexity subarachnoid spaces most
Key Differential Diagnosis Issues common location
• Age of patient is very helpful in o May involve cisterns> parenchyma>
differentiating lesions of the 4th ventricle ventricles
• For many pediatric 4th ventricle masses, o Intraventricular cysts are often isolated,
imaging of entire neuraxis prior to surgery is 4th ventricle most common
recommended (medulloblastoma, choroid o Imaging varies with stage, host response
plexus tumors, ATRT) • Epidermoid Cyst

• MR with contrast is best imaging modality o Congenital epithelial inclusion cyst
• Sagittal images helpful to determine tumor o 90% intradural, primarily in basal cisterns
origin (location in 4th ventricle) • CPA: 40-50%; 4th ventricle 15-20%
o Nonenhancing, lobular, extra-axial mass
Helpful Clues for Common Diagnoses o Follows CSF on all sequences except FLAIR
• Medulloblastoma (PNET-MB) &DWI
o Arises from vermis or roof of 4th ventricle
• Hemangioblastoma
(superior medullary velum) o Intra-axial posterior fossa mass with cyst &
o Small round blue cells: Hyperdense on CT
enhancing mural nodule abutting pia
o 50% have CSF dissemination at diagnosis
o Associated with von Hippel-Lindau disease
o Solid, enhancing mass within 4th ventricle
o 90-95% posterior fossa: 80% cerebellar
o Hydrocephalus in > 90%
hemispheres; 15% vermis, 5% other
• Ependymoma (medulla, 4th ventricle)
o Arises from floor of 4th ventricle
o 7-10% of posterior fossa tumors
o "Plastic" tumor squeezes out lateral
060% cyst & "mural" nodule; 40% solid
recesses, foramen of Magendie • Metastasis, Intraventricular
I o Intratumoral cysts, hemorrhage common
o 2/3 are infratentorial within 4th ventricle
o Intraventricular metastases often involve
choroid plexus
3
32
FOURTH VENTRiClE MASS CIl
"
c:
o Gray-white junction lesions most common o Rarely involves 4th ventricle

o Primary tumor often known • Encephalocraniocutaneous Lipomatosis
• Atypical Teratoid-Rhabdoid Tumor o Rare congenital neurocutaneous syndrome
(ATRT) characterized by ipsilateral cranial, facial,
o 50% infratentorial, most off-midline; CPA, ocular, & CNS anomalies
cerebellum &/or brainstem o Unilateral hemispheric cerebral atrophy &
o Large mass with cysts &/or hemorrhage ventriculomegaly in a child with ipsilateral
o Variable enhancement alopecia overlying a scalp lipoma
o Very young patients, usually < 3 years o CNS lipomas occur inconsistently
o May mimic medulloblastoma • Rosette-Forming Glioneuronal Tumor
o Newly described rare tumor of 4th
ventricle, WHO grade 1
• "Trapped" 4th Ventricle
o Midline mass of 4th ventricle; may involve
o Related to extraventricular obstructive ;:0
brainstem, vermis ct>
hydrocephalus (EVOH) or <0
• Central Neurocytoma o·
"communicating" hydrocephalus :::J
o "Bubbly" mass in frontal horn or body of V>
o EVOH: Obstruction distal to 4th ventricle
lateral ventricle
outlet foramina
o 4th ventricle, extremely rare, < 1%
o Etiologies include thickened meninges
(often related to SAH, meningitis, CSF Alternative Differential Approaches
tumor seeding, venous obstruction, NPH) • 4th ventricle mass in a child
• Ependymal Cyst o Medulloblastoma, ependymoma, pilocytic
o Typically lateral ventricle: Body or atrium astrocytoma, brainstem glioma, ATRT
o 4th ventricle location rare • 4th ventricle mass in an adult
o Follows CSF on all sequences o Metastasis, choroid plexus papilloma,
• Dermoid Cyst subependymoma, hemangioblastoma
o Commonly sellar/parasellar/frontonasal • 4th ventricle mass, all ages:
o May occur as primary 4th ventricle mass Neurocysticercosis, epidermoid, dermoid,
o Fat appearance with droplets in cisterns, "trapped" 4th ventricle
sulci, ventricles if ruptured
• Lipoma
o Well-delineated lobulated extra-axial mass
with fat intensity
o 40-50% interhemispheric fissure
I
Sagittal T1 C+ MR shaws heterogeneous enhancement
of this 4th ventIicufar medulloblastoma. Hydrocephalus
Sagittal T1 c+ MR shows an enhancing 4th ventIicular
mass with extension through the foramen of Magendie.
3
& CSF seeding are characteristic of these WHO grade 4 Note ventIicufar obstIuction with an enlarged cerebral
tumors. aqueduct =::I & a dilated 3rd ventIide EI.
33
(f)
c FOURTH VENTRiClE MASS
.Q
Ol
Q)
0:::
~
Cll
:::J
U
'C Pilocytic Astrocytoma Brainstem Glioma, Pediatric
C (Left) Sagitlal T I C+ MR
Q)
>
'C
shows a mixed cystic & solid
Q) posterior fossa mass with
a.. patchy enhancement of the
(f)
Q)
tumor nodule. Note the 3rd
ventricular obstruction.
~ Multiplanar MR imaging is
C
Q) essential for characterization
> of a pediatric posterior fossa
C mass. Detecting the
III relationship of the mass to
~
ell the 41h ventricle is key.
"0 (Right) Sagitlal T2WI MR
C shows a focal glioma,
III
localed in the dorsal
pOnlomedullary junction
wilh mild mass effect on the
anterior 4th ventricle.
Choroid Plexus Papilloma

shows a typical T2
hyperintense, inferior 4th
ventricfe subependymoma
E!lI. Lack of hydrocephalus is
typical of subependymoma.
These intraventricular masses
are often asymptomatic.
(Right) Sagittal T1 C+ MR
shows a lobular, midline 4th
ventricular mass with robust
enhancement &
hydrocephalus. Other 4th
ventricular tumors would not
demonstrate such strong
enhancement. These tumors
may be in the 4th ventricle
or at the lateral recess.
Neurocysticercosis
(Left) Sagi!!al T1 WI MR
shows a cyst with a nodule
within the inFerior 4th
ventricle~. The lesion
showed no enhancement, in
keeping wilh the vesicular
stage. The protoscolex is the
viable larva within the
thin-walled cyst visible on
MR. (RighI) Axial FLAIR MR
shows the 4th ventricular
lesion & mild edema in the
adjacent brain E!lI. As Ihis
was a solitary lesion~ it was
resected for diagnosis.
Intraventricular NCC lesions
I are best seen on T7 & FLAIR

MR.
3
34
FOURTH VENTRICLE MASS ,.-c:
CJl
Ql
::l
Co
tll
...•
Hemangioblastoma III
::l
shows a non enhancing <
(1)
CSF-like mass expanding the ::J
4th ventricle. The ...•
"scalloped" expansion of the ~
(1)
4th ventricle suggests Vl
epidermoid. Most posterior

fossa epidermoids occur in
the CPA cistern, rather than
intraventricular. (Right)
Sagittal TI C+ MR shows a
cystic-appearing mass of the
vermis with an enhancing
nodule 81 adjacent 10 the :;0
(1)
compressed 4th ventricle !::ll. to
The mural nodule of o·
::J
hemangioblaslOma typically Vl
abuts a pial surface.
Atypical Teratoid-Rhabdoid Tumor

(ATRT) "Trapped" 4th Ventricle
(Left) Sagillal TI C+ MR
shows a typical posterior
fossa ATRT as an off-midline
mass with marked
heterogeneity &
enhancement. There is
compression & displacement
of the 4th ventricle. (Right)
Sagillal TI C+ MR shows
extraventricular obstructive
hydrocephalus (EVOH) with
enlargement of the 4th
ventriclel causing
displacement of the pons &
medulla. EVOII is caused by
blocked reabsorption of CSF
through the arachnoid villi.
(Left) Axial N[CT shows a

large, round CSF-like mass
filling the 4th ventricle.
Ependymal cysts are most
common in the lateral
ventricles & relatively rare in
the 4th ventricle. (Right)
Sagillal T I WI MR shows
encephalocraniocutancous
IipomalOsis, also known as
Fishman syndrome, which
may be characterized by
extensive intracranial
lipomas. There is a large
lipoma extending into the
upper cervical canal!::ll & a
prominent subcutaneous
lipoma. I
3
35
'"
c: "BUBBLY-APPEARING" INTRAVENTRICULAR MASS
o
Ol
Q)
0::: • Nearly 1/2 occur in the 3rd decade
• 75% between 2nd-4th decades
Common o Location
• Choroid Plexus Cysts • Arises from septum pellucid urn or lateral
less Common ventricle wall
• Neurocysticercosis • Anterior (near foramen of Monro),
'"
Q) • Central Neurocytoma mid-body> > atrium, temporal horn
U • Less common: 3rd ventricle
";:: • Ependymoma
C • Rare: Extraventricular central
Q) • Subependymoma
> • Epidermoid Cyst neurocytoma
c:
• Cavernous Malformation • 13% bilateral
....
'" o Imaging
a! • Ependymal Cyst
• Cyst-like areas seen in 2/3 of cases
"c: Rare but Important • Moderate enhancement is typical
'" • Choroid Plexus Papilloma • Punctate calcifications in up to 1/2
• Choroid Plexus Carcinoma • Hemorrhage not uncommon
• Parasites, Miscellaneous • Ependymoma
• Astroblastoma o WHO grade II neoplasms
o Arises from differentiated ependymal cells
ESSENTIAL INFORMATION lining ventricles, central canal of the
spinal cord
Key Differential Diagnosis Issues o Mean age - 6 years
• Purely cystic intraventricular masses are o Location
usually benign • 58% 4th ventricle
o Xanthogranulomas> > ependymal or • 42% lateral, 3rd ventricles
inflammatory cysts • Less common: Extraventricular
• Only truly common "bubbly-appearing" ependymoma
intraventricular masses = choroid plexus o Imaging
cysts (xanthogranulomas) • Ca++ in 40-80%
Helpful Clues for Common Diagnoses • Occasional intra tumoral hemorrhage
• Choroid Plexus Cysts yields blood-fluid levels
o Benign xanthogranulomas • Contrast-enhancement varies; usually
o Choroid plexus glomi, bilateral intense but spares the cyst-like regions
o Increased prevalence with age • Extension beyond ventricular margins
o Usually asymptomatic (rarely cause (paraventricular) not uncommon
obstruction) • Subependymoma
o Histologically most are xanthogranulomas o Middle-aged, older adults
• Benign degenerative process o Most located within the 4th, frontal horn
• Typically FLAIR hyperintense of lateral ventricles
• May restrict on DWI o Varied enhancement: None to intense,
• Inhomogeneous enhancement common calcification, cyst formation may occur
o Extension of a subependymoma beyond
the ventricular margins is rare, unlike for
ependymoma
o Often show rim enhancement
• Epidermoid Cyst
o Look for characteristic scolex,
o DWl most specific: Restricted diffusion
parenchymal/cisternal lesions
o FLAIR next most helpful sequence,
o Small intraventricular cysts best seen on
showing "gray" CSF or incomplete CSF
FLAIR
suppression
• Central eurocytoma
I o Who grade II neoplasm
• Cavernous Malformation
o Intraventricular location is uncommon
o Younger age patients
3
36
"BUBBLY-APPEARING" INTRAVENTRICULAR MASS
o Imaging appearance like cavernous Other Essential Information

malformations elsewhere • Enhancing intraventricular tumors may
oGRE or SWI sequence helpful to assess for require MR neuraxis screening for drop
susceptibility due to blood products metastasis, particularly when choroid plexus
• Ependymal Cyst <
CD
tumors and ependymoma are suspected ;;.
o Lacks enhancement • Nonenhancing cystic lesions with DWI :0.
Q.
o CSF signal all sequences (FLAIR most restriction characteristic for epidermoid cysts CD
(j)
specific) • Neurocysticercosis can rarely mimic other
Helpful Clues for Rare Diagnoses intraventricular cysts, such as colloid cyst
• Choroid Plexus Papilloma o Cryptococcal infection can present in a
o Nearly half present in 1st decade similar fashion to cysticercosis
o WHO grade I (carcinoma is WHO grade III)
o Presentation with hydrocephalus ;0
SELECTED REFERENCES CD
common; can be due to mechanical <C
obstruction and/or overproduction of CSF 1. Bell JW et al: Neuroradiologic characteristics of o'

:J
astroblastoma. Neuroradiology. 49(3):203-9, 2007 (j)
o Locations: Lateral ventricle most common 2. Mathews M et al: Intraventricular cryptococcal cysts
site (50% of cases) > 4th ventricle (40%; masquerading as racemose neurocysticercosis. Sueg eurol.
67(6):647-9,2007
most common in adults) > 3rd ventricle 3. Prayer D et al: MR imaging presentation of intracranial
(5%) disease associated with Langerhans cell histiocytosis. AJNR
o Imaging Am J Neuroradiol. 25(5):880-91, 2004
4. Koeller KK et al: From the archives of the AFII'. Cerebral
• Cauliflower-like lobulated tumor, usually intraventricular neoplasms: radiologic-pathologic
with moderate or intense enhancement correlation. Radiographies. 22(6):1473-505, 2002
5. Figarella-Branger 0, Soylemezoglu F, Kleihues 1', lIassounJ.
• Hemorrhage, cyst formation may occur cntral neurocytoma. In: Klcihues P, Cavenee W, eds.
• Necrosis and/or parenchymal invasion Pathology and genetics of tumours of the nervous system.
suggest choroid plexus carcinoma Lyon, France: IARC, 107-109,2000
6. Takara K et al: Intraventricular, cystic, atypical
• Flow voids common meningioma. Neurol Med Chir (Tokyo). 37(11):856-60,
• Pure "cystic" variant may occur within 1997
7. Furie OM et al: Supratentorial ependymomas and
ventricles, subarachnoid spaces subcpendymomas: cr and MR appearance. J Com put
• Astroblastoma Assist Tomogr. 19(4):518-26,1995
o "Bubbly" appearance common 8. Wichmann Wet al: Neuroradiology of central
neurocytoma. Neuroradiology. 33(2):143-8, 1991
o Parenchymal> > intraventricular 9. Morrison G et al: Intraventricular mass lesions. Radiology.
153(2):435-42, J984
Choroid Plexus Cysts Choroid Plexus Cysts
I
Axial T1 C+ MR shows multiple rim-enhancing cysts
=, some with solid-appearing nodules 8l in atria of
Axial OWl MR in another case shows bilateral choroid
plexus cysts that show diffusion restriction=, an
3
both laleral venlricles. llislologically these cysts are occasional finding in this entity.
xanthogranulomas. 37
(fl
c "BUBBLY-APPEARING" INTRAVENTRICULAR MASS
.2
OJ
Q)
cr
(LeFt) Axial T2WI FS MR

shows multiple cysts in the
quadrigeminal cistern ~
and atrium of righllareral
(fl ventricle ~. Note trapped
Q)
u temporal horn '2>, (Courtesy
'C
E. Bravo, MOJ. (Right) Axial
C T2WI MR shows multiple
Q)
> "bubbly" intraventricular
cysts = in a patient with
known NCe. (Courtesy B.
Villarreal, MOJ.
Central Neurocytoma
(Left) Coronal T2WI MR
central neurocytoma
a classic "bubbly"
-=
shows a typical MR case of
with
muJUcyslic appearance.
These tumors are typically
attached to the septum
pellucidum. (Right) Coronal
Tl C+ MR in the same case
as previous image shows
patchy enhancement 82
within the partly cystic,
"bubbly-appearing" mass
that arises from the septum
=
pellucidum.

shows a large,
"bubbly-appearing" 4th
mass =
ventricle/cisterna magna
in a 9 year old with
a 2 month history of morning
vomiting and worsening
headaches. (Right) Sagittal
T2WI MR shows a large,
"bubbly-appearing" mixed
cystic and solid 4th
ventricular/cisterna magna
mass = in a 40 year old
female with headaches.
I
3
38
"BUBBLY-APPEARING" INTRAVENTRICULAR MASS CJ)
c:
"""
III
:3
Co
..,
lD
III
(Left) Axial FLAIR MR shows :3

an inhomogeneous mass <
CO
filling the 4th ventricle =:II.
~
::!.
Incomplete suppression on
()
FLAIR gives this epidermoid ro-
VI
cyst a "cauliflower" or
"bubbly" appearance.
(Right) Axial T2WI MR
shows a lobulated fluid
signal intensity cyst in the
4th ventricle =:II. Although
an arachnoid cyst is a
possibility, the insinuating
margins are more typical (or
epidermoid.
Cavernous Malformation Cavernous Malformation

(LeFt) Axial T1WI MR shows
typical findings of a
cavernous malformation in
the atrium of the left lateral
ventricle 1m. Note the classic
mixed signal appearance,
with intrinsic -f 1 shortening.
(Right) Axial T2WI MR in the
same case as previous image
shows a mixed signal
intensity =
with areas of
high and low T2 signal,
characteristic of cavernous
malformation.
Choroid Plexus Papilloma Choroid Plexus Papilloma

(Leh) Coronal T1WI MR in a
43 year old female with
headaches shows a
well-delineated
inhomogeneously
hypointense mass in the 4th
ventricle cz.(Right) Axial
T2WI MR in the same case
shows the "bubbly"
appearance of mass caused
by multiple small cysts =:II.
Choroid plexus papilloma
was confirmed at surgery.
I
3
39
en EPENDYMAL ENHANCEMENT
c
.Q
0>
OJ
0::
~ DIFFERENTIAL DIAGNOSIS Helpful Clues for Less Common Diagnoses
.!!l
::J
U Common • Ventriculitis
·C
o Ventriculomegaly with fluid-debris level &
C • Normal Variant
OJ
> • Developmental Venous Anomaly enhancement characteristic
·C
OJ o Associated DWI restriction typical
0.. • Multiple Sclerosis
o May complicate meningitis, abscess, or
vi
OJ Less Common shunt
~ • Ventriculitis • Opportunistic Infection, AIDS
C
OJ • Opportunistic Infection, AIDS o CMV commonly causes ventriculitis
> • Neoplasm with CSF Seeding
C
o TB may cause ventriculitis
1tI
~
• Lymphoma, Primary CNS o Toxoplasmosis may extend to ependyma &
CO • Tuberculosis mimic lymphoma
"t:l
c
1tI Rare but Important • Neoplasm with CSF Seeding
• Subependymal Venous Congestion o Many parenchymal tumors result in
o Sturge- Weber Syndrome ependymal spread as they abut ventricular
o Thrombosis, Deep Cerebral Venous surfaces
o Arteriovenous Malformation or Dural A-V o Ependymal spread most common in
Fistula childhood tumors: Medulloblastoma>
• Vasculitis ependymoma, pineal & choroid plexus
• Neurosarcoid tumors
• Langerhans Cell Histiocytosis o Malignant gliomas in adults (GBM,
anaplastic
astrocytoma/ oligod en drogli oma)
ESSENTIAL INFORMATION commonly spread along ependyma
Key Differential Diagnosis Issues o Metastases from extra cranial primary:
• Pre-operative neuraxis MR (imaging) Breast & lung most common
recommended in patients suspected of • Lymphoma, Primary CNS
having CSF seeding of tumor o Enhancing lesion(s) within basal ganglia,
periventricular WM
Helpful Clues for Common Diagnoses o Frequently abut, extend along ependymal
• Normal Variant surfaces
o Subependymal veins enhance normally & o Often involves, crosses corpus callosum
may be mistaken fur pathol9GY • Tuberculosis
• Developmental VenousAnomaly o Typically basal meningitis, may be
o Enhancing "Medusa head" (dilated
complicated by ventriculitis
medullary white matter veins) o Dural & parenchymal disease common
o May have enlarged subependymal veins
o Almost always unilateral, focal lesion Helpful Clues for Rare Diagnoses
o Angle of ventricle common location • Sturge-Weber Syndrome
• Multiple Sclerosis o May cause subependymal venous
o Common locations: Subependymal, congestion
peri ventricular, posterior fossa o Cortical Ca++, atrophy, & enlarged
o Ovoid or round enhancing lesion with no ipsilateral choroid plexus

significant mass effect o UsuaJly a sporadic congenital
o "Horseshoe" (incomplete ring malformation in which fetal cortical veins
enhancement) characteristic of fail to develop normally
demyelination • Thrombosis, Deep Cerebral Venous
o Tumefactive MS may mimic neoplasm, o Hyperdense internal cerebral veins on
and enhancement may extend to ECT
o Usually affects bilateral internal cerebral
I ependyma
veins and variably involves vein of Galen
& straight sinus
3
40
EPENDYMAL ENHANCEMENT
o Deep gray nuclei, internal capsule, o Rare subependymal involvement by

medullary WM typically affected perivascular space infiltration
o Venous stasis in deep WM (medullary) o May affect choroid plexus
veins seen as linear enhancing foci Alternative Differential Approaches
radiating outwards from ventricles <
C1l
• Neoplasm with CSF seeding:
o May cause subependymal venous ~
congestion
Medulloblastoma, ependymoma, Q:
germinoma, GBM, metastases, lymphoma, C1l
en
• Arteriovenous Malformation or Dural A-V anaplastic astrocytoma, anaplastic
Fistula oligodendroglioma, choroid plexus tumors,
o AVM: Vascular malformation with pineoblastoma, leukemia
arteriovenous shunting • Ependymal enhancement in a child:
• Tightly packed mass of enlarged, Medulloblastoma, ependymoma, choroid
enhancing vascular channels plexus or pineal tumor, leukemia ;:0
• May cause subependymal venous • Ependymal enhancement in an adult: C1l
<0
congestion o·
High-grade gliomas, metastases, lymphoma, ::l
o DAVF: Network of tiny vessels in wall of en
multiple sclerosis
thrombosed dural venous sinus • All ages: Normal variant, developmental
• Transverse sinus> cavernous sinus venous anomaly, ventriculitis
• May thrombose, resulting in venous
infarct
• May cause subependymal venous SELECTED REFERENCES
congestion 1. Fukui MB et al: CT and MR imaging features of pyogenic
• Vasculitis ventriculitis. AJNR Am J euroradiol. 22(8):1510-6,2001
2. Gomori JM et al: Leptomeningeal metastases: evaluation by
o Linear enhancement along course of gadolinium enhanced spinal magnetic resonance imaging.
penetrating vessels J eurooncol. 36(1):55-60, 1998
o Enhancement often extends to ventricular
margins
o Extensive T2 hyperintense white matter
common
• Neurosarcoid
o Leptomeningeal & dural enhancing masses
o May occur intraventricularly or along
ependyma
• Langerhans Cell Histiocytosis
Developmental Venous Anomaly Multiple Sclerosis
I
Axial n C+ MR shows an enlarged seplal vein =
this pa(jent with a prominent leh centrum semiovale
in Axial T7 C + M R shows mulliple foci of
contrasl-enhancemenl PJ:ll along the subependymal
3
developmental venous anomaly ~. Note also normal region, characteristic of multiple sclerosis.
subependymal veins PJ:ll.
41
(/)
c EPENDYMAL ENHANCEMENT
.Q
Ol
<ll
a:
~
co
:J
<.l
E Ventriculitis Opportunistic Infection, AIDS
c (Left) Axial T1 C+ MR shows
<ll
>
·C
ventriculomegaly & intense
<ll ventricular wall
a.. enhancement a
(/) characteristic of ventricu!Ws.
<ll
U This was due to right
·C temporal lobe abscess
C rupture. Note associated
<ll
> meningeal enhancement
along the pons =::I. (Right)
Coronal Tl C+ MR shows
multifocal ring E:I & nodular
= enhancing masses in this
AIDS patient with
toxoplasmosis. Note
:J ependymal enhancement !:;:l
-"CJ) in lesion adjacent to the
ventricular surface.
Neoplasm with (SF Seeding Neoplasm with (SF Seeding

shows metastatic seeding
along the ependyma of the
frontal horns of the lateral
ventricles =::I in this child
with medulloblastoma. Note
also {ocal intraventricular
lesion in the right frontal
horn. Pre~operaliveimaging
of the entire neuraxis is
recommended in patients
with medulloblastoma.
(Rig"') Axial T I C+ FS MR
shows thin linear
enhancement along the
ependymal margins of 4th
ventricle = due to tumoral
seeding.

a thick rind of enhancing
ependymal & subependymal
tumor common in
germinoma, which has a
propensity for CSF spread &
brain invasion. (Right) Axial
T1 C+ MR shows multifocal
linear enhancement in
leukemic infiltration of
cerebral microvasculature &
perivascular spaces. This
pallern of "carcinomatous
encephalitis II is a rare
manifestation of systemic
leukemia. Enhancement
extends lo lhe venlricular
I margins.
3
42
EPENDYMAL ENHANCEMENT (J)
7'C
c:
Tuberculosis
ependyrnalenhancen1enl
related to spread of
lymphoma 1lli\1. Primary CNS
lymphoma is classically
located in the periventricular
white maHer and abuts &/or
extends along the ependymal
surfaces. Involvement of the
leptomeninges or dura is
more common in sEcondary
lymphoma. (Right) Coronal
T1 C+ MR shows subtle
subependymal enhancement ::lJ
1m in addilion to more C1l
<0
classic basal meningeal c;-
::>
enhancement E!I in
tuberculosis. '"
Arteriovenous Malformation or Dural

A-V Fistula Vasculitis
(Left) Axial T 1 C+ MR shows
enlarged subependymal &
deep while maHer veins =
in this patient with dural
AVF This ependymal
enhancement is related to
subependymal venous
congestion. (Right) Sagittal
T I C+ M/? shows linear
enhancement = that
extends to the ependyma in
granulomatous angiitis, a
rare cause of vasculitis.
Sarcoid, amyloid, &
intravascular lymphoma
could mimic this
appearance.
shows septum pel/ueidum
thickening {.'{enhancement
Ea. There is a thickened
infundibular stalk Illi\1 &
septum pellucidum with
subtle adjacent ependymal
enhancement =. (Right)
Axial T 1 C+ MR shows
markedly enhancing masses
in the suprasellar cistern m
choroid plexus of both lateral
ventricfes =. and tentorial
apex Ea. The enhancing
choroid plexus masses
extend to the ependymal
surface, mimicking
I
3
43
en LARGEVENTRICLES
c
o
Ol
QJ
a: DIFFERENTIAL DIAGNOSIS • Intraventricular obstructive
~
Cll
:J
hydrocephalus (IVOH) =
'-'
'C
Common "non-communicating hydrocephalus":
C
QJ
• Aging Brain, Normal Due to obstructed CSF at level of
>
'C • Encephalomalacia, General ventricles from focal mass effect
QJ
Il. • Obstructive Hydrocephalus • Extraventricular obstructive
en o Meningitis hydrocephalus (EVOH) =
QJ
U o Subarachnoid Hemorrhage, NOS "communicating hydrocephalus": Due to
'C
C o Intraventricular Hemorrhage obstructed CSF resorption at level of
QJ
> • Cerebral Atrophy, NOS sulci, meninges/arachnoid granulations
c: o Chronic Hypertensive Encephalopathy
..
01
III
o Multiple Sclerosis
• CSF overproduction (choroid plexus
tumors)
"C o Alcoholic Encephalopathy o Meningitis
c:
01 o Radiation and Chemotherapy • Mild hydrocephalus typical, may be
o Diffuse Axonal Injury (DAI) earliest imaging finding (EVOH)
o Post-Meningitis • Leptomeningeal enhancement
o Drug Abuse • Complications: Cerebritis/abscess,
Less Common effusions, ischemia
• Alzheimer Dementia o Subarachnoid Hemorrhage, NOS
• Normal Pressure Hydrocephalus • Impaired CSF resorption (EVOH)
• Multi-Infarct Dementia • Subarachnoid blood, often aneurysmal
• Frontotemporal Dementia o Intraventricular Hemorrhage
• Impaired CSF resorption (EVOH)
Rare but Important
• Ventricular blood, often related to
• Choroid Plexus Papilloma trauma or AVM
• Megalencephaly Syndromes • Cerebral Atrophy, NOS
• Huntington Disease o Chronic Hypertensive Encephalopathy
• Creutzfeldt-]akob Disease (C]D) • Brain parenchymal changes due to
• Inborn Errors of Metabolism (End-Stage) long-standing effects of untreated or
poorly treated systemic hypertension
ESSENTIAL INFORMATION • May result in vascular dementia
• Diffuse white matter (WM) atrophy with
Key Differential Diagnosis Issues low density or high T2 signal
• Imaging most important to distinguish • May have hemorrhagic foci on GRE
acutely obstructive causes from (basal ganglia, thalamus, cerebellum)
non-obstructive causes o Multiple Sclerosis
• Dementias best diagnosed clinically • Periventricular WM pattern of T2
Helpful Clues for Common Diagnoses hyperintensities ± enhancement
• Aging Brain, Normal • Often dramatic callosal volume loss &
o Ventriculomegaly in proportion to sulci ventriculomegaly
o Reflects atrophy from parenchymal loss • Lesions generally lack mass effect
• Encephalomalacia, General o Alcoholic Encephalopathy
o Volume loss from many causes (prior • Chronic alcohol abuse results in
stroke, trauma, surgery) symmetric lateral ventricle enlargement
o Focal, in areas of parenchymal tissue loss & superior vermian atrophy
(with focal ventricular enlargement), or • Wernicke involvement: Mamillary
diffuse when global bodies, medial thalami, hypothalamus,
• Obstructive Hydrocephalus periaqueductal gray matter
o Surgically emergent condition o Radiation and Chemotherapy
I o Types of obstructive hydrocephalus • Late volume loss & diffuse T2

hyperintensity WM
3
44
LARGEVENTRICLES ,.-c:
CJl
III
• Spares subcortical "U" fibers • Frontotemporal Dementia ::l
0-
Diffuse Axonal Injury (DAI) o Anterior frontotemporal atrophy with WM
o
hyperintensity; "knife-like gyri"
..•III
lD
• DAI best seen on GRE, FLAIR,& DWI
::l
• Classic locations: Gray-white matter Helpful Clues for Rare Diagnoses
junctions, callosum, deep nuclei <
(1)
• Accompanied by late WM volume loss o Intraventricular enhancing mass in child
..•
3-
('j'
o Post-Meningitis o Hydrocephalus due to obstruction &/or
ro
CJ>
• Late WM volume loss diffusely CSF overproduction
• May have encephalomalacia related to • Megalencephaly Syndromes
abscess, ischemia o Ventricular enlargement ipsilateral to
o Drug Abuse enlarged hemisphere
• Consider in young patients with • Huntington Disease
ischemic or hemorrhagic strokes o Focal enlargement of frontal horns due to ;0
• Chronic: Volume loss caudate atrophy
(1)
to
0'
Helpful Clues for Less Common Diagnoses • Creutzfeldt-jakob Disease (CJD) ::l
CJ>
• Alzheimer Dementia o Hyperintensity involving deep nuclei &/or
o Parietal & temporal cortical atrophy cortex on DWI > FLAIR
with/disproportionate hippocampal • Inborn Errors of Metabolism (End-Stage)
volume loss is suggestive o Chronic ventriculomegaly from
• Normal Pressure Hydrocephalus parenchymal volume loss
o Clinical triad of dementia, gait apraxia, & Alternative Differential Approaches
incontinence • Ventriculomegaly may represent atrophy or
o Ventriculomegaly disproportionate to "compensated" hydrocephalus
sulcal prominence, normal hippocampus • Compensated hydrocephalus: Compressed
o CSF flow studies can detect increased or small sulci, little/no transependymal CSF
velocity migration, relatively stable over time
• Multi-Infarct Dementia • Acute hydrocephalus: Small or compressed
o Multifocal infarcts involving cortical gray
sulci, transependymal CSF migration (T2
matter, subcortical WM, & basal ganglia hyperintensity along ventricular margins),
o Strokes of multiple ages & lacunes ventricles enlarge over short time period
common o Acute obstruction usually requires urgent
o Often associated with arteriolosclerosis,
treatment
WM hyperintensity
Obstructive Hydrocephalus
I
Axial FLAIR MR shows mild ventricular enlargement ~
a
in proportion to the mild sulcal enlargement in an
Coronal T2WI MR shows massive acute obstructive
hydrocephalus, with ballooned ventricles &
3
elderly patient with expected atrophy, Note lack of transependymal CSF migration a
due to a tectal
significant white maller disease. glioma m obstrucUng the cerebral aqueduct.
45
C/)
c:: LARGE VENTRICLES
a
OJ
Q)
IX
~
ell
:::J
'-'
.;::
C (Left) Sagittal T1 C+ MR
Q)
> shows a dilated 4th ventricle
.;::
Q) m & extensive enhancement
a.. obliterating the basal cisterns
C/)
Q)
& Filling the cisterna magna
<3 ~ Meningitis may be
.;::
complicated by
C
Q) hydrocephalus, usually due
> to impaired CST resorption
(EVOH). (Right) Axial NECT
shows blood in the basal
cisterns E1 & subarachnoid
spaces ~. Note blood levels
in the occipital horns &
ventricular dilation due
to acute ("communicating")
hydrocephalus ([vOH).
Multiple Sclerosis
marked parenchymal volume
loss evidenced by ventricular
prominence 8lI & marked
white matter volume foss.
Note multiple while maller
T2 hyperintense plaques
related to the patient's MS.
Marked corpus callosum
atrophy is typical. (Right)
Axial FLAIR MR shows lateral
ventricle enlargement = &
diFFuseparenchymal volume
1055in a patient with chronic
alcohol abuse. White matter
disease is also noted, likely
arteriolosclerosis.
Radiation and Chemotherapy Post-Meningitis

(LeFt) Axial T2WI MR shows
diFFusehyperintensity
white matter =
throughout perivenlricular
sparing the
subcortical U-Fibers & corpus
callosum, in this young
patient who underwent
radiation & chemotherapy.
shows marked
venlriculomegaly = in a
patient with a history of
coccidioides meningitis. Lack
of transependymal CSF
migration suggests the
obstruction is likely chronic
I ("compensated") or low
grade.
3
46
LARGE VENTRiClES ,..c:
en
Ql
::l
a.
OJ
...•
Multi-Infarct Dementia Ql
(Lefl) Axial T2WI MR shows ::l

multiple high signal foci in <
(1)
the basal ganglia !::ill & white
maller caused by vasculitis ~
related to drug abuse. In Q.
(1)
young patients with en
ischemia, drug use should be
considered. Street drugs
such as amphetamines may
cause chemical vasculitis
with secondary infarcts.
multiple hypoinlensilies with
associated volume 1055
consistent with prior
territorial cortical infarctions.
Basal ganglia lacunes are
also typical.
Frontotemporal Dementia Choroid Plexus Papilloma

enlargement of the frontal
horns with "knife-like" gyri
8l characteristic of Pick
disease. Note relalive sparing
of the parietal & occipital
lobes. Selective frontal &
temporal atrophy is
Tl C+ MR shows
venlriculomegaly !::ill due to
an enhancing trigone mass
~ without obstruction.
Ventriculomegaly is related
to overproduction of CSF
that outpaces the ability of
arachnoid granulations to
resorb CSF.
Huntington Disease
enlarged right hemisphere &
characteristic ipsilateral
enlarged deformed lateral
ventricle -=
in
megalencephaly. (Right)
Axial TlWI MR shows
enlargement of both frontal
horns, with 1055of the
normal concave appearance
of the lateral ventricular
margins, consistent with
caudate head atrophy 1J::l.
I
3
47
Vl
c SMALLVENTRICLES
.Q
Ol
<IJ
a:: DIFFERENTIAL DIAGNOSIS o Cause shunted ventricle to collapse
~
.!:Q • Cerebral Edema, Traumatic
::J
U
'C
Common o Low density parenchyma with sulcal &
C • Normal Variant (Young Brain) ventricular effacement
<IJ
>
'C • CSF Shunts and Complications o Hyperdense cerebellum, "reversal sign"
<IJ
ll.. • Cerebral Edema, Traumatic • Herniation Syndromes, Intracranial
Vl
<IJ
• Herniation Syndromes, Intracranial o Ventricular effacement common
U
'C Less Common Helpful Clues for Less Common Diagnoses
C • Encephalitis (Miscellaneous)
<IJ • Encephalitis (Miscellaneous)
> • Intracranial Hypotension
C
o White matter T2 hyperintensity & edema
...
III • Intracranial Hypertension, Idiopathic o Mild restriction on DWI common
m • Intracranial Hypertension, Secondary • Intracranial Hypotension
"c
III
• HIE, NOS
• Meningitis
o "Slumping" midbrain, acquired tonsillar
herniation/ectopia, enhancing dura
::J
-'"
(/J Rare but Important • Intracranial Hypertension, Idiopathic
• Brain Death o "Pseudotumor cerebri"
• Inborn Errors of Metabolism (Acute o Dilated optic nerve sheaths, basal cisterns
Presentation) effaced, small ventricles
• Intracranial Hypertension, Secondary
o Etiology: Any causes of high intracranial
ESSENTIAL INFORMATION pressure or diffuse edema: Trauma, venous
Key Differential Diagnosis Issues outflow obstruction, anoxic or metabolic
• Clinical presenting features usually help encephalopathy, mass, brain death
define the category of disease in question • HIE, NOS
o Global anoxic/ischemic event results in
Helpful Clues for Common Diagnoses DWI changes
• Normal Variant (Young Brain) • Basal ganglia> diffuse cortex bright
o Ventricles in children, young adults can
• Diffuse white matter restriction (may be
normally appear quite small subacute manifestation)
• CSF Shunts and Complications o DWI abnormalities evolve slower than
o CSF diversion
thromboembolic infarction
• ± Reduced ventricular compliance
• Meningitis
o Compliance changes caused by
o Mild hydrocephalus> > > small ventricles
• Ependymal scar/adhesions
CSF Shunts and Complications Cerebral Edema, Traumatic
I
3 Axial NECT shows small ventricles= & indeterminate
shunt position 61. SymptomaUc ventJicular collapse is
=-
Axial NECT shows hyperdense foci of DAI which is
commonly associated with tJaumaUc cerebral edema.
known as "s/il·like venlfic1e syndrome" & suggests Note sulcal & ventricular effacement ffi Loss of
overshunting. gray-while differentiation is common.
48
SMALL VENTRICLES
Ql
:l
C.
..•
llJ
Ql
Herniation Syndromes, Intracranial Encephalitis (Miscellaneous)
(Left) Axial NECT shows low
:l
density subacute infarcts in
the cerebellar hemispheres.
Basal cisterns are effaced =
as is the 4th ventricle m in
this patient with
transtentoriaf herniation.
Herniation syndromes
typically result from trauma,
ischemia, or mass. (Right)
Axial fLAIR MR shows near
confluent T2 hyperintensity
in the deep white mailer =:J
& small ventricles Ell related
to mild mass effect from the
encephalitis.

symmetric small ventricles
= and smooth diffuse linear
pachymeningealthickening
and enhancement ~.
(Right) Coronal T1WI MR in
young adult female with
headaches, papilledema
shows very small lateral
ventricles EB Superficial
sulci ~ also look somewhat
less prominent than normal.
Pituitary gland is normal
for a young menstruating
female.
(Left) Axial PO FSEMR

shows enlarged bilateral
hyperintense deep nuclei =:J
& small ventricles ~ from
mass effect in HIE. Cortical
hyperintensity is less
prominent than on OWl (not
shown) except for more
advanced bilateral occipiwl
involvement liB (Right)
Axial T2WI MR shows diffuse
acute brain swelling in maple
syrup urine disease & small
ventricles due to subacute
thalami
capsules.
=
edema of deep white mailer
a and internal
I
3
49
rJ)
c ASYMMETRIC LATERAL VENTRiClES
o
Ol
Q)
0::: • Intraventricular Hemorrhage
ro o Involved ventricle may dilate early from
:J
U
·C
Common mass effect
C
Q)
• Normal Variant o Chronic dilation may be due to scarring
>
·C • Extrinsic Mass Effect from adhesions
Q)
Cl. • Encephalomalacia, General o Etiologies include trauma, AVM, basal
rJ)
Q)
• Intraventricular Hemorrhage ganglia hemorrhage
C3
·C
• Herniation Syndromes, Intracranial • Herniation Syndromes, Intracranial
CQ)
• Surgical Defects o Subfalcine herniation: Cingulate gyrus
> • Obstructive Hydrocephalus herniates under falx
• Choroid Plexus Cyst • Ipsilateral lateral ventricle compressed
Less Common • Foramen of Monro obstructs, causes
• Ventriculitis contralateral lateral ventricle
• CSF Shunts and Complications enlargement
:J
• Meningioma o Unilateral descending transtentorial
-"
en herniation (uncal): Herniation of medial
• Neurocysticercosis temporal lobe inferiorly
• Contralateral temporal horn becomes
Rare but Important entrapped & enlarges
• Intraventricular Synechiae/Adhesions o Entrapped ventricle: Typically temporal
• Choroid Plexus Carcinoma horn, by extrinsic mass effect
• Ependymal Cyst • Surgical Defects
• Dyke-Davidoff-Masson o Look for calvarial defect or "tract"
• Hemimegalencephaly o Typically related to resection of mass
o Ventricle enlarged unilateral to defect
ESSENTIAL INFORMATION • Obstructive Hydrocephalus
o Typically acquired & bilateral
Key Differential Diagnosis Issues o May be unilateral if shunt complication or
• Asymmetric lateral ventricles are most obstructing tumor is cause
commonly seen as a normal variant o Rare: Colloid cyst may obstruct unilateral
Helpful Clues for Common Diagnoses foramen of Monro & cause unilateral
• Normal Variant ventriculomegaly
o Asymmetric lateral ventricles seen in • Choroid Plexus Cyst
5-10% of normal population o Nonneoplastic, noninflammatory cyst of
o Asymmetry mild-moderate, left> right the choroid plexus
o Septum may be displaced across the o Common incidental finding in older
midline patients (40% prevalence)
o 0 associated mass effect, herniation, or o Typically bilateral, may be unilateral &
parenchymal atrophy enlarge lateral ventricle
o Must exclude underlying mass or Helpful Clues for Less Common Diagnoses
obstructing lesion • Ventriculitis
• Extrinsic Mass Effect o Ventriculomegaly with debris level,
o Etiologies include mass, hemorrhage,
enhancing ependyma
infarct, infection o May affect lateral ventricles
o Mass can cause ventricular deformity, asymmetrically, particularly if related to
subfalcine herniation shunt placement or abscess rupture
• Encephalomalacia, General • CSF Shunts and Complications
o Parenchymal loss results in compensatory
o Common complications include shunt
ventricular enlargement obstruction or breakage, infection,
I o Common etiologies include chronic
infarct, trauma, surgery
overdrainage
3
50
ASYMMETRIC LATERALVENTRICLES
III
o Asymmetric ventricles may result from • Ependymal Cyst ::::l
a.
overdrainage or underdrainage of an o Nonenhancing thin-walled cyst with CSF ro
...•
"isolated" ventricle density/intensity III
::::l
• Meningioma o Lateral ventricle most common location
o Intraventricular meningioma rare, • Dyke-Davidoff-Masson
typically left lateral ventricle o Antenatal unilateral hemispheric
o Associated with choroid plexus infarction causes cerebral hemiatrophy
o Smooth enhancing intraventricular mass o Ipsilateral calvarial thickening &
• Choroid Plexus Papilloma hyperpneumatized frontal sinuses,
o Enhancing, lobulated intraventricular mass temporal bones
in a child o Dilated ventricle from volume loss is
o 50% in lateral ventricle atrium, left> right ipsilateral to small hemisphere
o May obstruct CSF flow or overproduce CSF • Hemimegalencephaly
;:0
o May have CSF spread of tumor o Unilateral hemispheric enlargement C1>
<0
• Neurocysticercosis o Dilated, usually dysmorphic ventricle o'
::::l
o Intraventricular disease uncommon ipsilateral to enlarged hemisphere en
o Rarely may obstruct unilateral foramen of o Ipsilateral extra calvarial soft tissues may be
Monro & cause asymmetric lateral larger
ventricle Other Essential Information
o Cyst with "dot" representing scolex • High resolution "MR cisternography": CISS,
characteristic balanced FFE, FIESTA
o Tl & FLAIR best show intraventricular
o May detect small septations or arachnoid
cysts membranes causing obstruction
Helpful Clues for Rare Diagnoses • Cine CSF flow study may help detect
• Intraventricular Synechiae/Adhesions physiologic flow obstruction from arachnoid
o May be congenital or acquired (prior bleed, webs or membranes
infection, tumor) o May assess adequacy of drainage
o Look for enhancing septae, procedures
intraventricular cysts within ventricle
• Choroid Plexus Carcinoma
o Enhancing intraventricular mass &
ependymal invasion in young child
o CSF seeding common
Normal Variant Extrinsic Mass Effect
I
Axial T2WI MR shows asymmetrically large right
ventricular system I:] representing a normal variant.
Axial T1
horn lID
C+ MR shows compression of the left frontal
by a large periventricular enhancing mass !Ill 3
Note mild displacement of the septum pellucidum primary eNS lymphoma. Extrinsic mass effect is a
acrossmidline~. common cause of ventricular asymmetry.
51
en ASYMMETRIC lATERAL VENTRiClES
c
o
Cl
Q)
0::
~
.!l1
~
()
·C Encephalomalacia, General Intraventricular Hemorrhage
C (Left) Axial T2WI MR shows
Q)
>
·C
chronic MCA ischemia as
Q) encephalomalacia with
0.. gliotic hyperintense borders
en PJ:lI. The adjacent sulci are
Q)
U prominent and there is
·C
enlargement of the ipsilateral
C lateral ventricle SI related to
Q)
> volume loss. (Right) Axial
NECT shows a basal ganglia
C
III
~ hypertensive hemorrhage =
en with intraventricular
"C extension m. Associated
c midline shift results in
=
III
dilation of the contralateral
ventricles from foramen
of Monro obstruction.
Surgical Defects
shows a right hemispheric
subacute subdural
hematoma causing
subfalcine PJ:lI& uncal SI
herniation. Mass effect
compresses the right frontal
horn. The left ventricle ~ is
enlarged from foramen of
Monro obstruction. (Rig"')
Axial T2WI MR shows
=
widening of right foramen of
Monro seplum
pellucidum deviation &
enlarged right lateral
ventricle eJ in this tuberous
sclerosis patient with remole
tumor resection.
marked enlargement of the
left lateral ventricle with
bowing of seplum
=
peflucidum across midline
& transependymal CSF
migration EI indicating
acute obstruction. Findings
were related to a small atrial
diverticulum. (Right) Axial
T2WI MR shows a medial
atrial diverticulum =.
complication of severe
a rare
hydrocephalus. CSF pouch

herniates inferomedially
through tentorial incisura.
I
3
52
ASYMMETRIC LATERAL VENTRiClES
III
:J
Co
..•
OJ
III
(Left) Axial T' C+ MR shows

:J
a lobulated, nonenhancing <
(tl
mass =:I in the lateral ;:;
ventricle atrium, a choroid ::!.
()
plexus xanthogranuloma. ro-
This degenerative cyst of the en
choroid plexus is often found
incidentally in older patients.
shows ventriculitis with
asymmetric lateral ventricles
related to a temporal lobe
abscess = rupture &
meningitis rz. Note ;:0
(tl
ventriculomegaly & <0
ventricular wall o
:::J
enhancement a en
characteristic of ventriculitis.

isolated right lateral ventricle
with transependymal flow of
CSF p:;Jl indicating acute
obstruction. Note left shunt
=:I & completely
decompressed left lateral
ventricle. (Right) Axial T7 C+
MR shows enhancement
within the mass in the atrium
of the lateral ventricle =:I
with encysted
asymmetrically larger left
lateral ventricle.
shows a large mass in atrium
of right lateral ventricle p:;Jl
with trapped, encysted
occipital horn 81.
Ependymal enhancement
represents tumor spread
from choroidal metastasis.
(Right) Axial FLAIR MR
shows a cyst enlarging the
left lateral ventricle with
signal intensity isoinlens€ La
CSF =:I. There was no
enhancement of the cyst
wall, typical of ependymal
cyst.
I
3
53
CIl
C IRREGULAR LATERALVENTRICLES
o
Ol
C1l
a::: DIFFERENTIAL DIAGNOSIS o Deformity is chronic
o Overlying skull or scalp also shows defect
Common • Peri ventricular Leukomalacia
• CSF Shunts and Complications o "Wavy" margins or undulating lateral
• Surgical Defects ventricular contours typical
• Peri ventricular Leukomalacia o Cysts or ill-defined T2 hyperintensity in
CIl
C1l
• Cerebral Infarction, Chronic periventricular white matter (WM)
u • Porencephalic Cyst o Colpocephaly common & reflects
E
c
C1l
• Chiari 2 predominant posterior WM loss
> Less Common • Cerebral Infarction, Chronic
• Heterotopic Gray Matter o Vascular territory wedge-shaped area of
• Tuberous Sclerosis Complex encephalomalacia
• Metastases, Intracranial, Other o Results in compensatory or "ex vacuo"
• Intraventricular Webs or Adhesions dilation of the regional ventricle, due to
::::I volume loss
-"
• CMV, Congenital
l/)
• Schizencephaly • Porencephalic Cyst
o Cystic space in brain parenchyma with
Rare but Important
enlarged adjacent ventricle, may
• Hemimegalencephaly communicate with ventricle
• Holoprosencephaly o Cyst may cause mild mass effect (from CSF
• Holoprosencephaly Variants pulsations)
• Chiari 2
ESSENTIAL INFORMATION o Pointed anterior horns, colpocephaly
o Small posterior fossa, tecta I "beaking",
Key Differential Diagnosis Issues downward herniation of cerebellar tissue
• Irregular ventricles may be the result of through foramen magnum
obstruction, chronic volume loss &/or o Associated with a lumbar
congenital deformities myelomeningocele
o Obstruction: Mass effect, "ballooned"
appearing ventricles, & transependymal Helpful Clues for Less Common Diagnoses
CSF migration • Heterotopic Gray Matter
o Volume loss: Ventricle irregularity with o Subependymal nodules follow gray matter
brain parenchymal loss signal & do not enhance
o Congenital: Look for associated findings o May be seen with epilepsy or incidental
(colpocephaly, subependymal nodules) • Tuberous Sclerosis Complex
• Ventricular deformities may become o Subependymal nodules lining the
permanent despite relief of obstruction, due ventricles characteristic
to parenchymal atrophy or acquired • Mostly along striothalamic groove
ventricular non-compliance • Calcify with increasing age
• Enhancement may help differentiate o Cortical & subcortical tubers are usually
etiologies multifocal ± mild mass effect
• Tubers are most easily seen on FLAIR
Helpful Clues for Common Diagnoses • Rarely tubers may calcify or enhance
• CSF Shunts and Complications o Enhancing mass at foramen of Monro =
o Common complications include shunt subependymal giant cell astrocytoma
obstruction/breakage, infection, • Metastases, Intracranial, Other
overdrainage o CSF seeding of primary CNS tumors,
o Acquired ventricular non-compliance may lymphoma or systemic malignancy may
result in ventricle deformity cause irregular ventricles
• Surgical Defects o May result in ventricular nodules which
I o Often evident from prior shunt tract or
burr hole
can deform the ventricles
• Intraventricular Webs or Adhesions
3
54
IRREGULAR LATERAL VENTRiClES CJl
;><"
r::
III
o May be congenital or acquired (prior o Lobar: Anterior lateral ventricle may be ::::l
a.
hemorrhage, infection or tumor) deficient
..,
llJ
o Contours of ventricles may be rounded or • Holoprosencephaly Variants III
::::l
balloon-like due to obstructive symptoms o Middle interhemispheric (MIH) variant of
o Contrast ventriculography or cine CSF can holoprosencephaly <
CD
be helpful to assess for evidence of o MIH: 25% hyperintense dorsal cyst, ~
:0.
physiological flow obstruction obstructs third ventricle ~
CD
U>
• CMV, Congenital Alternative Differential Approaches
o White matter volume loss
• Tumors resulting in irregular ventricles are
o Periventricular calcifications are common
typically related to CSF dissemination
o Polymicrogyria & cortical malformations
• Adult tumors with CSF spread: GBM or other
may be seen malignant gliomas
• Schizencephaly • Pediatric tumors with CSF spread: ;;0
o Outward "dimpling" of lateral ventricle CD
Medulloblastoma, ependymoma, choroid CO
suggests schizencephaly plexus papilloma, pineal tumors o·
::::l
o Look for gray matter lining the CSF cleft U>
• Systemic malignancies with CSF spread:
Helpful Clues for Rare Diagnoses Lymphoma, breast or lung cancers
• Hemimegalencephaly • Gadolinium studies can differentiate among
o Hamartomatous overgrowth of part/all of a causes of ependymal nodules
hemisphere • Nonenhancing subependymal nodules may
o Lateral ventricle ipsilateral to enlarged represent gray matter heterotopia or TSC
hemisphere is usually bizarre-shaped & nodules
typically enlarged o Gray matter heterotopias follow gray
• Holoprosencephaly matter signal/density
o Congenital structural forebrain anomalies o TSC nodules follow white matter signal or
defined by degree of frontal lobe fusion are calcified
o All types have absent septum pellucidum • Enhancing nodules suggest ependymal
& frontal lobe fusion anomaly tumor seeding
o Alobar: Monoventricle, often incompletely
covered posteriorly by brain ("dorsal cyst")
o Semi/obar: Anterior horns absent, partial
occipital & temporal horns
CSF Shunts and Complications Surgical Defects
I
Axial NECT shows a right frontal ventricular drain that
traverses the right ventricle but is not decompressing the
left lateral ventricle, which remains irregularly enlarged
occipital horn =
Axial T2WI MR shows irregular enlargement of the left
due to left temporal and occipital
surgical defect & encephalomalacia from tumor removal
3
PJ:J. in this localion.
55
'"c IRREGULAR LATERAL VENTRiClES
.Q
C>
Q)
0:::
Periventricular leukomalacia
classic "wavy" or undulating
contours of the lateral
ventricles = in addition to
colpocephaly (enlargement
'"
Q)
u of the posterior portions of

·C lateral ventricles).
C Colpocephaly refleclS the
Q)
> predominantly posterior

C volume 1055. (Right) Axial
...
01
al
NECT shows irregular
enlargement of the left
"C frontal horn 81 due 10 focal
c regional parenchymal
01
volume los5 in this patient
with remote MCA infarct.
(Left) Axial CECT shows a

low density outpouching
from the right lateral
ventricle 1::1. While a thin
rim of cortex seems intact,
the cyst nearly reaches brain
surface & can be considered
a porencephalic dilation or
porencephalic lateral
ventricle cyst. (Right) Axial
NfCTshowsirregu~r~
dilated occipital horns 1::1
with interdigitation of
parietal & occipital
parenchyma across midline
PJ:ll due 10 a falx deficiency.
(Left) Axial T1 WI FS MR
shows multifocal nodularity
along ependymal margins of
both lateral ventricles 1:12.
These nodules follow gray
matter signal on all
sequences & do not enhance
or change over time. (Right)
Axial T2WI MR shows
multiple calcified
subependymalnodules
(SEN) 1:12 lining ventricles.
Note also subcortical tubers
PJ:ll. SEN calcify much more
commonly than
cortical/subcortical tubers.
Approximately 50% SfN are
I calcified by 10 years of age.
3
56
IRREGULAR lATERAL VENTRiClES CIl
""c:
Ql
:J
Co
tll
..,
Ql
CMV, Congenital
:J
near complete coating of the
ependymal lining of both
lateral
nodules =
venlricles with tumor
due to metastatic
seeding of anaplastic
oligodendroglioma. (Right)
Axial NECT shows
periventricuJar calcification
~ particularly along the
cauda-striatal groove in the
context of microcephaly &
developmental delay. This
strongly suggests congenital
CMV inFection. Note smooth
ventricular margins, unlike
calciFied nodules in TSC
complex.

Focal outpouchings of CSF
=
From both lateral ventricles
with a CSF cleFt
extending From lateral
ventricles to the subpial
surface. The
"pial-ependymal seam" is
gray matter-lined. (Right)
Axial T2WI MR shows
cortical dysplasia & open-lip
schizencephaly =.
Schizencephaly is closed-lip
with a Fusedgray matter
lined pial-ependymal seam
or open-lip with large, gray
matter-lined & Fluid-Filled CSF
cleFts.

enlargement of leFt cerebral
hemisphere accompanied by
an irregular ipsilateral
ventricle =. The body of the
leFt hemispheric white matter
is bulky. Note leFt Fornix ~
overgrowth. (Right) Axial
TlWI MR shows a large
/I horseshoe*shaped"
monovenlricle with fused
basal ganglia. There is no
interhemispheric fissure & no
identiFiable lobulation or
formation of ventricular
horns in this a/abar
holoprosencephaly patient.
I
3
57
IJ)
c: PERIVENTRICULAR ENHANCING LESIONS
o
Cl
Q)
0:: o May be identical to MS
Common o Enhancing periventricular WM or BG mass
• Multiple Sclerosis o Often extend along ependymal surfaces
• ADEM o Often crosses corpus callosum
• Lymphoma, Primary CNS o Solid appearing mass with low T2 signal,
IJ)
Q) Less Common mild DWI restriction
U o Hyperdense on CT
'C • Glioblastoma Multiforme
C
Q) • Abscess Helpful Clues for Less Common Diagnoses
> • Toxoplasmosis, Acquired
c: • Glioblastoma Multiforme
III • Germinoma o Peripherally enhancing WM mass with
'-
m • Metastases, Parenchymal central necrosis
"C
c: • Vasculitis o Surrounding T2 hyperintensity &
III
• Lyme Disease significant mass effect common
• Ependymoma o Often crosses corpus callosum
Rare but Important • Abscess
• Leukemia o Ring enhancing mass in peri ventricular
• Susac Syndrome WM
• Alexander Disease o Smooth, thin, linear enhancement
• Ependymal/Subependymal Veins (Mimic) o DWI restriction characteristic
• Toxoplasmosis, Acquired
o Multiple WM & BG ring enhancing masses
ESSENTIAL INFORMATION o May show "target" sign
o DWJ restriction variable
o Typically seen in HIV patients
• Germinoma
o Enhancing midline mass (pineal,
suprasellar) typical
o Occurs in BG or thalamus 5-10%
o Hyperdense on CT
o CSF spread common
• Metastases, Parenchymal
o Gray-white junctions & multiple
enhancing lesions typical
o May occur in periventricular WM
• Vasculitis
o Irregularities, stenosis & vascular
occlusions
o Multifocal cortical/subcortical & BG T2
hyperintensities; DWI restriction if acute
o Patchy enhancement typical
o Angiography remains gold standard for
diagnosis
• Lyme Disease
o Periventricular T2 hyperintensities +
enhancement in patient with skin rash &
flu-like illness
o Cranial nerve enhancement may occur
I • eN? often involved
o May be identical to MS
3
58
PERIVENTRICULAR ENHANCING LESIONS
ell
• Ependymoma • Venous thrombosis, vascular :J
0-
o Majority (2/3) infra tentorial malformations (AVM, DVA)
..,
OJ
• 4th ventricle in a child Alternative Differential Approaches ell
:J
• ± Extension through lateral recesses into
• Mass involving corpus callosum: GBM, <
CPA cisterns lymphoma, MS, ADEM CD
o 1/3 are supratentorial ..,
~
• Mass in immunocompromised patient: ~
• Most are extraventricular Lymphoma, abscess, toxoplasmosis, CD
(f)
• Typically periventricular WM metastases
o Heterogeneous enhancing mass • Single enhancing mass: MS (tumefactive),
o 50% are calcified
ADEM (tumefactive), lymphoma, GBM,
o Cysts, hemorrhage common
abscess, germinoma, ependymoma
Helpful Clues for Rare Diagnoses • Multiple enhancing masses: MS, ADEM,
• Leukemia lymphoma, abscess, toxoplasmosis, ;:0
CD
o Typically involves dura metastases, vasculitis, Susac syndrome to
o May see along penetrating vessels or o·
:J
(f)
ependyma
o Enhancing mass(es) in a child
SELECTED REFERENCES
1. Lucchinetti CF et al: Clinical and radiographic spectrum of
• Susac Syndrome pathologically confirmed tumefactive multiple sclerosis.
o Clinical triad: Encephalopathy, retinal Brain. 131(Pt 7):1759-75, 2008
artery occlusions, hearing loss 2. Hunt MA et al: Distinguishing primary central nervous
system lymphoma from other central nervous system
o Corpus callosum, BG, posterior fossa diseases: a neurosurgical perspective on diagnostic
lesions dilemmas and approaches. Neurosurg Focus. 21 (5):E3, 2006
o May be identical to MS 3. Do TH et al: Susac syndrome: report of four cases and
review of the literature. AJNR Am J Neuroradiol.
• Alexander Disease 25(3):382-8, 2004
o Diffuse symmetric bifrontal WM signal
abnormality & enhancement
o ear total lack of myelin
o Infant with macrocephaly, seizures,
developmental delay
• Ependymal/Subependymal Veins (Mimic)
o Normal periventricular venous structures
may become engorged with various
pathologies
Multiple Sclerosis Multiple Sclerosis
I
Axial Tl C+ MR shows numerous enhancing MS
plaques in the periventricular ~ & subcortical white
Axial T1 C+ MR shows characteristic tumefaClive MS
plaque with i((egula, thick, partial ring enhancement &
3
matter. Note typical lack of mass effect. ADEM & Lyme
disease may be idenUcal.
mass effect =. These lesions may cross the corpus
callosum & mimic tumors.
59
(/)
c PERIVENTRICULAR ENHANCING LESIONS
.Q
Ol
<ll
0:::
ADEM lymphoma, Primary eNS

shows numerous foci of
enhancement in the
subcortical & perivenlricular
white matter. Fuzzy
enhancing margins are
typical for demyelination.
ADEM typically follows an
infection or vaccination.
shows homogeneous
enhancement within multiple
perivenlricular white maller
~ foci. Lack of significant
surrounding T2 abnormality
(not shown) & mild mass &
corpus callosum involvement
is common.
Glioblastoma Multiforme
(Leh) Axial T1 C+ FS MR
shows a large
occipital lobe mass with
central necrosis. Note
extension across the
splenium of the corpus
ca/Josum B characteristic
of glioblastoma multiforme.
(Right) Axial T1 C+ FS MR
shows a ring enhancing mass
~ in the left frontal lobe.
Thin walled enhancement is
typical of abscess; note
impending intraventricular
ruplUre~.
Germinoma
shows multifocal masses
with ring-enhancement =.
Nodular enhancement is also
frequently seen EJ.
Toxoplasmosis often lacks
restricted diffusion on MR,
unlike most abscesses.
shows a large mixed solid &
cystic heterogeneously
enhancing mass involving
the right basal ganglia ~.
Up to 10% of CNS
germinomas arise within the
basal ganglia.
I
3
60
PERIVENTRICUlAR ENHANCING lESIONS en
"
r::
Ql
::l
0-
OJ
.,
Ql
::l
enhancing lesions in the
periventricuJar while maller
~ in this patient with a
history of breast cancer.
shows patchy mullifocal
enhancement consistent with
subacute inFarcts in this
patient with lupus vasculitis.
Vasculitis is often in the
cortical & subcortical white
matter, although basal
ganglia involvement is ;0
CD
common. Associated OWl <0
restriction may be seen. o
::l
'"
Lyme Disease Ependymoma

multifocal punctate foci of
=
perivenlricular enhancement
with associated T2
hyperintensity (not shown)
without significant mass
effect This pattern mimics
MS and ADEM. (Right) Axial
NECT shows a left
perivenlricular enhancing
mass = with small cystic
areas E1 that are commonly
present. [pendymomas more
commonly are in or near the
4th ventricle but may be
supratentorial (1/3 of cases).
Calcifications are seen in
50%.
Susac Syndrome Alexander Disease

(Left) Sagittal FlAIR MR
shows multiple hyperintense
lesions in the corpus
callosum, typical for Susac
syndrome & MS. Enhanced
scans typically show
leptomeningeal
T7 C+ MR shows
characteristic near-tota/lack
of while matter myelination
= & striking enhancement
of the deep peri ventricular
white matter a These
patients usually present with
a large head.
I
3
61
en INTRAVENTRICULARCAlCIFICATlON(S)
c
.Q
C)
Q)
0:: • Nodular calcified (healed) stage: Small,
Cll
:::J
Ca++ nodules
tl
.;:
Common o Typically subarachnoid spaces; may
C
Q)
• Physiologic Calcification, Choroid Plexus involve cisterns> parenchyma> ventricles
>
.;: • Choroid Plexus Cyst o Intraventricular cysts are often isolated;
Q)
0... • Neurocysticercosis 4th ventricle most common
en
Q)
• Neurofibromatosis Type 2 o Most common cause of cerebral Ca++
"0
.;:
• Tuberous Sclerosis Complex under 30 years
C less Common • Neurofibromatosis Type 2
Q)
> • Meningioma o Nonneoplastic cerebral Ca++ is
• Ependymoma uncommon manifestation

• Intraventricular Hemorrhage (Mimic) o Extensive choroid plexus Ca++ > cortical
• Choroid Plexus Papilloma surface Ca++ > ventricular lining Ca++

• Subependymal Giant Cell Astrocytoma • Tuberous Sclerosis Complex
:::J
• Subependymoma o Ca++ subependymal nodules (SEN), 98% of
.>0:
C/)
• Central Neurocytoma patients
• Cavernous Malformation • Along caudothalamic groove> atrial> >
• TORCH, General (Mimic) temporal
• 30-80% of SEN enhance, best seen on MR
Rare but Important o Cortical/subcortical tubers, WM lesions
• Medulloblastoma (PNET-MB) 70-95%
• Craniopharyngioma Helpful Clues for less Common Diagnoses
• Meningioma
o Calcified (20-25%): Diffuse, focal,
ESSENTIAL INFORMATION sand-like, sunburst, globular, rim
o Approximately 1% are intraventricular
o Most common in left lateral ventricle
• Ependymoma
o Soft or "plastic" tumor: Squeezes out
through 4th ventricle foramina
o Ca++ common (50%)
o 2/3rd infratentorial, arise from floor of 4th
o Hydrocephalus common; ± cysts,
hemorrhage
• Intraventricular Hemorrhage (Mimic)
o Typically associated with trauma
o May be primary presentation of AVM
o Acutely, hyperdense blood may mimic
intraventricular Ca++
o May result in Ca++ in chronic phase
o Intraventricular, papillary neoplasm
derived from choroid plexus epithelium
o Child with strongly enhancing, lobulated
intraventricular mass; Ca++ in 25%
o 50-70% - atrium of lateral ventricle
o 4th ventricle most common site in adults
• Sub ependymal Giant Cell Astrocytoma
o Enhancing mass at foramen of Monro
I o Ca++ common; hydrocephalus common
o Occurs in 15% of TSC patients
3
62
INTRAVENTRICULAR CALCIFICATlON(S) (J)
""r::
• Subependymoma o Ca++ in up to 20%

o Rare, benign, well-differentiated, and o Small tumor cysts/necrosis in 40-50%
intraventricular, ependymal tumor • Choroid Plexus Carcinoma
o T2 hyperintense lobular, nonenhancing o Child < 5 y, with enhancing
intraventricular mass intraventricular mass & ependymal
o May see cysts, hemorrhage, Ca++ invasion
o Inferior 4th (60%) > lateral ventricle o Ca++ in 20-25%
• Central Neurocytoma o Almost all in lateral ventricle
o Typical "bubbly" appearance; Ca++ o May see necrosis, cysts & hemorrhage
common • Craniopharyngioma
o Lateral ventricle, attached to septum o Partially Ca++, partially solid, cystic
pellucidum suprasellar mass in a child
o Moderate to strong enhancement o Typically sellar & suprasellar
• Cavernous Malformation o Rare within third ventricle
o Rarely intraventricular, 2.5-11 % of cases
o Ca++ & T2 hypointense hemosiderin rim
• Calcified intraventricular mass: Adult
common o Meningioma (lateral ventricle)
o Enhancement variable
o Subependymoma (4th> lateral ventricle)
• TORCH, General (Mimic) o Central neurocytoma (lateral ventricle)
o Acronym for congenital infections caused
o Cavernous malformation
by transplacental transmission of o Neurocysticercosis (4th ventricle)
pathogens • Calcified intraventricular mass: Child
o Taxa, CMV, HIV, & rubella cause
o Ependymoma (4th ventricle)
parenchymal &/or periventricular Ca++ o Choroid plexus papilloma (lateral> 4th
Helpful Clues for Rare Diagnoses ventricle)
• Medulloblastoma (PNET-MB) o Subependymal giant cell astrocytoma
o Malignant, invasive, highly cellular (foramen of Monro)
embryonal tumor o Medulloblastoma (4th ventricle)
o 4th ventricle tumor, arise from roof o Craniopharyngioma (3rd ventricle)
(superior medullary velum)
o Hydrocephalus common (95%)
o 90% hyperdense related to high
nuclear:cytoplasmic ratio
Physiologic Calcification, Choroid Plexus Choroid Plexus Cyst
I
Axial NECT in a padent who presented following
trauma. Note symmetric physiologic Ca++ ~ in the
Axial CECT shows bilateral choroid plexus cysts
(xanthogranulomas), a common incidental finding in
3
auia of the lateral ventricles in this young patient. older patients. The cysts are calcified =::I & show mild
rim-enhancement.
63
C/)
c INTRAVENTRICULAR CAlCiFICATION(S)
.Q
OJ
Q)
0:::
(Left) Axial T2' CRE MR

shows mullifocal Ca++ in
this patient with nodular
calcified NCe. Note focal
C/) intraventricular Ca++
Q)
u
·C
Ca++ typically occur at
convexity subarachnoid
CQ) spaces. (Right) Axial N[CT
> shows globular Ca++ within
C the ventricles in unusual
nl locations (foramen of
•....
1IJ Monro). In a young patient,
"C the presence of extensive
c &/o( unusual intraventricular
nl
Ca++ suggests NF2.

bilateral Ca++
subependymal nodules in
this tuberous sclerosis
patient. These occur along
caudothalamic groove, atria,
& temporal horns. 50%
calcify; progressive after I
year. (Right) Axial NECT
shows a hyperdense mass
with central ~ & rim
Ca++ in the left lateral
ventricle. Note associated
ventricular enlargement ~.-
Approximately I % of
meningiomas are
intraventricular.

partially calcified mass
within the 4th ventricle.
Ependymomas often partially
calcify (50%) &
characteristically extrude
through the 4th ventricular
foramen. (Right) Axial N[CT
shows a lobulated mass in
the atrium of the lateral
ventricle with focal Ca++
81. Note the marked
expansion & septation of the
lateral ventricle =.
I
3
64
I NTRAVENTRICU LAR CALCIFICATION (5) C/l
"
c:
Ql
:J
Co
..,
lJl
Ql

:J
calcified foramen or Monro <
<t>
mass 81. Note dilated lateral ;:l.
ventricle indicating :::!.
Cl
ventricular obstruction. CO
Often, hydrocephalus is first en
presentation of tuberous
sclerosis. (Rigl1t) Axial NECT
shows a densely calcified 4th
ventricular mass. Although
rare in subependymomas,
Ca++ is more commonly
seen in 4th ventricle
subependymomas and in ;:0
<t>
very large subependymomas. CO
o'
:::l
en
Central Neurocytoma Cavernous Malformation

variant case of a solid central
neurocytoma with no cystic
component Note mass at
the foramen of Monro with a
focal Ca++ =11. Lack of cysts
suggests a subependymoma
or SCCA (Right) Axial NECT
shows a hyperdense mass
centered in the lateral
ventricles with rim Ca++ m.
The mass consists of multiple
I'focu/es" or "cysts"
consistent with hemorrhages
of different ages.
Medulloblastoma (PNET-MB)
~eft)Ax~/NECTshowsa
large, 4th ventricular mass
I:llIthat is higher in
attenuation than brain
parenchyma. Note a small
focus of Ca++ 81 &
hydrocephalus in this child
with medulloblastoma.
(Right) Axial NECT shows a
hypodense mass centered
over a 3rd ventricle with a
delicate rim of Ca++ 1:llI.
Craniopharyngiomas are
typically sellar & suprasellar,
but they rarely occur in the
third ventricle.
I
3
65
(/)
c PERIVENTRICULAR CALCIFICATION
o
OJ
Q)
0::: DIFFERENTIAL DIAGNOSIS o Consider congenital HIV if bilateral
symmetric basal ganglia C++ identified in
Common child> 2 months old!
• TORCH, General o If congenital infection is diagnostic
o CMV, Congenital consideration, obtain NECT to detect Ca++
o Toxoplasmosis, Congenital • CMV, Congenital
(/) o Herpes Encephalitis, Congenital o Most common cause of intrauterine
Q)
u o HIV, Congenital infection in USA

·CO
C o Rubella, Congenital o Timing of infection predicts pattern of
Q)
> • Tuberous Sclerosis Complex damage

c o Hypomyelination
Less Common
•..
C1l
lrl • Neurocysticercosis o Cortical gyral anomalies
o Microcephaly
"c
C1l
• Tuberculosis
• Ventriculitis (Chronic) o Symmetric periventricular Ca++ in 30-70%
• Germinal Matrix Hemorrhage • Toxoplasmosis, Congenital

o Periventricular & scattered Ca++
Rare but Important o Hydrocephalus (colpocephaly-like)
• Radiation and Chemotherapy • Herpes Encephalitis, Congenital
• Pseudo-TORCH o Calcification pattern varies in HSV2
o Aicardi-Goutieres Syndrome
• Asymmetric periventricular
o Coats-Plus Syndrome
• Scattered periventricular and deep gray
• Subcortical white matter & cortex
ESSENTIAL INFORMATION • Calcification pronounced in foci of
hemorrhagic ischemia
Key Differential Diagnosis Issues • Like rubella, rare cause of "stone brain"
• Look for associations o Brain atrophy or cystic encephalomalacia
o Brain destruction
• Focal or diffuse
o Malformations
• HIV, Congenital
o Other loci of calcification o Vertical HIV infection
o History
o Basal ganglia Ca++, atrophy
Helpful Clues for Common Diagnoses o Consider congenital HIV if bilateral
• TORCH, General symmetric basal ganglia C++ identified in
o Classic acronym for congenital infections child> 2 months old!
• Caused by transplacental transmission of • Rubella, Congenital
pathogens o Periventricular and scattered
• TOxoplasmosis, Rubella, o Scattered or hazy basal ganglia Ca++
Cytomegalovirus, Herpes o Rare "stone brain"
• All cause parenchymal Ca++ • Extensive gyral calcification & gliosis
• Most can cause lenticulostriate o Micro-infarcts
mineralization, vasculopathy • Tuberous Sclerosis Complex
• Some (CMV) cause migrational defects o Look for cutaneous markers of TS
• Some (syphilis, herpes) cause meningitis, o Subependymal nodules
meningoencephalitis • Variable-sized periventricular
• Some (e.g., CMV) cause germinolytic calcifications
cysts o Cortical tubers also calcify
• Others (e.g., rubella, HSV) cause striking Helpful Clues for Less Common Diagnoses
lobar destruction/encephalomalacia • Neurocysticercosis
o Congenital HIV, syphilis also considered
o Best clue: Dot inside cyst
part of TORCH o Usually convexity subarachnoid space
I o Also gray-white junction, intraventricular
o Nodular calcified (healed) stage
3
66
PERIVENTRICULAR CALCIFICATION C/l
"
c:
III
• Shrinks to small Ca++ puncta or nodule o Coats-Plus Syndrome :l
Q.
• Tuberculosis • a.k.a., cerebroretinal microangiopathy
o Best diagnostic clue: Basal meningitis and with calcifications and cysts (CRMCC)
...
OJ
III
pulmonary TB :l
• Ocular coats: Retinal telangiectasia &
o Acute exudate
• Typically basal meningitis • CNS small blood vessel calcification
• ± Localized CNS tuberculoma • Extensive thalamic and gyraJ
o Chronic calcification
• Residual pachymeningeal • Defects of bone marrow & integument
• ± Localized Ca++ • Growth failure
o "Target sign"
• Calcification surrounded by enhancing
SELECTED REFERENCES
rim (not specific)
1. Briggs TA et al: Cerebroretinal microangiopathy with ;;u
• Ventriculitis (Chronic) calcifications and cysts (CRMCC). Am J Med Genet A.
Cll
(Q
o Areas of prior hemorrhagic infarction I 46A(2): 182-90, 2008 o·
:l
prone to dystrophic calcification 2. Crow YJ et al: Aicardi-Goutieres syndrome: an important (/)
Mendelian mimic of congenital infection. Dev Med Child

• Germinal Matrix Hemorrhage Neural. 50(6):410-6, 2008
o Occasional ependymal, germinal matrix 3. Rice G et al: Clinical and molecular phenotype of
calcific foci Aicardi-Goutieres syndrome. Am J Ilum Genet.
81(4):713-25,2007
Helpful Clues for Rare Diagnoses 4. Linnankivi T et al: Cerebrorelinal microangiopathy with
calcifications and cysts. Neurology. 67(8):]437-43, 2006
• Radiation and Chemotherapy 5. Abdel-Salam GM et al: Aicardi-Goutieres syndrome: clinical
o History! and neuroradiological findings of ]0 new cases.Acta
Paediatr. 93(7):929-36, 2004
o Mineralizing microangiopathy
6. Malinger Get al: Fetal cytomegalovirus infection of the
• Pseudo-TORCH brain: the spectrum of sonographic findings. AJNR Am J
o Aicardi-Goutieres Syndrome Neuroradiol. 24(1):28-32, 2003
7. Numazaki K et al: Intracranial calcification with congenital
• "Mendelian mimic of congenital rubella syndrome in a mother with serologic immunity. J
infection" Child Neurol. 18(4):296-7, 2003
• Multifocal punctate calcifications 8. Tanaka F et al: Association of osteopontin with ischemic
axonal death in periventricular leukomalacia. Acta
• Variable locations including Neuropathol. 100(1):69-74,2000
periventricular white matter, basal
ganglia, dentate nuclei
• Elevated CSF interferon (IFN-a)
• TREXI mutations in some
CMV, Congenital CMV, Congenital
I
Coronal NECT shows classic findings of TORCH. Note
linear periventricular Ca++ ~ with scattered Ca++ foci
Sagittal T2WI MR shows a thick cortex with small gyri,
hyperintense white maNer and a thin layer of 3
within cortex 1m in this deaf child, suggesting prior calcification!J:.:l in the same 18 month old deaf toddler.
intrauterine CMV exposure.
67
PERIVENTRICUlAR CALCIFICATION
'"c:o
OJ
Ql
0:::

basal ganglia SII and
perivenuicular calcifications
~ in a child with typical
colpocephalic dilation of the
U
'"
Ql
ventricles. (Right) Coronal
'C T2WI MR shows marked
C ventriculomegaly and loss of
Ql
> the perivenlricular while
c: malter. The periventricular
III and basal ganglia
•....
al calcifications are occult on
"0 MR but do involve the right
c: choroid plexus glomus
III

scattered and peri ventricular
calcifications. In this child,
there is unilateral left-sided
colpocephaly~. Note
severe cortical mantle
thinning SII over the
cofpocephalic ventricle.
(RighI) Axial T2' GRE MR
shows similar findings,
although the calcifications
e:I are not as well-visualized.
(Left) Axial NEeT in child

who survived congenital
herpes encephalitis shows
scattered parenchymal
calcifications ~. (Right)
Axial NECT in same patient
shows calcifications of the
infarcted Rolandic cortex SII.
They can be variable,
predominantly involving
damaged brain.
I
3
68
PERIVENTRICUlAR CALCIFICATION CJl
"
C
Rubella, Congenital
hazy, symmetric basal
ganglia calcification =with
diffusely prominent sulci and
cisterns consistent with
volume loss. In this one year
old, the findings are highly
suggestive of congenital I II V.
(Right) Axial NEeT shows
basal ganglia calcifications
81 and diffuse white matter
hypoinlensily. There are faint
bilateral subependymal
calcifications lining the
posterior horns =.

(Left) Sagittal ultrasound in
child with TSC,
subependymal giant cell
astrocytoma shows mass
indenting lateral ventricle
B. Tumor shows increased
echogenicity =.
(Right)
Axial NECT shows variable
calcification in the
subependymal nodules.
Calcification in these lesions
progresses over lime.

disseminated "miliary" form
of neurocysticercosis (NCC).
Note numerous cysts, each
with a hyperdense central
"dot" representing scolex
=. Innumerable small
calcific foci, some of which
are peri ventricular Eel cause
classic "starry sky"
appearance of healed NCe.
(Right) Axial T2' CRE MR
show scattered calcifications
throughout the brain. A few
are in the deep gray
structures =
and one is
intraventricular ~.
I
3
69
en PERIVENTRICULAR CALCIFICATION
c
.Q
Ol
Q)
0::
~
ro
:J
U
.0: Tuberculosis Tuberculosis
C
Q)
>
.0:
nodular calcification E2
Q) along the postero-medial
CL temporal lobe on the
en tentorial surface. (RighI)
=
Q)
u Axial CECT in same patient
E shows the calcification to
c be largely obscured by the
Q)
> thick rind of pachymeningeal

and leptomeningeal
thickening and enhancement
H2.
:J
-'"
III
(Leh) Axial T7 WI MR early in

the course of the disease
shows hemorrhagic
infarction H2 of the
ependyma and
subependymal brain. (RighI)
Axial NECT shows
subependymal tissue
necrosis and calciFication in
the same areas m.
Germinal Matrix Hemorrhage Radiation and Chemotherapy

aeft)Ax~/N[CTshows
while matter deficiency due
to perivenlricular
leukomalacia. The gray
matter I!:'J nearly
approximates the ventricular
surface. Small perivenlricular
calcifications Ea are present
at the site of prior germinal
matrix hemorrhage. (Right)
Axial NECT shows bilateral
symmetric calcifications at
the gray-white junction H2
due to mineralizing
microangiopathy following
radiation and chemotherapy.
I
3
70
PERIVENTRICULAR CALCIFICATION en
:0:-
r::
III
::s
Q.
.,
OJ
Radiation and Chemotherapy Aicardi-Goutieres Syndrome III
(Left) Axial T2WI MR from ::s

the same patient shows <
en
while mailer demyelination
;:!.
l:l:I. The calcificalions are ::::!.
Cl
occult. (Right) Axial NECT CD
(f)
shows brain alrophy and
bilaleralsymmelrical
calcifications in the basal
ganglia ~. Extension into
the corona radiata (nol
shown) was also present
;;u
en
to
o
::J
(f)
Aicardi-Goutieres Syndrome Aicardi-Goutieres Syndrome

shows extensive abnormal
signal of white maller and
volume 1055of gray & while
matter. Faint calcifications
~ are presenl, allhough
they are less well seen on
MR lhan on NECT (Right)
Coronal T2WI MR again
shows severe volume loss.
Faint perivenlricular
calcificalions ? and basal
ganglia calcificalions ~ are
present, mimicking the
appearance of TORCH
infections.
Coats-Plus Syndrome Coats-Plus Syndrome

extensive Byra!, brainstem,
and perivenlricular
calcifications. The brainstem
is also swollen ~ and low
density. Note post-operative
change of lhe righl globe.
dense perivemricular
calcification that extends to
involve the sparse
subcortical white maller
posleriorlya lhe fronlal
while maller, cortex, and
lhalami~. The pal/ern of
calcification is lypical,
although swelling occurs
first.
I
3
71
CI)
c PERIVENTRICUlAR T2/HAIR HYPERINTENSE lESIONS
o
Ol
(!)
0:: • Multiple Sclerosis
C1l
:::J
o Linear/ovoid callosal & perpendicular
U
·C
Common caIJososeptallesions
C
(!)
• Aging Brain, Normal • Infratentorial (esp. brachium pontis,
>
·C • Arteriolosclerosis brainstem), optic nerve, spinal cord
(!)
0.. • Multiple Sclerosis o T1 MR: Hyperintense rim: Chronic plague
CI)
(!)
• ADEM o T1 C+ MR: Enhancement with active
u • Diffuse Axonal Injury (DAI) disease: Nodular> ring> semilunar
E • Metastases, Parenchymal
c • ADEM
(!)
> less Common o Lesions have less mass effect than expected
c: for size; BG lesions common
• Radiation and Chemotherapy
~
'" o T1 C+ MR: Enhancement & appearance
aJ • Periventricular Leukomalacia (PVL)
"0
c: • Lyme Disease may mimic MS; often need flu exam
'" • Vasculitis o Clinical: Viral prodrome or recent
• Obstructive Hydrocephalus vaccination; monophasic
• Drug Abuse • Diffuse Axonal Injury (DAI)
• CADASIL oGRE: Multiple "black dots" at gray/white
• Susac Syndrome interface, CC, deep gray matter, brainstem
o Clinical: Trauma patient
Rare but Important • Metastases, Parenchymal
• Metachromatic Leukodystrophy (MLD) o T1 C+ MR: Multiple enhancing masses at
• X-Linked Adrenoleukodystrophy gray/white interface
• Mucopolysaccharidoses o T2/FLAIR: Hyperintensity has mass effect
• TORCH Infections (vasogenic edema)
ESSENTIAL INFORMATION • Radiation and Chemotherapy
Key Differential Diagnosis Issues o Numerous appearances based on injury
• Peri ventricular T2/FLAIR hyperintense • Periventricular leukoencephalopathy:
lesions are often nonspecific, with Confluent T2 hyperintensity, spares
significant overlap among etiologies subcortical V-fibers & CC
• These guestions help narrow differential • PRES: Symmetric posterior circulation
o How old is the patient? subcortical/peri ventricular T2
o Volume loss vs. mass effect? hyperin tensi ty
o Are there T2 * GRE "black dots"? • Radiation necrosis: Vasogenic edema
o Is there enhancement? surrounds irregular, enhancing lesion(s)
o Is the corpus callosum (CC) involved? • Periventricular Leukomalacia (PVL)
o Are the basal ganglia involved? o Early: Periventricular cystic changes
o Late: Undulating ventricular borders,
Helpful Clues for Common Diagnoses ventriculomegaly, WM volume loss
• Aging Brain, Normal o Clinical: Pre term birth, spastic diplegia,
o Smooth, thin rim of peri ventricular visual & cognitive impairment
hyperintensity, wide sulci, prominent • Lyme Disease
ventricles o T1 C+ MR: Multiple enhancing cranial
o Sparing of cortex, subcortical/deep white nerves; CN7 common
matter (WM) & basal ganglia (BG) o WM lesions may be identical to MS
• Arteriolosclerosis o Clinical: Meningoencephalitis, ± history of
o Patchy confluent & focal lesions; skin rash (erythema migrans); higher
subcortical/deep WM & BG involved; ± prevalence in New England
cortical infarcts • Vasculitis
I oGRE: Associated "black dots" (overlap with
chronic hypertension & amyloid)
o Restricted diffusion in acute phase
3
72
PERIVENTRICULAR T2/FLAIR HYPERINTENSE LESIONS CIl
~
c:
III
o T2/FLAIR MR: Ranges from normal to Helpful Clues for Rare Diagnoses
::l
Co
patchy asymmetric hyperintensity in • Metachromatic Leukodystrophy (MLD): tll
....•
multiple small vessel territories Confluent "butterfly-shaped" cerebral
III
::l
o DSA: Regions of alternating stenosis & hemispheric WM T2 hyperintensity
dilatation primarily involving 2nd, 3rd <
CD
• X-Linked Adrenoleukodystrophy: ~
order branches Enhancing peri-trigonal WM demyelination
....•
~
• Obstructive Hydrocephalus • Mucopolysaccharidoses: T2 hyperintensity CD
o Periventricular "halos": Fingers of CSF-like surrounds dilated MPS-filled PVS '"

hyperintensity most pronounced at • TORCH Infections: Variable WM T2
ventricular horns hyperintensity, ± calcification
o Ventricles dilated without sulcal widening
or cortical volume loss Alternative Differential Approaches
• Drug Abuse • Patient age
o Elderly: Normal aging, arteriolosclerosis, ;0
o Confluent peri ventricular WM; CD
<C
corticospinal tract & deep grey matter; metastases o·
::l
often hemorrhagic o Young adult: MS, ADEM, vasculitis, drug
abuse, CADASIL '"
o Cerebellar involvement in absence of
hypertension, characteristic of inhaled o Infant to child: ADEM, PVL, MLD, TORCH
heroin ("chasing the dragon") • Volume loss vs. mass effect
o Can cause a vasculitis o Volume loss: Normal aging,
• CADASIL arteriolosclerosis, MS, PVL, CADASIL

o Subcortical lacunar infarcts & o Mass effect: MS (active), ADEM,
leukoencephalopathy in young adult metastases, obstructive hydrocephalus
o Anterior temporal pole & external capsule • T2 * GRE "black dots" present
lesions highly sensitive/specific o Arteriolosclerosis, DAI, periventricular
o Frontal lobe has highest lesion load leukoencephalopathy (+ radiation-induced
• Susac Syndrome vascular lesions), chronic hypertension
o Central CC > callososeptallesions • Enhancement: MS, ADEM, Lyme disease,
o WM lesions may be identical to MS metastases, radiation necrosis
o Clinical triad: Encephalopathy, hearing • Corpus callosum involved: MS, ADEM, DAI,
loss, branch retinal artery occlusions Susac syndrome
• Basal ganglia involved: Arteriolosclerosis,
ADEM, DAI, vasculitis, drug abuse
I
Axial FLAIR MR shows prominent venlric/es, wide
cortical sulci, and a thin rim of periventricular while
Axial FLAIR MR shows confluent periventricular and
subcortical hyperintensity, focal right thalamus SI and
3
matter hyperintensity 1:::1 in an elderly individual. left putamen I!:ll hyperintensity with diffuse white
malLer volume 1055.
73
(/)
c PERIVENTRICULAR T2/FLAIR HYPERINTENSE LESIONS
o
Ol
Ql
ex:
Multiple Sclerosis
multiple
subcortical
callososeptal ~
=-
perivemricular
and
f
(/) hyperintense lesions. The

Ql
C3 perpendicular orientation at
·C
the callososeptal interface is
C along the penetrating
Ql
> venules (Dawson fingers).
C (Right) Axial FLAIR MR
shows a typical ADEM with
•...
III
lD numerous bilatera/,
'0 asymmetric ffocculent
c lesions. Lesions are typically
III
bilateral but asymmetric with
enhancemenl. Lesions often
exhibilless mass effect than
expected for size.
Diffuse Axonal Injury (DAI) Metastases, Parenchymal

hyperintensity in corpus
callosum splenium SI
caused by axonal injury. GRE
scan (not shown) disclosed
some focal hemorrhages.
shows two hyperintense
lesions It] representing lung
metastases that showed
enhancement following
contrast. Without contrast, it
may be difficult to
differentiate these lesions
from other WM diseases.
Radiation and Chemotherapy Periventricular leukomalacia (PVl)

treatment-related
leukoencephalopathy of the
periventricular & subcortical
WM with sparing of the
subcortical U-fibers ~ and
corpus callosum, which is
characteristic of this type of
injury. (Right) Axial T2WI
MR shows the typical
"square comers" of
periventricular leukomalacia
of prematurity at the junction
of the body and trigones of
the lateral ventricles ~. Also
note the typical
periventricular hyperinlensily
I SI
3
74
PERIVENTRICULAR T2/FLAIR HYPERINTENSE LESIONS CIl
"
c:
=
III
:l
C.
..•
OJ
III
Lyme Disease Vasculitis
:l
multifocal hyperintense <
CD
lesions in the subcortical &
perivenlricular WM & corpus ~
callosum =. Lesions did not ~
CD
enhance following contrast.
Lyme disease often mimics
'"
MS & can be confirmed with
laboratory tests such as PCR
& ELISA. (Right) Axial T2WI
MR shows multiple foci of
high signal in the
peri ventricular WM
basal ganglia caused by
= &
;u
CD
chemical vasculitis. These T2 CO
lesions are often associated o·
:J
with restricted OWl in acute
phase. '"
fingers of hyperintensity most
pronounced at the
ventricular horns ~ related
to transependymal flow of
CSF. The ventricles are
dilated without widening of
the cortical sulci. (Right)
Axial FLAIR MR shows
symmetric corticospinal tract
a corpus callosal &
confluent perivenlricular =
hyperintensity, often found
in drug-induced
leukoencephalopathy.
CADASIL Susac Syndrome

hyperintensity & volume 1055
in the subcortical anterior
temporal=&
periventricular WM in a 32
year old male with CADASIL,
confirmed by chromosomal
analysis. (Right) Sagiltal
fLAIR MR shows central
corpus callosum
hyperintensities = with
relative sparing of the
callososeplal imerface. Susac
syndrome often mimics MS
on MR but has a clinical
triad which confirms the
diagnosis.
I
3
75
SECTION 4
Extra-Axial Spaces and
Subarachnoid Cisterns
Cistern, Subarachnoid Space Normal Variants 1-4-2
Epidural Mass, Brain 1-4-4
Enlarged Sulci, Generalized 1-4-8
Effaced Sulci, Generalized 1-4-12
Effaced Sulci, Focal 1-4-16
Interhemispheric Fissure Cysts 1-4-20
CPA Mass, Adult 1-4-24
Cystic CPA Mass 1-4-28
Prepontine Cistern Mass 1-4-32
Cisterna Magna Mass 1-4-38
Foramen Magnum Mass 1-4-42

Enhancing Cranial Nerve(s) 1-4-46
CSF-like Extra-Axial Fluid Collection 1-4-50
CSF-like Extra-Axial Mass 1-4-52
Sulcal/Cisternal Enhancement 1-4-54
Fat in SulcijCisterns/Ventricles 1-4-58

Extra-Axial Flow Voids 1-4-60
T1 Hyperintense CSF 1-4-62
FLAIRHyperintense CSF 1-4-64
T2 Hypointense Extra-Axial Lesions 1-4-68
Hyperdense CSF 1-4-72
Hyperdense Extra-Axial Mass(es) 1-4-74
Hypodense Extra-Axial Mass(es) 1-4-76
C/l
C
~
CISTERN, SUBARACHNOID SPACE NORMAL VARIANTS
OJ
Ui
U • MR Artifacts, Flow-Related
"0 DIFFERENTIAL DIAGNOSIS
o o CSF flow artifact is common in basal
c Common
-'u
" cisterns, ventricles
ctl
~ • Cavum Septi Pellucidi (CSP) o Commonly seen on FLAIR MR
ctl
.n • Mega Cisterna Magna o Artifact often extends outside skull
:::J
(f) • MR Artifacts, Flow-Related • Enlarged Subarachnoid Spaces
"0
c • Enlarged Subarachnoid Spaces o Idiopathic enlargement of subarachnoid
ctl
C/l
OJ Less Common spaces (SAS) during first year of life
<J
ctl • Cavum Velum Interpositum (CVI) o Increased head circumference (> 95%)
a.
(f)
• Enlarged Optic Nerve Sheath a Resolves without therapy by 12-24 months
ctl
'x Rare but Important Helpful Clues for Less Common Diagnoses
ctl,
ctl
~ • Blake Pouch Cyst • Cavum Velum Interpositum (CVI)
X • Liliequist Membrane o Triangular-shaped CSF space between
W
r::
bodies of lateral ventricles, below fornices,
<ll
•... above 3rd ventricle
[0 ESSENTIAL INFORMATION o Often elevates, splays fornices & causes
"0
r:: Key Differential Diagnosis Issues inferior displacement of internal cerebral
<ll
• Normal variants have CSF density/intensity veins & 3rd ventricle
• Important to recognize normal variants & • Enlarged Optic Nerve Sheath
not mistake for more ominous pathology o May occur as normal variant
o Occurs in idiopathic intracranial
Helpful Clues for Common Diagnoses hypertension (pseudotumor cerebri), NFl
o Elongated finger-shaped CSF collection Helpful Clues for Rare Diagnoses
between frontal horns of lateral ventricles • Blake Pouch Cyst
o Posterior continuation between fornices o Failure of regression of Blake pouch cyst
often associated (cavum vergae) causes compression of basal cisterns
• Mega Cisterna Magna o Free communication of 4th ventricle with
o Enlarged cisterna magna communicates prominent inferior CSF space
freely with 4th ventricle & basal cisterns • Liliequist Membrane
o Large posterior fossa o Thin arachnoid membrane separates
o Normal vermis suprasellar, interpeduncular, & prepontine
o Cistern crossed by falx cere belli, tiny veins cisterns
o Occipital bone may appear scalloped
Cavum Septi Pellucidi (CSP)
I
4 Axial T1WI MR shows a cavum sepli pellucidi =
posterior extension into a cavum vergae B, seen as a
with Sagiaal T1WI M R shows a prominent retrocerebellar
CSF space Sl a mega cisterna magna. This normal
CSF-signalcollection that lies between the bodies of the variant requires no lreatment. Note normal vermis & 4th
lateral ventricles. ventricle.
2
CISTERN, SUBARACHNOID SPACE NORMAL VARIANTS CII
:>:"
c:
Ql
::l
a.
..•
OJ
Ql
::l
(Left) Axial TlWI MR shows
a mega cisterna magna ~ m
with scalloping & remodeling ..•~
of the adjacent occipital ,
Q)
Q)
bone, likely related to CSF ~.
pulsation. (Right) Axial fLAIR Q)
MR shows flow artifact in the CII

-0
3rd ventricle &. foramen of
Monro =, which can mimic
Ql
()
C1>
a mass. This artifact is often Ul
Q)
seen on FLAIR MR & can be ::J
confirmed on spin echo a.
sequences (T!). UJ
c:
0-
Ql
~
Q)
()
::T
::J
o
Ci
o
Ul
en~
::J
Cavum Velum Interpositum (CVll Ul
(Left) Axial T2WI MR

frontal CSF spaces.
Flow-voids due La traversing
veins ~ are seen,
conFirming that these are
enlarged subarachnoid
spaces & not subdural or
epidural collections. This
condition typically resolves
without therapy. (Right)
CVI =
Sagittal T! WI MR shows a
that flattens the
internal cerebral veins ::> &.
compresses the
quadrigeminal cistern ~.
Inferior displacement of the
3rd ventricle is also typical.
Enlarged Optic Nerve Sheath Blake Pouch Cyst

prominent, dilated optic
nerve sheaths & flattened
orbits. While patulous optic
nerve sheaths can occur as a
normal variant, the imaging
findings together with clinical
presentation are consistent
with idiopathic intracranial
hypertension. (Right) Axial
T2WI MR shows an enlarged
posterior fossa & Blake
pouch cyst ~ The vermis is
typically rotated but normal
in these patients.
I
4
3
en
c
~ EPIDURAL MASS, BRAIN
OJ
tl
u • "Swirl sign" from rapid bleeding,
"
"0
c Common
unretracted clot
.r:
u o Arterial EDH = 90%
ro
~ • Epidural Hematoma • With fracture, nearly always secondary to
ro
.0 • Meningioma MMA groove fracture
:J
(/) • Dural Metastasis o Venous = 10%
"
c
ro less Common • Adjacent to venous sinus
en • Meningioma
OJ • Lymphoma
u
ro • Neurosarcoid o Hyperdense (70-75%) because of tightly
Cl.
(/)
• Epidural Empyema packed cells ± calcification
ro o Homogeneous intense enhancement (>
"X Rare but Important
ro, 90%)
ro
~ • Tuberculoma o Vascular pedicle common/increased
X • Plasmacytoma
w vascular markings
C • Meningioma, Atypical and Malignant o Underlying hyperostosis may be present
ltl
~ • Hemangiopericytoma o Peritumoral edema (60%)
cc • Extramedullary Hematopoiesis
1:1 o MRS: Elevated alanine on short TE
c • Leukemia
ltl • Dural Metastasis
• Gliosarcoma
:J o Underlying bone destruction/scalp
.:.: • Rosai-Dorfman Disease
1Il involvement common
• Langerhans Cell Histiocytosis • Fat-saturation helpful to distinguish
• Neurosyphilis enhancement from normal hyperintense
marrow and scalp fat
ESSENTIAL INFORMATION o Often multiple lesions
o Often diffuse nodular enhancement
Key Differential Diagnosis Issues o Primary malignancy
• Pattern of enhancement • Breast, lung, melanoma, prostate most
o No enhancement: Hematoma common
o Rim enhancement: Abscess, rarely
leukemia Helpful Clues for less Common Diagnoses
o Heterogeneous enhancement: Atypical or • Lymphoma
malignant meningioma, o Dural-based lesions usually related to
hemangiopericytoma, gliosarcoma known systemic disease (secondary
o Diffuse enhancement: Most other lesions lymphoma) although occasionally seen in
• Hyperdense: ECT primary CNS lymphoma (PCNSL)
o Epidural hematoma • Often affects brain and spine
o Meningioma • PCNSL: Usually basal ganglia,
o Lymphoma periventricular WM
o Tuberculoma o Hyperdense on unenhanced CT/slightly
o Plasmacytoma: Mildly hyperdense hypointense on T2WI MR because of
o Meningioma, atypical and malignant tightly packed blue cells
o Hemangiopericytoma o Homogeneous enhancement common
o Leukemia • Neurosarcoid
o Epidural empyema: Sometimes o Dural, leptomeningeal> > parenchymal
disease
• Especially basal cisterns involving optic
• Epidural Hematoma chiasm, hypothalamus, infundibulum,
o Trauma most common etiology
cranial nerves (CN)
• Classic "lucid interval" in only 50% • Lacy leptomeningeal enhancement
• Most EDHs occur at impact ("coup") site typical
I • Overlying fracture common 85-95%
• Hypointense dural lesions and
subarachnoid space/sulci
4
4
EPIDURAL MASS, BRAIN
III
o Systemic disease usually present o Typically involve falx, tentorium, or dural :l
C.
• Chest radiograph may be helpful (lungs sinuses ..,
[Jl
affected in > 90% NS patients) o Marked enhancement, often III
:l
o African-American:Caucasian-American = heterogeneous
10:1 o Elevated myoinositol on short TE MRS
m
~
..,
o Gender: M:F = 2:1 may help to distinguish from meningioma 0>
0,
• Epidural Empyema • Extramedullary Hematopoiesis ~-
0>
o Extra-axial collection with rim o Juxta-osseous smooth homogeneous
UJ
enhancement masses in patients with chronic anemias or "0
0>
o MR best to demonstrate presence, nature, marrow depletion ()
CD
en
extent, and complications o Soft tissue filling paranasal sinus(es) 0>
::J
• Best imaging technique: T1 C+ and DWI o Homogeneous enhancement C.
UJ
• Complications: Cerebritis/cerebral • Leukemia c
C-
abscess, dural venous sinus thrombosis, o Homogeneous enhancement ..,
O>
0>
ischemia • Rarely mimic abscess with enhancing rim ()
::T
o Extra-axial collection, typically isodense to o Most often a complication of acute ::J
o
hyperdense to CSF myelogenous leukemia (AML) Ci
o Look for underlying sinusitis/mastoiditis • Gliosarcoma o
w-
o Rare malignant neoplasm with both glial, eD
..,
Helpful Clues for Rare Diagnoses ::J
mesenchymal elements en
• Tuberculoma
o Heterogeneously enhancing mass with
o Hyperdense on NECT CT/T2 hypointense
dural invasion, ± skull involvement
• Plasmacytoma
o Usually homogeneous, mildly hyperdense • Rosai-Dorfman Disease
o Rare disease of the lymphoid tissues
on NECT
o Neurologic involvement is rare, but typical
• Meningioma, Atypical and Malignant
dural-based lesions may mimic
o Bone/scalp/brain invasion common
meningioma
o Irregular heterogeneous enhancement
pattern
o Destruction of adjacent bone without
• Hemangiopericytoma
periosteal reaction
o Lobular, enhancing, extra-axial mass with
o Diabetes insipidus
dural attachment ± skull erosion
o May mimic meningioma, but without
• Neurosyphilis
o Dural-based gumma may mimic
Ca++ or hyperostosis
meningioma
I
Axial NEG sholVs a la'ge, slighUy inhomogeneously
hyperdense, right epidural hematoma C]_ Foci of
Axial T1 C+ MR sholVs an enhancing epidural mass on
the left C]_ Typical meningioma was found at surgery_
4
hypodensity I?J within the collection represent
hyperacute hemorrhage ("swirl sign").
5
en EPIDURAL MASS, BRAIN
c
~
Q)
~
U
"0
·0
C
£
U
Dural Metastasis Lymphoma
co
~ (Left) Axial T7 C+ MR shows
co an enhancing epidural mass
.n
::J
(f)
= related to a calvarial
"0
metastasis in this patient with
C renal cell carcinoma. (Right)
co Coronal T7 C+ MR shows a
en
Q) dural-based enhancing mass
u
co
Q.
= in a patient with systemic
(f) lymphoma.
co
·x
co,
co
~
X
w
C
III
"-
CO
"t:l
c
III
Neurosarcoid
a lobulated, dural-based
mass = that infiltrates the
brain, causing underlying
edema. Note subtle sulcal
enhancement~. (Right)
Coronal T7 C+ FS MR shows
two epidural fluid collections
with rim-enhancement =.
Note the underlying sinusitis
~
Tuberculoma
(Left) Axial NEeT a
hyperdense dural-based
mass =:I that enhanced
following contrast
administration (not shown).
Dura/tuberculoma was
found at surgery. (Right)
Axial T2WI MR shows a
solitary osteolytic skull
plasmacytoma with a large
tumoral component = that
displaces the relatively
normal dura ~
I
4
6
EPIDURAL MASS, BRAIN ,..
en
c:
III
:J
Co
Ol
....•
Meningioma, Atypical and Malignant III
(Left) Sagillal T1 C+ MR :J
shows a heterogeneously m
enhancing mass =
extension through the
with ~
....•
OJ,
OJ
calvarium and into the scalp x
and a "mushrooming" or
pattern of brain invasion UJ
-0
with associated edema. OJ
(Right) Axial T1 C+ MR ()
C1>
shows a large
=
(f)
hemangiopericyloma OJ
:J
with transcalvarial extension 0.
~ and heterogeneous UJ
c:
enhancement. 0-
OJ
....•
OJ
()
:T
:J
o
a:
o
(ii'
CD
....•
:J
Extramedullary Hematopoiesis leukemia (f)

lobulated, hyperdcnse,
dural-based mass 1::1. The
mass was profoundly
hypointense on T2WI and
enhanced strongly following
contrast administration.
(Right) Axial NEC r shows a
hyperdense bifrontal mass
1::1 with adjacent calvarial
destruction and frontal sinus
invasion
Gliosarcoma langerhans Cell Histiocytosis

a left frontal mass with
heterogeneous, thick,
irregular enhancement and
central necrosis, typical for
gliosarcoma. Note the dural
invasion SII. (Right) Axial T1
C+ FS MR shows a
destructive, avidly
enhancing, mastoid lesion
with epidural extension =.
I
4
7
(/)
c: ENLARGED SULCI, GENERALIZED
~
Q)
~
U
DIFFERENTIAL DIAGNOSIS o Metabolic/demyelinating disorders
"0
·0 (inherited or acquired, longstanding) may
c: Common
.!: cause volume loss, sulcal enlargement
u
ro
~ • Aging Brain, Normal
ro Helpful Clues for Common Diagnoses
.0 • Dementias
:J
o Alzheimer Dementia
• Aging Brain, Normal
CfJ
"0 o White matter volume decreases
c: o Vascular Dementia
ro o Mild/moderate ventricular, sulcal
(/) o Dementia with Lewy Bodies
Q)
u o Frontotemporal Dementia enlargement
ro o Thin periventricular hyperintense rim
Q.
CfJ
• Chronic Alcoholic Encephalopathy
o Scattered white matter hyperintensities
ro • HIV Encephalitis
·x increase with age, normal
ro Less Common
ro~ o "Black dots" on GRE/SWI are NOT normal
xw • Chronic Hepatic Encephalopathy • Chronic hypertensive encephalopathy
• Remote Generalized Insult • Cerebral amyloid angiopathy
.=~
Ol
o Trauma • Dementias
al o Hypoxic Ischemic Encephalopathy o Evaluate for other treatable (potentially
"0
c: o Meningitis treatable) causes of dementia (e.g.,
Ol o Encephalitis (Miscellaneous) repeated trauma with subdural hematoma)
:J o Multiple Sclerosis (Longstanding) • Endocrinopathy (e.g., hypothyroidism)
-"III o Radiation and Chemotherapy • Alcohol/drug abuse
o Other Toxic/Metabolic Insults • Depression ("pseudodementia")
• Enlarged Subarachnoid Spaces (Benign o General imaging findings
Macrocrania of Infancy) • Differentiation solely on basis of CT,
Rare but Important standard MR difficult
• Steroids • PET, fMRI helpful
• Volume Loss Secondary to Nutrition or o Alzheimer Dementia
Hydration Status • Temporal (especially hippocampal),
• Miscellaneous Neurodegenerative Disorders parietal atrophy
o Corticobasal Degeneration • Hypometabolic areas, perfusion deficits
o Parkinson Disease o Vascular Dementia
o Huntington Disease • Second most common dementia

o Multiple System Atrophy • Volume loss, multiple chronic infarcts,
• Creutzfeldt-]akob Disease (ClD) lacunes
• Multifocal white matter disease, often
confluent (arteriolosclerosis)
ESSENTIAL INFORMATION o Dementia with Lewy Bodies
Key Differential Diagnosis Issues • Visual/a uditory hallucinations, delusions
• Some age-related volume loss (especially • Entire brain hypo metabolic (including
cortical) normal visual cortex, cerebellum)
o Frontotemporal Dementia
• Location helpful
o Generalized or disproportionately affecting • Anterior frontotemporal atrophy
some parts of brain more than others? • "Knife-like" gyri
o Parieto-temporal/hippocampal • Up to 40% familial (tau mutations)
(Alzheimer), frontotemporal (FTD or Lewy • Chronic Alcoholic Encephalopathy
body disease) vs. parieto-occipital o Generalized & cerebellar (superior
(Heidenhain variant of C]D) vermian) atrophy

o Hyperintense basal ganglia on Tl WI
• Clinical information helpful
o History of trauma, drug abuse, stroke, suggests chronic hepatic encephalopathy
infection o Polydrug abuse common
I o Dehydration, steroids may cause o Methanol less common; causes
temporary sulcal enlargement hemorrhagic putaminal necrosis
4
8
ENLARGED SULCI, GENERALIZED en
;;r::
c:
• HIV Encephalitis Helpful Clues for Rare Diagnoses ':" l

Q.
o Most common imaging finding in brains
• Steroids ..•
OJ
of HIV/AIDSpatients
o Diffuse atrophy, "hazy" white matter
o May cause transient, reversible sulcal '"
:l
enlargement m
hyperin tensi ty • Volume Loss Secondary to Nutrition or ..•OJ
~
Helpful Clues for Less Common Diagnoses Hydration Status ,
OJ
x
• Chronic Hepatic Encephalopathy o Starvation, dehydration (may be reversible) Qj'
o History of alcohol abuse, liver disease • Miscellaneous Neurodegenerative Ul
'0
common Disorders OJ
()
o Atrophy (especially cerebellum), T1 o Multiple system atrophy (midbrain, l1>

(f>
shortening (especially globi pallidi) corticobasal degeneration) OJ

:l
Q.
• Remote Generalized Insult o Parkinson-associated dementia (midbrain
Ul
o Any longstanding, sufficiently severe with loss of pars compacta) C
CT
OJ
..,
disease may cause brain atrophy, sulcal • Creutzfeldt-]akob Disease (ClD) OJ
prominence o Early findings
()
:::T
:l
o Trauma, infection, demyelination, • Hyperintensity in anterior basal ganglia o
radiation/ chemothera py, • "Pulvinar sign" (hyperintensity in
a:
o
toxic/metabolic/hypoxic insult posterior thalamus) (f>
CD
..,
• If patients survive, brain often shrinks • FLAIR,DWI positive ::J
(f>
and sulci enlarge o Later findings
• Very chronic MS causes severe white • Rapidly progressive atrophy, ventricular
matter loss, sulci enlarge, basal ganglia dilatation
become hypointense o Heidenhain variant
• Enlarged Subarachnoid Spaces (Benign • Peripheral cortex, especially occipital
Macrocrania of Infancy)
o Enlarged SASscommon in infancy
• Bifrontal, symmetric
• Peaks about 7 months, tends to resolve
after age 1
o Danger signs
• Rapid t OFC or signs of t ICP
• Asymmetric, persisting after 1 year
• Asymmetric
I
Axial T2Wf MR shows mild sulcal prominence with
minimal while matter hyperinlensilies in this
Axial T2WI MR in a 63 year old man with Alzheimer
dementia shows large sylvian fissures, la/eral ventricles.
4
high-functioning 76 year old man. No/e normal sylvian The parie/o-occipital sulci are lessseverely affected.
fissures,/emporal horns, hippocampi =:11.
9
VJ ENLARGED SULCI, GENERALIZED
~
C
<ll
~
U
1:l
·0
C
.s=
u
Vascular Dementia Frontotemporal Dementia
CO
~ (Left) Axial T2WI MR shows
CO enlarged sulci/laleral
.0
::> ventricles~ cortical atrophy,
(f)
and multiple confluenl white
1:l
C maller hyperintensities
CO
(grade 3 on European Task
VJ
<ll Force on Age-Relaled White
u
CO Maller Changes rating scale).
a. (Right) Axial NECT shows
(f)
severely shrunken (rontal
CO
·x gyri, with classic" kni{e·like"
,
CO gyral configuration of
CO
~ frontolemporal demential.
X
UJ
C
III
"-
III
"l:l
c
III
(Left) Axial CECT in a 43

year old chronic alcoholic
shows enlarged ventricles,
sulci, withhypodensity in the
corpus callosum
peripheral while mailer ~
This is a classic appearance
for Marchiafava·Bignami
disease. (Right) Axial T2WI
MR in a 27 year old patient
who drank melhanol,
survived, shows generalized
atrophy plus symmetric
volume loss, hyperintensily
in pulamina =1 caudate
nuclei 81.
HIV Encephalitis
(Left) Axial FlAIR MR in
longstanding HIV/AIDS on
HAART shows diffuse
ventricular, sulcal
enlargement with while
mailer hyperinlensity and
volume loss. (Right) Axial
NECT shows prominent
bifronlal fluid collections.
Note sublle findings for
acute 7... subacute ::>
subdural blood in Ihis child
with repealed nonaccidental
trauma.
I
4
10
ENLARGED SULCI, GENERALIZED (fl
"
c:
III
:J
Co
tll
.,
III
(Left) Axial T2WI MR in a :J

patient with longstanding MS m
shows classic peri ventricular ~
.,
plaques ("Dawson fingers") ,
OJ
OJ
IIJI. Note generalized ><
ventricular, sulcal 0;.
enlargement. White matter (fl
-0
volume loss, steroids can OJ
cause sulcal enlargement. Cl
C1l
(Right) Axial T2WI MR en
following whole brain XRT OJ
:J
shows diffuse, symmetric C.
white matter hyperintensily, (fl
enlarged ventricles and sulci.
<=
rr
Two focal hypointensities = .,
OJ
OJ
are probably Cl
radiation-induced vascular ::T
::l
malformations. o
Ci
Enlarged Subarachnoid Spaces (Benign

Macrocrania of Infancy) Corticobasal Degeneration
-
0-
en
.,
C1l
::l
en
(Left) Axial CECT in a 7
month old with head at 95th
percentile shows very
prominent but normal
subarachnoid spaces. Note
enhanced veins crossing
fluid collection ell
confirming these are
subarachnoid spaces, not
subdural hematomas. (Right)
asymmetric enlargement of
frontal sulci, sylvian fissures
!l:ll with volume loss in both
putamina B:I.
Huntington Disease Creutzfeldt-Jakob Disease (CJD)

focal caudate atrophy ell
with convex frontal horns,
generalized volume 1055 with
enlarged sulci. (Right) Axial
T1 C+ MR in a patient with
rapid onset dementia shows
generalized left hemispheric
atrophy, diffuse gyral
enhancement. Basal ganglia
were normal. Variant
manifestation of C/O.
I
4
11
en
c EFFACED SULCI, GENERALIZED
~
OJ
Ul
(5
DIFFERENTIAL DIAGNOSIS o Easy to miss; when in doubt get CECT
:"2 (look for enhanced cortical veins displaced
o
c Common
.s:: away from skull) or MR (hyperintense on
u
~ • Generalized Cerebral Edema TlWI)
CO
.0 o Cerebral Edema, Traumatic • Acute Obstructive Hydrocephalus
::l
(fJ o Hypoxic-Ischemic Encephalopathy o Can be intra- or extraventricular
-0
C o Hypotensive Cerebral Infarction • Intraventricular (look for discrepancy in
CO
en o Toxic/Metabolic Encephalopathies (Many) size of ventricles indicating mass,
OJ
u
CO
• Subdural Hematoma, Subacute aqueductal stenosis, etc.)
"-
(fJ
• Acute Obstructive Hydrocephalus • Extraventricular (CSF absorption
CO • Meningitis alterations, e.g., with acute aneurysmal
·X
CO, • Aneurysmal Subarachnoid Hemorrhage SAH or meningitis): All ventricles
CO
~ Less Common enlarged ± transependymal CSF flow
X
w • Metastases, Skull and Meningeal o Any unexplained hydrocephalus on NECT
C
• Encephalitis scan should prompt CECT scan or MR
l'll
~ without, with contrast
CO • Thrombosis, Dural Sinus
"t:l • Thrombosis, Deep Cerebral Venous • Meningitis
c
l'll
• Acute Hypertensive Encephalopathy, PRES o Pyogenic, granulomatous (even neoplastic)
• Status Epilepticus meningitis appear similar on imaging
• Intracranial Hypertension, Idiopathic • Normal CSF spaces filled with pus or
neoplasm - isodense/isointense with
Rare but Important brain
• Neurosarcoid • Typically enhance strongly, uniformly
• Contrast Complications o Beware: Meningitis is clinical/laboratory
• Brain Death diagnosis; early meningitis may have
• Cerebral Hyperperfusion Syndrome normal imaging!
• Aneurysmal Subarachnoid Hemorrhage
ESSENTIAL INFORMATION o Basal, generalized vs. localized (with
traumatic SAH)
o Hyperdense on ECT scans
o Beware: Acute aSAH is isointense with
brain on Tl WI (fills normal hypointense
CSF spaces), isointense with CSF on T2WI
(may be difficult to detect)
• Metastases, Skull and Meningeal
o May fill, obliterate normal CSF spaces
o Enhance; look for adjacent skull, dura
lesions
• Encephalitis
o Temporal lobe, insula/cingulate gyrus
swelling, hyperintensity: Suspect herpes
o Other encephalitides may be nonspecific
but look for predilection (e.g., West Nile in
basal ganglia, thalamus)
• Thrombosis, Dural Sinus
o SSS > TS as cause for diffuse brain swelling
o TS + vein of Labbe may cause extensive
venous ischemia, hemorrhage, frank
I infarct
4
12
EFFACED SULCI, GENERALIZED en
~
c:
III
o NECT shows hyperdense sinus; CECT ~ o May mimic encephalitis, ischemic stroke, :J
C.
"empty delta sign" even neoplasm! OJ
.,
o Beware: Hyperacute thrombus is isointense o Follow-up scan shows resolution III
:J
on 1'1WI, hypointense on T2WI (may • Intracranial Hypertension, Idiopathic
mimic "flow void")! o Severe "pseudotumor cerebri" may cause
m
~
o T2* (GRE, SWI) best MR sequence to show diffuse brain swelling, papilledema, small OJ
0,
blooming clot ventricles ~,
III
• Thrombosis, Deep Cerebral Venous o Look for "empty sella" plus dilated optic
en
o Hyperdense ICVs, straight sinus nerve sheaths indenting posterior globe
o Hyperdense thrombosed rcvs can make
"
III
()
Helpful Clues for Rare Diagnoses <1>

en
NECT look like CECT scan! • Contrast Complications Q)
:J
o Hypodensity in thalami, basal ganglia, 0.
o Contrast overdose may cause diffuse
internal capsules, deep periventricular en
c:
cerebral edema 0-
white matter o Renal failure may cause gadolinium-based
Q)
.,
Q)
• Acute Hypertensive Encephalopathy, agents to accumulate in CSF, show sulcal ()
::r
PRES :J
enhancement on FLAIR o
o Bioccipital cortical/subcortical edema, • Cerebral Hyperperfusion Syndrome
Ci
sulcal obliteration most common o
o Rare complication following carotid iii'
o May affect brainstem, cerebellum, basal CO
endarterectomy 3
ganglia, watershed (sometimes ONLY these o Defined as a> 100% increase in CBF
en
areas without classic posterior cerebral • Occurs in 10-15% of patients but
territory involvement) minority become symptomatic
o Hypodense on NECT, hyperintense on
• Can develop immediately or within first
T2WI/FLAIR few days (mean = 5 days) although some
o Typically does not restrict on DWI
reports up to a month
• Status Epilepticus • Triad of ipsilateral headache, focal
o Prolonged seizure causes hypermetabolic
seizure, neurologic deficit in absence of
state, blood-brain-barrier leakage cerebral ischemia
o Imaging within 24 hours after ictus
• Most symptomatic patients are
• Cerebral edema (gyraJ swelling, sulcal hypertensive
obliteration) • Unilateral cerebral edema with gyral
• May cause transient enhancement swelling, vascular enhancement;
• May cause DWI restriction decreased MTT on perfusion CT, MR
Toxic/Metabolic Encephalopathies
Cerebral Edema, Traumatic (Many)
I
Axial NECT shows diffuse brain swelling with loss of
gray·while differentiation, diffuse sulcal effacement.
Axial NECT in a padent with chronic hepadc
encephalopathy and acute exacerbation shows diffuse
4
Small subdural hematoma is present ~. cerebral edema, obliterated sulci, and effaced
gray-while matler. 13
(/l
c EFFACED SULCI, GENERALIZED
'--
Q)
u;
o
-0
'0
C
~ Subdural Hematoma, Subacute Acute Obstructive Hydrocephalus
u
ro (Left) Axial NEeT shows
'--
ro
.n perfeclly isodense subdural
::J hematomas ~ same
(fJ
-0
attenuation as cortex. All
C sulci are obliterated except
ro one where CSF is seen in a
(/l
Q) sulcus displaced away Irom
u
ro inner table ffi (Right) Axial
n.
(fJ NECT shows absence of
visualized cerebral aqueduct
ro
'x ~ with enlarged 3rd, lateral
ro, ventricles and diffuse brain
ro swelling. "Blurred" margins
'--
X of lateral ventricles
w
indicate transependymal CSF
C flow.
...
l'Cl
al
"C
c
l'Cl
Meningitis Aneurysmal Subarachnoid Hemorrhage

sulcal ell a cement over /elt
convexity (contrast with
normal-appearing right sulci)
secondary to pyogenic
meningitis &. Asymmetric
involvement is unusual.
(Right) Axial TlWI MR
shows basal cisterns
sulci I:llI appear effaced
because they are lilled with
isointense acute blood, not
normal hypointense CSF
Note acute obstructive
hydrocephalus with
blood-fluid levels in dilated
lateral ventricles
Metastases, Skull and Meningeal

(Left) Axial FlAIR MR in a
patient with prostate cancer,
headaches, shows normal
right-sided sulci, thickened
dura and infiltrated sulci
m over entire left
hemisphere. (Right) Coronal
T I C+ MR in a patient with
viral encephalitis shows
diffuse right hemisphere
swelling, especially temporal
lobe. All surface sulci are
obliterated. Note subIa/cine
herniation from mass effect
I
4
14
EFFACED SULCI, GENERALIZED ,..c:
(Jl
Ql
:J
a.
III
...•
Ql
(Left) Axial NEeT shows 555

:J
m
occlusion SlI with
parenchymal =-
subarachnoid hemorrhage
~
...•
OJ,
OJ
PJ:iil. Note near-complete ~.
effacement of right OJ
hemisphere sulci compared UJ
-0
to more normal left side. OJ
(Right) Axial NEeT shows (1
CO
hyperdensity in both internal rJl
cerebral veins and straight OJ

::J
sinus =:I. Hypodensity in a.
bilateral thalami SlI is UJ
c
consistent with edema rr
and/or venous ischemia . ...•
OJ
OJ
Most sulci, cisterns appear ()
effaced by brain swelling.

:::r
::J
o
a:
o
w'
Acute Hypertensive Encephalopathy, eD
...•
::J
PRES rJl
(Left) Axial NECT in renal

transplant patient on
cyclosporin shows bilateral
parieto-occipital sulcal
effacement with hypodense
cortical/subcortical lesions
=:I consistent with PRES.
obtained after status
epilepticus shows temporal
lobe (and, to a lesser extent,
parietal lobe) gyral
hyperintensity CO> and mass
effect mimicking
encephalitis. Cyral swelling
has effaced adjacent sulci.
Intracranial Hypertension, Idiopathic

dilated optic nerve sheaths
elevation of optic nerve
head liB Suprasellar cistern,
sylvian fissure are small;
superficial sulci almost
effaced. (Right) Axial NECT
in a patient with right
arm/leg weakness 24 hours
after left carotid
endartereclOmy, shows
swollen gyri with generalized
decrease in left hemispheric
sulci. Note hypodense
parietal whitemaller=:l.MR
showed hyperintense
cortex/while matle"
decreased MTT I
4
15
(/)
c EFFACED SULCI, FOCAL
~
Q)
115
U o Look for focal traumatic SAH adjacent to
:2
o contusions
C
.!: Common • Cerebral Ischemia-Infarction, Acute
()
ro
~ • Cortical Contusion o Cortical branch occlusion - gyral swelling
ro
.0 • Cerebral Ischemia-Infarction, Acute o Difficult to see on ECT, Tl/T2WI
::>
CfJ • Spontaneous Intracranial Hemorrhage o DWI helps distinguish ischemia (restricts)
-0
C • Subdural Hematoma from neoplasm (usually doesn't)
ro
(/) • Epidural Hematoma • Spontaneous Intracranial Hemorrhage
Q)
()
ro • Neurocysticercosis o Children/young adult
0-
CfJ Less Common • Vascular malformation, venous
ro • Primary CNS Neoplasm occlusion, drug abuse
'xro
, o Meningioma o Middle-aged, older adults
ro
~ o Oligodendroglioma • Amyloid angiopathy, hypertension
X
W
o Ganglioglioma • Hemorrhagic neoplasm (metastasis,
r:: GBM)
III
o Diffuse Astrocytoma, Low Grade
~ o DNET • Subdural Hematoma
r:c
-0
o Pleomorphic Xanthoastrocytoma o Usually crescentic, spreads over
r::
III
• Metastases, Parenchymal hemisphere - more generalized sulcal
::> • Metastases, Skull and Meningeal effacement
-"1Il o Occasionally focal, mimics EDH
• Abscess
• Meningitis • Epidural Hematoma
• Focal Cortical Dysplasia o Focal, biconvex extra-axial hematoma
• Tuberous Sclerosis Complex o Severe compression of underlying sulci

• Thrombosed Cortical Vein(s) o Mimics: Plasmacytoma, extra-medullary
hematopoiesis, etc.
Rare but Important • Neurocysticercosis
• Extra-Axial Empyema o NCC cysts typically in subarachnoid
• Meningioangiomatosis spaces, depths of sulci
• Superficial Siderosis o Intense pial inflammatory reaction may
efface sulci
ESSENTIAL INFORMATION Helpful Clues for Less Common Diagnoses
Key Differential Diagnosis Issues • Primary CNS Neoplasms
• Focal = one or several sulci (not hemisphere o Any cortical, subcortical neoplasm causes
or whole brain) local mass effect, expanded

• Key concept: Is sulcal effacement caused by parenchyma/compressed sulci
lesion within sulcus itself or underlying o Age, history helpful
gyrus? • Child, young adult with longstanding

o Intra- vs. extra-axial causes seizures: Ganglioglioma (cyst, Ca++
o Parenchymal> > sulcal disease common), DNET ("bubbly" appearance),
• Imaging low grade astrocytoma
o Sulcal, gyral masses can be isodense on • Adult: Meningioma (dural-based, often
NECT, isointense on Tl-weighted MR - Ca++), oligodendroglioma (Ca++
difficult to detect!! common, variable enhancement), PXA
o CECT, T2WI, FLAIR, Tl C+ scans most (look for "dural tail")
helpful • Metastases, Parenchymal
o May cause focal mass, variable edema
Helpful Clues for Common Diagnoses o Almost always enhances
• Cortical Contusion • Metastases, Skull and Meningeal
o History of closed head injury
o Dural-based, usually isodense/isointense
I o Heterogeneous
gyri
hyper-/hypodense swollen with brain
o Look for skull lesions
4
16
EFFACED SULCI, FOCAL ,..
CJl
C
III
• Abscess • Thrombosed Cortical Vein(s) :l
C.
o Gray-white junction common site o Usually occurs with dural sinus occlusion III
.,
o Early stage (cerebritis) typically does not o May be isolated, solitary III
:l
enhance o Clinically devastating if vein of Labbe
m
o Late cerebritis/capsule stages - occluded ~
.,
ring-enhancement o Can mimic hemorrhagic ,
0>
0>
o Sulci compressed but don't enhance unless neoplasm/stroke/vascular malformation X
Qi"
meningitis also present o T2* scan (GRE, SWI) helpful
en
o DWI shows restriction early, helps • Petechial hemorrhage in cortex ± focal "0
0>
distinguish abscess from neoplasm SAH ()
CD
en
• Meningitis • Look for occluded dural sinus 0>
:l
o Diffuse> focal, symmetric> asymmetric • Look for "cord-like" blooming in a.
o Rarely affects solitary sulci; multiple thrombosed vessel en
c
0-
adjacent sulci typically involved Helpful Clues for Rare Diagnoses 0>
.,
0>
o FLAIR, Tl C+ stans best for detecting ()
• Extra-Axial Empyema -::r
subtle disease o Look for sinusitis, mastoiditis ± underlying
:J
o
• Focal Cortical Dysplasia meningitis
c:
o History of longstanding seizures o
o Subdural> > epidural en
o Perisylvian most common location CO
.,
• Meningioangiomatosis :J
o Follows gray matter on all sequences en
o Usually child/young adult with seizure
(occasionally slightly hyperintense on o Consider MA if calcified cortical lesion ±
FLAIR) cysts
o Does not enhance
o Typically hypointense "serpentine" cortical
o MRS usually normal
lesion
• Tuberous Sclerosis Complex o Enhances
o Cortical tubers expand gyri, blur
o May extend along PVSs, mimic neoplasm
gray-white interface • Superficial Siderosis
o Cortical/subcortical hyperintensity on o History of repeated SAH helpful but not
FLAIR, T2WI always present
o Tubers typically don't enhance
o Serpentine pial/cortical hypointensity on
o Taylor-type cortical dysplasia
T2* scan> mass-like lesion
• Considered "forme fruste" of TSC o Posterior fossa> supratentorial brain
• Solitary tuber
• Caution: Can mimic neoplasm!
Cortical Contusion Cerebral Ischemia-Infarction, Acute
I
Axial NEG scan shows a left frontal hyperdensity with Axial TIWI MR in patient "found down" several hours
4
surrounding hypodensily typical of cortical contusion.
Note effaced frontal sulci from focal mass effect. mass =
after "doing cocaine" shows a subtle, mostly isointense
drug·reJaled
with adjacent sulcal effacement. Acute
cortical inFarct.
17
(/)
c EFFACED SULCI, FOCAL
~
OJ
Ul
U
:2
o
c
.r: Spontaneous Intracranial Hemorrhage
II
~ (Left) Axial T1 WI MR in 68
CO yo man with sudden onset of
.0
:J right-sided weakness shows
(f)
mostly isoinlense
"C
CO
cortical/subcortical mass 6>
effacing adjacent sulci. T2
(/)
OJ showed numerous
II
CO peripherally-located
0.
(f) microbleeds consistent with
amyloid angiopathy. (Right)
CO
·X Axial NECT shows almost
CO, perfectly isodense right
~
CO
X
posterior frontal mass =.
Only indication of presence
w
of mass is focal effacement
c of the underlying sulci. This
~
'" is an easy lesion to miss.
aJ
"c
'"
:J
.:.;
(f)

effacement of left posterior
=-
frontal sulci by calcified mass
(Right) Coronal FLAIR
MR shows inhomogeneously
hippocampus,
=
hyperintense left temporal
lobe mass that infiltrates
compressing
temporal horn and effacing
the collateral sulcus
(compare with normal right
side).

hypointense left posterior
parietal cortical/subcortical
mass ~ with adjacent sulcal
effacement. Mass was
hyperintense on T2WI,
FLAIR. WHO grade II
fibrillary astrocylOma was
Axial T1WI MR shows
slightly "bubbly"
cOrLical-based mass ~ with
focal gyral expansion, sulcal
effacement.
I
4
18
EFFACED SULCI, FOCAL (fl
;><"
c:
III
::l
Q.
to
....•
III
::l
(Left) Coronal T2WI MR in a
22 year old with m
longstanding temporal lobe ~
....•
OJ
epilepsy shows hyperintense
cortically based mass 81
a,x
with adjacent sulcal w'
compression. (Right) Axial (fl
"0
T1 WI MR in a patient with Ol
()
known metastatic disease
CD
shows focal gyral expansion, en
sulcal effacement caused by Ol
::l
Tl isoinlenS€ metastasis. n.
(f)
c:
0-
Ol
....•
Ol
()
::r
::l
o
Ci
()
en
~
CD
3
en
Abscess
diffusely thickened,
infiltrated inhomogeneously
hypointense skull with
adjacent dural-based mass
81. Note focal effacement of
adjacent sulci. (Right) Axial
NECT shows hypodense
=
mass at gray-white junction
that showed ring-like
Thrombosed Cortical Vein(s)

gyral swelling, subarachnoid
hemoffhage causing focal
sulcal hyperintensity =.
T2'
scan showed isolated cortical
vein thrombosis. (Right)
cortical/subcortical mass
with effaced sulci,
hypoinlense area !3iJ
suggestive of calcification.
Lesion enhanced with
contrast.
I
4
19
en INTERHEMISPHERIC FISSURE CYSTS
c
~
Q)
~
U
"0 DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
·0
C
Common • Pineal Cyst
.r:
u o Glial-lined intrapineal cyst located in
ro
~ • Pineal Cyst
ro pineal recess
.n
:J Less Common o Common (23% of healthy adults)
(fJ
"0 • Callosal Dysgenesis o Multiple small « 2 mm) or larger
C
ro • Neurocysticercosis confluent cysts
en
Q) • Arachnoid Cyst o Usually isointense with CSF on 1'1-, T2WI;
u
ro FLAIR variable
Cl.
(fJ
Rare but Important
• Holoprosencephaly (HPE) o Wall thickness < 2 mm
ro
·x • Medial Atrial Diverticulum o Smooth rim-enhancement typical
'P o Thick/nodular enhancement may be
ro
~ • Atretic Cephalocele
X • Dermoid Cyst indistinguishable from pineocytoma
w
C • Epidermoid Cyst • Truly cystic pineocytomas are rare
lU
•... • Tumor-Associated Cysts • Some pineal cysts may have variant
l:ll
• Aicardi Syndrome appearance, may even hemorrhage (cyst
"0
c apoplexy)
lU

• Callosal Dysgenesis
Key Differential Diagnosis Issues o 3rd ventricle open dorsally
• Anatomic sublocation key o Two types of agenesis with
o Pineal/quadrigeminal region interhemispheric cyst
• Is it pineal cyst or cystic-appearing pineal • Type 1 (most common): Cyst is
tumor (e.g., pineocytoma) diverticulum of lateral ventricle,
• CSF-like: Arachnoid cyst, epidermoid density/signal like CSF, ependymal-lined
cyst, medial atrial diverticulum • Type 2: Multilocular/septated cysts
o Superior interhemispheric fissure within/adjacent to midline that do not
• Most common: Cyst associated with communicate with ventricles, typically
callosal dysgenesis, holoprosencephaly; hyperdense/hyperintense to CSF
neurocysticercosis • Neurocysticercosis
• Less common: Arachnoid cyst, atretic o "Racemose" cysts> solitary cysts
cephalocele, Aicardi syndrome • Convexity sulci
o Posterior interhemispheric fissure • Anteroinferior interhemispheric fissure
• More common: Holoprosencephaly, • Suprasellar/basal, quadrigeminal cisterns
medial atrial diverticulum • Arachnoid Cyst
• Less common: Epidermoid cyst o Only S% of ACs occur in parasagittal
o Anteroinferior interhemispheric fissure region/interhemispheric fissure
• Neurocysticercosis • Usually are convexity ACs that extend
• Dermoid cyst (more common in midline) medially
• Epidermoid cyst (less common in • Most are small, unilateral, asymptomatic
midline) o Large/symptomatic ACs in
• Two morphologically distinct types of interhemispheric fissure rare
interhemispheric CSF-containing cysts • Typically not associated with callosal
o Interhemispheric cyst associated with dysgenesis
callosal dysgenesis or holoprosencephaly • May also "straddle" falx, extend equally
o Parasagittal cyst unassociated with callosal on each side
dysgenesis • Do not communicate with ventricular
• Arachnoid cyst, medial atrial system
diverticulum
I • Tumor-associated cysts (macroadenoma,
• May cause progressive lower extremity
weakness
meningioma)
4
20
INTERHEMISPHERIC FISSURE CYSTS ,..c:
(IJ
III
o Look for fatty droplets in cisterns, sulci, ::::l
Helpful Clues for Rare Diagnoses Co
ventricles .,
III
• Holoprosencephaly (HPE)
• Epidermoid Cyst III
o Alobar HPE ::::l
o 4-9x more common than dermoid cyst
• Central monoventricle opens to large m
BUT ~
.,
dorsal CSF-filled cyst
• Off-midline> midline ,
Q)
• Cyst wall comprised of telencephalic roof Q)

• Rarely arises in interhemispheric fissure x
plate, tela choroidea remnants 0;"
o May adhere to surrounding structures like
o Semilobar HPE (fl
ACA, make resection difficult -0
• May occur with large dorsal CSF space Q)
()
o Resembles CSF on CT, MR en
• Medial Atrial Diverticulum
o Local herniation of posteromedial lateral
• Often very slightly hyperintense to CSF '"::::l
Q)
• Doesn't suppress on FLAIR Q.

ventricle (fl
• Restricts on DWI c:
o Typically associated with severe, 0-
• Insinuates/infiltrates along subarachnoid .,
Q)
long-standing hydrocephalus Q)
cisterns ()
o Massive ventricular enlargement - uni- or :;y
bilateral pulsion diverticulae of • Tumor-Associated Cysts ::::l

o
o Most common with pituitary 0:
inferomedial atrial wall o
macroadenoma, meningioma
o CSF-filled pouch herniates medially into
o Trapped pools of CSF (subarachnoid space) '"CD.,
quadrigeminal cistern ::::l
or interstitial fluid (perivascular spaces)
• Large medial atrial diverticulae may
• Aicardi Syndrome
'"
extend inferiorly through incisura into
o X-linked dominant
posterior fossa
o Associated with broad spectrum of cerebral
• Atretic Cephalocele
malformations (e.g., Dandy-Walker
o T2 hyperintense subscalp mass extends
continuum)
through midline calvarial defect
o Classic triad
o ± Primitive falcine vein
• Infantile spasms
• Dermoid Cyst
o Congenital inclusion cyst
• Chorioretinallacunae
• Agenesis CC ± interhemispheric cyst
o Fat & calcification
o Choroid plexus cysts, papillomas
o Location
• Midline> off-midline Other Essential Information
• Frontonasal, sella/parasellar, • FLAIR,DWI helpful to distinguish CSF-like
quadrigeminal cistern cysts from other types
Pineal Cyst
I
Sagiltal T7 c+ MR shows a unilocular cystic pineal
gland with r;m-enhancement =.
Note that cyst fluid is
Sagiltal T2WI MR shows multiple tiny cysts in the pineal
gland
4
slighlly hyperintense to CSF in adjacent
quadrigeminal/superior cerebellar cistern. 21
(/)
c
~ INTERHEMISPHERIC FISSURE CYSTS
Q)
U5
U
"0
'0
C
.L: Callosal Dysgenesis Callosal Dysgenesis
U
CO
~ (Left) Sagittal T2WI MR
CO
.n shows a dysgenetic corpus
::J callosum EJ with a large
(f)
Barkovich type 7
"0
c
CO
interhemispheric cyst =.
(/)
(Right) Axial CECT shows
Q) callosal dysgenesis with
u
CO widely-spaced, parallel,
c. nonconverging, lateral
(f)
CO
ventricles =. Barkovich type
'xCO 2b multilocular cysts EJ are
, slightly hyperdense and do
CO
~ not communicate with
X ventricles.
w
C
III
~
CO
"0
c
III
Neurocysticercosis Neurocysticercosis
NCC cysts in the
anleroinferior
interhemispheric fissure I::]
as well as suprasellar cistern
EJ. (Right) Sagittal T2WI FS
MR shows multiple
interhemispheric cysts =
in
a patient with known
neurocyslicercosis. (Courtesy
r. Bravo, MOJ.
a CSF-like mass =
over the
leFt cerebral convexity that
extends medially to the
interhemispheric fissure E1.
Iligh signal intensity Foci
lateral to cyst are small
chronic subdural
hematomas. (Right) Sagittal
TlWI MR shows large
CSF-like mass extending From
supravermian cistern ED into
cavum velum inlerposilUm
=.. flauening internal
cerebral veins ~.
I
4
22
INTERHEMISPHERIC FISSURE CYSTS (J)
""c:
III
::l
Co
..•
OJ
Medial Atrial Diverticulum III

::l
shows a semi/abar variant m
with a large dorsal cyst ...
~
open to monoventricle ~ ,
OJ
OJ
(Right) Axial NECT shows x
moderate but symmetric iii'
enlargement of both lateral (j)
"0
ventricles. A pouch of CSF OJ
SlI protrudes medially from ()
CD
the right lateral ventricle ~ C/l
into the interhemispheric OJ

::l
fissure, quadrigeminal, and CL
superior cerebellar cisterns. (j)
c:
cr
...
OJ
OJ
()
:=r
:::l
o
Ci
Q
C/l
ro
3
Atretic Cephalocele Dermoid Cyst C/l

shows a hyperintense atretic
parietal cephalocele I:]
extending through the
midline cranium bifidum.
Note persistent primitive
falcine vein [;8 (Right) Axial
NECT shows very hypodense
mass in the midline
anleroinferior hemispheric
fissure. Note the marginal
calcification =.
Tumor-Associated Cysts
a hyperintense extra·axial
mass = in the
posteroinferior
interhemispheric fissure that
displaces the occipital lobe
anteriorly and erodes the
skull posteriorly SlI. (Right)
Axial T2WI MR shows a
pituitary macroadenoma =
with superior extension into
the 3rd ventricle, anterior
extension into the
interhemispheric fissure.
Note trapped CSF-likc pools
of fluid SlI around the tumor
representing nonneoplastic
tumor-associated cysts.
I
4
23
1Il CPA MASS, ADULT
~C
OJ
~
U
"0
DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
'0 • Vestibular Schwannoma
C
.r: Common
() o Morphology: Ovoid intracanalicular mass
~ • Vestibular Schwannoma
ell (lAC); "Ice cream on cone" shape
.n Less Common
OJ
(/)
(CPA-lAC)
"0
• Meningioma, CPA-lAC o Tl C+ MR: Enhancing ± intramural cysts
C
ell • Epidermoid Cyst, CPA-lAC
1Il
OJ • Aneurysm, CPA-lAC
()
ell • Arachnoid Cyst, CPA-lAC • Meningioma, CPA-lAC
Q.
o Morphology: "Mushroom" dural-based
(/)
• Metastases, CPA-lAC
ell mass capping lAC asymmetrically
'xell Rare but Important o Tl C+ MR: Enhancing ± dural "tails" ±
,
ell
~ • Neurofibromatosis 2, CPA-lAC CSF-vascular cleft if CPA component is
X • Sarcoidosis, CPA-lAC larger
w
c • Choroid Plexus Papilloma, CPA • 25% of CPA meningiomas have
~ • Lipoma, CPA-lAC extension/dural tail into lAC
'"
CO
'tl
• Ependymoma, CPA • Epidermoid Cyst, CPA-lAC
c • Pseudotumor, Intracranial o Morphology: Insinuating ± scalloping
'"
OJ
• Schwannoma, Facial erve, CPA-lAC brainstem margin
-"en • Schwannoma, Jugular Foramen o Tl C+ MR: Nonenhancing; may be
• Hemangioma, lAC difficult to see
• Neurenteric Cyst o DWI: Restricted diffusion (high signal)
makes diagnosis
ESSENTIAL INFORMATION • Aneurysm, CPA-lAC
o Morphology: Ovoid or fusiform; rarely lAC
Key Differential Diagnosis Issues o Tl & T1 C+ MR: Complex signal mass
• Idealized imaging protocol in evaluating from wall calcification, clot & flow
CPA mass lesions o MRA, CTA, or angiography sort out
o Tl C+ fat-saturated MR is gold standard diagnosis
• Fat-saturation differentiates lipoma from • Arachnoid Cyst, CPA-lAC
vestibular schwannoma o Morphology: Fills cistern with rounded
• Add DWI for possible epidermoid margins
• Add GRE for aneurysm wall clot & o Imaging
calcification; tumor calcifications • Tl C+ MR: No enhancement
o T2 thin-section, high-resolution, MR gives • FLAIR attenuates
more surgical data when vestibular • DWI: No restricted diffusion
schwannoma diagnosed • Metastases, CPA-lAC
• Amount of CSF cap in lateral lAC o Morphology: Irregular, invasive margins
• Assessment of relationship to cochlear o Tl C+ MR: Single or multiple enhancing
nerve canal masses in CPA area
• If small schwannoma, nerve of origin • 4 sites primarily involved: Flocculus,
• Knowledge of relative incidence of lesions choroid plexus, arachnoid-dura, or pia
key in cerebellopontine angle
o Vestibular schwannoma - 90% all
CPA-lAC masses • Neurofibromatosis 2, CPA-lAC
o Morphology: Bilateral ovoid lAC or "ice
o Meningioma, epidermoid cyst, aneurysm,
arachnoid cyst together represent - 8% all cream on cone" CPA-lAC masses
o T1 C+ MR
CPA-lAC masses
o All other diagnoses in differential list - 2%
• Bilateral enhancing CPA-lAC masses
of CPA-lAC masses pathognomonic of NF2
I • Other schwannomas & meningiomas
may be present
4
24
CPA MASS, ADULT
III
• Sarcoidosis, CPA-lAC • Marginal enhancement of tumor cyst :J
a.
o Laboratory: CSF lymphocytosis; t t blood wall w
....•
angiotensin converting enzyme (ACE) • Pseudotumor, Intracranial III
:J
o Morphology: En plaque or nodular dural o Morphology: En plaque
o Tl C+ MR: Thickened, enhancing dura m
lesion(s) ?:S-
o Tl C+ MR: Enhancing multifocal o Caveat: May mimic meningioma, Ol
OJ
dural-based lesions sarcoidosis or metastatic disease x
Oi
• Choroid Plexus Papilloma, CPA • Schwannoma, Facial Nerve, CPA-lAC
en
o Morphology: Dumbbell shape with 4th o Morphology: CPA-lAC mass with "0
OJ
ventricle and CPA cistern components "labyrinthine tail" (')
CD
rJl
• Pear-shaped if begins in foramen of oCT: Labyrinthine segment CN? may be OJ
::>
Luschka enlarged a.
o Tl C+ MR: Avidly enhancing mass in 4th o Tl C+ MR: Enhancing tubular mass in en
c
CT
ventricle projecting through foramen of CPA-lAC and labyrinthine segment CN? OJ
...••
OJ
Luschka into CPA cistern o Caveat: If not labyrinthine segment CN? (')
:::,-
• Lipoma, CPA-lAC involvement, cannot differentiate from ::>
o
o Morphology: Ovoid if lAC; CPA lesion may vestibular schwannoma 0.:
be broad-based against brainstem • Schwannonla, Jugular Foramen Q
rJl
oCT: Fat-density lesion of CPA ± lAC ± o Tl C+ MR: Enhancing mass arising from co...••
::>
inner ear jugular foramen rJl
o T1 MR: High signal lesion disappears with • Mass projects cephalad into CPA cistern
fat-saturation • Hemangioma, lAC
o Caveat: If Tl C+ without fat-saturation, o Morphology: Ovoid lAC mass with
may be mistaken for vestibular punctate calcifications
schwannoma oCT: Punctate calcifications in lAC mass
• Ependymoma, CPA o Tl C+ MR: Enhancing lAC mass with focal
o Morphology: Irregular soft tumor squeezes low signal foci (calcifications)
out through 4th ventricle foramen of • Neurenteric Cyst
Luschka into CPA cistern o Morphology: Rounded ovoid mass in
• Tumor margins amorphous prepontine cistern
oCT: Calcifications in 50% o MR: Intermediate to high signal Tl
o Tl C+ MR: Heterogeneous enhancement of prepontine mass
solid tumor components o Caveat: Tl increased signal differentiates
from epidermoid cyst
Vestibular Schwannoma Meningioma, CPA-lAC
I
Axial T1 C+ MR ,eveals enhancing mass filling the CPA
=
Axial T1 C+ FS MR reveals an enhancing dural-based
4
nerve canal is involved
hearing preservation
=
& internal auditory canal 81. Note the cochlear
difficult.
making resection with
mass centered over the lAC but with minimal lAC
involvement
B make
=. The shape and the associated dural tail
meningioma diagnosis.
25
IJl
C
~
CPA MASS, ADULT
OJ
u;
U
"0
·0
c
.r: Epidermoid Cyst, CPA-lAC Aneurysm, CPA-lAC
o
~ (Left) Axial TI WI MR shows
ro a low signal mass in the right
.0
:J CPA cistern that insinuates
en and enlarges the Foramen of
"0
c
ro
Luschka = and scallops the
ventral cerebellar
IJl
OJ hemisphere 81. (Right) Axial
o
ro TI C+ MR demonstrates a
C>-
en large enhancing distal
ro vertebral artery aneurysm =
·x projecting up into the CPA
ro, cistern and compressing the
ro
~ area where CN? and CN8
X exit the brainslem ~.
w
C
•..
III
aJ
"0
C
III
Arachnoid Cyst, CPA-lAC Metastases, CPA-lAC

(Left) Axial T2WI FS MR
shows a high signal lesion
in low CPA cistern. Note the
=
anterior displacement of
proximal CN8 by arachnoid
cyst 81. The high signal
results From absence of CSF
(Jaw. (Right) Axial TI C+ FS
MR reveals an
in homogeneously enhancing
metastatic focus arising from
dura along the prepontine
cistern. This metastasis
reaches the anterior margin
of the porus acuslicus =.
Neurofibromatosis 2, CPA-lAC Sarcoidosis, CPA-lAC

bilateral enhancing CPA-tAC
schwannomas =. The leFt
schwannoma involves the
intra temporal facia! nerve HJ
indicating it is mosllikely a
facial nerve scl1wannoma.
(RighI) Axial TI C+ MR
shows heaped up,
dural-based, sarcoid deposit
in right CPA = that enters
the internal auditory canal
!l::I. Meckel cave is also
aFFected81. This lesion
mimics meningioma.
I
4
26
CPA MASS, ADULT Ul
"
c:
III
::l
Co
..,
III
lipoma, CPA-lAC III
(Left) Axial TI C+ MR ::l

reveals a pear-shaped m
inhomogeneously enhancing ~
..,
papilloma = projecting
from the lateral recess of the
OJ
0,
x
4th ventricle through the Cli'
foramen of Luschka into the en
"0
low CPA cistern 82. (Right) OJ
Axial T1WI MR shows a ()
(lJ
varianllhree-part
affecting the CPA cistern
lipoma
high anterior jugular foramen

=- CJ>
OJ
::l
0-
82 and the vestibule of the en
c
inner ear P.:Z. No surgery is 0-
OJ
done for these lesions.
OJ
()
::T
::l
o
c:
o
CJ>
CD
3
Pseudotumor, Intracranial CJ>
(Left) Axial TI C+ MR
demonstrates an aggressive
mixed cystic-solid enhancing
CPA cistern =-
ependymoma of the right
8l and cerebellar
4th ventricle
hemisphere 1J:!ll. (Right) Axial

T1 C+ MR demonstrates an
extensive area of enhancing
dural thickening = along
the right low CPA cistern.
The intracranial
pseudotumor also involves
the subjacent jugular
foramenB.
Schwannoma, Facial Nerve, CPA-lAC Schwannoma, Jugular Foramen

a variant facial nerve
schwannoma with
enhancing CPA-lAC
component II] extending
into the geniculate ganglion
82. Note associated
arachnoid cystlJ:!ll. (Right)
Coronal TI + rs
reveals a schwannoma
MR
projecting cephalad from the

=
jugular foramen 82 into the
CPA cistern. Note the normal
lAC IJ:!ll is at the level of
upper margin of the tumor.
I
4
27
I/l
CYSTIC CPA MASS
~
C
OJ
]2
U
DIFFERENTIAL DIAGNOSIS • Also sorts out solid and cystic
-0
·0 components of lesions
C
.r:: Common • May help with associated cranial nerve
()
co
~ • Epidermoid Cyst, CPA-lAC and arterial anatomy
co
.0 • Arachnoid Cyst, CPA-lAC
OJ Helpful Clues for Common Diagnoses
rJ)
-0
Less Common • Epidermoid Cyst, CPA-lAC
C
co • Vestibular Schwannoma with Intramural o Congenital rest of epithelial tissue in CPA
I/l
OJ Cyst(s) o Imaging
()
co
Q.
• Neurocysticercosis, CPA • Insinuating ± scalloping brainstem
rJ) • Hemangioblastoma margin
co • Large Endolymphatic Sac Anomaly (IP-2)
·x • Tl C+ MR: Nonenhancing, cystic
co,
co Rare but Important appearing; may be difficult to see
~
X • Vestibular Schwannoma with Arachnoid • DWI: Restricted diffusion (high signal)
W
Cyst makes diagnosis
r::
III
~ • Schwannoma, Facial Nerve, CPA-lAC with • Arachnoid Cyst, CPA-lAC
1IJ
Cyst o Congenital lesion resulting from failure of
"C
r:: • Neurenteric Cyst embryonic meninges to merge with cyst
III
• Schwannoma, Jugular Foramen with between split in arachnoid membrane
Intramural Cyst o Imaging: Fills cistern with rounded
margins
• Tl C+ MR: No enhancement
ESSENTIAL INFORMATION • Other MR: FLAIRattenuates; DWI: No
restricted diffusion
• Vestibular Schwan noma with Intramural
Cyst(s)
o Vestibular schwannoma may have either
intramural or extramural (arachnoid cyst)
cysts
o Imaging
• Solid CPA-lAC mass with intramural
cysts
• Tl C+ MR: Enhancing solid tumor
component ± intramural cysts (common)
± arachnoid cyst (rare)
• Neurocysticercosis, CPA
o Intracranial infection caused by pork
tapeworm (Taenia solium)
o Imaging
• Cysts with "dots" inside
• Appearance varies with stage
• Tl C+ MR: Cysts with enhancing thin or
thick wall
o Adult with intra-axial posterior fossa mass
abutting pia
o Imaging
• Cerebellar cystic & solid tumor
• Tl C+ MR: 60% of tumors with solid
I enhancing & cystic components (40%
solid only)
4
28
CYSTIC CPA MASS CJl
'"
c:
III
• Large Endolymphatic Sac Anomaly (IP-2) • Tl C+ MR: Enhancing tubular mass in ::::l
Co
o Bilateral congenital S HL that appears in CPA-lAC & labyrinthine segment of III
..,
child with cascading hearing loss pattern facial nerve; intramural or extramural III
::::l
o Most common congenital imaging cyst visible
m
abnormality • Neurenteric Cyst ~
..,
o Imaging o Incidental rounded to ovoid mass in OJ,
OJ
• CT: Enlarged bony vestibular aqueduct prepontine cistern X
0;.
• T2 high-resolution MR: Enlarged o Imaging
CJl
endolymphatic sac + mild cochlear • MR shows intermediate to high signal T1 -0
OJ
aplasia (modiolar deficiency, bulbous prepontine mass ()
CD
(f>
apical turn, scalar chamber asymmetry) • Schwannoma, Jugular Foramen with OJ
::::l
Helpful Clues for Rare Diagnoses Intramural Cyst a.
o Presents with some mixture of 9-12 cranial CJl
• Vestibular Schwannoma with Arachnoid c:
0-
Cyst neuropathy ..,
OJ
OJ
o Imaging ()
o Vestibular schwannoma with extramural :T
(arachnoid cyst) cyst • Bone CT: Enlarged sharply marginated :::J
o
jugular foramen 0:
o Neuro-otologist refer to as "herald cyst" ()
o Imaging
• Tl C+ MR shows enhancing mass with (f>
intramural cysts arising from jugular CO
• CPA-lAC mass with extramural cyst 3
foramen & projecting superomedially (f>
• Tl C+ MR: Enhancing solid tumor
component rare ± arachnoid cyst into CPA cistern often with brainstem
• Schwannoma, Facial Nerve, CPA-lAC with compression
Cyst
o Rare CPA-lAC mass with "labyrinthine tail"
involving labyrinthine segment of facial
nerve canal
o Often present with hearing loss before
facial nerve symptoms
o Imaging
• CT: Labyrinthine segment CN? may be
enlarged
Epidermoid Cyst, CPA-lAC
I
lhat insinuates into foramen of Luschka =
Axial T7 C+ MR reveals a low signal epidermoid cyst
and
cerebellar hemisphere E:I. OWl MR sequence would
Axial T7 C+ FS MR demonstrates a right CPA cistern
arachnoid cyst = displacing the proximal facial and
vestibu/ocochlear nerves anteriorly H2.
4
show restricted diffusion.
29
(/)
CYSTIC CPA MASS
E
ell
en
u
-0
·0 Vestibular Schwan noma with Intramural Vestibular Schwannoma with Intramural
C
~ Cyst(s) Cyst(s)
U
~
<Il (Left) Axial T1 C+ MR shows
<Il a large enhancing vestibular
.0
:J schwannoma projecting from
(f)
-0 the lAC 1:1'1 into the CPA.
C The tumor has a large
<Il
(/)
intramural cyst 81 &
ell compresses the brainstem
u
<Il and cerebellum. (Right) Axial
a. T1 C+ MR reveals the
(f)
inFerior aspect of a large
<Il
·x enhancing vestibular
<Il, schwannoma in the leFt CPA
~
<Il cistern. An unusually
X prominent intramural cyst is
w present 81.
C
III
~
III
"t:l
c
III
:J
-"rn
(LeFt) Axial T I C+ FS MR
demonstrates a cystic mass
in the right cerebellopontine
angle cistern with an
enhancing wall 1:1'1. Adjacent
enhancing, thickened
meninges are also seen 9.
(Right) Coronal T1 C+ rs
MR shows multiple cysts in
the right cerebellopontine
angle cistern -= causing
mass effect on the brainstem.
Secondary hydrocephalus is
present.
Hemangioblastoma Hemangioblastoma
(LeFt) Axial T1 C+ FS MR
shows an inlracerebelfar
mixed cystic-solid
hemangioblastoma
projecting into the leFt
cerebellopontine angle
cistern area. The solid
nodule is avidly enhancing
1:1'1 (Right) Axial T2WI MR
reveals an intra cerebellar
high signal
hemangioblastoma
projecting into the
cistern area. Contrast is
required to define enhancing
nodule if present.
I
4
30
CYSTIC CPA MASS CJl
"
c:
III
:l
a.
Vestibular Schwannoma with Arachnoid ...
OJ
III
Large Endolymphalic Sac Anomaly (IP-2) Cyst
:l
a large endolymphatic sac m
=:J within the posterior wall ...0>
~
of the T-bone. CT would ,
0>
reveal a large bony vestibular ~.
aqueduct in this patient with 0>
large endolymphatic sac en
-0
anomaly. (Right) Axial T2WI 0>
MR shows a vestibular ()
Cll
schwannoma =:J
projecting (fl
from the lAC into the CPA 0>

:l
cistern. An associated a.
arachnoid cyst is visible a en
c:
compressing the brainslem & c-
4th ventricle ~ . ...0>
O>
()
::J
:l
o
a:
o
Schwannoma, Facial Nerve, CPA-lAC
with Cyst
-
(fl
...:l
Cll
(fl
reveals a cerebellopontine
angle enhancing tumor =:J
with prominent intramural
cysts. The lesion did project
into the lAC but did not
involve the labyrinthine
facial nerve. (Right) Axial
TI WI MR shows small mass
anterior to the
pOnlamedullary junction =:J.
The neurenteric cyst is
well-delineated and does not
enhance significantly.
Schwannoma, Jugular Foramen with Schwannoma, Jugular Foramen with

Intramural Cyst Intramural Cyst
(Left) Axial T I C+ MR
demonstrates an ovoid
enhancing mass in low CPA
cistern =:J. Multiple
intramural cysts suggest the
diagnosis of schwannoma.
Extension into jugular
foramen is evident 81.
(Right) Axial T2WI FS MR
reveals large sharply
marginated lesion in the
jugular foramen E2. High
signal mass projects medially
into the low CPA cistern
where it compresses the
brainstem =.
I
4
31
en PREPONTINE CISTERN MASS
c
~
Q)
Cil
U
DIFFERENTIAL DIAGNOSIS o Assess real vs. artifact in other planes
"0
'0 o Minimize TOF losses: Use short TE, image
C
.c Common parallel to flow, acquire thicker slices
o
ro
~ • CSF Flow Artifact • Dolichoectasia (Vertebrobasilar)
ro • Dolichoectasia (Vertebrobasilar)
.n o Older patients
::J
(/) • Fusiform Aneurysm, ASVD o Look for ASVDin other vessels
"0
C • Meningioma o Ectasia often extends into branches
ro
en • Metastases, Skull and Meningeal o May have significant mass effect on pons
Q)
o • Fusiform Aneurysm, ASVD
ro
Cl
Less Common
(/)
• Epidermoid Cyst o Long segment fusiform arterial dilatation
ro • Chiari 2 ("Creeping Cerebellum") o Involves long nonbranching segments
·x
ro, • Exophytic Brainstem Glioma, Pediatric o Calcifications common
ro
~
• Pituitary Macroadenoma (Giant) o Lumen enhances strongly, clot does not
X
w • Neurocysticercosis • Meningioma
C
• Intracranial Hypotension o Clival dural-based enhancing mass
III
~ o Infratentorial (8-10%): CPA most common
aI Rare but Important
"0 o Causes cranial neuropathies or ataxia
c • Inflammatory Mass
III • Metastases, Skull and Meningeal
o Tuberculosis
o Enhancing lesion(s) with skull/meningeal
o Fungal Diseases
destruction/infil tra tion
o Neurosarcoid
o Manifestations: Smooth thickening,
• Clival Neoplasms nodularity, loculation, fungating masses
o Chordoma, Clivus
o Image entire neuraxis!
o Chondrosarcoma, Skull Base
o Plasmacytoma, Skull Base Helpful Clues for Less Common Diagnoses
o Nasopharyngeal Tumor (Invading Clivus) • Epidermoid Cyst
• Schwannoma o Usually extends medially from CPA cistern
• Arachnoid Cyst o Lobulated, irregular, insinuating CSF-like
• Craniopharyngioma mass
• eurenteric Cyst o Doesn't completely suppress on FLAlR;
• Ecchordosis Physaliphora restricts on DWI
• Chiari 2 ("Creeping Cerebellum")
o Small posterior fossa with low torcular
ESSENTIAL INFORMATION herophili
Key Differential Diagnosis Issues o Cerebellar hemispheres/tonsils herniate
• Anatomy anteriorly - "creeping"
o Extensive CSF space along ventral & lateral o Pons, cranial nerve roots often elongated
pons, dorsal to clivus (a.k.a, pontine • Exophytic Brainstem Glioma, Pediatric
cistern) o Nonenhancing mass markedly expanding
o Bounded superiorly by interpeduncular pons; may engulf basilar artery
cistern, inferiorly by subarachnoid space of o Infiltrative have poor survival
spinal cord, & continuous about medulla o Focal are uncommon, better prognosis
with cerebellomedullary cistern • Pituitary Macroadenoma (Giant)
• Many abnormalities, often from transpatial o No distinct pituitary gland
processes o Bone CT shows benign bony margins
o Early intense but heterogeneous CTST+
Helpful Clues for Common Diagnoses o Dural "tail" may mimic meningioma
• CSF Flow Artifact • Neurocysticercosis
o MR artifacts divided into 2 categories:
o Cisterns> parenchyma> ventricles
Time-of-flight effects & turbulent flow o Basal cistern cysts may be racemose
I o Worsens with thinner slices, longer TE,
and imaging perpendicular to flow
o Cysts variable, typically 1 cm, range from
5-20 mm, contain a 1-4 mm scolex
4
32
PREPONTINE CISTERN MASS (/)
~
c:
Ql
o Most are isointense to CSF • Hyperintense on T2WI, enhances j
Co
• Intracranial Hypotension strongly but heterogeneously I:D
...•
o Sagittal shows brain descent in 40-50% • Chondroid mineralization on CT (50%) III
j
o Pons may be compressed against clivus o Plasmacytoma, Skull Base
m
o Diffusely, intensely enhancing dura in • Solitary intraosseous osteolytic soft tissue ~
...•
85% mass with non-sclerotic margins OJ
ro
o Bilateral subdural fluid collections in 15% • Peripherally displaced osseous ~.
OJ
expansion/fragmentation may be seen
Helpful Clues for Rare Diagnoses (/)
o Nasopharyngeal Tumor (Invading -0
• Inflammatory Mass OJ
Clivus) Cl
(1)
o Tuberculosis
• Basilar meningitis, pulmonary TB
• Often squamous cell CA arising from '"
OJ
j
nasopharyngeal mucosal space 0.
• Thick basilar exudate ± (j)
• Multi-planar MR images best show c:
tu berculomas/ abscesses 0-
invasion of clivus OJ
...•
o Fungal Diseases OJ
• Schwannoma Cl
• Blastomycosis, coccidiomycosis, ::r
o T2 hyperintense, enhance j
histoplasmosis, candidiasis Q.
• Arachnoid Cyst 0.
• Meningeal enhancement, multiple ()
o Extra-axial cyst follows CSF
enhancing brain lesions '"CD...•
attenuation/signal
o Neurosarcoid j
o Suppresses completely with FLAIR;no DWI
• Classically infiltrates dura,
restriction
'"
leptomeninges, basal cisterns
• Craniopharyngioma
• Solitary or multifocal CNS mass(es) ±
o 90% Ca++, 90% cystic, 90% enhance
abnormal CXR
o May extend behind sella into posterior
• Clival Neoplasms
fossa
o Chordoma, Clivus
• Neurenteric Cyst
• Destructive midline mass centered in
o Round/lobulated nonenhancing, slightly
clivus with high T2 signal intensity
hyperintense to CSF mass
• Sagittal images show tumor "thumb"
o Benign malformative endodermal CNS cyst
indenting anterior pons
• Ecchordosis Physaliphora
o Notochord remnant
• Arises from petro-occipital fissure
o Extends from clivus into prepontine
• May extend posteriorly into prepontine
cistern
cistern
o Hyperintense on T2WI
I
Axial FLAIR MR reveals a hyperintense artifact= due
to CSF turbulent flow. Also note sulcal hyperintensity a dolichoectatic basilar artery=
Axial T1 C+ MR demonstrates luminal enhancement of
with associated
4
from subarachnoid hemorrhage H1 deformation of the pons SI.
33
(j)
E
PREPONTINE CISTERN MASS
QJ
lQ
()
"0
'0
C
.s:: Fusiform Aneurysm, ASVD
()
~ (Left) Sagittal TI WI MR
':::l"
.0 shows a large mass anterior
to the pons and medulla =
(f)
"0
Note mixed hyper-,
C isoinlense signal caused by
'"
(j)
QJ
slow flow & laminated clot in
this classic ASVD (usi(orm
()
aneurysm. (Right) Sagittal TI
'"
n.
(f) C+ MR demonstrates avid
meningioma enhancement
=::I as well as enhancing
dural tails~.
Metastases, Skull and Meningeal Metastases, Skull and Meningeal

demonstrates extensive renal
cell metastatic disease
overlying dura =
involving the clivus &
effacing
the prepontine cistern Ea.
(Right) Axial T I C+ MR
shows a typical MR case of
leptomeningeal seeding of
carcinoma along the folia of
the cerebellum and the
brainstem =as well as
within bilateral Meckel cave
ffi
(Left) Sagittal TI WI MR
depicts a nearly csr
isointense, nonenhancing,
multilobulated epidermoid
within prepontine,
interpeduncular, &
quadrigeminal cisterns =.
Note flattening of the pons
EllI. (Right) Axial T2WI MR
shows cerebellar
hemispheres herniating or
Ifcreeping" = anteriorly due
to a congenitally small
posterior fossa of Chiar; 2.
I
4
34
PREPONTINE CISTERN MASS Ul
;><"
c:
Ql
::::l
Co
..,
OJ
Ql
Exophytic Brainstem Glioma, Pediatric Pituitary Macroadenoma (Giant)
::::l
a diffuse brainslem glioma m
asymmetrically involving the ~
pons = with a small
anterior exophytic
OJ
0,
x
component extending into !il
the right prepontine cistern (f)
~. (Right) Sagillal T2WI MR "0
Q)
()
shows a giant
CD
macroadenoma
w/suprasellar extension =- '"::::l
Q)
invading anteriorfy into a.

basisphenoid 81 & (f)
c:
posteriorly into basi-occiput 0-
Q)
~ pons & basilar are
OJ
(fallenedffi ()
:::r
:J
o
0.:
o
(ii.
CD
..,
:J
Intracranial Hypotension
(Left) Axial T2WI MR shows '"
multiple racemose cysts in
the subarachnoid spaces
including the CPA and
quadrigeminal & prepontine
cisterns =.Also note cysts
within suprasellar cistern ~.
(Right) Sagittal Tf C+ MR
demonstrates obliteration of
the suprasellar & prepontine
cisterns
midbrain,
=with a sagging
pontine flattening
against the clivus, dural
enhancement, &. tonsillar
descent.
(Left) Axial Tf C+ MR
demonstrates typical TB
enhancing exudative
meningitis filling the basilar
cisterns =.(Right) Sagittal
Tf C+ MR shows TB
abscesses within the basal &
prepontine cisterns =
as
well as 3rd ventricle 81.
I
4
35
rn PREPONTINE CISTERN MASS
c
~
QJ
U;
U
:Q
o
c
.r: Fungal Diseases Fungal Diseases
o
ro
~ (Left) Axial TI C+ MR shows
ro thick enhancement in the
.J:J
:J subarachnoid space & along
CI)
the pia /illing the prepontine
-0
C
ro
cistern= and extending
into the le/tlAC 81.
rn
QJ Diagnosis: Cocci meningitis.
o
ro (Right) Axial TI C+ MR
c. demonstrates fine linear
CI)
.~
x
ro,
=
enhancement along the pia
from candida meningitis.
~
X
w
c:
.n;
•..
1XI
"c:
III
:J
""I/) Neurosarcoid Chordoma, Clivus
(Le/t) Sagittal TI C+ MR
demonstrates a typical
neurosarcoid appearance &
location with marked
multi/ocal dural-based
enhancement =;
sella/parasellar & basal
cisterna/location is classic.
(RighI) Sagittal T I C+ MR
shows a "honeycomb"
pallern of enhancement with
replacement 0/ the clivus a
posteriorly =
"thumbing" of the pons
& anterior
extension into the sphenoid
sinus !im.
Chondrosarcoma, Skull Base Plasmacytoma, Skull Base

reveals chondrosarcoma =
originaling from
petro-occipital fissure,
extending posterosuperiorly
into Meckel cave a
prepontine and
cisterns. (Right) Sagittal
TlWI MR demonstrates
plasmacytoma = expanding
the clivus and elevating the
pituitary gland P!:J.
I
4
36
PREPONTINE CISTERN MASS CJl
""c:
III
::l
a.
..,
[D
Schwan noma III

::l
(Left) Sagiltal T7 C+ MR
demonstrates m
nasopharyngealSSCA ?:$.
..,
infiltration of the mucosal
space ~ as well as
'r"o
x
abnormal marrow signal and iii'
cortical destruction involving CJl
an expanded clivus =.2. "0
(Right) Axial T7 C+ MR '"

()
(1)
trigeminal If] schwannomas '"':":l
in a patient with a.
neurofibromatosis type 2. (JJ
c:
c:r
..,
'"
'::r"
()
::l
o
Ci
o
'"CD
3
Arachnoid Cyst Craniopharyngioma
(Left) Sagittal T7WI MR '"
demonstrates a primarily
suprasellar cistern arachnoid
cyst=.2 extending into the
interpeduncular SI and
prepontine cisterns r:=. Note
flaltening of the pons &..
(Right) Sagiltal T7 WI MR
demonstrates hyperintense
mass in prepontine cistern
~ that is connected to
suprasellar mass ~ by a thin
stalk Craniopharyngioma
was found at surgery.
Predominance of tumor mass
in posterior fossa is unusual.
(Left) Sagiltal T7 WI MR
reveals a well-delineated,
slightly ovoid, lobulated
mass = that was
hyperintense to CSF on all
sequences. (Right) Axial
T2WI FS MR shows a
lobulated mass in prepontine
cistern that indents pons =-
is hyperintense to CSF.Note
subtle dehiscence of clivus
B from which lesion arose.
I
4
37
(/)
c CISTERNA MAGNA MASS
~
Q)
u;
U
DIFFERENTIAL DIAGNOSIS o Treatment aim = restore normal CSF flow
"0
·0 at foramen magnum (FM)
C
.<: Common • Chiari 2
u
CIl
~ • Herniation Syndromes, Intracranial o Small PF ~ contents shift j.
CIl
.0 • Chiari 1 o "Cascade" of tissue (vermis, not tonsil)
:::J
CfJ • Chiari 2 herniates j. through FM
"0
C • Dandy-Walker Continuum (DWe) o - 100% associated myelomeningocele
CIl
(/)
Q) Less Common • Dandy-Walker Continuum (DWe)
U o DWC a broad spectrum of cystic posterior
CIl
Cl.
• Arachnoid Cyst
CfJ • Ependymoma fossa (PF) malformations
CIl o DW malformation: Large posterior fossa
·x • Meningioma
,
CIl
• Metastasis and large CSF cyst, normal 4th ventricle
~ absent, lambdoid-torcular inversion
x • Intracranial Hypotension
w o OW variant: Failure of "closure" of 4th
c: Rare but Important Ventricle, vermian hypoplasia
ltl
~ • Subependymoma o Mega cisterna magna: Communicates
!Xl • Epidermoid Cyst
"0 freely with 4th ventricle, basal
c: • Dermoid Cyst
ltl subarachnoid spaces
• Hemangioblastoma o 2/3 have associated C Sand/or
• Neurenteric Cyst extracranial anomalies
ESSENTIAL INFORMATION • Arachnoid Cyst
Key Differential Diagnosis Issues o Sharply demarcated extra-axial cyst that
• Cisterna magna (CM) between medulla follows CSF attenuation/signal

(anterior), occiput (posterior) (a.k.a., o FLAIRsuppresses; no diffusion restriction
cerebellomedullary cistern) o Size varies from a few mms to giant

o Below/behind inferior vermis o Often asymptomatic, found incidentally
o Large medullary cistern masses may extend o CPA location> CM
laterally, posteriorly into CM • Ependymoma

• Most common adult lesions are o Cellular ependymomas more common in
tonsillar-associated children
o Indirect (secondary effect on tonsil) > o Soft or "plastic" tumor squeezes out of 4th
direct (lesion in tonsil) ventricle foramina into cisterns
• MR and clinical information helps DDx o Ca++ common (50%); ± cysts, hemorrhage
o Sagittal imaging can distinguish origin as
Helpful Clues for Common Diagnoses floor vs. roof of 4th ventricle
• Herniation Syndromes, Intracranial o Heterogeneous Tl/T2 signal with mild to
o Most often 2° to posterior fossa (PF) mass
moderate enhancement
effect • Meningioma
o Tonsils pushed down into CM o CM rare PF location (CPA, medullary
o "Peg-like" configuration of tonsils cisterns more common)
o Tonsil folia usually oriented horizontally ~
o CM meningiomas usually arise from
become vertically oriented when herniated occipital squamosa
o 4th ventricle may obstruct, cause o Well-demarcated, lobulated/rounded
obstructive hydrocephalus enhancing mass with dural attachment
• Chiari 1 o Hyperostosis, tumoral calcifications, t
o Pointed cerebellar tonsils "- 5 mm below vascular markings
foramen magnum • Metastasis
o Posterior fossa (PF) usually normal size o Linear or nodular meningeal enhancement
I o Age-related tonsil descent below
"opisthion-basion line" common
o MR CSF flow may be helpful establishing
location and degree of CSF obstruction
4
38
CISTERNA MAGNA MASS CIl
'"
c:
III
o Primary tumors include breast, lung, • Dermoid Cyst ::l
Q.
melanoma, prostate o Fat appearance: Use fat suppression
sequence to confirm
...
to
o Lymphoproliferative malignancy = III
::l
lymphoma and leukemia o With rupture find fat droplets in cisterns,
m
o Primary CNS tumor seed basal cisterns sulci, ventricles with extensive MR
...~
(drop metastases) enhancement possible from chemical ,
QJ
QJ
o Image entire neuraxis! meningitis ~.
QJ
• Intracranial Hypotension o Rare: < 0.5% of primary intracranial
CIl
o Sagittal shows brain descent in 40-50% tumors
o Caudal displacement of tonsils in 25-75% o Rupture can cause significant
'"
QJ
()
CD
en
o Diffusely intensely enhancing dura in 85% morbidity/mortality QJ
:J
o Bilateral subdural fluid collections in 15% o Rare malignant degeneration into Q.
squamous cell carcinoma CIl

o Frequently misdiagnosed syndrome of c:
c:r
headache caused by • intracranial CSF • Hemangioblastoma ...
QJ
QJ
pressure from spontaneous spinal CSF leak o Intra-axial posterior fossa mass with cyst, ()
or
Helpful Clues for Rare Diagnoses enhancing mural nodule abutting pia :J
o
o Classified as meningeal tumor of uncertain c:
• Subependymoma o
histogenesis (jj.
o T2 hyperintense lobular, nonenhancing
o Familial = von Hippel-Lindau CD
intraventricular mass 3
o 7-10% of posterior fossa tumors en
o Arises from 4th ventricle floor, may extend
posteroinferiorly into cisterna magna
o Round/lobulated nonenhancing, slightly
o More common in middle-aged, older
hyperintense to CSF mass
adults
o Most intracranial NECs found in posterior
00.7% of intracranial neoplasms
fossa
• Epidermoid Cyst
o Benign malformative endodermal CNS cyst
o Lobulated, irregular, CSF-like mass with
o Part of split spinal cord malformation
"fronds" insinuates cistern
spectrum; persistent neurenteric canal
o FLAIRusually doesn't completely null;
o Location
diffusion yields high signal restriction
• Thoracic (42%), cervical (32%)
00.2-1.8% of all primary intracranial tumors
• Others: Lumbar spine, basilar cisterns,
o Congenital inclusion cysts; rare malignant
brain parenchyma
degeneration into squamous cell
• Anterior medullary, CPA cisterns> CM
carcinoma
Herniation Syndromes, Intracranial
I
Sagittal TI WI MR shows cerebellar tonsillar herniation
!J:l:l from a large left posterior fossa mass. Note
Sagittal T2WI MR shows a classic case of Chiari I with
pointed cerebellar tonsils ~ protruding through the
4
4th ventricle H:I. Supratentorial foramen magnum and effacing the cisterna magna.
compression of
=.
ventricles are enlarged
39
CISTERNA MAGNA MASS
Chiari 2 Dandy-Walker Continuum (DWC)

shows caudal descent of
cerebellar verm;an tissue =
and elongated 4th ventricle
!:ll as well as callosal
dysgenesis 81 and a small
posterior fossa. (Right)
Sagittal T1WI MR
demonstrates markedly
enlarged posterior fossa with
huge cisterna magna cyst B:I
in continuity with 4th
ventricle. Note upwardly
rotated superior vermian
remnant 11].
Arachnoid Cyst
(Left) Sagittal T1 WI MR
shows a CSF isointense
arachnoid cyst 81 filling the
cisterna magna, flattening
junction =-
the cervicomedullary
extending
caudally into the upper
cervical canal. (Right)
enhancing tissue extruding
through the foramen of
magna =-
Magendie, filling cisterna
and causing
=
enlarged cerebral aqueduct
dilated 3rd ventricle 81.
Metastasis
tumor =
demonstrates dural-based
with significant
mass effect compressing and
displacing the cerebellum.
Note the /rapped CSF clefts
!:ll. The tumor encroaches
on cisterna magna. (Right)
Axial T1 C+ MR shows a
typical case of primary CNS
lymphoma with
subependymal tumor spread.
Note a posterior fossa mass
near the foramen of Luschka
= as well as a 2nd
dural-based mass 81.
I
4
40
CISTERNA MAGNA MASS
III
:J
Co
Ol
.,
III
(Left) Sagitlal TI C+ MR
:J
shows obliteration of the m
suprasellar cistern =
sagging/fat midbrain with
~
~
,
Q)
Q)
closed angle between the x
0;'
dural enhancement =-
peduncles and the pons 8l
and
tonsillar descent Ii8 (Right)
(fJ
l:l
Q)
()
Sagiual TI C+ MR in 40 yo
Ctl
male shows an enhancing (J)
Q)
mass at the bottom of the ::J
4th ventricle =:2
filling the n.
cisterna magna. (fJ
c
rr
Q)
~
Q)
()
:::r
::J
o
a:
o
(J)
CD
~
::J
Dermoid Cyst (J)
(Left) Sagitlal TlWf MR

shows a typical case of a
large 4th ventricular
epidermoid cyst =-
which
follows CSF intensity but is
often slightly brighter and
mildly heterogeneous in
signal. (Right) Axial T2Wf
MR demonstrates a T2
hyperintense mass =:2
encroaching laterally upon
the cisterna magna. There
was evidence of rupture (not
shown) causing recurrent
meningitis.
Hemangioblastoma
demonstrates a mostly solid
hemangioblastoma =:2
involving the cerebellar
tonsils and effacing the
cisterna magna. (RighI) Axial
T f C+ MR shows a
neurenteric cyst encroaching
upon the cisterna magna EB
Although most often these
are located anteriorly, when
large they may extend
posteriorly as in this case.
I
4
41
(/)
c
~
FORAMEN MAGNUM MASS
Q)
(j)
o DIFFERENTIAL DIAGNOSIS • Chiari 1
"0
·0 o Small posterior fossa, crowded FM
C
.r: Common o Low-lying, pointed cerebellar tonsils; > 5
()
co
~ • Acquired Tonsillar Herniation mm below FM
co
.0 • Dolichoectasia (Vertebrobasilar) • Chiari 2
::J
CJ) • Chiari 1 o Complex malformation of hindbrain with
"0
C • Chiari 2 lumbar myelomeningocele
co
(/) • Diffuse Astrocytoma, Low Grade o Tissue herniates through FM behind upper
Q)
()
co Less Common cervical cord
a.
CJ) • Meningioma o Elongated, "straw-like" 4th ventricle
co o Associated with dural abnormalities,
·x • Schwannoma
co,
• Ependymoma "beaked" tectum, "towering" cerebellum,
co
~
X • Metastases, Intracranial, Other dysgenic corpus callosum
w • Diffuse Astrocytoma, Low Grade
• Subependymoma
c o Primary astrocytic brain tumor with
co • Hemangioblastoma
"-
CO • Intracranial Hypotension intrinsic tendency for malignant
-0
• Skull Base Masses progression
c
o Chordoma, Clivus o 50% of brain stem "gliomas" are low-grade
'" astrocytoma; occur in pons & medulla of
o Giant Invasive Pituitary Macroadenoma children
o T2 hyperintense mass; ± enhancement
Rare but Important
• Epidermoid Cyst Helpful Clues for Less Common Diagnoses
• Dermoid Cyst • Meningioma
• Syringomyelia o Extra-axial, enhancing, dural-based mass
• Neurenteric Cyst with dural "tails"
o Often occur along clivus with extension
through FM
ESSENTIAL INFORMATION • Schwannoma
Key Differential Diagnosis Issues o Benign encapsulated nerve sheath tumor
• Foramen magnum (FM) is posterior skull composed of differentiated neoplastic
base aperture in occipital bone Schwann cells
o Transmits medulla oblongata, vertebral o Enhancing extra-axial mass; T2
arteries & accessory nerves (CNll) hyperintense
• FM mass can be divided into intra-axial, o Often occur along cranial nerves at skull
extra-axial, & skull base masses base with extension into FM
• Cisterna magna is skull base cistern between • Ependymoma
medulla anteriorly & occiput posteriorly o Soft or "plastic" tumor, squeezes out
through 4th ventricle foramina
Helpful Clues for Common Diagnoses 02/3 infratentorial, 4th ventricle
• Acquired Tonsillar Herniation o Heterogeneously enhancing 4th ventricle
o Secondary to posterior fossa mass effect or
mass
severe hydrocephalus • Metastases, Intracranial, Other
o Tonsils pushed inferiorly, impacted into
o Enhancing mass, usually multiple
FM o Primary tumor typically known
o Cisterna magna obliterated • Subependymoma
o 4th ventricle may obstruct causing o Rare, benign, well-differentiated,
hydrocephalus intraventricular, ependymal tumor
• Dolichoectasia (Vertebrobasilar) o Intraventricular, inferior 4th ventricle
o Dilated, ectatic vessels in older patient
typical (60%)
I o Typically affects vertebrobasilar system
o May mimic a PM mass
o T2 hyperintense lobular mass
o Usually middle-aged or elderly male
4
42
FORAMEN MAGNUM MASS en
~
c:
Ql
• Hemangioblastoma o CSF-like, lobular, extra-axial mass :J
C-
o Posterior fossa mass with cyst, enhancing insinuates into cisterns, encases
mural nodule (60%); 40% solid mass
.,
O:!
nerves/vessels Ql
o 80% cerebellar hemispheres; 15% vermis, o CPA 40-50%, 4th ventricle 15-20% :J
5% medulla, 4th ventricle m

• Dermoid Cyst ~
.,
o Often extend through FM o Midline mass with fat, may rupture OJ,
OJ
• Intracranial Hypotension o May involve posterior fossa, vermis, 4th X
0;.
o Brain descent with tonsillar herniation ventricle
(fJ
&/or "sagging midbrain" in 40-50% • Syringomyelia l:l
OJ
o Diffuse, intense dural enhancement 85% o Cystic spinal cord cavity not contiguous ()
CD
en
o Headache caused by reduced intracranial with central cord canal OJ
:J
CSF pressure o Expanded spinal cord with dilated, beaded, C>-
• Chordoma, Clivus or sacculated cystic cavity (fJ
c:
<J
o Rare malignant tumor arising from • Neurenteric Cyst OJ
.,
remnants of primitive notochord o Round/lobulated nonenhancing, slightly OJ
()
::T
o Destructive, T2 hyperintense midline mass hyperintense mass in front of medulla, :::J
o
in clivus near pontomedullary junction c:
o May extend into FM o
Alternative Differential Approaches (ji"
• Chondrosarcoma, Skull Base • Intra-axial mass: Diffuse astrocytoma,
CO
o Chondroid malignancy of the skull base, 3
en
hemangioblastoma, metastases
typically centered on petro-occipital fissure
• Extra-axial mass: Meningioma,
o Chondroid matrix on CT 50%; > 50% bone
schwannoma, epidermoid, dermoid,
destruction
neurenteric cyst, dolichoectasia
o T2 hyperintense mass, heterogeneous
• Skull base mass: Chordoma,
enhancement
chondrosarcoma, invasive pituitary
o May extend into FM from adjacent bone
macroadenoma
• Giant Invasive Pituitary Macroadenoma
• Ventricular mass: Ependymoma, metastases,
o Pituitary macroadenoma with inferior
subependymoma, hemangioblastoma
extension to basisphenoid & basiocciput
• Tonsillar herniation: Chiari 1 & 2,
o Central skull base enhancing mass
intracranial hypotension
o No normal pituitary gland seen

• Epidermoid Cyst
Acquired Tonsillar Herniation Dolichoectasia (Vertebrobasilar)
I
Axial T2WI MR shows tonsillar herniation with the Axial T1WI MR shows ectasia of the vertebral arteries.
4
=-
tonsils completely impacted into the foramen magnum
obliterating the cisterna magna. This is commonly
related to a posterior fossa mass.
enlarged, tortuous vertebral & basilar arteries
consistent with slow flow.
=-
There is high signal (entry slice phenomenon) within
43
(/l
c FORAMEN MAGNUM MASS
~
Q)
en
o
"0
·0
C
.I::
U
ro
~ (Left) Sagittal T1 WI MR
ro shows herniaUon with
.0
::J diminished posterior fossa
CfJ
CSF The bony posterior
"0
C fossa is small leading to a
ro "mismatch" with the
(/l
Q) normal-sized cerebellum.
u
ro The pointed cerebellar
D-
CfJ tonsils ~ protrude through
the foramen magnum.
ro
·x (RighI) Sagittal T2WI MR
ro, shows dysgenesis of the
ro
~ corpus callosum ~ small
X posterior fossa, "beaked"
w tectum & downward
C shift of the pons, 4th
III
~ ventricle, & cerebellum.
III Note also cortical dysplasia.
"tl
c::
III
shows marked enlargement
of the medulla ~ with
foramen magnum, related to
a brainstem glioma. Note
encasement of the basilar
artery. (Right) Sagittal T1 C+
MR show5 a clival
meningioma with marked
enhancement & a dural tail
that extends through the
foramen magnum 11):],
Schwan noma
a large, enhancing extra-axial
mass extending through the
foramen magnum with a
small lobule projecting
anteriorly into the jugular
foramen =- shown to be
glossopharyngeal
schwannoma. When farge,
5chwannomas may extend
through the foramen
magnum. (Righi) Sagittal T1
C+ MR shows a 4th
ventricular heterogeneously
enhancing mass extending
posleroinferiorly into the
cisterna magna & foramen
I magnum!:].
4
44
FORAMEN MAGNUM MASS
Ql
;j
Co
...
OJ
Hemangioblastoma Ql
(LeFt) Sagittal T2WI MR

::I
shows a large; m
heterogeneous 4 th ~
Q],
ventricular subependymoma
= with extension through
the foramen magnum.
OJ
X
OJ
Heterogeneity is usually seen (f)

'0
in larger lesions, related to OJ
()
cystic changes, blood (1)
products, &Ior calciFication. (/)
(Right) Sagillal n C+ MR OJ
:::J
shows an enhancing vermis C.
mass extending through the (f)
C
Foramen magnum Ell with IJ'
OJ
associated hydrocephalus. ~
OJ
These primary tumors are ()
::J'
most common in the ;j
cerebellar hemispheres. Q.
c.
o
(/)
m
~
;j
Dermoid Cyst (/)
(LeFt) Coronal T2WI MR

shows a lobulated
hyperintense mass extending
through the Foramen
magnum =.Bright OWl
conFirms the diagnosis of
epidermoid. (Right) Sagiual
nWI MR shows a
hyperintense extra-axial mass
at the foramen magnum =.
Fat-saturation technique
confirms fat in this dermoid
cyst.
Syringomyelia Neurenteric Cyst

shows syringomyelia
extending into the brainstem
(syringobulbia). There is T2
hyperintense signal with
expansion of the spinal cord
extending From the medulla
to the cervical spinal cord.
(Right) Sagittal nWI MR
shows a large,
well-delineated extra-axial
foramen magnum mass =
elevating & displacing the
pons & medulla. The mass is
very slightly hyperintense
compared to CSF. Typical
location for neurenteric cyst.
I
4
45
(/l
c ENHANCING CRANIAL NERVE(S)
~
OJ
u;
(5 o Known neoplasm
'0 o Flu-like illness (ADEM, viral neuritis)
C
L
Common
U Helpful Clues for Common Diagnoses
~ • Metastases
ro
• Neurofibromatosis Type 2 • Metastases
.0
:J o Most common: CSF spread
(j) • Neurofibromatosis Type 1
"0
o Plexiform eurofibroma • Involves pia, CNs, may extend along
c
ro
o Optic Nerve Glioma
perivascular spaces
(/l
OJ • Multiple thickened nerves> solitary
u
ro
• Multiple Sclerosis
0. o Optic Neuritis
involvement
(j)
• Fundus of CPA/lAC most common site
ro Less Common
·x o Less common: Perineural tumor extension
ro,
ro
• Viral, Post-Viral Neuritis from extracranial primary
~ o Bell Palsy
X • Extension into cisternal CN uncommon
w o Herpes Zoster • Squamous cell, adenoid cystic carcinoma
c o ADEM
•..
ro (CNS, ? involvement most common)
lD • Lyme Disease • Neurofibromatosis Type 2
"C
c: • Lymphoma o Multiple schwannomas
III
• Neurosarcoid o Bilateral acoustic schwannomas diagnostic
• Opportunistic Infection, AIDS o Acoustic schwannoma plus schwannoma
• Leukemia of one other CN highly suggestive
Rare but Important o Schwannoma of "small" CN (e.g., C 3, 4)
• Ischemia should raise consideration of F2

o Diabetes • Neurofibromatosis Type 1
o Arteriolosclerosis (Microvascular Disease) o Plexiform Neurofibroma
• Langerhans Cell Histiocytosis • Intracranial involvement less common
• Chronic Inflammatory Demyelinating than scalp, orbit, face (e.g., parotid
Polyneuropathy (ClOP) gland)
• Plexiform neurofibromas of CN3 or CNS
may extend intracranially, involve
ESSENTIAL INFORMATION cavernous sinus
Key Differential Diagnosis Issues o Optic Nerve Glioma
• Enhancement of cisternal, cavernous sinus • Most are typical pilocytic astrocytomas
CN segments always abnormal (PAs)
• Which cranial nerve(s) affected? • 15-20% of NFl patients develop PA
o Optic nerve: MS, NFl (optic glioma), (most commonly in optic pathway)
viral/post-viral • Up to 1/3 of patients with optic pathway
o C 3, 6: Often ischemia (diabetes, PA have Nfl
arteriolosclerosis) • Enhancement varies from none to
o CN?: Bell palsy, Herpes zoster (Ramsay striking
Hunt) • May be uni- or bilateral, extend to/from
o CN8: Schwannoma (sporadic or NF2 orbit, involve
associated), metastasis nerves/ chiasm/h ypotha lam us
• If multiple nerves involved, consider • Multiple Sclerosis
o Metastases, lymphoma, leukemia o Optic nerve (ON) most commonly affected
o NF2 o 50-60% of patients with optic neuritis
o Lyme disease ultimately develop MS
o ClOP (especially if nerves massively o Imaging
enlarged) • Mildly enlarged, enhancing ON
• History important • 40% extend to intracanalicular,
I o Optic neuritis (majority have or develop prechiasmatic/chiasmatic segments
MS)
4
46
ENHANCING CRANIAL NERVE(S) en
"
c:
III
• Other CNs (e.g., trigeminal nerve) less o Most common intracranial involvement = ::::l
Co
commonly affected optic nerve/chiasm/hypothalamus lD
....•
o Non-MS associated optic neuropathy o Other CNs rare III
::::l
• Infectious (viral) • Opportunistic Infection, AIDS
o Tuberculous meningitis, CMV neuritis
m
• Anterior ischemic optic neuropathy ~
....•
(AION) (retina, optic nerve) Q)
,
Q)
x
Helpful Clues for Less Common Diagnoses Helpful Clues for Rare Diagnoses 0;"
• Viral, Post-Viral Neuritis • Ischeluia (f)
"0
o Bell Palsy o Diabetes, microvascular disease Q)
()
<tl
• Enhancement of intratemporal facial • CN3, 6 most commonly affected Ul
nerve • Optic nerve (anterior ischemic optic Q)

::::l
Co
• "Tuft" of enhancement in lAC less neuropathy) less common (f)
common o Transient enhancement, then atrophy C

cr
Q)
o Herpes Zoster • Langerhans Cell Histiocytosis iil
()
• Ramsay Hunt syndrome (Herpes zoster o Usually children :J"
:::l
oticus) = vesicular rash of pinna, o Optic o
nerve/ ch iasm/h ypo thala m us/ infundibular
a:
involvement of CN?, 8 in lAC, cochlea o
• Other CNs (e.g., 5) less common stalk most common Ul
CD
....•
o ADEM • Infiltrated, thickened structures enhance :::l
Ul
• Rare manifestation of post-viral strongly, uniformly
demyelination o Disseminated intracranial LCH rare
• Affected nerve minimally enlarged, • Sulcal/cisternal enhancement
enhances transiently • Multiple enhancing C s
• Lyme Disease • Chronic Inflammatory Demyelinating
o Most common = MS-like lesions in patient Polyneuropathy (CIDP)
with skin rash, flu-like illness following o Typical setting = chronic MS
deer tick bite o Serial demyelination, remyelination -
o Can involve multiple CNs (CN? most "onion bulb" thickening of affected nerves
common) o Massive enlargement, enhancement of
• Lymphoma, Leukemia spinal, cranial nerves (spinal> > C s)
o Diffuse pial tumor spread - multiple CNs
• Neurosarcoid
Metastases
I
Axial TI C+ MR in a patient with disseminated Axial TI C+ F5 MR shows thickened, enhancing V2 in a
patient with adenoid cystic carcinoma with perineural
4
metastases covering brain, CPA/lACs
abducens nerves ~.
=.
malignant glial neoplasm shows diffuse enhancing
both tumor spread in pterygopalatine fossa
along foramen rotundum
=. extending
into Meckel cave ~
47
(/)
c
~
ENHANCING CRANIAL NERVE(S)
Q)
U5
u
:g
o
c
-<: Neurofibromatosis Type 2 Neurofibromatosis Type 2
<..l
l1l
l1l bilateral acoustic
..c
:::l schwannomas with classic
(fJ
"ice cream on cone"
"0
C
l1l
appearance m. Note
(/)
arachnoid cyst associated
Q) with left lesion 82. (Right)
<..l
l1l Coronal T1 C+ FS MR in a
0- patient with known NF2
(fJ
shows trigeminal
l1l
'x schwannomas in both
,
l1l
l1l
Meckel caves =as well as
~ multiple schwannomas
X involving cervical spinal
w
nerve roots ~.
C
III
~
aJ
"tl
c
III
:::l
oX:
en Plexiform Neurofibroma Optic Nerve Glioma
(Left) Axial T1 C+ FS MR in a
patient with NF 1 shows
unusually extensive plexiform
neurofibroma of CN3
branches, extending from
orbit through markedly
enlarged orbital fissure into
expanded cavernous sinus
=. Note scalp plexiform
neurofibroma 82. (Courtesy
M. Martin, MOJ. (Right)
Axial CECT in a child with
NFl shows bilateral optic
nerve gliomas extending
through optic canals £0
chiasm =. The right optic
nerve is noticeably enlarged,
enhancing ED.

shows enhancement of
almost the entire length of
the left optic nerve =:I,
including segment within
optic canal 82. (Right)
Coronal T1 C+ FS MR in a
patient with MS, left
trigeminal neuralgia, shows
enhancing left CNS =.
Compare to normal
nonenhancing right side ED.
I
4
48
ENHANCING CRANIAL NERVE(S) 00
~
c::
III
:::l
C-
..,
O:!
Lyme Disease ~,
(Lefl) Axial T7 C+ rs
MR
:::l
with magnified view shows m
~
"(undaltuft" in lAC
enhancing labyrinthine
=-
variant case with enhancing
with
OJ,
OJ
><
segment 81 leading to Qi'
geniculate ganglion § 00
-0
(RighI) Axial T7 C+ FS MR OJ
()
shows enhancement in left (1)
lAC involving both CN7 and (J)
CN8 =. Note pial OJ

:J
enhancement along pons 81 C.
extending along CN6 from its [f)
<=
brainstem exit to Dorelia rr
OJ
canal PJ:].
OJ
()
::r
:J
o
Ci
o
w·
eD
..,
:J
Neurosarcoid (J)
(Lefl) Axial T7 C+ FS MR in a
patient with known systemic
lymphoma, right 3rd nerve
palsy shows thickened,
enhancing right oculomotor
nerve =- intraconaf
retrobulbar enhancing tumor
81. (RighI) Axial T7 C+ MR
shows enhancemen/ of both
thickened optic nerves
extending from optic cana/to
optic chiasm =.
Chronic Inflammatory Demyelinating

Opportunistic Infection, AIDS Polyneuropathy (ClOP)
(Lefl) Axial T7 C+ MR in a
patient with HIV/AIOS who
presented with confusion,
seizures, shows tubercular
meningitis r.:= that thickens,
encases the righllrigeminal
nerve [;B (RighI) Coronal T I
C+ FS MR in a 39 year old
woman with longstanding
MS, left facial pain shows
both trigeminal nerves are
thickened, enhancing ffi
I
4
49
en CSF-liKE EXTRA-AXIAL FLUID COLLECTION
c
~
Q)
Ul
U • Mega Cisterna Magna
'0 o Cisterna magna measuring> 10 mm
C
£
Common o Vermis intact
U
~
<1l • Aging Brain, Normal • Subdural Hematoma, Chronic
<1l
.0 • Enlarged Subarachnoid Spaces o Hypodense subdural collection; may be
::::J
(fJ • Mega Cisterna Magna hyperdense to CSF & have septations
"0
C • Subdural Hematoma, Chronic • Subdural Hygroma
<1l
en • Subdural Hygroma o Results from tear in arachnoid; CSF density
Q)
u
<1l
n.
(fJ • Subdural Effusion • Subdural Effusion
<1l
• Dandy-Walker Continuum o Sterile CSF-like collection associated with
'",,
<1l
• Arachnoid Cyst
~ meningitis
X • Intracranial Hypotension • Dandy-Walker Continuum
w
Rare but Important o Large posterior fossa with big CSF cyst
C
III • Extra-Axial Empyema o 4th ventricle appears contiguous with cyst
~
CO • Cephalocele/Meningocele • Arachnoid Cyst
'tl
c
III
• Epidermoid Cyst (Mimic) o CSF density/intensity ± bone remodeling
• Intracranial Hypotension
o Characteristic postural headache related to
ESSENTIAL INFORMATION reduced intracranial CSF pressure
Key Differential Diagnosis Issues o Subdural collections in 15%
• Absence of mass effect & veins traversing o "Slumping midbrain", low tonsils, dural
subarachnoid space suggests normal variant enhancement
• Aging Brain, Normal • Extra-Axial Empyema
o Decreased brain volume; mild low o Peripherally enhancing extra-axial
density/high intensity periventricular rim collection; DWI bright!
o No mass effect • Cephalocele/Meningocele
• Enlarged Subarachnoid Spaces o Congenital herniation of intracranial
o Physiologic enlargement of subarachnoid structures through a skull defect
spaces • Epidermoid Cyst (Mimic)
o Benign macrocephaly of infancy o CSF-like extra-axial mass; basal cisterns
o Head circumference> 95% common
Aging Brain, Normal Enlarged Subarachnoid Spaces
I
4 Axial T2WI M R shows prominence of subarachnoid
spaces (SAS) due to age-related cerebral involution.
Axial T2WI MR shows prominent CSF spaces in this
infant with macrocrania. Small linear flow voids g..
Lilck of mass effect & veins traversing SAS IdI is represent veins traversing the SAS. Enlarged SASresolve
characteristic. withoUltherapy by 12-24 month,.
50
CSF-liKE EXTRA-AXIAL FLUID COLLECTION en
"
c:
Ql
;,
Co
..,
OJ
Subdural Hematoma, Chronic Ql
;,
shows a prominent m
retrocerebellar CSF space 81 ~
..,
without compression. There ,
OJ
OJ
is a normal 4th ventricle & ><
vermis ~. Mega cisterna 0;'
magna is a normal variant & (f)
requires no treatment.
(Right) Axial NrCT shows
"
OJ
(1
(l)
acule-an-chronic right en
frontoparietal subdural OJ
;,
hematoma. The anterior C.
portion shows the (f)
C
hypodense chronic 0-
component I!:i'l with
m
~
OJ
associated mass effect. The (1
more acute blood layers ::T

:J
posteriorly, o
1i
o
iii'
CD
3
Dandy-Walker Continuum Arachnoid Cyst en
shows a large posterior fossa
cyst continuous with the 4th
ventricle. Note also the
superiorly rotated vermian
remnanlldl. classic for
Dandy-Walker malformation.
Patient a/so has macrocrania
& hydrocephalus. (RighI)
Axial T1 WI MR shows CSF
intensity extra-axial lesion
causing thinning of the
adjacent calvarium
arachnoid cyst. Arachnoid
=-
cysts follow CSF signal on all
MR sequences.
Intracranial Hypotension
shows small bilateral
subdural effusions = over
the cerebral convexity. Note
the diffuse dural thickening &
enhancement a
characteristic for intracranial
hypotension, (Right) Axial T1
C+ MR shows a peripherally
enhancing subdural
empyema = in this sinusitis
patient. OWl MR (not
shown) shows restricted
diffusion which can help
differentiate empyema from
more benign extra-axial fluid
collections.
I
4
51
VJ
C
CSF-L1KE EXTRA-AXIAL MASS
L-
Q)
~
()
"0 DIFFERENTIAL DIAGNOSIS Helpful Clues for less Common Diagnoses
·0
C
Common • Pineal Cyst
£
U o Lies dorsal to midbrain at pineal gland
Cll • Arachnoid Cyst
L-
Cll o Usually asymptomatic, less than 2 cm
.n • Neurocysticercosis
::::J
CfJ
• Schwannoma (Cystic)
"0
less Common o Commonly located in cerebellopontine
C
Cll • Pineal Cyst angle (CPA) cistern
VJ
Q) • Schwannoma (Cystic) o Enhancement typical
U
Cll
Q.
• Epidermoid Cyst • Epidermoid Cyst
CfJ
Rare but Important o Lobular, insinuating nonenhancing mass
Cll
·x • Neurenteric Cyst o Restricted diffusion & FLAIR
'P hyperintensity differentiates from
Cll
L-
• Leptomeningeal Cyst
X • Callosal Dysgenesis arachnoid cyst
W
c: • Holoprosencephaly (Dorsal Cyst) Helpful Clues for Rare Diagnoses

III
L- • Neurenteric Cyst
a!
'tl ESSENTIAL INFORMATION o Posterior fossa: Anterior to brainstem, CPA
c: o Nonenhancing midline or paramedian cyst
III
Key Differential Diagnosis Issues o MR signal variable (protein content)
• Enhancement is helpful to differentiate • Leptomeningeal Cyst
CSF-like extra-axial masses o Underlying brain shows encephalomalacia
Helpful Clues for Common Diagnoses o Communicates with subarachnoid space
• Arachnoid Cyst o Well-marginated skull defect at site of cyst
o Nonenhancing CSF-like mass, bone • Callosal Dysgenesis
remodeling o Interhemispheric cyst common
• Neurocysticercosis o Parallel lateral ventricles, colpocephaly,
o Cyst with a scolex is pathognomonic high riding 3rd ventricle
o Racemose (grape-like) in basal cisterns: No • Holoprosencephaly (Dorsal Cyst)
scolex is typical o Hydrocephalus is almost always present
o Subarachnoid & intraventricular disease o Look for fused thalami, absence of
often symptomatic from hydrocephalus interhemispheric fissures, septum
&/or meningitis (enhancing) pellucidum
o May see corpus callosum agenesis
I
4 Sagittal T1WI MR shows an extra-axial mass causing
'-=.
thinning of the inner table of the skull Arachnoid
cysts are benign & usually found incidentally. They
=
Sagittal T1WI MR shows a large frontal arachnoid cyst
with associated mass errect. Vast majority of
arachnoid cysts are incidentally found & require no
follow CSFon all MR sequences. treatment.
52
CSF-liKE EXTRA-AXIAL MASS
III
::::l
C.
...
OJ
III
Neurocysticercosis Pineal Cyst
::::l
multiple hypointense cysts m
with mild peripheral ~
...
Ql
enhancement. Note
Q,
interhemispheric I:] & ~.
sylvian fissure E!lI cysts. Ql
Subarachnoid spaces are the (fJ

"t)
most common location for Ql
(')
NCC cysts. Cisternal NCC (l)
may be complicated by en
Ql
meningitis, hydrocephalus, :J
or vasculitis. (RighI) Sagillal C.
T1 WI MR shows a cystic (fJ
mass = in the pineal region.
C
0-
...
Ql
These are typically less than
Ql
2 em & incidental. (')
Enhancement of compressed
::T
::::l
pineal gland may be seen. o
c:
o
(jj'
...
CD
:J
Neurenteric Cyst en
wel'·circumscribed
extra-axial mass ~ which is
isointense to CSF. FLAIR &
OWl MR can differentiate
this lesion from an arachnoid
cyst. (Right) Sagittal T1 C+
MR shows a mildly
hyperintense non enhancing
cistern =-
lesion in the prepontine
typical location
for neurenteric cyst. MR
signal is dependent on
protein content of cyst. They
are typically T I hyperintense
or isointense & T2
hyperintense (to CSf).
Callosal Dysgenesis
corpus callosum dysgenesis
with a large dorsal
interhemispheric cyst"" &
prominent azygous artery
The large dorsal cyst &
the parallel lateral ventricles
E!lI are typical of callosal
dysgenesis. (Right) Axial
NECT shows a large dorsal
cyst associated with alobar
holoprosencephaly~. Note
absence of septum
pellucidum 1:]. Streak
artiFacts ~ are due to shunt
(not shown) inserted into the
cyst. I
4
53
rJJ
SULCAL/CISTERNAL ENHANCEMENT
E
Q)
]2
U
DIFFERENTIAL DIAGNOSIS o Use imaging to detect complications (e.g.,
-0
'0 ventriculitis, hydrocephalus, subdural
C
.L: Common empyema, cerebritis/abscess, secondary
U
l\l
~ • Meningitis ischemia, dural venous thrombosis)
l\l
.0 • Meningeal Carcinomatosis • Meningeal Carcinomatosis
:J
en • Lymphomatous Meningitis o CNS neoplasms (e.g., GBM,
-0
c • Neurocysticercosis medulloblastoma, pineal tumors, choroid
l\l
rJJ • Tuberculosis Meningitis plexus tumors), extra-CNS primary tumors
Q)
U
l\l less Common (breast, lung, melanoma common)
n.
en • Neurosarcoid o Look for other lesions (parenchyma, bone)
l\l
• Sturge-Weber Syndrome • Lymphomatous Meningitis
'xl\l
, • Fungal Diseases o Involvement of leptomeninges or dura,
~l\l
• Aneurysmal Subarachnoid Hemorrhage more commonly in secondary lymphoma
X
w (Subacute May Enhance) • Primary CNS lymphoma: Typically
c periventricular parenchymal disease
• Opportunistic Infection, AIDS
~
'" o Often affects both brain, spine
llJ • Leukemia
-0 • Neurocysticercosis
c Rare but Important o Cysts often in deep sulci, may incite
=':J" • Neurocutaneous Melanosis intense inflammatory reaction
-'en
" • Meningioangiomatosis o Cisternal NCC may appear racemose
• Contrast Leakage (multilobulated, grape-like), typically lacks
scolex
ESSENTIAL INFORMATION • Complications: Meningitis,
hydrocephalus, vasculitis
Key Differential Diagnosis Issues o Cisterns> parenchyma> ventricles
• All meningitides (infectious, granulomatous, o Best diagnostic clue: Cyst with "dot"
neoplastic) have similar imaging appearance (scolex) inside
(enhancing pia ± sulcal/cisternal • Tuberculosis Meningitis
enhancement) o Most common presentation of active CNS
• Location, pattern only minimally helpful TB
• Nodular "leptomeningeal" (pial) o Predilection for basal cisterns
enhancement o Complications: Hydrocephalus, ischemia
o Meningeal carcinoma tosis
common
o Lymphomatous meningitis o Look for extracerebral TB (pulmonary)
o Tuberculosis meningitis
o TB often mimics other diseases like
o Leukemia
neoplasm
o eurosarcoid
o Fungal diseases Helpful Clues for less Common Diagnoses
• Thick basal cistern enhancement • Neurosarcoid
o Tuberculosis meningitis o Dural, leptomeningeal> > parenchymal
o Fungal diseases disease
o eurosarcoid o Lacy leptomeningeal enhancement typical
o Pyogenic meningitis o Look for infundibular stalk involvement
o Lymphoma o CXR may be helpful to assess for
o Neurosyphilis hilar/paratracheallymphadenopathy (most
have systemic disease)
Helpful Clues for Common Diagnoses • Sturge-Weber Syndrome
• Meningitis o Atrophy of affected hemisphere
o Clinical-laboratory (not imaging) diagnosis o Pial angioma enhances
• Positive CSF by lumbar puncture o Ipsilateral choroid plexus often enlarged
I o Imaging may be normal
helpful)
early (FLAIR o Abnormally prominent medullary (deep
white matter), ependymal veins
4
54
SULCAL/CISTERNALENHANCEMENT en
""C
Cll
• Fungal Diseases Diffuse/focal pial enhancement; may
o ~
Co
o Coccidioidomycosis, cryptococcus often extend into parenchyma via perivascular
basilar spaces
...
OJ
Cll
• Aneurysmal Subarachnoid Hemorrhage o Pre-contrast 1'1WI sulci/cisterns may be ~

(Subacute May Enhance) normal, iso-, or hyperintense m
o 1'2* GRE: Hypointense hemosiderin • Meningioangiomatosis
...
~
0>
deposition in 70-75% of patients with o Neurofibromatosis found in Yz of patients

dJ
><
00·
prior SAH (particularly NF2)
en
• Opportunistic Infection, AIDS o Rare, hamartomatous -0
0>
o Meningeal involvement in AIDS (HIV or cortical/leptomeningeal malformation ()
<0
rn
opportunistic infection> tumor) o Best diagnostic clue: Cortical mass with 0>
::J
• Acute aseptic HIV meningitis Ca++ (with or without cysts) Co
• Cryptococcal or TB meningitis • Contrast Leakage en

c
C-
• Lymphoma: Extension of parenchymal o Increased signal in CSF on 1'1WI and ...
O>
disease FLAIR 0>

()
::r
• Other fungal: Candidiasis, aspergillosis, o Dialysis-dependent patient with end-stage ::J
o
coccidiosis renal disease Ci
• Consider neurosyphilis o Contrast overload Q
rn
• Leukemia o Leakage from tumor ro...
::J
o Meningeal disease, usually with acute
lymphoblastic leukemia (ALL)
Other Essential Information '"
• Thin, curvilinear enhancement over brain
o Multiple lesions at multiple sites are
surface reflects pial disease
suggestive of diagnosis • Predilection for basal cisterns in
Helpful Clues for Rare Diagnoses inflammatory, granulomatous meningitis
• Neurocutaneous Melanosis
o Giant or multiple cutaneous melanocytic
nevi (GCMN) and
SELECTED REFERENCES
1. Fukui MB et al: MR imaging of thc mcningcs. Part II.
o Benign, malignant CNS melanotic lesions
Neoplastic disease. Radiology. 20] (3):60S-12, 1996
occur 2. Meltzer CC et al: MR imaging of the meninges. Part I.
o Foci of 1'1 hyperintensity (parenchymal orrnal anatomic features and nonneoplastic disease.
Radiology. 201(2):297-308, ] 996
melanosis) in amygdala or cerebellum
Meningeal Carcinomatosis
I
Axial T1 C+ MR shows extensive leptomeningeal
enhancement of the sulci
Axial T1 C+ MR reveals extensive leplOmeningeal
carcinomatosis with a basal predominance. There is
4
diffuse coaUng of the cerebellar folia with additional
nodular areas of enhancement E2.
55
(/)
c SULCAL/CISTERNAL ENHANCEMENT
~
Ql
~
o
"0
'6
c
J::
()
ro
~ (Left) Sagittal T1 C+ MR
ro shows extensive
--"::J leptomeningeal
(f)
carcinomatosis with diffuse
"0
C coating of the cerebellar folia
ro ffi Scattered nodular areas
(/)
Ql of enhancement are evident
()
ro
n.
in the supratenlorium =.
(f) (RighI) Axial T I C+ FS MR
shows enhancement in the
ro
'x
ro,
internal auditory canal =
and in Meckel cave on the
ro
~ right !G. Note extensive
X fetro-orbital enhancement in
w
this patient with lymphoma
c ffi
~
'"
III
"0
c
'::J"
en
""
shows ring·enhancing right
CPA cistern cysts 1:;;1 and
thickened enhancing
meninges 81, (RighI) Axial
T1 C+ FS MR shows small
areas of ring-enhancement in
the subarachnoid space 1:;;1.

intense basal meningeal
enhancement ffi (RighI)
Axial T 1 C+ MR shows linear
and nodular coating of the
midbrain 1:;;1, Note
thickening of the
infundibular stalk PJ:J:l,
I
4
56
SULCAl/CISTERNAL ENHANCEMENT
III
::l
a.
CD
.,
Sturge-Weber Syndrome Fungal Diseases III
(Left) Axiat T7 C+ MR shows ::l

serpentine leptomeningeal m
enhancement ffi feft ~
.,
III
cerebrat atrophy, thickening o
III
o( the catvariat diptoic space X
Qj.
=:1 and hypertrophy of the
ipsilateral choroid plexus •. en
-0
(Right) Axiat T7 C+ MR III
shows thick enhancement of o
the basal cisterns = in this
<1l
VI
III
patient with ::l
coccidioidomycosis a.
meningitis. en
c
rr
.,
III
III
o
:T
::l
o
0.:
o
(ii.
CD
.,
::l
Fungal Diseases Neurocutaneous Melanosis VI
(Left) Axiat T7 C+ MR shows

thick enhancement in the
subarachnoid space and
atong the pia =:1
Coccidioidomycosis
meningitis. (Right) Axiat TI
C+ MR shows intense
enhancement of the en/ire
surface of the brain and
adjacent subarachnoid
space. Note associated
communicating
hydrocephatus.
Meningioangiomatosis Contrast leakage

(Left) Sagittat T7 C+ MR
shows serpentine cortical
enhancement 1m. Consider
meningioangiomalosis when
a calciried corUea/lesion
\.vill1 or without cysts is
delected. (Right) Axiat FLAtR
MR in patient with renal
failure, contrast-enhanced
MRA of the abdomen (\.'1'0
days earlier shows contrast
accumulation in the CSF EE
which appears diffusety
hyperintense.
I
4
57
rJ)
C
L
FAT IN SULCI/CISTERNS/VENTRICLES
Q)
]i
U
DIFFERENTIAL DIAGNOSIS o Blood products show "blooming" artifact
"0
·0 on GRE sequence
c Common
.r.
()
o Does not suppress with fat suppression
co • Lipoma
L
co Helpful Clues for Less Common Diagnoses
.n • Subacute Hemorrhage (Mimic)
:::J
(fJ
• Dermoid Cyst (Ruptured)
"0
Less Common o Fat droplets in sulci
C
co • Dermoid Cyst (Ruptured) o Signal nulled with fat suppression
rJ)
Q)
()
• Teratoma • Teratoma
co o Midline mass containing Ca++, soft tissue,
Cl. Rare but Important
(fJ
• Lipoidal Contrast (Mimic) cysts, & fat
co
·x • Metaplastic Meningioma (Lipomatous) • Soft tissue component enhances
co,
co • Choroid Plexus Xanthogranuloma (Mimic) o Pineal region common; suprasellar less
L
X • Encephalocraniocutaneous Lipomatosis common

W
c: Helpful Clues for Rare Diagnoses

III
L
ESSENTIAL INFORMATION • Lipoidal Contrast (Mimic)
a:l
"'C o Oil-based contrast agent
c: Key Differential Diagnosis Issues o High Tl signal intensity
III
• Review brain CT; fat may have confusing • Metaplastic Meningioma (Lipomatous)
MR signal intensity o Dural-based enhancing mass with fat
• MR fat suppression technique helps density/signal intensity
differentiate lesions o Look for adjacent hyperostosis
Helpful Clues for Common Diagnoses • Choroid Plexus Xanthogranuloma
• Lipoma (Mimic)
o Well-defined nonenhancing fatty mass o Nonneoplastic, noninflammatory cysts of
o Locations: lnterhemispheric/pericallosal, choroid plexus
suprasellar, quadrigeminal, & o Low density on CT may mimic fat
cerebellopontine angle (CPA) • Encephalocraniocutaneous Lipomatosis
o Bulky interhemispheric/pericallosal o Scalp lipomas ipsilateral to brain
lipomas often associated with anomalies
agenesis/dysgenesis of corpus callosum o CPA, Meckel cave, & foramen magnum
• Subacute Hemorrhage (Mimic) lipomas
o Tl shortening in subacute blood may
mimic fat
I
4 Sagittal TlWI MR shows a lipoma = with corpus
callosum hypoplasia. Majority are supratentorial (80%),
Sagittal TI WI MR shows an asymptomatic ribbon-like
pericallosaJ lifX>ma ~. Lipomas are congenital
most common along interhemispheric fissure. malformations, not true neoplasms. 20% are
Suprasellar & pineal region are less common. infra tentorial, most commonly in the CPA.
58
FAT IN SULCI/C1STERNS/VENTRICLES 00
"
c:
(Left) Axial T I WI MR shows

a ruptured dermoid 81 with m
characteristic fat droplets ~
~
throughout the subarachnoid Ol
Q,
space 111.1. Ventricular X
fat-fluid levels are common. iii'
Chemical meningitis is a 00
-0
common complicalion. Ol
(Right) Axial NECT shows a ()
CD
suprasellar mass I'll] en
containing fat & Ol
:J
calcifications, teratoma. C.
These midline masses are en
c
most commonly in the pineal CT
Ol
region as are other germ cell ~
Ol
tumors. The sort tissue ()
components of these lesions ::r

:J
enhance. o
c:
Q
en
CO
~
:J
Teratoma en
a heterogeneous lesion in the
pineal region with small
hyperintense foci = related
to fat. The lateral & 3rd
ventricles are enlarged due
to compression of the
cerebral aqueduct. (Right)
Sagittal T1 WI MR shows a
metaplastic (lipomatous)
meningioma with
characteristic T1
hyperinlensily related to fat
Ea. Signal characteristics are
from triglyceride fat droplets
within metaplastic
adipocyles.
Choroid Plexus Xanthogranuloma

(Mimic)
choroid plexus cysts in the
atria of the lateral ventricles.
These are commonly seen as
incidental findings. On CT,
the cysts may mimic fat.
(Right) Sagittal T1WI MR
shows
encephalocraniocutaneous
lipomatosis, a rare congenital
neurocutaneous syndrome,
which may be characterized
by extensive intracranial
lipomas. A large lipoma
extends into the upper
cervical canal P1t] & another
in the CPA 81.
I
4
59
(/)
c EXTRA-AXIAL FLOW VOIDS
~
Q)
Ul
o DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
"0
·0
C Common • CSF Pulsation
.r:
() o Ill-defined signal loss near artery
ro
~ • Normal (Normal Arteries, Veins)
ro • CSF Pulsation • Saccular Aneurysm
.Q
:J o Typically involve major branch points
(f) • Saccular Aneurysm
"0 • Fusiform Aneurysm, ASVD
C • Fusiform Aneurysm, ASVD
ro o Long segment & focal outpouching (BA >
(/) • Arteriovenous Malformation
Q) ICA/branches)
()
ro
• Developmental Venous Anomaly
0-
• Arteriovenous Malformation
(f) Less Common o Extra-axial feeding, draining vessels
ro • Dural A-V Fistula
·x o Look for aneurysms (feeding arteries,
ro
• Thrombosis, Dural Sinus intranidal), venous varices
~
>< • Fusiform Aneurysm, Non-ASVD • Developmental Venous Anomaly
l1J
• Dissecting Aneurysm o Draining vein & enlarged medullary veins
c
III
• Pseudoaneurysm o Tl C+ best sequence
~
al Rare but Important
"0
c • Vein of Galen Malformation • Dural A-V Fistula
III
:J
• Venous Varix o Older; usually prior dural sinus thrombosis
-"(f) o Direct AV shunt
ESSENTIAL INFORMATION • Thrombosis, Dural Sinus

o Prominent collateral veins
Key Differential Diagnosis Issues • Fusiform Aneurysm, Non-ASVD
• Vascular vs. CSF flow void (FV) o Often more distally located than ASVD
o Vascular FVs sharply demarcated from o Vasculopathy, vasculitis, mycotic, oncotic
surrounding CSF • Dissecting Aneurysm
o If large, vascular FVs may cause phase o Extra- > intracranial; VA > supra clinoid
artifact ICA
• Vascular FV vs. acutely thrombosed
artery/vein
• Vein of Galen Malformation
o Thrombus iso- on Tl, hypointense on
o t VOG, feeding/draining vessels
T2WI, can mimic FV
o Do T2* (GRE/SWI) - clot "blooms"
• Venous Varix
o Seen with AV shunting, venous strictures
Normal (Normal Arteries, Veins) Normal (Normal Arteries, Veins)
I
4 Axial T2WI MR shows paired ACA flow voids "on end"
.2b curvilinear MCA flow voids a.
veins 1'71 proximal straight sinus ~
internal cerebral
& superior sagittal
=-
Axial T2WI MR shows superior sagittal sinus flow void
cortical veins entering sinus ~ .•. & superficial
cortical veins over the convexities ~.
sinus !:ll.
60
EXTRA-AXIAL FLOW VOIDS ,...
Ul
c:
III
::l
Co
III
.,
III
CSF Pulsation Saccular Aneurysm
::l
localized signal loss in the m
prepontine cistern CSF ~ ~
.,
Q)
due to pulsations from the
Q,
basilar artery =:II. (Right) ~.
Axial T2WI MR shows a Q)
rounded flow void in the Ul

-0
lower interhemispheric Q)
fissure It] representing a ()
ro
(f)
saccular anterior
Q)
communicating artery ::J
aneurysm. 0-
Cf)
c
0-
.,
Q)
Q)
()
::T
::J
o
Ci
o
(jj.
CD
.,
::J
Fusiform Aneurysm, ASVD Arteriovenous Malformation (f)

an ovoid mass that involves
the horizontal segment of the
left middle cerebral artery
=:II. Note tortuous, elongated
"flow voids" in both middle
cerebral arteries. (Right)
Axial PO FSEMR shows
enlargement of the internal
cerebral veins ~ as well as
prominent areas of flow void
in an AVM nidus located in
the lateral basal ganglia 8:1.
Developmental Venous Anomaly Dural A-V Fistula

a solitary prominent flow
void near the vertex ~ that
is substantially larger than
other vascular flow voids at
this level =:II. (Right) Axial
T2WI MR shows high signal
in the left transverse sinus &
a number orpunctate &
curvilinear signal voids
within it These small
flow voids are part of a dural
AVF within a chronically
thrombosed dural sinus.
Compare with the normal
flow void of right transverse
sinus=.
I
4
61
rn
c 11 HYPERINTENSE CSF
~
OJ
U;
U
DIFFERENTIAL DIAGNOSIS • Subarachnoid Hemorrhage
"0
'0 o May be traumatic, aneurysmal, or
C
.r:: Common nonaneurysmal perimesencephalic
u
~ • MR Artifacts, Flow-Related • Location helps determine etiology
Cll
..Q • MR Artifacts, Magnetic Susceptibility o Typically isointense to brain, "dirty CSF"
::J
(/J • Subarachnoid Hemorrhage • Intraventricular Hemorrhage
"0
C • Intraventricular Hemorrhage o Typically hyperintense to CSF & isointense
Cll
rn • Meningitis to brain with a fluid level
OJ
u o May be T1 hyperintense, related to age
Cll
a.
Less Common
(/J • Ventriculitis • Meningitis
Cll o Typically isointense to brain, "dirty CSF"
'xCll Rare but Important o Meningeal enhancement classic
ro~ • Dermoid Cyst (Ruptured)
x
w • Carcinomatous Meningitis Helpful Clues for Less Common Diagnoses
C • Contrast Complications, NOS • Ventriculitis
ltl • Retained Pantopaque o Debris in ventricles from sediment, cells
~
al o Typically hyperintense to CSF & isointense
"t:l
C to brain with a fluid level
ltl ESSENTIAL INFORMATION
::J Helpful Clues for Rare Diagnoses
...:
(/J
Key Differential Diagnosis Issues • Dermoid Cyst (Ruptured)
• MR artifact common at high field strengths o Fat droplets within CSF spaces
• CSF hemorrhage & infection often causes o Suppress with fat-saturation
"dirty CSF", hyperintense to CSF & • Carcinomatous Meningitis
isointense to brain parenchyma o Rare, related to blood, cells, melanoma
o CSF FLAIRhyperintensity more common • Contrast Complications, NOS
than true T1 CSF hyper intensity o Chronic renal failure causes delayed
Helpful Clues for Common Diagnoses excretion & hyperintensity from
• MR Artifacts, Flow-Related recirculation
o Pulsation artifact in phase encoding o Gadolinium leak from lack of intact
direction blood-brain barrier: Infection, PRES

o Confirm artifact when seen outside skull • Retained Pantopaque
• MR Artifacts, Magnetic Susceptibility o Often focal T1 hyperintensity in CSF
o "Black holes" with T1 bright rim o Older adults (not used since 1980s)
o Changing phase encode direction confirms
I
4 Axial TlWI MR shows CSFpulsation artifact
spin echo Tl sequence (3T magneO. Anifact is
=
on this
artifact=
Axial T I C+ MR shows localized magnetic susceptibility
from an aneurysm clip. This results in
confirmed by periodic high SII and low !l:?Jl signal localized Tl hyperintensity within the suprasellar cistern
artifacts in phase encoding direction. SII.
62
T1 HYPERINTENSE CSF
Ql
::I
Q.
..,
I:D
Subarachnoid Hemorrhage Ql
(Left) Axial TI WI MR shows ::I

"dirty" CSF in the m
suprasellar cistern, isointense ~
..,
with brain, related to ,
Ql
Ql
aneurysm rupture. Note X
hydrocephalus with Oi
blood-fluid level ~ in lateral (j)
-0
ventricle. (Right) Axial TI WI Ql
()
MR shows heterogeneous
C1l
hyperintense signal anterior V>
to the medulla. This is a Ql
:J
typical distribution for Q.
nonaneurysmal (j)
c:
perimesencephalic 0-
Ql
subarachnoid hemorrhage,
Q]
which tends to collect ()
around the midbrain &

::T
:J
anterior to the pons. o
Ci
o
V>
CD
..,
::J
Intraventricular Hemorrhage V>

hyperintense hemorrhage
layering in the occipital
horns 11II] & 3rd ventricle.
Focal clot is seen in the
frontal horn ~ in this
patient with posterior fossa
AVM rupture. (Right) Axial
TlWI MR shows "dirty" CSF,
isointens€ to brain
parenchyma in the basal
cisterns ~ in this fungal
meningitis patient. The CSF
is also FLAIR hyperintense &
enhances. Meningitis is a
clinical-laboratory diagnosis.
Ventriculitis
debris layering posteriorly
within the occipital horns =
in this 2 year old with
ventriculitis. Note signal is
mildly hyperintense to CSF &
isointense to brain. (Right)
Sagittal TI WI MR shows
=
numerous hyperintense foci
in the subarachnoid
spaces & supraselJar cistern
SI related to rat droplets
from dermoid rupture.
Hydrocephalus is caused by
associated chemical
meningitis.
I
4
63
en FLAIR HYPERINTENSE CSF
c
~
Q)
Ul
U DIFFERENTIAL DIAGNOSIS o May be complicated by hydrocephalus,
"
"0
C Common
ventriculitis, abscess, vasculitis
J:: o Remains a clinical-laboratory diagnosis
U
~ • Subarachnoid Hemorrhage, OS • MR Artifacts, Magnetic Susceptibility
'" • Intraventricular Hemorrhage
':::J"
.0 o Regionally adjacent metal, blood, air-bone
(f) • Meningitis interfaces causes FLAIRhyperintensity
"C • MR Artifacts, Magnetic Susceptibility o Distorts local magnetic field, altering null
'e"n
Q)
• MR Artifacts, Flow-Related point for fluid (Tl), resulting in
u • MR Artifacts, Patient-Related inappropriate high signal
'"
Cl.
(f) • Metastases, Meningeal o Often seen close to aerated frontal sinuses
• Ventriculitis & temporal bones
'",
";;:
o Common surrounding aneurysm clips
'~" Less Common
X'" • Gadolinium in CSF due to • MR Artifacts, Flow-Related
w o Blood-Brain Barrier Leakage o CSF flow artifacts are common in basal
c: o Chronic Renal Failure cisterns, foramen of Monro, aqueduct, &
t'll
~ 4th ventricle
In • Cerebral Ischemia-Infarction, Acute
o Periodic artifacts extending outside skull in
"C
t'll
Rare but Important phase encoding direction is diagnostic
• Dermoid Cyst (Ruptured) o Usually absent on spin echo sequences (Tl,
• Moyamoya T2); helpful to confirm artifact
• MR Artifacts, Patient-Related
ESSENTIAL INFORMATION o Diffuse FLAIRhyperintensity
o Common etiologies: Head motion,
Propofol, 50% or greater supplemental
oxygen (4-5x t signal with 100% 0,)
• Metastases, Meningeal
o Usually due to cellularity &/or increased
protein content within CSF
o May be focal or diffuse
o Meningeal enhancement typical
o Adjacent bone changes common
o Breast & lung most common distant
primary tumors
• Ventriculitis
o Ventriculomegaly with debris level
o OWl bright & ventricular enhancement
o Complication of meningitis, abscess,
ventricular catheter
• Blood-Brain Barrier Leakage
o Etiologies include:
Infection/inflammation, ischemia, tumor
• Cerebritis, posterior reversible
encephalopathy syndrome (PRES)may
cause BBBleak
• Acute/subacute stroke (poor prognostic
sign suggests hemorrhagic
transformation)
• Neoplasms uncommon, usually with
I delayed imaging
4
64
FLAIR HYPERINTENSE CSF (/I
;YC
r::
Q)
o Gadolinium accumulates in CSF due to o Leptomeningeal enhancement (contrast :l
C.
BBB leakage "ivy sign") OJ
..,
o May cause focal or diffuse FLAIR Q)
Other Essential Information :l
hyperintensity & enhancement • Causes of pathologic FLAIR hyperintense m
• Chronic Renal Failure CSF: Blood, elevated protein, or cells ~
..,
o Increased FLAIR related to delayed ,
Ql
• FLAIR hyperintensity can be due to T2 Ql
gadolinium clearance from circulation prolongation or Tl shortening X
oj"
o May augment other pathologic causes of
• "Fast" FLAIR can cause artifactual FLAIR (fJ
FLAIR hyperintensity
o Usually seen with delayed imaging (may
hyperintensity "CD
Ql
()
Alternative Differential Approaches en

also be seen in normal patients) Q)
:l
• Cerebral Ischemia-Infarction, Acute • FLAIR hyperintensity with enhancement: 0.
o May see hyperintense CSF related to vessel Meningitis, metastases, ventriculitis, (fJ
r::
0-
occlusion or slow flow blood-brain barrier leakage, chronic renal ..,
Ql
o "Dot sign" related to occluded MCA failure, acute ischemia, moyamoya Ql

()
::r
branches in Sylvian fissure :l
o
o Enhancement related to slow flow SELECTED REFERENCES c:
o
00·
Helpful Clues for Rare Diagnoses 1. Morris JM et ai: Increased signal in the subarachnoid space
on fluid-altenuated inversion recovery imaging associated m
..,
• Dermoid Cyst (Ruptured) with the clearance dynamics of gadolinium chelate: a
~
en
o Fat-containing lesions are FLAIR bright potential diagnostic pitfall. AJNR Am J Neuroradiol.
from Tl shortening effects 28(10): 1964-7,2007
2. Stuckey SL et al: Hyperintensity in the subarachnoid space
o Tl foci in subarachnoid spaces on FLAIR MRI. AJR Am J Roentgenol. ]89(4):913-21,2007
pathognomonic 3. Cian[oni A et al: Artifact simulating subarachnoid and
• Moyamoya intraventricular hemorrhage on single-shol, fast spin-echo
fluid-attenuated inversion recovery images caused by head
o Progressive narrowing of distal ICA & movement: A trap for the unwary. AJNR Am J Neuroradiol.
proximal circle of Willis with collateraIs, 27(4):843-9,2006
anterior> posterior circulation 4. Frigon C et al: Supplemental oxygen causes increased
signal intensity in subarachnoid cerebrospinal fluid on
o "Ivy sign": Bright FLAIR signal related to brain FLAIR MR images obtained in children during
slow-flowing engorged pial vessels, general anesthesia. Radiology. 233(1):S]-S, 2004
S. Bozzao A et al: Cerebrospinal fluid changes after
thickened arachnoid membranes intravenous injection of gadolinium chelate: assessment by
• More commonly seen in frontal & FLAIR MR imaging. Eur Radiol. 13(3):592-7,2003
parietal lobes
I
Axial flAIR MR shows abnormal hyperinlensily wilhin
=.
lhe lefl-sided sulci The pauern of peripheral sulcal
Axial flAIR MR shows high signal in lhe basal cislerns
= & along the sylvian fissure !:ll caused by
4
blood is more characteristic (or traumatic hemorrhage subarachnoid blood relaled La aneurysm rupWre. Note
than aneurysm rupture. also acule hydrocephalus 81.
65
Cfl
E
FLAIR HYPERINTENSE CSF
OJ
§
U
"0
'0
C
.r:: Intraventricular Hemorrhage Intraventricular Hemorrhage
u
~
Cll (Left) Axial FLAIR MR shows
Cll
increased signal surrounding
..0
:J
en the midbrain = & in the
suprasellar cistern 81. A
"0
C small amount of
Cll
Cfl
intraventricular hemorrhage
OJ is presenl p:;J layering in the
u
Cll occipital horns. (Rigl1t) Axial
Cl.
en fLAIR MR shows a basal
Cll
·x
ganglia hematoma =in a
patient with a hypertensive
,
Cll
hemorrhage. Hyperintensity
~Cll
in the atrium of the left
X lateral ventricle B is
w
indicaUve of intraventricular
C extension.
III
~
aJ
"0
C
III
MR Artifacts, Magnetic Susceptibility

diffusely abnormal signal
pial surfaces =
throughout the sulci 81 &
caused by
pyogenic meningitis.
Hyperintensity in the choroid
plexi p:;J suggests choroid
plexitis. FLAIR hyperintense
CSF may be more apparent
than abnormal enhancement
on contrast images in
meningitis. (Right) Axial T2*
GRE MR shows magnetic
susceptibility artifact
to aneurysm clip placement
=due
in this patient with recent

subarachnoid hemorrhage.
MR Artifacts, Flow-Related MR Artifacts, Patient-Related

prominent round
hyperinlense focus in the 4th
ventricle =. Periodic
artifacts in the phase
encoding direction EJ
confirm the suspicion of CSF
pulsation artifact. (Rigl1t)
=
hyperintensity within the CSf
due to high levels of
inspired oxygen at the time
of imaging. This is a relatively
common artifact in patients
requiring sedation for an MR
study.
I
4
66
flAIR HYPERINTENSE CSF en
""c:
'Co"
:J
..,
lJl
Ventriculitis
Metastases, Meningeal
'"
:J
scattered hyperintense signal m
at the sulci PJ:J:l & along the ..,
~
dura 1::1 related to meningeal OJ
metastatic disease. Enhanced

0,
1:5.
images (not shown) revealed OJ
thickened, enhancing dura en
"D
wilh subtfe sulcal OJ
()
enhancemenl. (Right) Axial
CD
FLAIR MR shows
hyperintense material with '":J
OJ
the righllaleral venlricle ~ 0..
in this patient with en

c
meningoencephalitis & rr
ventriculitis . ..,
OJ
OJ
Ventriculomegaly with debris ()
::r
level is most common :J
imaging appearance. o
c:
o
'"10..,
:J
Blood-Brain Barrier leakage Blood-Brain Barrier leakage
(Left) Coronal FLAIR MR
'"
shows focal hyperintense
CSF 1::1 from local conlrast
accumulation overlying a
small parenchymal mass E!llI
due 10 focal cerebritis.
Contrast accumulation is
relaled 10 blood-brain barrier
leakage. (Rigl1t) Axial FLAIR
hyperinlensity =
MR shows diffuse CSf
due 10
gadolinium leakage in PRES.
Note classic vasogenic
edema in bOlh occipilal
lobes ~ & extensive right
temporal involvement. Renal
function was normal.
Chronic Renal Failure

diffuse hyperinlensity within
the sulci = in a patient with
brain MR 2 days
post-gadolinium injection for
abdominal MRA (patient had
a creatinine of 3.0). If history
not known, would consider
other meningeal processes.
shows brighl CSF 1::1 in lhis
patient with a hyperacute
right MCA infarct. This
abnormal signal is thoughllo
be relaled 10 slow flow
(luxury perfusion).
I
4
67
rn
c 12 HYPOINTENSE EXTRA-AXIAL LESIONS
~
<1l
Ul
<.) DIFFERENTIAL DIAGNOSIS o Common surrounding aneurysm clips
"0
"0 • Pneumocephalus
C
.r::: Common o Evidence of recent craniotomy or trauma
u
co
~ • MR Artifacts, Flow-Related o Completely black signal
co • MR Artifacts, Magnetic Susceptibility
.0
:::J
o Non-dependent location
en • Pneumocephalus • Physiological Calcification, Dura
"0
c • Physiologic Calcification, Dura o Anterior parafalcine region most common
co
rn • Meningioma o Ossification may demonstrate T1
<1l
u
co
• Metastases, Skull and Meningeal hyperintensity centrally due to fatty
0-
en • Schwannoma marrow (mimics blood or lipoma)
"~ Less Common o Associations with chronic renal failure,
x
co, • Epidural Hematoma where it may be more extensive
co
~
;( • Subdural Hematoma, Mixed • Meningioma
W
• Saccular Aneurysm o Enhancing extra-axial mass with dural tail
c o Often T2 hypointense from high
ro • Lymphoma, Metastatic, Intracranial
~ cellularity or intrinsic calcification
co Rare but Important
"C • Metastases, Skull and Meningeal
c • Neurosarcoid
ro o Enhancing extra-axial mass
:::J
• Dural A-V Fistula o Meningeal metastases typically associated
..l< • Leukemia
en with skull involvement
• Hypertrophic Pachymeningitis o T2 hypointense if associated blood
• Extramedullary Hematopoiesis products (melanoma, renal cell carcinoma)
• Hemangiopericytoma o Primary tumor often known
• Retained Pantopaque • Schwannoma
o Homogeneously enhancing extra-axial
ESSENTIAL INFORMATION mass along cranial nerves, CPA most
common
o May show T2 hypointensity
o T2 hyperintense cystic change is common
• Epidural Hematoma
o Epidural collection in a trauma patient
o Hyperacute, mixed & chronic hematomas
may be T2 hypointense
oGRE may show susceptibility artifact
• Subdural Hematoma, Mixed
o Subdural collection in a trauma patient
o Hyperacute, mixed age & chronic
hematomas may be T2 hypointense
oGRE may show susceptibility artifact
• Saccular Aneurysm
o Round/ovoid T2 hypointense mass
o Flow artifact in phase encoding direction
o When thrombosed, challenging diagnosis
• Maintain high suspicion when
anatomically near vascular structures!
o Often a T2 hypointense dural lesion
o Hypointensity related to high nuclear to
I cytoplasmic ratio
o Systemic disease usually present
4
68
12 HYPOINTENSE EXTRA-AXIAL LESIONS CJl
"
c:
III
o Mimics other metastases o Typically T2 hyperintense; rarely T2 :J
a.
hypointense tll
.,
• Hemangiopericytoma III
• Neurosarcoid :J
o Lobular, enhancing extra-axial mass with
o Hypointense durallesion(s) ± m
dural attachment, ± skull erosion ~
leptomeningeal disease> > parenchymal
o May mimic meningioma, but without OJ
disease Q,
o Dural, leptomeningeal, subarachnoid space Ca++ or hyperostosis ~.
OJ
o Typically heterogeneously T2 hypointense
enhancement CJl
o 5% present as solitary dural-based
• Retained Pantopaque 1:l
OJ
o Signal parallels fat (shortens Tl/T2)
()
CD
extra-axial mass en
o Usually older patients since not in use
o Majority of patients have systemic disease OJ
:J
since late 1980s C.
• Dural A-V Fistula CJl
o Network of tiny vessels in wall of Alternative Differential Approaches c:
0-
thrombosed dural venous sinus • Diagnosis by signal intensity .,

OJ
OJ
()
o Isointense thrombosed sinus ± "flow voids" • "Hypointense" T2 lesions: Meningioma, ::r
:J
o Look for serpiginous foci in CSF cellular metastases, schwan noma, Q.
c.
• Leukemia lymphoma, leukemia o
o Usually a dural-based enhancing mass • "Black" hypointense lesions: Air, iji.
CD
o Commonly hypointense calcification, (cortical) bone, dense fibrous 3
en
o Most often a complication of acute tissue, flow voids from vessels or CSF flow
myelogenous leukemia • Diagnosis by location
• Hypertrophic Pachymeningitis • Dural lesions: Physiologic Ca++,
o Diffuse dural thickening without known meningioma, metastases, epidural/subdural
etiology hematoma, neurosarcoid, hypertrophic
o Involves at least 75% of dural surface pachymeningitis, extramedullary
o Typically T2 hyperintense hematopoiesis
o Dense fibrosing pseudotumor may appear • Osseous lesions: Hyperostosis frontalis
"black" (rare) intern a, metastases, fibrous dysplasia,
o Diagnosis of exclusion osseous metaplasia, exostosis, myelofibrosis
• Extramedullary Hematopoiesis
o Juxta-osseous smooth homogeneous
masses in chronic anemias or marrow
depletion patients
MR Artifacts, Flow-Related MR Artifacts, Magnetic Susceptibility
I
artifact=
Axial T2WI MR shows hypointense flow-related MR
due to CSF pulsations in the premedullary
cistern. This artifact is not present on spin echo (Tl)
=
Axial T2WI MR shows typical magnetic susceptibility
artifact due to aneurysm clips. This artifact is also
present close to aerated frontal & temporal bones.
4
sequences.
69
(f)
c 12 HYPOINTENSE EXTRA-AXIAL LESIONS

~
QJ
u;
(3
"0
·0
C
L
U
Pneumocephalus Meningioma
ro
~ (Left) Axial T2' GRE MR
ro shows intraventricular blood
.D
:J SII & pneumocephalus 1:].
(f)
"0
Pneumocephalus may be a
C cause of II blooming" artifact
ro & multiple" black dots" on
(f)
QJ T2' (GRE or SWI) scans.

u
ro (Right) Sagitlal T2WI FS MR
Q.
(f) shows a T2 hypointense
lenlOrial-based mass m.
ro
·x Note lhe lectum [;8 is
ro, superiorly displaced A CSF
ro
~ clefl ~ supports the
X extra-axial location. Flow
w
voids are common in
c meningioma. Marked
ro
~ enhancement of the mass
r:n was seen (not shown).
'tl
c
III
Metastases, Skull and Meningeal

hyperostosis in a plaque-like
meningioma =
along the
lefl inner calvarium.
Calcified/ossified
meningiomas rarely enhance
except for a small dural tail.
CT can help exclude a more
malignant process. (Right)
Axial T2WI MR shows
hypoinlenS€ extra-axial
masses bilaterally I:] in this
patient with osseous & dural
metastases. There was
marked enhancement
following contrast. Note
associated righl-lo-Iefl
midline shift
Schwannoma
a large hypointense right
CPA mass SII. A subtle rim
of T2 hyperintense CSF (CSF
"cleft") ~ helps to delineate
this as an extra-axial mass.
shows a giant
heterogeneously hypointense
mass which causes mass
effect on lhe pons, creales a
waist SII as it goes through
porus trigeminus into a
massively enlarged Meckel
cave, trigeminal
schwannoma. The normal
left Meckel cave ~ is seen.
I
4
70
12 HYPOINTENSE EXTRA-AXIAL LESIONS ,..
(fl
c
OJ
::l
Q.
OJ
..,
Subdural Hematoma, Mixed Saccular Aneurysm OJ

a hypoinlense subdural m
hematoma =
ill lhis trauma ~
..,
OJ
patient T2 hypoinlensily
Q,
may be presenl in subdural ><
hematomas of varying ages. Qi.
(RighI) Axial T2WI MR (fl
shows a giant aneurysm of
the right middle cerebral
"CD
OJ
C1
artery =. If thromboses, rJl
OJ
these may be poorly seen or ::l
non-visualized on 0..
angiography. Lack of flow (fl

C
arlifact in the phase r::r
encoding direction suggests ..,
OJ
OJ
that this aneurysm is C1
lhrombosed. This was
::T
::l
conFirmed surgically. o
0.:
o
rJl
CD
..,
::l
lymphoma, Metastatic, Intracranial Neurosarcoid rJl

subtle dural-based mass
along the right sphenoid
=
wing. NOle similar signal
intensity in the involved
masticator space E1 & orbit
~. (RighI) Axial T2WI MR
shows both Meckel caves
are filled with hypoinlense
tissue = instead of normal
hyperintense csrin lhis
sarcoid patient
Neurosarcoid affecting both
trigeminal nerves without
other identifiable lesions is
unusual.
leukemia Extramedullary Hematopoiesis

(Lefl) Axial T2WI MR shows
a hypoinlense extra-axial
bifrontal mass ~ wilh
adjacent calvarial destruction
related to leukemia in this
pediatric patient Leukemia
oFten presents as a
dural·based enhancing mass.
(RighI) Axial T2WI FS MR
shows strikingly hypointense
extra-axial masses = along
the dura in this patient with
extramedullary
hematopoiesis. These
patients lypically have
anemia or another
depletion process.
marrow
I
4
71
C/l
HYPERDENSE CSF
~C
OJ
~
U
DIFFERENTIAL DIAGNOSIS o Gyri swollen, cisterns compressed
"0
·0 o "Cerebellar reversal sign": Density of
r.
C
Common cerebellum> > hemispheres
t.l
OJ
~ • Subarachnoid Hemorrhage (SAH), Traumatic • Brain Death (Mimic)
OJ
.0 • Aneurysmal Subarachnoid Hemorrhage o Diffuse low density in supratentorial brain
:::J
(f) • Streak Artifact causes "pseudo SAH"
"0
C • Diffuse Cerebral Edema (Mimic) o Gyri swollen, cisterns compressed
OJ
C/l • Brain Death (Mimic) o "Cerebellar reversal sign": Density of
OJ
t.l
OJ Less Common cerebellum> > hemispheres
D-
(f)
• Contrast Material o Clinical criteria for confirmation
OJ
x • Chronic Renal Failure Helpful Clues for Less Common Diagnoses
,
OJ
• Ventriculitis • Contrast Material
OJ
~
;( • Meningitis o Noncontrast CT follows recent contrast
W
• Metastases, Meningeal procedure (myelogram, cisternogram)
t:
III Rare but Important • Chronic Renal Failure
'-
CO o Causes contrast recirculation from recent
"0
• Nonaneurysmal Perimesencephalic SAH
t: • Superficial Siderosis IV contrast injection
III
• Ventriculitis
:::J
o Ventriculomegaly with debris level,
""(f) ESSENTIAL INFORMATION enhancing ependyma
Helpful Clues for Common Diagnoses • Meningitis
• Subarachnoid Hemorrhage, Traumatic o Normal CT or mild ventriculomegaly
o Peripheral sulci, interpeduncular cistern o May see hyperdense CSF, especially in

o Less extensive than aneurysmal blood fungal infections & TB
• Aneurysmal Subarachnoid Hemorrhage • Metastases, Meningeal
o Typically basal cisterns, may be diffuse o May see hyperdense CSF, effaced sulci
o Location may indicate causative aneurysm Helpful Clues for Rare Diagnoses
• Streak Artifact • Nonaneurysmal Perimesencephalic SAH
o Non-anatomical distribution o Small volume hemorrhage in basal cisterns
o Due to metal & dense bone interfaces • Superficial Siderosis
• Diffuse Cerebral Edema (Mimic) o Atrophy; hyperdensity along brain surface
o Diffuse low density in supratentorial brain
causes "pseudo SAH"
Subarachnoid Hemorrhage (SAH),

Traumatic Aneurysmal Subarachnoid Hemorrhage
I
4 Axial NEeT shows extensive traumatic SI\H
subdural hematomas ~
1m
Trauma is the most common
& Axial N£eT shows cisternal=& intraventricular E1
hemorrhage from recent aneurysm rupture. The
cause of SAH & is typically less extensive than location of the blood often indicates the causative
72 aneurysmalSAH. aneurysm.
HYPERDENSE (SF CIl
"
l:
OJ
::::l
a.
l:D
...•
Streak Artifact Diffuse Cerebral Edema (Mimic) OJ
(Left) Axial NECT shows a ::::l

subtle linear hyperdensity in m
the left frontal extra-axial ~
space 1:1 suspicious for OJ
Q,
possible acute blood. This x
was negative on short 0;'
interim follow-up CT. Streak Ul
-0
artifact is typically in a OJ
()
non-anatomic location.
CD
(Right) Axial NEeT shows U>
multifocal subtle linear foci OJ

::::l
of high density =:I that may a.
be mistaken for SAH. This is Ul
l:
due to residual normal cortex r::r
& surrounding diffuse ...•
OJ
OJ
cerebral edema in this ()
::r
near-drowning patient ::::l
o
0:
o
U>
CD
...•
::::l
Brain Death (Mimic) Contrast Material U>

diffuse edema & complete
loss of gray-white matter
differentiation which
accentuates the vascular
structures. The density of the
MCAs =:I may also be partly
due to stasis or thrombosis.
There is a "cerebellar
reversal sign" ~ which
reflects relative sparing of the
posterior Fossa contents.
extensive contrast in the CSF
spaces = & right temporal
horn E!ilI from recent
ventriculography.
Nonaneurysmal Peri mesencephalic SAH

increased density within the
left sulci &J due to
proteinaceous content nearly
isodense with the underlying
brain. Compare to normal
hypodense CSF over the
right hemisphere. (RigM)
Axial NECT shows minimal
=
prepontine cisternal blood
in this patient with a
negative angiogram. The
volume of blood in
perimesencephalic SAH is
usually minimal & confined
to the basal cisterns.
I
4
73
rn
c
~ HYPERDENSE EXTRA-AXIAL MASS(ES)
Q)
~
U
u DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
'0
c Common • Subdural Hematoma, Acute
.r:
u o NECT: Homogeneously hyperdense
~ • Subdural Hematoma, Acute
CO
.n • Epidural Hematoma crescent-shaped extra-axial collection
:::l
(/) • Meningioma o May cross sutures, not dural attachments,
U
C • Metastases, Meningeal may extend along falx & tentorium
CO
rn
• Epidural Hematoma
Q) less Common o NECT: Hyperdense biconvex extra-axial
u
CO
a.
• Thrombosis, Dural Sinus collection in acute phase
(/)
• Thrombosis, Cortical Venous o Does not cross sutures unless sutural
.~ • eurosarcoid
X diastasis/fracture, can cross falx &
,
CO
CO
~ tentorium
X • Tuberculosis • Meningioma
w • Dural A-V Fistula o 70-75% hyperdense on NECT, sharply
c
Cll
~ Rare but Important circumscribed smooth mass abutting dura
aI • Extramedullary Hematopoiesis o > 90% enhance homogeneously &
-c
t: • Leukemia intensely on CECT
Cll
• Venous Varix (Isolated) • Metastases, Meningeal
:::l
..ll:
• Hemangiopericytoma o NECT: Hypercellular or hemorrhagic
(/)
• Malignant Nonmeningothelial Tumors o Skull/dura often/but not always infiltrated
o Often known extra cranial malignancy
ESSENTIAL INFORMATION Helpful Clues for less Common Diagnoses

• Thrombosis, Dural Sinus
Key Differential Diagnosis Issues o Hyperdensity along expected location of
• Is it hemorrhage? dural sinuses
• Or is it hyperdense mass(es) masquerading o May be associated with venous infarcts
as hemorrhage? • Neurosarcoid
• CECT/Tl C+ MR helpful in differentiating o Multifocal dural-based foci, presence of
between the two leptomeningeal enhancement additional
o 0 contrast-enhancement - hemorrhage clue
o Contrast-enhancement within hyperdense o Abnormal CXR, raised ESR, ACE levels
mass excludes simple hemorrhage
Subdural Hematoma, Acute Epidural Hematoma
I
4 Axial NEU shows a crescentic hyperdense extra-axial
fluid collection typical for acute subdural hematoma
Axial NECT shows a classic
epidural hematoma EB
biconvex hyperdense
74
HYPERDENSE EXTRA-AXIAL MASS(ES) ,..
(JJ
c:
III
:J
0-
..,
llJ
Meningioma Metastases, Meningeal III
(Left) Axial NECT in a patient

:J
with multiple m
meningiomalosis syndrome ~
~
III
shows several hyperdense,
lobulated, dural-based x
masses Bt,. (Right) Axial '"
iii'
NECT shows a mildly en
-0
hyperdense extra-axial mass III
(")
overlying the cerebral (1)
convexity with adjacent en
calvaria/thickening [;8 in a III
:J
patient with a prostate 0-
metastasis. en
c:
CT
III
~
III
(")
::T
:J
Q,
0-
o
en
ro~
::J
Thrombosis, Dural Sinus Tuberculosis en
dural sinus thrombosis with
hyperdensity along the
expected location of the right
transverse sinus ffi (Right)
Axial NECT shows a
hyperdense extra-axial mass
=:J found to be a dural
tuberculoma at surgery
(Courtesy R, Ramakantan,
MD)
Extramedullary Hematopoiesis leukemia

(Left) Axial NECT shows the
typical appearance of
extramedullary
hematopoiesis with
hyperdense, dural-based
masses = mimicking
subdural hematomas in a
patient with myelofibrosis.
multiple hyperdense
extra-axial masses
(chloromas) ~ in a patient
with leukemia, CECT showed
homogeneous enhancement.
I
4
75
en HYPODENSE EXTRA-AXIAL MASS(ES)
c
~
Cll
Ul
U
DIFFERENTIAL DIAGNOSIS • Post-Operative Epidural Fluid, Effusion,
"0
'0 Fat, or Air
C
.<: Common o Fat/muscle used to repair craniofacial
u
C1l
~ • Arachnoid Cyst defects may have "mass-like" appearance
C1l
.0 • Subdural Hematoma, Chronic o Post-operative fluid collections often
OJ
(/) • Post-Operative Epidural Fluid, Effusion, Fat, contain blood products &/or protein
"0
C or Air resulting in hypodense collections
C1l
en • Pneumocephalus o Surgical or traumatic arachnoid tear may
Cll
u permit CSF to collect in subdural space
C1l
0.
less Common
(/) • Neurocysticercosis • Pneumocephalus
ro
.;;: • Lipoma o Typically related to trauma or post-surgical
,
C1l
• Pineal Cyst o Air may become trapped & expand
['! resulting in "tension pneumocephalus"
x
w
• Schwan noma
• "Mount Fuji sign": Subdural air
c:
• Epidural Hematoma separates/compresses frontal lobes,
•..'"
aJ • Epidermoid Cyst creating widened interhemispheric space
'tl • Rathke Cleft Cyst between frontal lobe tips that mimics
c:
silhouette of Mount Fuji
'" Rare but Important
OJ
• Extra-Axial Empyema Helpful Clues for less Common Diagnoses
-"(/)
• Arachnoid Granulations, Dural Sinuses • Neurocysticercosis
o Convexity subarachnoid spaces most
• Dermoid Cyst
• Neurenteric Cyst (and Other Epithelial common location
Cysts) o Commonly involves basal cisterns
o Racemose form less common: "Grape-like"
cystic masses in basal cisterns
ESSENTIAL INFORMATION o Imaging varies with stage & host response
Key Differential Diagnosis Issues • Lipoma
• Hypodense extra-axial masses can often be o Well-delineated, lobulated, fat density,
best characterized using FLAIR & DWI MR extra-axial mass
• Wide window CT settings are important for o 40-50% along interhemispheric fissure
differentiating air, fat, & water densities • Peri callosal & cisternal locations are
• Contrast-enhancement is key for common
differentiating cystic neoplasm & most • Perisylvian location may be associated
infectious etiologies from benign or with seizures
developmental cysts o Midline lipomas should prompt search for
other abnormalities
Helpful Clues for Common Diagnoses • Callosal dysgenesis
• Arachnoid Cyst • Azygous anterior cerebral artery
o Round/oval CSF density extra-axial mass
• Aneurysms
o May remodel adjacent calvarium • Pineal Cyst
050-60% middle cranial fossa; 10% CPA o Homogeneous fluid-filled pineal mass
o DWI, FLAIR MR differentiate from o 25% have associated calcification
epidermoid cyst o Rare enhancement along rim or in
• Subdural Hematoma, Chronic adjacent compressed pineal gland
o Hypodense, lentiform subdural
• Schwan noma
collection(s) o Most common CPA mass (85-90%)
o Can be uni- or bilateral o Enhancing mass with extension into
o May be loculated, septated internal auditory canal ("ice cream on
o Can have mixed density fluid-fluid layers cone")
I o Enhancement along dural margins &
septations common
o Intratumoral cysts in about 20% of cases
o Associated arachnoid cysts rare
4
76
HYPODENSE EXTRA-AXIAL MASS(ES) en
""
r::
III
• Craniopharyngioma o Scalloping of inner calvarium is common ::l
C-
o Calcified, cystic/solid suprasellar mass in a • Dermoid Cyst
child o Fat &/or calcifications are key to diagnosis
..•III
OJ
::l
o Rim &/or solid portions enhance o Commonly midline location
o Look for pathognomonic "fat droplets" in m
• Epidural Hematoma ...~
o Extra-axial biconvex lesion ruptured dermoid cysts ,
III
OJ
o Usually hyperdense; late subacute/chronic • Neurenteric Cyst (and Other Epithelial x
fii·
or rapid acute bleeding ("swirl sign") may Cysts)
en
be partially hypodense o Neurenteric cyst: Round/lobulated -0
OJ
• Epidermoid Cyst nonenhancing, slightly hyperintense to ()
C1l
VJ
o Lobulated, insinuating CSF density mass CSF mass in posterior fossa, typically OJ
::l
with potential deformity of surrounding anterior to pons/medulla C-
structures o Epithelial cysts not adequately en

c::
0-
o DWI MR hyperintensity differentiates from differentiated by imaging: Characterized OJ
by histologic wall make-up 0;

other lesions (arachnoid cyst, cystic mass) ()
OJ
• Rathke Cleft Cyst o Internal signal depends on contents ::l
o
o Sellar/suprasellar cystic mass with Other Essential Information c:
intracystic nodule o
• MR with DWI & FLAIR sequences helpful en·
o No calcification or enhancement
when considering these diagnoses:
m
3
VJ
Helpful Clues for Rare Diagnoses Arachnoid cyst, epidermoid cyst, neurenteric
• Extra-Axial Empyema cyst, extra-axial empyema
o Subdural much more common than Alternative Differential Approaches
epidural empyema • "Cystic" masses: Arachnoid cyst,
o Peripherally enhancing extra-axial lesion neurocysticercosis, pineal cyst,
o DWI can help differentiate from other schwannoma, craniopharyngioma, Rathke
more benign lesions cleft cyst, epidermoid cyst, dermoid,
o 15% of cases have both epidural &
neurenteric cyst
subdural components • Enhancing lesions: Subdural hematoma,
o Complication of paranasal sinus disease & neurocysticercosis, schwannoma,
bacterial meningitis craniopharyngioma, epidural hematoma,
• Arachnoid Granulations, Dural Sinuses extra-axial empyema
o Fluid signal cysts in or near dural sinuses
• DWI MR "bright" lesions: Epidermoid cyst,
o No enhancement
extra-axial empyema
Arachnoid Cyst Subdural Hematoma, Chronic
I
Coronal NECT shows an extra-axial CSF collection over
the left convexity =::I with local mass effect. Note
Axial NEeT shows crescentic hypodense extra-axial
=.
collection compressing the left hemisphere chronic
4
expansion & thinning of the regional overlying skull 81. subdural hematoma. Chronic hematomas &
hygromas/effusions may appear similar.
77
rn
<=
~
HYPODENSE EXTRA-AXIAL MASS(ES)
QJ
u;
U
-0
·0 Post-Operative Epidural Fluid, Effusion,
<=
.c Fat, or Air Pneumocephalus
'-'<Il~ (LeFt) Axial NECT shows a
<Il hypodense extra-axial mass
.0
:J anterior 10 both frontal lobes
(fJ
-0 =. Note that on brain
<= windows, air & fat are not
<Il
rn easily differentiated. Bone
QJ windows confirm the
'-'<Il epidural fat packing. (Right)
0-
(fJ Axial NECT shows
hypodense extra-axial masses
<Il
·x bifrontally, characteristic of
<Il, tension pneumocephalus.
~<Il
Note stretched bridging
X veins ~ & Mount Fuji sign
w
E:!:2 where the frontal lobe
c: lips resemble the mountain
....
III
peaks .
eo
'tl
c:
III
Neurocysticercosis
extra·axial cyst in the middle
cranial fossa = without
enhancement. Racemose or
grape-like NCC occurs in the
basal cisterns & typically
contains no scolex & does
not enhance unless there ;s
associated meningitis. (Right)
Axial NECT shows a midline
extra-axial hypodense mass
=. Bone windows (not
shown) confirmed fat.
Incidentally found lipoma in
chis trauma patient. Midline
location is typical for these
congenital lesions.
Pineal Cyst
(LeFt) Axial NECT shows a
small pineal cyst =
with
mild rim calcification. Unless
nodularity is present, this is
usually incidental, though if
over 7 em, serial follow-up
studies (over )-] years) is
advisable to exclude growth
(to avoid missing a cystic
pineal tumor). (Right) Axial
NECT shows a hypodense
mass centered over the 3rd
ventricle with a thin rim of
calcification Itl. A cystic
mass, which extended from
the suprasellar region, is
I typical.
4
78
HYPODENSE EXTRA-AXIAL MASS(ES) en
"
c:
III
:J
Co
OJ
.,
Epidural Hematoma III
(Leh) Axial NECT shows a :J
biconvex right frontal mass m
with a hyperdense inner ~
~
componenl =:I and ,
Q)
Q)
hypodense outer component X
representing a very iii'
rapidly bleeding epidural (f)
hematoma. (Right) Axial "0
Q)
NECT shows CST density o
(1)
extra-axial mass deforming en
the brainstem =:I. Q)
:J
Insinuating margins are C.
classic for epidermoids. OWl (f)
c:
& FLAIR MR confirm 0-
Q)
diagnosis. ~
Q)
o
::r
:J
o
a:
o
(ii'
ro~
:J
Rathke Cleft Cyst en
(Left) Axial NfCT shows a
hypodense suprasellar cyslic
mass 1:]. An inlracystic
nodule is commonly seen on
MR. No enhancement ;s
typical. (Right) Axial CECT
shows a lefl fronlal subdural
empyema with enhancement
along lhe deep margin =:I. A
tiny focus of air is seen
wilhin the collection Ii8
Underlying left fronlal white
mailer hypodensily is
consistent with vasogenic
edema ~. Associated mass
effect is evident with midline
shifllO the righl.
Arachnoid Granulations, Dural Sinuses Dermoid Cyst

(Leh) Axial NfCT shows a
well-circumscribed round
cyst =:I within the superior
sagillal sinus which followed
CSF, arachnoid granulation.
The density & location are
lhe key imaging findings for
lhese lesions, which should
nol be confused with
intraluminal thrombus.
(Right) /lxial CECT shows a
low density pineal region
mass a Fat droplets are
present in the subarachnoid
space =:I. due to dermoid
rupture. A shunt is presenllo
treat the hydrocephalus, I
4
79
SECTION 5
Multiple Enhancing Lesions, General 1-5-2
Ring-Enhancing Lesion, Solitary 1-5-6
Ring-Enhancing Lesion, Multiple 1-5-12
Solitary Cystic Parenchymal Mass, General 1-5-16
CSF-like Parenchymal Lesion(s) 1-5-22
Cyst with Nodule 1-5-28
Fat-like Lesion(s), General 1-5-32

Solitary Parenchymal Calcification 1-5-34
Multiple Parenchymal Calcifications 1-5-40
Solitary Hyperdense Parenchymal Lesion 1-5-44
Multiple Hyperdense Parenchymal Lesions 1-5-50
Solitary Hypodense Parenchymal Lesion 1-5-56
Multiple Hypodense Parenchymal Lesions 1-5-60
Multiple Brain Hyperintensities (T2/FLAIR), Common 1-5-64
Multiple Brain Hyperintensities (T2/FLAIR), Less Common 1-5-70
Multiple Brain Hyperintensities (T2/FLAIR), Rare but Important 1-5-76
Multiple Hypointense Foci on T2 1-5-80
Multiple Hypointense Foci on GRE/SWI 1-5-82
T1/T2 Hyperintense Parenchymal Lesions 1-5-86
T1 Hypointense, T2 Hyperintense Parenchymal Lesions 1-5-90
T1/T2 Isointense Parenchymal Lesions 1-5-94
Restricted Diffusion 1-5-98
T1 Hyperintense Parenchymal Lesion(s) 1-5-102

Brain Tumor in Newborn/Infant 1-5-106
Brain Tumor in Child> 1 Year 1-5-112
Epilepsy, General 1-5-118
<1l
~ MULTIPLEENHANCING LESIONS, GENERAL
Ql
c
Ql
<.9 • May be nodular, ring, or semilunar
Common o Cyst with scolex in convexity
• Metastases, Parenchymal subarachnoid spaces is typical
• Multiple Sclerosis o Four stages: Vesicular, colloidal vesicular,
• Neurocysticercosis granular nodular, nodular calcified
• Abscess (Multiple) o Vesicular: No enhancement typical; may
c: Less Common see discrete, eccentric scolex enhancement

Oro o Colloidal vesicular: Thick cyst wall
•... • ADEM
lD • Opportunistic Infection, AIDS enhances; enhancing marginal nodule
't:l
c: • Tuberculosis o Granular nodular: Thickened, retracted
ra
• Lymphoma, Primary CNS cyst; nodular or ring enhancement
• Neurosarcoid o Nodular calcified: Small calcified lesion,
• Glioblastoma Multiforme rare minimal enhancement
• Abscess (Multiple)
Rare but Important
o DWI + & T2 hypointense rim classic
• Vasculitis o Four stages: Early cerebritis, late cerebritis,
• Lyme Disease early capsule, late capsule
• Lymphoma, Intravascular (Angiocentric) o Early cerebritis: No/patchy enhancement
• Parasites, Miscellaneous o Late cerebritis: Intense but irregular rim
• Susac Syndrome enhancement
o Early capsule: Well-defined, thin-walled
ESSENTIAL INFORMATION enhancing rim thicker on side near cortex
o Late capsule: Cavity collapses, thickened
Key Differential Diagnosis Issues enhancement of capsule especially side
• Superficial enhancement is usually vascular near cortex
or inflammatory o Septic emboli ~ multiple lesions
• Nodular cortical/subcortical enhancement is
characteristic for hematogenous metastases Helpful Clues for Less Common Diagnoses
& embolic disease • ADEM
• Ring-enhancing lesions have numerous o Multifocal T2 hyperintense lesions 1-2
etiologies: Gliomas (40%), metastases (30%), weeks after viral infection or vaccination
abscesses (8%), demyelinating disease (6%) o Variable patterns of enhancement,
• Thick, irregular ("shaggy") rim-enhancing incomplete ring classic
lesions are usually malignant • May be punctate, ring, or peripheral
• OWl MR may help differentiate lesions o Predilection for subcortical white matter
o Bilateral, but asymmetric lesions
Helpful Clues for Common Diagnoses • Opportunistic Infection, AIDS
• Metastases, Parenchymal o Toxo: Multiple ring-enhancing lesions
o Discrete enhancing parenchymal masses at
with surrounding edema in deep &
gray-white interface superficial brain typical
o Account for up to 50% of all brain tumors
• Enhancement: Smooth, nodular or target
o 80% hemispheres, 15% cerebellum, 3%
(central nodule & peripheral rim)
basal ganglia (BG) • Involves BG & gray-white junctions
o Enhancement: Punctate, solid, or ring
o Aspergillosis: Hemorrhagic, multifocal,
poorly defined, enhancing lesions
• Multiple Sclerosis • Solid or rim enhancement
o Multifocal periventricular & callososeptal
• Tuberculosis
T2 hyperintensities in a young adult o TB meningitis is most frequent
o Active demyelination enhances transiently
manifestation, more common in children
I o Incomplete ring or "horseshoe shaped"
enhancement is classic
o Basilar meningitis & parenchymal lesions
highly suggestive of TB
5
2
MUlTIPLE ENHANCING lESIONS, GENERAL ,..c:
VI
III
o Tuberculomas: Typically parenchymal, o Multifocal areas of mildly irregular stenosis ::::l
Co
supratentorial; solid or ring-enhancing alternating with dilated segments
..,
OJ
• Lymphoma, Primary CNS o Multifocal subcortical ischemia, ± patchy III
::::l
o Enhancing lesions in periventricular white or gyriform enhancement
OJ
..,
matter (WM) or BG o DWI + in acute setting
o Majority supratentorial but deep gray • Lyme Disease '"
::::l
-U
nuclei are commonly involved o Lesions simulate multiple sclerosis in a ..,
o Often involve corpus callosum & extend patient with skin rash & flu-like illness '"
CO
:J
()
along ependymal surfaces o Some enhancement in WM lesions &/or ::T
'<
o Immunocompetent: Strong homogeneous meninges 3
enhancement o Cranial nerve enhancement may be seen 'Q
"
o lmmunocompromised: Peripheral • Lymphoma, Intravascular (Angiocentric) co
:J
enhancement with central necrosis or o Multifocal abnormal T2 hyperintensity in co
Q)
homogeneous enhancement deep WM, cortex, or BG
• Neurosarcoid o Enhancement: Linear, patchy, nodular,
o Solitary or multifocal CNS mass(es) & gyriform, homogeneous, meningeal
abnormal CXR classic o Supratentorial location typical
o Typically leptomeningeal &/or dural • Parasites, Miscellaneous
enhancement o Amebic encephalitis: Single or multiple
o Rarely causes parenchymal nodules focal, nodular, or ring-enhancing masses
• Glioblastoma Multiforme o Malaria: Punctate & ring hemorrhages,
o Rapidly enlarging malignant tumor infarcts, cerebral edema
characterized by necrosis & neovascularity o Paragonimiasis: Conglomerated, multiple
o Thick, irregular rim enhancement ring-enhancing lesions
surrounding necrotic core classic o Trichinosis: Eosinophilic
• May be solid, ring, nodular, or patchy meningoencephalitis, vascular thrombi,
o Rarely may be multifocal or multicentric infarcts
o Supratentorial WM most common location • Susac Syndrome
o Encephalopathy, visual changes, hearing
loss
• Vasculitis
o "Holes" in middle of corpus callosum
o Heterogeneous group of CNS disorders
o Multifocal enhancing WM lesions
characterized by non-atheromatous
inflammation & necrosis of blood vessels
Metastases, Parenchymal Multiple Sclerosis
I
Axial T7 C+ MR shows multiple
the corticomedullary junctions,
enhancing masses at
a classic location for
Axial T7 C+ MR shows the classic incomplete ring or
"horseshoe-shaped" enhancement of demyelination in
5
metastatic disease. Significant associated vasogenic a patient with MS plaques. enhancement is transient &
edema is typical. OWl is typically negative. indicates active disease.
3
co
~ MULTIPLE ENHANCING lESIONS, GENERAL
Q)
c
Q)
c:>
co
E
>.
.r: Neurocysticercosis
(.)
c (Left) Coronal TI C+ Fs MR
~
Q)
shows multiple small
co
0.. peripherally enhancing
c
co
lesions =
in the
~ subarachnoid spaces relaled
ell 10 nodular calcified slage of
c NCe. NOle lack of edema.
Lesions may be in different
'"
"-
ell stages in the same patient.
"0 (Right) Axial TI C+ (5 MR
c shows mullifocal enhancing
'" lesions related to septic
::3 emboli. OWl is Iypically
..><:
en positive. Contrast MR mimics
metastases as the lesions are
at gray·white interfaces.
ADEM Opportunistic Infection, AIDS

mullifocal subcorlical
enhancement in this child
wilh ADEM. Bilaleral bUI
asymmetric involvement is
Iypical. The deep gray nuclei
are involved in 50% of
cases. (Right) Axial TI C+ (5
MR shows multifocal
ring-enhancing lesions, some
with a classic "target"
appearance Ell in Ihis
patient with toxoplasmosis.
Lesions are most often seen
in Ihe BG & cerebral
hemispheres. Patients
respond well 10 Iherapy.
Tuberculosis
multiple tuberculomas in the
corlex & BG wilh ring
nodular enhancement H2.
=&
Classic TB caseating
granulomas are T2
hypointense, which helps
distinguish them from other
enhancing lesions. (Right)
Axial TI C+ MR shows solid
& ring·enhancing lesions in
this immunocompromised
patient with primary eNS
lymphoma. Ilemorrhage,
necrosis, & ring-enhancing
lesions are more common in
I immunocompromised
palien/s.
5
4
MULTIPLE ENHANCING LESIONS, GENERAL
Cll
:J
Co
OJ
....•
Glioblastoma Multiforme Cll
Neurosarcoid
:J
nodular & linear OJ
....•
enhancement with III
surrounding edema. :J
Granulomatous II
III
....•
leptomeningitis is the most (t)
common pathologic feature :J

()
in neurosarcoid. ::r
Leptomeningeal
'<
3
enhancement is III
characteristic. Periventricu/ar G)
(t)
WM T2 hyperintensities are :J
seen in approximately 50% (t)
....•
of cases. (RighI) Coronal T I III
C+ MR shows mult/focal
enhancing masses related to
GBM with involvement of
Ihe perivascular spaces.
Vasculitis
(Left) Sagittal T1 C+ MR
shows multiple linear
enhancing foci.
Granulomatous angiitis was
found al biopsy. Imaging
differential diagnosis includes
sarcoid, amyloid angiopathy,
vasculitis, & intravascular
lymphoma. (RighI) Axial T1
C+ MR shows nodular
enhancement & subtle
patchy 81 enhancement
typical of intravascular
lymphoma. This rare
diagnosis should be
considered in patients with
dementia, T2 hyperintense
lesions, & enhancement.

mulUfocal enhancing lesions
in this patient with amebic
encephalitis. Note nodular
!:ll & ring enhancement
typical for this parasite.
=-
(RighI) Coronal T1 C+ MR in
a 27 year old woman with
dizziness, headaches,
blurred vision shows
multjfocal enhancing lesions
=.
I
5
5
~
C1J RING-ENHANCING lESION, SOLITARY
Ql
c
Ql
c.9 o T2 hypointense rim & thin enhancing rim
C1J
E o DWI + in pyogenic abscess
>-
.r=
Common o Look for other signs of infection & source
u
c • Metastases, Parenchymal in mastoids & paranasal sinuses
~
Ql
• Glioblastoma Multiforme
C1J o Proton MR spectroscopy (MRS) within
0-
c • Abscess pyogenic abscess cavity shows elevated
~
C1J • Intracerebral Hematoma (Subacute) cytosolic amino acids (0.9 ppm), acetate
III
• Cerebral Infarction, Subacute (1.92 ppm), and succinate (2.4 ppm)
• Radiation Necrosis • Intracerebral Hematoma (Subacute)
less Common o History of trauma, coagulopathy, amyloid
• Tumefactive Demyelinating Lesion angiopathy
• Neurocysticercosis o Ring enhancement common subacutely
• Lymphoma, Primary CNS o Look for blood products on MR (especially
• Toxoplasmosis, Acquired on GRE/T2*/SWI sequence)
• Tuberculoma • Cerebral Infarction, Subacute
• Aneurysm (Thrombosed) o Signal changes in a vascular territory
• Arteriovenous Malformation (Thrombosed) o May see gyriform Tl hyperintensity
• Ganglioglioma o Enhancement: Ring-like &/or gyriform
• Pilocytic Astrocytoma o At this stage, DWT has normalized
• Radiation Necrosis
Rare but Important o Occurs months after radiotherapy in site of
• Lacunar Infarction (Subacute) radiation portal
• Fungal Diseases o Perfusion MR may discriminate between
• Parasites, Miscellaneous radiation necrosis & tumor
• Radiation necrosis: Hypoperfusion
ESSENTIAL INFORMATION • Tumor: Hyperperfusion
Key Differential Diagnosis Issues Helpful Clues for less Common Diagnoses
• Solitary ring-enhancing lesions most often • Tumefactive Demyelinating Lesion
related to tumor, infection, or o Seen in multiple sclerosis & ADEM
demyelination o Often incomplete ring enhancement, little

• Location of lesion often helpful for diagnosis mass effect or vasogenic edema; resolves
• Metastatic lesions are typically subcortical, with steroid therapy
while primary tumors are often deep o Often mimics neoplasm
• Smooth rim enhancement suggests abscess • Neurocysticercosis
• Irregular, thick rim suggests tumor o Cyst with a scolex is pathognomonic
o Ring enhancement seen in colloidal
Helpful Clues for Common Diagnoses vesicular & granular nodular stage
• Metastases, Parenchymal • Lymphoma, Primary CNS
o Often significant vasogenic edema
o Ring-enhancing pattern seen in
o Gray-white matter junction typical
immunocompromised patients
o Generally does not restrict on DWI
o Typical locations: Periventricular, corpus
o Multiple> single lesion callosum, basal ganglia (BG)
• Glioblastoma Multiforme o Hyperdense on CT, hypointense on T2 MR
095% of primary GBMs have central due to hypercellularity
necrosis, rim enhancement, DWI negative o MRS may differentiate from toxo
o Heterogeneous white matter (WM) tumor o Lymphoma: Elevated choline level
with irregular, thick rim enhancement • Toxoplasmosis, Acquired
o Strong tendency to infiltrate widely
o Solitary or multiple lesions with nodular or
• Abscess ring enhancement
I o Can be pyogenic, fungal, or
granulomatous
o Occurs in immunocompromised,
especially HIV+ patients
5
6
RING-ENHANCING lESION, SOLITARY en
"
c:
• Tuberculoma o Associated with neurofibromatosis type 1

o Associated with TB meningitis in 50%
o Can be solitary or multiple
• Lacunar Infarction (Subacute)
• Aneurysm (Thrombosed) o Typically in BG, thalamus, or deep white
o May be partially or completely
matter
thrombosed o May enhance subacutely
o Laminated appearance of thrombus
• Fungal Diseases
o May see pulsation artifact on MR
o Rare infections that occur primarily in
• Arteriovenous Malformation immunosuppressed patients
(Thrombosed) o Includes nocardia, blastomycosis,
o May be partiaJly or completely
coccidioidomycosis, histoplasmosis, G)
thrombosed candidiasis
<ll
:J
o Blood products, calcium are common <ll
o Multiple lesions> single lesion iil
o Serpiginous nidus seen as flow voids on
• Parasites, Miscellaneous
MR, large draining veins o Rare infections occur at aJi ages, most
• Ganglioglioma common in children & young adults
o May be solid, cystic, or mixed solid-cystic
o Patient's travel history important
o 1/3 have calcifications
o May cause solitary or multiple
o Temporal lobes & cerebellar hemispheres
ring-enhancing lesions
most common locations o Amebic encephalitis: Single or multiple
o Temporal lobe lesions present with
nodular or ring-enhancing masses
seizures o Paragonimiasis: Hemorrhage or infarct
• Pilocytic Astrocytoma with granuloma formation; ring
o Common locations: CerebeJlum,
enhancement
hypothalamus, optic pathway
o 4 predominant imaging patterns
• Mass with enhancing cyst wall & SELECTED REFERENCES
intensely enhancing mural nodule (46%) 1. Smirniotopoulos JG et al: Patterns of contrast
• Mass with a non enhancing cyst & enhancement in the brain and meninges. Radiographies.
27(2):525-5 1,2007
intensely enhancing mural nodule (21 %)
• Necrotic mass with central
nonenhancing zone (16%)
• Predominantly solid mass with minimal
cyst-like component (17%)
Metastases, Parenchymal
I
Axial T1 C+ [5 MR shows a solitary, thick-walled mass
in the right cerebellum =. A thick enhancing rim
Coronal T1 C+ M R shows a cystic mass with large
mural nodule in the cerebellum 1:]. While this lesion
5
suggestsWmor. Biopsy proved metastatic melanoma. resembles hemangioblastoma, the wall of most cystic
hemangioblastomas rarely enhances.
7
ctl
~ RING-ENHANCING LESION, SOLITARY
Q)
c
Q)
~
ctl
E
>-
.c Glioblastoma Multiforme Glioblastoma Multiforme
u
c (Left) Axial T7 C+ MR shows
~ a histologically proven
ctl
0.. glioblastoma multiforme in
c
ctl
the left thalamus =. Note
~ irregular wall & central
OJ necrosis. CBMs lend to
C occur in the deep white
III matler or deep nuclei &
"-
OJ infiltrate widely beyond the
"'C enhancing margins. (Right)
C
III Axial T7 C+ MR shows a
large glioblastoma
multiforme E!2 with
subependymal involvement
=. Note the irregular
peripheral rim enhancement
in the tumor.
Abscess
a solitary ring-enhancing
pyogenic abscess IclJ with
perilesional vasogenic edema
=. A smooth, thin
enhancing wall & a T2
hypoinlense rim is
characteristic of abscess.
Often abscess walls are
thinner along ventricular
side, which may predispose
to ventricular rupture.
(RighI) Axial OWl MR shows
a mass demonstrating
restricted diffusion on OWl,
which is typical of a
pyogenic abscess R8
(Left) MRS shows Iypical

MRS spectrum of an abscess
with volume of interest
placed within the abscess
cavity. MRS was obtained
with TR20001TE35. Note the
large lactate doublet peak
resonating at /.3 ppm =. A
large acetate peak is present
at 2 ppm E!2. The peak at
0.9 ppm IJ::l represents
cylosolic amino acids
(leucine, isoleucine, valine).
ring enhancement in a
subacute left parietal
hematoma 1J::l.
I
5
8
RING-ENHANCING LESION, SOLITARY
Ql
:J
a.
..,
OJ
Ql
Cerebral Infarction, Subacute Radiation Necrosis
:J
an evolving infarct in the left IJl
..,
temporal lobe ~ that was OJ
initially thought to represent :J
-U
a tumor. Follow-up MR (not
shown) shows interval lesion
..,
OJ
C1l
involution with resolution of :J
()
contrasl·enhancemenl. ::T
'<
3
shows radiation necrosis E2 OJ
occurring in the site of a G)
previous arteriovenous C1l
:J
malformation that was ..,
C1l
treated with gamma knife. OJ

Radiation necrosis often
mimics tumor.
Tumefactive Demyelinating Lesion Neurocysticercosis

a biopsy-proven tumefactive
demyelinating lesion
secondary ta multiple
sclerosis. (Right) Coronal T1
C+ MR shows a thick
enhancing lesion =.
Note
the linear enhancing area
that appears ta extend ta the
brain surface E:I. This is a
solitary neurocysticcrcosis
cysllhal is actually within
the depths of a sulcus, not
actually in the brain
parenchyma. The linear
enhancement is
inflammation along the pial
surface of the sulcus.
shows an irregular
ring-enhancing mass in the
body of corpus callosum
with extension into adjacent
=
perivenlricufar while matter
in an HIV patient.
Periventricular location may
help differentiate from taxa.
shows a ring·enhancing mass
=:I & ependymal
enhancement ~ in this II/V
patient. Hemorrhage,
necrosis, & ring-enhancing
lesions are common in
patients with HIV/AIOS who
develop CNS lymphomas. I
5
9
CIl
~ RING-ENHANCING LESION, SOLITARY
Q)
C
Q)
C)
CIl
E
>.
.r:
u
c (Left) Coronal T7 C+ MR
~
Q)
shows a left frontal
CIl
D... tuberculoma ~. Meningitis
c occurs in approximately
~ 50% of patienlS with CNS
co TB. TB is more common in
c: children &, young adullS.
ra~ (Right) Axial CECT shows an
co irregular, ring-shaped mass in
"'C
c
the suprasellar cistern =.
ra Note adjacent pial
enhancement extending
around the suprasellar
cistern & into the sylvian
fissure m in this patient with
suprasel1ar tuberculoma with
tuberculous meningitis.
Aneurysm (Thrombosed) Aneurysm (Thrombosed)

shows a large extra-axial
basilar artery aneurysm
anterior to the pons &
medulla =:I with some
nodular & rim enhancement.
This mass is markedly
hypointense on T2 MR. A
laminated appearance may
help with the diagnosis.
ring enhancement in this
partially thrombosed "giant"
aneurysm (> 2.5 em) =:I.
Giant aneurysms are more
likely to thrombose.
Arteriovenous Malformation Arteriovenous Malformation

(Thrombosed) (Thrombosed)
heterogeneous,
ring-enhancing mass =:I with
a fluid level SlI related to
recent hemorrhage. Note
surrounding edema.
Thrombosed AVMs account
for only 1-2% of all AVMs of
the brain. When they occur,
they often mimic neoplasm.
shows a partially treated
right parietal arteriovenous
malformation that contains
serpentine flow voids ffi
typical of AVM.
I
5
10
RING-ENHANCING lESION, SOLITARY VI
"
c:
Cll
:l
Co
.,
llJ
Cll
:l
shows a large partially llJ
~
rim-enhancing cystic mass OJ
8lI in the frontal lobe, :l
"U
compressing the frontal horn OJ
of the left lateral ventricfe. ro:l
There is a strongly enhancing ()
mural nodule within this ::r
'<
cystic mass (not shown), 3
typical of ganglioglioma. OJ
(Right) Axial T1 C+ MR Gl
shows a ring-enhancing mass CD
:l
with a solid mural nodule CD
~
OJ
~, a cfassic ganglioglioma.
Gangliogliomas usually
present in children & young
adults, typically younger
than 30 years.
Pilocytic Astrocytoma Pilocytic Astrocytoma

shows a cavitary cerebe/Jar
pHocytic astrocytoma with
tumor cyst wall ~ and
nodular r.:= enhancement.
shows a ring·enhancing mass
with an enhancing mural
nodule that abuts dura.
Pilocylic astrocytoma (PA)
Supratentorial PA are
uncommon in the cerebral
hemispheres. Differential
diagnosis includes
ganglioglioma &
pleomorphic
xanthoastrocytoma.
Fungal Diseases Parasites, Miscellaneous

an irregular, mildly
rim·enhancing mass with
surrounding edema &
Aspergilloma was found at
surgery. (Right) Axial T1 C+
MR shows a heterogeneous
ring-enhancing mass =
with
mild leptomeningeal
enhancement ~. Amebic
meningoencephalitis was
found at biopsy.
I
5
11
co
~ RING-ENHANCING LESION, MULTIPLE
Q)
c
Q)
CJ o Mass effect usually less than expected for
co DIFFERENTIAL DIAGNOSIS
E size of lesion
>-
.r:
Common o Coexistence of enhancing &
<.>
c
Q)
• Metastases Parenchymal nonenhancing lesions due to relapsing,
~ • Abscess
co remitting nature of disease
a.. • Multiple Sclerosis
c o Perivenular location "Dawson fingers" &
.~ • ADEM undersurface of corpus callosum typical
co • Neurocysticercosis
c • ADEM
.<0 Less Common o Usually monophasic
~
co • Tuberculosis o History of recent viral illness or
"'C
c • Opportunistic Infection, AIDS immunization
<ll
• Lymphoma, Primary CNS o Multifocal white matter (WM) &/or basal
• Radiation and Chemotherapy ganglia (BG) lesions
• Multifocal Glioblastoma Multiforme o May have with punctate, ring, incomplete
• Subacute Intracerebral Hematomas ring, or peripheral enhancement
• Subacute Cerebral Infarctions o May mimic multiple sclerosis (MS)
Rare but Important
o Parasitic infection caused by pork
• Fungal Diseases tapeworm, Taenia solium
• Parasites, Miscellaneous o Cyst with a scolex is pathognomonic
• Lyme Disease o 4 stages: Vesicular, co]]oidal vesicular,
granular nodular, nodular calcified
ESSENTIAL INFORMATION o Ring enhancement seen in colloidal
vesicular & granular nodular stages
• Ring-enhancing lesions are most commonly Helpful Clues for Less Common Diagnoses
related to tumor, abscess, & demyelination • Tuberculosis
• Smooth, thin ring enhancement is typical of o Associated with TB meningitis in 50%
an organizing abscess o Caseating TB granulomas often have
• Thick, irregular rings suggest a necrotic markedly T2 hypointense centers
neoplasm o Infants, children, & immunocompromised
are predisposed
Helpful Clues for Common Diagnoses o Review CXR to exclude miliary TB or
• Metastases Parenchymal primary TB infection
o Associated with substantial vasogenic
edema for relative size of lesion o Multiple ring-enhancing lesions in HIV+
o Ring-enhancing lesions at patient: Consider toxoplasmosis, TB,
corticomedu]]ary junctions pyogenic/fungal abscess, & lymphoma
• Abscess o Toxoplasmosis is most common
o Thin T2 hypointense rim characteristic opportunistic infection
o DWI shows restriction within abscess
• BG & gray-white matter junctions
o Ventriculitis, meningitis may be present • Asymmetric "target sign": Enhancing
o Proton MRS of abscess cavity: Presence of
eccentric nodules within abscess cavity
cytosolic amino acids (0.9 ppm), succinate o MRS may differentiate Toxo from
(2.4 ppm), & acetate (1.92 ppm) lymphoma; NAA & choline usua]]y nearly
o Risk factors: Sepsis, immunocompromised,
absent (Toxo)
right to left pulmonary shunt • Lymphoma, Primary CNS
o Multifocal disease often caused by septic
o Subependymallocation of lesions
emboli or paranasal sinus infection o Ring enhancement seen in HIV+ patients
• Multiple Sclerosis with lymphoma
I o Enhancement
demyelination
indicates acute o MRS: Elevated choline peak
o PET: Hypermetabolic
5
12
RING-ENHANCING lESION, MULTIPLE
o Perfusion MR: Hyperperfusion Meningitis common

o
• Radiation and Chemotherapy Often multiple ring-enhancing lesions
o
o Radiation necrosis may cause multiple o Most common in immunosuppressed
enhancing lesions patients
o Often difficult to differentiate from • Parasites, Miscellaneous
recurrent tumor o Amebic encephalitis: Meningoencephalitis;
o MRS & MR perfusion may be useful single or multiple focal, nodular, or
• MRS: No elevated choline ring-enhancing masses
• MR perfusion: Hypoperfusion o Malaria: Punctate & ring hemorrhages,
• Multifocal Glioblastoma Multiforme infarcts, cerebral edema, + enhancement
o Seen in malignant transformation of low • Lyme Disease Gl
grade glioma & spread of primary GBM o Multifocal T2 hyperintense periventricular CD
:J
o Metachronous lesions uncommon WM lesions ± enhancement CD
~
OJ
• Subacute Intracerebral Hematomas o Cranial nerve enhancement is common
o History of trauma, coagulopathy, amyloid o Mimics MS in patient with skin rash &
angiopathy flu-like illness
o Look for blood products on MR (especially
on GRE/T2*/SWI sequence)
SELECTED REFERENCES
• Subacute Cerebral Infarctions
1. Smirniotopolllos JG et al: Patterns of contrast
o Exclude vasculitis & embolic phenomenon enhancement in the brain and meninges. Radiographies.
as cause for multiple infarcts 27(2):525-5 I, 2007
o Enhancement pattern is ring-like & 2. Siskas N et al: Cortical laminar necrosis in brain infarcts:
serial MR1.Nellroradiology. 45(5):283-8, 2003
gyriform 3. Kamiyama M et al: Cortical laminar necrosis in brain
o Gyriform Tl hyperintensity due to cortical infarcts: chronological changes on MRI. ellroradiology.
laminar necrosis seen as early as 2 weeks 39(7):474-9, 1997
post infarct
o Contrast-enhancement of laminar lesions
may be seen up to 8 months
• Fungal Diseases
o Includes nocardia, blastomycosis,
coccidioidomycosis, histoplasmosis,
candidiasis
Metastases Parenchymal Abscess
I
Coronal T1 c+ FS MR shows multiple brain metastases
from metastatic breast carcinoma. Significant associated
Axial T1 C+ MR shows multiple brain abscesses =-
ventriculitis a & meningitis m. Ventriculit.is is a
5
vasogenic edema is common. complication of meningitis or a cerebral abscess that
ruptures into the ventricular system.
13
~ RING-ENHANCING LESION, MULTIPLE
OJ
c
OJ
(9
ro
E
>-
.r: Abscess Multiple Sclerosis
u
c (Lefl) Axial T1 C+ MR shows
~
OJ
abscesses with thin smooth
ro
0... enhancing waifs =.
The thin
c waif sugges15infection rather
ro
~ than neoplasm. A T2
en hypointense rim & OWl
c restriction is characteristic of
•..
III
en
abscess. (Right) Axial T1 C+
MR shows a
"'C horseshoe-shaped or
c U-shaped enhancement
=
III
typical of demyelinating
lesions. Another lesion is
partially visualized in this
image. Enhancing &
nonenhancing lesions often
coexist in MS.
ADEM Neurocysticercosis
a large, tumefactive ADEM
lesion in the left cerebral
hemisphere with mild
incomplete enhancement
E!iJ. Mass effect is less than
that expected for lesion size.
Another clue to its
nonneoplastic nature is a
second lesion on the right
~. (Right) Axial T1 C+ MR
shows ring-enhancing right
CPA cistern cysts
thickened enhancing
& =
meninges E2.
Opportunistic Infection, AIDS

multiple ring-enhancing foci
= due to tuberculomas.
Caseating tuberculous
granulomas with solid
centers may be profoundly
hypoinlense on T2 MR (not
shown). (Right) Coronal T1
C+ Fs MR shows multiple
ring-enhancing lesions in =
an 1-11 V patient with
toxoplasmosis. An eccentric
target sign may be seen,
typical of toxoplasmosis.
MRs may help differentiate
this from lymphoma.
I
5
14
RING-ENHANCING LESION, MULTIPLE CJl
c:
""
III
:l
a.
lP
...•
III
(Left) Coronal T1 c+ MR
:l
shows ring enhancement in OJ
Ihe basal ganglia =. OJ
:::J
Hemorrhage & necrosis
-U
occur in AIDS-related
...•
Cll
lymphoma, which leads to CD
ring enhancement :::J
Cl
AIDS-relaled lymphoma ::T
'<
occurs at a younger age than 3
primary CNS lymphoma. Cll
(Right) Axial T1 C+ FS MR (j)

shows 2 ring-enhancing CD
:::J
lesions in Ihe frontal lobes CD
...•
9: Ihal have been stable for Cll
2 years. These lesions

occurred within the radiation
portal in this palient with
sinonasaf adenocarcinoma.
Multifocal Glioblastoma Multiforme Subacute Cerebral Infarctions

shows multi/ocal
glioblastoma multi/orme ~
in a patient who has
previous tumor resection r:=.
Ependymal spread is
common in GBM. (Right)
Sagiaal T1 C+ FS MR shows
multiple enhancing =
watershed infarcts. Some 0/
these infarcts demonstrate
gyri/arm T1 hyperintensity
(nolshown) secondary to
cortical laminar necrosis.
shows multifocal
ring-enhancing lesions in an
immunocompromised
patient. Blood cultures were
positive for Nocardia in this
rena/transplant patient.
shows ring ~ & punctate
enhancement in this patient
with Amebic encephalitis.
This infection may be focal
or diffuse with multiple
ring-enhancing lesions.
I
5
15
ro
~ SOLITARY CYSTIC PARENCHYMAL MASS, GENERAL
Ql
c
Ql
c.9 • Key imaging issues
ro DIFFERENTIAL DIAGNOSIS
E a Is cystic mass exactly like CSF?
£
>- Common • Enlarged perivascular space,
U
c • Enlarged Perivascular Space encephalomalacia, porencephalic or
~
Ql
• Encephalomalacia
ro neuroglial cyst
0..
c • Neurocysticercosis a Is cystic mass hypodense to parenchyma
ro
~ • Porencephalic Cyst but hyperdense compared to CSF?
OJ
• Glioblastoma Multiforme • Cystic neoplasm, abscess, tumefactive
C
nl • Metastasis demyelination, epidermoid or
~
OJ • Pilocytic Astrocytoma neurenteric cyst, parasites
"0
C • Abscess a Is density/signal intensity of surrounding
ro
Less Common brain abnormal?
• Intracerebral Hematoma (Resolving) • Encephalomalacia, infection, neoplasm
• Multiple Sclerosis a Does lesion enhance?
• Ganglioglioma • Yes: Neoplasm, abscess, resolving

• DNET (subacute) hematoma, tumefactive
• Pleomorphic Xanthoastrocytoma demyelination
• Hemangioblastoma • No: Enlarged perivascular space (PVS),
• Meningioma (Cystic) encephalomalacia, porencephalic or
• Epidermoid Cyst neuroglial cyst
a Does cyst have mural nodule?
• Dermoid Cyst
• Neuroglial Cyst • Neurocysticercosis (NCe), neoplasm
• Ependymoma, Supratentorial Helpful Clues for Common Diagnoses
Rare but Important • Enlarged Perivascular Space
• Parasites, Miscellaneous a Multiple lesions, clusters of variable-sized
• Schwan noma (Cystic) cysts> > solitary enlarged PVS

• eurenteric Cyst a Well-delineated round/ovoid
• Desmoplastic Infantile Ganglioglioma a Basal ganglia> white matter, midbrain,
temporal lobe, dentate nucleus
a Follows CSF density/signal intensity
ESSENTIAL INFORMATION • Encephalomalacia
Key Differential Diagnosis Issues a Trauma, infarct, surgery
a Follows CSF
• Definition
a Includes all cyst-like parenchymal masses a Adjacent parenchyma often hyperintense
a Excludes extra-axial cysts on T2WI, FLAIR
• Cisternal (e.g., arachnoid cyst), • Neurocysticercosis
intraventricular (ependymal cyst) a Multiple small> solitary small or large cyst
a Includes "pseudoparenchymal" lesions that ± visible scolex

can invaginate into brain, mimic cystic a Cyst fluid typically proteinaceous, not
parenchymal mass exactly like CSF
• Epidermoid, dermoid cysts; cystic a ± Enhancement, edema
meningioma a Look for multiple parenchymal
• Key clinical issue: Effect of age on diagnosis calcifications ("starry sky")

a Most common in child • Porencephalic Cyst
• Encephalomalacia, infection (abscess, a CSF-containing cyst contiguous with
parasite), neoplasm (primary> > ventricle
metastatic) • Glioblastoma Multiforme
a Most common in adult a 95% central necrosis ± hemorrhage
a Thick, irregular rim enhancement
• Enlarged perivascular space,
I encephalomalacia, neoplasm (GBM, • Metastasis
metastasis), infection (abscess, parasite) a Rim enhances
5
16
SOLITARY CYSTIC PARENCHYMAL MASS, GENERAL
• Pilocytic Astrocytoma o Looks like CSF on NECT

o Child, young adult o Does not suppress on FLAIR,restricts on
o Cerebellar cyst + mural nodule DWI
• Abscess • Dermoid Cyst
o Appearance depends on stage o Fat ± Ca++
o Rim enhancement typical in late cerebritis, o Look for fat "droplets" (rupture)
capsule stages • Neuroglial Cyst
o Well-delineated CSF-like parenchymal cyst
o No enhancement
• Intracerebral Hematoma (Resolving)
• Ependymoma, Supratentorial
o Slightly hyperdense to CSF on NECT
o 1/3 of ependymomas
o Hyperintense on Tl-, T2WI G)
o 80% parenchymal, not necessarily related ([)
o Rim enhancement common ::J

to ventricular wall ([)
~
• Multiple Sclerosis OJ
o Usually large, ± cysts, hemorrhage
o "Tumefactive" MS has "horseshoe-shaped"
o Ca++ seen in 50%
enhancing rim
o Variable heterogeneous enhancement of
• Ganglioglioma
cyst wall, solid component
o Cortically based cyst + enhancing nodule
o ± Ca++; may remodel skull Helpful Clues for Rare Diagnoses
• DNET • Parasites, Miscellaneous
o NECT: Cortically based hypodense mass o Solitary or conglomerate cyst(s)
• Hyperdense to CSF o Some (e.g., hydatid cyst) very large
o MR: "Bubbly" appearance • Schwan noma (Cystic)
• Pleomorphic Xanthoastrocytoma o Only 1-2% of schwannomas are in brain
o Cortically based cyst + nodule parenchyma
o Look for adjacent "dural tail" o Peripheral cyst + enhancing nodule
• Hemangioblastoma • Neurenteric Cyst
o Middle-aged adult o Most are extra-axial, posterior fossa
o Posterior fossa cyst + enhancing nodule o Do occur in supratentorial brain (rare)
that abuts pia o Well-delineated cyst hyperintense to CSF
• Epidermoid Cyst • Desmoplastic Infantile Ganglioglioma
o Irregular "cauliflower-like" margins o Infant with cystic supratentorial mass
o Sylvian fissure, quadrigeminal mass can o Dural-based enhancing mural component
mimic intra-axial mass
Enlarged Perivascular Space Enlarged Perivascular Space
I
Coronal T2WI MR shows a solitary cystic left temporal
lobe lesion ~ that followed CSF on all sequences. Note
Coronal T1WI M R shows a solitary giant midbrain cyst
~ that compresses aqueduct Sl causing obstrucUve
5
the farge pedvascufar space. hydrocephalus 1:2. Enlarged pial-lined cyst was found at
surgery
17
ro
~ SOLITARY CYSTIC PARENCHYMAL MASS, GENERAL
Q)
c
Q)
19
ro
E
>-
.!:
U
C (Left) Axial FLAIR MR in a
Q)
~ patient with history of
ro
0- remote right MCA infarct
c shows cystic
[ll encephalomalacia 81 with
co spongiosis and gliosis, seen
c here as FLAIR hyperintensity
CIl
~ = surrounding the infarcted
co brain. (Right) Axial CECT in
"'C a patient with history of
c systemic cysticercosis and
CIl
seizure shows a large
CSF-like right temporal lobe
cyst =:Ii. No other lesions
were identified.
(Left) Coronal TI C+ MR
shows a large leFt temporal
lobe cyst 81 that thins,
expands overlying skull =:Ii.
NOle compression of the
lateral ventricle 1J:ll. Surgery
disclosed cyst lined by gliotic
brain. (Right) Axial NEeT in
patient with two·day history
of increasing headache,
leFt-sided weakness had CT
scan to "rule out stroke".
NECT shows low density
right temporal lobe mass E±.
Enhancing rim was seen on
TI C+ MR (not shown).
Biopsy disclosed
glioblastoma mufliforme.

cyslic·appearing mass with
thin enhancing rim HI
edema =. Preoperative
diagnosis was abscess, but
biopsy disclosed
adenocarcinoma. Right
parahifar mass was Found on
chest radiograph. A
bronchogenic carcinoma
primary was diagnosed.
(Right) Axial NEeT in a 7
year old shows a hypodense
leFt cerebellar mass that is
hyperdense compared to
CSF Patchy enhancement of
solid component [;g was
I seen on (fU (no{ shown).
5
18
SOLITARY CYSTIC PARENCHYMAL MASS, GENERAL en
,.-
r::
III
:l
C.
...
llJ
III
(Left) Axial CECT shows :l

ill-defined cyslic lesion
with surrounding edema in
= ...OJ
llJ
:l
patient with pyogenic
-U
meningitis, enhancement
basilar cisterns E'J. These
in
...
OJ
CD
findings are characteristic of :l
()
late cerebritis stage of ::r
'<
abscess formation. (Right) 3
Axial CECT shows low OJ
density mass that is not quite G)
as hypodense as CSf in CD
:l
adjacent ventricles. Thin rim CD
enhancement is seen I:}:I OJ
IOgether with some adjacent
edema 81. MR disclosed
features of late subacute
hematoma.
Multiple Sclerosis
cyslic-appearing right
posterior parieta/lobe mass
~ Several other subtle
hypointense lesions are
present Faint rim
enhancement was seen on
TI C+ (not shown). (Right)
Axial NECT shows
hypodense right posterior
parietal mass E1 with
extensive
edema =. while maller
Partial
(" horseshoe") rim
enhancement seen on T1 C+
MR is characteristic of
tumefaCl;ve demyelination.
(Left) Axial T 1 C+ MR shows

classic ganglioglioma with
cortically based enhancing
nodule E:I, nonenhancing
cyst =. (Right) Axial CECT
in a 16 year old with
long·standing seizures shows
nonenhancing
cystic·appearing cortical
mass =. Note subtle
remodeling 01 adjacent skull
81. Both the patient's history
and this CT image are classic
ONn
I
5
19
l'll
L
SOLITARY CYSTIC PARENCHYMAL MASS, GENERAL
Q)
C
Q)
(9
l'll
E
>-
.<: Pleomorphic Xanthoastrocytoma Hemangioblastoma
<.)
c (Left) Axial TI C+ MR shows
Q)
L
l'll
a cystic mass in right medial
0... temporal lobe 1:::1 with
c enhancing cortically based
l'll
L nodule 82. (Right) Axial TI
[D C+ FS MR in a 42 year old
C shows posterior fossa
nl
•... parenchymal cystic mass 82
[D with enhancing nodule 1:::1
"'C that abuts pia.
C
nl

hyperintense cystic mass II]
with solid dural-based
nodule 82. This cystic
meningioma invaginales into
the brain, making
differentiation between intra-
and extra-axiallocalion
difficult. (Rigllt) Axial NECT
shows left temporal lobe
CSF-like mass. Note that the
margins are irregular, slightly
lobulated 1:::1. Mass did not
suppress on FLAIR, showed
strong restriction on OWl.
Sylvian fissure epidermoid
Dermoid Cyst
calcified hypodense frontal
mass 82 that is like fat (not
CSF). Note fat droplets in
subarachnoid space 1:::1. This
was diagnosed as a ruptured
dermoid. (Right) Axial FLAIR
MR shows a left temporal
lobe cyst 82 that suppresses
completely on FLAIR. This
could be a solitary enlarged
perivascular space or
neuroglial cyst
I
5
20
SOLITARY CYSTIC PARENCHYMAL MASS, GENERAL en
"
r::
III
:l
Q.
III
.,
Ependymoma, Supratentorial III
(Left) Axial FLAIR MR shows :l

a cyst of CSF-intensity in the OJ
.,
right medial temporal lobe t\)
=. These 50-called choroid :l

-0
fissure cysts are probably a t\)
.,
variant of arachnoid cyst. C1l
(Right) Axial NECT in a :l
=
()
young child shows cystic ::T
mass in right hemisphere
'<
3
=
that has solid component
8l Ca++ severe white
matter edema. WI 10 grade
t\)
Gl
C1l
:l
'" cellular ependymoma was .,
C1l
the diagnosis. t\)
Parasites, Miscellaneous Schwan noma (Cystic)

large, unilocular, CSF-like
parenchymal cyst
without edema or
=
enhancement. Echinococcus
cysts grow slowly and may
attain very large size. (Right)
occipital cystic mass =

Axial T1 C+ MR shows right
with
a cortically based enhancing
nodule 81. Parenchymal
schwannoma was found at
surgery.
shows large, somewhat
lobulated, CSF-like,
nonenhancing,
intraparenchymal cyst =.
Neurenteric cyst found at
surgery. (Right) Coronal T1
C+ MR in infant with large
head shows cystic mass with
enhancing dural-based
nodule =.(Courtesy M.
Sage, MO).
I
5
21
~ CSF-liKE PARENCHYMAL LESION(S)
'"
OJ
C
OJ
<.9 • "Clusters" of variably sized CSF-like cysts
'E" characteristic
>-
.!:
Common • Can occur anywhere but most common
U
C • Enlarged Perivascular Spaces locations = basal ganglia, hemispheric
OJ
~ • Encephalomalacia white matter, midbrain, dentate nuclei
'"
0..
• Lacunar Infarction • Variant (mostly in elderly) = "etat crible"
c
~ • Neurocysticercosis ("cribriform state") with multiple tiny
co'"
C
Less Common cysts in basal ganglia (BG)
•..
III • Porencephalic Cyst • Encephalomalacia
CXl • Multiple Sclerosis o Etiology varies (trauma, infarction, etc.)
"tl
c: • Normal Variant o Can be solitary, multifocal, multicystic
III
o Hippocampal Sulcus Remnants o CSF-like ± adjacent FLAIR hyperintensity
o Connatal Cysts • Lacunar Infarction
o Solitary or multiple
Rare but Important o Typically along single long unpaired
• Neuroglial Cyst penetrating arteries &/or vascular
• Cryptococcosis watershed zones
• Parasites, Miscellaneous • BG, thalamus, white matter (WM)
• Mucopolysaccharidoses common
• Germinolytic Cysts • Multifocal BG infarcts + surrounding
• Miscellaneous Congenital Malformations gliosis = "etat lacunaire" or "lacunar state"
ESSENTIAL INFORMATION o Most neurocysticercosis (NCC) cysts are
actually in sulci
o Cysts in vesicular stage smooth,
thin-walled, with scolex generally visible
as "dot" within cyst
o Multiple lesions in mixed stages common
• Some enhance, some do not
• Ca++ (multiple = "starry sky" pattern)
• Porencephalic Cyst
o Communicates with ventricle &/or pial
surface
o Does not enhance
o Chronic "burned-out" lesions
o Appear as CSF foci with hyperintense rinds
on FLAIR/PD
o Look for faint hyperintensity surrounding
lesions on Tl WI ("lesion within a lesion")
o Do sagittal FLAIR or T2WI to look for other
lesions along callososeptal interface
• Hippocampal Sulcus Remnants
o "String of beads" cysts medial to temporal
horns of lateral ventricles
o Developmental variant, incidental
• Remnants of vestigial primary embryonic
hippocampal sulcus
I o Imaging
• Between hippocampus, dentate gyrus
5
22
CSF-L1KE PARENCHYMAL LESION(S)
• Follow CSF on all sequences • Mucopolysaccharidoses

• No surrounding gliosis o Multiple, bilateral
• Connatal Cysts o Dilated PVSs in deep periventricular WM
o Single or multiple • Germinolytic Cysts
o Location o Periventricular/subependymal cysts
• Intra- or periventricular (may actually be • Cyst(s) along caudothalamic groove
cysts of anterior choroid plexus) probably result from germinolysis
• Small cyst adjacent to tip of frontal horn • Glial (not ependymal) lined
may be normal anatomic variant cysts/pseudocysts resulting from
o Lined with ependyma germinolysis
o Present at birth • Distinguish from "connatal" cysts
Gl
o Usually transient (intraventricular anterior choroid plexus Cll
:::J
o Occasionally seen in older patients cysts) Cll
Ql
o No septations, no hemosiderin • Many etiologies, including inherited
o Generally isolated without associated metabolic disorders (e.g., Zellweger,
abnormalities infantile Refsum), congenital infections
Helpful Clues for Rare Diagnoses (CMV)
• eSF-like; ± septations, hemosiderin; do
• Neuroglial Cyst
o onenhancing CSF-like cyst not enhance
o Look for associated abnormalities
o 0 surrounding signal abnormality
o Does not communicate with ventricle
• Leukoencephalopathy
o Subcortical WM, choroidal fissure
• Delayed myelination
common sites • Polymicrogyria, pachygyria, heterotopias
• Miscellaneous Congenital Malformations
• Cryptococcosis
o Several have parenchymal CSF-like cysts as
o Nonenhancing gelatinous pseudocysts in
perivascular spaces (PVS) part of syndrome
o Multifocal > > solitary lesions
• Van der Knaap leukoencephalopathies
o Most patients have HIV/AIDS
(megaloencephalic leukoencephalopathy
with subcortical cysts, anterior temporal
• Parasites, Miscellaneous
o Other than NCC, parasitic brain cysts
lobe cavitations)
uncommon • Congenital muscular dystrophy
o Hydatid cyst = large non enhancing
(cerebellar cysts common, may represent
unilocular cyst dilated perivascular spaces)
Enlarged Perivascular Spaces Encephalomalacia
I
Coronal T2WI MR shows cluster of variable-sized
CSF-like cysts in lefl parieral subcortical white matter
Axial TlWI MR in a patient with old left internal artery
occlusion shows multicystic encephalomalacia. FlAIR.
5
m. Lesions did not enhance. Follow-up scan 5 years T2-weighted scans showed extensive hyperinlensity in
later showed no change. residual parenchyma secondary to gliosis, spongiosis.
23
ro
~ CSF-L1KE PARENCHYMAL LESION(S)
Q)
c
Q)
19
ro
E
>-
£:
U
C (Left) Coronal T7WI MR in
~
Q)
an elderly patient with
ro
0.. bilateral chronic subdural
c hematomas ~ shows
ro
~ multiple lacunar infarcts ~
CD in while mailer, basal
c ganglia. (Right) Axial T7 C+
ro
~ MR shows several
CD nonenhancing CSF-like cysts
"'C ~ of variable sizes in a
c patient with NCe. Several
ro
may be cisternal,
invaginating into brain.
(Courtesy E. Bravo, MO).

fluid replacing a portion of
the anteromedia"eft
temporal lobe =. The cystic
space communicates with
the lateral ventricle ~ and
the pial surface of the brain
SJ. (Right) Axial FLAIR MR
shows a classic
porencephalic cyst =
suppresses completely on
that
FLAIR. Some gliosis is

present, seen here as a faint
area of increased signal
intensity SJ.

(Left) Axial T7 WI MR in a
patient with long-standing
MS shows multiple
hypointense foci that are
almost (but not quite)
CSF-like. Note the faint
hyperintense rims ~ that
surround plaques. (Right)
Axial TlWI MR in the same
patient shows that some
lesions are CST intensity SJ.
Several others are "bright"
= but clearly do not
resemble the other lesions
SJ or CSF in the lateral
ventricles.
I
5
24
CSF-L1KE PARENCHYMAL LESION(S) en
,...
c:
III
::J
a.
ro
.,
III
(Lelt) Axial T2WI MR shows ::J
both hippocampi =-
multiple CSF-like cysts in
just
medial to temporal horns of
OJ
.,
OJ
::J
-U
lateral ventricles. This was an
incidental finding on MR .
.,
OJ
(1)
(Right) Axial T2WI MR ::J

()
shows an array of several ::r
'<
tiny round and ovoid 3
CSr-like cysts in both OJ
hippocampi just medial Gl
(1)
LO temporal horns of lateral
::J
ventricles. FLAIR scan (not .,
(1)
shown) demonstrated that OJ
the cysts suppressed

completely.
Connatal Cysts Con natal Cysts

(Left) Coronal ultrasound in
a 7 day old premature infant
shows a CSF-like intra- or
periventricular cyst I:] with
a tiny strand of tissue 811 that
connects the walls of
anterior horn. (Right) SagiLtal
T2WI MR in same infant
shows that the cyst ~ is
definitely CSF-like.
Con natal Cysts

(Left) Axial T7 WI MR in an
asymptomatic patient shows
a CSF-like cyst ~ adjacent
to, but separated from, left
frontal horn. A smaller cyst
present posteriorly
(Right) Axial T2WI MR in
same patient shows cysts are
surrounded by mild
hyperintensity 811. Whether
these are
connalal/germinolytic cysts
persisting into adulthood or
neuroglial cyst is uncertain.
Regardless of etiology, such
asymptomatic cysts are
benign and typically
nonprogressive. I
5
25
CIl
~ CSF-liKE PARENCHYMAL LESION(S)
Q)
C
Q)
(9
CIl
E
>.
.r: Neuroglial Cyst
=
u
c (Left) Axial flAIR MR shows
Q)
~ a large cystic mass that
CIl
0.. suppresses completely but
c neither enhanced nor
CIl
~ restricted. At surgery cyst
CD wall was composed of
c benign glial cells. (Right)
CIl
~ Sagiual T2WI MR shows a
CD variant case of neuroglial
"'C cyst that appears to arise
C
CIl from the tectum, which
appears stretched ~ around
the cyst.
Parasites, Miscellaneous
(Left) Axial T2WI MR in
patient with HIV/AIOS
shows several hyperintense
cystic areas, representing
dilated perivascular spaces
~J from cryptococcosis.
fungi and gelatinous material
collect within the spaces.
There is typically liu/e to no
unilocular cyst =
in the
right cerebral hemisphere
with no surrounding edema
or enhancement, typical of
echinococcus (hydatid
disease).
Mucopolysaccharidoses
multiple enlarged
perivascular spaces in this
young child with MPS 1H
and minimal neurological
symptoms. Note severe
perilrjgonal, callosal
involvement. (Right) Axial
FlAIR MR shows] findings
typical of
mucopolysaccharidosis:
CSF-like dilated perivascular
spaces filled with
mucopolysaccharides ffi
hyperintense while maller,
and global atrophy.
I
5
26
CSF-L1KE PARENCHYMAllESION(S) CJl
"
c::
III
::::l
Co
...
to
III
(Left) Axial T2WI MR in an

::::l
inFant with congenital CMV ...ro
to
shows hyperintense
germinolytic cysts ~ and ::::l
-U
extensive perisylvian cortical
dysplasia ~. Unexplained
...
ro
CD
periventricular T2 ::::l
()
hyperintensity ::r
perivenlricular cysts, and
'<
3
neuronal migration and ro
organization abnormalities G>
should suggest congenital CD
::::l
CMV inFection. (Right) Axial CD
T2WI MR in another inFant Q]
with congenital CMV
inFection shows multiple
perivenlricular germinolytic
cysts ffi
(Left) Coronal fLAIR MR in a

patient with inFantile ReFsum
disease shows bilateral
perivenlricular germinolytic
cysts a.."
mimicking
Zellweger syndrome. (Right)
Axial T2WI MR in an inFant
with Zellweger syndrome
shows germinolytic cysts at
the caudothalamic groove
The hyperintense white
maller is indicative of
demyelination. Also note the
perisylvian polymicrogyria
Ii8
Miscellaneous Congenital Malformations Miscellaneous Congenital Malformations

(Left) Axial T2WI MR in a
child with congenital
muscular dystrophy shows
multiple small cystic lesions
in the dysplastic cerebellum
=. The pons is hypoplastic
with dorsal cleFting ~
Hypomyelination of the
temporal lobes is present 81.
(Right) Coronal FLAIR MR in
an 78 month old inFant with
van der Knaap
leukoencephalopathy shows
cystic changes in both
temporal lobes
characteristic
=.
of this
condition.
I
5
27
['(l CYST WITH NODULE
Q)
c
Q)
(9 o Imaging appearance varies with stage;
increased enhancement & edema when
Common organism dies (inflammatory host
• Neurocysticercosis response)
• Pilocytic Astrocytoma o Location: Convexity subarachnoid space>
• Ganglioglioma > cisterns> parenchyma> ventricles
• Hemangioblastoma • Pilocytic Astrocytoma
Less Common o Cerebellar cystic mass with mural nodule
• Metastases, Parenchymal in a child; rarely supratentorial
• Glioblastoma Multiforme o Tl C+: Nodule shows intense but
• Pleomorphic Xanthoastrocytoma heterogeneous enhancement
• Abscess • Ganglioglioma
• Opportunistic Infection, AIDS, o Cortically based, slow-growing enhancing
Toxoplasmosis mass in older child or young adult
• Parasites, Miscellaneous o Cyst with nodule most common, may be
• DNET solid
o Most common tumor to cause temporal
Rare but Important lobe epilepsy
• Desmoplastic Infantile Ganglioglioma • Hemangioblastoma
• Schwannoma, Intraparenchymal o Parenchymal posterior fossa cyst with
• Arteriovenous Malformation (AVM) nodule mass in an adult
o Tl C+: Nodule abuts pial surface & shows
ESSENTIAL INFORMATION intense, homogeneous enhancement
o Multiple in von Hippel-Lindau syndrome
Key Differential Diagnosis Issues (VHL) (25-40% of hemangioblastomas)
• Cystic lesions with solid nodular
components can be divided into 2 categories Helpful Clues for Less Common Diagnoses
o Lesions that typically demonstrate cyst • Metastases, Parenchymal
with nodule morphology o Discrete, gray-white interface mass(es) with
• Neurocysticercosis (NCC), pilocytic adjacent vasogenic edema
astrocytoma, ganglioglioma, o Multiplicity, history of primary
hemangioblastoma, pleomorphic malignancy, helpful if present
xanthoastrocytoma (PXA), desmoplastic o Solitary metastasis may mimic GEM
infantile ganglioglioma (DIG), • Glioblastoma Multiforme
intraparenchymal schwannoma o Malignant white matter mass with central
o Lesions that may demonstrate cyst with necrosis
nodule morphology o Predilection to spread across midline along
• Metastases, glioblastoma multiforme corpus callosum; "butterfly glioma"
(GEM), abscess, toxoplasmosis, parasites, o Tl C+: Thick, irregular, nodular enhancing
DNET, thrombosed AVM margins
• Although metastases, abscesses, & GEMs do o T2/FLAIR: Surrounding hyperintensity &
not classically present as "cysts with mass effect reflect edema + infiltrative
nodules", they are included because of their tumor
overall prevalence • Pleomorphic Xanthoastrocytoma
o Statistically, the atypical form of these o Cortically based cyst + nodule ±
common diseases may be more likely than involvement of adjacent meninges
some of the other "classic" cyst with o Tl C+
nodule lesions • Enhancing nodule
• Look for thickening, enhancement of
Helpful Clues for Common Diagnoses adjacent meninges
I • Neurocysticercosis
o Cyst with "dot" inside representing scolex
• 70% have "dural tail"
o Temporal lobe predominance; young adult
5
28
CYST WITH NODULE C/I
c:
""
Dl
• Abscess • Schwan noma, Intraparenchymal ::l
Q.
o T2 Hypointense rim with surrounding o Only 1-2% of schwannomas are lJl
...•
edema classic parenchymal Dl
::l
o Tl C+: Enhancing capsule thinnest at o Cyst with strongly enhancing nodule
lJl
...•
ventricular side • Arteriovenous Malformation (AVM) Q)
o DWI: Cystic component bright (diffusion o When hemorrhagic with partial or ::l
-0
restriction) complete thrombosis, may present as cyst ...•
Q)
• Opportunistic Infection, AIDS, with nodule <1l

::l
()
Toxoplasmosis o Blood breakdown products of various ages; :T
'<
o Toxoplasmosis: Enhancing central nodules fluid-fluid levels 3
Q)
with peripheral rim = "target" lesions Alternative Differential Approaches G)

o Location: Basal ganglia> hemispheres <1l
• By location ::l
o Clinical: Immunocompromised patient ...•
<1l
o Posterior fossa: Pilocytic astrocytoma, Q)
• Parasites, Miscellaneous hemangioblastoma, metastasis

o Multiple enhancing lesions typical o Temporal lobe: Ganglioglioma,
o May mimic brain tumor
pleomorphic xanthoastrocytoma, DNET
o Travel history critical
o Gray-white junction: Metastases, abscess
• DNET o Hemispheric: NCC, Metastases, GBM,
o Bubbly, wedge-shaped, cortically based infections, DIG, AVM
mass "points" toward lateral ventricle • Patient age
o T2: Very hyperintense; nodular, septate; o Child & young adult: Pilocytic
no surrounding edema astrocytoma, ganglioglioma, PXA, DNET
o Tl C+: No to minimal enhancement, may o Adult: Hemangioblastoma, GBM,
be nodular metastases
o Temporal lobe predominance
o Any age: Neurocysticercosis, abscess, other
Helpful Clues for Rare Diagnoses infections
• Desmoplastic Infantile Gangiiogiioma • Multiple lesions
o Supratentorial cystic/nodular mass with o Metastases (50-55%), NCC (50-70%),
dominance of the cyst hemangioblastoma (VHL), abscesses (septic
o Cortically based nodule with intense emboli), toxoplasmosis, parasites
enhancement & dural tail
o May be massive
o Peak age 3-6 months
Neurocysticercosis
I
Axial T1WI MR shows a frontal ~ & left laleral
ventricular BI "cyst with dot". The "dot", or scolex,
Axial Tl C+ MR shows
intense, heterogeneously
a cystic mass ~
enhancing
with an
mural noc/ule HI in
5
may be TI hyperintense m. Edema &. enhancement the posterior fossa of a child. Note associated temporal
vary with stage & host response. horn dilatation related to U1etumor.
29
ro
~ CYST WITH NODULE
(l)
c
(l)
C)
ro
E
>-
£
()
Hemangioblastoma
C (Left) Coronal T7 C+ MR
~
(l)
shows a circumscribed cystic
ro
CL and solid mass in the
c tempora/lobe with intense
ro
~ enhancement of the solid
III mural nodule !:l. Note
C cortical location and lack of
1'0
~ significant mass effect and
III edema. Gangliogliomas
"0 commonly cause temporal
C
1'0 lobe epilepsy. (Right) 5agi((al
T7 C+ MR shows a cystic
mass ~ with an intensely
and homogeneously
enhancing mural nodule a
in the posterior fossa of an
adult. The nodule typically
abuts the pial surface.
shows a cystic mass with a
large enhancing nodule in
the cerebellar hemisphere
with rim enhancement 11].
This is an atypical
appearance for a metastasis.
Primary malignancy history &
presence of other lesions are
helpful for diagnosis. (RighI)
Axial CECT shows a
heterogeneous mass = with
irregular peripheral
enhancement containing a
nodular component ~.
Aggressive features help
diagnose this malignant
tumor.
Pleomorphic Xanthoastrocytoma Abscess

shows a cortically based left
temporal lobe cystic mass
liB with an enhancing
nodule ~ in a young adult.
Enhancement & thickening
of the adjacent dura !:l help
diagnose PXA & differentiate
from a ganglioglioma. (Right)
Axial T7 C+ F5 MR
demonstrates a
ring-enhancing lesion with a
small enhancing mural
nodule!:l. OWl MR (not
shown) showed
characteristic diffusion
I restriction in the central

nonenhancing component.
5
30
CYST WITH NODULE en
c
""
ell
::l
a.
Opportunistic Infection, AIDS, lP
..,
Toxoplasmosis ell
(Left) COlOnal Tl C+ MR ::l

shows basal ganglia, OJ
..,
lhalamic, & parenchymal
ring-enhancing lesions
an immunocompromised
in -= tlJ
::J
-U
tlJ
patient. Note f1target" CD
appearance with central ::l
()
nodule in the 'ight ::T
tempo,allobe lesion. (Right)
'<
3
Axial CECT demonstrates a tlJ
ring-enhancing lesion with G)
an associated nodule ~ & CD
::l
surrounding vasogenic CD
edema. Multiple punctate ill
lesions = are also apparent
in this patient with amebic
encephalitis.
(Left) Axial Tl C+ MR shows

a left tempo,allobe mass
with a small focus of mild
enhancement I:] within the
bubbly, cystic mass. Faint
nodular enhancement can
be seen in 20% of ONETs.
Lesions a,e typically T2
hyperintense & may erode
the adjacent calvarium, as in
this case. (Right) Coronal Tl
C+ MR shows a large cyst
with cortically based,
intensely enhancing mural
nodule = in an infant. Note
enhancement
DIG.
=
adjacent dural thickening &
typical of
Schwannoma, Intraparenchymal Arteriovenous Malformation (AVM)

fLeft} Axial T1 C+ MR shows
a cystic parenchymal mass
= with intensely enhancing
mural nodule SI in the right
occipital lobe. Although
ganglioglioma was the
pre-operative diagnosis,
schwannoma was found on
pathology. (RigI1l) Axial
CECT shows a mixed density
cystic and solid lesion with
rim enhancement =. There
is a lIuid-fluid level within
one of the cysts Ell
representing hemorrhage in
this partially thlOmbosed
I
AVM.
5
31
FAT-LIKElESION(S), GENERAL
DIFFERENTIAL DIAGNOSIS • Usually Tl hypointense

ro • Lipoma
E
>-
..c::
Common o Subpial mass (-SO to 100 HU, short Tl)
t.l
c • Choroid Plexus Xanthogranuloma o 50% interhemispheric ± agenesis CC
~
Ql
• Lipoma • Craniopharyngioma
ro
0..
c
• Craniopharyngioma o Cyst contains high cholesterol fluid
ro
~ • Teratoma o Variable signal on MR
co • Dermoid Cyst • Teratoma
c
'iij • Ossified Falx o Midline mass with Ca++, adipose tissue
~
co less Common • Dermoid Cyst
't:l
c • Asymmetric Marrow, Petrous Apex o ± Cisternal fat droplets
III
• Cholesterol Granuloma, Petrous Apex o NECT: 20-40 HU ± Ca++
o MR: Heterogeneously hyperintense
Rare but Important • Ossified Falx
• "White" Epidermoid Cyst o Osseous metaplasia, fatty marrow
• Meningioma, Lipomatous
• Encephalocraniocutaneous Lipomatosis Helpful Clues for less Common Diagnoses
• Retained Pantopaque • Asymmetric Marrow, Petrous Apex
o Asymmetric aeration
o Fatty marrow, no expansile change
ESSENTIAL INFORMATION • Cholesterol Granuloma, Petrous Apex
Key Differential Diagnosis Issues o Expansile PA mass
• Fat vs. cholesterol-containing lesion o Tl/T2 hyperintense
o Fat (lipoma, dermoid, teratoma) Helpful Clues for Rare Diagnoses

o Cholesterol (craniopharyngioma, • "White" Epidermoid Cyst
xanthogranuloma, cholesterol granuloma) o t Protein - short Tl/T2
• Fat vs. mimic (lesions with short Tl) • Meningioma, Lipomatous
Helpful Clues for Common Diagnoses o Rare, inhomogeneously hyperintense
• Choroid Plexus Xanthogranuloma • Encephalocraniocutaneous Lipomatosis
o Common (70% of autopsies) o Scalp lipoma, hemispheric atrophy,
o Incidental MR finding variable intracraniaillpomas
o Older patient with bilateral choroid plexus • Retained Pantopaque
cysts o Tl hyperintense; T2 iso-/hypointense
• Hypodense, Ca++ on NECT o Spine> > > brain
I
5 Axial N[CT shows bilateral hypodense, calcified
choroid plexus cysts ~ in an elderly paUent. Cysts are
Sagittal T1WI MR shows a small curvilinear
interhemispheric lipoma =:I above the corpus callosum.
xanthogranulomas and look more like CSFthan fat.
32
FAT-LIKE lESION(S), GENERAL en
,.-
c:
IU
::::l
Co
...IU
III
Teratoma
(Left) T1WI MR shows
::::l
...OJ
craniopharyngioma =-
classic adamantinomatous
with
striking T 7 shortening caused
OJ
::::l
-U
by thick, brownish
("crankcase") fluid
...
OJ
CD
containing high cholesterol. ::::l
()
(Right) Sagillal T1 WI MR ::r
'<
fat=- =-
demonstrates hyperintense
hypointense focal
calcification and soft
3
OJ
G)
tissue ~ components in a CD
::::l
suprasellar teratoma. CD
Q]
Dermoid Cyst Ossified Falx

(Left) Sagillal Tf WI MR
demonstrates a lesion of
mixed signal in the
quadrigeminal cistern Q in
keeping with a dermoid cyst.
There is evidence of rupture
with lipid droplets noted
throughout the subarachnoid
space PJ:?]. A fat-fluid level
was present in the lateral
ventricle (not shown).
(Right) Sagittal T1 WI MR
shows hyperintense foci in
the midline caused by fatty
marrow in the osseous
metaplasia i:l2.
Asymmetric Marrow, Petrous Apex Cholesterol Granuloma, Petrous Apex

V
increased signal within leFt
petrous apex = without
expansion. Compare to the
normal aerated right petrous
apex 81. This is a "leave me
alone" pseudolesionl (Right)
Axial Tf WI FS MR shows
expansile, hyperintense
lesion in pelrous apex
Lesion did not saturate,
=.
which lipoma or fat in
asymmetric, unaerated
petrous apex would have
done.
I
5
33
~
<1l SOLITARY PARENCHYMAL CALCIFICATION
Ql
C
Ql
<.9
<1l
E • Neurocysticercosis
>- Common
-'u= o Nodular calcified (healed) stage
C • Neurocysticercosis
~
Ql o Multiple ("starry sky") > solitary lesions
<1l • Tuberculosis
CL o Most NCC cysts are actually cisternal
.!: (within depths of superficial sulci) > brain
~
<1l • Oligodendroglioma
[]) parenchyma, ventricles
• Ganglioglioma
c
• Diffuse Astrocytoma, Low Grade • Tuberculosis
~ o Healed gran uloma
co'" • Pilocytic Astrocytoma
• Can be single or multiple
-0
c Less Common • Many fewer lesions than CC
'" • Arteriovenous Malformation • Occasionally solitary tuberculoma can be
• Ependymoma mass-like, mimic neoplasm
• Parasites, Miscellaneous • Cavernous Malformation
Rare but Important o Solitary> multiple
• Physiologic Calcification, Brain o Ca++ can be dot-like, clumped, or scattered
• "Brain Rock" within single lesion

o Do MR with T2* scan (GRE, SWI) to look
• Calcified Embolus
• Saccular Aneurysm for hemorrhage, multiplicity
• Metastasis, Parenchymal • Oligodendroglioma
• TORCH Infection o Cortical/subcortical mass
o Slow-growing; may erode adjacent skull
• DNET
• Meningioangiomatosis o 70-90% calcify (nodular, clumped)
o Adult> child
• Ganglioglioma
ESSENTIAL INFORMATION o Slow-growing, cortically based neoplasm
Key Differential Diagnosis Issues o Child/young adult with epilepsy
• Solitary brain calcification includes o Common: Ca++ nodule, ± cysts
o True parenchymal calcification o May erode/remodel adjacent skull

o Some lesions that may look like they are in • Diffuse Astrocytoma, Low Grade
brain itself but are not actually in o Hemispheres> posterior fossa
parenchyma o Solid> > cystic mass
• Lesion in deep sulcus (neurocysticercus o 10-20% calcify
cyst) o Infiltrates brain
• Lesion in vessel (calcified embolus, o Intrinsic tendency to undergo malignant
saccular aneurysm) degeneration

• Key question: Is Ca++ solitary focus or are • Pilocytic Astrocytoma
there multiple calcified foci in solitary o Cerebellum> optic nerve/chiasm, 3rd
mass-like lesion? ventricle> pons
• Solitary "dot-like" or globular Ca++ o Cyst with nodule (cerebellum)
o Typically infectious (neurocysticercosis, o Solid mass (optic chiasm/hypothalamus,
TB, occasionally other rare parasites) pons)

o Less common o Ca++, hemorrhage uncommon (unless
• Physiologic (habenular commissure, pilomyxoid variant)
unilateral basal ganglia) Helpful Clues for Less Common Diagnoses
• Vascular (AVM, cavernous malformation, • Arteriovenous Malformation
Ca++ embolus) o Little/no mass effect unless hemorrhage
o Rare = brain "rock" o Look for enlarged feeding arteries, draining
• Solitary mass-like lesion with clustered Ca++ veins
I o Neoplasm (many) o Occasional Ca++ in nidus, draining veins
o Cavernous malformation (phlebolith)
5
34
SOLITARY PARENCHYMAL CALCIFICATION C/)
~
r::
ll>
• Ependymoma • Metastasis, Parenchymal j
C-
o 3rd most common posterior fossa o Untreated metastases rarely calcify
..,ll>
OJ
neoplasm in children (after o Breast, mucinous carcinoma, osteosarcoma
j
medulloblastoma, pilocytic astrocytoma) metastasis may calcify spontaneously
OJ
02/3 infra tentorial (4th ventricle) • TORCH Infection OJ
o 1/3 supratentorial (extra-ventricular, o Multiple> > solitary :J
-U
hemispheric WM) o CMV most common OJ
• Large, extensively calcified cystic/solid o Cortical Cil

:J
(")
hemispheric mass in young child? Think • DNET ::r
'<
ependymoma first! o Almost all patients < 20 years 3
OJ
o 50% of all ependymomas calcify o Chronic epilepsy
Gl
o Cysts, hemorrhage also common o Well-delineated, "bubbly" appearing <1>
:J
• Parasites, Miscellaneous cortical mass ..,
<1>
OJ
o Except NCC, parenchymal Ca++ rare • May remodel overlying skull
o Any healed parasitic infection can calcify • Gross Ca++ uncommon, hemorrhage rare
Helpful Clues for Rare Diagnoses • < 20% enhance
• Physiologic Calcification, Brain • May have adjacent cortical dysplasia
o True solitary, unilateral normal
• Meningioangiomatosis
o Child/young adult with seizures
parenchymal Ca++ unusual
o Hamartomatous cortical/leptomeningeal
• Basal ganglia usually bilateral,
malformation
occasionally unilateral
o Meningovascular proliferation along
• Habenular commissure may Ca++
perivascular spaces (PVSs)
• "Brain Rock"
o 50% associated with neurofibromatosis
o Dense globular parenchymal Ca++
o Cortical mass with Ca++ (often gyriform)
o No infection, neoplasm, degeneration
o T2 hypointense
• Calcified Embolus
o Plaque-like pial, linear enhancement along
o In artery within sulcus, not brain
parenchyma PVSs
o Huge, bizarre-appearing, extensively
calcified mass in adult? Think
partial/completely thrombosed giant
saccular aneurysm
Neurocysticercosis Neurocysticercosis
I
Axial N[CT shows solitary calcified NCC cyst
probably in depths of sulcus. This was an incidental
=- Axial NECT shows small right medial frontal calcification
= in a patient with known neurocysticercosis.
5
finding in an immigrant from endemic area who has Although lesion looks intraparenchymal, it is most likely
systemic Nee. No other brain lesions were identified. within a deep sulcus.
35
<1l
~ SOLITARY PARENCHYMAL CALCIFICATION
Q)
c
Q)
c.?
<1l
E>,
J:: Tuberculosis Tuberculosis
U
C (Left) Axial NECT in patient
Q)
~ with known TB shows
<1l
0.. parenchymal calcification 811
c with surrounding
<1l
~ hypodensity, characteristic of
a:J healed caseating granuloma.
c (Right) Axial NEeT shows
~
l'Cl large bifrontal densely
lD calciFied lesion =:2
withoul
"'C mass eFFect.Note
c encephalomalacia HJ in
l'Cl
adjacent parenchyma.
Solitary luberculoma was
Found at surgery.
Cavernous Malformation
(LeFt) Axial NEeT in child
w/Family history of multiple
cavernous malformation
syndrome shows solitary,
densely calcified right
posterior frontal/anterior
parietal lobe lesion =:2. One
month later lesion
hemorrhaged. Cavernous
malformation was found at
surgery. (Right) Axial NECT
shows large solitary
hyperdense mass =:2
that
contains multi(ocal punctate
calcifications E:I. "Popcorn"
appearance within
hyperdense mass is typical
for cavernous malformation.
(LeFt) Axial NECT shows a
partially calcified leFtparietal
mass ::3> with edema. MR
disclosed cavernous
malFormation, but NECT
findings are indistinguishable
From oligodendroglioma.
cortically based leFt Frontal
hypodense mass with
calcification =. Calcification
is seen in the vast majority of
oligodendrogliomas, typically
nodular or clumped.
I
5
36
SOLITARY PARENCHYMAL CALCIFICATION CIl
'"
c:
Ganglioglioma
(Lefl) Axial CECT shows
cystic left parietal mass
with calcification m in
=
enhancing mural nodule.
Ganglioglioma was found at
surgery. (RighI) Axial NEeT
in child with refractory
temporal lobe epilepsy
shows calcified temporal
lobe lesion =:1 no significant
mass effect. Ganglioglioma Gl
was found at surgery. CD
::>
Solitary calcification without CD
associated cyst is less Gl
common appearance.

solitary right thalamic mass
with central clump of
calcification =. Note severe
obstructive hydrocephalus
with transependymal CSF
migration 81. WHO grade /I
fibrillary astrocytoma was
found at surgery. (RighI)
Axial NEeT in a child with
headache shows mass with
rim =:1 globular 81 Ca++.
Pilomyxoid variant of
pilocytic astrocytoma was
found at surgery.
(Lefl) Axial NECT in a patient

with first seizure shows
slightly hyperdense right
medial temporal lobe mass
= with focus of globular
calcification 81. CECT scans
(not shown) demonstrated
that the mass consisted of
enhancing serpentine vessels
characteristic of an AVM
nidus. (RighI) Axial NECT in
a young child shows a large,
right hemisphere, multicystic
mass with marked
surrounding edema and
dense clump-like
calcification. Ependymoma
was found at surgery. I
5
37
ro
~ SOLITARY PARENCHYMAL CALCIFICATION
<lJ
c
<lJ
CJ
ro
E
>-
£ Parasites, Miscellaneous
U
C (Left) Axial NECT shows a
~
<lJ
large left frontal mass with
ro
0.. extensive rim = and
c globular calcification EJ.
ro
~ (Right) Axial NECT shows a
co mixed hypo- & hyperdense
C right posterior frontal mass
~III with early clump-like

al calcification =.
Ameboma
"'0 was found at surgery.
C
III
Physiologic Calcification, Brain "Brain Rock"

(Lefl) Axial NEeT in a 67
year old woman who
presented with dizziness
shows a solitary "speck" of
physiologic calcification in
the left basal ganglia EJ.
densely calcified lesion
without mass effect Lesion
=
did not enhance on MR.

with acute right middle
cerebral artery territory
infarct = shows
calcification EJ that is
actually in M 1 MCA
segment. Note distal
thrombus in vessel =.
solitary calcification in right
posterior frontal region =.
Lesion appears to be at
gray-white junction but is
actually in a small cortical
artery within depths of deep
sulcus EJ.
I
5
38
SOLITARY PARENCHYMAL CALCIFICATION en
"
c:
III
::::I
Co
.,
lJl
Metastasis, Parenchymal III
Saccular Aneurysm
(Left) Axial NECT shows a ::::I
la'ge, mostly isodense mass lJl
.,
with striking rim calcification Q)
8l which proved to be a ::::I

-0
giani, chronically Q)
.,
thrombosed aneurysm . C1>
(Right) Axial NECT in a ::J
()
patient with prior brain ::r
melaslases from clear cell
'<
3
Q)
carcinoma, primary site
unknown. Six months after G)
radialion therapy one of the C1>
::J
metastases has calcified 1m. C1>
OJ
TORCH Infection DNET

calcificalion =-
subtle lefl perivenlricular
Note broad,
flal, fronloparielal gyri,
suggesling a corlical
neuronal migrational
abnormalily ~ Note
moderate ventricular
dilatalion 1!:lI. (Right) Axial
NECT shows a hypodense,
right posterior fronlallobe,
corlically based mass with
adjacenl remodeling of lhe
calvarium and a dOL of faint
calcificalion ~ The
diagnosis was ONET.
(Left) Axial NECT in a 75

year old with chronic
epilepsy shows dense
gyriform calcificalion
enlargement of adjacent
=-
subarachnoid space m.
Meningioangiomalosis found
at surgery. (Right) Axial
NECT in young adult wilh
chronic epilepsy shows
superficial cortical
calcificalion =.
MR
demonstrated enhancing
mass in adjacent pia that
infiltrated deep into brain
along perivascular spaces.
Meningioangiomatosis
identified at surgery.
I
5
39
[1:1 MUlTIPLE PARENCHYMAL CALCIFICATIONS
OJ
C
OJ
19 • Tuberous sclerosis complex
E Helpful Clues for Common Diagnoses
>-
.c
Common
u
c • Normal • Normal
~
OJ
• Neurocysticercosis o Microscopic brain Ca++
ro
0..
• Cavernous Malformation (Multiple) ("calcospherocytes")
c • Ca++, iron deposits in microvessels
ro
~
co Less Common • Common in elderly, especially basal
C • Tuberculosis ganglia (BG)
ltl
~ • Tuberous Sclerosis Complex • Except for BG, macroscopic brain
l%l
"t:l
• Sturge- Weber Syndrome parenchymal calcifications usually
c • Metastases, Parenchymal
ltl abnormal
Rare but Important o Basal ganglia
• Remote Brain Injury • Ca++ common in adults
• Opportunistic Infection, AIDS • Physiologic> > metabolic derangement
• TORCH Infections (e.g., thyroid/parathyroid disorders)
• Lymphocytic Choriomeningitis • Uni-/bilateral
• Metabolic (Inherited or Acquired) • Symmetric or asymmetric
o Fahr Disease • Neurocysticercosis
o MELAS o Nodular calcified stage of
o Hypothyroidism neurocysticercosis (NCe)
o Hyperparathyroidism o Multiple, small ("starry sky" pattern) >
o Hypoparathyroidism solitary, large Ca++
o Pseudohypoparathyroidism o Lesions appear to be parenchymal but
oX-linked Adrenoleukodystrophy most actually in depths of sulci!
• Pseudo-TORCH Syndromes • Cavernous Malformation (Multiple)
• Radiation and Chemotherapy o Multiple (familial) CM syndrome
o 10-30% of cases
o Variably-sized hyperdense/Ca++ lesions
ESSENTIAL INFORMATION • Can be small/almost invisible,
Key Differential Diagnosis Issues occasionally very large
• Discrete, multifocal/scattered Ca++ • Homogeneous or "salt and pepper"
• Hyperdensities on NECT, variably o T2* (SWI > GRE) best to detect
"blooming" hypointensities on T2*/GRE Helpful Clues for Less Common Diagnoses
• Location helpful in differential diagnosis • Tuberculosis
o Basal ganglia (physiologic in adults) o Ca++ uncommon ('" 20%)
• Abnormal Ca++ can be congenital, • Represents healed granuloma
acquired • Solitary> multiple small Ca++ more
• End result of toxic/metabolic (e.g., common
thyroid/parathyroid disorder), • Ca++ often somewhat larger (can be
inflammatory/infectious etiologies (e.g., giant) compared to NCC
TORCH) • Few scattered, larger Ca++ (TB) vs.
o Cortex: Neurocysticercosis (sulci), TB, numerous multiple small (NCe)
Sturge-Weber o "Target sign" = central Ca++ surrounded by
o Gray-white junction enhancing rim
• Fahr disease • Tuberous Sclerosis Complex
• Tuberous sclerosis complex o 98% have Ca++ subependymal nodules
• Metastases (treated> > untreated) • Most along caudothalamic groove
• Radiation/chemotherapy • 30-80% enhance
o Periventricular
I • Fahr disease
• Enhancing lesion near foramen of Monro
needs follow-up (growth indicates
• TORCH, pseudo-TORCH subependymal giant cell astrocytoma)
5
40
MULTIPLE PARENCHYMAL CALCIFICATIONS CIl
"
c:
Ql
o Tubers in cortex, subcortical white matter • Lymphocytic Choriomeningitis :J
C-
• Up to 50% show some Ca++ by age 10 o Rodent-borne OJ
.....
• Enhancement less common (10-15%), o Causes necrotizing ependymitis, Ql
:J
does not presage malignancy aqueductal obstruction
OJ
.....
• Sturge-Weber Syndrome o Can be indistinguishable from CMV III
o Gyral (cortex, subcortical white matter) • Fahr Disease :J
lJ
Ca++ (not in pial angioma!) o Cerebrovascular ferrocalcinosis III
o Extensive bilateral BG Ca++ CO
o Atrophy/prominent subarachnoid spaces :J
()
o Look for enlarged, enhancing ipsilateral o Can involve dentate nuclei, cerebral white ::T
'<
choroid plexus, prominent medullary matter 3
III
veins • MELAS Gl
o 20% bilateral o Stroke-like cortical, basal ganglionic C1>
:J
C1>
• Metastases, Parenchymal lacunar infarcts .....
III
o Typically post-treatment (e.g., XRT for o Basal ganglia Ca++
breast metastases) • Hypothyroidism
o Untreated metastases rarely Ca++ o May cause BG, cerebellar, subcortical white
o Exceptions matter Ca++
• Mucinous adenocarcinoma • Hyperparathyroidism
• Malignant bone neoplasms o Rare; BG Ca++
• Breast (rare) • X-Linked Adrenoleukodystrophy
o Chronic lesions may Ca++
• Pseudo-TORCH Syndromes
• Remote Brain Injury
o Types
o Rare cause of Ca++
• Baraister-Reardon
o Can occur with trauma, infarction
• Aicardi-Goutieres
o BG, cerebellar> periventricular Ca++
o Most acute, not chronic; Ca++ rare
o Co-infection with TB may cause Ca++ if
• Radiation and Chemotherapy
o Mineralizing microangiopathy
patient survives
o BG, gray-white junction Ca++
• TORCH Infections
o CMV most common intrauterine infection
in developed countries
o Others rare (e.g., toxoplasmosis, rubella,
herpes)
Neurocysticercosis
I
Axial NEeT shows multiple calcifications typical for
healed cysticercosis. While most lesions look as if they
Axial NEeT scans in same patient at low ventricular
fleft), high left frontal (right) regions show healed,
5
are in brain parenchyma, many are actually within calcified TB granulomata 1::1.
cerebral sulci.
41
OJ
~ MUlTIPLE PARENCHYMAL CAlCIFICATIONS
OJ
c
OJ
(9
Tuberous Sclerosis Complex Sturge-Weber Syndrome

multiple parenchyma/l:lll
and subependymal
calcifications 811. (RighI)
Axial NECT shows variant
case of Swrge-Weber
syndrome with focal sulcal
enlargement ffi linear
calcifications in underlying
thinned cortex SlI. Most
patients show much more
extensive atrophy and
calcification.
Metastases, Parenchymal Remote Brain Injury

untreated calcified
metastases = in a patient
with breast carcinoma,
decreased mental status.
Multiple lesions enhanced on
CECT scan, including these
lesions. (RighI) Axial NECT
shows focal right temporal
lobe infarct as a
wedge-shaped area of low
density encephalomalacic,
gliotic brain 1:llI. Associated
dystrophic calcification !J:gI is
very rare. Ipsilateral ventricle
is mildly enlarged related to
volume 1055SlI.
TORCH Infections
extensive perivenlricular.
basal ganglia cerebellar
IaI calcification. The
"primitive" appearance of
sylvian cisterns are due to
bilateral opercular
polymicrogyria ~ (RighI)
Axial NECT shows
periventricular, thalamic
calcifications with
venlriculomegaly.
Lymphocytic
choriomeningilis can mimic
cytomegalovirus.
I
5
42
MUlTIPLE PARENCHYMAL CALCIFICATIONS
III
:J
a.
..,
OJ
Fahr Disease MELAS III
(Left) Axial NECT shows :J

mulliple nearly symmeuic CD
..,
calcifications in basal OJ
ganglia, gray-while malter :J
"U
junclions. (Right) Axial NECT
shows bilaleral basal ganglia
..,
OJ
calcifications =.. bioccipilal

Ctl
::J
()
encephafomalacic areas m ::r
'<
in a child with MELAS, 3
mulliple strokes. OJ
Gl
Ctl
::J
Ctl
ID

diffuse hyperdense
calcifications within basal
ganglia and subcorlical white
maller in a patient with
proven hypothyroidism.
dense laminar calcifications
of lentorial dura
as faint parenchymal
= as well
calcification in basal ganglia

E2.
Pseudo- TORCH Syndromes Radiation and Chemolherapy

brainslem, parenchymal
calCIfications more than
perivenlricular calci(;cations,
suggesling a pseudo-TORCIf
syndrome such as
Aicardi-Coulieres. (Right)
Axial NECT shows striking
symmetrical calcifications in
basal ganglia, gray-white
matter junction in a patient
who had received prior
radialion chemotherapy.
I
5
43
OJ
~ SOLITARY HYPERDENSE PARENCHYMAL lESION
QJ
C
QJ
<.9 • Anterior inferior frontal, temporal lobes
OJ
E most common
>.
.J:::
Common • Multiple> > solitary lesion
()
c • Cerebral Contusion o Evolves over time; 24-48 hours existing
QJ
~ • Hypertensive Intracranial Hemorrhage
OJ lesion may enlarge, become more
0...
c
• Cerebral Amyloid Disease hemorrhagic
OJ
~ • Glioblastoma Multiforme • Hypertensive Intracranial Hemorrhage
co • Metastasis, Parenchymal o Older hypertensive patient
c
• Thrombosis, Dural Sinus o Location important
~
'"
aJ • Thrombosis, Cortical Venous • Deep> superficial lesion
"C
c: less Common • Nearly 2/3 striatocapsular
'" • Cavernous Malformation • Thalamus 15-25%
• Developmental Venous Anomaly o Look for multifocal"microbleeds"
• Arteriovenous Malformation • 1-5%
• Medulloblastoma (PNET-MB) • Best seen on T2* MR
• Ependymoma, Supratentorial • Cerebral Amyloid Disease
• Melanoma o Causes 15-20% of all"spontaneous"
• Ganglioglioma intracranial hemorrhages (ICHs) in

• Lymphoma, Primary CNS normotensive elderly patients
• Germinoma o Classic = lobar hemorrhage (vs. basal
• Anaplastic Oligodendroglioma ganglia in hypertension)
o Look for "microbleeds" (do T2* MR)
Rare but Important • Cortical/subcortical vs. basal ganglia,
• Drug Abuse cerebellum (chronic hypertension)
• Tuberculoma • Glioblastoma Multiforme
• Neurosarcoid o Necrosis, hemorrhage common
• Leukemia • Metastasis, Parenchymal
• Tuberous Selerosis Complex o Can be hemorrhagic or non hemorrhagic
• Meningioangiomatosis o Hypercellular, electron dense
non hemorrhagic metastases
ESSENTIAL INFORMATION • Thrombosis, Dural Sinus
o Multifocal > solitary hemorrhage
Key Differential Diagnosis Issues o Parenchymal elot(s) adjacent to dural sinus
• Hyperdense parenchymal lesions (transverse sinus> superior sagittal sinus)
o t Attenuation compared to normal brain • Thrombosis, Cortical Venous
• Caused by o Multifocal > solitary hemorrhage
o Clotted blood (most common)
o Can occur with or without dural sinus
o Nonhemorrhagic hypercellular (electron occlusion
dense) mass (less common)
o Calcification (excluded here) Helpful Clues for less Common Diagnoses
• History essential • Cavernous Malfornlation
o Age o Variable presentation
o Trauma, hypertension, drug abuse, o Acute hemorrhage

dementia, known extracranial primary • Common cause of spontaneous ICH in
neoplasm children, young adults
o Sudden onset vs. subacute/chronic o Epilepsy
• Hyperdense calcified or noncalcified
Helpful Clues for Common Diagnoses parenchymal mass
• Cerebral Contusion • Developmental Venous Anomaly
o Trauma o Hemorrhage rare unless mixed with
I o Location important
• Cortex, subcortical white matter
5
44
SOLITARY HYPERDENSE PARENCHYMAL LESION CIl
c:
""
o Blood in transcortical draining vein o Densely cellular tumor but may also
slightly hyperdense to brain hemorrhage
• Arteriovenous Malformation o Hyperdense basal ganglia mass in
o Common cause of spontaneous ICH in child/young adult? Think germinoma!
children, young adults • Anaplastic Oligodendroglioma
o Rupture of intranidal aneurysm, o Mixed density common
stenosis/occlusion of draining veins o May Ca++, hemorrhage
• Medulloblastoma (PNET-MB) Helpful Clues for Rare Diagnoses
o Electron dense tumor with high
• Drug Abuse
nuclear:cytoplasm ratio o Striatocapsular hemorrhage in
o Midline hyperdense posterior fossa mass in
young/middle-aged adult? Consider drug Gl
child? Suspect PNET-MB abuse
ctl
:J
o Lateral (cerebellar) mass in older ctl
~
• Tuberculoma OJ
child/young adult? Suspect desmoplastic o Granuloma mildly hyperdense
variant of medulloblastoma o Can mimic intra- or extra-axial neoplasm
• Ependymoma, Supratentorial • Neurosarcoid
o Most ependymomas are intraventricular,
o Multifocal > solitary
but up to 40% are supratentorial, o Extra-axial> parenchymal mass(es)
parenchymal> intraventricular
• Leukemia
o Large hyperdense calcified solid/cystic
o Extra-axial> intra-axial lesion
hemispheric tumor in young child? Think o Hyperdense parenchymal lesion can be
ependymoma! hemorrhagic complication (more
• Melanoma common) or chloroma (less common)
o Metastatic> primary CNS melanotic lesion
• Tuberous Sclerosis Complex
o Melanin or hemorrhage - t density
o Cortical, subcortical tubers can be
• Ganglioglioma hyperdense &/or calcified
o Child/young adult with epilepsy
o Multifocal > solitary
o Most are partially cystic, contain Ca++
o Solitary large, "lobar-type" hyperdense
• Lymphoma, Primary CNS tuber ± Ca++ can mimic neoplasm
o Corpus callosum, basal ganglia
o Hemorrhage rare unless HIV/ AIDS
o Cortical-based, gyriform hyperdensity
• Germinoma o May be densely calcified
o Pineal> infundibulum> basal ganglia o Can mimic neoplasm!
Hypertensive Intracranial Hemorrhage
I
Axial NECT shDws a left frDntal hyperdensity with
surrDunding hypodensity, typical Df corUcal contusion.
Axial NECT demDnstrates the high density mass
surrounding tow density edema E:I in the most
= wid,
5
NDte effaced frDntai sulci from focal mass effect. common location for hypertensive hemorrhage. Note
compression of the right lateral ventricle by the mass.
45
Q)
c
Q)
(9
ctl
E
>-
..c Cerebral Amyloid Disease
=
<.l
c aefOAx~/NECTshows
~
Q)
focal lobar hematoma in
ctl
0.. a 68 yo normotensive, mildly
c demented patient with
~ sudden onset of right-sided
IJJ weakness. T2* MR scan
c: showed multifocal peripheral
l'll
~ ,jblack dots" characteristic of
IJJ amyloid angiopathy. (RighO
"'C Axial NECT shows
c: inhomogeneously
l'll
hyperdense hematoma ~
surrounded by edema =.
MR showed thick, irregular
enhancing rind of tissue.
Surgery disclosed G8M with
intralesional hemorrhage of
different ages.
Metastasis, Parenchymal Metastasis, Parenchymal

(LefO Axial NECT shows
hematoma =
right temporal lobe
in this elderfy
normotensive nondemented
patient wilh decreasing
mental status and right 3rd
nerve palsy. Hemorrhagic
metastasis from unsuspected
colon carcinoma was found
at surgery. (RighO Axial
mass =
NECT shows hyperdense
with speckled
calcifications [?J.
Nonhemorrhagic metastasis
from mucinous
adenocarcinoma was Found
at surgery.
Thrombosis, Dural Sinus Thrombosis, Cortical Venous

(LefO Axial NECT in a
postpartum woman wiLh
sudden headache followed
by seizure shows left
posterior temporal lobe
hemorrhage 1:1 edema.
Transverse sinus is
hyperdense ~. MR showed
leFt transverse sinus
thrombosis. (RighO Axial
NECT shows hyperdense left
posterior parietal mass 9.
Note superior sagittal sinus
~ appears normal.
I lemorrhagic neoplasm was
suspected. Ilemaloma with
adjacent thrombosed cortical
I vein was found at surgery.
5
46
SOLITARY HYPERDENSE PARENCHYMAL LESION en
,...
c:
III
::::l
Co
.,
O::J
Cavernous Malformation Cavernous Malformation III
(Left) Axial NECT shows a ::::l
small, hyperdense left OJ
.,
parietal lesion =.
The OJ
::::l
diagnosis was cavernous
malformation without gross \J
OJ
hemorrhage. (Right) Axial CD
NECT in a young girl with 2 ::::l
()
day history of headache, ::T
visual changes shows mixed
'<
3
density lesion in the right OJ
occipital lobe =.MR Gl

(l)
documented hemorrhage but ::::l
no other lesions. Cavernous .,
(l)
malformation with acute, OJ

subacute, and chronic
hemorrhage was Found at
surgery.
(Leh) Axial NEeT shows a

rounded, well-delineated,
mildly hyperdense lesion
in the left cerebellar
=
hemisphere. CECTshowed
strong enhancement with
"Medusa head" dilated
venous tributaries. (Right)
Axial NECT shows mixed
density parenchymal
hematoma =
in 24 year old
with sudden severe
headache, decreased
consciousness, and right 3rd
nerve palsy. DSA disclosed
arteriovenous malformation
with oullet vein stenosis.
Medulloblastoma (PNET-MB)
(Leh) Axial NECT shows
slightly hyperdense mass in
the 4th ventricle = with
solitary faint calcified focus
BI. Note obstructive
hydrocephalus with dilated
temporal horns~. (Right)
Axial NECT shows
=
heterogeneously hyperdense
partially calcified ~
periventricular mass with
surrounding edema.
Ependymoma adjacent to,
but not within, lateral
ventricle was Found at
surgery.
I
5
47
ro
Q)
c
Q)
t?
ro
E
>-
J:: Melanoma
U
C (Left) Axial NECT in palient
Q)
~ with known metastatic
ro
0.. melanoma shows
c hyperdense left temporal
ro
~
[IJ
lobe lesion =.(Right) Axial
NECT in a 5 year old with
C possible seizure shows a
III
~ hyperdense mass that
al thickens, distorts cortex =.
"0 Lesion showed minimal
c enhancement on MR, and on
III
NECT, it was
indistinguishable from
Taylor·type cortical
dysplasia.
Germinoma
(Left) Axial NECT shows an
infiltrating mass 1:1 centered
on the corpus callosum, that
extends into adjacent deep
periventricular white maller
o( both hemispheres. The
mass is hyperdense
compared to white maller,
minimally hyperdense
compared to cortex. (Right)
Axial NECT shows a
hyperdense periventricular
lesion = in the region o( the
right caudate head/anterior
limb o( the internal capsule.

biFrontal hemorrhagic
"butterfly" lesion involving
corpus callosum =. Imaging
appearance is
indislinguishable (rom
glioblastoma multiforme,
which was the pre-operative
diagnosis. (Right) Axial
NECT shows striatocapsular
hematoma 1:'.1 typical (or
hypertensive intracranial
hemorrhage. This 22 year
old presented to the
emergency department with
blood pressure 260/720
I subsequent to a cocaine
overdose.
5
48
SOLITARY HYPERDENSE PARENCHYMAL lESION en
"
c:
III
:J
a.
...
OJ
III
Tuberculoma Neurosarcoid
:J
mixed hyper-, hypodense ...OJ
OJ
mass =. Tuberculoma was
:J
-U
Axial NECT shows
hypodense right posterior
...
OJ
frontal mass = with a mildly

hyperdense cortical
CO
:J
Cl
::r
'<
component 81. MR showed 3
minimal palchy OJ
enhancement. Infiltraling Gl
sarcoid was Found at surgery. CO
:J
...
CD
OJ
(Left) Axial NECT shows very

hyperdense mass
cerebral
= with
in left
while maller
adjacent edema ~ in a 79
year old with known history
of AML, leukemic relapse,
presented with new onset
seizure, right-sided
weakness. The finding was
presumed chloroma. (Right)
Axial NECT shows a variant
case of tuberous sclerosis
complex with hyperdel1se
=-
calcified posterior fossa mass
a large cortical ruber.

hyperdense, parlially
calcified lobar hamartoma
= in this patient with
tuberous sclerosis complex.
This rare manifestation may
mimic neoplasm. (Right)
Axial NECT in a 16 year old
with long-standing seizures
shows thickened,
hyperdense corlex =-
focally effaced sulci. The
cortex was hypointense on
T2WI, with sulcal
hyperintensity and
enhancement on MR.
I
5
49
ro
~ MULTIPLE HYPERDENSE PARENCHYMAL LESIONS
Ql
c
Ql
C)
DIFFERENTIAL DIAGNOSIS o Other: Corpus callosum, deep gray nuclei,
ro
E midbrain/brainstem
>,
.r:
Common o T2* scan (GRE/SWI) helpful
'-'
c • Cerebral Contusion • Hypertensive Intracranial Hemorrhage
~
Ql
ro o Solitary hematoma> patchy/multifocal
11.
c
• Hypertensive Intracranial Hemorrhage hemorrhage
ro
~ • Cerebral Amyloid Disease o Deep> superficial lesions
co • Metastases, Parenchymal
C
• Nearly 2/3 striatocapsular
III
• Cavernous Malformations • Thalamus 15-25%
~
III Less Common o Look for multifocal"microbleeds" (1-5%),
"t:l
c • Cerebral Infarction, Subacute best seen on MR with GRE/SWI sequence
III
• Thrombosis, Cortical Venous • Basal ganglia, cerebellum (vs. cortical,
• Acute Hypertensive Encephalopathy, PRES peripheral in amyloid)
• Anticoagulation Complications • Cerebral Amyloid Disease
• Glioblastoma Multiforme o Causes 15-20% of primary non traumatic
• Lymphoma, Primary CNS intracranial hemorrhage in older patients
• Tuberous Sclerosis Complex o Classic = lobar hemorrhages of different
ages
Rare but Important o Most common manifestation actually
• Tuberculomas "microbleeds"
• Neurosarcoid • Do T2* (GREor SWI) scan to detect
• Leukemia • Metastases, Parenchymal
• Thrombotic Microangiopathies (HUS/TTP) o Electron dense (hypercellular or
• Thrombolysis Complications hemorrhagic)
• Parasites, Miscellaneous o Some enhancement usually present
• Acute Hemorrhagic Leukoencephalopathy • Cavernous Malformations
o Multiple (familial) lesions
ESSENTIAL INFORMATION o NECT often normal unless acute
intralesional hemorrhage
o Iso-/hyperdense ± Ca++
o Mass effect absent unless hemorrhage
o Do MR with T2* (GREor SWI) for optimal
imaging
• Cerebral Infarction, Subacute
o Hemorrhagic transformation
• Typically 2-3 days after ischemic infarct
• Patchy petechial hemorrhages in cortex,
basal ganglia
• Thrombosis, Cortical Venous
o With or without dural sinus thrombosis
o Patchy cortical/subcortical petechial
hemorrhages
• Acute Hypertensive Encephalopathy,
PRES
o Most common: Patchy hypodense
cortical/subcortical foci
• Occipital lobes > basal ganglia>
brainstem, cerebellum
I o Less common: Petechial hemorrhages
(gross hematomas rare)
5
50
MULTIPLE HYPERDENSE PARENCHYMAL LESIONS en
"
c:
Ql
• Anticoagulation Complications • Leukemia :I
a.
o Mixed density hemorrhages o Most parenchymal hyperdensities are III
...,
o Fluid-fluid levels, unclotted blood hemorrhages Ql
:I
• Glioblastoma Multiforme o Hypercellular parenchymal masses
III
...,
o ecrosis, hemorrhage common (chloromas) < extra-axial tumor Q)
• Low density center, thick irregular high • Thrombotic Microangiopathies (HUS/TTP) :I

-U
density hypercellular rim o Thrombocytopenia, intravascular ...,
Q)
o Multifocal GBM, "butterfly" GBM of corpus hemolysis characteristic of 3 disorders CD

:I
()
callosum • Malignant hypertension (often with :r
'<
• Both can appear to have separate HUS) 3
Q)
hyperdense regions • Disseminated intravascular coagulation G)
• Can be either hemorrhage or (DIC) CD
:J
hypercell ular regions • Thrombocytopenic thrombotic purpura ...,
CD
Q)
• Lymphoma, Primary CNS (TIP)

o Iso-/hyperdense lesions in corpus o Patchy petechial hemorrhages,
callosum, basal ganglia, periventricular predominately cortical
WM • Thrombolysis Complications
o Frank hemorrhage? Suspect HIV/ AIDS o 10-lS% hemorrhage
• Tuberous Sclerosis Complex • Petechial> gross lobar
o 98% have Ca++ subependymal nodules o Post-procedural T1 C+ MR may predict
o Some cortical, subcortical tubers calcify hemorrhagic transformation (HT)
o Occasional noncalcified cortical, • If present, risk of HT t
subcortical hyperdensities seen • Parasites, Miscellaneous
Helpful Clues for Rare Diagnoses o Cysts> hyperdensities
o Consider travel history, especially in
• Tuberculomas
o Meningitis> parenchymal lesions endemic area
o Mildly hyperdense (rim> solid) ± edema o Beware: Conglomerate parasitic masses can
o Healed granulomas may calcify mimic brain tumor!
• Neurosarcoid • Acute Hemorrhagic Leukoencephalopathy
o Infiltrates along perivascular spaces -> o Fulminant variant of ADEM
parenchymal mass o Hyperintensities in/along perivascular
o May cause focal patchy hyperdense spaces
mass(es) o Microhemorrhages > gross lesions
oCT, MR may not show hemorrhage
Cerebral Contusion Diffuse Axonal Injury (OAf)
I
Axial NECT shows several hemorrhagic contusions =
in the inferior frontal lobes, anterior right temporal lobe, =-
Axial NECT shows scattered hyperdense foci of OAI at
gray-white interfaces left thalamus Sl and
5
and posterior righllemporal lobe. midbrainP.::D.
51
co
~ MULTIPLE HYPERDENsE PARENCHYMAL lESIONS
QJ
C
QJ
o
co
E
>,
-'u=
c (Left) Axial NECT shows a
QJ
~ large high density mass in
co
0- the leit cerebellar
c hemisphere =:I. The right
co
~ cerebellar hematoma oi
[D slightly lesser increased
c attenuation ~ indicates
co
•... active hemorrhage. (Right)
[JJ Axial NECT in a hypertensive
"tl patient shows patchy
c pontine =:I and cerebellar
III
hemorrhages PJ:].
Cerebral Amyloid Disease Cerebral Amyloid Disease

spontaneous leitlobar
hemorrhage =:I in a
demented, normotensive
patient. (Right) Axial NECT
at a higher level in the same
patient shows a right lobar
hemorrhage =:I. Multiple
lobar hemorrhages suggest
amyloid angiopathy.

heterogeneous, slightly
hyperdense lesion =
in the
leit temporal lobe, with a
central iocus oi hemorrhage
~ and surrounding
vasogenic edema. This
patient has metastatic
bronchogenic carcinoma.
(Right) Axial NECT in the
same patient shows 2 other
slightly hyperdense lesions
=:I in the leit iron tal lobe,
one with central hemorrhage
ffi Significant surrounding
vasogenic edema is present.
I
5
52
MUlTIPLE HYPERDENSE PARENCHYMAL LESIONS ,..
en
c:
III
::::l
Q.
..,
OJ
Cavernous Malformations III
::::l
(Left) Axial NECT shows faint
hyperdensities in the septum ..,
OJ
pe//ucidum and left medial Ql
frontal cortex =. MR with ::::l

II
SWI showed multiple
cavernous malformations
..,
Ql
<ll
mixed with large venous ::::l
()
malformation. (Righi) Axial ::r
'<
NECT in a child with known 3
multiple cavernous Ql
malformation syndrome G)
shows 2 faint hyperdense <ll
lesions
lobe.
= in left parietal
::::l
..,
<ll
Ql
(Left) Axial NECT obtained

one week after acute
ischemic inFarction shows
hemorrhagic transformation,
seen here as mulLifocal
gyriform hyperdensities =.
acute thrombosis of the
superior sagittal sinus ~
with multifocal
cortical/subcortical
hemorrhages = caused by
cortical vein occfusions.
Acute Hypertensive Encephalopathy,

Thrombosis, Cortical Venous PRES
(Leh) Axial NECT shows
multiple hemorrhagic fod in
the left temporal lobe =.
MR disclosed thrombus in
the left transverse sinus that
extended into a large
anastomotic vein of Labbe
(VorL), causing massive
parenchymal hemorrhages.
This location is very
characteristic of VorL
occlusion. (Right) Axial
NECT in 24 year old renal
transplant patient on
cyclosporine shows bilateral
hypodensities in both
occipital lobes = with
hemorrhagic foci Ell.
I
S
53
~
Q) L
MUlTIPLE HYPERDENSE PARENCHYMAL LESIONS ---!
c
Q)
<.9
<Il
E
>-
.r::
()
~ (Lefl) Axial NECT in this 71
ro year old woman with
Cl.. laboratory-documented
c coagulopathy shows bilateral
~ intracerebral hematomas
III with blood-fluid levels =.
c (RighI) Axial NECT shows
~ bilateral hemorrhages E:I
CD into "butterfly" lesion of the
"'C corpus callosum genu.
C
III

(Left) Axial NECT shows 2
hyperdense periventricufar
lesions It] with some
surrounding vasogenic
edema. These lesions are
hypercellular, not
hemorrhagic. (RighI) Axial
NECT shows multifocal,
discrete, hyperdense,
non calcified subcortical
hyperdensiUes =. Other
scans showed typical
nodules.
Tuberous Sclerosis Complex Tuberculomas

(Lefl) Axial NECT in a child
with known tuberous
sclerosis complex shows
hyperdense masses in
thickened cortex and basal
ganglia =. The tuber in the
caudate head is partially
calcified E:I. (RighI) Axial
NECT shows left frontal
edema = adjacent to
several ring-like hyperdense
lesions BiI in patient with
known tuberculous
meningitis.
I
5
54
MULTIPLE HYPERDENSE PARENCHYMAL lESIONS en
"
l:
III
::l
Co
..,
OJ
III
::l
hype,dense right occipital lJJ
..,
lesions 6tIthat showed OJ
strong but patchy ::l
-0
enhancemenl. Infiltrating
neurosarcoid was proven at
..,
OJ
C1l
biopsy. (Coullesy M. ::l
()
Hemmati, MDJ. (Right) Axial ::T
'<
NECT shows extensive 3
multiiocal pa,enchymal OJ
hemo(lhages in a ,apidly Gl
deteriorating teenager with C1l
::l
acute myelogenous leukemia ..,
C1l
who presented in the OJ
emergency department with
visual problems. CBC
revealed the patient had
almost no platelets.
Thrombotic Microangiopathies
(HU5/TTP)
(Left) Axial NECT in septic
patient with disseminated
intravascular coagulopathy
hemo(lhages =-
shows multiiocal petechial
p,edominately right irontal

with lesser involvement of
leit irontallobe 81.
Innumerable bilateral cortical
infarcts were seen on OWl.
(Right) Axial NECT obtained
several hours after
thrombolysis ior M 1 MCA
thrombus with ischemic
territorial infarction shows
petechial hemo(lhages =.
Acute Hemorrhagic
Parasites, Miscellaneous Leukoencephalopathy
(Leit) Axial NECT shows
patchy hyperdense lesions in
the right posterior irontal
lobe =. Amebiasis was
iound at surgery. (Right)
Axial NECT was obtained
just prior to death in this 70
year old patient patient with
mullifocal hyperinlensilies
along perivascular spaces, as
seen on MR. Diiiuse brain
swelling but no iocal
hemorrhages were seen.
Autopsy iound acute
hemo(lhagic
leukoencephalitis.
I
5
55
SOLITARY HYPODENSE PARENCHYMAL LESION
DIFFERENTIAL DIAGNOSIS • Cerebral ischemia-infarction (adult>

CIl
E child)
>-
J:: Common
U Helpful Clues for Common Diagnoses
C • Cerebral Contusion
Ql
L-
• Cerebral Ischemia-Infarction, Acute • Cerebral Contusion
CIl
Cl.. o Cortical/subcortical hypodensity
c • Cerebral Infarction, Subacute
o ± Petechial hemorrhages
CIl • Cerebral Infarction, Chronic
o Multifocal > solitary, confluent
L-
en • Glioblastoma Multiforme
c o Look for
• Anaplastic Astrocytoma
...
ns
aJ • Metastasis • Overlying scalp swelling (coup) or
"'C
• Oligodendroglioma opposite lesion (contrecoup)
C
ns • Adjacent traumatic subarachnoid
Less Common hemorrhage
• Diffuse Astrocytoma, Low Grade o Lesions "bloom" (become more prominent)
• Pilocytic Astrocytoma with time
• Cerebritis • Cerebral Ischemia-Infarction, Acute
• Encephalitis o Look for dense MCA, dot signs
• Intracerebral Hematoma (Resolving) o Subtle effacement of gray-white interfaces
• Thrombosis, Cortical Venous • Insular ribbon sign
Rare but Important • Hypodense/"smudged" basal ganglia
• Multiple Sclerosis • Cerebral Infarction, Subacute
o Hypodensity increases
• ADEM
• Tuberculoma o Mass effect increases
o Wedge-shaped hypodensity in vascular
distribution
ESSENTIAL INFORMATION o Involves both gray, white matter; extends
Key Differential Diagnosis Issues to cortex
• Definition • Cerebral Infarction, Chronic
o Includes solitary focal hypoattenuating o Gliotic, encephalomalacic brain
parenchymal lesions that are hypodense to o Hypointense on FLAIRbut often has
brain but hyperdense compared to CSF hyperintense borders
o Excludes cysts, cyst-like lesions • Glioblastoma Multiforme
o Excludes multifocal, diffuse/confluent o Glioblastoma multiforme (GBM) usually
white matter diseases tumor of middle-aged, older adults
• History key o 95% central necrosis, thick enhancing
o Trauma (contusion, resolving hematoma)? rind, edema
o Sudden (e.g., stroke) vs. gradual onset o Ca++ rare; gross hemorrhage common
(tumors, infection, demyelinating diseases) • Anaplastic Astrocytoma
• Effect of age on differential diagnosis o Poorly-delineated, infiltrating
o Child o Ca++, hemorrhage less common
• Diffuse astrocytoma, low grade o If any enhancement, suspect GBM
• ADEM • Metastasis
o Adult o Iso- to hypodense mass, variable edema
• Multiple sclerosis o Enhances (solid, ring, nodular)
• ADEM • Oligodendroglioma
• Glioblastoma multiforme o Hypodense cortical/subcortical mass
• Anaplastic astrocytoma o 50% calcify
• Metastasis o Enhancement variable
o Both Helpful Clues for Less Common Diagnoses
• Contusion
I • Infection (cerebritis, encephalitis)
o Hypodense, nonenhancing
o 2/3 supratentorial (hemispheres)
5
56
SOLITARY HYPODENSE PARENCHYMAL lESION Ul
c"
:
III
o 1/3 posterior fossa (brainstem, cerebellum) o Hypodense cortex/subcortical white matter ::;,
0-
• Pilocytic Astrocytoma lesion(s) ..•
lJl
o Cerebellum = cyst + nodule o Patchy petechial hemorrhage common III
::;,
o Hypothalamus/optic pathway o Do CECT/CTV
• Lobulated hypodense mass oMR
• Enhances strongly, uniformly • Include T1 C+
• Cerebritis • Do T2* (GRE/SWI), look for blooming
o First, earliest stage of abscess formation clot in thrombosed cortical vein
o Poorly marginated hypodense mass Helpful Clues for Rare Diagnoses
o Enhancement none or minimal • Multiple Sclerosis
• Encephalitis o Multiple> solitary lesion
o Mostly viral o Solitary tumefactive MS plaque can mimic
• General imaging findings = hypodense neoplasm
mass, variable enhancement o Hypodense on ECT
o Herpes encephalitis most common
o MR
• Limbic system predilection (both • Do sagittal FLAIR
temporal lobes, cingulum, subfrontal • T1 C+ may show "horseshoe"
cortex) enhancement
• Cortex, subcortical white matter
• ADEM
• Enhancement, hemorrhage absent in o Follows viral illness, vaccination
early stage o Multifocallesions > solitary
• MR with FLAIRmost sensitive o Solitary tumefactive demyelination can
• Intracerebral Hematoma (Resolving) mimic neoplasm
o Hypodense to brain but hyperdense to CSF
• Tuberculoma
o May show ring enhancement o Can be parenchymal or dural-based mass
o MR shows evidence for resolving o Can be hyper- or hypodense or mixed
hemorrhage o Variable enhancement (can mimic
• Thrombosis, Cortical Venous neoplasm)
o Can be solitary or multiple
o Can occur with or without associated dural
sinus occlusion
o May show "cord sign" (thrombosed cortical
vein)
I
=
extensive cortical/subcortical hypodense mass
petechial hemorrhages ~.
=
Axial NEeT in this patient 24 hours after trauma shows
with
Note intraventricular
Axial NEG shows hypodense right insular lesion
with loss or gray-white dirrerenUation("insular ribbon
sign") in this elderly patient who presented to the
5
blood-fluid level r=;J. emergency department with acute stroke symptoms.
57
C1l
~ SOLITARY HYPODENSE PARENCHYMAL LESION
Q)
C
Q)
C)
Cerebral Infarction, Subacute Cerebral Infarction, Chronic

(Left) Axial NECT 2 days
after a stroke shows
well-demarcated
hypodensity in the cortical
territory of the leFt middle
cerebral artery 1:]. (Right)
Axial NECT shows
encephalomalacia I:] in leFt
MCA distribution. Note
enlargement of lateral
ventricle '-=secondary to
= volume loss.
(Left) Axial NEC!, in a 65
year old in the emergency
department with progressive
headache & leFt-sided
weakness; was obtained to
"rule out stroke". It shows
hypodense right temporal
lobe mass 1:1 hypedense to
C5f MR (not shown)
disclosed enhancing rind
around non enhancing center
of mass. (Right) Axial CECT
in a child shows a
hypodense nonenhancing
mass that enlarges the pons,
flattens & compresses the 4th
ventricle 1:]. /-ligh grade
glioma was Found at biopsy.
Oligodendroglioma Diffuse Astrocytoma, Low Grade

nonenhancing, noncalcified
hypodense leFt Frontal mass
I:] that involves both corlex
and subcortical white maller.
Oligodendroglioma with no
atypical Features was Found
at surgery. (Right) Axial
CECT shows a hypodense
diFFuselyinfiltrating
non enhancing white matter
mass I:] in leFt Frontal lobe.
The cortex appears relatively
spared in this patient with
W/-IO grade II astrocytoma.
I
5
58
SOLITARY HYPODENSE PARENCHYMAL lESION VI
"
c:
III
::J
0.
III
.,
Cerebritis III
(Leh) Axial NECT in this 3 ::J

year old shows large III
.,
lobulated hypodense mass III
1m centered in the ::J

-U
hypothalamus. MR showed III
that the mass enhanced ~
CD
strongly, uniformly. (Right) ::J
()
Axial NECT in teenager with ::r
2 day history of headache,
'<
3
nausea, & vomiting shows an III
ill-defined hypodense area in G)

right posterior temporal lobe CD
::J
=:2. OWl restriction, early CD
rim enhancement were seen OJ
on MR (not shown).
Thrombosis, Cortical Venous

relatively well-delineated
hypodense right hemisphere
mass ~ that is not quite
CSF-like. CECT (not shown)
demonstrated rim
enhancement; T 1 WI showed
lesion contained
homogeneously hyperintense
fluid consistent with dilute
free methemoglobin. (Right)
Axial NECT in patient with
occluded vein of Labbe
shows hypodense left
posterior temporal venous
infarct=:2 with patchy
hemorrhage 81.
Multiple Sclerosis ADEM

low density lesion =:2
isolated to the left frontal
white matter in a patient
with multiple sclerosis.
large, tumefactive ADEM
lesion =:2. MR demonstrated
"horseshoe" enhancement
around the lesion margins.
I
5
59
~ MULTIPLE HYPODENSE PARENCHYMAL LESIONS
<ll
C
<ll
<.9 o Trauma history is usually known
• Cerebral Contusion
Common o Brain surface injuries involving superficial
• Cerebral Infarction gray matter (GM) & contiguous subcortical
• Trauma white matter (WM)
o Cerebral Contusion o Classic location: Anterior inferior frontal
o Diffuse Axonal Injury (DAI) lobes & inferior temporal lobes
• Metastases, Parenchymal o Hemorrhagic> nonhemorrhagic
..
C
l'Cl
aI
Less Common
o Soft tissue injury in 70% of patients
"'C
c • Infection o Punctate hemorrhages at corticomedullary
l'Cl
o Encephalitis (Miscellaneous) junction, corpus callosum, deep GM, &
o Abscesses upper brainstem classic
o Opportunistic Infection, AIDS oCT often normal acutely (50-80%)
o Tuberculosis o May see small hypodense edematous foci
• ADEM o Petechial hemorrhage in up to 50%
• Acute Hypertensive Encephalopathy, PRES • Metastases, Parenchymal
• Vasculitis o Multifocal enhancing lesions with edema
at corticomedullary junctions
Rare but Important
• Glioblastoma Multiforme Helpful Clues for Less Common Diagnoses
• Osmotic Demyelination Syndrome • Multiple Sclerosis
• Tuberous Sclerosis Complex o Multiple hypodense periventricular lesions
• Lyme Disease o Variable enhancement
• Systemic Lupus Erythematosus o Young adult presentation common
• CADASIL • Infection
• Rickettsial Diseases o Pattern of brain involvement may help
• Lymphoma, Intravascular (Angiocentric) differentiate various etiologies
o Fungal & parasitic infections less common
• Encephalitis (Miscellaneous)
ESSENTIAL INFORMATION o Viral agents most common
Key Differential Diagnosis Issues o Many involve deep gray nuclei
• Includes multiple parenchymal lesions o Hypodense lesions with patchy
hypodense to brain but hyperdense enhancement common
compared to CSF o Herpes encephalitis most common agent
• Cysts & cyst-like lesions are excluded • Predilection for limbic system
• Involves cortex and subcortical WM
Helpful Clues for Common Diagnoses • Bilateral, asymmetric involvement
• Cerebral Infarction • Abscesses
o Wedge-shaped area of hypodensity in a o Four pathologic stages: Early cerebritis, late
vascular distribution classic cerebritis, early capsule, late capsule
o Hypodensity increases with age of infarct o Imaging varies with abscess stage
• Acute: Subtle hypodensity o Bacterial> > fungal/parasitic
• Subacute: t Hypodensity & edema o Multiple often related to septic emboli
• Chronic: Gliosis/encephalomalacia with o Frontal, parietal lobes commonly involved
volume loss typical • Opportunistic Infection, AIDS
o Cerebral hemispheres> posterior fossa o Toxoplasmosis: Multiple ring-enhancing
o Often in a single vascular distribution lesions of varying size with surrounding
o May appear as multiple lesions if embolic edema in deep & superficial brain
• Trauma o PML: Large multifocal subcortical WM
I o DAI & cerebral contusions typically
hemorrhagic (hyperdense)
lesions without mass effect, enhancement
5
60
MULTIPLE HYPODENSE PARENCHYMAL LESIONS en
'"
r::
Ql
o TB & fungal: Solid, mildly hyperdense or • Osmotic Demyelination Syndrome ::J
0-
hypodense masses o Acute demyelination caused by rapid shifts
.,
lD
• Tuberculosis in serum osmolality Ql
o 50% in pons (CPM): Central fibers

::J
o Basilar meningitis + parenchymal lesions
highly suggestive involved; peripheral fibers spared ....
lD
Q)
o Tuberculomas: Hypodense parenchymal o 50% extra-pontine sites (EPM): BG, WM :::J

-u
masses with solid or ring enhancement • Tuberous Sclerosis Complex ...•
Q)
o Cortical/subcortical tubers, WM lesions CD

o Meningitis is most frequent manifestation :::J
()
of CNS TB & is more common in children o Frontal> parietal> occipital> temporal ::T
'<
• ADEM o Calcified subependymal nodules typical 3
Q)
o Multifocal WM &/or basal ganglia (BG) • Lyme Disease
lesions after infection or vaccination o Small hypodense periventricular lesions
o Hypodense flocculent, asymmetric lesions o Cranial nerve enhancement common
o Initial CT normal in 40% • Systemic Lupus Erythematosus
• Acute Hypertensive Encephalopathy, o Small multifocal hypodense WM lesions
PRES o Focal infarcts of various sizes; symptomatic
o Patchy cortical/subcortical PCA territory "migratory" edematous areas
lesions in a hypertensive patient o Frontal, parietal subcortical WM common
o Posterior parietal, occipital lobes > BG, • CADASIL
posterior fossa o Characteristic subcortical lacunar infarcts
o Usually bilateral, often asymmetric & leukoencephalopathy in a young adult
• Vasculitis o Anterior temporal pole & external capsule
o Characterized by non-atheromatous lesions (high sensitivity & specificity)
inflammation & blood vessel wall necrosis o Subcortical hypodense lesions typical, may
o May see multifocallow density areas in be confluent
subcortical WM, BG • Rickettsial Diseases
o Initial CT often normal; angiography o Rocky Mountain spotted fever most
remains gold standard common (skin rash)
o III-defined areas of WM & GM
hypodensity ± petechial hemorrhage
o Variable enhancement
o Single hypodense mass with central
• Lymphoma, Intravascular (Angiocentric)
necrosis & rim enhancement common
o Multifocal WM lesions + enhancement
o Multifocal or multicentric disease rare
o May mimic chronic small vessel ischemia
Cerebral Contusion
I
Axial NECT
hypodensities
shows muldple wedge-shaped
= related to chronic ischemia in this contusions -=
Axial NECT shows hemorrhagic & nonhemorrhagic
related to deceleration injury from a
5
multi-infarct dementia patient. The multiple vascular mOlOr vehicle crash. NOle involvement of the fronlal &
distributions suggest a central embolic source. lemporallobes, classic locadon.
61
cu
~ MULTIPLE HYPODENSE PARENCHYMAL LESIONS
Q)
c
Q)
c..?
cu
E
>-
J:::
<..l
=
C
~
Q)
cu hemorrhagic &
a.. non hemorrhagic ~ foci of
c OAI in typical locations,
~ most commonly at the
co gray-white interfaces.
c: CRE/SWI MR often shows
I'll additional lesions. (Right)
~
CO Axial NECT shows multiple
"c: hypodense lesions

related to lung cancer
=
I'll
metastases in this palient
with altered mental status.
Parenchymal metastases
enhance after contrast &
typically have significant
edema.
Encephalitis (Miscellaneous) Abscesses

hypodensity in the temporal
lobes bilaterally & inferior
right frontal lobe a related
to herpes encephalitis.
Cortex & subcortical white
matter involvement is
typical. Associated
hemorrhage is common.
multiple parietal lobe
hypodensities = related to
multiple abscesses. The
frontal & parietal lobes are
most commonly involved.
MR shows OWl restriction
centrally.
Opportunistic Infection, AIDS Tuberculosis

multiple ring-enhancing
lesions with surrounding
hypodensity in this If/V
patient with toxoplasmosis.
Toxoplasmosis is the most
common opportunistic
infection in the CNS. (Right)
Axial NECT shows multiple
hypodensilies in both
hemispheres related to a
combination of edema
surrounding T8 granulomas
~ & infarcts secondary to
T8 meningitis =.
I
5
62
MULTIPLE HYPODENSE PARENCHYMAL lESIONS ,...
Ul
c:
III
::l
Co
Acute Hypertensive Encephalopathy, ..,
CD
PRES III
::l
hypodensity in the deep gmy OJ
..,
nuclei I:] & perivenlricular OJ
while maller E1 in this ::l
-0
young patient with acute
..,
OJ
symptoms after a recent viral C1>
illness. /nvolvement of white ::l
()
maller & deep gray or
'<
structures ;5 common in 3
ADEM. (RighI) Axial NECT OJ
shows hypodense lesions I:] G)
in the parieta/lobes C1>
::l
bilaterally in this C1>
..,
hypertensive patient, typical Ol
of PRES.PRESis commonly
OWl negative & reversible.

multiple infarcts in this
patient with angioinvasive
fungal vasculitis related to
aspergillosis. Multiple low
density lesions in the
subcortical white matter &
deep gray nuclei is common.
OWl MR may be positive
acutely. (Right) Axial N[CT
shows multiple parenchymal
hypodensities I:] in the
cortex & subcortical white
maller related to tubers.
Note the multiple calcified
subependymal nodules,
characteristic of tuberous
sclerosis complex.
Rickettsial Diseases
multiple hypodense lesions
in the while maller related to
hypertensive
encephalopathy secondary
to severe renal involvement
in this patient with lupus.
low density in the deep gray
nuclei bilaterally, with areas
of petechial hemorrhage 1:].
White maller hypodensity is
also seen. Rickettsial diseases
often a((ect the basal ganglia
& show small infarct-like
lesions in both the deep gray
& white matter.
I
5
63
ell
~ MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), COMMON
Q)
c
Q)
t? o Encephalomalacia is a "hole" that follows

CSF signal, often surrounded by gliosis
Common • Atherosclerosis, Intracranial
• Aging Brain, Normal o Results in distal emboli or hypoperfusion
• ormal Myelination infarcts
• Reactive Astrocytosis (Gliosis) & o Variable infarct location, depends upon
Encephalomalacia vessel involved
• Atherosclerosis, Intracranial • Neurofibromatosis Type 1
• Neurofibromatosis Type 1 o Nonenhancing T2 hyperintensities in basal
o Myelin Vacuolization ganglia (BG) & deep cerebellum most
• Enlarged Perivascular Spaces commonly (myelin vacuolization)
o Mucopolysaccharidoses o No mass effect, unlike astrocytoma, the
• Lacunar Infarction main differential in NFl
• Chronic Hypertensive Encephalopathy o Develops in early childhood, peaks around
• Acute Hypertensive Encephalopathy, PRES age 8, & usually regresses by late teens
• Cerebral Infarct, Subacute • Enlarged Perivascular Spaces
• Cerebral Infarct, Chronic o Commonly symmetric & peripheral in
• Hypotensive Cerebral Infarct WM, but can be unilateral focal & deep
• Cerebral Edema, Traumatic o Inferior BG, near anterior commissure
• Cerebral Contusion common location
• Diffuse Axonal Injury (DAI) o Sharp margins & lentiform, follows CSF on
• Multiple Sclerosis T2/FLAlR in young patients
• Metastases, Parenchymal o Often associated with gliosis in the elderly
• Lymphoma, Primary CNS (FLAIRhyperintense)
• Radiation and Chemotherapy o MucopoIysaccharidoses
• Periventricular Leukomalacia • Dilated PVS usually with surrounding
gliosis presenting in infancy
ESSENTIAL INFORMATION • CC & peri atrial WM most common
• Lacunar Infarction
Helpful Clues for Common Diagnoses o Usually in lenticular & caudate nuclei,
• Aging Brain, Normal thalamus, internal capsules, periventricular
o White matter (WM) hyperintensities are WM
normally seen Acute: T2 hyperintense, diffusion positive
o
• Rule of thumb: 1 per decade to age SO o Chronic: Focal encephalomalacia with
o Increase in number & size is exponential surrounding gliosis
from age SO to 100 years • Chronic Hyperintensive Encephalopathy
o Due to gliosis, leukoariosis, & enlarged o Usually deep & periventricular WM
perivascular spaces (PVS) confluent hyperintensities
• Normal Myelination o Often associated with T2 hypointensities
o T2 hyperintense myelin at birth, except from microhemorrhage on GRE images
posterior fossa, optic radiations, & • Acute Hypertensive Encephalopathy,
corticospinal tracts PRES
o Corpus callosum (CC) myelinates from 4 o Peripheral subcortical confluent
to 9 months, splenium to genu hyperintensities, mild mass effect
o Parietal & frontal myelination from center o Bilateral occipital parietal is common, but
to periphery until around 2 years of age many variations including hemorrhage
• Reactive Astrocytosis (Gliosis) & • Cerebral Infarct, Subacute
Encephalomalacia o Embolic infarcts usually cortical,
o Brain's only response to insults: Infectious, wedge-shaped with mass effect
stroke, trauma
I o Gliosis is T2 hyperintense without mass
o Microembolic infarcts are usually
peripheral centrum semiovale or BG
effect, encephalomalacia often associated
5
64
MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), COMMON
III
o Enhancement typical o Acute tumefactive lesion: Large with T2 ::J
a.
• Cerebral Infarct, Chronic hypointense ring that enhances, usually
o Results in focal encephalomalacia & gliosis little mass effect
..•
lJl
III
::J
o Typically in a major vascular distribution • Metastases, Parenchymal
OJ
• Hypotensive Cerebral Infarct o Hyperintensities may be punctate to
~.
o Watershed infarcts massive, with variable surrounding edema, ::J
II
• Parasaggitallinear "string of pearls" in mass effect ..•
OJ
the centrum semiovale o Hyperintensity, edema, & mass effect less CD

:::J
()
• Wedge-shaped regions in the border prominent in posterior fossa, but risks :::J"
'<
zone between vascular distributions higher 3
OJ
o Diffuse or multifocal cortical infarcts & BG • Lymphoma, Primary CNS Gl
o Diffusion positive acutely o Central region nearly T2 isointense due to CD
:::J
• Cerebral Edema, Traumatic high nuclear to cytoplasmic ratio ..•
CD
OJ
o Cerebral swelling without T2 change early, o Surrounding edema variable, usually
may develop hyperintensities crossing or around CC in
o Contusion & DAI commonly with immunocompetent
hemorrhage o Immunocompromised PCNSL will have
• Cerebral Contusion multifocal ring-like "glioblastoma" look
o Cortical, subcortical hyperintensities with • Radiation and Chemotherapy
developing hemorrhage o Radiation leukomalacia: Confluent poorly
o Regions of injury: Temporal, frontal lobe, marginated regions in the radiation field
superficial brain with direct trauma without enhancement
• Diffuse Axonal Injury (DAI) o Radiation necrosis: Irregular
o Shear stress deceleration injury: ring-enhancing lesions with variable mass
Gray-white, midbrain hemorrhage; effect, may grow, CBV/choline low
diffusion positive early • Peri ventricular Leukomalacia
o Typically in older children to young o WM volume loss, gliosis, & focal cystic
adults, as there is minimal subarachnoid lesion in the periatrial WM
space & brain movement o Associated with prematurity
o CC & peri 4th ventricular involvement
characteristic
o Radiating periventricular location,
"Dawson fingers"
Aging Brain, Normal
I
Axial FLAIR MR shows minimal deep while maIler
hyperintensilies I:'.] & minimal gyral atrophy in this
Axial FLAIR MR shows more extensive & confluent
regions of hyperintensity including perivascular
5
healthy 76 year old patient. These hyperinlensilies may "leukoariosis" in this 96 year old healthy individual.
be seen as parI of the aging process. Note the minimal atrophy.
65
ro
~ MUlTIPLE BRAIN HYPERINTENSITIES (T2/FlAIR), COMMON
Q)
c
Q)
(9
ro
E
>.
.<:: Normal Myelination Normal Myelination
u
c (Left) Axial T2WI MR shows
Q)
~ a normal myelin pattern at 5
ro
n.. months of age. There;s
c hyperintensity throughout
ro
~ the frontal & parietal white
ell maller & hypointellsity of
c normal myelination within
III
•... the centrum semiovale =
ell emanating from the internal
"'C capsules. (Right) Axial T2WI
C
III MR at 12 months of age
shows normal residual
hyperintense signal in the
the frontal lobe & insula

and in the peripheral white
=
juxta cortical white maller of
maller of the parietal lobes

81.
Reactive Astrocytosis (Gliosis) & Reactive Astrocytosis (Gliosis) &

Encephalomalacia Encephalomalacia
profound asymmetric
perivenlricufar while matter
volume loss & hyperintensity
indicative of gliosis l:ll along
with generalized left greater
than right atrophy ill this
microcephalic 14 year old.
shows volume loss with
enlarged subarachnoid,
sylvian, & ventricular CST
spaces @ CSF isointense
cystic encephalomalacia Ii8
& mixed intensity gliolic
brain in this patient with
chronic hemispheric
infarction.
Atherosclerosis, Intracranial Neurofibromatosis Type 1

parasaggital deep white
maller hyperintensities in the
right hemisphere, almost
Forming a distinct line =
due to low-flow infarcts
along watershed 7ones. This
patient had an ICA occlusion
with inadequate coJlalerals.
shows multiple foci of
parenchymal hyperintensities
in the globus pallidi
subinsular
= =-
while maller
and
characteristic of myelin
vacuolization of NF I.
I
5
66
MULTIPLE BRAIN HYPERINTENSITIES (T2/FlAIR), COMMON ,..
(JI
r::
III
::::l
0-
ro
.,
Myelin Vacuolization Enlarged Perivascular Spaces III
(Left) Axial FLAIR MR shows ::::l

numerous focal areas of OJ
increased signal intensity in iil
OJ
Ihe midbrain & lemporal
lobe =:I due 10 myelin lJ
vacuolization, common in
.,
OJ
CD
OJ
Ihe BG & deep cerebellum. o
These are Iransienl & usually ::T
resolve in lale childhood.
'<
3
They have variable margins OJ
& rarely enhance. (RighI) G:l
Axial T2WI MR shows CD
OJ
mulliple sharply demarcaled CD
~
enlarged PVS =:I wilh a OJ
characteristic appearancel
being sharply marginaled &
oval, allhough markedly
asymmetric.
Mucopolysaccharidoses Mucopolysaccharidoses
enlarged PVS in the periatrial
WM eXlending into
posterolateral margin of lhe
ee splenium 1J:2. These have
a typical radialing, linear,
eSF-isoimense appearance.
(RighI) Axial (LAIR MR
shows diffuse hyperintensily
of the deep WM due CO
gliosis & mullifocal
eSF-intensily enlarged PVS
filled wilh unmelabolized
mucopolysaccharide. The
degree of callosal & seplal
involvement = is rarely
seen in olher forms of PVS
enlargement
Lacunar Infarction
very sublle increased signal
in an acute lacunar infarct
=:I (OWl posilive). A more
well-defined chronic lacunar
infarct ~ & chronic while
matter disease are also seen.
shows hyperintensities in the
periventricular while malle'
= with areas of chronic
hyperlensive hemorrhage IJ:2
in the putamina. GRE/SWI
MR (not shown) often
demonstrates additional
hemorrhagic foci.
I
5
67
MUlTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), COMMON
ro
E Acute Hypertensive Encephalopathy,
>-
.!:
(J
PRES Cerebral Infarct, Subacute
C (Left) Axial FLAIR MR shows
Q)
~ marked juxtacorUcal while
ro
0.. matter hyperintensity =:II &
c modest gray matter
ro
~
(l)
C
=
hyperintensity & thickening
typical for acute
hypertensive
nl
•.... encephalopathy. (RighI)
(l) Axial T2WI MR shows
"C subacute cerebral infarction
c
nl
=
involving the middle cerebral
&. anterior cerebral artery
~ vascular distributions
with hyperintensity & gyral
swelling and sulcal
effacement. The while matter
is less hyperintense than that
seen in PRES.
(Leh) Axial fLAIR MR shows

a chronic middle cerebral
artery infarct with
due to gliosis =
surrounding hyperintensilies
CSF intensity due to

& central
encephalomalacia IJ:J.
shows hyperintensilies in a
parasaggital WM
corresponds to the
=-
linear "string of beads" in the
which
watershed zone between

basal perforating arteries &
penetrating cortical vessels.
The small central
hypointense areas are due to
encephalomalacia.
Diffuse Axonal Injury (DAI) Multiple Sclerosis

hyperintensilies in the medial
peripheral frontal lobes at
the gray-white matter
junction, typical for OAI =.
A small contusion I!:e is also
seen. Associated
hemorrhagic foci are beller
seen with CRE/SWI. (Right)
Axial FLAIR MR shows a
large hyperintense lesion
with a marked hyperintense
rim = with lesions in the
lobe =
corpus callosum & frontal
typical for a large
acute demyelinating plaque
I
with smaller more chronic
lesions.
5
68
MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), COMMON en
~
c:
Multiple Sclerosis Metastases, Parenchymal

(Left) Sagittal FLAIR MR
shows numerous
hype,intense plaques
=-
involving the juxtacortical
deep, & peri ventricular
white matter. The marked
callosal involvement &
perpendicular orientation at
the callososeptal interface
~ are highly specific for
MS. (RighI) Axial FLAIR MR G)
shows multiple hemispheric CD
:J
hyperinlensiUes with central ,
CD
isoinlense masses ~ typical OJ
for parenchymal metastases.
The prominent edema is also
suggestive of metastatic
disease.
scattered foci of T2
hyperintensity in the central
while matter II}] that
enhanced with gadolinium in
this patient with metastatic
breast cancer. This "miliary"
pattern is more commonly
seen with small cell lung,
thyroid, and melanoma.
shows hyperintense
perivenlricuJar lesions m.
The mixed intensity of the
splenial callosal lesion PJ::I is
due to a high nuclear to
cytoplasmic ratio within the
tumor.

periventricufar while maller
& centrum semiovale
hyperintensWes with sparing
of the subcortical U-fibers
= due to treatment-related
shows enlargement of the
lateral ventricular trigones &
periventricular
hyperintensities due to gliosis
PJ::l in this young adult who
was born prematurely.
Pedalrial white matler
volume loss, gliosis, &
macrocystic change in a
premie are characteristic. I
5
69
ro
L
MULTIPLE BRAIN HYPERINTENSITIES (T2/FlAIR), LESS COMMON
Q)
C
Q)
C)
DIFFERENTIAL DIAGNOSIS o Granulomatous (PACNS), drug-induced, &
ro
E infectious vasculitis usually moderate-sized
>-
.L:
Less Common vessels: M1 to cortical surface, may involve
U
C
Q)
• Cerebral Amyloid Disease basal structures
L
ro • ADEM o Lupus & radiation-induced vasculitis are
[L
c • Vasculitis small vessel & usually angiographically
~ • Sickle Cell Disease occult with punctate to confluent
co • Leigh Syndrome hyperintensi ties
c
ro • Thrombosis, Cortical or Deep Venous • Sickle Cell Disease
•...
In • CMV, Acquired o Creates a moyamoya pattern of vascular
"'C
C
• CMV, Congenital stenosis & occlusion with infarcts in MCA
C'Il
• Cerebritis territory or watershed
• Encephalitis (Miscellaneous) o Demographic & family history
• Herpes Encephalitis differentiate it from classic moyamoya
• Septic Emboli • Leigh Syndrome
• Neurocysticercosis (NCC) o Symmetric hyperintensity in regions of
• Parasites, Miscellaneous oxidative activity
·PML o Putamina & periaqueductal gray> caudate
• Opportunistic Infection, AIDS > globi pallidi, brains tern, thalami, dentate
• Glioblastoma Multiforme • Thrombosis, Cortical or Deep Venous
• Gliomatosis Cerebri o T2 hyperintensity without diffusion
• Osmotic Demyelination Syndrome restriction unless infarction has developed
• CO Poisoning o Lesions usually solitary when isolated
• Drug Toxicity, NOS cortical venous
• Tuberous Sclerosis Complex o Dural sinus: Multiple lesions
• Susac Syndrome o Deep venous: Bilateral thalamic
• CMV, Acquired
ESSENTIAL INFORMATION o Opportunistic infection with
periventricular (4th> lateral) & cerebellar
Helpful Clues for Less Common Diagnoses > cortical hyperintensity with mild
• Cerebral Amyloid Disease enhancement
o Multifocal juxtacortical small infarcts & • CMV, Congenital
hemorrhages of varying ages o Multifocal deep band-like T2
o Little to no deep white matter (WM) or hyperintensity with microcephaly &
basal ganglia (BG) involvement calcifications
o Acute lobar hemorrhage, the usual o Cortical dysplasia, agyria, myelination
presenting symptom, typically large delay, periventricular cysts
o May see confluent WM hyperintensity • Cerebritis
• ADEM o Early stage of bacterial infection, prior to
o Multifocal WM lesions, punctate to cavitation & enhancement seen in abscess
flocculent, with enhancement, faint & o Peripheral, poorly marginated large lesion
fuzzy early, ring-like later with mass effect
o May mimic MS, but lesions are often more • Encephalitis (Miscellaneous)
peripheral WM & all at same stage o Most non-herpes encephalitides involve
o Usually 10-14 days following infection or the BG, thalamus, midbrain, & WM
vaccination o Variable enhancement
• Vasculitis • Herpes Encephalitis
o Multiple hyperintensities typical; pial & o Cortical & subcortical WM with bilateral,
subarachnoid hemorrhage common asymmetric involvement of the medial
o Less cortical involvement & more
I enhancement than embolic stroke
temporal & inferior frontal lobes & insula
o Pial-cortical enhancement; OWl positive
5
70
MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), LESS COMMON en
"
r::
III
• Septic Emboli o Heterogeneous mass with irregular ::J
a.
o Scattered small juxtacortical enhancement III
.,
hyperin tensi ties o May cross the corpus callosum III
o Develop into small ring-enhancing ::J

• Gliomatosis Cerebri
OJ
.,
micro-abscesses o Extensive multilobar or diffuse cerebral
III
• Neurocysticercosis (NCC) hyperintensity with mild mass effect ::J
-U
o Vesicular phase: Small 10 mm cysts with o Preservation of underlying architecture III
central dot- or comma-shaped scolex, no • Osmotic Demyelination Syndrome ro::J

()
edema, follows CSF o Central pontine hyperintensity sparing the ::r
'<
o Colloidal phase: Cyst may enlarge, is periphery & cortical spinal tract, round or 3
III
hyperintense to CSF,+ surrounding trident-shaped (CPM)
edema, enhancement o BG & WM lesions with extra-pontine
o Granular nodular & calcified phase: Cyst myelinolysis (EPM)
retracts, wall thickens, edema resolves, • CO Poisoning
calcifies o Bilateral globi pallidi hyperintensity ±
• Parasites, Miscellaneous adjacent hemorrhage
o Cystic mass or masses with hypointense o May see putamen, caudate, & WM
rim & surrounding edema hyperintensity
o Many with hemorrhage, which is • Drug Toxicity, NOS
uncommon in bacterial infection o WM multifocal strokes: Cocaine,
·PML amphetamine
o Multifocallarge WM lesions that lack mass o Diffuse leukoencephalopathy: Inhaled
effect, rarely enhance heroin
o Involves subcortical U-fibers • Tuberous Sclerosis Complex
• Opportunistic Infection, AIDS o Cortical tubers: juxtacortical
o Toxoplasmosis: Peripheral ring-enhancing hyperintensities
"abscesses" o Calcified subependymal nodules
o Cryptococcus: Enlarged perivascular spaces • Susac Syndrome
o CMV: Subtle ventriculitis, pial o Callosal involvement always; central rather
inflammation than at callosal septal margin seen in MS
o Tuberculosis: Meningitis, tuberculous o Will leave "holes" in central callosum in
abscesses chronic cases
• Glioblastoma Multiforme o Involves BG in 70%, much more than MS
o Rarely multifocal or multicentric
I
Axial FLAIR MR shows patchy & confluent T2 Axial FLAIR MR shows numerous peripheral
5
hype,intensities 1:2 in the deep and subcortical white
matter bilaterally. The lesion distribution is often more
peripheral than in arteriolosclerosis.
=-
hyperintensities generally sparing the cortex & extending
around the subcortical U-fibers typical for AD[M.
Bilateral, asymmetric involvement is common.
71
MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), LESSCOMMON
(Lefl) Axial FLAIR MR shows

confluent while maller
hyperinlensity primarily
affecling the fronlal lobes
with a small amounl of old
hemisphere =-
hemorrhage in the right
due to
granulomatous angiitis.
(Right) Axial PO FSEMR
shows bilateral subfrontal
infarctions -=with increased
flow voids in paramedian
sulci ~ due to pial collateral
engorgement in this African
American child. The Findings
are similar to moyamoya in a
differenl demographic.
Thrombosis, Cortical or Deep Venous

bilaleral putaminal
hyperintensity = & swelling
classic for acute Leigh
syndrome with periatrial
signal abnormality~.
shows hyperinlensity &
swelling in the lhalami,
putamina, & caudate heads
= bilaterally with
hypointensity of the internal
cerebral & thalamOSlriate
veins due to deep venous
thrombosis.

shows thin regular linear
hyperintensities in the
immediate perivenlricular
while maller & caudate rim
= =
of the lateral & 3rd
ventricles typical for
acquired CMV ventriculitis in
this AIDS patient. (RighI)
Axial T2WI MR shows
hyperintensity =
extensive periventricular
with
germinal matrix cysts ~ &
perisylvian cortical dysplasia
~. Microcephaly &
calcifications are also
common in congenital CMV.
I
5
72
MUlTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), LESS COMMON ,.-c:
CIl
Dl
:l
Q.
l:D
....•
Dl
Cerebritis
:l
abnormal hyperintense signal OJ
....•
in the cerebellar hemispheres OJ
:l
~ due to cerebellitis.
-U
Enhanced images showed OJ
....•
marked enhancement. CD
Cerebellitis is often a disease :l
()
of children & is typically ::r
bilateral. (Right) Axial FU\IR
'<
3
MR shows symmetric OJ
hyperintense signal within Gl
the thalami = with
involvement of the deep WM
CD
:l
CD
....•
E!lI in this EBVencephalitis OJ
patient. Viral encephalitis

typically involves the BG,
thalami, cortex, &/o{
brainstem.
(Left) Axial FU\IR MR shows

symmetric hyperinlensily in
the medial temporal lobes &
hippocampi bilaterally =.
Sparing of the basal ganglia
& brainstem is typical of
herpcs enccphalitis. (RighI)
Axial T2WI MR shows the
typical appearance of a small
brain abscess with a
hypointense rim
necrosis, & modest
=-central
surrounding edema,
occurring in a patient with
streptococcal endocarditis
with an associated cervical
cord abscess.
Neurocysticercosis (NCC) Parasites, Miscellaneous

shows numerous CSF
isoinlense cysts with a
discrete, eccentric,
=
hypoinlense scolex in each
& lack of edema, due to
disseminated or "miliary"
form of NCe. (Right) Axial
FU\IR MR shows mixed
frontal mass =
hypo-/hyperintense right
with multiple
smaller supratentorial masses
due to amoebiasis.
Hypoinlense hemorrhage or
calcification, common in
parasitic infections, is
atypical for other infections.
I
5
73
~ MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), LESSCOMMON
Q)
c
Q)
CJ
ro
E
>.
.r:
()
c (Left) Axial T2WI FS MR
~
Q)
shows confluent, high signal
ro
n.. in the fronlallobes wilhout
c significant mass effect. The
ro
~ subcorlical U-fiber
III involvement leads to a
c "scalloped" appearance to
ell
~ the gray-white junction (;8
CO (Right) Axial FLAIR MR
't:l shows numerous mixed
C
ell hyperintense lesions m
commonly seen with
toxoplasmosis, the most
common opportunistic eNS
infection in AIDS. Ring
enhancement is a/so typical.
in the BG = =
mu/tifocal high signa/lesions
& subcortical WM
midbrain E!:l
characteristic of gelatinous
"pseudocysts" caused by
cryptococcosis due to
dilated PVS filled with fungi,
mucoid material, &
infiammalOry cells. (Right)
extensive hyperintensity
infiltrating the cerebral WM
& corpus callosum 1::1 wilh
mass effect due 10 atypical
GBM.
Gliomatosis Cerebri Osmotic Demyelination Syndrome

mullifocal hyperinlensily
infiltrating Ihe thalamus,
basal ganglia, insula, &
fronla/lobe while & gray
matter with mild associated
enlargement of the involved
structures, typical for
gliomatosis cerebri.
Involvement of more than
one lobe is common. (Right)
Axial T2WI MR shows high
signal intensity in the pons
geographic pal/ern =
with characteristic symmetric
typical for centra! pontine

myelinolysis (CPM).
I
5
74
MULTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), LESSCOMMON
III
:J
0-
III
.,
Osmotic Demyelination Syndrome CO Poisoning III
(Left) Axial FLAIR MR shows :J
hyperintensity in the bilateral OJ
putamina E:II and caudate 03
:J
nuclei !:l'l due to osmotic
-U
demyelination, extra-pontine. OJ
Central and extra-pontine CD
myelinolysis are often seen in :J
()
the same patient. (Right) ::r
Axial T2WI MR shows
'<
3
hyperintensity 8. decreased OJ
size of the globus pallidi =.1 G)

surrounded by a hypointense CD
:J
rim Sltypical for chronic CD
.,
carbon monoxide poisoning. OJ

multiple hyperintense foci
involving the basal ganglia
=.1 8. cerebral white maUer
!:l'l caused by
amphetamine-induced
vasculitis. (Right) Axial T2WI
MR shows multiple
subcortical hyperinlensilies
=.1 due to peripheral tubers.
The hypointense
subependymal nodules!:l'l 8.
heterogeneous giant celt
astrocytoma at the foramen
of Monro E:II are diagnostic
of tuberous sclerosis.
Tuberous Sclerosis Complex Susac Syndrome

normal immature myelin in
this infant with subtle
premature hypointensity in a
tuber of the medial left
frontal white maUer
along with multiple low
=-
signal intensity
subependymal nodules 81.
shows hyperintensities in the
white maller with
callosum =-
involvement of the corpus
always
associated with Susac
syndrome. Imaging often
mimics multiple sclerosis.
I
5
75
ro
~ MUlTIPLE BRAIN HYPERINTENSITIES (T2/FLAIR), RARE BUT IMPORTANT
QJ
c
QJ
<.9 o Parenchymal lesions can extend to the
E periventricular WM; usually confluent
>.
.r:
Rare but Important o Associated T2 hypointensity in dura &
u
c • CADASIL leptomeninges is characteristic, but can be
~
QJ
• Neurosarcoid
ro seen with secondary lymphoma &
Cl..
c
• Hashimoto Encephalopathy metastasis
ro
~ • Granulomatous Angiitis • Hashimoto Encephalopathy
OJ
• Lyme Disease o MR positive in 25%, involves
C
ltl
• West Nile Encephalitis hippocampus, WM, cerebellum
~
OJ • Wegener Granulomatosis, Brain o Lesions usually ill-defined, no
• Paraneoplastic Syndromes
"C
ltl
• Lymphoma, Intravascular (Angiocentric)
enhancement
o May mimic olivopontocerebellar
• Olivopontocerebellar Degeneration degeneration (OPCD)
• Subacute Sclerosing Panencephalitis • Granulomatous Angiitis
• Rasmussen Encephalitis o Multiple subcortical & cortical infarcts,
• Kernicterus often with peripheral subarachnoid
hemorrhage
o Peripheral segmental symmetric stenoses
typical, not seen in CADASILor chronic
Key Differential Diagnosis Issues hypertensive disease
• Lesion location is critical: Gray vs. white • Lyme Disease
matter (WM), basal ganglia (BG) vs. o Scattered lesions 2-3 mm typical, usually
periphery, or specific locations less than 10 mm
• Treatment in these diagnoses is often o May be DWI + & may enhance
specific & consideration of these rare o Cortical involvement unusual
diagnoses is important o Myalgia, arthralgias, petechial rash of the
• Enhancement helps separate inflammatory palms & soles suggest Lyme disease
from noninflammatory lesions • West Nile Encephalitis
Helpful Clues for Rare Diagnoses o Midbrain, substantia nigra, cerebellum, &
• CADASIL anterior horn of the spinal cord

o Subcortical bilateral anterior temporal involvement typical
poles involved early o Moderate-sized lesions, ill-defined,
o Diagnosis age 20-40 years is common, leptomeningeal enhancement

unique to CADASIL • Wegener Granulomatosis, Brain
o External capsule involvement somewhat o Similar to neurosarcoid in distribution, T2
specific, but other WM regions, thalamus, signal, & enhancement

BG, pons also commonly involved o Necrotizing vasculitis with paranasal sinus
o Frontal lobe predominant involvement & orbital involvement

developing into confluent lesions will • Para neoplastic Syndromes
become more prominent after age 50 o Limbic encephalitis: Hyperintensity in
o Migraine-like symptoms common, but amygdala, hippocampus, cingulate gyrus,

CADASILlesions larger than typical & inferior frontal lobe WM
punctate lesions in migraineurs o Paraneoplastic cerebellar degeneration:
o Can have a multiple sclerosis-like Bilateral peripheral cerebellar & pontine

appearance early in the disease, although involvement
callosal involvement is rare o Mild edema in the acute phase; atrophy in
• Neurosarcoid the chronic phase

o Pial & leptomeningeal involvement with • Lymphoma, Intravascular (Angiocentric)
extension via perivascular spaces o Multifocal, often confluent periventricular
I o Peripheral WM hyperintensities, intense

enhancement
hyperintensity
5
76
MULTIPLE BRAIN HYPERINTENSITIES (T2/FlAIR), RARE BUT IMPORTANT en
,...
c:
III
a Radiating enhancement pattern along Alternative Differential Approaches
;,
Cl.
deep medullary veins
• Characterize lesions by enhancement O::J
....•
• Olivopontocerebellar Degeneration a Enhancing multiple rare T2 lesions
III
;,
a Cruciate T2 hyperintensity in lower pons
• Neurosarcoid O::J
a Cerebellar hemispheres more involved
• Wegener granulomatosis OJ
than vermis, with "fine comb" cerebellar :::J
• Granulomatous angiitis lJ
folia in dominant form Q)
• Lymphoma, intravascular ....•
a Lateral cerebellar hemisphere atrophy with CD
a Nonenhancing multiple rare T2 lesions :::J
()
"fish mouth" deformity in recessive form :::r
• CADASIL '<
• Subacute Sclerosing Panencephalitis • Hashimoto encephalopathy 3
Q)
a Multifocal large or diffuse T2
• Lyme disease Gl
hyperintensity extending into the gyri CD
• West Nile encephalitis :::J
with callosal involvement; no CD
• Paraneoplastic syndromes OJ
enhancement
• Olivopontocerebellar degeneration
a Similar features to progressive multifocal
(OPCD)
leukoencephalopathy with differing past • Subacute sclerosing panencephalitis
medical history
• Rasmussen encephalitis
a Diffuse atrophy with severe WM volume
• Kernicterus
loss late
• Characterize lesions by location
a Presents in childhood or early adolescence
a Anterior temporal lobe: CADASIL,trauma
• Rasmussen Encephalitis o Limbic system/cerebellum: Paraneoplastic
a Early focal cortical swelling & gray-white
syndromes, herpes
differentiation loss, usually does not a Olive, pons, cerebellum: OPCD,
enhance multisystem atrophy
o Atrophy of the cerebral hemisphere or a
a Unilateral hemisphere: Rasmussen
lobe late encephalitis, Sturge-Weber,
a Begins in childhood, progressive seizures,
Dyke-Davidoff-Mason
hemiparesis, cognitive deterioration o Deep white matter: Granulomatous
• Kernicterus angiitis, intravascular lymphoma,
o Globus pallidus, hippocampi, substantial
Hashimoto, multiple sclerosis,
nigra & dentate nuclei, T2 & T1 arteriolosclerosis
hyperintensity a Basal ganglia: Kernicterus, hypoxia, West
o Encephalopathy due to deposition of
Nile, Leigh, Wilson
unconjugated bilirubin
CADASIL
I
=
Axial FLAIR MR shows hyperintensity in the subcorUcal
white matter of the anterior temporal lobes typical of
Axial T2WI F5 MR shows extensive confluent frontal
white matter hyperintensity in this 57 year old woman.
5
CAOASft along with periventricular lesions in this 32 The extensive, confluent involvement is atypical for
year old woman. chronic hypertensive change or MS.
77
MUlTIPLE BRAIN HYPERINTENSITIES (T2/FlAIR), RARE BUT IMPORTANT
ell
E
>-
J:: Neurosarcoid Neurosarcoid
U
C (Left) Axial FLAIR MR shows
~
Q)
unusual signal abnormality
ell
(L along the corpus callosum
c m caudate nucleus, a
ell
~
[!J =-
thickened septum
pellucidum & bilateral
..
C parieto-temporal white
III mailer. (Right) Coronal T1
[!J C+ MR shows enlargement
"C of the choroid plexus I:] &
c enhancement in the
III
cerebellum. The left
convexity lesion has typical
pial-leptomeningeal
enhancement with extension
into the parenchyma ~ via
perivascular spaces.
Granulomatous Angiitis
multiple confluent
hyperintensities in the frontal
& parietal white matter that
extend into the gyri but spare
the immediate juxtacortical
white maller = related to
Ilashimoto encephalopathy
(Rigl1t) Axial T2WI MR show
confluent while matter
hyperintensity primarily
affecting the (rontallobes
with smaller regions on the
right posteriorly. Old
hemorrhage in the right
hemisphere I:] suggests
vasculitis.
Lyme Disease West Nile Encephalitis

(Left) Axial fLAIR MR shows
small white maller
hyperintensity in the deep,
peripheral, & juxtacortical
white malter. The scattered
peripheral nature with small
foci is typical for Lyme
disease. (Right) Axial FLAIR
MR shows multiple
hyperinlensities surrounding
the red nuclei !:ll & in the
basal ganglia 1:]. The
combination of basal ganglia
& midbrain involvement is
lypical for a viral
encephalitis, in this case due
to West Nile virus.
I
5
78
MUlTIPLE BRAIN HYPERINTENSITIES (T2/FlAIR), RAREBUT IMPORTANT en
'c":
III
:3
..
C.
lXl
III

:3
shows typical limbic
encephalitis involving the
medial temporal lobes =:I &
right insular cortex PJ:I. This
mimics herpes encephalitis,
but lack of hemorrhage as
we/J as cingulate
involvement (not shown)
favors limbic encephalitis.
shows multiple, poorly
marginated, (.f/.- confluent
hyperintensilies in the
periventricular, deep, &
peripheral white mailer =:I
with an outwardly radiating
pattern seen in lymphoma.

disproportionate cerebellar
=:I & pontine atrophy with
cruciform T2 signal within
t.he lower pons, the" hot
cross bun" sign E±I
characteristic for OPCD.
Note the normal
supratentorial brain. (Right)
Axial T2WI MR shows
subcortical white maller
hyperintensities III which
have ill-defined margins &
spare the cortex. This is
atypical for MS or stroke.
SSPEusually ocwrs after a
clinically silent period of
months to years.
Rasmussen Encephalitis Kernicterus

(Leh) Axial T2WI MR shows
ill-defined whit.e matter
hyperintensities in the {rontal
lobe within a larger
region of striking atrophy of
the frontal & parietal lobes.
Rasmussen encephalitis.
I-femicranium hypoplasia of
Dyke-Davidoff-Mason &
cortical hypointensity of
Sturge-Weber are absent.
shows abnorrnal
hyperintensity in the
hippocampus =:I & globus
pallidi PJ:I in a patient with
age·appropriale immature
myelin. I
5
79
MULTIPLE HYPOINTENSE FOCI ON 12
ro DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses

E • Lymphoma
£
>- Common
() o Both primary & secondary CN5 lymphoma
C • Neoplasm
~ o Lymphoma
may present as intermediate 51masses
ro
CL
o Metastases, Parenchymal
• PCN5L often limited to brain
c parenchyma
ro
~ o Multifocal Glioma
co • Atypical Infection • 5CN5L more likely to involve
r::
o Bacterial (TB, Nocardia)
leptomeninges, dura, bone
ell
~ • Metastases, Parenchymal
III o Fungal Diseases
o Highly cellular, non-necrotic metastases
"'C
r:: o Toxoplasmosis, Acquired
ell o Breast & lung mets often T2 intermediate
Less Common • Atypical Infection
• Neurosarcoid o Pyogenic abscesses typically have central t
• Neoplasm-like Conditions 51on T2WI because of pus
o Post-Transplant Lymphoproliferative o Atypical non-pyogenic "abscesses" often
Disorder (PTLD) have intermediate 51on T2WI
o Lymphomatoid Granulomatosis • In TB, due to caseous material
• Fungal: Due to absence of pus,
ESSENTIAL INFORMATION concentration of paramagnetic ions
• Toxo: May show "eccentric target sign"
Key Differential Diagnosis Issues o Variable reduced diffusion
• These lesions show mild T2 hypointensity or
"intermediate" signal intensity (51) Helpful Clues for Less Common Diagnoses
o Lesions are often isodense or mildly
• Neurosarcoid
o Parenchymal nodules & masses often
hyperdense to gray matter (GM) on CT
• Lesions in this ddx often associated with intermediate T2 51due to high cellularity
o Look for dural/leptomeningeal disease
vasogenic edema & "bright" on T2/FLAIR,
but are centrally iso- or hypointense to GM • Post-Transplant Lymphoproliferative
• Neoplasms included are generally small Disorder (PTLD)
o Parenchymal lesions resemble lymphoma
round blue-cell tumors (e.g., lymphoma) or
highly cellular metastases with high • Lymphomatoid Granulomatosis
o Rare lymphoproliferative disorder
nuclear-to-cytoplasmic ratio
o Typical: Punctate & linear enhancement
• DWI variable; may be mildly reduced due to
o Large coalescent nodules T2 intermediate
t cellularity of some of these lesions
I
5 Axial T2WI MR shows multiple brain parenchymal
masses lID with intermediate SI & variable associated
Axial T2WI MR shows multiple lesions with associated
vasogenic edema. The 2 posterior lesions 1:.1 show fairly
vasogenic edema. The lesions enhanced intensely 8.. homogeneous intermediate 51, while the left frontal
homogeneously- typical of primary eNS lymphoma. lesion I:i.'.l has a rim of low SI.
80
MULTIPLE HYPOINTENSE FOCI ON 12
III
::l
a.
[ll
.,
III
Multifocal Glioma
(Left) Axial T2WI MR shows ::l
areas of vasogenic edema in OJ
the right frontal & left OJ
temporal lobes, with central ::J
intermediate 51 ~ & \J
.,
OJ
associated mass effect The CD
T2 hypointense central ::J
()
masses enhanced ::T
'<
post-gadolinium. (Right) 3
Axial T2WI MR shows OJ
multiple lesions that are Gl

intermediate in 5/ I:] & CD
::J
associated with vasogenic <ll
.,
edema. These lesions ~
showed ring enhancement.
This patient had evidence for
pulmonary TB as well as
epididymo-orchitis.
Fungal Diseases
multifocallesions =
with
intermediate 51centrally &/or
involving the rim with
significant vasogenic edema.
Blood cultures were positive
for Nocardia, a gram-positive
bacillus, in this
immunocompromised
patient. (Righi) Axial T2WI
MR shows multiple centrally
T2 hypointense lesions 1::1
with associated vasogenic
edema. Only minimal
enhancement was seen, &
this patient with
disseminated aspergillosis
was severely neutropenic.

multiple intermediate 5/
lesions =with associated
edema & mass effect in an
HIV+ man. The lesions
enhanced post-gadolinium.
shows mass-like areas of
intermediate Sllissue &
adjacent 10 the lateral
ventricles & involving the
choroid plexus. These
masses enhanced intensely
post-gadolinium. Confluent
areas of increased 51
surrounding the temporal
horns are consistent with
transependymal flow of C5F. I
5
81
~
ell MUlTIPLE HYPOINTENSE FOCI ON GRE/SWI
Q)
c
Q)
<.9 Predominate in basal ganglia, thalami,
ell
DIFFERENTIAL DIAGNOSIS o
E brainstem (esp. pons), cerebellum
>.
.!:
Common • Cerebral Amyloid Angiopathy (CAA)
u
C
Q)
• Chronic Hypertension o Usually affects age> 6S years unless
~ • Cerebral Amyloid Angiopathy (CAA)
ell familial
0..
c • Diffuse Axonal Injury (DAI) o Lesions predominantly juxta-cortical,
~
ell • Metastases, Parenchymal cerebellar
co • Pneumocephalus o Relative sparing of deep gray nuclei,
C
lU
~ Less Common brainstem
co • Vascular Malformations o May coexist with HTN changes &
"0
c o Cavernous Malformation, Multiple Alzheimer disease
lU
o Multiple Micro-Arteriovenous o Often accompanied by moderate to severe
Malformations small vessel ischemic changes in
• Infections hemispheric white matter (WM)
o Neurocysticercosis • Diffuse Axonal Injury (DAI)
o Tuberculomas o Classic triad: Lobar WM, corpus callosum,
o Fungal Diseases dorsolateral brainstem
o Septic Emboli o History of severe head injury with
• Vasculitis acceleration-deceleration mechanism
• Vasculopathy o Often associated with cerebral contusions,
• Radiation and Chemotherapy EDH/SDH, SAH, IVH
o Radiation-Induced Telangiectasia • Metastases, Parenchymal
o Mineralizing Microangiopathy o Classically hemorrhagic mets: Melanoma,
thyroid carcinoma, renal cell carcinoma,
Rare but Important choriocarcinoma
• Coagulopathy o Lung & breast cancer so prevalent, account
• Leukemia for many cases of hemorrhagic metastasis
• Metastatic Atrial Myxoma o Hemorrhage may be seen at presentation
• Devices and Complications or following treatment
• Pneumocephalus
ESSENTIAL INFORMATION o Obvious on CT, can be confusing on MR
o Often high signal edge surrounding low
Key Differential Diagnosis Issues signal center, suggesting artifact
• NECT may help with differential diagnosis o Seen post-trauma, post-surgical, CSF leak,
o Air black on CT, calcification (Ca++) dense,
spinal intervention
hemosiderin staining not appreciable
• GRE/SWI susceptibility generally greater for Helpful Clues for Less Common Diagnoses
hemosiderin than for Ca++ • Vascular Malformations
• Distribution of GRE/SWI hypointensities o Cavernous Malformation, Multiple
o CAA typically peripheral/subcortical, while • Occur both supra- & infratentorially
hypertension (HT ) changes are central • Autosomal dominant inheritance pattern
o Subarachnoid involvement suggests • Not associated with developmental
pneumocephalus, cysticercosis venous malformation
• Gadolinium enhancement o Multiple Micro-Arteriovenous
o eoplasm & infection generally enhance, Malformations
whereas CAA, HTN changes, DAI do not • Occur in setting of HHT
• Associated with vascular shunts & AVMs
Helpful Clues for Common Diagnoses in other organ systems
• Chronic Hypertension • Infections
o Increased prevalence of GRE/SWI
o Neurocysticercosis
I hypointensities related to "microbleeds" • Stage 4 lesions (chronic, healed) present
as punctate & rounded Ca++ on CT
5
82
MULTIPLE HYPOINTENSE FOCI ON GRE/SWI CIl
r::
""
• Variable hypointensity on GRE Helpful Clues for Rare Diagnoses

o Tuberculomas
• Coagulopathy
• Active lesions: Often central intermediate o May cause hemorrhage into underlying
Sl on T2WI lesions (metastasis, CAA)
• Treated lesions: Often calcified, GRE/SWI o "Spontaneous" hemorrhage may also occur
hypointense
• Leukemia
• Often present with TB meningitis o Microhemorrhages may indicate blast
o Fungal Diseases
crisis
• Invasive fungal infection is associated • Metastatic Atrial Myxoma
with multifocal brain parenchymal o "Oncotic" aneurysm may lead to SAH,
hemorrhage parenchymal hematoma, or Gl
• Usually seen in severely microhemorrhages
C1l
:J
imm unocompromised patients • Devices and Complications
C1l
~
III
o Septic Emboli
o Cardiac valves; cardiopulmonary bypass
• Associated with multifocal infarction, • Patients who have been on bypass pump
often hemorrhagic often have nonspecific punctate GRE
• May result in microabscesses hypointensities
• Vasculitis o Coils, methacrylate, other foreign
o Brain micro hemorrhage may be due to materials
primary or secondary CNS vasculitis • Aneurysm clips & coils usually cause GRE
• Vasculopathy hypointensity outside & at base of brain
o Small vessel vasculopathy (e.g., CADASIL • Coiling of more peripheral aneurysms
or sickle cell disease) is associated with may lead to signal loss that appears to be
cerebral microbleeds & hemorrhage parenchymal
• Radiation and Chemotherapy • Embolic material in AVM
o Brain radiation is associated with
formation of multiple telangiectasias Alternative Differential Approaches
• Distribution conforms to radiation port • Patient's age
• Increase over time o Older patient: CAA, HTN changes,
o Chemotherapy metastatic disease, infection
• In combination with radiation may lead o Younger patient: DAl, infection, familial
to mineralizing microangiopathy vascular malformations, iatrogenic
• Dense Ca++ on CT, variable loss of signal
on GRE/SWI
I
=-
Axial T2 CRE MR shows multiple hypointense foci in
the central pons a characteristic location for
Axial T2' CRE MR more superiorly in the same patient
shows characteristic hypertensive microhemorrhages in
5
hypertensive microhemorrhages. This patient also had a the thalami and basal ganglia =::I, as well as the remote
remote lobar hemorrhage Ei:I. right temporal hematoma Ei:I.
83
co
~ MUlTIPLE HYPOINTENSE FOCI ON GRE/SWI
Q)
c
Q)
(9
co
E
>-
.r: Cerebral Amyloid Angiopathy (CAA)
u
c (Left) Axial T2' CRE MR in a
=
Q)
~ patient with a right frontal
co
c.. lobe hematoma shows
c innumerable
co
~ microhemorrhages located
IJ) predominantly in the
periphery of the brain. This
patient also has small vessel
ischemic changes in the
cerebral while maller.
shows that amyloid
cerebellum =
angiopathy may involve the
but typically
spares the brainslem. In this
case cerebellar involvement
is mild, 8, the supratentorial
involvement is severe.

shows multiple punctate foci
of low signal intensity in the
bifrontal parasagittal white
matter =. This distribution
is typical of OAI. The frontal
lobes are often preferentially
effected. (Right) Axial T2'
CRE MR shows multiple foci
of susceptibility = in a
patient with lung cancer
metastases. Even if
metastases are not initially
hemorrhagic, they may
hemorrhage after treatment
8, mimic pathology such as
amyloid angiopathy.
Pneumocephalus
shows multiple rounded foci
of low signal intensity = in
the subarachnoid space
(SAS). The patient had IVH
E::I & recent posterior fossa
craniotomy. The round
shape of the lesions, their
"shiny" periphery, 8, their
SAS distribution suggest air.
shows multiple foci of low
signal intensity in the frontal
& parietal lobes. There are 2
=
dominant lesions on the left
8, punctate nonspecific
I ks0nsonther~ht~
5
84
MULTIPLE HYPOINTENSE FOCI ON GRE/SWI (JJ
"
c:
III
::l
Q.
Multiple Micro-Arteriovenous OJ
....•
Cavernous Malformation, Multiple Malformations III
::l
(Left) Axial T2WI MR in the
prior patient shows OJ
...••
"mulberry" appearance & OJ
peripheral hemosiderin ::l
-0
of one
staining
malformation = cavernous
& a
fluid-fluid level in another
OJ
...••
(t)
::l
()
1J:!lI. The punctate additional ::T
cavernous malformations are
'<
3
not seen on this FSE T2WI. OJ
(Right) Axial T2* CRE MR G)
(t)
shows several large ::l
hemorrhagic lesions in the (t)
brain = as well as multiple

punctate foci of
...••
OJ
susceptibility This HHT

patient had prior brain &
pulmonary hemorrhages.
Neurocysticercosis Fungal Diseases

shows multifocal
hypointensities scattered
throughout the sulci,
parenchyma, & ventricles.
Some of these lesions
showed ring enhancement
on T1 C+ scans, & many
were calcified on CT (not
shown). (Right) Axial T2'
CRE MR shows multiple foci
of hemorrhage along the
course of the penetrating
medullary vessels in a patient
with AML & fungal sepsis.
Autopsy confirmed
disseminated aspergillus
infection.
Vasculitis Radiation-Induced Telangiectasia

(Left) Axial T2 CRE MR
shows punctate foci of CRE
susceptibility =
in a patient
with known lupus vasculitis.
(Right) Axial T2* CRE MR
shows multiple foci of CRE
hypointensity in the brain
parenchyma =
& signal loss
due to a right cranioplasty
~. This patient had prior
radiation treatment of an
astrocytoma as well as
surgical resection of a
radiation-induced
meningioma. These lesions
are consistent with
radiation·induced
telangiectasias. I
5
85
ro
~ 11/12 HYPERINTENSE PARENCHYMAL lESIONS
OJ
c
OJ
l') • Rim "ages" faster than center
ro
E o Early subacute parenchymal hemorrhage
>.
.<=
Common • Typically 3-6 days
()
c • Intracerebral Hematoma • Contains methemoglobin within RBCs
OJ
~ • Cavernous Malformation • Tl shortening in periphery
ro
0..
c
• Cerebral Amyloid Disease • Isointense centrally
ro
~ • Profound T2 hypointensity
(JJ
less Common
• Multiple Sclerosis o Late subacute/early chronic hemorrhage
C
III
~ • Neurofibromatosis Type 1 • Cells lyse, release methemoglobin
(JJ
• Metastases, Parenchymal • Extracellular dilute free methemoglobin
"t:l
c • Cerebral Infarction, Subacute demonstrates diffuse Tl shortening, T2
III
prolongation
Rare but Important • Hematoma demonstrates hyperintensity
• Lymphoma, Primary CNS on both Tl/T2WI
• Lipoma • Develops hypointense rim
• Fahr Disease • Cavernous Malformation
o Zabramski type 1 = subacute hemorrhage
ESSENTIAL INFORMATION • Hyperintense on Tl WI
• T2 signal depends on hematoma stage
• Early subacute: Hypointense on T2WI
• Late subacute: Hyperintense on T2WI
o Zabramski type 2 = mixed signal (classic
"popcorn" ball)
• Fluid-fluid levels in multiple "caverns"
• Iso-/hyperintense on Tl WI
• Hypo-/hyperintense on T2WI
• Complete T2-hypointense hemosiderin
rim surrounds lesion
• Important: Do T2* scan (GRE/SWI) to
look for multiple lesions
• Cerebral Amyloid Disease
o Elderly normotensive demented patient
o Look for multiple parenchymal
hemorrhages of different ages
• Subacute hematomas are hyperintense
on both Tl/T2Wls
• Do T2* sequence!
• > 50% have multiple cortical/subcortical
"black dots" (micro hemorrhages)
• CAA microbleeds rare in cerebellum,
basal ganglia (typical for chronic
hypertensive encephalopathy)
o Most MS plaques are hypointense on
Tl WI, hyperintense on T2WI
o Chronic plaques may develop faint
hyperintense "ghost" or "rim" on Tl WI
that surrounds hypointense lesions
I o Deep periventricular white matter most
common location
5
86
11/T2 HYPERINTENSE PARENCHYMAL lESIONS ,..
en
r::
• Neurofibromatosis Type 1 a CNS lipomas are congenital

a Bilateral basal ganglia hyperintensity malformations, not neoplasms
common in NFl a Typically located in subpial space along
a Foci of abnormal signal intensity ("FASIs") brain surfaces
on T2WT represent myelin vacuolization, a On standard spin-echo imaging, fat is
clumping, disappear with age hyperintense on Tl WI, hypointense on
• Metastases, Parenchymal T2WI
a Most are iso-/hypointense on Tl WI a Because of ]-coupling, lipomas are
a T2 signal intensity variable hyperintense on both Tl and T2-weighted
a Metastases with subacute hemorrhage or fast spin echo scans
melanin may display Tl shortening a Look for chemical shift artifact
G)
• Cerebral Infarction, Subacute a To confirm, do fat-suppressed sequence (1)
:::l
a Hemorrhagic transformation • Fahr Disease (1)
~
Ql
• Typically occurs between 2-5 days a Also known as cerebrovascular
• Foci of punctate or gyriform Tl ferrocalcinosis or bilateral
shortening striopallidodentate calcinosis
• T2 hyperintensity typically much larger a Degenerative neurologic disorder with
• Basal ganglia, cortex most common sites extensive, typically bilaterally symmetrical
Helpful Clues for Rare Diagnoses nonarteriosclerotic calcifications
a Some cases have bizarre-appearing
hyperintensities on both Tl/T2WIs
a Classic primary CNS lymphoma is solid
corresponding to dense parenchymal
infiltrating tumor
calcifications
a Typically isointense with gray matter on
both Tl/T2WIs
a AIDS-related lymphoma
• Increasing prevalence
• Hemorrhage, necrosis common
• Hyperintense on both Tl/T2WTs
• Ring or "target" enhancement
• Lipoma
a Fat is not normal in CNS (i.e., inside
arachnoid) anywhere!
Intracerebral Hematoma
I
Axial T1WI MR showstypicaJ late subacute intracerebral
hematoma with homogeneous hyperintensity due to
Axial T2WI MR in the same patient as the previous
image shows that the hematoma remains hyperintense.
5
extracellular dilute methemoglobin.
87
<1l
~ T1/T2 HYPERINTENSE PARENCHYMAL LESIONS
Q)
c
Q)
<.9
<1l
E
>-
.r::
u
Cavernous Malformation Cavernous Malformation
c (Left) Axial T7 WI MR shows
Q)
~ mostly hyperintense left
<1l
D- parietal mass ~ with a small
c mixed signal intensity nodule
<1l
~ ~ (Right) Axial T2WI MR
co in the same patient as the
c previous image shows the
III
~ mass remains mostly
CO hyperintense on T2WI with
"t:l nodule ~ demonstrating
c typical "popcorn ball" mixed
III
signal intensity.

a subacute hemorrhage
in right temporal lobe. A
more acute left parietal
hemorrhage = is almost
completely isoimense with
brain. (Right) Axial T2WI MR
shows that subacute right
tempora/lobe hematoma
remains hyperintense to
brain while more acute left
parietal hemalOma 11Im
appears inhomogeneously
hypointense.

(Left) Axial T7 WI MR in a
MS shows multiple ovoid
white maller lesions. Lesions
are mostly hypointense, have
faint but definite "ghost-like"
hyperintense rims ~
("lesion within a lesion"
appearance). (Right) Axial
T2WI MR in the same patient
as the previous image shows
lesions are uniformly
hyperintense. Note classic
perivenous demyelinating
plaques = within prominent
I
5
88
11/T2 HYPERINTENSE PARENCHYMAL LESIONS ,..c:
Ul
III
:1
Co
...III
lJl
:1
patient with known ...
CD
Q)
metastatic melanoma shows
multiple hyperintense foci :1
= at the gray-white matter
junction. (Right) Axial T2WI
-0
...<1>
Q)
MR in the same patient as :J

o
the previous image shows ::r
'<
Jargesllesion remains 3
hyperiniense ffi Chronic Q)
hemorrhage is seen around G)

second metastasis =- <1>
:J
left-sided lesion barely visible ...
<1>
Q)
with mild edema ~.
Cerebral Infarction, Subacute

(Left) Sagittal T7WI MR in a
patient with subacute right
middle cerebral infarct
shows faint hyperintense foci
in cortex !:J indicating
hemorrhagic transformation.
(Righi) Axial T2WI MR
shows farge hyperintense
right MCA infarct~. A
small focus of more acute
hemorrhagic transformation
is seen 1m.
fLeft) Axial T7 WI MR in a
patient with HIV/AIOS
shows bilateral
inhomogeneously
hyperintense lesions in basal
ganglia, suggesting subacute
hemorrhage =. (Right) Axial
T2WI MR in an HIV/AIOS
patient shows moderately
but inhomogeneousJy
hyperintense lesions in both
basal ganglia CNS
lymphoma in
immunocompetent patients
is usually isointense with
gray matter on both
T7/T2WI.
I
5
89
~
Cll 11 HYPOINTENSE,12 HYPERINTENSE PARENCHYMAL LESIONS
Q)
C
Q)
C)
DIFFERENTIAL DIAGNOSIS • Location generally less helpful (some
Cll
E exceptions like herpes encephalitis, Fl,
>.
.r::
Common TSC, enlarged PVSs)
u
c • Enlarged Perivascular Spaces
Q)
~ • Arteriolosclerosis Helpful Clues for Common Diagnoses
Cll
(l.
• Chronic Hypertensive Encephalopathy • Enlarged Perivascular Spaces
C
• Cerebral Amyloid Angiopathy o All locations, all ages but most common in
~
Cll
co • Lacunar Infarction basal ganglia/around anterior commissure,
c
• Demyelinating Disease in midbrain, dentate nuclei, hemispheric
cu
white matter
co"- o Multiple Sclerosis
"'C o ADEM o Contain interstitial fluid; follow CSF signal
c
cu o Susac Syndrome on all sequences
• Encephalomalacia o May cause focal mass effect (expanded
o Post-Traumatic gyri, occasionally cause aqueductal
o Post-Ischemic obstruction)
• Neurocysticercosis o May look bizarre, mimic neoplasm but
• Cerebral Contusion spare cortex, do not enhance
• Diffuse Axonal Injury (DAI) • Arteriolosclerosis
o Small vessel ischemic changes
Less Common ("microvascular disease")
• Primary Brain Tumor o Scattered or confluent white matter/basal
o Diffuse Astrocytoma, Low Grade ganglia hypointensities on Tl WI,
o Anaplastic Astrocytoma hyperintense on T2WI
o Glioblastoma Multiforme o No enhancement
o Oligodendroglioma o Patients generally older, often
o Gliomatosis Cerebri hypertensive
• Metastases, Parenchymal • Chronic Hypertensive Encephalopathy
• Abscess o Look for confluent lesions around atria of
• Cerebral Amyloid Disease lateral ventricles
• Encephalitis o Do T2* (GRE or SWI) to look for
o Herpes Encephalitis microbleeds (central> peripheral)
o Encephalitis (Miscellaneous) • Cerebral Amyloid Angiopathy
• Cerebritis o Elderly normotensive demented patients
• Vasculitis o Hemorrhages of different age, peripheral
• Neurofibromatosis Type 1 microbleeds on T2*
• Tuberous Sclerosis Complex • Demyelinating Disease
Rare but Important oMS> > ADEM
• Neurosarcoid • History of viral illness, recent
• Radiation and Chemotherapy immunization suggests ADEM
• Inherited Leukodystrophies (Many) o Susac Syndrome
• Rare; often mistaken for MS!
• Young to early middle-aged females
ESSENTIAL INFORMATION • Progressive encephalopathy,
Key Differential Diagnosis Issues sensorineural hearing loss, visual
• Very broad differential diagnosis symptoms
• Most parenchymal masses, benign or • "Holes" in middle of corpus callosum
malignant, are hypointense on Tl-, Helpful Clues for Less Common Diagnoses
hyperintense on T2WI • Primary Brain Tumor
• Look for presence/absence of mass effect, o Most primary brain neoplasms typically
enhancement, blooming on T2* GRE/SWI,
I diffusion restriction, etc., to help narrow
hypointense on Tl WI, hyperintense on
T2WI; may be difficult to distinguish
differential diagnosis neoplastic from nonneoplastic etiologies
5
90
T1 HYPOINTENSE,12 HYPERINTENSE PARENCHYMAL lESIONS en
"
c:
• DWI helpful (neoplasms generally don't • Temporal lobes, insular cortex

restrict; ischemia/infarction, infection • Cingulate gyrus, subfrontal cortex
typically do) o Look for "sequential bilaterality" in
• MRS helpful in some cases (t Cho) temporal lobes
o Presence/absence/pattern of enhancement o Preferentially involves cortex
helpful but often nonspecific o FLAIR,DWI most sensitive for early
o Tend to be infiltrative rather than discrete, detection
round masses o Hemorrhage with TI shortening in late
• Metastases, Parenchymal acute/subacute stages
o Tend to be round rather than infiltrative • Vasculitis
o Gray-white junction common location o Can be primary CNS or secondary to
Gl
o Almost always enhance (ring, punctate, systemic disorder CD
:J
solid) o Combination of cortical/subcortical, basal CD
~
Q)
o May cause multifocal white matter ganglia disease suggestive
hyperintensities, mimic "small vessel o Punctate/linear enhancement common
disease" • Neurofibromatosis Type 1
o Difficult to detect or differentiate from o Foci of abnormal signal intensity best seen
vascular disease without contrast on T2WI, FLAIR
• Abscess o Hypointensities on TI WI less common;
o Early cerebritis stage can be difficult to basal ganglia may have hyperintensity
distinguish from ischemia, neoplasm o Typically represent myelin vacuolization,
o Late cerebritis to late capsule stages show not demyelination; are transient (rarely
ring enhancement seen in adults)
o DWI restriction at all stages typical o No enhancement; if present, suggests
o MRS often shows lactate, amino acid peaks possibility of astrocytoma (usually
• Cerebral Amyloid Disease pilocytic)
o Can be multifocal, diffuse (amyloid • Tuberous Sclerosis Complex
angiopathy) o Cortical/subcortical tubers hypointense on
• Do T2* (GRE/SWI) to detect micro bleeds TI, hyperintense on T2WI (similar signal
• Peripheral> central (basal ganglia) to WM lesions of NFl)
o Lobar (hemorrhages of different ages) o Look for other stigmata of TSC (e.g.,
o Mass-like ("amyloidoma" rare) subependymal nodules, lesions along
• Herpes Encephalitis radial glial bands)
o Affects limbic system
Enlarged Perivascular Spaces Arteriolosclerosis
I
Axial T2WI MR shows bizarre va,iable-sized
hyperintense white matter cysts with gyral expansion
Sagittal TI WI MR in a patient with clinical diagnosis of
Binswanger vasculaNype dementia shows mu/tjfocal
5
cortical sparing lesions followed CSFon TI WI, did discrete and confluent lesions in subcortical, deep
not enhance. perivent/ieu/ar white maller _
91
T1 HYPOINTENSE,12 HYPERINTENSE PARENCHYMAL lESIONS
co
E
>.
.s::
u
c (Leh) Axial T2WI MR shows
•...
Q)
several types o( T2
co
0.. hyperintense lesions:
c Chronic hypertensive
co
•... encephalopathy (typically
[]:J periatrial changes) 1C>1
c lacunar infarcts [;>1
•...
l'Cl prominent perivascular
aJ spaces ffi (RighI) Axial
"'C T2WI MR shows multifocal
c hyperintensities in
= =.
l'Cl
subcortical white matter
Presence of acute
chronic 81 hemorrhage plus
peripherallocalion is
characteristic for CAA.
(Lefl) Sagittal T7 WI MR in
this patient with known MS
shows deep perivenlricular
hypointense lesions oriented
perpendicular to the
ventricular margin These
lesions are perivenular
demyelinating MS plaques.
shows discrete, ill-defined
hypointense foci ~ in a
patient with a history of
recent viral illness. Many
additional lesions were
present on fLAIR, T2WI.
Susac Syndrome Metastases, Parenchymal

(Lefl) Sagittal T7 WI MR
shows multifocal
hypoinlensilies in the middle
of the corpus callosum I:] in
this 31 year old man with
encephalopathy,
sensorineural hearing loss,
visual symptoms. (Courtesy
P. Rodriguez, MO). (RighI)
Axial T2WI MR in a patient
with decreasing mental
status shows mulliFocal white
maller hyperinlensilies lID.
Severa/lesions enhanced
with contrast. Breast
carcinoma was found on
I
Further evaluation.
5
92
11 HYPOINTENSE,12 HYPERINTENSE PARENCHYMAL lESIONS
III
::l
Co
..,
OJ
III
::l
(Left) SagiLral T1 WI MR in
polydrug abuser shows 2 ..,
IJl
inhomogeneously tlJ
hypointense lesions
enhanced slrongly with
= that ::J
\J
contrast and showed
..,
tlJ
C1l
reSlriction on DWI. (RighI) ::J
()
Axial T1WI MR shows diffuse :::r
cortical swelling,
'<
hypointensity = in left
temporal lobe with less
3
tlJ
Gl
prominent involvement of C1l
::J
right temporal lobe SI. ..,
C1l
Bilateral disease suggests tlJ
herpes encephalitis.
Cerebritis Vasculitis
(Lefl) Axial T1 WI MR in a 16
yo with headache, nausea
developing 2 weeks after
URI shows in homogeneously
hypointense mass in right
temporal lobe T1 C+
scan (nol shown)
demonstrated poorly
delineated enhancing rim
characteristic for early
cerebritis stage of abscess.
shows hyperintense basal
ganglia, thalami in this young
female patient with known
systemic lupus
erythematosus and probable
SLE vasculitis.
(Lefl) Axial T1 WI MR shows
=-
an optic chiasm astrocytoma
hypointense foci in pons
[;8 Pontine lesions were
hyperintense on T2WI.
(RighI) Axial T1 WI MR
shows a large, flat gyri with
hypointense juxtacorlical
lesions in muflipfe tubers
and white matter, as well as
numerous calciried
hyperintense subependymal
nodules ffi Subcortical
lesions were hyperintense on
T2WI, fLAIR.
I
5
93
~ 11/12 IsOINTENsE PARENCHYMAL lESIONS
Q)
c
Q)
c.9 • Look for "dot sign" (intravascular high

l\l
E signal intensity caused by occlusion/slow
>-
.c Common flow)
u
c • Cerebral Ischemia-Infarction, Hyperacute • Found in 10% of patients with acute
~
Q)
• Intracerebral Hematoma (Hyperacute)
l\l stroke
Cl..
C
• Capillary Telangiectasia • Intracerebral Hematoma (Hyperacute)
l\l
~ • Developmental Venous Anomaly o Clot contains intracellular
co • Meningioma oxyhemoglobin, which is diamagnetic
C
ltl less Common o Although hyperacute clot can be
~
co • Metastases, Parenchymal isointense on Tl WI, most hematomas are
"'0
C • Lymphoma, Primary CNS inhomogeneous, often hyperintense on
'" Rare but Important
T2WI
• Capillary Telangiectasia
• Neurosarcoid o Can be anywhere
• Heterotopic Gray Matter • Pons, medulla> supratentorial cortex,
• Tuber Cinereum Hamartoma white matter
• Tuberous Sclerosis Complex o Imaging
• Cerebral Infarction, Subacute • Unless unusually large, typically invisible
on Tl/T2WI
ESSENTIAL INFORMATION • Use T2* sequence (become hypointense
on GRE, SWI)
• Tl C+ shows "brush-like" enhancement
• May see tiny central draining vein within
lesion
o Most common cerebrovascular anomaly
o Imaging
• If small, often invisible on Tl/T2WI
• Larger DVAsmay have discernible flow
void or flow-related enhancement
• If slow flow in "Medusa head" (medullary
veins), may become hypointense on T2*
(GRE/SWI)
• Best seen on Tl C+
• Meningioma
o Not truly a parenchymal lesion although
some may invaginate into brain
o Included because often isointense to
cortex, difficult to detect on nonenhanced
TlWI, T2WI
o Look for signs of extra-axial location
• Gray-white matter "buckling"
• CSF-vascular "cleft"
o Most enhance on Tl C+

• Metastases, Parenchymal
o Most hyperintense on FLAIR,T2WI
o Gray-white matter junction distortion
• Few are isointense on both Tl/T2WI
I • Most (not all) have detectable edema
5
94
T1/12 ISOINTENSE PARENCHYMAL lESIONS (J)
""c:
III
• Look for subtle alteration in gyral shape, o Beware: Masses of heterotopic gray matter :l
Co
sulcal effacement can distort ventricle, mimic tumor!
• Tuber Cinereum Hamartoma
..•
OJ
o Most enhance III
:l
• Lymphoma, Primary CNS o Typical clinical presentation
o Hypercellular tumor, high • Young male with isosexual precocious ..•
OJ
III
nuclear:cytoplasm ratio puberty :J
-u
• Isointense (cortex, basal ganglia) on both • Gelastic seizures III
CD
Tl/T2WI o Imaging :J
()
• Hemorrhage, necrosis rare unless • > 90% isointense with cortex on all ::T
'<
HIV/AIDS sequences 3
III
o Look for anatomic distortion of deep • 10% cystic, slightly hyperintense on PD, GJ
periventricular structures FLAIR,T2WI ct>
:J
• Tuberous Sclerosis Complex ct>
~
o Almost always enhances III
o Cortical "tubers"
• Thickened gyri
• Neurosarcoid
• "Blurred" gray-white interface
o Can be anywhere, look like almost
• Mostly isointense with cortex,
anything!
occasionally hyperintense
o Dural-based masses> > parenchymal
o Subependymal nodules
lesions
• Mostly isointense with white matter
o Infiltration along perivascular spaces -
• Variable, often heterogeneous intensity if
parenchymal masses
densely calcified
o Isointense on Tl WI
• May enhance on Tl C+
• Typically hyperintense on T2WI, FLAIR
• If enhancing SEN at foramen of Monro,
• Exception: Lesions in infundibular stalk
surveillance to watch for giant cell
usually isointense on all sequences
astrocytoma warranted
o Enhance strongly, sometimes
• Cerebral Infarction, Subacute
heterogeneously
o Imaging
• Heterotopic Gray Matter
• 10 days to 2 weeks after ictus
o Isointense to cortex on all sequences, no
• MR "fogging effect" may render stroke
enhancement
isointense on Tl/T2WI
o Can be cortical, subcortical white matter,
• DWI may pseudonormalize
subependymal
• Lesion typically enhances
Cerebral Ischemia-Infarction,
Hyperacute Intracerebral Hematoma (Hyperacute)
I
Axial T2WI MR shows very subtle focus of white matter
hyperintensity in right posterior frontal lobe ~ tI,at is
Axial T7WI FS MR in a patient with AML, acute clinical
deterioration with normal NEeT minutes before this
5
isointense with gray maHer. OWl showed anterior MCA scan shows left frontal lesion ~ isointense with cortex.
division infarct. T2W/showed expanding hematoma. 95
ro
~ 11/12 ISOINTENSE PARENCHYMAL LESIONS
Q)
c
Q)
o
ro
E
>-
.r:
()
Developmental Venous Anomaly
~ no discernible abnormality.
ro
0... T2' CRE scan (not shown)
c disclosed hypointense
ro
~ pontine lesion with
CO "brush-like" enhancement
c following contrast
~ administration. Most
'"
CO capillary telangiectasias are
"tl not detectable on either T1
c or T2Wls. (RighI) Axial T1 WI
ro
MR shows flow void of
OVA transmantle draining
vein. Enlarged medullary
radicles constituting OVA ~
are almost invisible but
enhanced strongly on T1 C+
scan.
left parietal sulcal effacement
by an isointense, dural-based
mass ~ (RighI) Axial T1 WI
MR in a patient with known
metastatic breast cancer
shows expansion of left
posterior frontal gyri by
mass that is so completely
;sointense with brain that it
can't be identified separately
from surrounding normal
parenchyma.

corpus callosum thickening
and expansion by an=
;sointens€ mass that
demonstrated strong
homogeneous enhancement
(not shown). Primary CNS
lymphoma was documented
on stereotaxic biopsy. (RighI)
Axial T2WI MR in the same
patientas previous image
shows corpus callosum
splenium lesion remains
mostly isointense with cortex
but is slightly hyperintense to
I white maller. Adjacent

edema Ell is hyperintense.
S
96
11/12 ISOI NTENSE PARENCHYMAL lESIONS en
"
c:
III
:l
Co
OJ
.,
III
Heterotopic Gray Malter Heterotopic Gray Malter
:l
extensive bilaleral OJ
.,
subependymal nodules of OJ
:l
heterotopic gray mailer 8
that are isointense with lJ
.,
OJ
cortex. (RighI) Axial T2WI (1)
MR in the same patient as :l

()
the previous image shows :r

'<
the nodules of heterotopic 3
gray maller .:= remain OJ
isointense with cortex. G)

(1)
:l
.,
(1)
OJ
Tuber Cinereum Hamartoma

(Left) Sagittal Tf WI MR in a
9 year old boy with
precocious puberty shows a
sessile mass =in the
hypothalamus/Jrd ventricfe
floor. (RighI) Axial TlWI MR
shows multiple cortical
tubers isointense with gray
mailer subependymal
nodules [;8 mostly isoinlense
with white maller.
Cerebral Infarction, Subacute Cerebral Infarction, Subacute

(Left) Axial Tf WI MR 2
weeks aFter right occipital
infarct shows no definite
abnormality. (RighI) Axial
as the previous image shows
only slight hyperintensity =:I
with most of the affected
cortex /lOW isoinlense with
normal brain because of T2
1/ Fogging" effect in subacute
infarction.
I
5
97
RESTRICTEDDIFFUSION
<ll
E • Cerebral Ischemia-Infarction, Acute
>.
.!:
Common
() a Abrupt clinical onset
C • Cerebral Ischemia-Infarction, Acute
~
Q)
a Occur in a vascular distribution
<ll • Abscess
a Punctate white matter (WM) lesions often
D-
c
• Empyema
<ll • Epidermoid Cyst of small vessel origin
~
co • May be clinically silent
Less Common a Venous ischemia may have increased or
• Intracerebral Hematoma mixed DWI changes; often hemorrhagic
• Diffuse Axonal Injury (DAI) • Abscess
• Encephalitis (Miscellaneous) a Restriction centrally in "cystic" or
• Meningioma ring-enhancing lesions
• Primary CNS Lymphoma a T2 hypointense rim characteristic
• Acute Hypertensive Encephalopathy, PRES a DWI restriction may be seen in bacterial,
• Creutzfeldt-]akob Disease (C]D) granulomatous, or parasitic infections
• Multiple Sclerosis (e.g., neurocysticercosis)
• Osmotic Demyelination Syndrome • Toxoplasmosis has variable DWI
• Status Epilepticus • Empyema
• Hypoglycemia a Peripheral rim enhancement typical
• Wernicke Encephalopathy a Extra-axial fluid coJJections that restrict are
usually pus-filled
ESSENTIAL INFORMATION • Mimic: Extra-axial hematomas
• Epidermoid Cyst
Key Differential Diagnosis Issues a Lobular extra-axial mass follows CSF
• Clinical history can help differentiate intensity except on FLAIR& DWI
between various etiologies: Infection, stroke, a DWI (usually markedly bright) is more
and neoplasm specific than FLAIR(may be bright or
• Morphology &/or location useful subtle "dirty CSF"); both show increased
a Vascular distribution or wedge-shaped: signal relative to CSF
Ischemia a Cholesteatoma of middle ear or petro us
a Round "cystic" T2 hyperintense lesions: apex histologically same & DWI bright
Abscess, septic emboli (thin slice DWI helpful)
a Solid intermediate-low signal T2 round
lesions: Solid ce]Jular masses (e.g., Helpful Clues for Less Common Diagnoses
lymphoma, metastases, meningioma) • Intracerebral Hematoma
a DWI signal variable; bright or "black"
a Extra-axial cyst: Epidermoid
a Conventional Tl/T2 sequences & clinical
(cholesteatoma in temporal bone)
a Central pontine &/or deep nuclei:
history help to distinguish
a GRE sequence may clarify (susceptibility
CPM/EPM, deep venous ischemia, PRES
• Degree of DWI hyperintensity is useful reflects blood products in most stages of
a Subacute & evolving strokes have less
hemorrhage evolution except early
intense DWI brightness as cytotoxic hyperacute)
changes fade over time & are replaced by • Diffuse Axonal Injury (DAI)
a Classic locations: Gray-white junction,
progressively increasing vasogenic edema
a Hypoperfusion infarcts usually have less deep WM, corpus callosum, brainstem
a Typically bright on DWI
intense DWI brightness
a Other useful sequences: FLAIR,GRE, SWI
a Inflammatory/infectious causes for
diffusion restriction are characteristically • Some foci appear only on some MR pulse
less hyperintense than acute stroke sequences
I • Check ADC map to confirm true restriction! • DAI may be hemorrhagic or
nonhemorrhagic
a Trauma history
5
98
RESTRICTED DIFFUSION
• Encephalitis (Miscellaneous) • Osmotic Demyelination Syndrome

o DWI signal is variable: Increased, mixed, or o May restrict acutely
decreased o Classic locations (pons, BG) & clinical
o Bright DWI signal is usually less intense picture diagnostic
than seen with acute ischemia & abscess • Status EpiIepticus
o T2 hyperintense lesions o DWI restriction occurs in the
• Meningioma acute-subacute phases, involving cortex &
o Mild restriction common due to cellularity hippocampi most commonly
o Enhancing extra-axial mass o Usually a patient in status for prolonged
• Primary CNS Lymphoma time period (often 24+ hours)
o Often DWI bright due high cellularity • Hypoglycemia G)
o Periventricular location & homogeneous o Bioccipital, parietal lesions typical Cl>
:J
Cl>
enhancement typical o Clinical history usually confirmatory ~
0>
• Acute Hypertensive Encephalopathy, • Wernicke Encephalopathy
PRES o Restriction in/around 3rd ventricle &
o T2 hyperintensity in posterior circulation midbrain
bilaterally in a hypertensive patient o Mamillary body, medial thalamus,
o Usually doesn't restrict on DWI!! hypothalamus, & periaqueductal gray
• Vasogenic edema (t diffusion) > > bilateral T2 hyperintensity &
cytotoxic edema (restricted diffusion) enhancement
• If DWI restriction present - poor Other Essential Information
prognosis (indicating progression to • Round foci of DWI restriction that resemble
infarction) abscess MUST be correlated with
o Critical to assess ADC to separate the 2
conventional MR images
components, both may be present o Homogeneously enhancing solid masses
• Creutzfeldt-Jakob Disease (CJD) that restrict are usually cellular neoplasm
o DWI restriction in basal ganglia (BG),
• Especially if relatively T2 iso- to
thalami ± cortical ribbon (esp. insula) hypointense
o DWI hyperintensity increases over time
o Densely cellular tumors can restrict (due to
o Older patient with rapidly t dementia
high nuclear:cytoplasmic ratio)
• Multiple Sclerosis • Lymphoma, PNET, medulloblastoma;
o Demyelination rarely causes restriction
some metastatic diseases, meningioma
o Most show increased diffusion on ADC
o Callososeptallesions characteristic
Cerebral Ischemia-Infarction, Acute Cerebral Ischemia-Infarction, Acute
I
Axial OWl M R shows
poste,ior temporal region
restriction in the caudate &
=::I related to acute middle
Axial OWl MR shows high signal
Labbe thrombosis & venous
=::I
ischemia.
due to vein of
OWl in acute
5
cerebral artery ischemia with involvement of the venous ischemia more commonly demonstrates
lenticulostriate arteries. vasogenic or mixed vasogenic & cytotoxic edema.
99
~ RESTRICTED DIFFUSION
<IJ
c
<IJ
<.9
ell
E
>-
.s::: Abscess Empyema
u
c (Left) Axial OWl MR shows
<IJ
~ central restriction within a
ell
ring·enhancing left parietal
0...
c lesion =.. consistent with
~ abscess. This abscess was
CI) complicated by
c intraventricular rupture and
ell
~ ventriculitisa which has a
1IJ poor prognosis. (Right) Axial
't:l OWl MR shows restriction in
c bifrontal epidural fluid
III
collections =::I related 10
empyemas, a complication
of this patient's frontal
sinusitis. Epidural
hematomas may have a
similar imaging appearance.
Epidermoid Cyst Diffuse Axonal Injury (DAI)

(Left) Axial OWl MR shows
classic findings of markedly
restricted diffusion within an
anterior to the medulla =-

extra-axial cystic structure
consistent with epidermoid.

An arachnoid cyst, a mimic
on conventional imaging,
would show dark CSF signal
on OWl MR. (Right) Axial
OWl MR shows a typical
case of OAI involving the left
thalamus =::I & right
temporal deep white maller
near the gray-white matter
junction 81. CRE or SWI
may show additional OAI
foci.
Encephalitis (Miscellaneous) Primary CNS Lymphoma

(Left) Ax;al OWl MR shows
increased signal in the
medial left temporal lobe =:I
in this 25 year old with
herpes encephalitis. Herpes
encephalitis typically
involves the gray matter of
the limbic system & is
bilateral, but asymmetric.
(Right) Axial OWl MR shows
restricted diffusion in a
parenchymal & dural-based
left anterior temporal mass
=:I in this patient with
secondary Nt-Ii. Both
primary & secondary
lymphoma may show OWl
I restriction.
5
100
RESTRICTED DIFFUSION (JJ
"
c:
Acute Hypertensive Encephalopathy, Acute Hypertensive Encephalopathy,

PRES PRES
posterior circulation
bilaterally =:I in this patien!
with known PRES. The
presence 01 cytotoxic edema
in PRESindicates a poor
prognosis and usually reflects
irreversibly infarcted tissue.
Conlirmation with AOC
maps is important, however. Gl
(Right) Axial AOC shows CO
:J
mixed difFusion CO
~
Ql
characteristics, with areas of
(bright) vasogenic edema 8lI
& (dark) cytotoxic edema 1:::1
in the same patient as the
previous image.
Creutzfeldt-Jakob Disease (CJD) Multiple Sclerosis

(Lelt) Axial OWl MR shows
increased signal without
caudate nuclei =-
mass effect involving the
typical 01
CIO. Symmetric involvement
01 the caudate & putamen is
more common than
involvemen! 01 the globus
pallidus or thalamus. (Right)
Axial OWl MR shows a
presumed acutely restricting
plaque =:I in a young patient
with known MS and recent
exacerbation. These focaf
lesions may be dillicult to
differentiate from acute
ischemia.
Osmotic Demyelination Syndrome Status Epilepticus

acute restriction = in the
central pons in this patient
with a rapid correction of
hyponatremia. Central
pontine myelinolysis may
show restricted diffusion &
enhancement in the acute
selling. (Right) Axial OWl
MR shows mild dilluse linear
hyperintensity along the lelt
parietal and temporal cortex
= in this patient with status
epilepticus. These MR
changes may resolve
completely or result in mild
regional atrophy. I
5
101
ro
~ 11 HYPERINTENSE PARENCHYMAL LESION(S)
Q)
c
Q)
<.9 a Melanin
ro
E a Hypoxic-ischemic injury as well as
>-
.<::
Common nonhemorrhagic cerebral infarction
u
c • Mineral Deposition a Remyelination/hypermyelination
~
Q)
a Physiologic Calcification a Macrophage infiltration
ro
0..
a Trace Element Deposition • Phagocytosis, paramagnetic free radicals
c
ro
~ • MR Artifacts, Flow-Related
OJ Helpful Clues for Common Diagnoses
• Intracerebral Hematoma (Late Subacute)
C • Mineral Deposition
ltl Less Common a Bilateral, symmetrical
"-
OJ
"0
• Multiple Sclerosis a Basal ganglia most common location
c • Metastases • MR Artifacts, Flow-Related
ltl
• Cerebral Amyloid Disease a Look for propagation across image
• Cavernous Malformation a Entry phenomena, phase artifact
• Neurocutaneous Syndromes • Intracerebral Hematoma (Late Subacute)
a Neurofibromatosis Type 1 a Age-related causes
a Tuberous Sclerosis Complex • Young patients: Vascular malformation,
Rare but Important neurocutaneous syndrome, blood
• Hypoxic-Ischemic Injury dyscrasias, metabolic disorders
a HIE, NOS • Elderly patients: Hypertension (basal
a Cerebral Infarction, Chronic ganglionic), amyloid (lobar, peripheral)
a Cortical Laminar Necrosis hemorrhagic metastases
• Acute Hypertensive Encephalopathy, PRES a Check history
• Encephalitis • Trauma: Hemorrhagic DAI, contusions

a Herpes Encephalitis (typical locations)
a Encephalitis (Miscellaneous) • Infection: Abscess, encephalitis
• Melanin Deposition Helpful Clues for Less Common Diagnoses
a Melanoma Metastases • Multiple Sclerosis
a Meningeal Melanocytoma a Look for hazy "rim" or "ghost" of Tl
a Neurocutaneous Melanosis shortening around chronic lesions
• Thrombotic Microangiopathies (HUS/TTP) • Metastases
• Fabry Disease a Hemorrhagic (renal cell, melanoma)
• Fahr Disease a Melanoma (hemorrhagic vs. intrinsic Tl
• Fungal Diseases shortening from melanin)
• Kernicterus • Cerebral Amyloid Disease
• Leukemia a Lobar, cortical/subcortical
• Dermoid Cyst (Ruptured) a Hemorrhages of different ages
a Can be single or multiple, large or small,
homogeneous or "popcorn" appearance
Key Differential Diagnosis Issues • Neurocutaneous Syndromes
• Short Tl on Tl WI scan related to a Neurofibromatosis Type 1
a Deposition of paramagnetic substances • Basal ganglia, internal capsules
• Methemoglobin • Symmetric Tl shortening due to myelin
• Non-heme iron (e.g., ferritin) clumping or microscopic calcification
a Mineral deposition (e.g., calcium) a Tuberous Sclerosis Complex
• Calcification • Subependymal nodules often
• Trace element deposition hyperintense on noncontrast Tl WI
a Fat • Cortical tubers hyperintense early
a Melanin
I a Proteinaceous materials
(unmyelinated brain), variable later
• Streaky or wedge-shaped white matter
a Increased lipid or cholesterol content hyperintensities (unmyelinated brain)
5
102
11 HYPERINTENSE PARENCHYMAL LESION(S) CIl
c:
""
Ql
• Taylor-type cortical dysplasias may o Hemorrhagic lesions :;j
a.
initially be hyperintense (unmyelinated • Hematoma (subacute)
brain) • Infarct (hemorrhagic transformation)
..•
OJ
Ql
:;j
Helpful Clues for Rare Diagnoses • Trauma (contusion, axonal injury)
• Vascular malformation ...
OJ
• Hypoxic-Ischemic Lesions OJ
o Hemorrhagic transformation in ischemic • Neoplasm (primary, metastatic) :;j

\J
o Protein-containing lesion ...
OJ
stroke (cortex> basal ganglia)
o Hypotension - cortical laminar necrosis • Colloid cyst (l)
:;j
n
(gyriform Tl shortening) • Craniopharyngioma ::r
'<
o Heat stroke - thermal injury, Tl
• Rathke cleft cyst 3
OJ
shortening in external capsules, • Atypical epidermoid Gl

o Fat-containing (l)
paraventricular thalami, cerebellum :;j
• Acute Hypertensive Encephalopathy, • Lipoma ...

(l)
OJ
PRES • Dermoid
o Gross hemorrhage rare; petechial • Meningioma with lipomatous
uncommon differentiation
o Calcification &/or ossification
o Typically occipital lobes
• Encephalitis • Metabolic
o Herpes encephalitis
• Calcified neoplasm (e.g.,
oligodendroglioma)
• Hemorrhagic cortical necrosis
• "Sequential bilaterality" in temporal lobes • Infection (TB, NCe)
highly suggestive • Dural ossification
o Other mineral accumulation
• May also involve cingulate gyrus,
subfrontal region • Liver failure
o Melanin-containing lesions
o Other: West Nile may cause basal
ganglionic necrosis, Tl shortening
Other Essential Information
• Do T2* (GRE or SWI) scan in all patients
with unexplained intracranial hemorrhage
to look for additional lesions
• Spontaneously hyperintense intracranial Tl
lesions
I
Axial T1WI MR shows symmetrical foci of TI shortening
= In the basal ganglia in this patient with proven
Axial T1WI MR in this patient wilh chronic liver failure
shows T 1 hyperintense lesions in the basal ganglia and
5
hypothyroidism. posterior thalami (pulvinar).
103
~ T1 HYPERINTENSE PARENCHYMAL LESION(S)
Q)
<=
Q)
<9
'E>-"
.r:
u
<= (Left) Axial T I WI MR shows
~ a classic lale subacute
8:. intracerebral hematoma with
<= TI shortening caused by
~ extracellular melhemoglobin.
CO (Right) Sagiual TI WI MR
l: shows multiple hyperintense
CO foci in the midbrain and
"-
CO Fornix ~ in this patient with
"0 closed head trauma and
lii dj(fuse axonal injury.
(Left) Coronal TI WI MR
shows a striking flow artifact
within the 3rd and lateral
ventricles =. If you look at
adjacent brain parenchyma,
you see propagation of a
phase artifacl [;> across the
scan indicating that this is
flow related. (Right) Axial
T1WI MR shows multiple
hypoinlense lesions in the
white matter. Note slight,
hazy "rings" of subllc T7
shortening around many of
the lesions a presumably
due to coagulative necrosis
in the periphery of chronic
MS plaques.
(ieft) Axial TI WI MR in
patient with known
metastatic renal cell
carcinoma shows multiple
foci of TI shortening at
gray·white maller junction.
Findings are characteristic of
metastases with subacute
hemorrhage. (Right) Axial
TI WI MR in elderfy
normotensive demented
patient with history of
"multiple strokes" & clinical
diagnosis of "vascular
dementia II shoW's multiple T 1
hyperintense lesions in
patient with both lobar &
I microhemorrhages =.
5
104
11 HYPERINTENSE PARENCHYMAL LESION(S) CIl
~
c:
III
::l
Co
..,
tD
Cavernous Malformation Neurofibromatosis Type 1 III
(Left) Sagittal T7 WI MR in a ::l
patient with multiple ..,
OJ
Q)
syndrome shows a typical ::J
1)
"popcorn"·fike lesion II]
along with a much smaller
..,
Q)
<1l
hyperintense focus E!lI of ::J
()
subacute hemorrhage. ::r
'<
3
Q)
shows bilateral pallidal,
thalamic~ and internal Gl
capsule hyperintensities ffi <1l
::J
commonly seen in NF ,. ..,
<1l
These probably represent ~
myelin clumping or T7
shortening caused by
microcalcifications.

Tuberous Sclerosis Complex PRES
shows radial white matter
lines ~ and subependymal
hamartomas ~ as areas of
increased signal intensity on
unenhanced T7Wls prior to
myelin maturation. Following
myelination they are best
seen on FLAIR. (RighI) Axial
T7WI MR shows bioccipital
subacute hemorrhages ~ in
patient with severe PRES.
Frank ischemia/infarction,
hemorrhage are rare
complications; most lesions
resolve spontaneously with
blood pressure
normalization.
Encephalitis (Miscellaneous) Melanoma Metastases

bilateral foci of T I shortening
It] in this patient with West
Nile encephalitis. (Right)
Axial T7 WI MR shows 3 foci
of T7 shortening =::I in a
patient with known
melanoma. Melanin has an
intrinsic short T7, but
melanoma metastases often
hemorrhage as well.
I
5
105
~ BRAIN TUMOR IN NEWBORN/INFANT
'"
Ql
C
Ql
<.9 • Sparse Ca++ '" 20%
'"
E
• Enhancement usual (may be late/slow)
>-
.<:
Common • Hemorrhage rare
u
c • Anaplastic Astrocytoma a Hypercellularity reflected on imaging
Ql
~ • Teratoma • Hyperdense (NECT), hypointense (T2)
'c"
0... • Medulloblastoma (PNET-MB) a Medulloblastoma with extensive
~ • Supratentorial PNET nodularity
'"
[]:J
• Supratentorial Ependymoma • Subtype with expanded lobular
c
• Choroid Plexus Papilloma architecture
'"
~
[]:J
Less Common • Grape-like enhancement
"C
c • Subependymal Giant Cell Astrocytoma • Better prognosis
'" • Desmoplastic Infantile Ganglioglioma • Supratentorial PNET
a Large complex mass
• Desmoplastic Infantile Astrocytoma
• Glioblastoma Multiforme • Restricts on DWI (differentiates from
ependymoma)
Rare but Important • Heterogeneous signal, enhancement
• Choroid Plexus Carcinoma • Ca++ more common than in posterior
• Atypical Teratoid-Rhabdoid Tumor fossa PNETs
• Neurocutaneous Melanosis • Hemorrhage, necrosis common
(Mela noma/Melanocytoma) a Hemispheric
• Pineo blastoma • Mean diameter 5 em
• Brainstem Glioma, Pediatric • Especially newborn/infants
• Medulloepithelioma • Minimal peritumoral edema
a Suprasellar
ESSENTIAL INFORMATION • Early neuroendocrine, visual

disturbances
a Pineal (pineoblastoma)
• Hydrocephalus, Parinaud syndrome
• Supratentorial Ependymoma
a Peri/extraventricular> intraventricular
• Periventricular ependymal rests
• Large, bulky
• Ca++ '" 50%
• Variable necrosis, hemorrhage
a CPP: Lobulated intraventricular mass
• Lateral> 4th> 3rd
• NECT: [so- to dense
• Iso- to slightly hyperintense on T2WI
• Vividly enhancing
a Hydrocephalus common
• Subependymal Giant Cell Astrocytoma
a Enhancing mass near foramen of Monro
a Found in tuberous sclerosis complex
a Look for
• Subependymal Ca++ nodules
• Tubers (best on FLAIR)
• Desmoplastic Infantile Ganglioglioma
I a DIGs often have large cyst
a Cortically based enhancing tumor nodule
5
106
BRAIN TUMOR IN NEWBORN/INFANT
III
o Enhancing adjacent pia & dura • Small cysts :J
Co
• Desmoplastic Infantile Astrocytoma • Inhomogeneous enhancement
o Similar to (but rarer than) DIG o Invades adjacent structures
..,
lJl
III
• Glioblastoma Multiforme :J
• Corpus callosum, thalamus, midbrain,
OJ
o Bulky irregular enhancing tumor vermis Ql
o Peritumoral edema, mass effect o Hydrocephalus usual at diagnosis :::J
"U
o Hemorrhage, central necrosis, cysts • Brainstem Glioma, Pediatric ..,
OJ
o t Glucose metabolism, avid FDG o Imaging appearance, prognosis vary with CD
:::J
()
accumulation on PET tumor type, location :T
'<
o Tectal 3
Helpful Clues for Rare Diagnoses OJ
• Choroid Plexus Carcinoma • Pilocytic astrocytoma
Gl
o Similar to CPP PLUS
• Clinically indolent course (may cause CD
:J
• Brain invasion obstructive hydrocephalus) CD
~
OJ
• Ca++, cysts, bleed • Variable enhancement/Ca++

o Focal tegmental mesencephalic
• Ependymal, subarachnoid space seeding
(can be seen with both CPP, CPC) • Pilocytic astrocytoma
• Atypical Teratoid-Rhabdoid Tumor • Cyst + nodule
o PNET-MB-likePLUS
• Surgery, radiation, or chemotherapy
• Metastases at diagnosis more common • Patients generally do well
o Diffuse pontine glioma
• Cysts, hemorrhage more common
• Cerebellopontine angle cistern location • Diffusely infiltrating fibrillary
more common astrocytoma
• Neurocutaneous Melanosis • Nonenhancing early in course
(Melanoma/Melanocytoma) • Enhancement with malignant
o Giant or multiple cutaneous melanocytic
progression
nevi PLUS • Survival generally poor
• Melanosis: Bright Tl amygdala, • Medulloepithelioma
o Rare malignant embryonal brain tumor
cerebellum
o Young children « 5 years)
• Melanoma: Melanosis + diffuse
o Histologic differentiation varies
leptomeningeal enhancement
• Pineoblastoma • Neuronal, astrocytic, ependymal,
o Large heterogeneous pineal region mass
melanotic, etc.
o Imaging appearance reflects variable
• Peripheral Ca++
differentiation
Anaplastic Astrocytoma
I
Coronal CECT in this 7 month old shows obstructive Coronal T2WI MR in same case shows mass E:I is
5
hydrocephalus and a large, i"-defined midline mass SI
with ring enhancement and central necrosis. hyperintensity
hydrocephalus
=-
extensively infiltrating, with bithalamic and upper
midbrain
with transependymal
causing obstructive
CSF migration.
107
ro
Q)
c::
Q)
C)
ro
E
>-
.r: Teratoma Teratoma
u
c:: (Left) Axial T7WI MR in Ihis
~ 7 day old infanl shows T7
ro
0...
c::
brighl signal from fal
scallered Ihroughoullhe
=
~ lesion. (Right) Axial NECT in
Q) Ihe same child al 15 monlhs
c: shows a complicaled pineal
C1l
~
III
"'C
c:
a solid lissue
calcificalion PJgI.
=
region mass consisting of fat
and
C1l
Medulloblastoma (PNET-MB) Medulloblastoma (PNET-MB)

monlh old infant shows
intermediate to low signal
mass that splays and encases
posterior communicating E.1
and superior cerebellar 11Im
arleries. (Right) Coronal T7
C+ MR in Ihis 10 monlh old
shows grape-like nodular
enhancement lID.
Medul/oblaslOma wilh
extensive nodularity is a
PNET-MB varianllhal has
somewhat betler prognosis.
(Lefl) Axial T2WI MR in a 12

week old infanl shows a
mixed helerogeneily lefl
lemporallobe mass. (Right)
Axial T2* CRE MR shows
multifocal hemosiderin and
calciFic foci ~.
I
5
108
BRAIN TUMOR IN NEWBORN/INFANT CJl
'"
c:
III
::::l
C-
..,
O!
Choroid Plexus Papilloma III
(Left) Axial T2WI MR shows ::::l
a large cyst coloboma CD
8l and temporal lobe til
=
subependymal heterotopia
in a 4 day old girl with
Aicardi syndrome. (RighI)
::::l
\J
w
..,
(1)
Coronal T I C+ MR shows ::::l

(")
bilateral choroid plexus ::r
papillomas. The left ~ is
'<
3
bulky and frond-like, while w
the right 81 is stretched by G)
(1)
the associated cyst. ::::l
(1)
til
Subependymal Giant Cell Astrocytoma

(Lefl) Sagittal ultrasound
shows a bulky
subependymal giant cell
astrocytoma 81 at the
foramen of Monro in this
newborn with cardiac
rhabdomyoma and tuberous
sclerosis. There are multiple
additional tubers ~ on the
same image. (RighI) Coronal
T7 C+ MR in a 7 month old
infant shows a massive right
(ronlal cystic tumor with a
solid enhancing component
that involves the medial
frontal cortex = and falx.
Desmoplastic Infantile Astrocytoma Desmoplastic Infantile Astrocytoma

(Lefl) Axial T2WI MR in a 9
month old infant shows a
right temporal cystic and
solid ~ tumor with
surrounding edema. (RighI)
Coronal T7 C+ MR in the
same infant shows
encasement of the right
middle cerebral artery ~ by
the avidly enhancing solid
component 81 of the tumor.
I
5
109
CIl
Ql
C
Ql
t9
CIl
E
>- Glioblastoma Multiforme
.r::
u
c (Left) Axial T2WI MR in this
~
Ql
6 week old infant shows a
CIl
c.. markedly heterogeneous
c bifrontal mass lesion with
CIl
~ hemorrhages of various ages
(lJ §. There is obstruction of
C both foramina of Monro and
III enlargement of the lateral
~
CO ventricular trigones. (Righi)
"'C Axial T7 C+ MR shows
c: extensive enhancement of
III
thislumor.
Choroid Plexus Carcinoma

(Left) Axial T7 C+ MR in this
9 month old infant shows a
large, bulky, avidly
enhancing left
intraventricular tumor ~
with invasion of the
overlying brain ED. There are
multiple intraventricular
metastases ~ (Right)
Anteroposterior angiography
performed as a part of
pre-operative embolization
shows hyper vascularity ~
and multiple areas of
contrast puddling ~.

(Left) Sagittal T2WI MR in
this 7 month old inFant
shows hydrocephalus and a
complicated solid & cystic
tumor filling the 4th
ventricle, supravermian
cistern and extending
through the tentorial incisura
E!llI. (Right) Coronal T1 C+
MR in the same 7 month old
shows a right frontal
metastatic deposit B.
I
5
110
BRAIN TUMOR IN NEWBORN/INFANT
III
~
C-
Neurocutaneous Melanosis Neurocutaneous Melanosis ..•
O:!
III
(Melanoma/ Melanocytoma) (Melanoma/ Melanocytoma)
(Left) 5agiltal T1WI MR
:l
shows increased signal ...OJ
OJ
intensity of the hippocampus
E!l:I in this 70 month old with ~
"U
a large cutaneous nevus.
Pachymeningealthickening
...
OJ
= is present
(1)
prior to ~
()
contrast administration. ::r
'<
(Right) Coronal T1 C+ MR 3
during the same examination OJ
shows diffuse pachy· and Gl
(1)
leptomeningeal metastatic :l
melanoma. ...
(1)
OJ
Pineoblastoma Pineoblastoma
7 month old infant shows a
mass in the pineal region
traversing the tentorial
incisura into the
supravermian cistern. There
;s compression of the
aqueduct of 5ylvius with
resultant hydrocephalus.
Acute edema along the fiber
tracts of the corpus callosum
renders a striated pattern El
(Right) Axial OWl MR in the
same patient shows typical
diffusion restriction.
Brainstem Glioma, Pediatric Medulloepithelioma

(Left) 5agiltal T1 C+ MR in
this newborn shows massive
expansion of the pons and
medulla by a nonenhancing
mass. (Right) 5agiual T1WI
MR in a 5 day old infant
shows a massive
hemorrhagic tumor replacing
and expanding the upper
cervical spinal cord, the
brainslem, and the
cerebellum. The tumor
protrudes through the
incisura and displaces the
straight sinus E!l:I.
I
5
111
~ BRAIN TUMOR IN CHILD> 1 YEAR
QJ
C
QJ
~ o Atypical teratoid-rhabdoid tumor (ATRT)
o Germinoma
,.,
E
£
Common o Epidermoid
U
C • Pilocytic Astrocytoma • May present with hemorrhage into tumor
~
QJ
o Cerebellar JPA
ro o Primary CNS sarcoma
a.. o Optic Pathway Glioma
c o Supratentorial PNET
~ o Pilomyxoid Astrocytoma (Rare) o Neuroblastoma metastatic to brain tissue
(]J
• Medulloblastoma (PNET-MB) o Pilomyxoid variant of pilocytic
C
III
• Ependymoma astrocytoma
~
III • Brainstem Glioma, Pediatric
"0 • Diffuse Astrocytoma, Low Grade Helpful Clues for Common Diagnoses
c
III
• Subependymal Giant Cell Astrocytoma • Pilocytic Astrocytoma
o Low density NECT
• DNET
o High signal T2
• Medulloblastoma (PNET-MB)
less Common o Hyperdense 4th ventricle (V) mass on
• Germinoma NECT
• Choroid Plexus Papilloma o Restricts on DWI
• Ganglioglioma • Ependymoma
• Oligodendroglioma o 60% posterior fossa
• Neurofibromatosis Type 2 • "Plastic" tumor in 4th ventricle, extrudes
o Meningioma through foramina
o Schwannoma o 40% supratentorial
• Pineoblastoma • Mixed cystic, solid mass with Ca++
• Pleomorphic Xanthoastrocytoma • Brainstem Glioma, Pediatric
• Anaplastic Astrocytoma o Location predicts pathology, prognosis
• Glioblastoma Multiforme • Infiltrating pontine glioma worst
• Gliomatosis Cerebri • Diffuse Astrocytoma, Low Grade
• Supratentorial PNET o Hemispheres, thalami (can be bithalamic),
• Teratoma tectum, brainstem (pons, medulla)
Rare but Important • 50% of brainstem "gliomas" are low
• Astroblastoma grade, diffusely infiltrating astrocytomas
• Choroid Plexus Carcinoma o Poorly marginated
• Atypical Teratoid-Rhabdoid Tumor o Hypo- on Tl WI, hyperintense on T2WI
• Primary CNS Sarcoma o No enhancement
• Metastases • Subependymal Giant Cell Astrocytoma

o Metastases, Skull and Meningeal o Location at foramina of Monro typical
o Metastases, Parenchymal o Look for cortical/subcortical tubers
o Leukemia o Look for subependymal nodules
o Neuroblastoma, Metastatic • DNET
o Neurocutaneous Melanosis (Melanoma, o Almost all in patients < 20 years
Melanocytoma) o Chronic epilepsy
• Central Neurocytoma o "Bubbly appearing" cortically based mass
• Dysplastic Cerebellar Gangliocytoma o Ring sign on FLAIR
o Nearly half of pediatric suprasellar masses
ESSENTIAL INFORMATION o 90% Ca++/cystic/enhance
• Diffusion weighted imaging helpful • Germinoma
• All of the following restrict on DWI
I o PNET-MB
o Suprasellar + pineal masses together best
clue
o Pineoblastoma (pineal PNET) o Early ependymal infiltration
5
112
BRAIN TUMOR IN CHILD> 1 YEAR
• Choroid Plexus Papilloma Helpful Clues for Rare Diagnoses

o Densely enhancing
• Astroblastoma
o Cotyledon- or frond-like surface o Large, hemispheric
• Neurofibromatosis Type 2 o Well-circumscribed
o If multiple schwannomas, think NF2+
o "Bubbly" solid and cystic
o Look for "hidden", dural-based
meningiomas with C+ o Similar to CPP
• Pineoblastoma • Invades ependymal surface & brain
o Restricts on DWI
• Less homogeneous than CPP
o Look for CSF spread (ventricles, ependyma)
• Atypical Teratoid-Rhabdoid Tumor
• Pleomorphic Xanthoastrocytoma o Heterogeneous intracranial mass in infant G)
o Cortically based tumor (temporal lobe CD
o 50% infra tentorial, early CSF spread ::J
CD
most common site) • Metastases
~
Q)
o Dural reaction ( "tail") common
o Pial, leptomeningeal
o Enhancing ill-defined mass plus cyst
• PNET
• Anaplastic Astrocytoma • Ependymoma
o Diffusely infiltrating
• Anaplastic astrocytoma
o Classic do not enhance
• Germinoma
• Glioblastoma MuItiforme • Choroid plexus carcinoma
o Typically arises from lower grade
o Falx
astrocytoma • Leukemia involves both sides of the falx
• Gliomatosis Cerebri o Bone & dura: Neuroblastoma> leukemia
o Less likely to enhance
• CT: Bone spiculation, "hair on end"
o More likely bilateral
• MR: Bone expanded and marrow
o More likely to spread across callosal tracts
replaced
• Supratentorial PNET • Central Neurocytoma
o Infant with large, bulky, complex
o "Bubbly" lobulated mass in body of lateral
hemispheric mass ventricle
o Ca++, hemorrhage, necrosis common
• Dysplastic Cerebellar GangIiocytoma
o Peritumoral edema sparse/absent o Look for evidence of Cowden disease
• Teratoma o Striated cerebellum
o Neonate with large bulky midline mass
• Enlarged low signal cerebellar folia
o Ca++, soft tissue, cysts, fat
Cerebellar JPA Cerebellar JPA
I
Axial NEG shows typical midline cystic tumor with
large low density mural nodule =. There is
Axial T2WI MR shows the nodule to be high signal
intensity, a clue to the high nuclear-to-cytoplasm ratio in
5
hydrocephalus with interstitialedema. cerebellarIPAtumors.
113
co
E
>-
.r: Optic Pathway Glioma Pilomyxoid Astrocytoma (Rare)
u
~
(1)
poorly marginated
co
a.. hyperintensity =:I that
c extends posteriorly from
co
~ optic chiasm/hypothalamus
(D along both optic radiations.
c:: (Right) Axial T2WI MR
~
Cll shows a large, hyperintense,
(D well-circumscribed mass. It
"0
arises from the hypothalamic
c:: region and demonstrates no
Cll
edema of adjacent
structures.
Medulloblastoma (PNET-MB) Medulloblastoma (PNET-MB)

a Jow signal midline tumor.
There is an associated cyst
=:1_ (Right) Axial OWl MR
shows diffusion restriction
within the tumor nodule, an
excellent clue to the
aggressive nature of the
lesion.
Brainstem Glioma, Pediatric

shows a large,
heterogeneous, low signal
mass that widens the
tegmenta-cerebellar angle
and extends through the
inferior recesses of the 4th
ventricle. There is extension
into the upper cervical spinal
canal =:1_ (Right) Sagittal
T2WI MR shows diffuse
expansion of the pons and
medulla due to an infiltrating
glioma_
I
5
114
BRAIN TUMOR IN CHILD> 1 YEAR en
,.-
c::
ll>
:J
Q.
OJ
.,
Subependymal Giant Cell Astrocytoma DNET ll>
(Lcfl) Coronal T1 C+ MR
:J
shows bilateral, asymmetric tAl
.,
enhancing lesions at the III
foramina of Monro. The :J
location is characteristic for lJ
III
.,
subcpendymal giant cell CD
astrocytoma. The child also :J
()
had skin and other brain ::r
lesions typical of tuberous
'<
3
sclerosis. (RighI) Coronal III
FLAIR MR in a child with Gl
seizures shows an CD
:J
insular·based
partial bright ring
ONET FLAIR ring sign.
=-
lesion with a
the
CD
.,
III
Germinoma
(Lcfl) Sagittal T1WI MR
shows a suprasellar
collection of cysts of many
signal intensities. One!:] is
very high signal intensity,
likely due to protein; another
extends behind the clivus
81; and the remainder
herniate into Jrd ventricle.
Calcification 1:1:1 is noted in
the solid component above
the dorsum sella. (RighI)
Sagittal T1 C+ MR shows a
medium-sized pineal mass
with central necrosis 1m.
There is a very small
enhancing mass in the
infundibular recess e=.

(Lefl) Coronal T1 C+ MR
shows a large enhancing
mass within the right lateral
venlricle. The surface is
frond-like, and there is no
brain invasion. The
appearance is typical for a
choroid plexus papilloma.
(RighI) Axial TI C+ MR
shows a cystic and solid
thalamic mass. This lesion
was heavily calcified on
NECT (not shown).
I
5
115
ro
~ BRAIN TUMOR IN CHILD> 1 YEAR
Ql
c
Ql
o
ro
E
>.
.r: Neurofibromatosis Type 2 Pineo blastoma
u
c (Left) Coronal T2WI MR
~
Ql
shows multiple dural-based
ro
a.. meningiomas ED at the
c vertex. There are a/50
ro
~ bilateral, asymmetric,
co vestibular schwannomas ~
C in this teen with NF2. (Right)
III Sagittal T2WI MR shows a
~
CO low signal pineal mass that
"'C obstructs the aqueduct. This
c lesion was dense on NEeT
III
and restricted on DWI.
shows a cortically based
temporal lobe tumor. It is
ill-defined, invades adjacent
brain tissue, enhances, and
contains a rim-enhancing
cyst ~. (Right) Axial T2WI
MR shows bithalamic
involvement by
homogeneous lUmor, which
did not enhance on T I C+
image (not shown).
Supratentorial PNET
(Left) Coronal T1 WI MR
shows marked expansion of
the left temporal lobe by a
hemorrhagic ED mass.
shows a mixed solid, cystic,
and calcified pineal region
mass Blthat obstructs the
aqueduct of Sylvius. This
teenaged patient presented
with Parinaud phenomenon.
There is acute edema
involving the septal-callosal
interface =:II.
I
5
116
Choroid Plexus Carcinoma Atypical Teratoid-Rhabdoid Tumor

a large heterogeneously
enhancing trigonal mass with
brain invasion and
ependymal spread 811.
shows a mixed signal mass
obstructing both the right 811
and left foramina of Monro.
Gl
ct>
::J
ct>
~
OJ

(Left) Axial OWl MR in the
same patient shows
extensive diffusion restriction
in the left frontal ATRT.
(RighI) Axial CECT in
metastatic PNET-MB shows
"comb-like" enhancement of
the interfoliate sulci ~ Note
moderately enlarged lateral
ventricles 1:1 caused by
extraventricular obstructive
hydrocephalus from diffuse
cisternal metastases.
leukemia Neuroblastoma, Metastatic

(Lefl) Axial T1 C+ FS MR in a
child with ALL shows
involvement of the posterior
= and anterior 811 falx by
densely enhancing tissue.
Both sides of the falx are
involved ventrally. (RighI)
Coronal FLAIR MR shows
expansion of the lesser wing
of sphenoid by
neuroblastoma. There is an
additional calvarial and
dural-based focus at the
vertex EJ.
I
5
117
•...
CIl EPILEPSY, GENERAL
OJ
c
OJ
(9 o MTS: Small, hyperintense hippocampus
CIl
E associated with temporal lobe epilepsy
>,
.s;;: Common o Causative vascular malformations include
u
c • Acquired Causes AVM & cavernous malformations
~ o Trauma
CIl o Toxic-metabolic & drug abuse patients
0..
o Remote Stroke may present with seizures
c
~ o Remote Infection • Heterotopic Gray Matter
co o Neoplasms o Gray matter (GM) nodules, follow GM
C
t'll
o Mesial Temporal Sclerosis (MTS) signal on all MR sequences
"-
co o Vascular Malformations o Subependymal most common location
o Toxic/Metabolic Insult, NOS
"c:
t'll
o Drug Abuse
o Can be found incidentally in patients
without seizures
• Heterotopic Gray Matter • Perisylvian Dysplasia
• Perisylvian Dysplasia o Common site for cortical dysplasia
• Schizencephaly o Typically bilateral
• Septo-Optic Dysplasia o ± Septo-optic dysplasia, schizencephaly
• Tuberous Sclerosis Complex (TSC) • Schizencephaly
• Focal Cortical Dysplasia, Taylor Type o CSF cleft extending to ventricular
(Balloon Cell Dysplasia) ependyma, GM-lined
• Focal Cortical Dysplasia o Outpouching or "dimpling" of lateral
• Pachygyria-Polymicrogyria ventricular contour "points" to cleft
• Lissencephaly Type 1 o Two morphologic varieties
• Band Heterotopia • Closed lip: GM ependymal seams touch
• Hemimegalencephaly • Open lip: GM seams separated by cleft
Less Common o May be unilateral or bilateral
• Neuronal & Mixed Neuronal-Glial Tumors o Absent septum pellucidum common

o DNET o Associated with septo-optic dysplasia
o Ganglioglioma • Septo-Optic Dysplasia
• Pleomorphic Xanthoastrocytoma o Some consider mildest form of
holoprosencephaly
Rare but Important o Septum pellucidum absence + optic nerve
• Sturge-Weber Syndrome hypoplasia, ± pituitary dysfunction
• Status Epilepticus o Common associated malformations:
Schizencephaly, perisylvian dysplasia
ESSENTIAL INFORMATION • Tuberous Sclerosis Complex (TSC)
o T2 hyperintense cortical/subcortical tubers
Key Differential Diagnosis Issues o Subependymal nodules follow white
• Generalized seizure disorders usually matter (WM) signal until calcified
nonlocalizing o 10-15% develop giant cell astrocytoma
• Partial complex (focal) epilepsy usually due • Focal Cortical Dysplasia, Taylor Type
to focal structural abnormality (i.e., MTS) (Balloon Cell Dysplasia)
• High-resolution MR necessary to fully o Imaging & histology = tubers in TSC
evaluate epilepsy • Histology shows "balloon cell" dysplasia
Helpful Clues for Common Diagnoses o Solitary dysplasia; lack other TSC features
• Acquired Causes o T2 hyperintense "comet tail" from cortex
o Trauma is most common cause in adults to ventricle; best seen on FLAIR> T2 > T1
o Trauma, remote stroke, or infection results • Focal Cortical Dysplasia
in encephalomalacia &/or gliosis, which o Thickening &/or nodular cortex
may cause epilepsy o Blurred gray-white junction
I o Benign, malignant tumors • Pachygyria-Polymicrogyria

o Pachygyria: Thick, smooth cortex
5
118
EPILEPSY, GENERAL ,...
C/)
c:
III
o Polymicrogyria: Small, "pebbly", o Well-circumscribed, no surrounding :J
Co
cobblestone or micronodular appearing edema OJ
..,
gyri (cortical dysplasia) o Involvement of adjacent meninges typical III
:J
• Lissencephaly Type 1 Helpful Clues for Rare Diagnoses OJ
..,
o "Smooth" brain lacking normal gyral
• Sturge-Weber Syndrome OJ
infolding; thick cortex :J
o Malformation of cortical & pial veins "U
o Spectral continuum with OJ
..,
o Clinical diagnosis by trigeminal
C1l
po Iymicrogyria -pach ygyr ia distribution facial "port-wine" stain :J
n
• Band Heterotopia o Earliest intracranial finding = ipsilateral ::r
'<
o Most genetic; X-linked inheritance 3
enlarged choroid plexus OJ
o Most (90%) are female
o Later = ipsilateral hemiatrophy Gl
• Males severely affected, rare survival C1l
:J
• Status Epilepticus C1l
o Band of incompletely migrated GM ..,
o Focal cortical (& subcortical) edema, T2 OJ
between cortex & ventricle (double cortex) hyperintense
o GM band size inversely proportional to • Varied cortical enhancement
overlying cortex thickness • Usually DWI & FLAIR bright
• Hemimegalencephaly o Persistent seizures, often 2: 24 hours
o Unilateral hemispheric overgrowth o May show hyperperfusion: High CBV &
o Dysplastic enlarged ipsilateral ventricle
CBF, delayed MTT
o Overlying skull & soft tissues overgrown
o Most resolve in days-weeks
Helpful Clues for Less Common Diagnoses o Long term atrophy may result
• DNET Other Essential Information
o Discrete T2 hyperintense "bubbly" cortical • "New onset seizures" require routine brain
mass, low grade neuronal neoplasm MR with & without contrast
o Associated cortical dysplasia common
o Rule out acute lesions: Hemorrhage,
o Medial temporal lobe most common
tumor, infection, & stroke
• Ganglioglioma • "Epilepsy" high resolution MR evaluation
o Cystic/solid enhancing, cortically based o High resolution Tl/T2 (3D techniques at 1
mass, mixed neuronal-glial tumor mm slices preferred) through entire brain
o Temporal lobe most common site
o IR techniques improve gray-white matter
o Associated cortical dysplasia common
contrast (STIR, FLAIR, & Tl FLAIR)
• Pleomorphic Xanthoastrocytoma o High field strength (3T) preferred
o Cyst + enhancing nodule classic
Mesial Temporal Sclerosis (MTS) Mesial Temporal Sclerosis (MTS)
I
Coronal FlAIR MR shows high signal in the right
hippocampus 1:2 related to this paUent's MTS. The
Coronal T1WI MR shows typical decreased
parenchymal volume 1:2 of U,e hippocampus in MTS.
5
primary MR features are T2 hyperintense signal, atrophy Internal architecture remains preserved in this case. Mild
of the hippocampus, & loss of internal architecture. enlargement of the adjacenllemporal horn is common.
119
EPILEPSY, GENERAL
<Il
E
>-
.c
()
Vascular Malformations Vascular Malformations
c (Left) Axial Tl WI MR shows
Q)
~ hyperintensity related to
<Il
a.. recent hemorrhage in a
c cavernous malformation =-
~
<Il Seizures are often the
co presenting symptom for
C vascular lesions such as a
III
~ cavernoma or AVM. (Right)
CO Axial T2' GRE MR shows
"t:l susceptibility artifact in this
c cavernous malformation It]
III
with recent hemorrhage.
GRE/SWI MR is helpful to
search for additional lesions
that may be occult on other
sequences.
Heterotopic Gray Matter Heterotopic Gray Matter

(Left) Axial Tl WI MR shows
mu/tiFocal gray maller
nodules lining both lateral
ventricles =. Note a/50
heterotopic gray matter
within the left frontal lobe
white matter PlB.
I feterotopic gray matter
follows gray matter signal on
all MR sequences & does 110t
enhance. (Right) Coronal
foci of cortical gray matter
lining the ependymal margin
of both lateral ventricles =.
These may be associated
with seizures or may be
asymptomatic.
(Left) Sagittal Tl WI MR
shows multifocal dysplastic
cortex =. Perisylvian
involvement (perisylvian
dysplasia) BlI is common.
Such focal abnormalities are
found in many patients with
partial complex epilepsy.
shows symmetric frontal and
opercular bilateral
polymicrogyria =- also
known as cortical dysplasia.
Note additional bands of
laminar heterotopic gray
matterE:l.
I
5
120
EPILEPSY, GENERAL ,.-
CIl
c:

a classically located
perisylvian open lip
schizencephaly, with a wide
CSF cleft Ell lined with gray
matter =. The cleft margins
do not lOuch in open-lip
schizencephaly. (Right) Axial
T2WI MR shows a closed-lip
schizencephaly lined by
dysplastic gray matter
Note the characteristic
=. Gl
ct>
:J
ventricular outpouching ~ ct>
~
Q)
Flow voids from embryonic
vessels lay adjacent to the
lateral margin of the
schizencephalic cleft P.::l.

shows seplO-optic dysplasia,
with small optic chiasm 8-
absent septum pellucidum
68 Note that the sella is also
small =.These patients
frequently also have pituitary
hypofunction. (Right)
right perisylvian
polymicrogyria = in this
seplO-optic dysplasia patient,
a common association.
However. schizencephaly is
nearly always associated
with polymicrogyria,
adjacent 10 the
schizencephalic cleft.
Tuberous Sclerosis Complex (TSC) Tuberous Sclerosis Complex (TSC)

shows numerous subcortical
hyperinlensilies consistent
with tubers =
patient Several
in this TSC
subependymal nodules
(SEN) Ell are also present.
Before they calcify, SEN
follow white matter signal.
shows a subependymal giant
cell astrocytoma =.. seen in
10-/5% of patients with
TSC. Note the associated
ventriculomegaly. Multifocal
subcortical tubers P1tJ are
seen in the left hemisphere.
I
5
121
~ EPILEPSY, GENERAL
Q)
c:
Q)
<.9
<1l
E Focal Cortical Dysplasia, Taylor Type Focal Cortical Dysplasia, Taylor Type
:>,
.J::: (Balloon Cell Dysplasia) (Balloon Cell Dysplasia)
U
c: (Left) Coronal T2WI MR
~ shows classic findings in
<1l
0.. Taylor dysplasia,
c: demonstrating juxtacorlical
~
<1l
(!J
high signal =
with a thin
"seam' of high signal E!ilI
c: tracking along the expected
ltl
~ course of the radial glial
(!J fibers to the subependymal
"0 margin. FLAIR is often more
c: sensitive to these dysplasias.
ltl
(Rig"') Coronal FLAIR MR
shows a single focus of mild
gyral expansion ~ and
classic thin high signal seam
= extending to the ventricle
E!ilI.
Focal Cortical Dysplasia

shows thickened, ill-defined
frontal cortex = with mild
blurring of the gray-white
junctions related to [ocal
cortical dysplasia. Such
findings should be confirmed
with multipJanar imaging or
isovoxel reconstructions.
shows small disorganized
perisylvian gyri =with a
cobblestone appearance,
characteristic for
polymicrogyria. Other areas
of cortex appear thickened
E!ilI & indistinct related to
pachygyria.
Band Heterotopia Band Heterotopia

a thin band of gray matter in
the deep white matter of
both hemispheres
month
=
in a 6
old. Some consider
band heterotopia to be in the
gray matter heterotopia
spectrum. (Right) Coronal
T2WI MR shows decreased
sulcalion, primitive sy/vian
fissures a & thick bands of
incompletely migrated cortex
= consistent with band
heterotopia ("double
cortex"). Note thickness of
overlying cortex is inversely
I proportional to band
heterotopia.
5
122
EPILEPSY, GENERAL
III
::::l
C-
..•
OJ
Hemimegalencephaly III
(Left) Coronal T1WI MR ::::l

show an enlarged right ...
III
hemisphere and ventricle
compared to the left. Note
= OJ
::::l
1:)
ipsilateral dysplastic OJ
appearing gray matter I:] in CO
this hemimegalencephaly ::::l
(')
patient. (Right) Coronal ::r
T1 WI MR shows a nearly
'<
3
cystic-appearing mass in the OJ
mesial right temporal lobe Gl
81. This was a proven DNET CD
::::l
(dysembryoplastic ...
CD
OJ
neuroepithelial tumor), a
neuronal tumor commonly
associated with dysplastic
cortex.
Pleomorphic Xanthoastrocytoma
a circumscribed cystic &
solid mass in the anterior
temporal lobe 1:]. This
well-differentiated
neuronal-glial tumor is the
most common tumor to
cause temporal lobe
epilepsy. (Right) Axial T1 C+
MR shows a cystic and solid
enhancing temporal mass
8l typical of pleomorphic
xanthoastrocytoma (PXA),
recurrent in this case. PXAs
often extend to the adjacent
meninges & have a "dural
tail".
Sturge-Weber Syndrome
shows right hemiatrophy,
angiomatosis =
pial enhancement, and
of CSF
spaces. This congenital
malformation has failure of
cortical venous development
that leads to progressive
venous occlusion and
ischemia. (Right) Coronal
FLAIR MR shows marked
hyperintensity involving
temporal cortex and adjacent
subcortical while matter =
in a patient with persistent
status epilepticus. These
changes resolved slowly over
the following weeks. I
5
123
SECTION 6
Asymmetric Cerebral Hemispheres 1-6-2
Thick Cortex 1-6-8
Thin Cortex 1-6-14
Focal Cortical Mass 1-6-20
Cortical Hyperintensity T2/FLAIR 1-6-24
Cortical Enhancement 1-6-28
Solitary White Matter Lesion 1-6-30
Confluent White Matter Lesions 1-6-34
Thin Corpus Callosum 1-6-40
Abnormal Shape/Configuration of Corpus Callosum 1-6-46
Corpus Callosum Holes 1-6-52
Corpus Callosum Lesion without Mass Effect 1-6-54
Corpus Callosum Mass 1-6-56
Corpus Callosum Splenium Lesion 1-6-58
Basal Ganglia Calcification 1-6-62
T1 Hyperintense Basal Ganglia 1-6-66
T2 Hyperintense Basal Ganglia 1-6-70
Enlarged Perivascular Spaces 1-6-74
Perivascular Space Enhancing Lesions 1-6-76
Bilateral Basal Ganglia Lesions 1-6-80
Putamen Lesion(s) 1-6-84
Globus Pallidus Lesion(s) 1-6-86
Unilateral Thalamic Lesion 1-6-90
Bithalamic Lesions 1-6-92
"Pulvinar Sign" 1-6-96
Tectal (Quadrigeminal Plate) Lesion 1-6-98
Midbrain Lesion 1-6-100
ro ASYMMETRICCEREBRALHEMISPHERES
E
>-
~
u
c • Post-ischemic loss of tissue following
~
Q)
ro
0..
parenchymal hypoxic cell death
c Common • Post-traumatic loss from parenchymal
ro
~ • ormal Variant
CD
irreversible traumatic insult
ro
• Encephalomalacia, General • Post-inflammatory loss by irreversibly
'C
o o Post-Ischemic Encephalomalacia injured tissue
-
C
Q)
ro
~
c.
::J
o Post-Traumatic Encephalomalacia
o Post-Inflammatory Encephalomalacia
• Contusion/Traumatic Cerebral Edema
o Post-Traumatic Encephalomalacia
• Parenchymal loss replaced by CSF
• Occur in characteristic locations where
(/)
• Cerebral Ischemia-Infarction, Acute brain is adjacent to bony protuberance or
C
III
~
• Cerebral Infarction, Chronic dural fold
!Xl • Alzheimer Dementia • Contusion/Traumatic Cerebral Edema
"C
C • Multi-Infarct Dementia o Patchy superficial hemorrhages within
III
• CMV, Congenital edematous background, loss of gray-white
::J
• Frontotemporal Dementia distinction
""(/) • Dyke-Davidoff-Masson o Swelling with loss of sulci, fissures, &
less Common cisterns
• Hypoxic Ischemic Encephalopathy • Cerebral Ischemia-Infarction, Acute
• Encephalitis o Early cortical swelling in defined vascular
• Sturge-Weber Syndrome distribution(s)

• Plagiocephaly o DWI restriction with correlating ADC map
• MELAS • Cerebral Infarction, Chronic

• Hemimegalencephaly of Tuberous Sclerosis o Volume loss with gliosis along margins
o Loss in a defined vascular distribution
Rare but Important
• Alzheimer Dementia
• Hemimegalencephaly (Sporadic or Familial) o Parietal & temporal cortical atrophy with
• Pachygyria-Polymicrogyria disproportionate hippocampal volume loss
• Gliomatosis Cerebri o Often affects brain asymmetrically
• Epidermal Nevus Syndrome • Multi-Infarct Dementia
• Schizencephaly o Multifocal infarcts of gray matter, white
• Encephalocraniocutaneous Lipomatosis matter, basal ganglia, pons
• Proteus Syndrome o Usually bilateral, but may be unilateral
• CMV, Congenital
ESSENTIAL INFORMATION o Microcephaly, cerebral calcification,
cortical gyral abnormalities, cerebellar
Key Differential Diagnosis Issues hypoplasia, & myelin delay or destruction
• Differential diagnosis list is vast and could o Gestational age at time of infection
logically be subdivided as follows determines pattern of CNS injury
o One hemisphere larger than the other
• Frontotemporal Dementia
o One hemisphere smaller than the other o Caused by focal cortical atrophy involving
Helpful Clues for Common Diagnoses frontal &/or temporal lobes
• Normal Variant o Worse atrophy of dominant hemisphere
o Minor asymmetry of otherwise normal • Dyke-Davidoff-Masson
appearing density/intensity parenchyma o Cerebral hemiatrophy with ipsilateral
o Substantial individual diversity of hypertrophy of the skull and sinuses
left-right gyral cerebral cortex asymmetries o Caused by an intrauterine or perinatal
o Cerebral asymmetry patterns are not carotid artery infarction
universal & show variation based on origin Helpful Clues for less Common Diagnoses
• Encephalomalacia, General • Hypoxic Ischemic Encephalopathy
I o All etiologies appear as CSF replacing
destroyed parenchyma due to
o Acquired neonatal condition generally
attributed to cerebral hypoperfusion
6
2
ASYMMETRIC CEREBRAL HEMISPHERES en
""
C
III
o Several brain injury patterns attributed to o Defect of cellular organization, neuronal ::::J
C.
differing clinical variables migration
• Pachygyria-Polymicrogyria
..•
OJ
• Encephalitis III
::::J
o Abnormal T2 hyperintensity of gray matter o Findings range from incomplete
lissencephaly to excessively small & en
± white matter, or deep gray nuclei c
"0
o Diffuse brain parenchymal inflammation prominent gyral convolutions OJ
caused by a variety of pathogens, most o Disorder of neuronal migration ro
::::J
commonly viruses • Gliomatosis Cerebri o
::::J.
• Sturge- Weber Syndrome o T2 hyperintense infiltrating mass with III
CD
o Cortical Ca++, atrophy, and enlarged enlargement of involved hemisphere OJ
ipsilateral choroid plexus o Typically hemispheric white matter ::::J
-0
o Unilateral 80%, bilateral 20%; occipital> involvement, involves cortex in 19% ...
OJ
CD
parietal> frontal/temporal lobes > • Epidermal Nevus Syndrome ::::J
()
diencephalon/midbrain> cerebellum o Hemimegalencephaly is most common ::T
'<
• Plagiocephaly CNS abnormality 3
OJ
oCT: Osseous asymmetry with thickened & o Also migration abnormalities, vascular
sclerotic suture margins malformations, corpus callosal agenesis,
o Premature unilateral closure of coronal Dandy-Walker, myelomeningocele, Chiari
&/or lambdoidal sutures malformations, & tumors
• MELAS • Schizencephaly
o Stroke-like cortical lesions crossing typical o Transmantle gray matter lined clefts
vascular territories o "Closed-lip" (small) or "open-lip" (large)
o Acute - gyriform swelling; chronic - • Encephalocraniocutaneous Lipomatosis
atrophy o Hemispheric atrophy, ventriculomegaly
• Hemimegalencephaly of Tuberous with ipsilateral alopecia overlying a scalp
Sclerosis lipoma
o Unilateral lobar/hemispheric overgrowth o Hydrocephalus is frequently present
o Look for other markers of TSC (e.g., • Proteus Syndrome
subependymal nodules) o Complex hamartomatous disorder
involving half the body
o CNS: Hemimegalencephaly, subependymal
• Hemimegalencephaly (Sporadic or
calcified nodules, & periventricular cysts
Familial)
o Hamartomatous overgrowth of hemisphere
Normal Variant
I
Axial T2WI MR shows normal asymmetry, especially
involving the left temporal/occipital lobes =:I as
Axial T2WI MR shows typical MCA distribuUon chronic
infarct as encephalomalacia WiUl gliotic hyperintense
6
compared to the right. in this paUent with headache and margins !:ll. Adjacent sulci & ventricle SI are
a normal MR. prominent from volume loss.
3
ASYMMETRIC CEREBRAL HEMISPHERES
Post- Traumatic Encephalomalacia Post-Inflammatory Encephalomalacia

(Left) Axial NECT
demonstrates posHraumalic
encephalomalacia of
bilaleral reclus gyri ~ & lefl
temporal tip ~ in
characteristic locations
adjaCenllO bony surfaces.
(Right) Axial Tl C+ MR
shows extensive cavitation of
bilateral hemispheric white
matter = with extreme
volume los5 and cavity
retraction bilalerally, right
more lhan left, all sequelae
from Citrobacler meningitis.
Contusion/Traumatic Cerebral Edema Cerebral Ischemia-Infarction, Acute

diffuse hypodensity,
decreased gray-white matter
differentiation, & diffuse
sulcal effacement in the righl
hemisphere. Note a/50
hemorrhage
=-=-
traumatic subarachnoid
hemorrhage subdural
mass effect,
& leftward midline shift.
classic wedge-shaped acute
=-
infarction with hypodensity
loss of gray-while
interface, & insular ribbon, as
well as effacemenl of sulci &
ipsilateral ventricle.
Cerebral Infarction, Chronic Alzheimer Dementia

right lemporallobe infarcl as
a wedge-shaped
encephalomalacic
low density margins
gliOlic brain. Associated
=
brain with
of
dystrophic calcification is.=

rare. Ipsilateral ventricle ;s
mildly enlarged from volume
loss 8:1. (Right) Axial FLAIR
MR shows typical findings of
Alzheimer dementia with
more pronounced atrophy
involving the temporal lobes,
left more than righI, besl
evidenced as asymmetry of
I the cortices & sylvian fjssures

8:1.
6
4
ASYMMETRIC CEREBRAL HEMISPHERES en
7';
c:
III
:l
a.
lXl
.,
CMV, Congenital III
Multi-Infarct Dementia
(Left) Axial NECT shows the
:l
classic appearance of en
c:
multi-infarct dementia with -0
perivenlricular while matter m
hypodensity =:I as well as CO
multiple bilateral MCA
distribution cortical infarcts
-
:l
o
.,
iil
~. (Right) Axial NECT
shows bilateral OJ
.,
III
perivenlricular calcifications
=
=:I and ventriculomegaly
left.
right more involved than
:l
-U
III
.,
CD
:l
()
::r
'<
3
III
Dyke-Davidoff-Masson
(Left) Axial NEeT
demonstrates a classic CT
appearance of
frontotemporal dementia,
also known as Pick disease,
with bilateral frontal and
temporal lobe atrophy
right side more involved than
=-
left. (Right) Axial NEeT
demonstrates left-sided
hemispheric atrophy with
ipsilateral ventricular
enlargement =:I and osseous
hypertrophy with
hyper-pneumatization of the
sinuses~.

demonstrates asymmetric
perivenlricular white matter
infarction and loss from
HIE. (Right) Coronal T1 C+
MR reveals a typical MR case
of viral encephalitis =:I
without significant
enhancement, mimicking a
low grade glioma or infarct.
I
6
5
'>,"
E
ASYMMETRIC CEREBRAL HEMISPHERES
.!:
U
C
<ll
~
0.. 'c"
Sturge-Weber Syndrome
~
'" (Left) Coronal TI C+ MR
(D
demonstrates right
·C 'o" hemiatrophy with extensive
serpentine pial enhancement
C
<ll from pial angiomatosis =.
"§ (Right) Coronal oblique 3D
a. CT reconstruction shows
:J unilateral right coronal
(/)
synostosis resulting in
c:
asymmetry. Craniosynostosis
co
~ of one suture leads to
[JJ
excessive growth of unfused
"tJ
c sutures and significant
co plagiocephaly.
:J
-"(/)
Hemimegalencephaly of Tuberous
MElAS Sclerosis
right temporal lobe cortical
hyperintensily and swelling
with relative sparing of
underlying while mailer =::I.
Under/ying white matter
sparing, MRS is helpful in
making distinction. (Right)
Axial NECT reveals Ihal the
en/ire lefl frontal lobe is
replaced by a
hamartomatous overgrowth
of disordered and partially
calcified neural tissue =.
Hislologically Ihese lesions
share characteristics with
hemimegalencephalyand
are uncommon.
Hemimegalencephaly (Sporadic or
Familial)
confirms enlargement of leFt
cerebral hemisphere with left
Fornix = overgrowth. In this
patient, there is normal
signal inlensily of gray and
white matter despile the
asymmetry. (Right) Axial
FLAIR MR demonstrates
cerebral asymmetry resulting
from right perisylvian cortical
dysplasia =::I.
I
6
6
ASYMMETRIC CEREBRAL HEMISPHERES Ul
""c:
III
::;,
Co
.,
[Jl
III
Gliomatosis Cerebri Epidermal Nevus Syndrome
::;,
hyperinlensily involving bOlh en
c:
the cortex and subcortical .,
"0
while mailer of the right Ol
tempora1- parietal, and CD
occipital lobes =.NOle
::J
8"
.,
infiltration into the insula,
w·
basal ganglia, and internal
capsule !:l as well as mild .,
III
Ol
mass effect upon lhe right
::J
lateral ventricle. (Right) Axial -0
T2WI MR shows left .,
Ol
hemimegalencephaly Sl
diffuse gyralthickening
& hyperintense
=- CD
::J
(")
::r
'<
demyelination !:l ipsilaleral 3
Ol
to facial hemihyperlrophy.
Encephalocraniocutaneous Lipomatosis
a small dimple on the lateral
wall of lhe lateral ventricle
"poin!ing" to the site of the
fused pial-ependymal seam
The aperlUre of the clefl
is lined by helerolopic gray
mailer 81. (Right) Axial
NECT demonstrates
unilateral, lefl-sided
hemispheric atrophy wilh
associated enlargement of
the left lateral ventricle and
subarachnoid space over the
hemisphere =. An overlying
scalp lipoma is not shown.
Proteus Syndrome Proteus Syndrome

(Left) Axial low field T2WI
MR shows righl
hemimegalencephaly in a 6
year old girl with normal
karyotype and PrOleus
syndrome. Note mild
ipsilateral venlriculomegaly
81 and prominenl soft
!issues =. (Right) Coronal
low field T1WI MR shows
right hemimegalencephaly in
lhe same pa!ien!. Note mild
ipsilateral ventriculomegaly
81 and prominent skull/sofl
tissues =.
I
6
7
ro THICK CORTEX
E
>-
-'o=
c o Enhancement, hemorrhage follow
~
Q)
ro
CL
c
.~
• Encephalitis • Hypomyelination (Pseudo Thick Cortex)
CO o Diminished/absent white matter (WM)
ro
• Herpes Encephalitis
'C myelination for age
o Less Common
C • Lacks peripheral "arborization" of white
Q)
• Hypomyelination (Pseudo Thick Cortex) matter
ro~ • Tuberous Sclerosis Complex
a. o Can be primary or secondary
~
CfJ • Taylor Cortical Dysplasia • Primary hypomyelination (e.g.,
c: • Pachygyria-Polymicrogyria Pelizaeus-Merzbacher )
ns
~ • Hemimegalencephaly
CO
• Secondary (prematurity, malnutrition)
"0 • Lissencephaly Type 1 o Imaging
c:
ns Rare but Important • "Pseudo" thick cortex appearance
• eoplasms Associated with Cortical • Poor gray-white differentiation on Tl WI
Dysplasia in children> 1 year
o DNET • Poor gray-white differentiation on T2WI
o Ganglioglioma in children> 2 years
o Dysplastic Cerebellar Gangliocytoma • Small brain with thin corpus callosum
• Glioblastoma Multiforme • Tuberous Sclerosis Complex
• Gliomatosis Cerebri o Flattened, thickened gyri with "blurred"
• Meningioangiomatosis GM/WM border
• Congenital Muscular Dystrophy o Can be calcified, involve entire mantle
o Look for subcortical WM hyperintensities,
subependymal nodules
ESSENTIAL INFORMATION • Taylor Cortical Dysplasia
Key Differential Diagnosis Issues o Also known as focal cortical dysplasia
• EXCLUDES transient (e.g., MELAS, cortical (FCD) type 2A/B
edema from stroke/seizure, etc.) o "Balloon cell" dysplasia
• Is cortex thick on both Tl and T2W o Malformation of cortical development
sequences? o Refractory focal epilepsy
• Does cortex follow gray matter signal o Thickened cortex with Tl hyperintensity,
intensity (malformations)? or is it T2 hypointensity in infancy
hyperintense (infection, neoplasm)? • Rare Ca++
• Is thickened cortex very focal (think o Lesion conspicuity decreases with WM
neoplasm)? or more generalized maturation
(malformation) ? • Pachygyria-Polymicrogyria
o Polymicrogyria ...•excessively small,
Helpful Clues for Common Diagnoses prominent convolutions ("gyri on gyri")
• Encephalitis o Pachygyria (sometimes called incomplete
o Commonly identified agents: Enterovirus, lissencephaly) ...•thickened, dysplastic
HSVl, Mycoplasma pneumonia, cortex
Epstein-Barr, HHV-6, influenza o Both cause appearance of "thick cortex" on
o Etiology not found in '" 50%
imaging
o Hyperintense on T2WI, FLAIR o Density/signal intensity of affected cortex
o Thickened, hyperintense temporal same as normal gray matter
lobe/insular cortex • Hemimegalencephaly
• Herpes Encephalitis o Hamartomatous overgrowth of part/all of a
o Often bilateral, asymmetric
hemisphere
o Look for cingulate gyrus, subfrontal cortex
o Enlarged hemisphere with thickened,
I involvement
o Restricts strongly on OWl
often dysplastic cortex
6
8
THICK CORTEX CIl
"
C
III
o Ipsilateral ventricle often enlarged, • Glioblastoma Multiforme ::::l
Co
abnormally shaped o White matter> > gray matter
o Tumor infiltration of cortex, subpial
..•
OJ
o White matter often overgrows, is III
::::l
hypermyelinated extension may occur late
o Hemorrhage, enhancement common en
• Lissencephaly Type 1 c
"0
o Most severe type (complete agyria) is o Primary GBM (older patient) 95% necrotic OJ
Miller-Dieker syndrome with thick irregular enhancing rim CD
OJ
o Thick, multilayered cortex o Secondary GBM (younger patient) shows 0-

OJ.
o "Hour glass" configuration with shallow enhancing focus within lower grade tumor Ql
CD
sylvian fissures in severe cases • Gliomatosis Cerebri OJ
o Tumor infiltrates but preserves underlying OJ
Helpful Clues for Rare Diagnoses \J
brain architecture Ql
• DNET o Two or more lobes affected CD

OJ
o Young patient, longstanding seizures ()
o T2 hyperintense infiltrating mass enlarges ::T
o Well-demarcated "bubbly" intracortical '<
cortex, basal ganglia 3
mass Ql
o MRS shows elevated myo-inositol (mI)

o Often associated with adjacent cortical
o Most are WHO grade II or III diffusely
dysplasia
infiltrating astrocytoma
• Ganglioglioma
o Child/young adult, seizures • Meningioangiomatosis
o Cortical mass with variable Ca++
o Superficial hemispheres, temporal lobe
o Linear &/or gyriform enhancement
o Cyst with nodule, ± Ca++, enhancement
o Perivascular proliferation of vessels in
typical
meninges, cortex
o Solid ganglioglioma can resemble Taylor
o May infiltrate along perivascular spaces,
cortical dysplasia (TCD does not enhance)
cause mass effect
• Dysplastic Cerebellar Gangliocytoma
• Congenital Muscular Dystrophy
o Thickening, overgrowth of cerebellar folia
o Cobblestone lissencephaly (overmigration)
o Gyriform "layered" or "striated" pattern
o Z-shaped brainstem
o Can cause significant mass effect
o Hypoplastic rotated cerebellum (similar to
o Cowden-Lhermitte-Duclos (COLD)
Dandy-Walker continuum)
syndrome is considered new phakomatosis
• Multiple hamartoma-neoplasia syndrome
• Long term cancer screening (breast,
thyroid)
I
hippocampal SI, temporal lobe cortex =-
Coronal FLAIR MR shows subl!c, but bilateral
and insular
Coronal FLAIR MR shows swollen, hyperintense
temporal lobe cortex ~ with relative sparing 01 the
6
COrlex ;>J signal increase and swelling in a child with underlying white matter. OWl (not shown) revealed
proven Mycoplasma encephalitis. restricted diffusion in insular cortex, cingulale gyri.
9
co THICK CORTEX
E
>-
.r:
u
c
~
OJ
co
ll.
c
~ (Left) Axial NECT in a 4
co month old with
co hypomyelination ~ shows
'C
o decreased volume and while
C matter density. The thin
OJ
ro~ arbors of while maller give a
c. false impression that the
:J cortex, especially in occipital
CJ)
poles, is thickened 81.
C
CO
~ an 18 month old with
al Pelizaeus-Merzbacher
"0
c disease (PMD) shows white
CO maller hypomyeJinalion in
cerebellum =-
occipital lobes 81 and
giving the
appearance of prominent
thick cortex.
Tuberous Sclerosis Complex Tuberous Sclerosis Complex

multiple large, (fat, thickened
gyri with classic subcortical
hyperinlensilies E1
characteristic for cortical
tubers. (Right) Axial T2WI
MR in an 8 month old shows
two maniFestations of
tuberous sclerosis complex:
Densely calcified, thickened
transmantle hamartoma =
in the right parietal lobe and
2) characteristic "tubers" ~
in the left. Note multiple
subependymal nodules 81.
(Left) Coronal PO FSf MR

shows focaf cortical
thickening with high signal of
the expanded gyrus 81.
(Right) Axial CECT in the
same child shows a focal low
density, noncalcified
cortical/subcortical mass Ea.
There is no enhancement,
and there are neither
subependymal nodules nor a
foramen of Monro giant cell
astrocytomas.
I
6
10
TH ICK CORTEX en
c"
:
III
::l
Q.
..•
OJ
III
(Left) Axial T2WI MR in a 10 ::l

month old with refractory (j)
c
"...
seizures shows bilateral
perisylvian foci of
polymicrogyria =- giving
the appearance of thick
III
ro::l
o
cortex. Note abnormal veins
...
!:ll and subtle laminar ~
heterotopia 81. (Right) ...
OJ
III
Sagittal T1WI MR shows a
::l
thick cortex ~ lining the -U
sylvian fissure in another ...
Q)
child with bilateral primitive Ctl

:J
sylvian fissures and (')
:r
perisylvian polymicrogyria. '<
3
III
pachygyria- Polymi crogyria

unilateral fronto-parietal
polymicrogyria with blurring
of the gray-white junction 81
and a nodular appearance
=. (Right) Axial T2WI MR
in a different child shows a
much more extensively
involved brain. Both
hemispheres have a diffusely
thickened, striated cortex
due to polymicrogyria.
Hemimegalencephaly
(Lcft) Axial T2WI MR shows
expanded left hemisphere
with diffuse overgrowth of
while maller = and some
gray matter as well =.
shows a diffusely thickened,
partially calcified left frontal
cortex 81. The remainder of
the left hemisphere has
decreased signal intensity
throughout gray and white
matter~
I
6
11
co THICK CORTEX
E
>,
£
U
C
~
Q)
co
0..
c
co
~ (Left) Axial T1 WI MR in a 2
(])
week old shows layered
co appearanCe of cortex with
'C
o thick inner band of gray SI
C mailer and thin outer layer
Q)
ro~ ~.
sparse!1
In between ;s the "cell
while matter zone
a.
:::l
(/) =::I. (Right) Coronal T1 WI
MR shows a thickened
c "cobblestone" cortex ~ and
•..
C1l
(])
a hypoplastic cerebellum .
The 4th ventricle =::I is
"0
C opened inferiorly due to
C1l vermian hypoplasia and
cephalad rotation.
DNET
thickened, hyperintense
cortically based mass with
"rim sign" of hyperintensity
on FLAIR =::I. Lack of edema
also is characteristic for
ONET. (Right) Axial T7WI
MR shows typical
multinodular low signal
intensity mass SI focally
expanding the cortical
mantle and remodeling the
inner cortex ~ of the
calvarium.
(Left) Axial PO rSf MR

shows thickened,
hyperintense cortex =
in a
S year old with epilepsy.
Without contrast-enhanced
scan, this image would be
indistinguishable from Taylor
cortical dysplasia. (Right)
Axial T7 C+ MR in the same
patient shows several small
enhancing foci =.
Ganglioglioma was found at
surgery.
I
6
12
THICK CORTEX ,..
en
c:

a striated ;50- and
hypointense posterior fossa
mass E!l2 that displaces the
4th ventricle~. There is an
additional epidermoid cyst
1:11. (Right) Coronal T2WI
MR shows thickened,
striated-appearing cerebellar
{olia ~ in a patient with
Lhermiue·Ouc/os disease. In
this case, there was no
association with Cowden
syndrome.
(Left) Coronal T2WI MR in a
74 year old shows iso- &
hyperintense right temporal
lobe & insular mass 1:11
involving both gray & white
maller. Note necrosis, Focal
hemorrhage liB Tumor
spread across anterior
commissure thickens the left
temporal lobe cortex ~
shows a typical case of
meningioangiomatosis, most
commonly found in NF2.
Fine gyriform increased
density was present on
NECT FLAIR MR shows
linear increased signal ~.

adult shows involvement of
the temporal pole cortex Sl
hippocampus ffi &
mesencephalon
Involvement of more than
one lobe or region is typical
of gliomatosis cerebri.
(Right) Axial T2WI F5 MR in
a 12 year old shows
hyperintense, swollen gyri
I:] with involvement of the
midbrain E!l2 related to
gliomatosis cerebri. WI 10
grade III diffusely infiltrating
astrocytoma was found.
(Courtesy M.
WarmUlh·Metz, MOr I
6
13
ell THIN CORTEX
E
>-
.r:
u
c • Pre- and post-central gyri myelinate early
~
Q)
ell
0..
• Hyperintensity on Tl WI, hypointensity
c Common on T2WI normal
ell
~ • Aging Brain o Note: White matter injury of prematurity
(D
ell
• Prematurity spares GM
.t:
o • Obstructive Hydrocephalus • Undulating ven tricular borders,
C • Cerebral Infarction, Chronic ventriculomegaly
Q)
Til • Encephalomalacia, General • Generalized volume loss due to " WM

Q.
::J
(f) Less Common • Obstructive Hydrocephalus
• Multiple Sclerosis o "Maximal" hydrocephalus thins cortical
C
Ol
~ • Alzheimer Dementia mantle
CO o May be difficult to distinguish from
"'C • Multi-Infarct Dementia
C
Ol • Frontotemporal Dementia hydranencephaly on NECT
• MR diagnostic
::l Rare but Important • Cerebral Infarction, Chronic
-"
en • Microcephaly o Usually wedge-shaped, involves both
• Subcortical Laminar Heterotopic Gray cortex & underlying WM
Matter o "Hierarchy" of vulnerability to territorial or
• Inborn Errors of Metabolism (Gray Matter hypotensive ischemia
Disorders) • CAI hippocampus most sensitive
• GM generally more vulnerable than WM
ESSENTIAL INFORMATION o Collateral flow across pial watershed
(border zones) may permit cortex within
Key Differential Diagnosis Issues ischemic penumbra to survive
• Is cortical thinning focal (typical for o Thin rim of cortex may persist adjacent to
encephalomalacia) or generalized? densely ischemic core of infarct
• Is cortex thin but normal signal intensity? o Often hyperintense on T2/FLAlR,
o If abnormal, consider infection, infarction,
reflecting spongiosis/gliosis
trauma, etc. • Encephalomalacia, General
• Child vs. adult o Trauma, infection, toxic-metabolic insults
o Child: History important o May primarily affect GM, WM, or both
• Prematurity, family history of inborn o Can be generalized (e.g., following global
error of metabolism hypo perfusion) or focal
• Seizures (heterotopias,
encephalomalacia) Helpful Clues for Less Common Diagnoses
o Adult: Normal cognitive function or • Multiple Sclerosis
demented? o Multiple T2/FLAlR hyperintensities
perpendicular to callososeptal interface
Helpful Clues for Common Diagnoses o Chronic, severe multiple sclerosis (MS)
• Aging Brain causes variable brain atrophy
o White matter (WM), not gray matter (GM)
• WM»GM
volume loss predominates in normal • But normal-appearing GM may have
"successfully aging" brain abnormal metabolic profile with" NAA
• Posterior vermis, cerebellum> cerebral • Cortical loss in secondary-progressive MS
hemispheres common
• Cortical thinning minimal • Alzheimer Dementia
o "Black line" in visual, motor/sensory cortex o Alzheimer dementia (AD) is most common
common in normal older patients of all dementias
• Prematurity o Best diagnostic clue = temporoparietal
o Hemispheric WM almost completely cortical atrophy + disproportionate
I unmyelinated ("wet brain")
o Cortex always appears thin
hippocampal volume loss
• Perihippocampal fissures widen
6
14
THIN CORTEX ,.-c:
C/l
• Hippocampal, entorhinal cortex thins • Primary (genetic) microcephaly (e.g.,

• Temporal horns enlarge microlissencephaly, many syndromes)
• Perfusion MR, FDG, & PET can identify • Secondary (nongenetic) microcephaly
hypometabolic areas (e.g., TORCH infection, fetal alcohol
• Multi-Infarct Dementia syndrome)
o Also known as "vascular" dementia • Subcortical Laminar Heterotopic Gray
o Second most common dementia after AD Matter
• 10-30% of all dementing disorders o "Band" heterotopia ("double cortex"): LlS1
o Imaging findings vary or LISX1
• Generalized, diffuse atrophy • Thick inner band of dysplastic GM in
• Large ventricles, superficial sulci subcortical WM
• Generalized cortical thinning • Overlying cortex thin (not all neurons
• Focal territorial &/or lacunar infarcts "arrive")
• Subcortical WM T2/FLAIR o Classic lissencephaly: (LIS1)
hyperintensities • Shallow sylvian fissure ("hourglass"
• Diffuse bilateral, confluent deep WM configuration of hemispheres)
hyperintensity secondary to • Thin outer layer of GM
arteriolosclerosis • "Cell sparse" WM zone
• Frontotemporal Dementia • Thick inner band of GM
o One of several tauopathies, also known as • Inborn Errors of Metabolism (Gray Matter
Pick disease Disorders)
o Frontotemporal dementia (FTD) causes o Includes inborn errors of metabolism that
disproportionate frontotemporal atrophy affect WM > > GM
o "Knife-like" gyri with very thin cortex o Many "poliodystrophies"; all uncommon
o Subcortical WM usually hyperintense o All have similar imaging appearance
o Parietal, occipital lobes relatively spared • Generalized atrophy with t sulci,
Helpful Clues for Rare Diagnoses thinned cortex
• Microcephaly • Cortical signal generally normal
o Small head size, • craniofacial ratio
• BUT WM often hyperintense due to
o Sutural overlap common
secondary axonal degeneration
o Lysosomal (example: Neuronal ceroid
o Simplified gyri with thin cortex
o Shallow sulci
lipofuscinosis) clue
o Many causes
• Hypointense thalami (best seen on
standard T2WI, not FSET2WI)
I
Axial FLAIR MR in an intellectually normal 65 year old
shows mild ventricular, sulcal enlargement. Thin rim of
Axial T2WI MR in an elderly demented patient with
su/xordcal arteriosclerodc leukoencephalopathy shows 6
periventricular hyperintensity =::I is normal. Very mild diffuse confluent hyperintensity in hemispheric white
cordcal thinning E1 is present. matter but only mild cortical thinning E1.
15
co THIN CORTEX
E
>-
J::
U
C
Q)
L
co
0..
c Prematurity Prematurity
co
L (Left) Sagittal T2WI MR in a
co normal 28 week premalUre
co
·C infant shows thin cortical
o ribbon 81. The brain is
C smooth, and only the central
Q)
115
L
~, calcarine and
a. parielOoccipital It] fissures
:J are present. (Right) Axial
CfJ
c:
..
III
CO
shows age-appropriate,
undersulcated brain. The
shallow, "squared" sylvian
"C
c: fissures are normal, as is the
III very thin cortical mantle
overlying almost completely
unmyelinated hemispheric
while matter.
Prematurity
week normal but premature
infant shows more advanced
5ulcaliofl, with deepening of
the sylvian fissures. WM is
stiff largely unmyelinated,
and cortex appears thin 81.
(Right) Axial T2WI MR in the
same premature baby shows
thin cortical mantle overlying
almost completely
unmyelinated white matter
with the exception of
hypointense WM Ii8 deep to
the central sulci. Mild
hypointensity of the cortex of
pre-, post-central gyri E±I is
normal.
Obstructive Hydrocephalus Obstructive Hydrocephalus

(Left) Coronal NECT in an 11
week old infant shows
"maxima/" hydrocephalus.
Note massively enlarged
ventricles within huge
cranium. Very thin, almost
imperceptible cortical mantle
am surrounds ventricles.
Posterior fossa appears
comparatively small but is
actually normal in size.
the same patient after
shunting shows ventricles
remain large, cortical mantle
very thin E±J.
I
6
16
THIN CORTEX ,..c:
CII
01
:J
C.
...
OJ
01
Obstructive Hydrocephalus Obstructive Hydrocephalus
(Left) Axial T2WI MR in a :J
patient with severe
congenital hydrocephalus
after shunting shows
stenogyria with thinned,
"crenelated" cortex along
the same patient shows more
clearly the stenogyria ~
with thinned cortex along lhe
Cerebral Infarction, Chronic Cerebral Infarction, Chronic

(Left) Axial T2WI MR,
obtained many years after
near-tolallefl hemisphere
infarction secondary to
internal carotid artery
occlusion, shows thin rims of
gliolic hyperintense cortex
~ surrounding cystic
encephalomalacia. (Right)
Axial FLAIR MR in a patient
with systemic lupus
erylhemalosus and multiple
old infarcts shows diffusely
atrophic right hemisphere
wilh enlarged sulci, shrunken
gyri, and markedly lhinned
cortexB.
Cerebral Infarction, Chronic Cerebral Infarction, Chronic

(Left) Axial NEeT in a child
wilh Slurge-Weber syndrome
shows small left hemisphere
with very atrophic, calcified
cortex. Dystrophic Ca++ is in
brain (nolleptomeningeal
angioma), and cortical
thinning is secondary to
chronic venous (not arteria/)
ischemia. (Right) Axial T2WI
MR in the same patient
shows how thin the affeeled
cortex
normal
-=
is compared to the
right side.
I
6
17
ro THIN CORTEX
E
>-
J:::
()
c:
~
Q)
ro
Il.
c: Encephalomalacia, General Encephalomalacia, General
ro
~ (Left) Coronal T2WI MR
OJ
obtained in a child 5 months
ro after initial neonatal group B
'C
o
~ Streptococcal meningitis
c: shows generalized volume
Q)
CO loss with gliosis and thinned

~ cortex ~ in the leFt temporal
n.
:J lobe. (Right) Coronal T2WI
CJJ
MR in child with Rasmussen
c: encephalitis shows thinned
01
~ cortex around the left sylvian
1IJ
Fissure=:I compared to the
"l:l
c: normal right side.
01
:J
""
1Il

hypointense bodies of
plaques =
caudate nuclei =..confluent
and thin cortex
81. (Right) Axial T2WI MR
shows disproportionate
atrophy of occipital lobes
with striking cortical thinning
[;8 The Heidenhain variant
of Alzheimer dementia
primarily a(Fects the occipital
cortex.
Multi-Infarct Dementia Frontotemporal Dementia

classic mulli·infarct dementia
with multi-territorial cortical
infarctions. Peri ventricular
white matter hypodensity,
multiple cortical infarcts EB
thinned cortex, shrunken
parielooccipilal gyri E:II are
all seen. (Right) Axial FLAIR
MR shows predominate
Frontal lobe atrophy with
striking cortical thinning.
Some gyri demonstrate a
classic" knife-like II
appearance =:I. There is also
associated white matter T2
hyperintensity 81.
I
6
18
THIN CORTEX
Microcephaly
infant wlhead circumference
3 standard deviations below
mean shows simplified gyral
pattern, thin corlex i7 ~
shallow sulci, & broad flat
gyri. The infant had familial
autosomal recessive
microcephaly. fRight) Axial
T2WI MR in an 8 month old
with microcephaly related to
congenital CMV shows thin
cortex [;8 delayed
myelination. Germinolytic
cysts ffi periventricular
calcifications a & large
subarachnoid spaces are also
seen.
Subcortical laminar Heterotopic Gray Subcortical laminar Heterotopic Gray

Matter Matter
week old with Miller-Dieker
syndrome shows
"hourglass-shaped"
smooth thin cortex =-
brain,
band of subcortical laminar

thick
heterotopic gray matter [;8

and primitive veins in sylvian
fissures !:ill. (Right) Sagiltal
T1 WI MR shows subcortical
"bands II or II ribbons II of
heterotopic gray matter ~
separated from thinned
overlying cortex S'I by a
strip of myelinated white
maller
Inborn Errors of Metabolism (Gray Inborn Errors of Metabolism (Gray

Matter Disorders) Matter Disorders)
child with neuronal ceroid
lipofuscinosis (CLN3 or
Batten variant) shows
markedly thinned cortex S'I
throughout both
hemispheres. Thalami are
shrunken, very hypointense
=. fRight) Axial T2WI MR
in a child with lysosomal
storage disorder (CLN 7 )
shows generalized atrophy
with very thin cortex !:ill,
classic "dark"thalamiG &
basal ganglia S'I.
I
6
19
FOCAL CORTICAL MASS
DIFFERENTIAL DIAGNOSIS o Usually solid, may be complex with central

cystic or necrotic areas
Common o May be hemorrhagic with increased Tl SI
• Cerebral Ischemia-Infarction, Acute o May be solitary but frequently are multiple
(Cortical) & bilateral
• Metastases, Parenchymal • Oligodendroglioma
• Oligodendroglioma o T2 hyperintense mass, variable
• Cerebritis enhancement
• Diffuse Astrocytoma, Low Grade o Calcification is common
Less Common o Frontal> other lobes; usually a single mass
• Venous Infarction • Cerebritis

• Pleomorphic Xanthoastrocytoma o Gray & white matter are often involved
• Tuberous Sclerosis Complex together
• Pachygyria-Polymicrogyria (Focal Cortical o T2 hyperintense with variable
Dysplasia) enhancement & variable DWI appearance
o Cerebritis essentially represents a
• DNET
• Ganglioglioma developing brain abscess & is commonly
caused by pyogenic bacteria
Rare but Important o May be solitary or multifocal
• Pilocytic Astrocytoma • Diffuse Astrocytoma, Low Grade
• Cavernous Malformation o T2 hyperintense WM mass, may involve
• Desmoplastic Infantile Ganglioglioma gray matter
• Viral Encephalitis o May mimic stroke; however ADC values
• Astroblastoma typically normal to elevated
o No or minimal enhancement is typical
ESSENTIAL INFORMATION o Usually a solitary mass
o Bilateral disease may be seen in gliomatosis
cerebri, a rare infiltrative process
• Venous Infarction
o T2 hyperintense lesion
o Associated hemorrhage is very common,
often at gray-white junctions
o Typically related to dural sinus thrombosis
o May be multiple & bilateral if the superior
sagittal sinus is involved
• Pleomorphic Xanthoastrocytoma
o Cortical enhancing mass with adjacent
cyst, classic appearance
o Enhancement extends to meninges,
causing a "dural tail"
o Temporal lobe is most common location
o Occurs in young adults
• Tuberous Sclerosis Complex
o Multiple cortical "tubers" = cortical
hamartomas are T2 hyperintense &
nonenhancing
o Calcified subependymal nodules ±
enhancing giant cell astrocytoma at the
I foramen of Monro is classic
o Usually a multiple & bilateral process
6
20
FOCAL CORTICAL MASS en
"
s::
III
o When solitary, consider Taylor cortical • Cavernous Malformation :l
C.
dysplasia o Heterogeneous mass with a "mulberry"
• Pachygyria-Polymicrogyria (Focal Cortical appearance related to blood products
..•
tll
III
:l
Dysplasia) o Hemosiderin ring "blooms" on GRE; Tl
(J)
o Limited to gray matter; focal or regional bright locules s::
"0
thickening of the cortex o May have increased CT density &/or Q)
o Variable T2 appearance; no enhancement punctate calcifications CD
:::J
o Many have deep sulci with thickened o Sometimes associated with a 8"
00.
Ol
cortex that mimics a mass developmental venous anomaly
o Occasionally a linear region of increased o May be deep as well as cortical ..•
CD
Ol
T2 signal connects the focal cortical o May be solitary or multiple, bilateral :::J
-U
dysplasia with the ependymal surface • Desmoplastic Infantile Ganglioglioma ..•
Ol
• DNET o Frontal/parietal locations common (t)

:::J
o
o Multicystic cortical mass, frequently seen o Cystic mass with enhancement ::T
'<
in the temporal lobe o May be massive, occupy majority of 3
Ol
o "Bubbly" appearance classic hemisphere
o Variable enhancement o Presentation occurs when younger than 6
o Solitary lesion in a young adult typical months
• Ganglioglioma • Viral Encephalitis
o Enhancing (multi)cystic mass; may be o Cortical swelling; minimal enhancement
solid or have a cyst & nodule appearance o Not in a typical vascular territory
o Calcification is common o Temporal, frontal, cingulum are often seen
o Temporal lobe is most common location in herpes simplex virus
o Solitary lesion • Astroblastoma
o Large hemispheric solid & cystic mass with
heterogeneous enhancement of solid
• Pilocytic Astrocytoma
o Enhancing nodule with or without an
portion
o Superficial mass involves cortex &
associated cyst, most common appearance
subcortical WM typical
o Children> adults
o Children & young adults
o Cerebellum & optic pathways are frequent
locations
o May rarely occur in the cortex
o Solitary lesion
Cerebral Ischemia-Infarction, Acute

(Cortical) Metastases, Parenchymal
I
Axial OWl MR shows hyperinlensily & mass effecl in the
right middle cerebral artery vascular distribution =
Axial
junction
CECT shows
=..
2 masses localed al Ihe gray-while
each with low density in the adjacent
6
related to acute ischemia. A wedge-shaped lesion in a while maller representing vasogenic edema H2.
vascular territory is classic. 21
co FOCAL CORTICAL MASS
E
>-
.r:
u
c
~
co
a..
c Cerebritis
~ (Left) Axial FLAIR MR shows
(lJ
a high signal mass SI
co containing a {ocal area of
'C
o lower signal:±" representing
C a calcification within the
OJ
1§a. tumor. A calcified frontal
lobe mass involving the
:::J cortex & subcortical while
(/)
maller is typical of
C
III
'-
III
patchy enhancement
"0
c significant edema, & mass
III effect. A mature abscess wall
& central cavity are not yet
present, differentiating
cerebritis from abscess.
Diffuse Astrocytoma, Low Grade Venous Infarction

a well-circumscribed frontal
lobe diffuse astrocytoma,
low grade Ea. There was no
significant enhancement of
the mass following contrast
injection. (Right) Axial NECT
shows ill-defined low density
~ associated with
subcortical hemorrhages
and a hyperdense superior
=
sagittal sinus E:I.
Ilemorrhage is common in
venous infarction. The
parenchymal findings can
mimic a primary tumor or
metastases.
Pleomorphic Xanthoastrocytoma Tuberous Sclerosis Complex

enhancing parenchymal
nodule SI associated with a
cyst = in the temporal lobe.
These features are
nonspecific but are typical of
PXA. (Right) Axial T2WI MR
shows several areas of high
T2 signal & slight mass effect
representing cortical
hamartomas ("tubers")~.
There are several
subependymal nodules,
some with dark signal
suggesting calcification ~
Subependymal nodules often
I enhance, while cortical

tubers rarely do.
6
22
FOCAL CORTICAL MASS CJ)
:0:-
c:
Pachygyria-Polymicrogyria (Focal
Cortical Dysplasia) DNET
bilateral deep sulci lined with
pebbly dysplastic cortex =.
Band-like heterotopic gray
mailer is also seen bilaterally
E2. The lack of
normal-appearing gyri &
unusual cortex makes this a
mimic of focal mass. (Right)
mass in the
parieto-lemporal-occipital
junction with a central
cystic area liB The mass did
not enhance with contrast
material. A mullicystic
"bubbly" appearance is
common.
Pilocytic Astrocytoma
(Left) Coronal T I C+ MR
shows an enhancing nodule
~ associated with a tumor
cyst E2. The findings are not
specific but are typical of
ganglioglioma. The temporal
lobe is a very common
location for ganglioglioma.
Patients typically present
with seizures. (Right) Axial
T7 C+ MR shows an
occipital lobe enhancing
nodule E2 associated with a
small cyst =. The findings
are not specific but are
typical of pilocytic
astrocytoma.
(Left) Coronal T2 CRE MR
shows typical hypointense
appearance of a cavernous
malformation [;8 The lesions
may be calcified but usually
"bloom" 0/1 CRE due to
contained blood products.
They may be associated with
anomaly. (Right) Coronal T7
C+ MR shows a very large
right hemispheric,
predominantly cystic mass
with an enhancing mass
along the medial wall =.
Findings are nonspecific but
typical of this entity.
I
6
23
co CORTICAL HYPERINTENSITY T2/FLAIR
E
>-
.r:
l>
c o T2 hyperintense cortically based,
Q)
co
0...
wedge-shaped lesions at border zone
c Common between vascular territories
co
~ • Cerebral Ischemia-Infarction, Acute o Edematous gyri with local mass effect
I:!l
co • Cerebral Contusion o May involve basal ganglia (BG) & thalamus
·C
o • Hypotensive Cerebral Infarction o DWI positive acutely
C • Status Epilepticus • Status Epilepticus
Q)
CO
~ • Herpes Encephalitis o T2 hyperintensity in GM &/or subcortical
a.
:::J
(/) Less Common WM with mild mass effect
• Diffuse Astrocytoma, Low Grade o May focally involve hippocampus or
C
CO
• Acute Hypertensive Encephalopathy, PRES corpus callosum
'-
I:!l o DWI positive acutely; variable
"t:l • Vasculitis
C
CO • Oligodendroglioma enhancement
• Anaplastic Oligodendroglioma • Herpes Encephalitis
• Hypoxic-Ischemic Encephalopathy, NOS o T2 hyperintensity in the limbic system &
• DNET temporal lobes; DWI positive
• Pleomorphic Xanthoastrocytoma o Subtle blood products, patchy
• Tuberous Sclerosis Complex enhancement common
o Typically bilateral, but asymmetric
• Cerebritis
o Acute onset, often with fever; may present
• Hypoglycemia
with seizures
Rare but Important
• MELAS(Acute Presentation) Helpful Clues for Less Common Diagnoses
• Creutzfeldt-jakob Disease (C]D) • Diffuse Astrocytoma, Low Grade
• Dysplastic Cerebellar Gangliocytoma o Infiltrating T2 hyperintense WM mass
o May extend to involve cortex
o No enhancement typical
ESSENTIAL INFORMATION • Acute Hypertensive Encephalopathy,
Key Differential Diagnosis Issues PRES
• Vast majority of cortical lesions are related o Patchy cortical/subcortical PCA territory
to ischemia & trauma lesions in a patient with severe
• Remainder of lesions much less common acute/subacute hypertension (HTN)
and include primarily tumors & infections o Parietooccipital T2 hyperintense cortical
• DWI may help differentiate lesions lesions in 95%

o DWI: Usually normal
Helpful Clues for Common Diagnoses o Variable patchy enhancement
• Cerebral Ischemia-Infarction, Acute o Diverse causes, clinical entities with HTN
o T2 hyperintensity in a typical vascular • Vasculitis
distribution (ACA, MCA, PCA) o Multiple small areas of T2 hyperintensity
o Wedge-shaped, involves gray matter (GM) in deep & subcortical WM, often bilateral
& white matter (WM) o GM involvement common
o DWI restriction o DWI positive in acute setting
• Cerebral Contusion o Variable enhancement
o T2 hyperintensity in inferior frontal & • Oligodendroglioma
temporal lobe GM & subcortical WM o Calcified T2 hyperintense frontal mass
o Blood products nearly always present o Slowly growing but diffusely infiltrating
oCT: Patchy superficial hemorrhages with cortical/subcortical mass
surrounding edema o Variable enhancement
o History of trauma • Anaplastic Oligodendroglioma
• Hypotensive Cerebral Infarction o Calcified frontal lobe mass involving
I o "Border zone" or watershed infarct related
to insufficient cerebral blood flow
cortex/subcortical WM, ± enhancement
o May appear discrete, but always infiltrative
6
24
CORTICAL HYPERINTENSITY T2/FlAIR C/l
;J("
c:
Ql
o Difficult to differentiate from o Parietal, occipital lobes > temporal or BG ~
c.
oligodendroglioma o OWl: Restricted diffusion, decreased AOC
..,
OJ
• Hypoxic-Ischemic Encephalopathy, NOS (may be transient) Ql
o Bilateral cortical involvement common ~

Helpful Clues for Rare Diagnoses C/l
o Oeep gray nuclei often involved
• MELAS (Acute Presentation) C
..,
'0
o OWl positive in acute setting
o Mitochondrial encephalopathy, lactic OJ
• DNET 10
acidosis, and stroke-like episodes ::J
o Well-demarcated, wedge-shaped "bubbly" 8'
..,
o Multifocal bilateral 1'2 hyperintensities, 0;'
cortical mass typically reversible OJ
o Temporal & parietal lobes most common
o Predominantly GM involvement, may OJ
o May remodel overlying bone ::J
involve subcortical WM -0
o Typically a young patient with OJ
o MRS shows lactate peak
longstanding seizures CD
::J
• Creutzfeldt-jakob Disease (CjD) o
• Pleomorphic Xanthoastrocytoma o Rapidly progressing, fatal, potentially
::r
'<
o Supratentorial 1'2 hyperintense cortical 3
transmissible dementing disorder OJ
mass with adjacent enhancing dural "tail" o Progressive 1'2 hyperintensity of BG,
o Enhancing nodule abuts pia
thalamus, & cerebral cortex (gyriform)
o Temporal lobe most common site
o OWl positive
o Found almost exclusively in young adults
o Frontal & temporal lobe cortex most
• Tuberous Sclerosis Complex commonly involved
o 1'2 hyperintense cortical & subcortical
o Occipital lobe involvement in Heidenhain
tubers variant
o Calcified subependymal nodules nearly
• Dysplastic Cerebellar Gangliocytoma .
always present
o Enlarged 1'2 hyperintense cerebellum with
o Subependymal giant cell astrocytoma 15%
preservation of folia
o Taylor cortical dysplasia: Solitary tuber in
o Striated, laminated, or "tigroid" appearance
cortex & subcortical WM o Associated with Cowden syndrome
• Cerebritis
01'2 hyperintense "mass" with mass effect Alternative Differential Approaches
o Typically DWI positive • Temporal lobe cortical lesions: Ischemia,
o Patchy enhancement contusion, status epilepticus, herpes
• Hypoglycemia .. encephalitis, ONET, PXA
o Severe parietooccipital edema or mfarcts m
a newborn with seizures
I
Axial T2WI MR shows a local cortical hyperintensity &
edema ~ in the medial posterior Iron tal lobe. OWl
Coronal T2WI MR shows a large hyperintense
involving the cortex & subcortical while matter ~
lesion
with 6
restriction & history
cerebral artery inlarct.
confirmed this acute anterior central blood products
Additional contusions =
related to a
are also present.
contusion.
25
co CORTICAL HYPERINTENSITY T2/FLAIR
E
>-
.r:
u
c
~
co
11.
c
co
(lJ
hyperinlensily in the cortex &
co
·C
o
subcortical white matter =
in a patient with a severe
C hypotensive event & a
Q)
ro~ Iypical walershed patlem of
a. ischemia. (Righi) Coronal
:::l FLAIR MR shows
(f)
c: subcortical while maller of
•..
Ol
10
Ihe temporal lobe in a
parienl imaged following a
"0
c: long episode of slatus
Ol epi/epricus. OWl may be
:::l positive acutely. Perfusion
..I< MR shows marked
en hyperemia on Ihe side of Ihe
epilepric focus aculely.
Diffuse Astrocytoma, Low Grade

(Left) Axial rLAIR MR shows
difruse swelling &
hyperintensity in Ihe righl
temporal lobe & cingulate
gyri. Ilerpes encephaliris
typically allecls Ihe limbic
system & is commonly
bilateral. OWl is posirive
acutely. (Right) Axial T2WI
MR shows a difluse
hyperintense fronlallobe
mass E1 with involvement of
the corlex & underlying
white malter. Allhough Ihese
tumors may appear discrete,
they are infiltrative. Tumor
cells eXlend beyond Ihe
region of signal change.

PRES
marked hyperinlensily &
swelling 01 Ihe bilaleral
fronlO·parietal cortex II::] in
Ihis palient wilh PRES.OWl
was negalive. PRESIypically
involves the posterior
circulation but may extend
into Ihe fronlallobes when
severe. (Right) Axial FLAIR
MR shows abnormal
subcortical white maller of
Ihe parielallobes in rhis
parienl with vasculiris. OWl
is positive aculely. Bi/aleral
involvement is common.
I
6
26
CORTICAL HYPERINTENSITY T2/FLAIR
III
::l
C.
OJ
.,
DNET III
::l
a heterogeneous frontal lobe
mass. Calcification was
present on the
corresponding CT.
Enhancement is noted in
about 50% of these tumors.
Imaging of grade If & grade
Ifl (anaplastic) tumors is
often similar. (Right) Coronal
FLAIR MR shows a cortically
based, hyperintense
"bubbly" mass in this young
patient. These low grade
tumors are most common in
the temporal & parietal lobes
& often remodel the adjacent
skull.
Pleomorphic Xanthoastrocytoma Tuberous Sclerosis Complex

a heterogeneous temporal
lobe mass with a large cystic
component =. Post-contrast
imaging typically shows an
enhancing nodule abutting
the pial surface. Surgical
resection of PXA is usually
curative. (Right) Axial FLAIR
MR shows multiple
hyperintense cortical &
subcortical tubers, typical of
TSC. Calcified subependymal
nodules are present 81 but
are better seen on T1 & T2
sequences as well as CT.

hyperintensity & swelling of
the posterior temporal,
opercular, parietal, &
occipital cortex = with
blurring of gray & white
matter. Involvement of the
basal ganglia is also noted.
Imaging is typical of
profound hypoglycemia.
(Rigllt) Axial T2WI MR
shows marked enlargement
of the cerebellum with
preservation of the cerebellar
folia pattern, giving a
characteristic "striated
cerebellum" or "tigroid"
appearance. I
6
27
CIl
E
CORTICAL ENHANCEMENT
>-
~
u
c
~
Q)
DIFFERENTIAL DIAGNOSIS • Status Epilepticus
CIl
a.. o Patchy or gyriform enhancement
c Common o Underlying white matter (WM) spared
~ • Cerebral Infarction, Subacute • Acute Hypertensive Encephalopathy,
co
CIl
• Herpes Encephalitis PRES
'C
o • Hypotensive Cerebral Infarction o Patchy cortical/subcortical PCA territory
C • Status Epilepticus
Q) lesions in a patient with hypertension
CO
~ • Acute Hypertensive Encephalopathy, PRES o Patchy enhancement, may be gyriform
Cl.
::J
(fJ
• Cerebritis • Cerebritis
c: Less Common o T2 hyperintense lesion with mass effect &
ns
~ • Malignant Gliomas patchy enhancement; DWI +
CO
"tl • Vasculitis Helpful Clues for Less Common Diagnoses
c: • Hypoglycemia
ns • Malignant Gliomas
Rare but Important o May involve cortex or have subpial spread
• MELAS • Vasculitis
• Cerebral Hyperperfusion Syndrome o Multiple small areas of T2 hyperintensity
• Osmotic Demyelination Syndrome in deep & subcortical WM, often bilateral
o Enhancement patchy or gyriform
• Hypoglycemia
ESSENTIAL INFORMATION o Severe parietooccipltal edema/infarcts
Helpful Clues for Common Diagnoses o Patchy enhancement
• Cerebral Infarction, Subacute Helpful Clues for Rare Diagnoses
o Gyriform enhancement characteristic • MELAS
o Petechial hemorrhage or pseudolaminar o Multifocal bilateral T2 hyperintensities
necrosis often seen (Tl hyperintense) o Patchy enhancement
o DWI has typically normalized • Cerebral Hyperperfusion Syndrome
• Herpes Encephalitis o Carotid endarterectomy, angioplasty, or
o Predilection for limbic system post-stenting patient
o Typically bilateral, asymmetric; DWI + o Increased vessel & patchy enhancement
o Enhancement patchy or gyriform • Osmotic Demyelination Syndrome
• Hypotensive Cerebral Infarction o May rarely involve cortex
o Commonly at cortical "border zones" o Pseudolaminar necrosis &/or gyriform
o Gyriform enhancement subacutely enhancement rare
Cerebral Infarction, Subacute
I
6 Axial T7 C+ MR shows marked gyri/arm enhancement
in this subacute infarct. Remember the "2-2-2 rule" for
Coronal T7 c+ MR shows gyri/arm enhancement in the
temporal lobes & insular cortex =but
in this herpes
strokes: Enhancement begins at 2 days, peaks at 2 encephalitis patient. Bilateral asymmetric
weeks, & generally disappears by 2 months. involvement of the limbic system is most common.
28
CORTICAL ENHANCEMENT ,.-
Ul
c:
Status Epilepticus
(Lcft) Coronal T7 C+ MR
shows diffuse gyriform
cortical enhancement &
basal ganglia enhancement
~. T7 hyperintensity
representing pseudolaminar
cortical necrosis is common
in this type of ischemia.
shows gyriform & meningeal
enhancement in the right
parietal & occipital lobes,
related to status epileplicus.
Ten days after imaging, once
the patient's seizures were
controlled, there was
resolution of enhancement

PRES
multifocal areas of punctate
enhancement =.. indicating
active blood-brain barrier
disruption in this case of
PRES. PRESis typically
completely reversible but
may become complicated by
hemorrhage or infarcts.
shows patchy enhancement
SII within an ill-defined
"mass ". The lesion showed
restriction on OWl (not
shown), typical of cerebritis.
This represents the early
cerebrilis stage of abscess
{ormation.
Vasculitis
gyriform & patchy
enhancement. OWl images
(not shown) reveal bright
diffusion restriction
indicating acute ischemia.
Multiple vascular
distributions are commonly
involved. (Right) Corolla I T 1
C+ MR shows increased
vascularity in the left
hemisphere with ill-defined
punctate enhancement
suggesting blood-brain
=.
barrier leakage in this carotid
endarterectomy patiellt. OWl
is normal, & there is
increased perfusion (rCBT). I
6
29
ctl SOLITARY WHITE MATTER LESION
E
>-
.r:
u
<= Usually in deep & periventricular WM
~
Q)
ctl
ll.
o Associated with lacunar infarcts
<=
Common • Multiple Sclerosis
~ • Enlarged Perivascular Spaces (PVS) o Corpus callosum (CC) & peri 4th
IJ)
ctl
• Lacunar Infarction ventricular involvement in a young adult
"C
o • Arteriolosclerosis o Acute tumefactive lesions large with
C • Multiple Sclerosis
Q) hypointense T2 ring that enhances,
ro~ • Metastasis usually with little mass effect
a.
:J
(/J
• ADEM o Solitary lesion commonly in deep or
• Reactive Astrocytosis (Gliosis) peripheral WM & at the onset of typical
c:
CIl
~
• Glioblastoma Multiforme disease or with tumefactive lesions
IJ)
Less Common o Enhancement may be ring-like or "U"
"'0
c: • Encephalitis (Miscellaneous) shaped in the subcortical fibers
CIl
:J • Oligodendroglioma • Metastasis
• Diffuse Astrocytoma, Low Grade o May be punctate to massive, with variable
""C/)
• Anaplastic Astrocytoma surrounding edema, mass effect
• Oligoastrocytoma o Hemorrhagic in renal cell, melanoma,
choriocarcinoma
Rare but Important
o Hyperintensity, edema, & mass effect less
• Thrombosis, Cortical Venous prominent in posterior fossa, but risks
• Osmotic Demyelination Syndrome higher
• Gliomatosis Cerebri o Solitary at presentation in 45-50%
• ADEM
ESSENTIAL INFORMATION o Usually multifocal WM lesions, but can be
solitary
o Range from punctate to flocculent, with
• Majority of solitary white matter (WM) enhancement, faint & fuzzy early, ring-like
lesions are vascular or neoplastic later
Helpful Clues for Common Diagnoses o Usually 10-14 days following infection or
• Enlarged Perivascular Spaces (PVS) vaccination
o Sharp margins & lentiform, follow CSF on o Often occurs in children 3-5 years, but can
all sequences occur at any age
o May be associated with gliosis in elderly • Reactive Astrocytosis (Gliosis)
(FLAIRhyperintense rim) o Gliosis is T2 hyperintense without mass
o Solitary enlarged PVS unusual, smaller effect & often associated with focal
characteristic lesions often seen elsewhere atrophy (encephalomalacia)
in the brain o FLAIRhelpful in separating microcystic
o Usually in lentiform nuclei, rarely in encephalomalacia & gliosis (hyperintense)
thalamus from macrocystic changes (hypointense)
• Lacunar Infarction o Brain's only response to insult: Infectious,
o Usually in basal ganglia (BG), thalamus, stroke, trauma
internal capsules, less commonly in • Glioblastoma Multiforme
periventricular WM o Irregular WM mass with ring
o Mildly irregular, but sharp margins, T2 enhancement, hemorrhage
hyperintense rim, ± GRE hypointense o Mass effect, heterogeneous signal typical
hemosiderin rim o Often involves, extends across CC
o Often associated with more confluent WM
arteriolosclerotic or hypertensive changes • Encephalitis (Miscellaneous)
• Arteriolosclerosis o Most non-herpes encephalitides involve
I o Usually multiple & confluent, but can be
solitary early in the disease
BG, thalamus, midbrain, & WM
o Poorly marginated, mild mass effect
6
30
SOLITARY WHITE MATTER LESION ,.-r:::
CIl
o Usually multiple, but may be solitary in o Deep venous: Bilateral thalamic

midbrain, or with solitary cerebritis o T2 hyperintensity without diffusion
o Variable enhancement of the parenchyma restriction unless infarct has developed
or meninges o Usually subcortical WM, sparing the
• Oligodendroglioma cortex, often hemorrhagic
o Peripheral lesion, often with significant o Look for the thrombosed cortical vein
cortical involvement which may be hyperintense on Tl or
o Frontal & temporal lobes, often with skull FLAIR,hypointense on GRE
changes due to slow growth • Osmotic Demyelination Syndrome
o Calcification common, enhancement from o Central pontine myelinolysis: Pontine
none to intense hyperintensity sparing the periphery &
• Diffuse Astrocytoma, Low Grade cortical spinal tract, round or
o Often peripheral, but occurs in any lobe & trident-shaped, usually solitary
brainstem o Extra-pontine myelinolysis: BG & WM
o Poorly marginated, cortical involvement lesions usually bilateral, but may be
less common solitary
o Usually no enhancement, hemorrhage, or • Gliomatosis Cerebri
calcification o Extensive multilobar or diffuse cerebral
• Anaplastic Astrocytoma hyperintensity with minimal mass effect
o WM tumor midrange between GBM & low o Unilateral multilobar disease may appear
grade with significant overlap to be a large solitary lesion
o Typically more enhancement & mass effect Alternative Differential Approaches
than low grade astrocytoma • Solitary white matter lesions in a child:
• Oligoastrocytoma Enlarged PVS, ADEM, gliosis, encephalitis,
o Similar to low grade or anaplastic
low grade astrocytoma
astrocytoma in appearance • Solitary white matter lesions in an adult:
o May arise from a lower grade
Enlarged PVS, lacunar infarct,
oligodendroglioma or astrocytoma arteriolosclerosis, MS, metastasis, ADEM,
Helpful Clues for Rare Diagnoses gliosis, gliomas, encephalitis, venous
• Thrombosis, Cortical Venous thrombosis, osmotic demyelination
o Lesions usually solitary when isolated syndrome, gliomatosis cerebri
cortical venous
o Dural sinus: Multiple lesions
I
Axial T2WI MR shows a sharply demarcated CSF-like
hyperintensity near the anterior commissure = & lower
Axial T2WI MR shows an acute lacunar infarcUon
involving the corticospinal tract in the cerebral peduncle 6
internal capsule. This is a typicallaealian & appearance r:=.Lacunar infarctions most commonly occur in the
for a solitary enlarged PVS. basal ganglia and thalamus.
31
Cll SOLITARY WHITE MATTER LESION
E
>-
L
U
C
~
Q)
Cll
CL
c Arteriolosclerosis Multiple Sclerosis
(()
hyperintensity in the pons
Cll
·C without mass effect =:I
o related to arterioloscferosis.
C These WM lesions are most
Q)
iii common in peri ventricular &

~
Q. subcortical WM.
:J Arteriolosclerosis is expected
(fJ
in patients with a history of
C
hypertension &lor diabetes.
ltl
~ (Right) Axial FLAIR MR
(()
shows a large hyperintense
"t:l
c =
ltl
while matler lesion
a linear isointense rim =with
an
isointense juxta cortical core
:J
~ & mass effect due to a
(fJ
"" lUmefactive MS lesion.
Metastasis ADEM
a solitary T2 hyperintense
lesion in the juxta cortical
right frontal lobe white
maller. There is a small
central focus of isointensity
=:I that may be due to
hemorrhage in this testicular
embryonal carcinoma
metastasis. (Right) Axial
FLAIR MR shows a large,
tumefactive ADEM lesion =:I
with hyperinlensily sparing
the cortex. The mass effect is
less than expected for lesion
size. Gadolinium
enhancement was at the
peripheral margin.
Reactive Astrocytosis (Gliosis) Glioblastoma Multiforme

increased signal intensity in
the medial left temporal lobe
=:I (gliosis), with dilatation
of the left temporal horn !J:il
in this seizure patient with
mesia/temporal sclerosis.
shows a heterogeneous,
discrete appearing mass =
in the posterior
temporal/occipital region.
Lack of surrounding edema is
very unusual for CBM. The
hypointensity is likely related
to blood products, common
I in CBM.
6
32
SOLITARY WHITE MATTER LESION en
~
r::
III
::l
a.
III
.,
III
Encephalitis (Miscellaneous)
::l
shows edema & en
c
hyperintensity of the u
.,
temporal lobe & insula with OJ
involvement of gray & white CD
matter = with significant
::J
o
.,
mass effect due to a viral 0;'
encephalitis. The lateral
neocortical location is rare in OJ
.,
OJ
herpes. (Right) Axial FLAIR
::J
MR shows a hyperintense -0
white maller mass involving OJ
.,
the cortex with mild mass (!l
::J
effect Although this may ()
::r
mimic acute stroke, '<
extension into the ACA 3
distribution = makes that
OJ
diagnosis unlikely
Diffuse Astrocytoma, low Grade Anaplastic Astrocytoma

a frontal lobe mass centered
in the white matter with
focal low signal likely
related to cystic change.
& expansion of
Involvement
the overlying cortex =
is
less prominent than a typical
Axial fLAIR MR shows a
hyperintense WM mass
involving the insula.
Although the mass appears
discrete, tumor cells often
extend beyond the signal
abnormality =.
Imaging
mimics a low grade
astrocytoma.

a WM lesion with mild
cortical involvement & mass
effect =
ischemia.
related to venous
T2 appearance is
nonspecific, but OWl &
cortical vein abnormality
were definitive. (Right) Axial
T2WI MR shows striking
hyperintensity within the
effect =
central pons with mild mass
due to central
pontine myelinolysis (CPM).
The mass effect & sharp
geographic appearance
favors CPM over
arteriolosclerosis or
neopbsm. I
6
33
ro CONFLUENT WHITE MATTER LESIONS
E
>-
.r::
u
c • Arteriolosclerosis
~
Q)
ro o Confluent periventricular & deep WM
CL
c Common o Spares corpus callosum (CC)
ro
~ • Aging Brain, Normal
co • Chronic Hypertensive Encephalopathy
ro
• Arteriolosclerosis o Basal ganglia (BG) lacunae typical
·C
o • Chronic Hypertensive Encephalopathy o Usually deep, periventricular confluent T2
CQ)
• Multiple Sclerosis hyperintensities
ro~ • Multi-Infarct Dementia o Hypointense micro hemorrhages on T2*
0.
:J • Hypotensive Cerebral Infarction common
(f)
• Cerebral Amyloid Disease • Multiple Sclerosis
c:
<ll
~ Less Common o Radiating peri ventricular location,
co "Dawson fingers"
"0 • Glioblastoma Multiforme
c:
<ll • Radiation and Chemotherapy o Acute tumefactive lesions large with
• HIV Encephalitis hypointense T2 ring that enhances
:J
-"(f) ·PML variable mass effect
• Encephalitis (Miscellaneous) • Multi-Infarct Dementia
• CADASIL o Similar to arteriolosclerosis & chronic
• Inherited Metabolic Disorders hypertensive encephalopathy, but usually
o Metachromatic Leukodystrophy (MLD) with peripheral & cortical infarcts
oX-linked Adrenoleukodystrophy (XLD) o BG & pons infarcts common
o Alexander Disease • Hypotensive Cerebral Infarction
o Canavan Disease o Chronic hemodynamic hypotensive
o Zellweger lesions are multifocal or confluent
o Van der Knaap Leukoencephalopathies parasagittal WM lesions
o Hypomyelination o Acute hypotension may result in confluent
• ADEM juxta cortical or diffuse WM lesion often
• Enlarged Perivascular Spaces associated with cortical necrosis
• Cerebral Amyloid Disease
Rare but Important o Confluent WM hyperintensity less
• Lymphoma, Primary C S common than peripheral multifocal
• Lymphoma, Intravascular (Angiocentric) lesions
• Gliomatosis Cerebri o Multifocal juxtacortical small infarcts &
• Hypothyroidism hemorrhages of varying ages common,
• CO Poisoning with little to no BG involvement
• Subacute Sclerosing Panencephalitis
• Drug Abuse Helpful Clues for Less Common Diagnoses
• Maple Syrup Urine Disease • Glioblastoma Multiforme
o Large confluent mass that may cross CC
o Can have unusual spread patterns:
ESSENTIAL INFORMATION Ependymal, pial, which can create large
Key Differential Diagnosis Issues confluent regions
• Confluent white matter (WM) lesions are all • Radiation and Chemotherapy
T2/FLAIR hyperintense & CT hypodense o Radiation necrosis may mimic high grade
neoplasm; has low cerebral blood volume
Helpful Clues for Common Diagnoses o Leukoencephalopathy: Diffuse confluent
• Aging Brain, Normal hyperintensity
o Usually multiple T2 hyperintensities, but • HIV Encephalitis
can become confluent in late elderly o Confluent diffuse WM hyperintensity with
o Less severe for age than arteriolosclerosis atrophy classic; spares subcortical U-fibers
or chronic hypertensive encephalopathy ·PML
I o Lack history of hypertension, diabetes, or
other vascular disease
o Large multifocal or confluent subcortical
WM lesions without mass effect
6
34
CONFLUENT WHITE MATTER LESIONS en
"
c:
III
• Encephalitis (Miscellaneous) • Lymphoma, Intravascular (Angiocentric) ::>
0-
o Herpes encephalitis: Medial temporal & o Often confluent radiating periventricular OJ
.,
inferior frontal confluent T2 hyperintense hyperintensity along deep medullary veins III
::>
• Predominantly cortical, but involves WM • Gliomatosis Cerebri
Ul
o Most non-herpes encephalitides involve o Confluent or diffuse with minimal mass c:
-0
.,
BG, thalamus, midbrain, & WM effect is typical OJ
• Hypothyroidism CD
• CADASIL ::>
o Onset at age 20-40 is common o Diffuse WM hyperintensity in Hashimoto 8"
.,
iij"
o Bilateral anterior temporal subcortical encephalopathy
CD
.,
lesions appear eaL"lyin diagnosis • CO Poisoning OJ
o External capsule involvement somewhat o Diffuse WM hyperintensity in severe cases ::>
"U
specific o Globi pallidi hyperintensity classic OJ
o After age SO, frontal lobe involvement • Subacute Sclerosing Panencephalitis co::>
()
develops into confluent lesions o Diffuse T2 hyperintensity extending into ::T
'<
• Inherited Metabolic Disorders the gyri with CC involvement 3
OJ
o Usually diffuse, confluent o Diffuse atrophy with severe WM volume
o Mitochondrial usually multifocal loss late
o All present in infancy, childhood, or rarely o 0 enhancement
in young adults (Alexander disease, MLD) • Drug Abuse
• ADEM o Periventricular or diffuse WM pattern with
o Multifocal lesions, punctate to flocculent inhaled heroin or rare vasculitis
o May become confluent when massive • Maple Syrup Urine Disease
o Enhancement: Faint & fuzzy early, o Diffuse cerebellar & brainstem WM T2
ring-like later hyperintensity with lesser supratentorial
o Usually 10-14 days following infection or involvement
vaccination Alternative Differential Approaches
• Enlarged Perivascular Spaces • Inherited metabolic disorders
o Variable-sized clusters, CSF-like o Macrocephaly: Canavan, van der Knaap,
o Can cause focal mass effect
Alexander disease, mucopolysaccharidoses
Helpful Clues for Rare Diagnoses o Frontal: Alexander disease
• Lymphoma, Primary CNS o Occipital: XLD
o Callosal peri ventricular, may be peripheral,
central isointense mass, modest mass effect
I
Axial T2WI MR shows diffuse hyperintensity with
sparing of the juxlacorlical =
& deep central while
matter E:I. Findings are typical for extensive age-related
the perivenlIicular while matter =
Axial T2WI MR shows diffuse patchy hyperintensily in
due to elderly
microangiopathy, a mixed eUology of arteriolosclerosis,
6
changes in this elderly gentleman. venous collagenosis, and amyloid.
35
Cll CONflUENT WHITE MATTER lESIONS
E
>-
-'u=
c
OJ
~
Cll
D-
c Multiple Sclerosis
~ (lefl) Axial T2WI MR shows
CJ
patchy & conlluentloci 01
ro hyperintensity in the centrum
'C
C
o semiovale =
& atrophy.
Although nonspecilic, these
OJ
ro~ findings are characteristic of
Cl. chronic hypertensive
:J encephalopathy. Associated
(/)
basal ganglia inlarcts &
C
Cll
hemorrhage are common.
~ (RighI) Axial T2WI MR
CJ
shows significant,
"C
c predominantly while maller
==
nl atrophy and confluent
:J periventricular &
-'"
(/)
juxta cortical hyperintense
plaques of severe chronic
multiple sclerosis.
Multi-Infarct Dementia Hypotensive Cerebral Infarction

confluent periventricular (.~
subcortical while malter
hyperintensities It] with
minimal callosal involvement
PJ::I
& significant atrophy.
typical for arteriolosclerosis
in this multi-infarct dementia
patient. (RighI) Axial FLAIR
MR shows confluent linear
hyperintensity of the cortex,
the subcortical "U-fibers"
hypointel1sity
profound hypoxic
=
I<±. & diffuse white mailer
due to
encephalopathy in this child

with a hypotensive event.
Cerebral Amyloid Disease Glioblastoma Multiforme

confluent hyperinlensilies in
the periventricular while
matter bilaterally & severe
thinning of the involved
corpus callosum PJ::I.
Demyelination (callosal) &
small vessel disease
(periventricular) cannot be
differentiated from amyloid
angiopathy with this pattern.
(RighI) Axial PO FSf MR
shows thick hyperintense
periventricular signal
related to diffuse ependymal
=
spread of glioblastoma
I mulliforme.
6
36
CONFLUENT WHITE MATTER LESIONS CJl
""
c:
HIV Encephalitis
diffuse cloud-like CJl
c:
hyperintense signal u
throughout the centrum OJ
~
semiovale ~
the subcortical V-fibers
due to treatment-related
=
with sparing of C1l
:J
S
~
Qi.
CD
(Right) Axial FLAIR MR ~
OJ
shows conffuent high signal
:J
I:] in the periventricular & II
subcortical white matter, OJ
~
sparing the V-fibers 81. The C1l
:J
diffuse cortical & white ()
:J"
malter atrophy is typically '<
seen in lale II/V encephalitis. 3
OJ
CADASll
symmetric hyperintense
signal of the deep white
matter 81 in this patient with
EBVencephalitis. Typical
imaging fealUres include
symmetric T2 hyperintense
signal in the basal ganglia,
thalami, cortex, &/or
brainstem. (Right) Axial
abnormal hyperintense
the white malter =

conffuent lesions throughout
in the
later stage of CADASIL Note
the lack of atrophy despite
extensive disease.
Metachromatic leukodystrophy (MlD)

conffuent occipital & parietal
hyperintensities & volume
loss due to gliosis. This
distribution is classic for
persistent uncontrolled
neonatal hypoglycemia.
shows conffuent
hyperintensity in the white
matter involving the
subcortical V-fibers =.
There is normal appearing
cortex & significant white
maller volume loss due to
MLD.
I
6
37
co CONFLUENT WHITE MATTER lESIONS
E
>-
.r:
()
c
~
Q)
co
ll..
c Canavan Disease
co
CD
extensive confluent
ro
'C hyperinlensity due to
o
~ demyelination of the
c peritrigonal while maller II.]
Q)
1il
~ & corpus callosum splenium
n.
::>
= in a characteristic
(f) distribution for XLD. (Right)
Axial T2WI MR shows
c: demyelination throughout
Ol
"- the entire white maller
CD
incfuding the subcortical
"t:l
c: U-fibers in this
Ol macrocephalic infant with
Canavan disease. MR
spectroscopy would show a
characteristic elevated NAA
peak.
Zellweger Van der Knaap leukoencephalopathies

confluent white maller
hyperintensity =.:I extending
into gyri with small
caudothalamic cysts ~ &
symmetric sylvian cortical
dysplasia 8l cfassic for
Zellweger. (Righi) Axial
T2WI MR shows white
maller hyperintensity in
nearly all of the hemispheric
white maller =with partial
sulcal effacement, sparing
the corpus callosum
suggesting mild white mailer
=-
volume expansion typical of
van der Knaap
ADEM
confluent while maller
hyperintensity & atrophy =.:I
with marked caudate
atrophy ~ due to
hypomyelination with
atrophy of the basal ganglia
and cerebellum (I-I-ABC).
shows poorly marginated
hyperinlensily with some
sparing of the subcortical
U·fibers = in a patient with
chronic ADEM. This is
somewhat more symmetric
than is typically seen.
I
6
38
CONflUENT WHITE MATTER lESIONS

marked expansion of the
cingulate =
corpus callosum =1
& occipital gyri
by innumerable clusters of
CSF-signal enlarged
perivascular spaces. Cyral
expansion with sparing of the
overlying cortex is common.
(Courtesy L. Valanne, MO).
shows confluent
hyperintensity in the right
temporal and parietal lobe
while matter with a nearly
isoinlenS€ mass ~ crossing
the corpus callosum
splenium.
Gliomatosis Cerebri
patchy confluent areas of
hyperintensity in the deep &
subcortical white maller in a
somewhat radiating pattern
=1 along with some mild
dilated perivascular spaces
PJ:l:l. (RighI) Axial FLAIR MR
shows extensive, confluent
hyperintensity throughout
the majority of the cerebral
whiLe matter
=
with mass effect
& callosal thickening
related to gliomatosis
cerebri. Preservation of the
underlying architecture is
typical.

confluent, symmetric
hyperintensity extending
peripherally = into the
subcortical areas, a very rare
manifestation of
hypothyroidism known as
Ilashimoto encephalopathy.
shows a striking paLLern of
edema in the cerebellar
while mailer & brainstem
=1 typical for maple syrup
urine disease. There was
relative sparing of the
supratentorial structures, also
common in this disease.
I
6
39
THIN CORPUS CAllOSUM
DIFFERENTIAL DIAGNOSIS o Sagittal section slightly off-midline can

make CC appear mildly thinned
Common • Immature Brain
• Normal Variant o Hemispheric WM in newborn
• Immature Brain unmyelinated, CC thin and hypointense
• Encephalomalacia on TlWI
• Multiple Sclerosis o As myelination progresses, CC thickens,
• White Matter Injury of Prematurity becomes hyperintense on Tl WI
• Callosal Dysgenesis • CC splenium at 4 months
• Callosectomy/Callosotomy • CC genu at 6 months
• Obstructive Hydrocephalus • By 8 months CC essentially like an
Less Common adult's
• Hypomyelination • Encephalomalacia
• Alcoholic Encephalopathy o Holohemispheric WM volume loss,
• Injury (Any Cause) regardless of etiology, causes diffuse CC
thinning
Rare but Important
o Focal WM loss can cause focal CC
• Susac Syndrome thinning
• Holoprosencephaly • Multiple Sclerosis
• Inherited Metabolic Disorders o Look for T2/FLAIR hyperintense lesions
• Hereditary Spastic Paraplegia with Thin along callososeptal interface
Corpus Callosum (HSP-TCC) o Ependymal "dot-dash" sign along
callosoventricular border occurs early
ESSENTIAL INFORMATION o Long-standing MS with decreased
hemispheric WM volume results in
Key Differential Diagnosis Issues thinned CC
• Diffuse corpus callosum (CC) thinning can • White Matter Injury of Prematurity
be normal o CC thinning secondary to periventricular
o Newborn (immature brain)
white matter infarction
• Abnormally thin CC can be inherited or o Posterior CC disproportionately affected
acquired • Callosal Dysgenesis
o Seen in many congenital malformations,
o Hypoplasia or absence of part or all of CC
inherited metabolic disorders o CC remnants vary in size, shape
o Check history for trauma, surgery,
o Most common abnormality associated
ischemia- infarction with other malformations
• Thin CC, normal signal hyperintensity • Chiari 2 malformation
o Normal variant, immature brain
• Heterotopias
o Secondary to hemispheric white matter
• Interhemispheric lipoma
(WM) volume loss • Cephaloceles
o Dysgenesis
• Callosectomy/Callosotomy
• Thin CC, abnormal signal intensity o History important!
o Hypomyelination or demyelinating disease o Look for surgical changes of craniotomy,
(chronic MS, Susac syndrome) ventriculostomy
o Injury (trauma, ischemia, radiation,
• Obstructive Hydrocephalus
toxic-metabolic insult) o Obstructive hydrocephalus causes two
o Obstructive hydrocephalus
kinds of CC abnormalities, stretching &
Helpful Clues for Common Diagnoses intrinsic signal abnormality
• Normal Variant o As lateral ventricles enlarge, CC is
o Focal thinning of corpus callosum at stretched, appears thinned
I "isthmus" (junction between posterior
body, splenium) is normal
• Look for associated signal abnormality in
CC (sagittal T2WI/FLAlR best)
6
40
THIN CORPUS CAllOSUM ,.,.
CJl
c:
III
o Post-shunt decompression may show CC • Vision problems (retinal artery ;j
Co
thinning, signal abnormality occlusions)
..•
OJ
• Can appear bizarre, causing horizontal • Hearing loss III
;j
hyperintense "streaks" in CC on axial o Always involves CC
CJl
imaging • Central> callososeptal interface lesions c:
"0
• Can extend into periventricular WM • Middle callosal "holes" ~
III
(subacute/chronic) CD
• Theories: Impingement of CC against
falx cerebri with resulting ischemia or
axonal stretch
• Holoprosencephaly
o Many variants; often affect CC
-
::J
o
~
0;'
OJ
• Inherited Metabolic Disorders ~
Helpful Clues for Less Common Diagnoses Cll
o Focal or diffuse atrophy ::J
• Hypomyelination \J
• Focal: X-linked adrenoleukodystrophy Cll
~
o Undermyelination, delayed myelin CD
• Diffuse: Many ::J
maturation ()
• Hereditary Spastic Paraplegia with Thin ::T
o Diminished/absent WM myelination '<
Corpus Callosum (HSP-TCC) 3
o Can be primary or secondary Cll
o HSP-TCC is one of many hereditary spastic
• Alcoholic Encephalopathy
paraplegias
o Marchiafava-Bignami disease
• Autosomal recessive with SPGll gene
• Alcohol toxic to WM
mutations on chromosome 15
• Necrosis in middle layers of CC
• Progressive neurodegenerative disorder
• Thinned, hypointense CC seen on T1 WI
o Clinical
o Look for other associated abnormalities
• Slow t spastic paraparesis
• Superior vermian atrophy
• Adolescent-onset cognitive decline
• Wernicke encephalopathy
• Pseudobulbar dysfunction
• Injury (Any Cause)
o Imaging
o Trauma (e.g., axonal injury,
• Thin CC (especially genu, body) with
radiation-induced leukoencephalopathy)
progressive atrophy
o Ischemia
• Cerebral, cerebellar atrophy often
Helpful Clues for Rare Diagnoses associated
• Susac Syndrome
o M<F
o Classic triad
• Encephalopathy (headache, confusion,
memory loss)
Immature Brain
I
Sagittal T7WI MR in term infant imaged at 2 days of age
shows thin corpus callosum I:'] with no discernible shows very thin corpus callosum genu =.
Axial Tl WI MR in 32 week gestation premature infant
reflecting
6
myelination. This is the normal appearance of an total lack of hemispheric myelination,
immature, largely unmyelinated brain. 41
THIN CORPUS CALLOSUM
(Left) Axial OWl MR in a
newborn shows extensive
diffusion reslriction of Ihe lefl
hemisphere following
perinatal stroke. Acute
axonal degeneration of Ihe
corpus callosum 81 is
present. (Right) Coronal
T2WI MR al follow-up shows
a large area of cystic
encephalomalacia ~ and a
very thin corpus callosum
81
::J
-"en
(Left) Sagittal OWl MR in a
neonale wilh group B strep
meningitis shows multifocal
brain ischemia~. There is
diffuse restriction of the
corpus callosum I!:ll due 10
axonal degeneration. (Right)
Sagittal T I WI MR in same
child al follow-up imaging
shows severe thinning of the
corpus callosum 81.

(Left) Sagillal FLAIR MR in a
leenager wilh MS shows
severe atrophy of the corpus
callosum with increased
signal intensity of the corpus
callosum Sllhe
seplal-callosal interface, and
Ihe fornix =. (Right) Axial
FLAIR MR shows extensive
demyelinating plaques 81 in
the same teen.
I
6
42
THIN CORPUS CALLOSUM en
~
r::
III
:::l
Co
.,
OJ
III
White Matter Injury of Prematurity White Matter Injury of Prematurity
:::l
shows extreme thinning of
corpus callosum = in a
child with cerebral palsy and
history of premature birth &
prolonged stay in NICU.
shows typical scalloping of
the ventricles due to
indentation by gray matter
81. The peritrigonal white
maller is severely deficient in
this same ex-premature
infant with perivenlricular
leukomalacia. Note relative
sparing of genu =.

child with Chiari 2
malformation shows thin,
dysgenetic-appearing corpus
callosum ~ (Right) Coronal
T2WI MR shows severe
thinning of the dysgenetic
corpus callosum ~ in the
same child with Chiari 2
malformation. Note absence
of the leaflets of the septum
pellucidum.
Callosectomy/Callosotomy Callosectomy/Callosotomy
shows absent midline corpus
callosum, post-callosotomy
for seizure control. Note
normal cingulate gyrus 81
and pericallosal artery =.
(Right) Corolla I T1WI MR
shows a farge callosotomy
defect 81 in the same child
in treatment of intractable
epilepsy due to
Lennox-Gastaul syndrome.
I
6
43
C1l
E
THIN CORPUS CALLOSUM
>-
.r:
()
c::
Q)
~
C1l
a..
c:: Obstructive Hydrocephalus
C1l
~ (Left) Sagiltal T2WI MR in
(])
palient with long-standing
C1l
·C
o
aqueduclal stenosis =
shows thinned, stretched
C corpus callosum with some
Q)
ro~ hyperintensity posteriorly
Cl. !:.2. Note hyperdynamic CSF
::l
(f) with "flow voids" 81. (Right)
Sagittal T7 WI MR shows very
c::
..
l'Cl
(])
thin corpus callosum III
with hypomyelination,
minimal T7 shortening 81
"0
c:: indicative of minimal
l'Cl myelination in the splenium.
Other images showed
striking lack of myelination in
this 5 month old infant.
(Left) Sagiltal T7 WI MR in
this chronic alcoholic shows
thinned corpus callosum
with striking hypointensity in
the middle layers ffi
characteristic for
Marchiafava-Bignami
disease. (Right) Sagittal T7 WI
MR shows thinned body
=
splenium of corpus callosum
following neonatal
parietooccipital ischemia
from combination of Hlf
hypoglycemia.
Susac Syndrome
same infant reflecls sequelae
of HIE and hypoglycemia.
There is extensive posterior
atrophy. The genu !:.2 of the
corpus callosum is norma! in
size, the splenium severely
atrophied 81. (Right) Sagittal
FLAIR MR shows moderately
thinned corpus callosum
with multiple
hyperintensilies, especially in
the middle and posterior
segments =. Note several
middle callosal" holes" 8l
characteristic for Susac
I syndrome.
6
44
THIN CORPUS CAllOSUM
Ql
::l
Co
OJ
..,
Ql
(Left) Sagittal TI WI MR ::l

shows layers of white E!ilI (J)
C
and gray maller comprising "0
..,
anterior corpus callosum in OJ
this child with semi/abar CD
:::l
holoprosencephaly. (Right) 0-
..,
(ii'
layering of white E!ilI and
gray matter in expected OJ
..,
OJ
region of the genu of the
::l
corpus callosum in this same -0
child with semilobar OJ
holoprosencephaly. CD
:::l
()
::r
'<
3
OJ
Inherited Metabolic Disorders Inherited Metabolic Disorders

(Left) Sagittal TI WI MR in
child with urea cycle
disorder shows diffuse
thinning of corpus callosum,
most striking in the posterior
body and splenium =.
(Right) Sagittal TI WI MR in a
10 year old with cobalamin
C deficiency shows marked
volume loss of the body
of the well-myelinated
=
corpus callosum. This finding
and hypomyelination (mild
in this child) are
characteristic of this
disorder. It is important to
consider this diagnosis, as
treatment is available.
Inherited Metabolic Disorders

(Left) Sagittal TI WI MR in a
pre-teen boy with
symptomatic X-linked
adrenoleukodystrophy shows
focal thinning E!ilI and signal
loss in the splenium of the
corpus callosum. (Right)
Axial TI C+ MR in the same
child with classic X-ADL
shows enhancemef1l of the
leading edge of
demyelination E!ilI and focal
atrophy [;8 of the splenium
of the corpus callosum.
I
6
45
C1l ABNORMAL SHAPE/CONFIGURATION OF CORPUS CALLOSUM
E
>-
.r:
u
c • Pre-myelination
~
Q)
C1l
0..
• Gradually thickens with progressive
c Common myelination
~ • Normal Variant • Callosal Dysgenesis
(])
C1l
• Callosal Dysgenesis o One or all segments absent
'C
o • Callosotomy • Rostrum, splenium most likely deficient
C • Neoplasm • Remnants vary in size, shape,
Q)
ro~ o Lipoma configuration

c.
::J o Glioblastoma Multiforme o "Micro" CC
(fJ
o Lymphoma, Primary CNS • Small, but well-formed
C
• Decreased White Matter Volume • Often syndromic
'"
"-
III o Hypomyelination o "Mega"CC
"c o Periventricular Leukomalacia • Isthmus usually absent
'" o HIE, Term • Megalencephalic (bulky white matter)
o Cerebral Infarction, Chronic • Or small to normal brain (syndromic)
o Diffuse Axonal Injury (DAI) • Callosotomy
o Multiple Sclerosis o Surgical disruption
o Radiation and Chemotherapy • Focal: Approach to 3rd ventricle or
• Obstructive Hydrocephalus suprasellar tumor
Less Common • Diffuse: Surgery for intractable seizures
• Holoprosencephaly o Best seen on sagittal or coronal MR
• Holoprosencephaly Variants • Neoplasm
o Can be benign/focal or malignant/diffusely
Rare but Important infiltrating
• Hypertensive Intracranial Hemorrhage o Lipoma
• Marchiafava-Bignami • 40-50% interhemispheric fissure
• Common in callosal dysgenesis
ESSENTIAL INFORMATION • Can be bulky, mass-like ("tubonodular"
type, usually associated with CC
Key Differential Diagnosis Issues agenesis; may extend through choroidal
• Normal corpus callosum (CC) varies in fissures into lateral ventricles)
thickness, shape • Thin mass curving around CC
• Isolated callosal dysgenesis not common body/splenium ("curvilinear" type, CC
o Look for second lesion
present but may be dysgenetic)
o Associated CNS anomalies in > 50%
o Glioblastoma Multiforme
• Heterotopia • "Butterfly" glioma
• Cortical dysplasia • Central necrosis + thick irregular rim
• Noncallosal midline anomalies enhancement
• Abnormal brainstem or cerebellum o Lymphoma, Primary CNS
• If not congenital, history crucial! • Hyperdense on NECT
Helpful Clues for Common Diagnoses • Strong, uniform enhancement
• Normal Variant o Decreased White Matter Volume
o Size, shape, thickness of normal CC vary • Many causes (congenital, acquired)
• Splenium, genu are largest parts of • All may result in focal or diffuse callosal
corpus callosum thinning
• Narrowing between body, splenium o Hypomyelination
("isthmus") is normal • Chromosomal, inborn errors of
• Dorsal surface of fully developed, metabolism
normally myelinated corpus callosum o Peri ventricular Leukomalacia
I often "wavy"
o Immature corpus callosum is thin
• Premature infant
• "Scalloped" lateral ventricles
6
46
ABNORMAL SHAPE/CONFIGURATION OF CORPUS CALLOSUM (J)
c:
""
III
o HIE, Term • Middle CC body "dips" :J
C.
• Term infant with profound partial • Gray matter crosses at dip CD
.,
asphyxia - WM/cortex damaged • If severe, add bilateral perisylvian III
:J
o Cerebral Infarction, Chronic polymicrogyria
(J)
• Axonal loss - focal/diffuse thinning CC Helpful Clues for Rare Diagnoses c:
o Diffuse Axonal Injury (DAI)
.,
1:l
III
• Hypertensive Intracranial Hemorrhage CD
• 20% involve CC (splenium, undersurface o CC rare primary site :J
posterior body) 8'
.,
• Marchiafava-Bignami III
o Multiple Sclerosis
o Middle-aged alcoholic OJ
• Chronic, late .,
o CC demyelination, necrosis, atrophy III
• Obstructive Hydrocephalus :J
"U
o Acute III
• Corpus callosum (CC) stretched SELECTED REFERENCES CD

:J
(")
• CC bowed upwards ]. Pierson TM et al: Mega-corpus callosum, polymicrogyria, ::r

and psychomotor retardation: confirmation of a syndromic '<
• Forniceal columns bowed downwards 3
entity. Neuropediatrics. 39(2):123-7, 2008 III
o Chronic 2. Samaranch Let al: SPGll compound mutations in spastic
• Post-shunt encephalomalacia paraparesis with thin corpus callosum. Neurology.
71(5):332-6, 2008
• Sequela of acute callosal impingement 3. Matar6 M et al: Functional and magnetic resonance
against falx imaging correlates of corpus callosum in normal pressure
hydrocephalus before and after shunting. J Neurol
Helpful Clues for Less Common Diagnoses Neurosurg Psychiatry. 78(4):395-8,2007
• Holoprosencephaly 4. Hetts SW et al: Anomalies of the corpus callosum: an MR
analysis of the phenotypic spectrum of associated
o Corpus callosum absent in alobar
malformations. AJRAm J Roentgenol. 187(5):1343-8,2006
• Large dorsal "cyst" often present 5. Rollins N: Semilobar holoprosencephaly seen with
o Semilobar may have residual splenium diffusion tensor imaging and fiber tracking. AJNR Am J
Neuroradiol. 26(8):2]48-52, 2005
• Frontal fusion & hypoplasia 6. Kinsman SL: White matter imaging in holoprosencephaly
• Splenium may be present in children. CUff Opin Neurol. ] 7(2):1 ]5-9,2004
o Lobar 7. Barkovich AJ et al: Callosal agenesis with cyst: a better
understanding and new classification. Neurology.
• Genu mayor may not be present 56(2):220-7,200]
• Gray matter often crosses with genu 8. Kier EL et al: The normal and abnormal genu of the corpus
callosum: an evolutionary, embryologic, anatomic, and MR
• Holoprosencephaly Variants analysis. AJNR Am J Neuroradiol. 17(9):1631-41, 1996
o Middle interhemispheric variant 9. Mendelsohn DB et al: Corpus callosum lesions after closed
• a.k.a., syntelencephaly head injury in children: MR], clinical features and
outcome. Neuroradiology. 34(5):384-8, 1992
• Splenium, genu present, body deficient
Normal Variant Normal Variant
I
Sagittal Tl WI FSMR with a close-up view of the corpus
=-
Sagittal TlWI MR shows a normal neonatal corpus
6
focal thinning along posterior body
normal finding.
=-
callosum shows normal "wavy" dorsal surface. Note the
a common
callosum thin due to age-appropriate lack of myelin
maturation. The cingulale gyrus ~ is normal.
47
Cll ABNORMAL SHAPE/CONFIGURATION OF CORPUS CALLOSUM
E
:>.
.<:
()
c
<ll
~
Cll
a..
c
~
Cll
co shows callosal agenesis.
Cll
·C Note radial array of
o paracentral gyri "pointing"
C 10 the Jrd ventricfe as well as
<ll
"§ absence of identifiable
a. cingulate gyrus.
:J Hippocampal commissure is
CIJ
visualized posteriorly 81.
C
(Right) Coronal r2WI MR
nl
•... shows the absence of
co crossing callosal fibers, the
"t:l
C presence of Probst bundles
nl a and vertical hippocampi
:J ~
-'"
(f)
(Left) Sagiltal T1WI MR

shows only a residual genu
IJ:.:I of the corpus callosum,
with absence of the body
and splenium and truncation
of the rostrum. (Right)
Sagittal TlWI MR shows
absent rostrum, small
deformed genu, thick body
a and absent splenium in
this child with Chiari 2. Note
=-=
prominent massa inlermedia
inferiorly beaked tectum
and caudally displaced
4th ventricfe.
(Left) Sagiltal T1WI MR in a

child with severe
microcephaly shows a short,
thick corpus callosum =:I.
Note the normal narrowing
(isthmus) at junction of
body; splenium is absent
Actual callosal volume is
small. (Right) Sagittal T2WI
MR shows focal defect at the
junction of the genu and
body of the corpus callosum
a the site of surgical
approach to this child's
suprasellar tumor =.
I
6
48
ABNORMAL SHAPE/CONFIGURATION OF CORPUS CALLOSUM en
;K"
c:
Ql
::I
Q.
III
.,
Ql
::I
shows a large midline lipoma (JJ
c:
and a small remnant of the "0
.,
body SlI of the corpus Q)
callosum. (Right) Coronal T1 co::I

C+ MR shows classic S
"bullerfly" glioblastoma
.,
00'
multi/orme of the corpus
callosum =. Central OJ
.,
Q)
necrosis with an irregular :J
rind of enhancing tumor is
lJ
typical. Q)
.,
CO
::I
o
::T
'<
3
Q)

primary CNS lymphoma
involving splenium of the
corpus callosum.
Gadolinium enhancement
shows avid, solid
enhancement of splenial
tumor & extension into
adjacent parenchymal white
mailer. (Right) Sagittal T1 WI
MR shows marked callosal
thinning SlI & atrophy in a
child whose hydrocephalus
follows unilateral grade 4
intravenlricular hemorrhage.
Posteriorly there is more
severe callosa! volume loss
~.
Periventricular leukomalacia Cerebral Infarction, Chronic

same child shows marked
1055 of periventricular white
matter, septal destruction, &
focal porencephaly ~ at site
of prior grade 4 hemorrhage.
Posterior white maller IOS5
correlates with focal CC
atrophy. (RighI) Sagillal
T1 WI MR shows focal
thinning SlI of body &
splenium of corpus callosum,
following neonatal
parietooccipital ischemia &
gliosis from combination of
hypoxic ischemic
encephalopathy &
hypoglycemia.
I
6
49
ell
E
ABNORMAL SHAPE/CONFIGURATION OF CORPUS CALLOSUM
>.
.<::
()
c
[I:'
ell
Cl..
C Cerebral Infarction, Chronic Diffuse Axonal Injury (DAI)
~ (Left) Coronal T2WI MR
en shows parietal ulegyria E!lI
ell
'C and marked thinning of the
.8 corpus callosum allhe
c
(I) psalterium '-=. (Right)
ro~ Sagillal T1WI MR shows
a. swelling and signal loss of
::J
CfJ the expected region of the
isthmus E!lI of the corpus
C
callosum due 10 shear injury.
ell
'-
!Xl
"0
c
ell
::J
-"en
Multiple Sclerosis
(Left) Axial rLAIR MR shows
abnormal signal of crossing
callosal fiber tracts
fo/Jowing traumatic
'-=
shear
injury. (Right) Sagillal FLAIR
MR shows multiple
hyperintense foci in the
corpus callosum = as well
as a large pontine lesion E!lI.
The isthmus (posterior body)
of CC is thinned more than
normally because of axonal
loss from multiple centrum
semiovale lesions.
Radiation and Chemotherapy Obstructive Hydrocephalus

(Left) Sagillal T1 WI MR
shows diffuse thinning E!lI of
the rostrum, genu, and body
of the corpus callosum
following treatment for ALL.
(Right) Sagillal T2WI MR
shows mild stretching and
thinning of the corpus
callosum due to
hydrocephalus. There is
obstruction of the aqueduct
of Sylvius by a tectal glioma
Ii8
I
6
50
ABNORMAL SHAPE/CONFIGURATION OF CORPUS CAllOSUM CJl
"
c:
III
::::J
Co
...
OJ
III
::::J
(Left) Sagillal T2WI MR
shows the absence of corpus CJl
C
callosum. White mailer S'I
traverses the midline,
...OJ
1:>
although not in compact CD

OJ
bundle form. There is a large
dorsal cyst. Note the lack of
o...
0;.
vermian primary fissure due
to associated ...OJ
OJ
rhombencephalosynapsis. OJ
(RighI) Axial T1WI MR -0
shows the lack of midline OJ
fissure. White maller ~ is in CO
OJ
continuity along the midline. ()
::T
8asal ganglia S'I '<
approximate each other. 3
OJ
(Lefl) Sagillal T1WI MR

shows both white, gray
maller H2 crossing midline
anterior and posterior to
"dip" PJ:!.:I in CC where only
gray matter traverses. This is
a middle interhemispheric
variant (synte/encephaly).
(Right) Axial TI WI MR in the
same case shows gray·white
maller traversing together H2
in the expected location of
splenium. Gray matter
protrudes ~ into ventricular
system. Septum pellucidum
is absent

extensive hemorrhage into
the genu and splenium of the
corpus calfosum, with
extension along the septal
leaflets PJ:!.:I and into the
ventricles in this child
following cardiac transplant.
(Right) Sagittal FLAIR MR
shows linear bright signal at
=-
the callososeptal interface
demyelination of the
splenium 8l and an
otherwise generally thin
corpus callosum.
I
6
51
co CORPUS CAllOSUM HOLES
E
>-
.r:
u
c
OJ
~ DIFFERENTIAL DIAGNOSIS • ADEM
co o Both subcortical white matter (WM), deep
a.. Common
c gray nuclei often involved
co
~ • Multiple Sclerosis o May mimic multiple sclerosis
co
co
• Diffuse Axonal Injury (DAI) • Obstructive Hydrocephalus
'C
o Less Common o Dorsal, middle layers may show Tl
C hypointense & T2 hyperintense signal
OJ • Post-Surgical
ro~ • ADEM o May be related to CC compression against
0..
:J falx during acute ventricular obstruction
(f) • Obstructive Hydrocephalus
C • Lacunar Infarction • Lacunar Infarction
co
~ o Uncommon; rich blood supply to CC
III Rare but Important
o Focal ischemia with surrounding gliosis
"C
c • Enlarged Perivascular Spaces o Supplied by anterior communicating
co • Marchiafava-Bignami Disease
:J
artery, peri callosal artery, & posterior
• Susac Syndrome pericallosal artery
-"en
ESSENTIAL INFORMATION • Enlarged Perivascular Spaces
Helpful Clues for Common Diagnoses o Follow CSF on all sequences
• Multiple Sclerosis o When CC involved, adjacent brain often
o Callososeptal interface T2 hyperintensities involved
o "Burned out" chronic lesions have Tl • Marchiafava-Bignami Disease
hypointense center, very slight o Rare complication of chronic alcoholism;
hyperintense rim (lesion within lesion) CC demyelination & necrosis
• Diffuse Axonal Injury (DAI) o T2 hyperintense CC (middle layers)
o Punctate hemorrhages at gray-white virtually pathognomonic
interfaces & corpus callosum (CC) typical o Sudden onset of altered mental status,
o "Blooming" on T2*, GRE, SWI common seizures, dysarthria, ataxia, hypertonia,
o May result in focal encephalomalacia pyramidal signs
• Susac Syndrome
o Classic clinical triad = encephalopathy,
• Post-Surgical visual changes, hearing loss
o Small CC "holes" common after shunt
o Multifocal supratentorial WM lesions + CC
o Defects may result from transcallosal
o "Holes" in CC middle layers characteristic
surgery (e.g., for colloid cyst)
Diffuse Axonal Injury (DAI)
I
6 Sagittal Tf WI MR shows mulUple hypointense lesions in
U,e CC & deep white mailer perpendicular to the lateral
Sagittal T2' eRE MR shows muMocal hypointensilies at
& CC related to OAi. The
ventricle= in this young adult. These lesions may have
the gray-white interfaces
CC lesion will likely result in focal
a mildly hyperintense rim. encephalomalacia, causing a "ce hole".
52
CORPUS CALLOSUM HOLES
III
::l
a.
III
.,
Obstructive Hydrocephalus III
ADEM
::l
(Left) SagiLtal FLAIR MR
shows multifocal en
c
hyperintensiLies within the -0
.,
CC & pons in this ADEM Q)
patient with a recent flu-like CD

~
illness. Imaging mimics MS.
These lesions often result in
o:0.
Q)
"CC holes" chronically.
(Rigl1t) Axial T2WI MR OJ
.,
Q)
shows a peculiar transverse ~
"striated" appearance of the -U
CC body resulLing from Q)
~
prior severe obstructive CD
~
hydrocephalus. In about ()
::T
15% of patients with '<
shunted hydrocephalus, CC 3
Q)
signal abnormalities may be
seen.
(Left) SagiLtal T1 WI MR
shows a CC hole Il::l related
to a lacunar infarct in a
moyamoya patient. Note the
T1 shortening related to
additional anterior
circulation ischemia. Lacunar
infarcts are uncommon as
there is a rich CC blood
supply. (Right) Sagittal T1 WI
MR shows mulLiple "cysLic"
lesions that follow CSF in the
CC & cingulate gyrus. When
perivascular spaces are in
the CC, there is often
involvement of the adjacent
brain, cingulate gyrus in this
case.
Marchiafava-Bignami Disease Susac Syndrome

(Lelt) Sagittal T1WI MR
shows cla.5sic findings (or
Marchiafava-Bignami disease
with a thinned CC &
hypoinlensily in the middle
layers l:llI. NOle that the
genu, body, & splenium are
all involved. T2
hyperintensity that extends
to the deep white matter is
also common. (Right)
SagiLtal T2WI MR shows a
subtle hyperintense" hole" in
the central CC l:llI in this
young adult with Susac
syndrome. Iioies in the
middle layers of the CC are
characteristic.
I
6
53
co CORPUS CAllOSUM lESION WITHOUT MASS EFFECT
E
>.
.£
l)
C
~
Q)
DIFFERENTIAL DIAGNOSIS o Large multifocal subcortical white matter
co (WM) lesions without mass effect
0-
c Common • ADEM
co
~ • Multiple Sclerosis o 10-14 days after viral illness/vaccination
CD
CO
• Diffuse Axonal Injury (DAI) o Involves subcortical WM, deep gray nuclei
'C
o less Common o May mimic multiple sclerosis
C
Q)
·PML • Periventricular Leukomalacia
ro~ o Small CC typical, ± T2 hyperintensity
Cl. • ADEM
:J o Peritrigonal WM loss & "wavy" ventricular
en • Periventricular Leukomalacia
c margins
co
Rare but Important
~ Helpful Clues for Rare Diagnoses
co • Enlarged Perivascular Spaces
• Vasculitis • Enlarged Perivascular Spaces
"coc • Lyme Disease o Cystic lesions follow CSF on all sequences
:J • Susac Syndrome o May involve CC
-"
en • Vasculitis
• X-Linked Adrenoleukodystrophy
• Metachromatic Leukodystrophy (MLD) o Subcortical WM commonly affected
o DWI bright & enhancement typical
• Lyme Disease
ESSENTIAL INFORMATION o May mimic multiple sclerosis
Helpful Clues for Common Diagnoses o Cranial nerve enhancement common
• Multiple Sclerosis • Susac Syndrome
o Multiple perpendicular callososeptal T2 o Classic triad: Encephalopathy, retinal
hyperintensities characteristic artery branch occlusions, hearing loss
o Corpus callosum (CC) almost always o Multifocal supratentorial WM lesions + CC
involved, subcallosal striations early • X-Linked Adrenoleukodystrophy
• Diffuse Axonal Injury (DAI) o Enhancing peritrigonal demyelination
o Punctate hemorrhages at corticomedullary o Involves CC splenium early, followed by
junction & CC typical peritrigonal WM & WM tracts
o CC involvement in 20%; 75% involve • Metachromatic Leukodystrophy (MLD)
splenium/undersurface of posterior body o Confluent "butterfly-shaped" cerebral
hemisphere WM T2 hyperintense signal
o Late involvement of CC, V-fibers,
·PML pyramidal tracts, internal capsule
o Bilateral, asymmetric involvement typical
Multiple Sclerosis Diffuse Axonal Injury (OAf)
I
6 Sagittal fLAIR MR shows mu/tjfocal hyperinlense lesions
wilhin the CC = & sulx:orlical while mailer. typical {or
Sagiual T2WI MR shows hyperinlensily in lhe CC body
= & local hypoinlensily in lhe splenium E!ilI relaled 10
MS. Sagillal FLAIR MR helps idenlily sulx:allosal OAI. Correialion with eRE or SWI sequences lypically
striations seen in early disease stages. shows mulliple addilionallesions.
54
CORPUS CALLOSUM LESION WITHOUT MASS EFFECT ,.-c:
(J)
'a.:"l
...
OJ

':"l
confluent, high signal in the (J)
c:
frontal lobes that crosses the
CC without significant mass
...
"0
Ql
effect. There is involvement m
:l
of the subcortical U-fibers,
typical of PML. No
o...
iii'
enhancement is
characteristic. (Right) Axial ...
OJ
Ql
T2WI MR shows a "wavy"
:l
ventricular margin m& a lJ
small corpus callosum, ...
Ql
CD
typical of PVL. Note also
:l
perilrigonal while matter 1055 (")
:::r
& deep sulci. PVL often '<
occurs in premature infanl5 3
Ql
related to a hypoxic-ischemic
event

innumerable clusters of
CSF-signal cysts in the
corpus callosum & occipital
white matter related to
perivascular spaces. These
are rare in the corpus
callosum. (Right) Sagittal
FLAIR MR shows
middle layers of the CC,
typical of Susac syndrome.
Central CC involvement is
more common than
callososeptal interface
involvement. Imaging may
mimic MS, so clinical history
is important for diagnosis.

marked hyperintensity in the
CC splenium & peritrigonal
white maller related to
demyelination in this patient
with X-ALD. CC splenium is
involved early. Enhancement
is cfassic. (Right) Axial T2WI
MR shows confluent
hyperintense periventricular
white matter~ (butterfly
pattern) related to
demyelination. Note the
preservation of subcortical
U-fiber myelination SlI.
Hyperintensity & volume loss
CC is common.
of the
I
6
55
ro CORPUS CAllOSUM MASS
E
>-
L
U
C
Q)
L
DIFFERENTIAL DIAGNOSIS o Often involves, crosses CC
ro
CL
Common Helpful Clues for less Common Diagnoses
c
ro
L • Glioblastoma Multiforme • Oligodendroglioma
co o Calcified frontal lobe mass involving
ro
• Lymphoma, Primary C S
·C
• Anaplastic Astrocytoma cortex/subcortical WM
o
C o May extend into CC
Q) less Common o Heterogeneous enhancement 50%
ro
L
• Oligodendroglioma
Cl.
::J
• "Tumefactive" Multiple Sclerosis
(/J • "Tumefactive" Multiple Sclerosis o CC lesions characteristic
C • Gliomatosis Cerebri o Single tumefactive lesion common
ro
"- • Lipoma o Often incomplete, "horseshoe-shaped"
CO
Rare but Important enhancement, open toward cortex
"cro • "Tumefactive" ADEM • Gliomatosis Cerebri
• Enlarged Perivascular Spaces o 1'2 hyperintense infiltrating mass with
enlargement of involved structures
o May cross CC
ESSENTIAL INFORMATION o Typically nonenhancing at presentation
Helpful Clues for Common Diagnoses • Lipoma
• Glioblastoma Multiforme o Often associated with CC dysgenesis
o Heterogeneously enhancing mass o 1'1 hyperintense mass along CC
o Classically crosses corpus callosum (CC), Helpful Clues for Rare Diagnoses
results in a "butterfly glioma" • "Tumefactive" ADEM
o Central necrosis, blood products typical o 10-14 days after viral illness/vaccination
• Lymphoma, Primary CNS o Often involves subcortical WM & deep
o Homogeneously enhancing, 1'2 gray nuclei
hypointense mass o Incomplete ring enhancement
o Usually involves basal ganglia, characteristic
periventricular white matter (WM) • Enlarged Perivascular Spaces
o Often crosses CC, extends along o May cause mass effect, particularly in
ependymal surfaces midbrain
• Anaplastic Astrocytoma o Follow CSF signal on all sequences
o 1'2 hyperintense WM mass with variable o No enhancement
enhancement
Glioblastoma Multiforme lymphoma, Primary eNS
I
6 Axial
mass
T1 C+ M R
involving
shows
the
a
corpus
helerogeneously
callosum
enhancing
splenium & left
Axial T1 C+ MR shows a homogeneously
mass involving t.he corpus callosum splenium
enhancing
&
perialfial while maller. Cenlfaf necrosis is characteristic perialrial while malter. Lymphoma is typically T2
of these malignanllumors. hypointense &, enhances homogeneously.
56
CORPUS CALLOSUM MASS CJl
"
c:
Anaplastic Astrocytoma
a hyperintense mass that
involves the corpus callosum
splenium & parietal lobes.
Anaplastic astrocytomas
occur in hemispheric white
malter, and neoplastic cells
are almost always found
OJ
beyond the signal ~
Ql
abnormality. (Right) Axial
:J
T2WI MR shows a
lJ
heterogeneous frontal lobe Ql
mass that involves the ii3

:J
corpus callosum genu, (')
::r
cortex, & subcortical white '<
matter. These tumors are 3
Ql
typically calcified, which is
often better seen on CT.
"Tumefactive" Multiple Sclerosis Gliomatosis Cerebri

marked while maller
hyperintensity I:j] with
extension into the corpus
callosum. There is a central
hypointense mass
causing mass effect on the
adjacent ventricle.
Enhancement was an
incomplete ring, typical (or
demyelination. (Right) Axial
FLAIR MR shows extensive
hyperintensity in the white
matter with involvement of
the corpus callosum genu &
splenium. Gliomatosis
cerebri at biopsy. Bilateral
involvement is common.
shows a fat-intensity lesion
I:j] in the interhemispheric
fissure, wrapping around the
mildly hypoplastic corpus
callosum. The lipoma also
extends anteriorly along the
interhemispheric fissure to
involve the fronlallobes ~.
(Right) Sagiltal TI WI MR
the corpus callosum,
cingula Ie, & occipital gyri by
innumerable clusters of
CSF-signal cysts, perivascular
spaces. Involvement of the
corpus callosum is rare. I
6
57
ctl CORPUS CALLOSUM SPLENIUM LESION
E
>-
£
U
C
Q)
L DIFFERENTIAL DIAGNOSIS o Focal splenium lesion less common
ctl
Q..
o CC almost always involved, callosal
c Common striations seen early
ctl • Diffuse Axonal Injury (DAI)
L
OJ
o May have characteristic incomplete ring or
ctl
• Multiple Sclerosis horseshoe enhancement
'C
o • Status Epilepticus • Status Epilepticus
CQ)
• Drug Toxicity, NOS o T2 hyperintensity in supratentorial gray
10 matter &/or subcortical white matter (WM)
L
C.
Less Common
~ with mild mass effect typical
(/) • Transient Metabolic Derangement
r:: • Encephalitis (Miscellaneous) o May focally involve hippocampus or CC
C'<l
• Hypoxic-Ischemic Encephalopathy, NOS splenium
"-
OJ
"t:l • Alcoholic Encephalopathy • Drug Toxicity, NOS
r::
• Neoplasms o Multiple drugs have been associated with a
C'<l
·PML reversible splenium lesion

• Hypoglycemia • Anti-epileptic agents, metronidazole,
sympathomimetic-containing diet pills
Rare but Important o Focal T2 hyperintensity, DWI positive
• X-Linked Adrenoleukodystrophy o Metronidazole encephalopathy may also
• Acute Hypertensive Encephalopathy, PRES affect dentate, brainstem, & WM
• ADEM
• White Matter Disease with Lactate Helpful Clues for Less Common Diagnoses
• Enlarged Perivascular Spaces • Transient Metabolic Derangement
• Systemic Lupus Erythematosus o Focal T2 hyperintense splenium lesion,
DWI positive
o Typically reversible
ESSENTIAL INFORMATION • Encephalitis (Miscellaneous)
Key Differential Diagnosis Issues o Multiple infectious agents may cause focal
• Corpus callosum (CC) has 4 named parts: T2 hyperintense splenium lesion
Rostrum, genu, body, & splenium • Influenza type A, rotavirus, E. coli,
• Splenium is most likely portion to be measles, mumps, adenovirus, herpes,
affected by various pathologies varicella, EBV, West ile, salmonella
o Possibly related to posterior pericallosal o Typically reversible & DWI positive
artery vascular supply • Hypoxic-Ischemic Encephalopathy, NOS
• Splenium lesions may have similar imaging o Most common in deep gray nuclei
appearance, history often key to diagnosis o DWI positive acutely
• Many etiologies may cause a reversible T2 o Focal splenium lesion less common
hyperintense lesion • Alcoholic Encephalopathy
o Pathophysiology for reversible lesions is o Marchiafava-Bignami: Sudden onset of
thought to be cytotoxic edema altered mental status, seizures, dysarthria,
ataxia, hypertonia, pyramidal signs
• T2 hyperintense CC (middle layers)
• Diffuse Axonal Injury (DAI) virtually pathognomonic
o Punctate hemorrhages at gray-white o Toxic leukoencephalopathy with
interfaces, corpus callosum (CC), deep gray demyelination, rare complication, often
matter, & upper brainstem typical involves splenium & peri ventricular WM
o CC involved in 20%; 75% involve
o Superior vermian atrophy common
splenium & undersurface of posterior body • Neoplasms
o T2*/GRE & SWI typically shows multiple
o Lymphoma & glioblastoma (GBM)
additional lesions classically cross CC splenium or genu
• Multiple Sclerosis o Enhancing WM mass with CC extension
I o Callososeptal T2 hyperintensities
characteristic
o Lymphoma: Homogeneous enhancement
o GBM: Heterogeneous enhancement
6
58
CORPUS CALLOSUM SPLENIUM LESION (Jl
"
c:
III
·PML o May focally involve splenium :I
C.
o Occurs in immunosuppressed or o Typically multiple lesions OJ
...,
immunocompromised patients • White Matter Disease with Lactate III
:I
o T2 hyperintensity in subcortical & deep o Van der Knaap leukoencephalopathy
(Jl
WM, crosses ee splenium & genu subtype C
"0
...,
o Involves subcortical V-fibers o Diffuse periventricular, deep cerebral WM Ql
• Hypoglycemia T2 hyperintensity + spinal involvement CD

:::J
o Severe parietooccipital edema &/or infarcts o Posterior ee & posterior limb of internal o
...,
0;.
in a newborn capsule involved
OJ
...,
o T2 hyperintensity in occipital & parietal o Positive lactate peak Ql
lobes; commonly affects splenium • Enlarged Perivascular Spaces :::J
lJ
o DWI positive o May occur throughout ee Ql
...,
o May be reversible if treated early o Follow eSF on all MR sequences (1)
:::J
()
o When present in ee, adjacent brain often ::T
Helpful Clues for Rare Diagnoses '<
involved 3
• X-Linked Adrenoleukodystrophy Ql
o Enhancing peritrigonal WM
• Systemic Lupus Erythematosus
o May cause focal lesion in splenium related
demyelination
o Splenium involved early followed by
to vasculitis
peri trigonal WM & other WM tracts Alternative Differential Approaches
(corticospinal tracts/forn ix/ comm isural • Reversible splenium lesions
fibers/visual and auditory pathways) o Status epilepticus, drug toxicity, transient
o Typically spares subcortical V-fibers metabolic derangement, encephalitis,
• Acute Hypertensive Encephalopathy, hypoglycemia, PRES
PRES • Splenium lesions in a child
o Reversible WM edema induced by o DAI, status epilepticus, drug toxicity,
hypertension encephalitis, HIE, hypoglycemia, ALD,
o Typically affects cortex & subcortical WM ADEM, WM disease with lactate,
of parietal & occipital lobes perivascular spaces
o Posterior circulation • Splenium lesions in an adult
o Rarely affects splenium o DAI, status epilepticus, drug toxicity,
• ADEM encephalitis, alcoholic encephalopathy,
o Subcortical WM & deep gray nuclei neoplasms, PML, PRES, ADEM,
commonly involved perivascular spaces
Diffuse Axonal Injury (DAI) Multiple Sclerosis
I
Axial T2WI MR shows focal hyperintensity in the CC
splenium P.t] related to OAf. OWl is often positive in
Axial T7 C+ MR shows a tumefactive multiple sclerosis
(MS! plaque that extends into the splenium. The 6
acute OAi. T2*/CRE & SWI sequences often show incomplete ring of enhancement P.:JJ is characteristic of
multiple additional lesions. demyelination. The CC is almost always involved in MS.
59
<1l CORPUS CAllOSUM SPLENIUM LESION
E
>-
.c
o
c
Q)
~
<1l
a..
c Status Epilepticus
<1l
CD
shows focal hyperintensity in
<1l
'C the CC splenium =::lI caused
o by transient slaWs
C epilepticus. Acutely this
Q)
lesion is OWl positive &
~
Q. typically resolves completely.
::J (Right) Sagittal T2WI MR
C/)
shows hyperinlensily
r:: throughout the spleniurn
CIl
~ with extension into the body
CO of the CC in this patient with
"C
r:: renal failure & electrolyte
CIl imbalance. These MR
:J findings are usually
-"C/) completely reversible.
Enhancement is rarely
present

focal hyperintensity in the
CC splenium P:J:I related to
an Epstein-Barr virus
infection. This reversible
lesion does not enhance.
focal restriction in the
splenium in this patient with
viral encephalitis. The
patient's symptoms & MR
findings completely resolved,
as is typical of this process.
Imaging mimics status
epileplicus, anti-epileptic
medica lion toxicity. early
Marchiafava-Bignami
disease, & acute ischemia.

subtle focal hyperintensity in
the CC splenium E!i:I related
to West Nile virus
encephalitis. West Nife virus
typically involves the deep
gray nuclei & brainstem.
shows focal a ute ischemia
in the CC splenium E!i:I of
this 2 year old related to a
morphine overdose. Note
subtle hyperintensity in the
basal ganglia. Involvement of
the deep gray nuclei is
common in
hypoxic·ischemic
I encephalopathy.
6
60
CORPUS CALLOSUM SPLENIUM LESION en
"
c:
III
:l
Co
..•
lJl
III
Alcoholic Encephalopathy
:l
shows focal hyperintensity in en
c:
the central CC splenium -0
related to early ID
Marchiafava-Bignami CD
:l
disease. This disease often
affeclS the body & splenium
o
..•
0;'
of lhe Cc. Involvement of
the middle layers of the CC is lJl
virtually pathognomonic.
ID
:l
(Right) Axial T1 C+ MR -U
shows enhancement in the
splenium & forceps major of
..•
Q)
(t)
:J
the CC ~ as well as the ()
::r
perivenlricular while matter '<
related to acute 3
Q)
demyelination from severe
alcohol poisoning.

diffuse enhancement in the
splenium of lhe CC related 10
primary CNS lymphoma.
This tumor classically crosses
lhe CC & spreads along the
ependyma. Extension to the
adjacent while matter is
lypical. (Right) Axial T2WI
MR shows hyperintenshy in
the CC splenium &
perivenlricular while maller
in this immunosuppressed
patient. PML lypically does
not enhance. Note
involvement of the
subcortical U-fibers,
characteristic of PML.

focal increased signal
intensity in the splenium of
the CC =::I related to
demyelination in early
X-ALD. This typically
progresses to involve the
forceps major of the CC &
adjacent white matter. Bone
marrow transplant may help
to prevent progression of the
disease. (Right) Sagittal
FLAIR MR shows a focal
hyperintense lesion =
in the
splenium in this young
patient with a recent viral
illness. ADEM often mimics
MS, as in this case. I
6
61
co BASALGANGLIA CALCIFICATION
E
>.
.r:
u
c • Convexity subarachnoid spaces most
Q)
'-
co common
a.. Common
c o Imaging varies with pathologic stage
co • Aging Brain, Normal • Ca++ in nodular calcified (healed) stage
'-
co
co
• eurocysticercosis
'C
.8 less Common • Fahr Disease
c
Q)
• Fahr Disease o Bilateral symmetric BG Ca++, often with
1il
'-
a. • Hypoxic-Ischemic Injury, NOS Ca++ in other locations
:J
U) • MELAS o GP is most common site of Ca++ (lateral>
C • Congenital Infections medial)
III
'- o HIV, Congenital o Other locations: Putamen, caudate,
CO
"0
o CMV, Congenital thalami, dentate nuclei of cerebellum,
C
III • Endocrinologic Disorders cerebral white matter, internal capsule
:J o Hyperparathyroidism o Associated abnormalities: Parkinsonism in
-"
en o Hypoparathyroidism autosomal dominant FD
o Pseudohypoparathyroidism • Hypoxic-Ischemic Injury, NOS
o Pseudopseudohypoparathyroidism o HIE, term: Profound acute injury results in
o Hypothyroidism decreased BG and thalamic density, ±
• Toxoplasmosis, Acquired hemorrhage acutely
• Leigh Syndrome • Lateral thalami and posterior putamen
• Tuberculosis typical
• Radiation and Chemotherapy • May show Ca++ in chronic phase
• Cavernous Malformation (Mimic) o HIE in adults: Putamen> GP typically
• Vascular Calcification (Mimic) • May have history of "anoxic event"
• Tuberous Sclerosis Complex (Mimic) • MR > CT for acute changes
Rare but Important • May show Ca++ in chronic phase
• Hallervorden-Spatz Syndrome • MELAS
• CO Poison ing o BG Ca++ in child or young adult with
• Parasites, Miscellaneous cortical lesions (parietooccipital >
tem poroparietal)
• HIV, Congenital
ESSENTIAL INFORMATION o Symmetric BG Ca++ and cerebral atrophy
Key Differential Diagnosis Issues • GP and putamen> caudate
• Basal ganglia (BG) Ca++ is end result of o Subcortical WM Ca++ common
multiple toxic, metabolic, inflammatory, o Ca++ occur in a fairly symmetric fashion a
and infectious insults result of a calcific vasculopathy of medium
• Location of Ca++ helpful to determine and small arteries
underlying cause (globus pallidus [GP] vs. • CMV, Congenital
putamen vs. caudate) o Periventricular Ca++, microcephaly, and
• Patient age may impact differential diagnosis cortical dysplasia characteristic
o Periventricular > > BG Ca++
Helpful Clues for Common Diagnoses • Endocrinologic Disorders
• Aging Brain, Normal o Bilateral BG: GP and putamen, dentate
o Commonly affects GP more than putamen
nuclei, thalami, subcortical areas
o Seen in aging brain as normal variant
o Ca++ in primary hypoparathyroidism is
o Typically in patients older than 30 years
more diffuse than in other etiologies of
o If occurs with other Ca++, consider
Ca++
pathologic condition • Toxoplasmosis, Acquired
• Neurocysticercosis o Typically multifocal, but BG common site
I o May occur anywhere in brain
(up to 75%)
o Enhancing lesion most common acutely
6
62
BASAL GANGLIA CALCIFICATION ,..
en
c:
III
o Post-therapy, Ca++ is common o T2 MR characteristic: High signal within :::l
Co
• Leigh Syndrome bilateral GP with surrounding low signal,
"eye of the tiger"
..•III
llJ
o Bilateral, symmetric t T2/FLAIR putamina
:::l
and peri-aqueductal gray matter o CT may show mineralization in GP
(fJ
o Putamen> caudate> GP, Ca++ when • CO Poisoning c:
chronic o Typically hypodense, symmetric GP on ..•
"0
OJ
• Tuberculosis CT, T2 hyperintense CD

:::l
~
o Typically causes tuberculous meningitis o GP Ca++ occurs as end result o
~
&/or localized CNS infection, tuberculoma • Parasites, Miscellaneous iii:
llJ
o Approximately 20% of tuberculomas o Amebic encephalitis: Supratentorial, ~
OJ
calcify frontal lobes and basal ganglia :::l
\J
• Radiation and Chemotherapy • Typically enhancing lesions acutely, may OJ
o Mineralizing microangiopathy causes BG calcify in chronic phase CD
:::l
()
and subcortical WM Ca++, atrophy o Malaria: Predilection for BG, cortex :T
'<
o Mineralizing microangiopathy common • Hemorrhage, infarcts and cerebral edema 3
OJ
with chemotherapy and XRT • May show Ca++ in chronic phase
o Typically occurs 2 or more years after XRT o Paragonimiasis: Acutely often hemorrhage
• Cavernous Malformation (Mimic) or infarct, followed by Ca++ granulomas
o Hyperdense mass (Ca++ and blood
products) may occur in any location
• BG Ca++ in a child
• Vascular Calcification (Mimic) o Mitochondrial encephalopathies: MELAS,
o May relate to physiologic vascular
MERRF,Leigh syndrome
calcification, atherosclerosis, aneurysm, or o Congenital infections: HIV, CMV
vascular mass o HIE, term
• Tuberous Sclerosis Complex (Mimic) o Associated with Down syndrome
o Subependymal nodules are typically
o Aicardi-Goutieres syndrome
calcified; occur along caudothalamic (pseudo-TORCH)
groove, peri ventricular o Cockayne syndrome
Helpful Clues for Rare Diagnoses o Long-term complications of radiation
• Hallervorden-Spatz Syndrome therapy for childhood brain tumors and
o Rare neurodegenerative disorder with intrathecal chemotherapy
brain iron accumulation
I
Axial NECT shows typical basal ganglia calcification in
this 75 year old male who presented after minor trauma.
Axial CECT shows a calcified left putamen nodule =
that represents the nodular, calcified (healed) stage of
6
Note location within the globus pallidus, typical for NCe. Note right external capsule cyst with central "dot"
normal aging brain. representjng a scolex.
63
ell BASAL GANGLIA CALCIFICATION
E
>,
.c
u
c
Q)
~
ell
0...
c Fahr Disease
ell
~ (Left) Axial NECT shows
CIl
typical CT appearance of
ell Fahr disease with extensive
·C
o calcifications present in the
C
Q) basal ganglia, cerebral white
ro~ matler, and at subcortical
n. gray-white junclions. (Right)
::::J
CIJ Axial NECT shows
calcification of thalami and
c BC ~ from stalus
ra
"- marmQratus. There is
!XI atrophy and a collapsed
"0
c calvarium fof/owing remote
ra mixed HIE. Profound acute
HIE typically affects Be.

calcificalion of globus
pallidus bilaterally I:?] in this
child Note low density in
medial occipital lobes related
to ischemia. BC calcification
is abnormal in children and
young adults. (Right) Axial
NECT shows symmetric BC
calcification with scattered
foci of subcortical
calcification. Note typical
involvement of lentiform
nuclei greater than caudate
heads.

peri ventricular and basal
ganglia calcifications.
Periventricular calcifications,
venlriculomegaly, and
microcephaly strongly
suggest congenital CMV
infection. (Right) Axial NEeT
shows diffuse hyperdense
calcifications within the basal
ganglia, thalami, and
subcortical white matter.
Calcification related to
systemic disease is typically
symmetric.
I
6
64
BASAL GANGLIA CALCIFICATION
III
::s
a.
..•
m
III
(Lefl) Axial CECT shows an ::s

enhancing Be mass 111 in an Ul
c
AIDS patient. Post-lherapy,
enhancing lesions typically
..•
"0
Ql
calcify. Be is the most ro:::l
common location followed
by thalamus, then ..•
S
Ql
hemispheres. (RighI) Axial
T2WI MR shows symmetric OJ
T2 hyperintensity in the
OJ
:::l
basal ganglia E±I bilaterally in -U
this child with Ql
neurodegeneralion. CO
:::l
Calcification of the Be is ()
::r
seen in chronic cases. '<
3
Ql
Radiation and Chemotherapy Vascular Calcification (Mimic)

mineralizing
microangiopathy related to
radiation therapy and
chemotherapy for a posterior
fossa medulloblastoma. Note
symmetric Ca++ in Be and
subcortical while maller.
(RighI) Axial NECT shows
intracranial atherosclerotic
disease with extensive Ca++
in internal carotid and
middle cerebral arteries I:]
which mimics Be Ca++.
Posterior fossa aneurysm is
partially visible.
Hallervorden-Spatz Syndrome
nodules in the foramen of
Monro region bilaterally in
this child with seizures,
mimicking Be Ca++. S[N
occur in 98% of patients
with tuberous sclerosis.
(RighI) Axial NECT shows
mineralization in CP
bilaterally related to iron
accumulation in a patient
with pantothenate
kinase-associated
neurodegeneration (PKAN);
look for "eye of the tiger" on
T2 MR.
I
6
65
Cll 11 HYPERINTENSE BASAL GANGLIA
E
>-
.<:
u
c
DIFFERENTIAL DIAGNOSIS o T1 hyperintensity in GP, thought to be
~
Q)
Cll
Q..
related to FASI&/or mineralization
c Common o Tl hyperintensity increases with age, but
~
Cll • Physiologic Calcification, Brain may resolve by adulthood
al
Cll
• Neurofibromatosis Type 1 • Hepatic Encephalopathy
·C
a • Hepatic Encephalopathy o GP & substantia nigra (SN) hyperintensity
C
Q)
• Hyperalimentation o History of liver disease
ro~ Less Common • Hyperalimentation
0.
::>
• Hypoxic-Ischemic Encephalopathy, NOS o Abnormal manganese metabolism in
(f)
c o HIE, Term patients undergoing parenteral feeding

•...
Cll
o Hypotensive Cerebral Infarction o T1 hyperintensity in GP & SN
al
"C • CO Poisoning Helpful Clues for Less Common Diagnoses
c • Kernicterus
Cll • Hypoxic-Ischemic Encephalopathy, NOS
• Wilson Disease o Includes anoxia, hypoxia, near drowning,
Rare but Important & cerebral hypoperfusion injury
• Endocrine Disorders o Tl & T2 hyperintense BG & cortical lesions
o Hypothyroidism o DWI restriction if acute

o Hyperparathyroidism • HIE, Term
o Hypoparathyroidism o Cerebral hypoperfusion injury
o Pseudohypoparathyroidism o Several patterns of injury related to infant
o Pseudopseudohypoparathyroidism development, severity & duration of insult
• Hypoglycemia o Tl & T2 hyperintense BG & thalamus with
• Hallervorden-Spatz Syndrome profound insult
• Fahr Disease o May involve posterior mesencephalon,
• Encephalitis (Miscellaneous) hippocampi, & peri-Rolandic cortex

o Japanese Encephalitis • Hypotensive Cerebral Infarction
o HIV, Congenital o Insufficient cerebral blood flow
o Border zone between major arterial
terri tories typical
ESSENTIAL INFORMATION o May be isolated to BG or thalami
Key Differential Diagnosis Issues o T1 hyperintensity related to blood or
• Basal ganglia (BG) are paired deep gray pseudolaminar necrosis

nuclei & include caudate nuclei, putamen, & • CO Poisoning
globus pallidus (GP) o Bilateral, symmetric GP T2 hyperintensity
• Lentiform nucleus: Putamen & GP o May also involve putamen, thalamus,
• Corpus striatum: Caudate, putamen, & GP white matter (WM)

• BG Tl hyperintensity is usually symmetric, o If hemorrhagic necrosis, Tl hyperintense
related to calcification (Ca++) or other • Kernicterus
mineralization o Tl & T2 hyperintensity in GP in a neonate
o Acute: Tl & (subtle) T2 hyperintensity in
Helpful Clues for Common Diagnoses GP, hippocampi, SN
• Physiologic Calcification, Brain o MR changes may be reversible with
o Commonly affects GP more than putamen
exchange transfusion in some cases
o Seen as normal variant in aging brain
• Wilson Disease
o Typically in patients older than 30 years o Children: T1 hyperintensity in GP
• Neurofibromatosis Type 1 o Children & adults: Symmetric T2
o Focal areas of increased signal intensity hyperintensity or mixed intensity in
(FASI)characteristic, T2 hyperintense putamina, GP, caudate, & thalami
o FASIoccur in deep gray nuclei, GP most o Characteristic "face of the giant panda"
I common sign at midbrain level & T2 hyperintense
WM tracts
6
66
11 HYPERINTENSE BASAL GANGLIA

o May have hypoparathyroidism
• Endocrine Disorders • Hypoglycemia
o Neonatal hypoglycemic brain injury
o All 5 may result in BG Ca++, particularly
o Occipito-parietal edema or infarcts, ± BG
GP & putamen
o May also see Ca++ of caudate dentate
• Hallervorden-Spatz Syndrome
o Preferred terms: Pantothenate
thalamus, SN, & subcortical WM '
kinase-associated neurodegeneration
o Symmetric involvement is typical
o Variable Tl signal, often hyperintense,
(PKAN)or NBIA-l
o Progressive neurodegenerative disorder
related to phase of calcification
with brain iron accumulation
• Hypothyroidism
o "Eye of the tiger": Symmetric GP T2
01'1 hyper- & T2 hypointensity in BG & SN
hyperintensity surrounded by
o Etiologies include autoimmune disease &
post-therapy (thyroidectomy, XRT) hypointensity
o May see Tl hyperintensity in T2
hypointense areas (iron accumulation)
o BG Ca++ typical, ± dural Ca++ (rare)
o Etiologies include parathyroid adenoma &
• Fahr Disease
o Bilateral symmetric BG Ca++ on CT
chronic renal failure
o GP most common site for Ca++
• Hypoparathyroidism
o Putamen, caudate, thalami, cerebellum,
o Caudate nucleus> putamen & GP Ca++
o Dentate nuclei, centrum semiovale , cortex ,
cerebral WM may also be involved
& mesencephalic gray matter also involved
• Encephalitis (Miscellaneous)
o Rabies encephalitis: 1'1 hyperintensity in
o More diffuse Ca++ than other etiologies
bilateral BG, rare
• Pseudohypoparathyroidism
o BG Ca++ common
• Japanese Encephalitis
o T2 hyperintense foci in WM , brainstem ,
o May see pulvinar & dentate nuclei Ca++
o Resistance to parathyroid hormone
BG, thalami bilaterally typical
o If hemorrhagic, may see 1'1 hyperintensity
o Includes Albright hereditary
osteodystrophy (AHO) • HIY, Congenital
o BG Ca++ (30-85%) > frontal WM >
• Short stature, obesity, brachydactyly, &
cerebellum
ectopic ossifications
o Symmetric BG Ca++ & cerebral atrophy
• Pseudopseudohypoparathyroidism
o Patients with AHO with normal responses
• GP & putamen> caudate
o Tl hyperintensity related to Ca++
to parathyroid hormone
I
Axial TlWI MR shows subtle hyperintensity in the CP
BI related to physiologic calcification in this 76 year old
Axial Tl WI MR shows hyperintensity in the BC &
thalamus in this NF I paUenL The CP & internal capsule
6
patient. Calcification is a common normal variant in the are commonly involved. Note also large right BC FASI.
aging brain
67
ro 11 HYPERINTENSE BASAL GANGLIA
E
>-
.!:
U
C
Q)
~
ro
0..
c
ro
~ (Lefl) Axial T1 WI MR shows
CD
hyperintensi/y in the BG,
ro
·C
o
C
Q)
=-
most prominent in the CP
& blurring of the
gray-white junctions related
ro~ to acute edema in this
a. hepatic encephalopathy
:J patient. With treatment,
CIJ
reversal of the bright lesions
C
is often seen in 3-6 months.
=
III
~ (RighI) Axial T1WI MR
CO
shows hyperintense GP
"0
C in a paUent receiving TPN.
t'll The hyperintensity is likely
:J caused by manganese
~ deposition &/o{ an
en astroglioUc reaction to the
deposition.
HIE, Term
(Lefl) Coronal T1 WI MR
shows hyperinlensily in the
BG, predominantly at the
heads =
putamen 1::1] & caudate
in this patient with
hypoglycemia & hypoxia.
Whether the damage is from
the hypoglycemia or
seizure-induced hypoxia is
difficult to de/ermine. (RighI)
Axial T1WI MR shows bright
signal within the lentiform
nucleus = & lateral
thalamus E!2 bilaterally,
related to profound acute
HIE in this neonate.
CO Poisoning
(Lefl) Axial T I WI MR shows
hypointensity in the GP with
surrounding hyperintensity
-= in this patient with a
remote history of
hypoxic-ischemic
encephalopathy related to
hypotension. Imaging mimics
CO poisoning. (RighI) Axial
T1WI MR shows
heterogeneous signal in the
GP bilaterally with areas of
central hypoinlensily with a
surrounding rim of
hyperintensity =. The
heterogeneous signal is likely
I related to necrosis &/or

blood products.
6
68
11 HYPERINTENSE BASAL -GANGLIA
III
::::l
Co
..•
OJ
III

::::l
acute changes of kernicterus (f)
C
with T1 shortening in the GP
= & ventral thalami ~. A
..•
"0
Q)
history of sustained or CD
::::l
pronounced neonatal o
::>.
hyperbilirubinemia is typical.
Q)
OJ
shows mixed signal intensity
in the putamen bilaterally ~
OJ
::J
in a young adult with Wilson -U
disease. Wilson disease is an
inborn error of copper
..•
Q)
(1)
::J
metabolism characterized by ()
:T
liver cirrhosis, '<
Kayser·Fleischer rings in the 3
Q)
cornea, & Be degeneration.
Hypothyroidism Hallervorden-Spatz Syndrome

hyperintensity in the BG
related to hyperdense
calcifications in this patient
with hypothyroidism. (Right)
hypointense GP with
surrounding hyperintensily
~. This corresponds to the
"eye of the tiger" sign on T2
MR imaging in which T2
hyperintensity surrounded by
pallidal T2 hypointensity
(iron deposition).

hyperintensity in the BG,
predominantly involving the
Gp, in this patient with Fahr
disease. The corresponding
CT showed dense
calcification. (Right) Axial
NECT shows symmetric BG
calcification with scattered
foci of symmetric subcortical
calcification in the frOnial &
parietal lobes. Note typical
involvement of the lentiform
nuclei greater than the
caudate heads. T1 MR often
shows corresponding
hyperintensity in the Be. I
6
69
co 12 HYPERINTENSE BASAL GANGLIA
E
>-
.!:
U
c:
DIFFERENTIAL DIAGNOSIS o Border zone between major arterial
...co
Q)
territories typical
CL
c: Common o DWI restriction if acute
~ • Hypoxic-Ischemic Encephalopathy, NOS • HIE, Term
III
o Hypotensive Cerebral Infarction o Involvement of BG & thalamus typically
CO
·C
o o HIE, Term seen with profound insult
CQ)
• Neurofibromatosis Type 1 o T1 & T2 hyperintensity in BG & thalamus
~ • ADEM o Ventrolateral thalamus typically involved
n.
:::J • CO Poisoning o DWI restriction if acute
U)
• Vasculitis • Neurofibromatosis Type 1
o Systemic Lupus Erythematosus o Focal areas of increased signal intensity
o Hemolytic Uremic Syndrome (FASI)characteristic, BG typical
o Infectious Vasculitis o May also see FASIin brainstem
:::J less Common • ADEM

-"en • Drug Abuse o Multifocal white matter (WM) & BG
• Gliomatosis Cerebri lesions following infection/vaccination

• Osmotic Demyelination Syndrome o Bilateral, asymmetric T2 hyperintensities
• Encephalitis (Miscellaneous) • CO Poisoning
o Bilateral, symmetric GP T2 hyperintensity
Rare but Important o May also involve putamen, thalamus, WM
• Creutzfeldt-]akob Disease (CJD) • Vasculitis
• Acute Hypertensive Encephalopathy, PRES o Heterogeneous group of CNS disorders
• Metabolic, Inherited characterized by nonatheromatous
o Leigh Syndrome
inflammation & blood vessel wall necrosis
o Wilson Disease
o Angiography: Multifocal areas of smooth
o MELAS
or mildly irregular stenosis alternating
o MERRF
with dilatations
o Glutaric Aciduria Type 1
o T2 hyperintensity in BG & WM
• Huntington Disease o DWI restriction if acute
• Systemic Lupus Erythematosus
ESSENTIAL INFORMATION o CNS involvement in up to 75% of cases,
typically multifocal ischemia
Key Differential Diagnosis Issues o True vasculitis of CNS is rare in SLE
• Basal ganglia (BG) are paired deep gray o Small multifocal WM lesions ± BG
nuclei & include caudate nuclei, putamen, & • Hemolytic Uremic Syndrome
globus pallidus (GP) o May cause vasculitis or hypertensive
• Lentiform nucleus: Putamen & GP encephalopathy (PRES)
• Corpus striatum: Caudate, putamen, & GP o BG involvement typical in patients with
• Symmetric BG lesions suggest a neurological complications of HUS
toxic/metabolic process or hypoxia • Infectious Vasculitis
• DWI may help differentiate BG lesions o Bacterial meningitis: Infarct due to
Helpful Clues for Common Diagnoses vascular involvement seen in 25%
• Hypoxic-Ischemic Encephalopathy, NOS o Tuberculous meningitis: Skull base vessels
o Includes anoxia, hypoxia, near drowning, most commonly involved
& cerebral hypo perfusion injury o Lenticulostriate artery involvement
o T1 & T2 hyperintense BG & cortical lesions common
o DWI restriction if acute
• Hypotensive Cerebral Infarction • Drug Abuse
o Infarct resulting from insufficient cerebral
o Young/middle-aged patient with stroke
I blood flow to meet metabolic demands
o May be isolated to BG
o May cause stroke &/or vasculitis
o T2 hyperintensities or hemorrhage in BG
6
70
12 HYPERINTENSE BASAL GANGLIA
Ql
• Gliomatosis Cerebri o Patchy cortical/subcortical PCA territory ::J
Co
o Diffusely infiltrating glial tumor involving lesions
.,
OJ
2 or more lobes, frequently bilateral o BG involvement less common Ql
o Typically hemispheric WM with BG or o No diffusion restriction on DWI typical ::J

thalami (75%) • Leigh Syndrome en
c
o Often infiltrates beyond BG into WM o Symmetric T2 hyperintense lesions with .,
'tJ
III
• Osmotic Demyelination Syndrome onset in infancy/early childhood CD

::J
o 50% in pons (CPM) & 50% extra-pontine o BG: Corpus striatum> GP 8'
:>.
sites (EPM): BG & cerebral WM o Bilateral lesions in putamen & III
OJ
.,
o Symmetric hyperintensity in BG, WM peri-aqueductal gray are classic III
• Encephalitis (Miscellaneous) • Wilson Disease ::J
\l
o Many pathogens, most commonly viruses o Symmetric T2 hyperintensity in putamen, III
o Abnormal T2 hyperintensity of gray matter GP, caudate, & thalami ro::J

(')
± WM or deep gray nuclei o Characteristic "face of the giant panda" :::r
'<
o West Nile encephalitis: Symmetric BG, sign at midbrain level & T2 hyperintense 3
III
thalami, mesial temporal lobe, brainstem, WM tracts
& cerebellum T2 hyperintensities • MELAS
o Japanese encephalitis: High signal foci in o T2 hyperintensities in putamen, may be
WM, brainstem, BG, thalami bilaterally asymmetric or unilateral
o Epstein-Barr virus: Symmetric BG, thalami, o Multifocal T2 hyperintensities in BG, deep
cortex, or brainstem T2 hyperintensities WM in chronic phase
o Mycoplasma: May cause acute bilateral • MERRF
striatal necrosis o Propensity for BG, caudate nuclei
o Watershed ischemia/infarcts common
• Glutaric Aciduria Type 1
• Creutzfeldt-jakob Disease (C]D)
o T2 hyperintensities in corpora striata, GP,
o Progressive T2 hyperintensity of BG,
± WM disease
thalamus, & cerebral cortex
o Characteristic opercular widening
o Symmetric T2 hyperintense caudate nuclei,
• Huntington Disease
putamen> GP
o Hyperintense signal in caudate & putamen
• Acute Hypertensive Encephalopathy,
in juvenile HD
PRES
o Typically seen in patients with severe
hypertension
I
Axial T2WI MR shows symmetric hyperintensity &
edema of the corpus striatum=in this patient with
Axial FLAIR MR shows hyperintensity in the posterior
putamen = & lateral thalami in this neonate with
6
anoxic injury. Symmetry suggests a toxic/metabolic profound HIE. OWl findings are most sensitive at 2 to 6
process or hypoxic-ischemic injury. days after the HIE event.
71
<Il 12 HYPERINTENSE BASAL GANGLIA
E
>.
.r:
u
c
~
Ql
<Il
a..
c Neurofibromatosis Type 1 CO Poisoning
~
<Il
CD
foci of abnormal signal
<Il intensity (FASI) in the BC
·C
o B. Lesions are usually
C bilateral but asymmetric. The
Ql
10
~ CP is the most common
Q. location for FASI, though
:J they maya/so be seen in the
(f)
brainstem. (Right) Axial
C
T2WI MR shows bilateral CP
~
'"
CD
hyperintensities =& diffuse
hyperintensity throughout
1:1
c: the white matter 81 but
'::s" sparing of the subcortical

U-fibers, typical of CO
-"III poisoning.
Systemic Lupus Erythematosus Infectious Vasculitis

symmetric high signal
intensity in the BC & thalami
related to vasculitis, a rare
manifestation of SLE. OWl is
bright in the acute setting.
SLE usually results in
multifocal ischemia in the
white matter & Be. (Right)
Axial T2WI MR shows
confluent hyperintensity in
the BC bilaterally related to
meningitis·induced vasculitis.
OWl is bright in the acute
selling. Be involvemenl is
typical of lenticulostriate
artery disease.
Osmotic Demyelination Syndrome

multiple BC hyperintensities
B caused by vasculitis in a
young adult with a history of
amphetamine abuse. OWl is
bright in the acute setting.
Drug abuse should be
considered in a young adult
with stroke. (Righi) Axial
FLAIR MR shows
extrapontine myelinolysis
(EPM) as symmetric
caudate head ~ & putamen
81 related to rapid
correction of hyponatremia.
I EPM may occur without

central pontine myelinolysis.
6
72
T2 HYPERINTENSE BASAL GANGLIA en
,.-
c:
Encephalitis (Miscellaneous) Creutzfeldt-Jakob Disease (CJD)

the BC =-
symmetric hyperintensities in
thalami, & insular
cortex E1 in a West Nile
encephalitis patient.
Symmetric involvement of
the BC, thalami, mesial
temporal structures,
brainstem, & cerebellum ;s
typical. (Right) Axial T2WI
MR shows symmetric
caudate heads = &
putamen ~ in a patient with
progressive dementia, cia.
FLAIR & OWl are the most
sensitive for diagnosing CjD.

PRES leigh Syndrome
symmetric increased signal
intensity in the subcortical
WM 8:1 & BC PJ:.:I related to
PRES. OWl is typically
negative in PRES.PRES
usually involves posterior
circulation territory. Be
involvement is uncommon.
shows bilateral symmetric
caudate PJ:.:I & putamen =-

foci of abnormal signal in the
typical of Leigh disease. Lack

of associated mass effect
indicates chronic disease.
MERRF Glutaric Aciduria Type 1

mullifocal hyperintensities in
the cortical gray maller =..
putamen, & caudate head
PJ:.:I bilaterally. Muscle biopsy
disclosed findings consistent
with myoclonic epilepsy with
ragged red fibers (MERRF).
shows lentiform nuclei
enlargement & hyperimensily
8:1. Note the wide sylvian
fissures, typical of CA 1. OWl
(not shown) revealed
restricted diffusion within the
lentiform nuclei.
I
6
73
ENLARGED PERIVASCULAR SPACES
'"
E
>-
.s:::
u
c • Aging Brain, Normal
~
Ql DIFFERENTIAL DIAGNOSIS
o PVS are commonly seen as the brain loses
'c"
0...
Common volume as part of normal aging
~
'" • Normal Variant
[D Helpful Clues for less Common Diagnoses
• Aging Brain, Normal
• Cryptococcosis
"'o'"" less Common o Enlarged PVS in BG & superior brainstem
C
Ql • Cryptococcosis o May see DWI hyperintense rim
ro~
Cl.
:J Rare but Important Helpful Clues for Rare Diagnoses
(f)
• Mucopolysaccharidoses • Mucopolysaccharidoses
c: • Tumor-Associated Cysts, Nonneoplastic
III o Enzyme deficiency & inability to break
•...
al • CADASIL down glycosaminoglycan (GAG)
• Megalencephaly with Dilated Perivascular
"c:
III
Spaces
o PVS dilated by accumulated GAG
o CC & periatrial WM most common sites
• Hypomelanosis of Ito o Surrounding T2 hyperintensity common ±
additional patchy WM signal
ESSENTIAL INFORMATION • Tumor-Associated Cysts, Nonneoplastic
o "Cysts" caused by enlarged/obstructed PVS
Key Differential Diagnosis Issues reported with pituitary adenomas
• Perivascular spaces (PVS) are pial-lined • CADASIL
interstitial fluid-filled structures that o Subcortical lacunar infarcts &
accompany penetrating arteries leukoencephalopathy in young adults
• Most commonly seen as a normal variant o Dilated PVS are frequent in CADASIL,
Helpful Clues for Common Diagnoses involving temporal WM & BG
• Normal Variant o PVS dilation in CADASIL increases with
o Round/oval fluid-filled spaces that have age (may be related to aging or vascular
CSF density/intensity, no enhancement wall alterations)
o Rare mass effect (giant PVS) • Megalencephaly with Dilated Perivascular
o Most commonly seen at anterior Spaces
commissure, inferior basal ganglia (RG) o Enlarged WM PVS with surrounding T2
o Common: Midbrain, deep white matter hyperintensity
(WM), subinsular cortex, extreme capsule • Hypomelanosis of Ito
o Rare: Thalami, dentate nuclei, corpus o Large PVS with periventricular T2
callosum (CC), cingulate gyrus hyperintensity
Normal Variant
I
6 =
Axial T2WI MR shows a small cluster of C5F-like
slructures H1 along the anterior commissure at the
inferior basal ganglia, the most common locaUon for
Axial TI C+ FSMR shows no enhancement of the PVS
a which is typical. Occasionally, the penetrating
vessel may be seen centrally within the pvs. These
enlarged perivascular spaces. occur as normal variants at al1ages.
74
ENLARGED PERIVASCULAR SPACES
III
:l
C.
..,
OJ
Aging Brain, Normal III
(Left) Axial T2WI MR shows :l

multiple enlarged PVS in CIJ
white mailer = =.
typical locations: Subcortical
subinsular regions
BG 8l &
They
c
"0
..,
OJ
ro::J
are often bilateral &
S
symmetric and are :::!.
OJ
considered part of the
normal aging process. Up to OJ
..,
OJ
2S% may have a small T2 ::J
hyperintense rim. (Right)
=
II
Axial CECT shows multiple ..,
OJ
enlarged PVS in this <1l

::J
patient with cryplococcosis. ()
::r
Note lack of enhancement, '<
typical of this infection. 3
OJ
Patients are often
immunocompromised.
Mucopolysaccharidoses Tumor-Associated Cysts, Nonneoplastic

multiple enlarged PVS~
with surrounding
hyperintense confluent white
mailer disease. These PVS
are filled with unmetabolized
mucopolysaccharide. Note
callosum =-
involvement of the corpus
a typical
location for enlarged PVS in
this disorder. (Right) Coronal
T7 C+ FS MR shows a giant
macroadenoma m with
surrounding extratumoral
cysts representing enlarged
PVS = that contain trapped
pools of interstitial fluid.
Megalencephaly with Dilated

Perivascular Spaces Hypomelanosis of 110
bilateral perivenlricular
enlarged PVS 81 in a patient
with megalencephaly.
Findings suggest that PVS
enlargement refleclS an
underlying brain pathology
causing neuroaxonaf
damage. (Right) Axial FLAIR
MR shows enlarged PVS with
surrounding WM
hyperintensity in this patient
with incontinentia pigmenti
(hypomelanosis of Ito).
Patients with this rare
syndrome have typical
whorled skin lesions & may
have hemimegalencephaly.
I
6
75
co PERIVASCULAR SPACE ENHANCING LESIONS
E
>.
£
u
C
CD DIFFERENTIAL DIAGNOSIS a May cause a small vessel vasculitis
~ (involves penetrating arteries)
CO
D-
c Common • Tuberculosis
~
CO • Meningitis a Meningitis + parenchymal lesions
ro
• Neurosarcoid common appearance
.~
o • Tuberculosis a Inflammatory cells may extend along PVS
C • Vasculitis a May cause an infectious vasculitis
CD
1\1
~ • Skull base vessels most commonly
a. Less Common
:J
Cf) • Glioblastoma Multiforme involved (supracJinoid ICA & Ml)
C • Lymphoma, Intravascular (Angiocentric) • Vasculitis
ns
~ • Cerebral Amyloid Disease a Heterogeneous group of CNS disorders
aJ with inflammation & blood vessel necrosis
"0
C
Rare but Important a Primary or secondary to systemic disease
CO
• Metastases a Alternating stenosis, dilatation primarily
• Granulomatous Angiitis involving 2nd, 3rd order branches
• Langerhans Cell Histiocytosis a Angiography best for diagnosis
• Wegener Granulomatosis, Brain a Multifocal ischemia in subcortical white
• Moyamoya (Mimic) matter (WM) & basal ganglia (BG)
• Meningioangiomatosis a May cause PVS enhancement
• Neurocutaneous Melanosis
ESSENTIAL INFORMATION a Peripherally enhancing, centrally necrotic
Key Differential Diagnosis Issues WM mass typical
• Perivascular spaces (PVS) are pial-lined, a Often involves corpus callosum
fluid-filled structures that accompany a May metastasize along PVS
penetrating arteries • Lymphoma, Intravascular (Angiocentric)
• PVS follow CSF on all MR sequences a Rare malignancy characterized by
• Rarely an enhancing vessel may be seen intravascular proliferation of lymphoid
centrally within the PVS as a normal variant cells with a predilection for CNS & skin
• Enhancement of PVS is typically related to a Multifocal T2 hyperintensity in deep WM,
infection, vasculitis, or tumor cortex, or BG + enhancement typical
• Age of patient may help differentiate lesions a May see cortical infarct-like lesions
a May cause a vasculitis
Helpful Clues for Common Diagnoses • Cerebral Amyloid Disease
• Meningitis a Lobar hemorrhages of different ages &
a Enhancing leptomeninges typical multifocal "black dots" typical
a Hydrocephalus very common a Amyloid deposits may occur along PVS
a Inflammatory cells may extend along PVS a May cause a vasculitis
a More common in children a Occurs in elderly adults
a May cause an infectious vasculitis;
infarction due to vasculitis in 25% Helpful Clues for Rare Diagnoses
• Neurosarcoid • Metastases
a Multisystem inflammatory disease a Multifocal parenchymal enhancement at
characterized by noncaseating granulomas gray-white interfaces typical
a Meningeal enhancement typical a May rarely spread along PVS or involve
(leptomeningeal & dural) meninges
a May invade brain via PVS & cause diffuse a Primary tumor often known
or focal mass-like lesions • Granulomatous Angiitis
a Periventricular T2 hyperintense lesions a Primary angiitis isolated to the CNS
(idiopathic)
I common (50%)
a Manifests as multiple intracranial stenoses
a May cause PVS enhancement in BG or WM
6
76
PERIVASCULAR SPACE ENHANCING LESIONS CIl
"
c:
III
• Langerhans Cell Histiocytosis o NF2 in about 1/2 of patients ::l
Co
o Thick enhancing pituitary stalk is most o Children, young adults usually present to
..,
common CNS manifestation with seizures or headaches III
::l
o Lack of pituitary "bright spot" • Neurocutaneous Melanosis
CIl
o May extend along PVS o Rare phakomatosis: Giant or multiple C
cutaneous melanocytic nevi & melanocytic ..,

1:l
o Rarely causes enhancing choroid plexus, OJ
BG, &/or leptomeningeal nodules lesions of the leptomeninges & ro::l
• Wegener Granulomatosis, Brain parenchyma o..,
Qi"
o Chronic systemic arteritis involving lungs, o Melanocytes often confined to PVS in
to
..,
kidneys, & sinuses parenchymal melanosis OJ
o CNS involved in 15-30% due to direct o Amygdala, cerebellum, basis pontis, & ::l
lJ
invasion from nose/sinuses thalami common parenchymal sites ..,
OJ
o May cause intracerebral & meningeal ct>

Alternative Differential Approaches ::l
Cl
granulomas or vasculitis • PVS enhancing lesions in a child ::T
'<
o May cause meningeal & PVS enhancement :3
o Meningitis, TB, Langerhans cell OJ
• Moyamoya (Mimic) histiocytosis, moyamoya (mimic),
o Moyamoya is an angiographic pattern
meningioangiomatosis, neurocutaneous
o Idiopathic progressive arteriopathy of
melanosis
childhood
• PVS enhancing lesions in an adult
o Slowly progressive occlusion of the
o Neurosarcoid, TB, vasculitis, GBM,
supraclinoid ICAs intravascular lymphoma, metastases,
o T2 MR shows multiple dark flow voids in
cerebral amyloid disease, granulomatous
BG related to lenticulostriate collaterals angiitis, Wegener granulomatosis
o Contrast MIl.shows enhancement of these
• PVS enhancing lesions in an elderly adult
collaterals mimicking PVS enhancement
o GBM, intravascular lymphoma, metastases,
o Pattern has been reported with
cerebral amyloid disease
neu rofibromatosis, atherosclerosis,
radiation therapy
o Cortical mass with enhancement & Ca++
o Proliferation of blood vessels &
meningothelial cells around vessels in
meninges, cortex, & underlying WM
o Often extends into cortex via PVS
Neurosarcoid
I
Coronal Tl c+ MR shows striking enhancement in the
PVS 8lI along the penetrating arteries in the basal
Coronal T1 c+ MR shows nodular parenchymal
enhancement 8lI in the frontal lobe of this sarcoid
6
ganglia in this patient with bacterial meningitis. patient Parenchymal involvement is typically caused by
Diagnosis is made by lumbar puncture. PVS invasion of the granulomatous disease.
77
'" PERIVASCULAR SPACE ENHANCING lESIONS
E
>-
.r:
()
c
~
(l)
'"
a..
c Vasculitis
~ (Leh) Coronal T' C+ MR
co shows multiple punctate &
'o"
'C linear enhancing foci m
along the penetrating
C perivascular spaces in this TB
(l)
ro~ meningitis patient. TB may

cause a true vasculitis with
Cl.
:J muflifocallacunar & cortical
(/)
infarcts as sequelae. (Right)
C
Axial T' C+ MR shows
'"
L- striking enhancement in the
CO
"c
'"
brain parenchyma &
perivascular spaces
basal ganglia in this HIV
= of the
patient. I-{IV vasculitis is

increasing in incidence,
particularly in children.
(Left) Axial TI C+ F5 MR
shows multifocal
glioblastoma multiforme with
involvement of the PV5 as
patchy contrast
enhancement s::I in the basal
ganglia. (Right) Coronal TI
C+ MR shows linear
perivascular spaces ED
representing intravascular
lymphoma. This
enhancement occurs in areas
of T2 white mailer signal
abnormality. The linear
enhancement along PVS can
help suggest the diagnosis in
a dementia patient.
Cerebral Amyloid Disease

nodular enhancement =
representing intravascular
lymphoma involving the
Enhancement patterns are
variable in intravascular
lymphoma & may be linear,
punctate, patchy, nodular,
ring-like, gyriform, or
homogeneous. (Right) Axial
TI C+ MR shows nodular
enhancement in the basal
ganglia ~ related to
amyloid in the perivascular
spaces. Amyloid deposits are
I typically interstitial, vascular,

or perivascular.
6
78
PERIVASCULAR SPACE ENHANCING lESIONS
III
::l
a.
..,
III
III
(Left) Coronal T1 C+ MR ::l

shows linear enhancement (fJ
c:
along the perivascular spaces
..,
"0
=.2 of the frontal lobes. OJ
Imaging mimics sarcoid & CD
::J
intravascular lymphoma. 0"
Biopsy disclosed
..,
Qi.
(Right) Axial T7 C+ MR III
..,
III
shows punctate & linear ::J
enhancement in the -U
tempora/lobe & pons =.2 ..,
OJ
representing involvement of CD
::J
the perivascular spaces. ()
::r
Biopsy disclosed Langerhans '<
cell histiocytosis in this 3
OJ
young patient.
shows irregular
enhancement in the frontal
lobes of this patient with
Wegener granulomatosis of
the paranasal sinuses.
Invasion of the meninges &
brain from the sinuses occurs
in up to 30% of these
patients. (Right) Axial T7 C+
MR shows enhancing
lenticulostriate collateral
vessels in the basal ganglia
= related to the patienes
dista//CA stenosis bilaterally.
These colfalerals mimic
perivascular space
enhancement.
shows linear enhancement
=.2 related to a calcified
pial-based mass seen on CT.
Meningioangiomatosis
infiltrating the brain
parenchyma via the PVS was
identified at surgery. (Right)
strongly enhancing
superficial mass that fills the
adjacent sulci & extends into
the underlying brain. Surgery
disclosed exlensive
melanosis that had invaded
the brain via the perivascular
spaces.
I
6
79
Cll BILATERAL BASAL GANGLIA LESIONS
E
>-
.r::
u
c • Lacunar Infarction
<ll
Cll
0...
o Reduced diffusion if acute
c Common o May mimic enlarged perivascular space if
~ • Enlarged Perivascular Spaces chronic, but typically t SI on FLAIR
co
Cll
• Lacunar Infarction o Usually due to small vessel disease in
'C
o o Atherosclerotic patients with vascular risk factors
C o Other Vasculopathy; Vasculitis o May be due to vasculitis (infectious or
<ll
ro~ • Mineralization non-infectious) or non-atherosclerotic
Cl.
OJ • Manganese Toxicity vasculopathy (e.g., CADASIL)
(f)
o Liver Disease; Hyperalimentation • Mineralization
c:
l1l
~
• Hypoxic-Ischemic Encephalopathy o In normal aging, usually affects globus
CO • Neoplasm pallidus (GP)
"t:l
c: o CNS Lymphoma; Astrocytoma o Involvement of caudate &/or putamen
l1l
• Trauma suggests underlying metabolic condition
OJ
oX • Neurofibromatosis Type 1 o Check for radiation, chemotherapy history
(f)
• Toxin Exposure/Drug Abuse • Manganese Toxicity
Less Common o Attributed to t manganese (Mn) levels
• Infection o Also seen with total parenteral nutrition ~

o Cryptococcosis; Toxoplasmosis; Viral high serum Mn levels
Encephalitides o Bilateral symmetric GP t Tl SI
• Osmotic Demyelination Syndrome • Common in patients with chronic liver
• ADEM disease
• Posterior Reversible Encephalopathy • Hypoxic-Ischemic Encephalopathy
Syndrome (PRES) o Often also involves cerebral cortex,
• Venous Ischemia/Infarction hippocampi, thalami
o Reduced diffusion in acute phase
Rare but Important
• Neoplasm
• Neurosarcoidosis o CNS lymphoma commonly involves
• Creutzfeldt-]akob Disease (C]D) bilateral BG
• Mitochondrial Encephalopathies • Typically intermediate SI on T2WI,
o Leigh Syndrome; MELAS
enhance post-gad, mild. diffusion
• Huntington Disease o Astrocytoma may diffusely infiltrate BG
• Metabolic Disorders • Bithalamic involvement common
o Wilson Disease
• ± Extension into midbrain
o Pantothenate Kinase Associated
• Trauma
Neurodegeneration (PKAN) o Axonal stretch/shear vs. tearing of
o Organic Acidopathies
lenticulostriate vessels
o Variably hemorrhagic
ESSENTIAL INFORMATION o GRE/SWI useful
• Neurofibromatosis Type 1
Key Differential Diagnosis Issues o Areas of T2 t SI are common in the GP,
• Basal ganglia (BG) "lesions" may be normal brainstem, & cerebellar white matter (WM)
variants (e.g., perivascular spaces), normal o Represent areas of myelin vacuolization &
changes over time (e.g., Ca++, iron myelin dysplasia
deposition in the aging brain), or true • Toxin Exposure/Drug Abuse
pathology o CO poisoning characteristically causes
Helpful Clues for Common Diagnoses symmetrical T2 bright lesions of the GP
• Enlarged Perivascular Spaces o Drugs of abuse, notably heroin, may cause
o Very common, especially in older patients injury similar to CO poisoning
I o Follow CSF on all sequences
o If extensive in BG, so-called "etat crible"
o Cyanide may cause selective injury to GP,
subthalamic nuclei, cerebellum
6
80
BILATERALBASALGANGLIA LESIONS
III
Helpful Clues for Less Common Diagnoses • Mitochondrial Encephalopathies ::l
Q,
o Often symmetrical except MELAS OJ
• Infection ....•
o Reduced diffusion in acute phase of injury III
o Cryptococcal meningitis: Gelatinous ::l
pseudocysts cause multiple t T2 foci in BG • Huntington Disease
Ul
o T2 hyperintensity & severe atrophy of C
• Usually nonenhancing, no • diffusion, U
....•
bilateral caudate, putamina OJ
seen in HIV+ patients CO
o Toxoplasmosis: Ring-enhancing lesions
• Metabolic Disorders ::l
o Large number of inborn errors of o....•
o Viral encephalitis: Many types may affect 0;'
metabolism can affect bilateral BG
BG, often symmetrically OJ
....•
o Also acquired conditions such as
• Osmotic Demyelination Syndrome OJ
kernicterus, hypoglycemia ::l
o Caudate nuclei, putamina are common "U
o Wilson disease: Autosomal recessive (AR); • OJ
....•
locations for extrapontine myelinolysis
biliary excretion of copper; t T2 Sl in BG <1l
::l
o Typically symmetrical T2 hyperintensity ()
o PKAN:AR disorder of coenzyme A ::r
• ADEM '<
metabolism; "eye of the tiger" sign in GP; 3
o Patchy, asymmetrical BG t T2 lesions OJ
symmetrical t T2 surrounded by • T2
o Also subcortical WM, thalami, spinal cord,
optic nerves Alternative Differential Approaches
• Posterior Reversible Encephalopathy • Bilateral caudate and putamina I lesions
Syndrome (PRES) o Symmetrical: HIE; extra-pontine
o BG involvement usually accompanied by myelinolysis; Wilson disease
subcortical WM t T2 lesions o Variably symmetrical: CJD; toxic,
• Venous Ischemia/Infarction metabolic, or mitochondrial processes
o BG involvement usually occurs with severe o Asymmetrical: Enlarged perivascular
bithalamic involvement spaces; lacunar infarcts; vasculitis;
neoplastic infiltration; ADEM
o Reduced diffusion: HIE; vasculitis or
• Neurosarcoidosis
vasculopathy; C]D; encephalitis; metabolic
o Enhancing nodules with edema
or mitochondrial disorder
• Creutzfeldt-]akob Disease (C]D)
• Bilateral globus pallidus lesions
o T2 hyperintensity may variably affect
o Symmetrical: HIE; CO poisoning;
bilateral BG, thalami, & cerebral cortex
manganese toxicity; PKAN
o Cortical involvement usually asymmetric,
o Asymmetrical: Mineralization (variable);
while BG & thalami more symmetric
NFl (variable)
o Reduced diffusion; no enhancement
Lacunar Infarction
I
Axial T2WI MR shows multiple small punclale foci of t
51 in bilateral caudate nuclei & putamina that {ollow CSF
on all sequences. Thalami & perivemricular WM show
of • diffusion in the Be=
Axial OWl MR shows multiple small asymmetrical foci
& in the hemispheric WM
EZl This patient had meningitis & infectious vasculitis
6
evidence of chronic ischemic change. affecUng multiple small vessels.
81
'" BILATERAL BASAL GANGLIA LESIONS
E
>-
-'o=
c
OJ
~
'c"
Cl..
Mineralization
~
'" (Left) Axial NEeT shows
CO
stippled Ca++ of the bila!eral
'C
C
'o"
OJ
subcortical WM =
putamina i:llI & fron!al
as subtle Ca++ of the

as well
ro~ caudate nuclei, in a patient

a. with
::>
(fJ pseudohypoparathyroidism.
Ca++ associated with normal
c aging affec!s the Cp, usually
•...
'" symmetrically. (Right) Axial
ell T1WI MR shows symmelrical
-0
c t 51 in the CP in a patient
with end·scage liver disease
'::>" from hepatic cirrhosis. After
-"(fJ liver transplantation, the
signal abnormality regressed
over time.

symmetrical * diffusion in
the caudate nuclei 81 &
putamina = in a patient
who suffered cardiac arrest &
was comatose. There is also
~ diffusion in the cortical
ribbon, most evident in the
occipital lobes ~ (Right)
Axial CECT shows
contrast-enhancing masses
with associated vasogenic
edema involving the caudate
nuclei i:llI & the ependymal
surfaces of bilateral fron!al
horns. An enhancing mass
E1 is also seen in the atrium.
Trauma Neurofibromatosis Type 1

(Left) Axial T2 CRE MR
shows severe traumatic
injury, with scalp
hemalomas, 5AH, fVH,
bifrontal hemorrhagic
contusions, & hemorrhagic
shear injury of the BG i:llI &
!halamus 81. Edema is also
present in the putamina &
frontal lobes. Swelling of the
right temporal cortical ribbon
~ was due to vascular
injury & MCA infarct (Right)
Axial T2WI MR shows t 51 in
the CP = & lef! > right
thalami 81 in a child with
I Nfl, representing myeNn

vacuolization.
6
82
BILATERAL BASAL GANGLIA LESIONS ,,-c:
CJl
III
~
Q.
...III
OJ
(LeFt) Axial FLAIR MR shows

~
fairly symmetric t 51 in the Ul
C
GP I:] & hemispheric WM in
a severely altered patient
...
"0
OJ
days after being found in a CD
:J
mobile home with a faulty
propane heater. Imaging
o::!.
OJ
typical of CO poisoning.
(Right) Axial PO F5f MR ...
aJ
OJ
shows "fluffy" irregular t 51
:J
without mass effect involving
lJ
bilateral caudate nuclei &
putamina. There was no J..
...
OJ
CD
:J
diffusion or enhancement in ()
::r
this IIIV+ patient with '<
cryptococcal meningitis & 3
OJ
gelatinous pseudocys15.

diffuse symmetrical t 51 in
putamina in a patient who
had rapid correction of
hyponatremia. Diffuse t 51
of the inner
cortex/subcortical WM is
also seen. (Righi) Axial OWl
MR shows asymmetrical J.
diffusion in the caudate
nuclei & putamina ED.
Anterior> posterior
putamina! abnormality is
typical of C/O. Note also
asymmetrical ~ diffusion in
the frontal & temporal lobe
cortical ribbon 1:].
(LeFt) Axial FLAIR MR shows

patchy t 51 in bilateral
caudate & putamina in a
young child with pyruvate
dehydrogenase complex
deficiency & an acute clinical
decompensation. These
lesions showed J. diffusion &
no post-gadolinium
enhancement. (Right)
Coronal FLAIR MR shows
fairly symmetric t 51 in the
putamina in this patient with
Wilson disease, a rare
autosomal recessive disorder
characterized by impaired
biliary excretion of copper.
I
6
83
co PUTAMEN lESION(S)
E>,
.r::
u
c • Profound acute HIE - deep gray matter,
~
OJ DIFFERENTIAL DIAGNOSIS
co posterior mesencephalon, hippocampi, &
a.. Common
c peri-Rolandic cortex injury
co
~ • Hypertensive Intracranial Hemorrhage
CD
o Hypotensive Cerebral Infarction
CO
• Hypoxic-Ischemic Encephalopathy • May be isolated to deep nuclei, BG
.'B" o HIE, Term • Bilateral, symmetric T2 hyperintensity
c o Hypotensive Cerebral Infarction • DWI bright in acute setting!
OJ
<Ii~
Q.
less Common Helpful Clues for less Common Diagnoses
:J
en • Methanol Toxicity • Methanol Toxicity
c • Osmotic Demyelination Syndrome o Putaminal necrosis, ± hemorrhage
III
~ • Leigh Syndrome o Symmetric T2 hyperintense lesions
CD
"tl Rare but Important o Often subcortical WM lesions
c
co • Creutzfeldt-]akob Disease (C]D) • Osmotic Demyelination Syndrome
• Huntington Disease o Extrapontine myelinolysis results in T2
• Parkinson Disease hyperintensity in putamen & caudate
• Multiple System Atrophy • Leigh Syndrome
o Symmetric T2 hyperintense lesions with
onset in infancy/early childhood
ESSENTIAL INFORMATION o Lesions primarily in brains tern, BG & WM;
Helpful Clues for Common Diagnoses putamen> GP
• Hypertensive Intracranial Hemorrhage Helpful Clues for Rare Diagnoses
o Related to systemic hypertension • Creutzfeldt-]akob Disease (CJD)
o Putamen most common (60-65%) o Progressive T2 hyperintensity of BG,
o Look for underlying lesion if no thalamus, & cerebral cortex
hypertension! o Putamen & caudate> GP
• Hypoxic-Ischemic Encephalopathy • Huntington Disease
o Includes anoxia, hypoxia, near drowning, o Caudate atrophy, t T2 caudate/putamen
& cerebral hypoperfusion injury • Parkinson Disease
o T1 & T2 hyperintense basal ganglia (BG) & o Hypointensity of putamen (iron)
cortical lesions; may affect only putamen o ± T2 hyperintense foci in putamen & GP
o HIE, Term • Multiple System Atrophy
• Acquired, usually cerebral hypoperfusion o Posterior putaminal atrophy ± T2
hyperintensity or hypointensity (iron)
I
6 Axial NECT shows a large hemorrhage in the putamen
with extension laterally into adjacent while matter. If
Axial NEeT shows hypodensily in the putamen ~
bilaterally related to infarcts in this 2 month old who
there is no hyperlension hislory, an underlying lesion had a near drowning even/. This type of I liE often
should be considered. a(feelSthe deep gray nuclei.
84
(Jl
PUTAMEN lESION(S)
'"
c:
Ql
::l
0-
..,
OJ
Ql
::l
hyperintensity within the en
c
putamen !:ll & lateral ..,Ql
thalami = related to
profound asphyxia in this
"0
CD
::l
newborn. Several patterns of
HIE may occur related to
o..,
infant development, severity
w"
& duration of insult. ..,
OJ
Ql
Involvement of BG &
::l
thalamus is typically seen -0
with profound insult. (RighI) ..,
Ql
Axial NECT shows mixed CD

:J
density lesions in the BG. ()
::;,-
Note gross & petechial '<
3
=-
hemorrhage in the putamen
typical of acute
methanol toxicity.
Ql
Osmotic Demyelination Syndrome

extrapontine myelinolysis
([PM) with symmetric
putamen = & caudate
heads bilaterally. EPM may
occur with or without
pontine involvement. (Right)
Axial T2WI MR shows
symmetric hyperintensity in
the putamen ~ with
associated edema related to
acute Leigh syndrome.
Hyperintensity was also
noted in the periaqueductal
gray, which is sensitive for
diagnosis of Leigh syndrome.
Creutzfeldt-Jakob Disease (CJD) Huntington Disease

symmetric hyperintensity
within the putamen SI &
pulvinar of the thalamus !:ll
in this patiellt with C/O.
Involvement of the caudate
heads is also typical. FLAIR &
OWl are the most sensitive
MR sequences for this
diagnosis. (Right) Axial PO
FSE MR shows volume loss
of the caudate heads SI.
Note symmetric
heads & putamen =-

hyperintensity in the caudate
of juvenile HUnlingtof1
typical
disease.
I
6
85
co GLOBUS PALLIDUS LESION(S)
E
>,
.I::
()
C
DIFFERENTIAL DIAGNOSIS o Involvement of BG & thalamus typically
~
Q)
co seen with profound insult

D..
c Common o Tl & T2 hyperintensity in BG & thalamus
co
~ • Hypoxic-Ischemic Encephalopathy, NOS o Ventrolateral thalamus typically involved
aJ
ro • HIE, Neonate • CO Poisoning
·C
o • CO Poisoning o Bilateral, symmetric GP T2 hyperintensity
C • Neurofibromatosis Type 1 o May also involve putamen, thalamus,
Q)
ro~ Less Common white matter (WM)

Q.
:J
(/) • Drug Abuse o If hemorrhagic necrosis, Tl hyperintense
C • Hyperalimentation o Chronic: T2 hyperintensity in centrum

III
~ • Hepatic Encephalopathy semiovale, internal/external capsules, &
In corpus callosum often seen
"0 • Leigh Syndrome
c • Cyanide Poisoning • Neurofibromatosis Type 1
III
• Kernicterus o Focal areas of increased signal intensity

:J
-"(/) • Hypothyroidism (FASI)characteristic
• Fahr Disease o FASI:T2 hyperintensities within deep
nuclei, most commonly affecting GP
Rare but Important o May be present within brainstem
• eurodegeneration with Brain Iron o FASIare transient & rarely enhance
Accumulation (NBIA)
• Hallervorden-Spatz Syndrome Helpful Clues for Less Common Diagnoses
• Maple Syrup Urine Disease • Drug Abuse
• Methylmalonic Acidemia o Methylenedioxymethamphetamine (a.k.a.
• Wilson Disease MDMA, "Ecstasy") causes bilateral GP
ischemia from prolonged vasospasm
o Heroin: GP ischemia &/or toxic
ESSENTIAL INFORMATION leukoencephalopathy, hypoxic brain
Key Differential Diagnosis Issues injury
• Globus pallidus (GP) are paired deep nuclei o MDMA & heroin: T2 hyperintense GP
within the basal ganglia (BG) with lateral & o Heroin inhalation: Symmetric WM T2
medial segments hyperintensity
• Lentiform nucleus = putamen & GP • Hyperalimentation
• Corpus striatum = caudate, putamen, & GP o Abnormal manganese metabolism in
• Majority of GP lesions are symmetric patients undergoing parenteral feeding
indicating a toxic/metabolic process or o Tl hyperintensity in GP & substantia nigra
hypoxia (S ), related to manganese
• Lesions may be differentiated based on • Hepatic Encephalopathy
patient age or Tl/T2 signal abnormality o Tl hyperintensity in GP & SN
o History of liver disease
• Leigh Syndrome
• Hypoxic-Ischemic Encephalopathy, NOS o Symmetric T2 hyperintense lesions with
o Includes anoxia, hypoxia, near drowning,
onset in infancy/early childhood
& cerebral hypoperfusion injury o Lesions primarily in brainstem, BG & WM;
o Occurs in adult or child, pattern depends
putamen> GP
on severity of insult • Cyanide Poisoning
o Tl & T2 hyperintense BG & cortical
o Bilateral T2 hyperintense GP
lesions; may affect only GP o May involve cerebellar cortex
• HIE, Neonate o Causes hemorrhagic necrosis
o Acquired condition related to cerebral
• Kernicterus
hypoperfusion o Tl & T2 hyperintensity in GP in a neonate
I o Several patterns of injury related to infant
development, severity & duration of insult
o Acute: Tl & (subtle) T2 hyperintensity in
GP, hippocampi, SN
6
86
GLOBUS PALLIDUS LESION(S) CIl
7<'
c:
III
o Chronic: T2 hyperintensity in GP & o May affect thalamus, cerebral peduncles, :>
Co
dentate nucleus corticospinal tracts III
..,
o MRI changes may be reversible with • Methylmalonic Acidemia III
:>
exchange transfusion in some cases o Bilateral GP T2 hyperintensity, ±
(f)
• Hypothyroidism periventricular WM c
"0
..,
o T1 hyperintensity & T2 hypointensity in • Wilson Disease OJ
BG & SN related to calcification (Ca++) o Children: T1 hyperintensity in GP ro-
:J
~
o Diffuse WM T2 hyperintensity in o Children & adults: Symmetric T2 o
:::!.
OJ
Hashimoto thyroiditis hyperintensity or mixed intensity in
OJ
..,
• Fahr Disease putamina, GP, caudate, & thalami OJ
o Bilateral symmetric BG Ca++ on CT o Characteristic "face of the giant panda" :J
\J
o GP most common site sign at midbrain level & T2 hyperintense ..,
OJ
CD
o Putamen, caudate, thalami, cerebellum, WM tracts :J
o
cerebral WM may also be involved Alternative Differential Approaches
::T
'<
3
Helpful Clues for Rare Diagnoses • Tl hyperintense GP lesions: HIE, CO OJ
• Neurodegeneration with Brain Iron poisoning, hyperalimentation, hepatic

Accumulation (NBIA) encephalopathy, kernicterus (acute),
o Includes Hallervorden-Spatz, hypothyroidism, Wilson disease (child)
aceruloplasminemia, neuroferritinopathy • T2 hyperintense GP lesions: HIE, CO
o Progressive neurodegenerative disorder poisoning, NFl, drug abuse, Leigh
with extrapyramidal motor impairment & syndrome, cyanide poisoning, kernicterus
brain iron accumulation (chronic), PKA , MSUD, MMA, Wilson
o T2 hypointensity in GP & SN disease
• Hallervorden-Spatz Syndrome • GP lesions in a child: HIE, NFl, Leigh
o Preferred terms: Pantothenate syndrome, kernicterus, NBIA, PKAN,MSUD,
kinase-associated neurodegeneration MMA, Wilson disease
(PKAN)or NBIA-l • GP lesions in an adult: HIE, CO poisoning,
o "Eye of the tiger": Bilateral, symmetric GP t drug abuse, hyperalimentation, hepatic
T2 surrounded by hypointensity encephalopathy, cyanide poisoning,
o Symmetric T2 hyperintense SN hypothyroidism
• Maple Syrup Urine Disease
o T2 hyperintensity in cerebellar WM,
brainstem, GP
HIE, Neonate
I
Axial FLAIR MR shows hyperintensity in lhe GP
bilaterally E1 related to an acute hypoxic·ischemic
Axial T1WI MR shows brighl signal wilhin lhe Gp,
putamen, & latera/thalamus. Imaging pattern is typical
6
event. Imaging mimics CO fXJisoning or other drug for profound acute HIE, seen in an acute event such as
abuse. DWI is positive in the acute setting. uterine rupture or cord prolapse.
B7
GLOBUS PAlliDUS lESION(S)
CO Poisoning Neurofibromatosis Type 1

(Left) Axial FlAIR MR shows
heterogeneous
globus pallidus 81 bilaterally
related 10 CO poisoning. The
heterogeneity is likely related
to necrosis &/o( blood
produc15. (Right) Axial FlAIR
MR shows extensive Focal
c: areas of increased signal
IV
•... intensity (FASI) 81 in the GP
al
in this NFl patient GP is
"'C
c: most common location for
IV FASI. Enhancement of these
lesions is worrisome but does
nol always signal neoplastic
change.

shows hyperintense GP 81
related to heroin abuse in
this young adult, likely
related to ischemia. MOMA
would mimic this
appearance. (Right) Axial
T7 WI MR shows bilateral,
the BC, predominanlly in the
GP ~. This hyperintensity
resolved after therapy. The
patient's movement disorder
also resolved, showing that
both clinical & imaging
findings of hepalOcerebral
degeneration can be
reversible.

bilateral, symmetric
hyperintensilies in the
putamina & CP =.The
(;ndings are suggestive of
mitochondrial
encephalopathy. (Right)
Axial T2WI MR shows
symmetric hyperintensities in
the CP =
bilaterally in this
adult patient with a history of
cyanide poisoning history.
Differential considerations in
an adult would include CO
poisoning, drug abuse, &
hypoxia.
I
6
BB
(fl
GLOBUS PALLIDUS LESION(S)
"
c:
Q)
:l
Cl.
..,
lJl
Q)
Kernicterus
:l
hyperintensity in the GP
in this child with acute
= en
c:
.,
"D
kernicterus. There are many OJ
causes for elevation of CD
:l
bilirubin to toxic levels; the 8"
most common worldwide is :0.
OJ
erythroblastosis fetalis.
OJ
.,
OJ
shows hyperintensity in the
GP bilaterally
with treated
= in this child
:l
\J
OJ
.,
hyperbilirubinemia. MR C1l
:l
obtained at 6 month ()
::T
follow-up shows typical GP '<
hyperintensity of chronic 3
OJ
kernicterus.
Neurodegeneration with Brain Iron

Accumulation (NBIA)
(Left) Axial Tf WI MR shows
bilateral hyperinl€nsities in
the medial GP ~ in this
patient with hypothyroidism
related to prior
thyroidectomy. (Right) Axial
T2WI MR shows symmetric
hypointensity within the GP
81. The "eye of the tiger"
appearance is absent,
characteristic of NBIA
Although physiologic brain
iron accumulation in the GP
& SN may be identified in
young adults, the degree of
T2 hypointensily in this case
is abnormal.

classic "eye of the tiger"
appearance of PKAN.- Small,
=
symmetric hyperintense foci
in the anteromedial GP
on a background of
hypointensity r=.:l. This
appearance has a nearly 7.- I
correlation with the PKAN2
mutation, hence the new
designation of PKAN. (Right)
Axial T2WI MR shows
the GP = bilaterally in this
metlly/malonic acidemia
patient. Associated WM
hyperinlensily is variable. I
6
89
ro UNILATERALTHALAMIC LESION
E
>,
J::
II
C
~
Q)
DIFFERENTIAL DIAGNOSIS o Globus pallidus, white matter (WM),
ro
D-
thalami, hippocampi, brainstem
c Common o Bilateral> > unilateral
ro
~ • Lacunar Infarction
en o No enhancement!
ro
• Hypertensive Intracranial Hemorrhage
'C
o • Neurofibromatosis Type 1
C • Diffuse Astrocytoma, Low Grade
Q) Less Common o Nonenhancing T2 hyperintense mass
ro~ • Diffuse Astrocytoma, Low Grade
c. o May be bilateral
:J
en • Glioblastoma Multiforme • Glioblastoma Multiforme
C • Anaplastic Astrocytoma o Peripherally enhancing WM mass typical
Cll
• ADEM o May involve thalamus or BG
co"-
'tl Rare but Important • Anaplastic Astrocytoma
l::
Cll
• Multiple Sclerosis o T2 hyperintense mass ± enhancement
• Thrombosis, Deep Cerebral Venous • ADEM
• Germinoma o Muitifocal WM &/or BG lesions following
infection/vaccination
o Thalamic involvement common
ESSENTIAL INFORMATION o Typically bilateral, but asymmetric lesions
• Lacunar Infarction • Multiple Sclerosis
o Small, < 1.5 em T2 hyperintensity in o Periventricular WM, corpus callosum T2
thalamus or basal ganglia (BG) hyperintense lesions most common
o DWI restriction if acute o Rarely involves thalamus
o Related to ischemia of penetrating vessels • Thrombosis, Deep Cerebral Venous
• Hypertensive Intracranial Hemorrhage o Typically bilateral, related to internal
o BG > thalamus> pons/cerebellum> cerebral vein (ICV) thrombosis
hemisphere bleed in a hypertensive patient o T2 hyperintensity in thalamus
o 15-25% in thalamus o Hyperdense lCV on CT
o May enhance subacutely • Germinoma
o Intraventricular hemorrhage common o Enhancing mass in pineal or suprasellar
• Neurofibromatosis Type 1 region; 5-10% involve BG or thalamus
o Focal areas of signal intensity (FAS!)in
deep gray matter characteristic (60-85%)
Lacunar Infarction
I
6 Axial FlAIR MR shows a focal hyperintensity within the
thalamus =
related to an acute lacunar infarct. Note
Axial NEeT shows a hypertensive hemorrhage p:J with
associated intraventricular hemorrhage, a common
abnormal perivenlricular hyperintensity related to complication. The thalamus is the second most
chronic small vessel ischemia 81. common location for hypertensive hemorrhages.
90
UNILATERAL THALAMIC LESION en
t:
""
Dl
::l
Co
..,
llJ
Hypertensive Intracranial Hemorrhage Neurofibromatosis Type 1 Dl
(Left) Axial T2' eRE MR ::l
shows muttiFocal areas of (f)
C
"blooming" related to
-
"0
hemosiderin in this chronic OJ
hypertension patient. Note C1l
::J
large area in left thalamus ~
related to a prior
o
::!.
OJ
hypertensive hemorrhage.
(Right) Axial FLAIR MR ..,OJ
llJ
::J
abnormally increased signal
\J
..,
thalamus =
in the globus pallidus &
typical of NFl.
They are related focal areas
OJ
C1l
::J
()
::T
of signal intensity (FAS/), '<
which are most common in 3
OJ
the deep gray nuclei.
Diffuse Astrocytoma, Low Grade

a discrete basal ganglia &
thalamic hyperintense mass
with a distinct lack of
surrounding edema. 20% of
low grade astrocytomas
involve deep gray matter~
including the thalamus &
basal ganglia. (Right) Axial
T1 C+ MR shows an
enhancing right thalamic
mass, anaplastic astrocytoma
=. Although these usually
occur in white matter,
involvement of the deep gray
nuclei is not uncommon.
Thrombosis, Deep Cerebral Venous

large confluent regions of
hyperintense signal in the
white matter BI & thalami
=. ADEM predominantly
involves white matter.
Bilatera/ is more common
than unifateral disease.
shows bilateral thalamic
hyperintensity related to
internal vein thrombosis.
Bilateral disease is much
more common than
unilateral. Hemorrhage often
thrombosis
parenchymal.
=
accompanies venous
typically I
6
91
co BITHAlAMIC LESIONS
E,.,
.<:;
t.l
C
<ll DIFFERENTIAL DIAGNOSIS o Acute onset of symptoms, reduced
~
co diffusion
D-
c Common o Artery of Percheron infarct: Occlusion of a
co
~ • Arterial Ischemia common vascular trunk that arises from
CD
co • Venous Ischemia/Deep Venous Thrombosis one PI segment, supplies bilateral thalami
·C
o • ADEM o Infarction of midbrain often also present
C • Diffuse Astrocytoma/Gliomatosis Cerebri • Venous Ischemia/Deep Venous
<ll
ro~ less Common Thrombosis
c.
:J
• Hypoxic-Ischemic Encephalopathy, NOS o Usually thrombosis of vein of Galen,
(/)
C o HIE, Term Neonate straight sinus, bilateral internal cerebral

~
Cll
o Profound Hypoperfusion Injury, Adult veins
CD
• Acute Hypertensive Encephalopathy, PRES o Edema, swelling with venous ischemia
'tl
c • Lymphoma, Primary C S o Reduced diffusion, parenchymal
Cll
• Multiple Sclerosis hemorrhage with venous infarction

• Vasculitis o CTV or MRV useful to establish specific
• Wernicke Encephalopathy diagnosis

• Osmotic Demyelination Syndrome • ADEM
• Encephalitis/Encephalopathy o Often affects thalami bilaterally
o Viral (Multiple Agents) o May cause swelling, T2 hyperintensity,
o Acute Necrotizing Encephalopathy (ANE) variable enhancement
of Childhood o Usually associated with white matter (WM)
lesions elsewhere in brain, with T2 high
Rare but Important signal & variable gad enhancement
• Creutzfeldt-]akob Disease (CJD) • Diffuse Astrocytoma/Gliomatosis Cerebri
• Paraneoplastic Syndromes o Bithalamic infiltration by neoplastic cells
• Inborn Errors of Metabolism usually occurs with diffuse astrocytoma or
o Krabbe Disease
gliomatosis cerebri
o Wilson Disease
o GMI, GM with Gangliosidoses Helpful Clues for less Common Diagnoses
• Mitochondrial Disorders • Hypoxic-Ischemic Encephalopathy, NOS
• Solvent Inhalation, Toxic Ingestion o Commonly affects bilateral thalami when
• Fahr Disease profound

• Kernicterus • Diffuse thalamic injury in preterm
neonates
• Lateral thalamic injury in term neonates
ESSENTIAL INFORMATION o Thalamic injury in adults usually
Key Differential Diagnosis Issues accompanied by global severe injury to
• Reduced diffusion in bithalamic process: cortex, hippocampi, & basal ganglia
Artery of Percheron infarct; bilateral PCA • Acute Hypertensive Encephalopathy,
infarcts; encephalitis; HIE; vasculitis; PRES
metabolic disorder; mitochondrial disorder o Thalamic involvement typically occurs in
• Bithalamic lesions with hemorrhage: Deep patients who also have classic symmetrical
venous thrombosis; vasculitis; encephalitis parietooccipital T2 hyperintensity
• Symmetrical bithalamic lesions: Wernicke o Often bilateral, not necessarily
encephalopathy; osmotic myelinolysis; HIE; symmetrical
CJD; inborn errors of metabolism o T2 high signal, variable swelling; reduced
diffusion, gad enhancement atypical
Helpful Clues for Common Diagnoses • Vasculitis
• Arterial Ischemia o Patchy T2 high signal & reduced diffusion
o Often associated with vertebrobasilar
o CTA or MRA possibly abnormal; catheter
I disease, "top of the basilar" syndrome angio shows irregularity, narrowing
6
92
BITHALAMIC LESIONS en
'"
c:
o Primary angiitis of CNS vs. secondary o Diffusion usually reduced in C]D; no

(drug-induced, SL£, PAN, Wegener, etc.) enhancement
• Wernicke Encephalopathy • Paraneoplastic Syndromes
o T2 high signal in dorsal medial nucleus of o May cause symmetrical T2 hyperintensity
thalamus in posterior thalamus
o Enhancement usually absent; may show o May mimic prion disease, but. diffusion
variably reduced diffusion usually not seen
o Associated midbrain, mamillary body • Inborn Errors of Metabolism
abnormalities may be seen o Krabbe Disease
• Osmotic Demyelination Syndrome • Thalami typically dense on CT, have
o Extrapontine myelinolysis (EPM) often short T2 on MR
accompanied by central pontine o Wilson Disease
myelinolysis • T2 high signal in thalami may be seen
o EPM commonly affects thalamus; external • More commonly involves putamina &
capsule; putamen; caudate nucleus caudate nuclei
o Typically very symmetrical • Mitochondrial Disorders
• Encephalitis/Encephalopathy o Often symmetric reduced diffusion
o Many encephalitides may affect thalami: o Involvement of gray & white matter
EBV,Japanese encephalitis; West ile virus • Solvent Inhalation, Toxic Ingestion
o Acute necrotizing encephalopathy (ANE): o Toluene may cause thalamic hypointensity
Affects infants, children; thalamic due to iron deposition
involvement common Alternative Differential Approaches
• Controversial if viral etiology vs. more • Bithalamic process in a child: ADEM; HIE;
likely immune-mediated or metabolic diffuse astrocytoma; encephalitis; inborn
pathogenesis errors of metabolism; mitochondrial disease;
Helpful Clues for Rare Diagnoses toxin exposure; ANE
• Creutzfeldt-]akob Disease (C]D) • Bithalamic process in an adult: Deep venous
o May affect medial thalami & pulvinar, thrombosis; arterial infarction; astrocytoma;
giving so-called hockey stick appearance vasculitis; C]D; paraneoplastic syndrome
o Thalamic involvement initially suggested
to be typical of vC]D, but also described
with sC]D
Arterial Ischemia Arterial Ischemia
I
Axial OWl MR shows high 51 representing reduced
diffusion in the bilateral thalami I:j] & occipital lobes, as
Axial OWl MR shows bithalamic areas of • diffusion I:j]
in an elderly patient with confusion, R > L hemiparesis,
6
well as the corpus callosum splenium. MRA showed no & abnormal eye movements. LBrge vessels were normal,
flow in PCAs. Diagnosis was bilateral PCA infarction. and artery of Percheron inFarct was the diagnosis.
93
ro BITHALAMIC LESIONS
E
>,
-C
u
c
~
<ll
ro Venous Ischemia/Deep Venous
a.. Venous Ischemia/Deep Venous
c Thrombosis Thrombosis
ro
~ (Left) Axial NECT shows
co edema in bilateral thalami &
ro
.;:: right caudate with
o parenchymal &
C intraventricular hemorrhage
<ll
ro~ =. t Density in the internal
n. cerebral veins 81 & straight
:J
(f) sinus P.:i'l represent deep
venous thrombosis. (Right)
c Axial T2WI MR shows
C'O
"- bithalamic & corpus striatum
CO
edema, without hemorrhage.
=
"C
c Absent vein of Calen flow
C'O
void compared with
:J normal sagillal sinus flow
void 81. OWl was ~ in the
-"CJ)
thalami, related to venous
infarct (not shown).
Diffuse Astrocytoma/Gliomatosis
ADEM Cerebri
(Left) Coronal flAIR MR in a
child shows asymmetrical
hyperintensity in the thalami
=.1 as well as areas of t Sf
involving the subcortical
V-fibers 81. Patchy
enhancement was present,
but no ~ diffusion. LP: t
Protein & lymphocytes.
(Right) Axial T2WI MR in a
patient with cognitive
decline & left hemibody
paresthesia shows
asymmetrical enlargement &
T2 hyperintensity of the
thalami, right caudate, &
putamen in this patient
Anaplastic astrocytoma.
HIE, Term Neonate

severe swelling and
hyperintensity in the thalami
~ in a neonate who had
poor Apgar scores after a
complicated delivery.
Reduced diffusion was also
present. (Right) Axial OWl
MR shows ~ diffusion of the
thalami = as well as
diffusely in the cerebral
cortex in a patient who
suffered profound
hypotension after aortic
dissection & rupture. No
significant swelling or mass
effect is present at this lime.
I
6
94
BITHAlAMIC lESIONS en
,..
c:
Dl
::l
C.
Acute Hypertensive Encephalopathy, ...Dl
OJ
PRES
subcortical WM of the
& =
t 51 in the thalami
::l
(JJ
C
...
-0
parietaf lobes 81. No Ql
enhancement or + diffusion co::::>

was present. The patient was
a liver transplant recipient &
o...
iii'
had renal disease. (Right)
Axial FLAIR MR shows a ...
OJ
bithalamic mass
=with
Ql
::::>
II
edema. The lesion enhanced ...
Ql
intensely & homogeneously Ctl

::::>
post-gadolinium and showed o
or
mildly reduced diffusion '<
centrally on the basis of high 3
Ql
cellularity.

symmetrical t 51 in the
medial thalami bilaterally
without ! diffusion or
=
enhancement.
Periaqueductal gray matter
also showed t 51. The
patient was on TPN &
responded rapidly to
thiamine. (RighI) Axial OWl
MR shows! diffusion in the
thalami = in a /I hockey
stick" pallern in a patient
with rapidly progressive
dementia. Note! diffusion
in the caudate nuclei &
putamina, as well as right
temporal cortical ribbon E:I.
Paraneoplastic Syndromes Krabbe Disease

fairly symmetrical t 51 in the
thalami, caudate nuclei, &
frontal WM in a patient with
rapidly progressive dementia
& a movement disorder. No
! diffusion was present.
Work-up eventually led to a
diagnosis of non-small cell
lung carcinoma & a
paraneopJaslic syndrome
that improved after
treatment of the tumor.
thalami =
shows symmetrical .1- 51 in B
in a patient with
Krabbe disease. The thalami
were dense on N[eT. I
6
95
ro "PULVINAR SIGN"
E
:>,
.s::
u
c
DIFFERENTIAL DIAGNOSIS • Creutzfeldt-]akob Disease, Variant (vC]D)
~
ro o Bilateral T2 pulvinar hyperintensity
a.. Common
c o ± , T2 dorsomedial thalami,
ro
~ • Creutzfeldt-]akob Disease (C]D) periaqueductal gray, caudate nuclei
OJ
• Creutzfeldt-]akob Disease, Variant (vC]D)
ro
·C Helpful Clues for Less Common Diagnoses
o Less Common • Fabry Disease
CQ)
• Fabry Disease o Multisystem X-linked disorder with renal
ro~ • Thalamic Infarct (Mimic)
c. & cardiac dysfunction and stroke
:J
(fJ • Neoplasms (Mimic) o T1 hyperintensity in bilateral pulvinar
C • ADEM (Mimic) o CT may show mineralization in pulvinar
~
'" Rare but Important o May see ischemia, white matter (WM)
OJ
"0 • Periventricular Leukomalacia lesions, & vertebrobasilar dolichoectasia
C
• Status Epilepticus • Thalamic Infarct (Mimic)
':J" o Artery of Percheron infarct & internal vein
-"en thrombosis: Bilateral T2 hyperintensity
ESSENTIAL INFORMATION o HIE may affect only deep gray nuclei
Key Differential Diagnosis Issues o DWI bright in acute setting
• "Pulvinar sign": T2 hyperintensity in • Neoplasms (Mimic)
bilateral pulvinar, most sensitive for vC]D o Lymphoma or astrocytoma may cause
• T1 hyperintensity in pulvinar also called bilateral thalamic T2 hyperintensity
"pulvinar sign" (Fabry disease) • ADEM (Mimic)
o T2 hyperintensity in bilateral thalami
Helpful Clues for Common Diagnoses o WM lesions typically also present
• Creutzfeldt-]akob Disease (C]D)
o Rapidly progressive, fatal Helpful Clues for Rare Diagnoses
neurodegenerative disease • Periventricular Leukomalacia
o Prion protein accumulates in neurons o Pulvinar hyperintensity may be seen in
o 85% of cases sporadic; 15% genetic or association with PVL
familial o Thalamic involvement suggests more
o Infectious/iatrogenic cases, including severe motor & mental disabilities
vC]D, < 1% • Status Epilepticus
o , T2 in basal ganglia (BG), thalamus, o Peri-ictal T2 hyperintensity, DWI
cortex restriction in bilateral pulvinar, often with
o FLAIR& DWI MR most sensitive hippocampal & cortex involvement
I
6 Axial FU\/R
involving the pulvinar=-
MR shows abnormal hyperintensity
medial thalami, putamen = Axial FU\/R MR shows bilateral hyperintensities = in
the posterior UJa/ami, "pulvinar sign" of vCID. FU\IR &
& caudate, characterisUc for C/D. Thalamic involvement OWl MR are most sensiUve for diagnosis. vCIO is
is less commonly seen than in velD. primarily seen in the United Kingdom.
96
"PULVINAR SIGN" ,..c:
CIl
III
='c.
Creutzfeldt-jakob Disease, Variant ..,
OJ
(vCjD) III
(Left) Axial OWl MR shows ='

(JJ
symmetric OWl restriction in
C
the pulvinar bilaterally EE ..,
"0
characteristic for velD. vClO OJ
is caused by ingestion of ro::0
beef produc15 infected with 8"
bovine spongiform
encephalopathy. It is rare,
"'.
OJ
making up < 1% of all Clo

cases. (Right) Axial TI WI MR
shows symmetric
=-
hyperintensity in the pulvinar
the "pulvinar sign" of
Fabry disease.
Hyperintensity is also noted
in the basal ganglia.

hyperinlensily in the medial
thalami =- classic location
for major penetrating artery
of Percheron stroke. Some
patients have a dominant
large posterior perforating
artery instead of multiple
smaller ones. When these
arteries are occluded,
devastating midbrain &
thalamic infarcts may occur.
OWl is positive in the acute
selling. (Right) Axial T2WI
MR shows asymmetric
bithalamic hyperintensity
H2. Astrocytoma was found
at biopsy.
ADEM (Mimic) Periventricular leukomalacia

symmetric hyperinlensity in
the pulvinar 1:]. Note
involvement of the occipital
subcortical white matter E:I.
ADEM involves the deep
gray structures more often
than other demyelinating
processes. 1l is typically
bilateral but asymmetric.
shows hyperintensity in the
pulvinar I:] of the thalamus
bilaterally in this patient with
spastic quadriparesis & PVL.
Note wavy ventricular
margins, typical of PVL. I
6
97
ro TECTAl (QUADRIGEMINAL PLATE) lESION
E
>,
.r:
u
c
Q)
~ DIFFERENTIAL DIAGNOSIS Helpful Clues for less Common Diagnoses
ro
a.. Common • Lipoma
c
~ • Diffuse Astrocytoma, Low Grade
III
• Brainstem Glioma, Pediatric with fat attenuation/intensity
ro o Interhemispheric fissure most common
·C
o less Common
C location (30-40%)
Q)
• Lipoma o 20-25% pineal region (attached to tectum)
ro~ • Neurofibromatosis Type 1
Cl.
:J
CI) • Chiari 2 o Focal areas of signal intensity (FASI) in
C
Rare but Important white matter & deep gray matter
~
tn'" • Cavernous Malformation • Typically involve globus pallidus
"'C • Progressive Supranuclear Palsy • May involve brainstem
c
o Tectal gliomas are associated with Nfl
':J"
• Chiari 2
""CI) ESSENTIAL INFORMATION o Complex malformation of hindbrain
Key Differential Diagnosis Issues associated with neural tube closure defect,
• Tectum is dorsal portion of midbrain, dorsal usually lumbar myelomeningocele
to cerebral aqueduct o Small posterior fossa, "beaked" tectum
• Tectum includes superior & inferior colliculi o "Towering" cerebellum protrudes up
& periaqueductal gray matter through incisura, compresses tectum
• Diffuse Astrocytoma, Low Grade • Cavernous Malformation
o Nonenhancing T2 hyperintense mass o Heterogeneous "popcorn" mass with T2
o Supratentorial 2/3, infratentoriall/3 hypointense rim (hemosiderin)
o 50% of "brainstem gliomas" are diffuse o Brainstem lesions common when multiple
astrocytomas • Progressive Supranuclear Palsy
• Brainstem Glioma, Pediatric o Midbrain, superior colliculi, & superior
o Heterogeneous group of gliomas cerebellar peduncle atrophy
o Tectal glioma: Most indolent, often only o T2 hyperintensity in periaqueductal gray
need CSF diversion o Midbrain atrophy described as "penguin" &
• Expands tectum & obstructs aqueduct "hummingbird" sign on sagittal MR
• T2 hyperintense mass ± enhancement o "Morning glory sign": Concave lateral
tegmentum on axial images
I
6 Sagittal T2WI MR shows a hyperintense mass involving
the tectal plate along the posterior 3rd ventricle ~ in
Axial T2WI MR shows a hyperintense mass involving
the tectal plate =_
Lesions in this location often cause
this young adult. Sagittal imaging is helpful 10 define obstruction of the cerebral aqueduct, requiring
lesions in this location. shunting.
98
TECTAL (QUADRIGEMINAL PLATE) LESION
Ql
::::l
Co
...
OJ
Ql
(Left) Sagittal TI WI MR ::::l

shows a homogeneous mass en
c
colliculus =-
arising from the superior
a tectal
glioma. Tectal gliomas are
..•tlJ
u
CO
::J
the most benign of the
brainstem gliomas. They
o::l.
tlJ
often have an indolent
course & usually only require ..•tlJ
OJ
CSF diversion. They are most
::::l
often pilocytic astrocytomas.
\J
(Right) Sagittal T1WI MR .,
tlJ
shows a hyperintense mass CD
::::l
=-
along the inferior collicu/us
typical location for a
collicular lipoma. Fat
()
::T
'<
3
tlJ
suppression confirms the
diagnosis.
Neurofibromatosis Type 1 Chiari 2

multiple foci of abnormally
increased signal (FASt) in the
brainslem = & cerebellum,
typical of neurofibromatosis
type 7. FASI are most
common in the globus
pallidus but may also be
seen in the brainstem.
shows a beaked tectum E!ll
characteristic of Chiar; 2.
Note the smaJl posterior
fossa with caudal
displacement of brainstem &
4th ventricle IJ:.:l as well as
the cerebellar nodulus.
a hemorrhagic midbrain
cavernous malformation =
with low signal blood
products & surrounding
edema related LO a recent
hemorrhage. Blood products
of varying ages result in a
II popcorn II or "mulberry"
appearance. (Right) Sagittal

T2WI MR shows a severely
atrophic tectal plate in
this patient with PSP.PSP is
characterized by midbrain &
superior colficufus atrophy.
Parkinsonian-like symptoms
are common in PSP.
I
6
99
III MIDBRAIN lESION
E
>-
.r:
()
c
DIFFERENTIAL DIAGNOSIS o Often accompanied by lesion of basilar
~
Ql
III artery, so consider MRA or CTA
Cl..
C
Common • Trauma (Diffuse Axonal Injury,
~
III • Cerebral Ischemia-Infarction, Acute Contusion)
CO
III
• Trauma (Diffuse Axonal Injury, Contusion) o Appropriate clinical history; FLAIR,DWI
'C
o • Demyelinating Disease (MS, ADEM) particularly helpful to assess for edema
C • Metastasis (cytotoxic &/or vasogenic); GRE to assess
Ql
CO
~ • Cavernous Malformation for hemorrhage
0.
:J • Enlarged Perivascular Spaces o Brainstem DAI typically dorsolateral,
(/)
• Wallerian Degeneration usually seen with hemispheric & callosal
C
III
less Common involvement; check for additional sites of
"-
CO
• Aqueductal Stenosis injury
"C
III • Brainstem Tumor • Demyelinating Disease (MS, ADEM)
o Tectal Glioma o T2 bright lesions typically without reduced
:J
-"
(/) o Low Grade Neoplasm diffusion or GRE abnormality, often
• JPA, Diffuse Fibrillary Astrocytoma enhance post-gadolinium
o High Grade Neoplasm o Assess rest of brain for additional white
• Anaplastic Astrocytoma, GBM, PNET matter (WM) lesions
• Wernicke Encephalopathy o Consider MR of optic nerves, spinal cord
• Mitochondrial Cytopathy • Metastasis
o Typically enhance, associated with
Rare but Important vasogenic edema; additional lesions often
• Infection present in brain, meninges, or bone
o Progressive Multifocal
o May be hemorrhagic
Leukoencephalopathy (PML) • Cavernous Malformation
o Abscess, Encephalitis
o Often bright on T1 & T2WI;
• Vasculitis "mulberry-like" morphology; >SI on GRE
• Intracranial Hypotension o Associated developmental venous anomaly
• Progressive Supranuclear Palsy (PSP) (DVA)may be present
• Parkinson Disease • Enlarged Perivascular Spaces
• Amyotrophic Lateral Sclerosis (ALS) o Usually seen at base of cerebral peduncles
• Drug Toxicity o Follow CSF on all MR seq uences
• Wallerian Degeneration
ESSENTIAL INFORMATION o Acute: Variable> diffusion and t SI on T2
o Chronic: Volume loss; variable T2 SI
• Most common midbrain lesions are Helpful Clues for less Common Diagnoses
ischemic, traumatic, demyelinating, • AqueductaI Stenosis
vascular, or neoplastic o Cause of "congenital" hydrocephalus: May
• Hemorrhage usually due to trauma, vascular be due to a web or adhesion; often
malformation, or hemorrhagic metastasis; post-infJammatory or post-intraventricular
hypertensive hemorrhage rare in midbrain hemorrhage
o Assess tectum carefully on axial T2 &
Helpful Clues for Common Diagnoses FLAIRto exclude subtle nonenhancing
• Cerebral Ischemia-Infarction, Acute tectal glioma
o Acute onset of clinical symptoms, often
• Brainstem Tumor
hemiparesis (corticospinal tracts), cranial o Multiple histologies can affect midbrain &
neuropathy (nuclei of III, IV; a nucleus of other parts of brainstem
V), &/or ataxia (red nucleus) o Imaging varies with tumor histology
o Presence of reduced diffusion: High SI on
o "Tectal gliomas": Typically confined to
I DWI, low SI on ADC map tectum, nonenhancing, present with
chronic hydrocephalus
6
100
MIDBRAIN LESION en
,..
c:
• Generally better prognosis then other o Pyogenic abscess: Central. diffusion; also
brainstem tumors; associated with NFl ring enhancement, vasogenic edema
• Wernicke Encephalopathy • Vasculitis
o Thiamine deficiency; most commonly seen o Nonspecific t SI on T2WI; often I diffusion
in alcoholics; also malnutrition, • Intracranial Hypotension
malabsorption, HIV/AIDS o Downward displacement of midbrain, loss
o Classic clinical triad: Ataxia, of cisterns; "folding" if severe
encephalopathy, oculomotor dysfunction • Progressive Supranuclear Palsy (PSP)
o Symmetrical t T2 SI variably involves o Atypical Parkinsonian syndrome:
periaqueductal gray matter, dorsomedial Supranuclear ophthalmoplegia,
thalami, mamillary bodies pseudobulbar palsy, dysarthria, postural
o • Diffusion, post-gad enhancement instability, frontotemporal dementia
variably present acutely o Neuropathological hallmark: Midbrain
• Mitochondrial Cytopathy atrophy; tau + aggregates
o Typically affects deep gray nuclei of o MR: Midbrain atrophy; variable midbrain
cerebrum &/or gray matter structures of T2 hyperintensity
brainstem in symmetrical fashion • Parkinson Disease
o • Diffusion, t T2 SI typically present with a Imaging findings typically subtle; possible
acute flare of disease • volume of substantia nigra, •
o t Lactate peak may be seen with MR hypointensity of lateral margin of
spectroscopy substantia nigra
Helpful Clues for Rare Diagnoses • Amyotropic Lateral Sclerosis (ALS)
o Degenerative disease of upper and lower
• Infection
o Progressive multifocal
motor neurons in the motor cortex,
brainstem, and spinal cord
leukoencephalopathy (PML)
o Imaging hallmark: t T2 SI of corticospinal
• Usually severely immunocompromised
tracts; no mass effect, enhancement
patients (AIDS, organ transplant,
chemotherapy) • Drug Toxicity
o Notably metronidazole; symmetrical t T2
• Classic: WM lesions without
SI, variable. diffusion
enhancement or mass effect
o Dentate nuclei usually involved
• May cause pattern of "small dots" in WM
or brainstem that eventually coalesce
into more typical geographic lesions
Trauma (Diffuse Axonal Injury,

Cerebral Ischemia-I nfarction, Acute Contusion)
I
Axial OWl MR in a 71 year old shows high signal
intensity representing reduced diffusion in the midbrain
Axial NEG shows a shear hemorrhage I:!lI in the right
dorsolateral midbrain. This paUent with severe head
6
1GB This lesion sharply respects midline An AOC trauma has evidence of scalp injury 8J and
map confirmed lrue reduced diffusion. post-traumatic SAIl ffi among other injuries. 101
<tl MIDBRAIN lESION
E
>.
.<=
u
c:
~
Q)
<tl
CL
c:
en a focal lesion in the right
<tl
'C:
o
midbrain =-consistent with
an MS plaque. This lesion
C enhanced & was
Q)
"§ symplOmaticallyacute.
n. Periventricular white maller
:::J
Cf) lesions ~ are also present in
this young woman with MS.
s:: (Right) Axial NEeT shows a
•..
Ol
aJ
focal hemorrhage in the right
midbrain with surrounding
-0
s:: edema Additional
Ol hemorrhagic lesions are
present in the temporal lobe
~ This patient had
metastatic melanoma.

a well-circumscribed lesion
1::1 with a hemosiderin rim &
heterogeneous internal signal
due 10 blood products. The
trunk of a large associated
OVA that drains brainslem
and cerebellum Ii8 is also
seen. (Right) Axial f2WI MR
shows bilateral linear T2
bright structures at the base
of the cerebral peduncles
bilaterally =. These
followed CST on all
sequences. Small
perivascular or
V;rchow-Robin spaces are
common in this location.

a hyperintense & mildly
atrophic left cerebral
peduncle =. This patient
had a prior left MCA stroke,
& left temporal atrophy is
present. (Right) Sagittal
T2WI MR shows a
funnel-shaped aqueduct of
Sylvius
ventricle =
normal 4th
thinned &
stretched corpus callosum
Sl & downward
displacement of the floor of
the 3rd ventricle ~ The
aqueduclalobstruction is
due to a web or adhesion,
I and no mass is present.
6
102
MIDBRAIN lESION en
""r::
III
::::l
c..
..•
lIJ
III
Tectal Glioma
::::l
shows a high signal inlensily en
r::
mass ~ confined 10 lhe
tectum, causing severe
..•
l:J
OJ
obslructive hydrocephalus. CD
::J
There was no associated
enhancement or surrounding
o..•
OJ
edema. (Rig"') Axial T2WI
MR shows an expansile mass ..•OJ
OJ
of lhe midbrain =:I lhat
::J
exlends well beyond lhe -U
tectum. There is no
associated edema.
..•
OJ
(t)
::J
Surprisingly, no ()
::r
hydrocephalus is present. '<
The mass enhanced intensely 3
OJ
& homogeneously. Palhology
confirmed IPA.

an expansile lesion involving
the dorsal midbrain =:I. The
lesion has an ill-defined
interface with normal
midbrain. Severe obstructive
hydrocephalus is presenl 81
wilh lransependymal flow of
CSF~. (Rig"') Axial FLAIR
MR shows symmetrical t 51
of the dorsal midbrain &
periaqueductal gray matter
=:I as well as t Sloflhe
mamillary bodies 81. This
patient was severely
malnourished & responded
to thiamine treatment.

symmetrical t 51of the
dorsal midbrain &
periaqueductaf gray matter
=:I in a 2 year old. The
lesion demonstrated!
diffusion & no enhancement.
Additional symmetrical
lesions were present in the
putamina. (Right) Axial
FLAIR MR shows patchy t
T2 51in righl midbrain &
cerebral peduncle,
associated with mild volume
loss. Addilional multifocal
peripheral/subcortical
lesions are present in the
righltemporallobe.
WM
I
6
103
SECTION 7
Large Brainstem 1-7-2
Small Brainstem 1-7-4
Pontine Lesion 1-7-6
Medulla Lesion 1-7-10
Infratentorial Midline Cyst 1-7-14
Cerebellar Atrophy 1-7-18
Cerebellar Mass 1-7-22
Vermis Mass 1-7-28
Low Cerebellar Tonsils 1-7-32

"Cystic-Appearing" Posterior Fossa Lesion 1-7-34

Posterior Fossa Neoplasm, Adult 1-7-40
Posterior Fossa Neoplasm, Pediatric 1-7-44
ro LARGE BRAINSTEM
E
>-
.<::
<.l
c • Osmotic Demyelination Syndrome
Q)
ro o Typically involves central pons
a.. Common
c 01'2 hyperintense, ± enhancement, DWI
ro
~ • Brainstem Glioma
CD
• Cerebral Ischemia-Infarction, Acute
ro
• Hypertensive Intracranial Hemorrhage o "Top of the basilar": Midbrain & thalamic
'C
o Less Common infarcts ± temporal & occipital lobes
C o May have midbrain, pons, or medulla
Q)
ro~
.•... • Osmotic Demyelination Syndrome ischemia related to vertebrobasilar
c
• Cerebral Ischemia-Infarction, Acute perforator or cerebellar artery disease
c: 01'2 hyperintense edema, DWI bright
<Il • Demyelination
~ • Demyelination
OJ • Encephalitis
-0
• Cavernous Malformation o Includes multiple sclerosis & ADEM
c:
<Il o Brainstem enlargement with acute lesions
Rare but Important o Focal 1'2 hyperintensity ± enhancement
• Metastases, Parenchymal • Encephalitis
• Syringobulbia 01'2 hyperintensity & enhancement typical
• Hypertrophic Olivary Degeneration o Etiologies include Listeria monocytogenes,
• Hemangioblastoma enterovirus, West Nile virus, herpes, EBV,
adenovirus, Japanese encephalitis
ESSENTIAL INFORMATION • Cavernous Malformation
o Heterogeneously bright on 1'1 & 1'2
Helpful Clues for Common Diagnoses o Hemosiderin rim classic
• Brainstem Glioma
o Pontine> medulla> mesencephalic glioma Helpful Clues for Rare Diagnoses
o Enlarged, 1'2 hyperintense mass • Metastases, Parenchymal
• Hypertensive Intracranial Hemorrhage o Enhancing mass with edema
o Pons hemorrhage in a hypertensive patient o Multiple lesions common
o Basal ganglia> thalamus> pons • Syringobulbia
o Extension of cervical syrinx into brainstem
• Hypertrophic Olivary Degeneration
• Intracranial Hypotension o Unilateral or bilateral 1'2 hyperintensity &
o Downward displacement of brain through
enlargement of medullary olives
incisura ("slumping" midbrain) • Hemangioblastoma
• "Fat pons" can mimic neoplasm! o Nodular enhancement ± cyst
o ± Dural enhancement, SDH
Brainstem Glioma Hypertensive Intracranial Hemorrhage
I
7 Axial T2WI FS MR shows expansion and hyperintensity
of the pons by a diffusely infiltraUng glioma. Note that
Axial NEeT
the pons
shows a hypertensive hemorrhage within
=.=.
Note that ale blood has dissected into the
the pons engulfs the basilar artery 1:;'.1 typical of these 4th ventricle Extension of blood into the venlJicular
tumors. system is common.
2
LARGE BRAINSTEM en
c"
:
III
:l
Co
Intracranial Hypotension Osmotic Demyelination Syndrome

..•
OJ
III
(Lefl) Sagillal T7 c+ MR :l
shows classic intracranial ::J
hypotension with a ..•tll
....••
"slumping midbrain" ffi CO
dural engorgement, & ::J
downward tonsillar o::!.
displacement. Signal in the tll
brainstem is normal, which OJ
helps differentiate this from iil
other etiologies. (RighI) Axial ::J
T2WI MR shows high signal \J
in the centra! pons with
..•
tll
C1l
peripheral sparing. ::J
()
Preservation of the :::r
corticospinal tracts may
'<
3
result in a classic trident tll
configuration. OWl is often
positive acutely.
Cerebral Ischemia-Infarction, Acute Demyelination

acute pontine ischemia
related to occluded pontine
perforating arteries off the
basilar artery. There is mild
swelling & subtle high signal
= in the pons. Brainstem
ischemia often respects
midline. OWl is positive
acutely. (RighI) Axial T2WI
MR shows a large multiple
sclerosis plaque in the pons
BI & cerebellum 1::1.
Brainstem lesions are
commonly seen in addition
to supratentorialles;o17s. The
middle cerebellar peduncle
is often involved.
hemorrhage in the pons
secondary to a pontine
cavernoma. Even in a
hypertensive patient,
follow-up imaging to exclude
an underlying vascular lesion
is helpful. (RighI) Axial T2WI
MR shows bilateral inferior
olivary nuclei hyperintensity
& hypertrophy ffi following
radiotherapy to a midbrain
AVM. This rare degeneration
results from an insulllO the
dcntato-rubro-olivary
pathway. The causative
lesion is often in the pons or
midbrain. I
7
3
<1l SMALL BRAINSTEM
E
>-
£
<..l
C
<ll
~ DIFFERENTIAL DIAGNOSIS Helpful Clues for less Common Diagnoses
<1l
0..
Common • Multiple Sclerosis, Chronic
c o Brainstem atrophy ± T2 hyperintensity
~
<1l • Cerebral Infarction, Chronic
co
• Wallerian Degeneration • Multiple System Atrophy
<1l
·C o Includes olivopontocerebellar atrophy,
o less Common striatonigral degeneration, & Shy-Drager
C
<ll • Multiple Sclerosis, Chronic o MR features overlap
ro~
.•... • Multiple System Atrophy • Brainstem & cerebellar atrophy
c
o Olivo pontocerebellar Degeneration • Pons, middle cerebellar peduncle r T2
C
nl o Striatonigral Degeneration • Putamen: T2 hypointensity
"-
CO
Rare but Important o MSA-C: Cerebellar signs predominate
"0
c • Friedreich Ataxia (Spinocerebellar Ataxia) o MSA-P: Parkinsonism predominates
nl
• Progressive Supranuclear Palsy o Olivopontocerebellar Degeneration
• Congenital • Pons T2 cruciform hyperintensity
o Prematurity-Related Atrophy • Pons, olives, & cerebellar vermis atrophy
o Congenital Muscular Dystrophy o Striatonigral Degeneration
o Pontocerebellar Hypoplasias • • T2 signal in putamen & midbrain
ESSENTIAL INFORMATION • Friedreich Ataxia (Spinocerebellar Ataxia)
o Severe atrophy of spinal cord (posterior)
Helpful Clues for Common Diagnoses o Mild atrophy of medulla & vermis
• Cerebral Infarction, Chronic • Progressive Supranuclear Palsy
o May be lacunar, territorial, related to small o Midbrain, collicular & superior cerebellar
vessel disease, or hypertensive hemorrhage peduncle atrophy
o Brainstem supplied primarily by cerebellar o T2 hyperintensity in periaqueductal gray
arteries & vertebrobasilar perforators o Midbrain atrophy described as "penguin",
o Brainstem T2 hyperintensity & atrophy "hummingbird", & "morning glory sign"
• Wallerian Degeneration • Prematurity-Related Atrophy
o Chronic infarct along corticospinal tract o Cerebellar> brainstem atrophy
leads to volume loss of cerebral peduncle, • Congenital Muscular Dystrophy
ventral pons, & medullary pyramid o Kinked or notched brain stem
o Typically T2 hyperintense • Pontocerebellar Hypoplasias
o Cerebellar & brainstem hypoplasia
Cerebral Infarction, Chronic Wallerian Degeneration
I
7 Axial T2WI MR shows multiple hyperintensilies within
the pons related to chronic small vessel ischemia. Note
Axial T2WI MR shows hyperintensity 8, atrophy of the
cerebral peduncle ~ related to wallerian degeneration
the prominent 4th ventricle related to the brainslem secondary to a large remote right MCA distribution
atrophy. infarct.
4
SMAll BRAINSTEM
III
:::l
Co
..•
OJ
Multiple Sclerosis,Chronic III
(Le(t) Axial FLAIR MR shows :::l
mulli{ocal hyperinlensilies in
the brainslem &. subcortical
while maller. Note
associated atrophy o( the
brainstem related to chronic
MS in this young patient.
(Right) SagiLtal T1WI MR
shows a small pons &
cerebellar vermian atrophy
in this patient with cerebellar
signs & clinical diagnosis o(
MSA-C. Imaging (in dings
overfap between MSA
subtypes. Brainstem &
cerebellar atrophy with
sparing o( the cerebral
hemispheres is typical.
Olivo pontocerebellar Degeneration Olivopontocerebellar Degeneration

(Left) SagiLtal T1 WI MR
shows striking atrophy o( the
pons, medulla, &
cerebellum. Note normal
appearance o( the cerebral
hemispheres in this classic
imaging o( sporadic
olivoponlocerebellar atrophy
(MSA-C subtype). (Right)
Axial T2WI MR shows
cruciform hyperinlensily in
pons, "hot cross bun" sign
~ related to loss o(
myelinated transverse
pontocerebellar (ibers &
neurons in pontine raphe.
Note atrophy o( pons &
cerebellum, typical o( MSA.

typical abnormal T2
hypointensity in the
substantia nigra = & a small
midbrain in a patient with
slrialonigral degeneration, a
type o( MSA. MSA is
characterized by
dysautonomia, parkinsonism,
& cerebellar atrophy. (Right)
SagiLtal T1WI MR shows
midbrain =-
marked atrophy o( the rostral
causing a
"hummingbird" or
"penguin" sign. Note also
the superior collicu/us &
cerebellar atrophy, classic
findings o( PSP. I
7
5
ro PONTINE LESION
E
>.
~
u
c • Hypertensive Intracranial Hemorrhage
Q)
'- DIFFERENTIAL DIAGNOSIS
ro o Hypertensive hemorrhages usually central
0..
c Common o Acute pontine hemorrhage usually
~ • Arteriolosclerosis (Ischemic Rarefaction) hypertensive, but may be due to
co
ro • Cerebral Ischemia-Infarction, Acute cavernoma or AVM
·C
o • Hypertensive Intracranial Hemorrhage o CTA or MR/MRA to look for AVM
C • Brainstem Tumor • Brainstem Tumor
Q)
1§
.•... • Vascular Lesion o Massive expansion of pons, "engulfing"
c o Capillary Telangiectasia, Cavernous basilar artery, often nonenhancing
c: Malformation, AVM o Typically diffuse fibrillary astrocytoma
ctl
"-
CO Less Common • Vascular Lesion
o Capillary telangiectasia: Usually small,
"c:
ctl
• Demyelinating Disease (MS, ADEM)
• Malignant Neoplasm asymptomatic; "feathery" enhancement;
o Metastasis, High Grade Tumor, Lymphoma signal loss on GRE; common in pons
• Pilocytic Astrocytoma Helpful Clues for Less Common Diagnoses
• Wallerian Degeneration • Demyelinating Disease (MS, ADEM)
• Acute Hypertensive Encephalopathy, PRES o Often involvement of middle cerebellar
• Focal or Multifocal Infection peduncles; incomplete ring enhancement
o Pyogenic Abscess, Tuberculoma, PML o Additional lesions in corpus callosum,
• Osmotic Demyelination Syndrome hemispheric white matter (WM), spinal
• Neurofibromatosis Type 1 cord, optic nerves
Rare but Important • Malignant Neoplasm
• Brainstem Encephalitis o High grade tumor (GBM, PNET) often
• Vasculitis accompanied by edema, irregular

• Multiple System Atrophy enhancement, increased CBV
• Radiation Necrosis o Metastases to pons associated with edema,
• Mitochondrial Disorder often other enhancing lesions of brain

• Maple Syrup Urine Disease parenchyma, dura, bone
• Infiltrative Disorder o Lymphoma usually homogeneously
o Langerhans Cell Histiocytosis; enhances, may show mildly J, diffusion
Neurosarcoid; Whipple Disease • Pilocytic Astrocytoma
o Focal enhancing lesion without edema
ESSENTIAL INFORMATION o Acute: Variable • diffusion and t SI on T2
Key Differential Diagnosis Issues o Chronic: Volume Joss; variable T2 SI
• Pontine lesions that present acutely are • Acute Hypertensive Encephalopathy,

typically ischemic or hemorrhagic PRES
• Diffuse astrocytomas present in a more o Most commonly involves parietooccipital
insidious fashion subcortical WM

o Infratentorial T2 hyperintensity often
Helpful Clues for Common Diagnoses present in pons, cerebellum
• Arteriolosclerosis (Ischemic Rarefaction) o Best appreciated on FLAIR;usually no
o Ischemic rarefaction of pons very common
enhancement or DWI abnormality
in older patients with ASVDrisk factors • Focal or Multifocal Infection
o Mild diffuse t SI on T2WI without mass
o Pyogenic abscess will typically reduce
effect, enhancement, or J, diffusion diffusion, whereas tuberculoma may not
• Cerebral Ischemia-Infarction, Acute o PML often causes multiple small dots of T2
o Pontine infarct typically respects the hyperintensity in the brainstem
midline & shows reduced diffusion • Osmotic Demyelination Syndrome
I • Consider CTA or MRA to assess
vertebrobasilar circulation
o Commonly involves centra] pons, spares
corticospinal tracts, may show. diffusion
7
6
PONTINE lESION en
,...
c:
ll>
• Neurofibromatosis Type 1 o Symmetrical T2 hyperintensity that often ::::l
Co
o Common in dorsal pons, due to involves hemispheric WM, deep gray l:Xl
.,
dysmyelination/myelin vacuolization nuclei, & pons ll>
o No mass effect, enhancement o Often> diffusion acutely; volume loss in ::::l
Helpful Clues for Rare Diagnoses chronic phase ...•.

::::l
.,
Q)
• Brainstem Encephalitis • Maple Syrup Urine Disease CD
o Neonate: Cerebellar WM, brainstem > :::J
o Multiple causative agents including listeria o.,
monocytogenes, West Nile, HSV 1 supratentorial edema Qi.
o Acute presentation, swelling, irregular • Infiltrative Disorder OJ

.,
enhancement, variable> diffusion o Enhancing lesions typical ~.
::::l
• Vasculitis Other Essential Information iJ
.,
Q)
o May mimic demyelinating lesions; look for • MR is study of choice for pontine pathology C1l
::::l
n
reduced diffusion, vascular irregularity, • Parallel imaging techniques may be helpful ::r
'<
irregular enhancement to reduce susceptibility artifacts that can 3
Q)
• Multiple System Atrophy obscure pontine pathology
o Sporadic neurodegenerative disorder Alternative Differential Approaches
encompasses olivopontocerebellar atrophy,
• Pontine lesion in a child: Demyelination
striatonigral degeneration, & Shy-Drager (ADEM), brainstem encephalitis, or diffuse
o When Parkinsonism predominates, MSA-P;
astrocytoma; metabolic or mitochondrial
when cerebellar signs predominate, MSA-C disorder
o Imaging may show putaminal volume loss,
• Pontine lesion in an adult: Likely to be
"slit-like" lateral putaminal T2 ischemic or hemorrhagic
hyperintensity (MSA-P), or "hot cross bun" o Hypertensive hemorrhage in older adult
appearance, atrophy of pons/middle o Vascular malformation (AVM, cavernoma)
cerebellar peduncles (MSA-C)
in young adult
• Radiation Necrosis • Enlargement of pons: Diffuse astrocytoma;
o Correlate with history; look for evidence of
brainstem encephalitis; severe ADEM, PRES
a port (fatty marrow in skull base)
• Atrophy of pons: Prior injury (ischemic,
o May occur many years after radiation
hemorrhagic, infectious, metabolic);
• Mitochondrial Disorder walJerian degeneration; MSA; other
o May be congenital or acquired (e.g.,
neurodegenerative disorder
perinatal exposure to zidovudine)
Cerebral Ischemia-Infarction, Acute
I
high signal =
Axial T2WI MR shows i"-defined central pontine T2
in all elderly man. Cerebrum
demonstrated volume loss as well as pedvenlricular and
Axial OWl MR shows reduced diffusion ill the left pons
thai respects the midline = in a patienl wiU, aCLIte
onset right hemiparesis. A 2nd area of acute infarcll!l:1
7
subcortical while matter T2 hyperintensities. is seen in the temporal lobe.
7
PONTINE lESION
'E>-"
.r:
u
c:
~
Q)
'c:"
0..
~
'" (Lefl) Axial NECT shows
lD
central pontine high density
·C'o" B consistent with acute
hemorrhage. This
C hypertensive patient had an
Q)
-
ro~
c:
c:
abrupt onset of headache
followed by loss of
consciousness. (RighI) Axial
FLAIR MR shows massive
...
III
en
expansion of the pons in =
a young girl with gradual
"c:
III
onset di(ficulty walking &
cranial neuropathy. The pons
is diffusely bright, & the
basilar artery SI appears to
be "engulfed" by tumor. The
lesion did not enhance or
reduce diffusion.
(Leh) Axial T2WI MR shows

a central"mulberry-fike"
high signal lesion with a dark
rim of hemosiderin This =.
appearance is classic for a
cavernous malformation. A
anomaly is often seen
post-gadolinium. (RighI)
central pontine lesion with
"feathery" enhancement.
The T2 was normal, & the
eRE image (not shown)
showed signal 1055 in this
region. This constellation of
findings is typical o( capillary
telangiectasia.

numerous well-defined T2
bright lesions in the pons &
middle cerebellar peduncles
in a patient with known
multiple sclerosis. These
lesions showed no
enhancement or reduced
diffusion. (RighI) Axial T2WI
MR shows multiple large,
bright, somewhat ill-defined
lesions in the pons & middle
cerebellar peduncles. Several
of the lesions showed mild
enhancement but no
reduced diffusion. This child
was subsequently diagnosed
I with ADEM.
7
8
PONTINE LESION en
,.-
c:
a centrally hemorrhagic
lesion with a low signal
intensity rim & surrounding
vasogenic edema. The pons
is moderately expanded in
this /5 year old. Biopsy
confirmed GBM. (Right)
Axial TI C+ MR shows a
fairly weJl-circumscribed low
Silesian in the dorsal pons
= with central
enhancement~. The lesion
was T2 bright, & there was
no associated edema. Biopsy
showed juvenile pilocytic
astrocytoma in this young
boy.
Focal or Multifocallnfection Osmotic Demyelination Syndrome

(Left) 5agillal TI C+ MR
shows a large rim-enhancing
lesion in the dorsal pons. A
"daughter" lesion !1m is
beginning to form. There was
associated vasogenic edema
& central reduced diffusion.
Pyogenic abscess. (Right)
central pontine high·signal
intensity, with sparing of a
thin peripheral rim of
pontine tissue as well as the
descending corticospinal
tracts=. There was
reduced diffusion & no
enhancement in the lesion.
CPM.
Infiltrative Disorder
marked atrophy of the pons
& visualized cerebellum. The
pons shows a "hot cross
bun U appearance due to
selective loss of myelinated
transverse pontocerebellar
fibers & neurons in the
pontine raphe. Corticospinal
tracts are preserved. (Right)
irregular linear & nodular
enhancement throughout the
pons, extending to middle
cerebellar peduncles &
cerebellum. High signal on
T2 was present.
Neurosarcoidosis. I
7
9
ro MEDULLA LESION
E
>-
£
(.)
C
DIFFERENTIAL DIAGNOSIS o Typically dorsolateral, due to occlusion of
~
Q)
ro
0..
vertebral artery or PICA; check CTA or
c Common MRA
ro
~ • Lateral Medullary Infarct o Wallenberg syndrome: Deficits in
co
ro • Wallerian Degeneration pain/temperature sense, dysphagia,
'C
o • Demyelinating Lesion (MS, ADEM) hoarseness, vertigo, diplopia, Horner
C • Vascular Lesion syndrome
Q)
-
ro~
c
C
o Cavernous Malformation;
• Brainstem Glioma, Pediatric
AVM
o Diffuse Fibrillary Astrocytoma

o Acute wallerian degeneration may lead to
medullary pyramid T2 hyperintensity,
III
~ o Exophytic Cervicomedullary Glioma mildly reduced diffusion
IJJ
"C Less Common o Chronic infarction along corticospinal
c
III
• Brainstem Neoplasm, Adult tract leads to volume loss of medullary
o Glioma, High or Low Grade pyramid; variable T2 signal
o Hemangioblastoma • Demyelinating Lesion (MS, ADEM)
o Metastasis, Lymphoma o Usually associated with WM lesions in
• Vasculitis other parts of brain, may enhance,
• Medial Medullary Infarct diffusion typically not reduced
• Infection (Abscess, Tuberculoma, PML) • Vascular Lesion
• Syringobulbia o Cavernous malformation may be
associated with developmental venous
Rare but Important anomaly; GRE hypointense
• Hypertrophic Olivary Degeneration o CTA or MRA may help to evaluate for high
• Infiltrative Disorders (Langerhans Cell flow vascular malformation
Histiocytosis, Neurosarcoid) • Brainstem Glioma, Pediatric
• Mitochondrial Disorder o Diffuse infiltrative astrocytoma: Medullary
• Viral Encephalitis expansion, t T2 SI, usually nonenhancing
o Pediatric astrocytoma may also be
ESSENTIAL INFORMATION exophytic from cervicomedullary junction
• Dorsal or ventral; often enhancing
• Acute onset of cranial nerve deficits and Helpful Clues for Less Common Diagnoses
Horner syndrome in an older patient • Brainstem Neoplasm, Adult
suggests medullary infarction o Medullary expansion, areas of irregular
o CT suboptimal for evaluation of medulla; enhancement likely high grade glioma
MR with diffusion is indicated o Hemangioblastoma presents as nodular
o Posterior circulation should be assessed enhancement ± cyst
intra- & extracranially with CTA or MRA • Usually in setting of VHL; look for other
o Vertebral artery dissection a consideration lesions in cerebellum, spinal cord
in younger patient; add Ax Tl with fat-sat o Focal enhancing lesion + associated
• Reduced diffusion in focal medullary lesion edema: Consider metastasis, lymphoma
usually due to acute medullary infarction • Vasculitis
• Volume loss of medullary pyramides) usually o Multifocal T2 lesions, variable ~ DWl
due to wallerian degeneration o CTA or MRA may show vascular

o Look for remote infarct irregularity, but catheter angiography
• Expanded medulla? Neoplasm> infarction, generally indicated
demyelination, infection o Often associated with systemic symptoms,
abnormal CSF
Helpful Clues for Common Diagnoses • Medial Medullary Infarct
• Lateral Medullary Infarct o Less common vertebrobasilar stroke
I o Reduced diffusion; often subtle T2
abnormality in acute phase
syndrome
7
10
MEDULLA lESION
III
o Classic Ipsilateral hypoglossal palsy, o May mimic medullary encephalitis, or vice :J
a.
contralateral hem iparesis, contralateral versa ..•III
OJ
lemniscal sensory loss • Viral Encephalitis
:J
• Infection (Abscess, Tuberculoma, PML) o Typically symmetrical, nonspecific t 51on
o Medullary pyogenic abscess rare; reduced
diffusion, peripheral enhancement
T2WI; variably! diffusion
o Specific diagnosis usually made with CSF
-
:J
...
OJ
ro:J
o Tuberculoma: Ring or nodular analysis o..•
enhancement, central T2 hypointensity, Other Essential Information Qj.
diffusion variable • MR is always the imaging study of choice for ...OJ
OJ
o PML: Multifocal T2 abnormality, no mass
medullary pathology :J
effect, immunocompromised patient -U
• Syringobulbia Alternative Differential Approaches ...ro

OJ
• Medullary lesion with reduced diffusion :J

o Cervical syrinx may extend cephalad into ()
::r
medulla o Typically medullary infarct; assess '<
vertebrobasilar circulation 3
o Assess for Chiari 1 malformation, spinal OJ
cord tumor, other obstruction to CSF flow o Occasionally seen with demyelination:
Look elsewhere for typical lesions
Helpful Clues for Rare Diagnoses o May occur with mitochondrial disease or
• Hypertrophic Olivary Degeneration brainstem encephalitis (more diffuse,
o Insult to dentato-rubro-olivary pathway symmetrical)
o Classic symptom: Palatal tremor
• Medullary lesion with GRE hypointensity
o Uni- or bilateral enlargement, T2
o Typically cavernous malformation; give
hyperintensity of inferior olivary nucleus gadolinium to look for DVA
o No reduced diffusion, no post-gad
o Other possibilities: Hemorrhage due to
enhancement AVM,neoplasm, infection, prior trauma
o Chronic phase: Possible volume loss
• Medullary lesion with gadolinium
• Infiltrative Disorders (Langerhans Cell enhancement
Histiocytosis, Neurosarcoid) o Neoplasm, infection, demyelination
o T2 abnormality, irregular linear and
• Medullary expansion
nodular enhancement o Usually seen with diffuse infiltrative
o Diffusion typically not reduced, vascular
astrocytoma in a child or young adult
imaging studies normal
• Mitochondrial Disorder
o Symmetrical t T2 51, often ! diffusion
lateral Medullary Infarct lateral Medullary Infarct
I
Axial OWl MR shows high signal intensity =
consistent with reduced diffusion in the left lateral
Axial eTA shows narrowing of !he contrast-€nhanced
lumen of !he left vertebral artery =:I as well as
7
medulla of a young man with acute onset of dysphagia intermediate density intramural hematoma
and lefl vocal cord paralysis. consistent with arterial dissecUon.
11
ctl MEDULLA LESION
E
>-
.c
o
c
<I)
~
ctl
0...
c Wallerian Degeneration Demyelinating lesion (MS, ADEM)
(]J
a small, mildly hyperintense
ctl medullary pyramid ffi This
·C
.f! patient had a left MCA stroke
c with right hemiparesis 1 year
<I)
earlier. (Right) Axial T2WI
.•..
~
c MR shows extensive high
signal in the central medulla
c ~ & the right medullary
pyramid laC The lesion does
'"""
(]J not respect the midline or
"0 usual vascular boundaries.
c
This patient had known MS
'" & presented with subacute
...•::::l onset of left-sided weakness
en & lower cranial
neuropathies.
Cavernous Malformation; AVM Diffuse Fibrillary Astrocytoma

a well-circumscribed lesion
in the dorsolateral medulla
with peripheral hemosiderin
staining There is central
hyperintensity & subtle
surrounding edema. The
patient was acutely
symptomatic & had bled into
this cavernous malformation.
shows diffuse but
asymmetrical medullary
expansion & T2
hyperintensity =:I in a 7 year
old This medullary
astrocytoma did not
enhance.
Exophytic Cervicomedullary Glioma Glioma, High or low Grade

(Left) Sagiltal T I C+ MR
shows a lobulated, ventrally
exophytic, moderately
enhancing mass arising (rom
the medulla of a child. The
pons & upper spinal cord
were not involved by Wmor.
shows an irregular,
peripherally enhancing mass
It] with central necrosis
involving the medulla in a 39
year old man. The patient
had no symptoms of
infection, & diffusion was not
reduced in the lesion.
I Pathology confirmed
glioblastoma.
7
12
MEDULLA lESION ,.-c:
(J)
III
::l
a.
...
OJ
III
(Left) Axial T1 C+ MR shows ::l

a well·circumscribed ::J
intensely enhancing nodule ...
....,
= in the dorsal medulla.
Additional enhancing
OJ
CD
::J
nodules were present in the
6'
...
cerebellum in this von iii'
Hippel-Lindau disease ...
OJ
patient with multiple OJ
hemangioblastomas. (Right) ::J
-U
Axial OWl MR shows focal OJ
high signal intensity ro::J
consistent with reduced ()
diffusion in the medullary ::T
pyramid = in an elderly
patient with acute onset of
'<
3
OJ
left hemiparesis & right
vertebral artery occlusion.

a well-defined peripherally
enhancing lesion with a thin
regular rim II] involving the
left dorsal medulla. The
lesion was intermediate on
T2WI. This patient also had
lung nodules and
epididymo-orchitis.
Tuberculosis. (Right) Axial
small T2 hyperintense lesions
= scallered in the medulla.
There was no associated
enhancement or reduced
diffusion. This patient had
AIDS & progressive
neurological decline. PML.
(Lefl) Sagillal T2WI MR

shows an extensive cervical
spinal cord syrinx = with
extension cephalad to the
medulla 81. This syrinx was
secondary to
hemangioblastoma. (Right)
Axial T2WI MR shows
enlargement & hyperintensity
of the medullary olives R
> L, in a patient with prior
hemorrhage into a brainstem
cavernoma. An additional
left cerebellum =
cavernoma is present in the
&
branches of a large OVA are
faintly seen in the right
cerebellum ~.
I
7
13
co INFRATENTORIALMIDLINE CYST
E
>-
£
U
c:: o Suppresses on FLAIR,no DWI restriction
Q)
L
co o Size varies from few millimeters to giant
0...
c:: Common o Often asymptomatic, found incidentally
~ • Mega Cisterna Magna
en Helpful Clues for Less Common Diagnoses
co • Arachnoid Cyst
·C • Neurocysticercosis
o Less Common
C o Best clue: Cyst with "dot" inside
~Q)
• Neurocysticercosis • ± Discrete eccentric scolex
~
.•... • Dandy-Walker Continuum
c:: • Cyst slightly hyperintense to CSF
• Obstructive Hydrocephalus ("Trapped" or o Cisterns> 4th ventricle
c:
ltl "Encysted" 4th Ventricle) • Dandy-Walker Continuum
aI'- • Pilocytic Astrocytoma o DWC: Broad spectrum of cystic posterior
"0
c: • Hemangioblastoma fossa malformations
ltl
• Epidermoid Cyst o DW malformation: Large posterior fossa +
• Dermoid Cyst large CSF cyst, normal 4th ventricle
• Enlarged Perivascular Spaces absent, lambdoid-torcular inversion
Rare but Important o DW variant: Failure of "closure" of 4th
• Congenital Vermian Hypoplasia ventricle, vermian hypoplasia
• Ganglioglioma o Includes persistent Blake pouch cyst, mega
• Pleomorphic Xanthoastrocytoma cisterna magna
• Neurenteric Cyst 02/3 have associated CNS &/or extracranial
anomalies
• Obstructive Hydrocephalus ("Trapped" or
ESSENTIAL INFORMATION "Encysted" 4th Ventricle)
Key Differential Diagnosis Issues o Due to obstructing lesions of 4th ventricle;
• Is mass intra- or extra-axial? all foramina must be involved (Magendie,
• lf extra-axial, cistern or 4th ventricle? Luschka, aqueduct)
o CSF cistern (mega cisterna magna, o May be from hemorrhage, infectious,
Dandy-Walker continuum, arachnoid cyst, inflammatory, or neoplastic causes
epidermoid cyst) o Ventricle enlarged but maintains basic
o 4th ventricle (encysted ventricle, shape
neurocysticercosis, dermoid or epidermoid o CSF intensity/attenuation
cyst, cystic neoplasm) • Pilocytic Astrocytoma
• lf intra-axial, pons, vermis, or cerebellum? o Cystic cerebellar mass with enhancing
o Cerebellum (enlarged perivascular spaces, mural nodule
cystic neoplasm) o Cerebellum> vermis, 4th ventricle
o Vermis (cystic neoplasm, vermian o Child> adult
hypoplasia) • Hemangioblastoma
o Pons (cystic neoplasm> > enlarged o Best diagnostic clue: Adult with intra-axial
perivascular spaces) posterior fossa mass with cyst, enhancing
mural nodule abutting pia
Helpful Clues for Common Diagnoses o Size varies from tiny to several centimeters
• Mega Cisterna Magna o 1-2% of primary intracranial tumors,
o Enlarged posterior fossa CSF space
7-10% of posterior fossa tumors
o Normal vermis completely covers 4th
o May be associated with von Hippel-Lindau
ventricle (rules out Dandy-Walker syndrome
malforma tion/varian t) • Epidermoid Cyst
o May show striking scalloping of skull (due
o Congenital inclusion cyst
to CSF pulsations) o Lobulated, irregular, insinuating CSF-like
• Arachnoid Cyst mass with "fronds"
I o Sharply demarcated extra-axial cyst
o Follows CSF attenuation/signal
o CerebeUopontine angle cistern> 4th
ventricle
7
14
INFRATENTORIAl MIDLINE CYST
III
o FLAIR usually doesn't completely null; o "Molar tooth" brainstem; "bat wing" or :l
a.
restricts on DWI "umbrella" shaped 4th ventricle; vermian
..,
OJ
• Dermoid Cyst remnant variable size III
:l
o Congenital inclusion cyst o Midline anomalies common
o Looks like fat (holoprosencephaly, frontonasal dysplasia,
• Use fat-suppression sequence to confirm facial clefting)
• ± Rupture (fat droplets in cisterns, sulci, • Ganglioglioma
ventricles) o Best diagnostic clue: Partially cystic,
• May cause chemical meningitis, enhancing, cortically based mass in OJ
extensive enhancement child/young adult m
::J
• Enlarged Perivascular Spaces o Cortical dysplasia commonly associated "U
o Pial-lined interstitial fluid-filled structures o Excellent prognosis if surgical resection ..,

Ql
ct>
::J
that accompany penetrating arteries but complete ()
::T
do not communicate directly with o Malignant degeneration rare, '<
3
subarachnoid space approximately 5-10% (glial component) Ql
o Cluster of variably sized intra-axial cysts • Pleomorphic Xanthoastrocytoma

o Off-midline (dentate nuclei) > midline o Supratentorial cortical mass with adjacent
(vermis, pons) enhancing dural tail
o Follow CSF o Cyst and enhancing mural nodule typical
• Suppress completely on FLAIR o 98% supratentorial, rarely found in
• No restriction on DWI cerebellum
• No enhancement o Despite circumscribed appearance, tumor
o "Leave me alone" lesion that should not be often infiltrates
mistaken for serious disease • Neurenteric Cyst
o Benign malformative endodermal C S cyst
o Round/lobulated nonenhancing mass
• Congenital Vermian Hypoplasia
o Anterior to pontomedullary junction,
o Prototype = Joubert syndrome
slightly off-midline
o Inherited hypoplasia or aplasia of vermis
o Slightly/moderately hyperintense
characterized by transient episodic
hyperpnea, oculomotor abnormalities, compared to CSF
ataxia, variable mental retardation
Mega Cisterna Magna Arachnoid Cyst
I
Sagittal TI WI MR in the midline shows a very large
CSF·imensity space behind an intact vermis a=. Note
Coronal TlWI MR demonstrates a sharply demarcated
cyst in the midline posterior fossa just behind the vermis
7
the thinned inner table of the occipital bone 81. =:l. Contents followed CSF signal intensity on all
sequences.
15
III
INFRATENTORIAl MIDLINE CYST
E
>.
.J::
u
C
~
Q)
III
0..
c Neurocysticercosis Dandy-Walker Continuum
~
III
IJ)
shows a nonenhancing cyst
III
·C with a nodule inside the 4th
o ventricle Itl. The protoscofex
C is the viable larva within the
Q)
ro~ smooth thin-walled cyst SI.

NOle associated mild
"-c: obstructive hydrocephalus
with transependymal CSF
flow!:iJ. (Right) Sagillal
T2WI MR demonstrates a
markedly enlarged posterior
fossa with cephalad rotation
of superior vermian remnant
~ and a thinned inner table
of the occipital calvarium
~
Obstructive Hydrocephalus ("Trapped"

or "Encysted" 4th Ventricle)
CSF-filfed mass in the
posterior fossa midline, in
the expected location o( the
4th ventricle m. This is the
typical imaging appearance
of a "trapped" fourth
ventricle. Also note
encephalomalacia in the le(t
temporal lobe SI. (Right)
Sagittal T2WI MR
demonstrates a cystic mass
~ that expands the vermis
=. Note compression,
anterior displacement of 4th
ventricfe ~.
Hemangioblastoma Epidermoid Cyst

(Left) Sagillal T7 C+ MR
shows a cystic-appearing
midline mass II] with
enhancing mural nodule B
of hemangioblastoma.
demonstrates a typical MR
of a large
appearance
epidermoid cyst = as a
mildly lobulated lesion that
expands the 4th ventricle,
which is nearly isoinlense to
CSF but shows mild
heterogeneity.
I
7
16
INFRATENTORIAl MIDLINE CYST CIl
"
c:
Dermoid Cyst Enlarged Perivascular Spaces

midline, fat-density,
extra-axial mass = that -.
:J
OJ
extends into the middle
cranial fossa ~. Low density
ro
:J
8"
foci are scattered in the ~
subarachnoid spaces,
indicative of rupture~.
'OJ"
~
shows enlarged perivascular '"
:J
spaces in left dentate nucfeus \J

= with extension toward
OJ
~
CD
:J
midline~. ()
::r
'<
3
'"
Congenital Vermian Hypoplasia

(Left) Axial TI WI MR reveals
a portion
fossa midline CST space
a tiny vermian remnant
=-
of a large posterior
a.
and the typical" molar
tooth" appearance of the
brainstem 1::1. (Right)
Coronal T1 C+ MR at 0.6 T
reveals a cystic-appearing
lesion of the cerebellum 1::1
demonstrating thick ring-like
enhancement and ventricular
enlargement from
obstructive hydrocephalus
81.
Neurenteric Cyst Neurenteric Cyst

shows hyperintense
extra-axial ovoid mass 1m
anterior to
ponlomesencephalic
junction. (Right) Sagittal T 1
C+ MR shows a large
well-delineated extra-axial
mass = elevating and
displacing the pons and
medulla.
I
7
17
ro CEREBEllAR ATROPHY
E
>-
.r:.
u
c • Progressive Non-Familial Adult Onset
Q)
L
ro
CL
Cerebellar Degeneration
c Common o Chronic Vertebrobasilar Insufficiency
ro • Aging Brain, Normal
L
(D
• Vertebral artery stenosis, posterior
ro
• Encephalomalacia, NOS circulation ischem ia
·C
o • Progressive on-Familial Adult Onset • Posterior circulation ischemia of
C Cerebellar Degeneration hemodynamic or embolic etiology
Q)
ro
.•...
L
o Chronic Vertebrobasilar Insufficiency • Atrophy w/sulcal enlargement; DWI dark
C o Alcoholic Encephalopathy o Alcoholic Encephalopathy
c o Phenytoin (Dilantin) Use, Chronic • Primary (direct) effects of EtOH =
III
L o Paraneoplastic Syndromes neurotoxicity - cortical/cerebellar
aI
"C o Lithium Intoxication degeneration & atrophy
c
III o Radiation and Chemotherapy • Best clue: Disproportionate superior
o Hypothyroidism vermian atrophy
less Common • F-18 FDG PET:Significant decrease in
• Cerebellitis, NOS whole-brain metabolism
o Phenytoin (Dilantin) Use, Chronic
Rare but Important • Dilantin vs. seizures as cause of atrophy
• Multiple System Atrophy debated
• Ataxia, Hereditary, NOS • Dilantin induces organic cerebellar
• Ataxia Telangiectasia damage & may interfere w/intestinal
• Cerebellar Atrophy, Hereditary, OS absorption of folate causing folate
• Congenital Vermian Hypoplasia (Mimic) deficiency - cerebellar atrophy
• Seizures can cause cerebellar atrophy as
ESSENTIAL INFORMATION cerebellum is very sensitive to hypoxia -
cerebellar atrophy
Key Differential Diagnosis Issues • Normal orientation & anisotropy of
• Clinical history often more important in middle cerebellar peduncle & transverse
making diagnosis than imaging findings pontine fibers
Helpful Clues for Common Diagnoses o Paraneoplastic Syndromes
• Aging Brain, Normal • Remote neurological effect(s) of cancer,
o ~ Brain volume (including cerebellum) associated with extra-CNS tumors
with t age • Most common tumor: Small cell lung
• Relative t CSF spaces carcinoma
• Selective atrophy of WM (not gray • Manifestation of paraneoplastic
matter) predominates encephalomyelitis associated
o "Successfully aging brain": Thin w/cerebellar degeneration
periventricular high signal rim without o Lithium Intoxication
white matter hyperintensities • Lithium is a neurotoxin with a particular
o May find focal/confluent periventricular affinity for the cerebellum
white matter hyperintensities • Atrophy of internal granule and Purkinje
• Encephalomalacia, NOS cell layers with dentate gliosis -
o All etiologies appear as CSF replacing neuronal loss and spongiosis
destroyed parenchyma due to • Preceded by neuroleptic malignant
• Post-ischemic loss of tissue following syndrome
parenchymal hypoxic cell death o Radiation and Chemotherapy
• Post-traumatic loss from parenchymal • Injury may be divided into acute, early
irreversible traumatic insult delayed injury, late delayed injury
• Post-inflammatory loss by irreversibly • Diffuse white matter injury or necrosis
I injured tissue • Radiation - induces cryptic vascular
malformations; blood products
7
18
CEREBElLAR ATROPHY
III
o Hypothyroidism o Some etiologies (e.g., cerebrotendinous ~
Co
• Best diagnostic clue: Symmetrical xanthomatosis) may have diffuse white
..,III
OJ
pituitary enlargement reversible with matter T2 hyperintense lesions
thyroid hormone replacement therapy • Ataxia Telangiectasia ~
• May see generalized atrophy; o Progressive neurodegenerative disorder;
alternatively focal cerebellar vermis or onset in early childhood; 1 in 40,000
olivo pontocerebellar atrophy o Multisystem disease - cerebellar ataxia,
• • Cerebral perfusion & metabolism oculomucocutaneous telangiectasias, &
Helpful Clues for Less Common Diagnoses susceptibility to certain infections and
neoplastic processes
• Cerebellitis, NOS
o Purkinje cell loss, atrophy of dentate
o Rare inflammatory syndrome typically
nuclei, diffuse spongy degeneration,
occurring as primary infectious,
multiple foci of coagulative necrosis
post-infectious, post-vaccination, or
w/calcification in white matter
idiopathic disorder
o Bilateral diffuse hemispheric abnormalities
• Cerebellar Atrophy, Hereditary, NOS
o Middle-aged patients; severe superior
are most common (73%)
vermian atrophy
o Often results in moderate to severe
o Lesser involvement of cerebellar cortex
atrophy
o Severity of cerebellar atrophy correlates
Helpful Clues for Rare Diagnoses well with degree of ataxia
• Multiple System Atrophy • Congenital Vermian Hypoplasia (Mimic)
o Sporadic progressive neurodegenerative o Prototype = Joubert syndrome
disorder of adult onset, unknown etiology o Inherited hypoplasia or aplasia of vermis
o "Hot cross bun" sign: Cruciform pontine characterized by transient episodic
hyperintensity on T2WI hyperpnea, oculomotor abnormalities,
o Impaired orientation/anisotropy of middle ataxia, variable mental retardation
peduncle transverse pontine fibers o "Molar tooth" brainstem; "bat wing" or
• Ataxia, Hereditary, NOS "umbrella" shaped 4th ventricle; vermian
o Example: Friedreich ataxia - cerebellar, remnant variable size
spinal atrophy
o Can be divided into autosomal dominant,
autosomal recessive, X-linked,
mitochondrial
Encephalomalacia, NOS
I
Axial T2WI MR 3T MR obtained at age 76 if/ustrates
generalized alfophy changes of prominent folial =:I and
Axial NEeT demonslfates a typical case of right
cerebellar chronic cerebral infarction as focal low
7
subarachnoid spaces 81. Also note slfiking ectasia of attenuation in the right PICA vascular distribution =.
the basilar artery~
19
ro CEREBELLAR ATROPHY
E
>-
.r:
u
c
~
Q)
ro
IL
c Encephalomalacia, NOS
ro
~ (Lefl) Axial T1 WI MR reveals
ro focal left cerebellar atrophy
.~ = as a residua of closed
.2 head injury. (RighI) Sagittal
c T1 WI MR shows the classic
Q)
-
ro~
C
finding of significant
cerebellar atrophy =
supratentorial parenchyma
that appear normal.
with
::::l
-"1Il
Phenytoin (Dilantin) Use, Chronic Paraneoplastic Syndromes

(Lefl) Coronal T2WI MR
demonstrates significant
diffuse cerebellar atrophy
in this 4 I year old man with
=
chronic Oilantin use. (RighI)
Axial FlAIR MR
hyperintensities
paraneoplaslic
= of
cerebellili5,
which will likely result in
cerebellar degeneration.
Radiation and Chemotherapy

T2 hyperintense toxic
demyelination = in a 46
year old woman undergoing
chemotherapy for breast
cancer, which will likely
result in atrophy. (RighI)
Axial FlAIR MR shows T2
confluent hyperintensity of
leukoencephalopathy
cerebellar peduncles &
=
of
temporal lobes E!i:I in a

hypothyroid patient with
Hashimoto encephalopathy.
I
7
20
CEREBELLAR ATROPHY (/)
"
c
Dl
:J
C-
.,
OO
Cerebellitis, NOS Dl
(Left) Axial GCT :J
demonstrates a typical CT ::J
...••
case with enhancement of OJ
cerebella, hemispheres CD
bilaterally =:I. (Right) Sagittal ::J
0-
TI WI MR of spontaneous ::::!.
olivopontocerebellar atrophy III
shows striking atrophy of the OJ

.,
pons =:I,medulla 8l and III
cerebellar vermis =. Note ::J

'U
the normal appearance of III
cerebral hemispheres .
.,
CD
::J
n
::T
'<
3
III
(Left) Sagittal T7 WI MR of
hereditary
olivopontocerebellar atrophy
reveals striking vermian
atrophy =:I as well as severe
pontine atrophy with
flattening 81. (Right) Axial
T2WI MR reveals severe
diffuse atrophy and gliosis
=:I of cerebellar hemispheres
in a patient with
spinocerebellar ataxia.
(Left) Axial T7 WI MR
demonstrates diffuse
cerebellar =:I atrophy. Not
shown are the normal
cerebral hemispheres.
reveals hypoplasia of the
vermis, which could be
mistaken for cerebellar
atrophy =:I. Note the typical
"molar tooth" shape g>J of
the mesencephalon.
I
7
21
CIl CEREBELLAR MASS
E
>-
.J::
U
C
Q)
~ DIFFERENTIAL DIAGNOSIS • Pilocytic Astrocytoma
CIl
(L
o Best clue: Cystic mass + enhancing mural
C
Common nodule
CIl
~ • Cerebral Ischemia-Infarction, Acute o Childhood (not adult) tumor
IJ)
CIl
• Hypertensive Intracranial Hemorrhage • Hemangioblastoma
'C
.9
• Neoplasms o Adult with intra-axial posterior fossa mass
c
Q)
o Medulloblastoma (P ET-MB) with cyst, enhancing mural nodule
co~
.•... o Pilocytic Astrocytoma abutting pia
C o Hemangioblastoma o May be associated with von Hippel-Lindau
C o Metastases, Parenchymal syndrome
III
~
a:l Less Common • Metastases, Parenchymal
"0
• Enlarged Perivascular Spaces o Intra-axial posterior fossa mass in
c
III
• "Tumefactive" Demyelinating Disease middle-aged/older adult? Think metastasis!
o Multiple Sclerosis o Can be solitary but look for other lesions
o ADEM Helpful Clues for Less Common Diagnoses
• Abscess • Enlarged Perivascular Spaces
• Cerebellitis, NOS o Fluid-filled spaces that look like CSF,
• Vascular Malformation, with/without surround/accompany penetrating arteries
Hemorrhage o No diffusion; may have FLAIR
o Cavernous Malformation hyperintense parenchymal rim
o Arteriovenous Malformation • Multiple Sclerosis
o Dural A-V Fistula o Fulminant acute plaque or conglomeration
Rare but Important of acute plaques forming mass lesion(s)
• Tuberculosis o May display ring enhancement simulating
• Glioblastoma Multiforme tumor or abscess
• Dysplastic Cerebellar Gangliocytoma o Most common disabling CNS disease of
• Oligodendroglioma young adults; 1:1000 in developed
• Ganglioglioma countries
• Remote Cerebellar Hemorrhage • ADEM
o Lesions 10-14 days following
infection/vaccina tion
ESSENTIAL INFORMATION o Large flocculent FLAIRhyperintensity but
Key Differential Diagnosis Issues with less mass effect than that expected
• Child vs. adult o Punctate, ring, incomplete ring, peripheral
o Child: Neoplasm> infection, enhancement
demyelinating disease • Abscess
o Adult: Ischemia, hypertensive hemorrhage o Especially in children
> neoplasm o Ring-enhancing lesion
• High signal on DWl, low ADC
• T2 hypointense rim with surrounding
• Cerebral Ischemia-Infarction, Acute edema
o PICA distribution most common
o Central necrotic area may show presence
• DWI restriction w/correlating ADC map of acetate, lactate, alanine, succinate,
• Early cortical swelling pyruvate, amino acids on MRS
• "Hemorrhagic transformation" in 15-45% • Cere belli tis, NOS
• Hypertensive Intracranial Hemorrhage o Typically occurs as a primary infectious,
o Round/elliptical high density mass
post-infectious, post-vaccination, or
o 10% occur in pons, cerebellum
idiopathic disorder
• Medulloblastoma (PNET-MB) o Variable enhancement - none to intense;
I o 4th ventricle> cerebellum
o Desmoplastic variant
meningeal enhancement can be seen
o Abnormal T2 hyperintensity & swelling
7
22
CEREBEllAR MASS ,..
en
C
o Bilateral diffuse hemispheric abnormalities o Characterized by necrosis and

are most common (73%) neovascularity
• Cavernous Malformation o Viable tumor extends far beyond signal
o "Popcorn ball" appearance with complete abnormali ties
hypointense hemosiderin rim on T2WI MR
o ECT: 40-60% Ca++
o Widened cerebellar folia with a striated
-
:J
Q)
Cii
appearance on MR :J
• Arteriovenous Malformation 0"
o "Bag of black worms" (flow voids) on MR o Thinning of skull may be apparent ~
Qi-
with minimal/no mass effect o a.k.a., Lhermitte-Duclos disease, associated ro
~
o Flow-related aneurysm on feeding artery with Cowden syndrome Q)
:J
10-15%; intranidal "aneurysm" > 50% • Oligodendroglioma II
Q)
• Dural A-V Fistula o Partially Ca++ subcortical/cortical mass in ~
CD
:J
o Best imaging tool: DSA with superselective middle-aged adult n
::T
catheterization of feeders o Majority calcify -+ nodular or clumped '<
3
o Dural AVFinvolving the region of the Ca++ (70-90%) Q)
foramen magnum, tentorium, torcula o May expand, remodel, erode calvarium

Herophili, or posterior fossa veins (e.g., • Ganglioglioma
inferior vermian vein) may affect o Partially cystic, enhancing, cortically based
cerebellum mass in child or young adult
o Most often presents with hemorrhage o Ca++ common -+ 35-50%
o Cortical dysplasia is commonly associated
• Remote Cerebellar Hemorrhage
• Tuberculosis
o Occurs after supratentorial craniotomy
o CECT: "Target sign" -+ central Ca++ or
o Superior cerebellar folia
enhancement surrounded by enhancing
• Bilateral (33%)
rim
• Contralateral to side of surgery (29%)
o T1 C+: Solid homogeneous to rim
• Ipsilateral (22%); isolated vermian (9%)
enhancement; ± central necrosis
o MRS: Prominent lipid, lactate but no
amino acid resonances
o Thick irregular enhancing rind of
neoplastic tissue surrounding necrotic core
Cerebral Ischemia-Infarction, Acute Hypertensive Intracranial Hemorrhage
I
Axial T2WI MR demons!rales a lypical case of PICA Axial NEeT shows a large high densily mass in !he lefl
7
acute infarction as hyperintensity associated with
swelling in lhe righl cerebellar hemisphere SI and
laleral medulla =:I_
s/ighdy lesser increased auenualion
hemorrhage.
=
cerebellar hemisphere =:I wilh some adjacenl areas of
indica ling aclive
23
ro CEREBElLAR MASS
E
>-
.r:
u
c
~
(!)
ro
CL
c Medulloblastoma (PNET-MB)
ro
co a poorly defined mass with
ro
.;:: components in vermis, right
o cerebellar hemisphere with
C irregular pattern of
(!)
=.
-
ro~
c
c
enhancemenl Note
temporal horn enlargement
from obstructive
hydrocephalus 81. (Right)
•...
'" Axial T7 C+ MR shows
CO classic cystic cerebellar
"tl pilocylic astrocytoma with
C
nonenhancing rim
'" robustly enhancing mural
nodule 81.
Hemangioblastoma Metastases, Parenchymal

demonstrates a typical MR
appearance of cerebellar
hemangioblastoma with both
an avidly enhancing solid
nodule = and cystic
component 81. (Right) Axial
T7 C+ MR demonstrates left
cerebellar, temporal tip
intensely enhancing masses
=. T7 and T2 shortening
(not shown) demonstrated
hemorrhage. Pathology
confirmed metastases from
renal cell carcinoma.
Metastases, Parenchymal Enlarged Perivascular Spaces

solitary metastasis with thin
rim enhancement =.
no
edema. Numerous
supralentoriallesions were
also found (not shown).
Resection revealed
adenocarcinoma metastases
of unknown origin. (Right)
Axial T7 C+ MR
demonstrates a variably
sized cluster of
non enhancing CSF-like cysts
in left dentate nucleus,
cerebellum P.>J Note mild
mass effect on 4th ventricle
I
7
24
CEREBEllAR MASS ,...
CJl
c:
III
::::l
a.
..
01
III
::::l
variant case of MS with large
demyelinating plaques in
pons ~ and the right
.-.
::::l
III
CD
=.
cerebellar hemisphere
mild mass effect is present.
A
..
::::l
8"
Qi.
..
fRight) Axial FLAIR MR
demonstrates hyperintense 01
flocculent ADEM lesions
of the cerebellum.
= III
::::l
..
""1l
III
Ctl
::::l
(")
::::l"
'<
3
III
Abscess Abscess
fLeft) Axial T1 C+ MR shows
a thick rim of enhancement
I:] surrounding a
nonenhancing central core.
At surgery, a well-developed
cerebral abscess with thick
collagenous capsule was
drained. fRight) MRS of
abscess with TR2000/TE288
shows a large lactate peak
resonating at 1.3 ppm
large acetate peak at 2 ppm
a =-
1.5 ppm =
El a smaller alanine peak at
and a peak at
0.9 ppm ~ representing
cytosolic amino acids
(leucine, isoleucine, valine).
Cerebellitis, NOS Cavernous Malformation

a typical case 01 cerebellitis
as hyperinlensity and mild
swelling of bilateral
cerebellar hemispheres ~.
Post-contrast images showed
marked associated
T2WI FS MR demonstrates
the classic "popcorn II
appearance of a cavernous
malformation in the upper
vermis =. associated with a
anomaly (not shown). Note
T2 heterogeneity of
interstices with hypoinlense
hemosiderin rim.
I
7
25
CEREBElLAR MASS
(Left) Axial SWI in patient
with multiple cavernous
malformation syndrome
illustrates sensitivity of
susceptibility-weighted
sequence by revealing
innumerable cavernous
malformations, many of
c: which were not apparent on
•...
'" CRE or T2 imaging. (Right)
al Axial NECT in a young
1J woman with severe
c:
headache and collapse
'" shows cerebellar
hemorrhage with upward
herniation causing
obstructive hydrocephalus.
Arteriovenous Malformation Dural A-V Fistula

(Left) Anteroposterior CTA in
the same patient with 3D
reconstruction demonstrates
a large right cerebellar AVM
= with a prominent
draining vein 8:1. (RighI)
prominent flow voids
impacting the inferior vermis
Ell multiple serpentine flow
=-
voids adjacent to the cord
&, cord hyperintensity
with mild fusiform cord
expansion from C7 to C4~.
Dural A-V Fistula Tuberculosis

(Left) Lateral angiography of
left vertebral artery in arterial
phase shows a dural fistula
IG>lsupplied by posterior
meningeal branches ffi
reveals irregular rim
enhancement around a
tuberculoma = with
associated leptomeningeal
enhancement around the
pons and 3rd cranial nerves
~.
I
7
26
CEREBElLAR MASS CJI
"
c
reveals CBM CSF spread as a :J
deFined vermian enhancing ~
-;,
nodule = as well as an
enhancing coaling along
Ol
m
:J
numerous subarachnoid
6"
:J.
space structures~. (Right) Ol
Axial T2WI MR shows a large OJ
~
Ol
nonenhancing mass
involving the left cerebellar :J
hemisphere =.The most
-U
Ol
~
characteristic imaging feature Ctl
is preservation of the :J
C1
cerebellar folia pattern or ::r
"stria/ed cerebellum ", typical
'<
3
for Lhermille-Duclos. Ol

variant case of 4/h
ventricular
oligodendroglioma that
mimics ependymoma.
Images reveal heterogeneous
enhancement of mass Ea
involving 4th ventricle
foramen of Luschka.
Intraventricular
oligodendrogliomas are very
rare, occurring in 1 to 10%
of cases. (Right) Axial T7 C+
MR at 0.6 T reveals a
cyst-like lesion that
demonstrates thick ring-like
enhancement = and
significant local mass effect.
Remote Cerebellar Hemorrhage Remote Cerebellar Hemorrhage

(Left) Axial NECT obtained
immediate status post
supratentorial craniotomy
reveals spontaneous
superficial cerebellar
hyperdense hemorrhage =.
A linear configuration
following the cerebellar folia
is the most typical pattern
observed. (Right) Axial T2*
CRE MR performed 2 days
following craniotomy shows
to better advantage a
hemorrhage in a superficial
configuration lit] in a linear
pattern of blood products,
which appears to follow the
cerebellar folia. I
7
27
ro VERMIS MASS
E
>.
.s::
u
c o Hemispheres> vermis
~
Q)
ro o Ca++ 20%, hemorrhage rare
a..
c Common
ro Helpful Clues for Less Common Diagnoses
~ • Medulloblastoma (PNET-MB)
co • Metastasis
ro
'C o ALWAYSinclude metastasis in differential
o Less Common diagnosis of posterior fossa parenchymal
C
Q)
• Metastasis mass in adult!
ro
~
.•... • Hemangioblastoma
c • Seen in 25% of cancer patients at
Rare but Important autopsy
• Dural A-V Fistula • Location approximately 80%
• Arteriovenous Malformation hemispheres, 15% vermis, 5%
• Cavernous Malformation pons/midbrain
• Cerebellitis o Metastases have rounded configuration
• Atypical Teratoid-Rhabdoid Tumor • Usually displace rather than infiltrate
• Dermoid Cyst tissue
• Glioblastoma Multiforme • Virtually 100% enhance
• Ganglioglioma • Variable edema
• Dysplastic Cerebellar Gangliocytoma o Can be hematogenous or originate from
• Rhombencephalosynapsis (Mimic) leptomeningeal carcinomatosis
o Adult with intra-axial posterior fossa mass
ESSENTIAL INFORMATION = metastasis vs. hemangioblastoma
Key Differential Diagnosis Issues • Classic imaging of hemangioblastoma =
• Patient age cyst + enhancing mural nodule abutting
o Child: PNET-MB, pilocytic astrocytoma pia
(PA), ATRTmost common • Solid mass ± hemorrhage less common
o Adult: Metastasis, hemangioblastoma most • Size varies (tiny to several centimeters)
common o Only 1-2% of 1 intracranial tumors but
0
• Does mass originate in vermis or 4th 7-10% of posterior fossa tumors

ventricle (V)? • 80% cerebellar hemispheres
o Vermis: PA, metastasis, • 15% vermis, 5% other (medulla, 4th V)
hemangioblastoma, cerebellitis, ATRT o ± von Hippel-Lindau syndrome
o 4th ventricle: PNET-MB (from superior • Hemangioblastomas in VHL typically
medullary velum), ATRT don't develop until young adulthood,
middle age
• Rare in children
o 30-40% of childhood infratentorial tumors Helpful Clues for Rare Diagnoses
o Round, hyperdense 4th ventricle mass • Dural A-V Fistula
• Arises from 4th ventricle roof o 10-15% of all cerebrovascular
• Posteroinferior spread into cisterna malformations
magna o Dural AVF involving foramen magnum,
• Distinguishes P ET-MBfrom tentorium, torcula Herophili, or posterior
ependymoma (arises from floor, extrudes fossa veins (e.g., inferior vermian vein)
laterally) may affect vermis
• Look for early subarachnoid spread o May be occult, cause tinnitus
o Lateral cerebellar hemisphere location o Can present with hemorrhage
• Desmoplastic variant o Rare: Dementia
• More common in older children, adults • Arteriovenous Malformation
I • Pilocytic Astrocytoma
o Cystic mass with enhancing mural nodule
o "Bag of black worms" on MR with
minimal/no mass effect unless hemorrhage
o Posterior fossa < hemispheres
7
28
VERMIS MASS CIl
""c:
III
o Headache, hemorrhage in 50% • Dermoid Cyst ::l
Co
o Rare: < 0.5% of 1 intracranial tumors
0
• Cavernous Malformation OJ
..,
o Benign vascular hamartoma with masses of o Fat appearance: Use fat-suppressed III
::l
immature blood vessels ("caverns"), sequence to confirm
intralesional hemorrhages, no neural tissue o With rupture find fat droplets in cisterns, ..•.
:J
..,
III
o Seizure 50%, neurologic deficit 25%, sulci, ventricles w/extensive enhancement CD
possible from chemical meningitis :J
asymptomatic 20% 8"
..,
o NECT: 40-60% Ca++ • Glioblastoma MuItiforme iii'
o MR o Rapidly enlarging tumor with necrosis, OJ
..,
• Most common pattern = "popcorn ball" neovascularity III
:J
with hypointense rim o Peak 45-70 years but may occur at any age -u
III
..,
• May present initially with large o Cerebellum uncommon primary site CD
:J
hematoma o 95% have thick, irregular enhancing rind ()
::r
o Can be familial, multiple (multiple of neoplastic tissue surrounding necrotic '<
3
cavernous malformation syndrome) core III
• Do T2* scan (GRE or SWI) in all cases of • Ganglioglioma

spontaneous, "unexplained" intracranial o Well-differentiated, slowly growing
hemorrhage! neuroepithelial tumor composed of
• Cerebellitis neoplastic ganglion cells & glial cells
o Rare inflammatory syndrome o Partially cystic, enhancing, cortically based
• Can be primary infectious, mass in child or young adult
post-infectious, post-vaccination, or o Hemispheres> > cerebellum
idiopathic o Ca++ common (35-50%)
o Imaging often nonspecific • Dysplastic Cerebellar Gangliocytoma
o MR > > CT o Also known as Lhermitte-Duclos disease
• Bilateral hemispheric involvement (75%) o Thick cerebellar folia with "striated"
• T2 hyperintensity appearance on MR
• Variable enhancement (none to intense) o Mass effect may be striking
• Atypical Teratoid-Rhabdoid Tumor o Associated with Cowden syndrome
o Infant/young child • Rhombencephalosynapsis (Mimic)
o 50% infra tentorial o Single lobed cerebellum w/transverse folia
o Off-midline> vermis o Dentate nuclei, superior cerebellar
o Mass often large, heterogeneous peduncles fused
o Can mimic PNET-MB o Vermis absent
I
Axial NECT shows a rounded hyperdense mass ~ Sagiual T1 C+ MR shows a midline cystic mass ~ with
7
within expanded
temporal horns
hydrocephalus,
=
4th ventricfe 81, Note enlarged
indicative of obstructive
solid enhancing nodule E2 in vermis. Note
and tonsillar herniation

=
compression, anterior displacement of 4th ventricle
29
co VERMIS MASS
E
;>,
.r:.
U
c
~
Q)
co
a..
c Metastasis Hemangioblastoma
co
~ (Left) Sagiltal T1 C+ MR in
OJ
an adult with headache,
co papilledema demonstrates
'C
o inferior vermian metastasis
C
Q) with strong but
-ro
c
c
~ heterogeneous enhancement
=. Pathology confirmed
adenocarcinoma of
unknown primary. (Right)
ro
~ Sagittal T1 C+ MR in an
OJ adult with headache,
"C papilledema demonstrates
c
ro cystic mass involving vermis,
with a strongly enhancing
mural nodule SlI. Note
compression, anterior
displacement of 4th ventricle
!:J.
Dural A-V Fistula Arteriovenous Malformation

shows prominent flow voids
within the posterior fossa m
that impact the inferior
vermis as well as mulliple
serpentine {Jow voids
adjacent to the cervical cord
=. Also note extensive cord
hyperintensity and mild
fusiform cord expansion from
C1 to C4 !:J. (Right) Axial
CECT show an enlarged
feeding artery in the CPA
cistern E'l a
acute hemorrhage
round
=-
focus
and a
large posterior draining vein
of
adjacent to the vermis !t].
Cavernous Malformation Cerebellitis

(Leh) Axial T2WI FS MR
demonstrates a mixed signal
intensity lesion or the vermis
It] with a "popcorn"
appearance and classic
peripheral hemosiderin
staining. (Right) Axial CECT
shows diffuse enhancement
of the cerebellum ~ in a
young patient with
cerebellitis.
I
7
30
VERMIS MASS en
"
c:
Dermoid Cyst
(Left) Sagittal T1 C+ MR in
lhis 2 year old shows a
mass in the 4th ventricle
-
:J
~
OJ
CD
:J
Appearance mimics
medulloblaslOma. (Right) o
::::!.
Axial NECT shows a bi/obed, OJ
=
fat density, extra·axial mass
lhal involves bOlh lhe lefl
middle cranial fossa &
OJ
OJ
:J
cerebellopontine angle. This II

OJ
lesion extends into the ~
C1l
ambient quadrigeminal, & :J
n
superior vermian cisterns. :,-
'<
Low densily foci are 3
scattered in the OJ
subarachnoid space,
indicative of rupture ~.
reveals GBM CSF spread as a
defined
nodule =
vermian enhancing
as well as an
enhancing coaling along
numerous subarachnoid
space slructures 8\. fRight)
Sagittal T1 C+ MR al 0.6 T
reveals a cysl-like lesion
centered within the vermis,
demonslrating lhick ring-like
enhancement =.1and
significanllocal mass effect

a classic appearance for
dysplaslic cerebellar
gangliocylOma as a
hyperintense mass with
dislinct strialed morphology
D11. The vermis is a less
common site than the
cerebellar hemisphere.
shows fusion of cerebellar
midline
vermis.
=
while maller across the
wilh absence of
I
7
31
C1l lOW CEREBEllAR TONSilS
E
>,
.r:
(J
c • Sagittal phase contrast MR best
Cl)
C1l
(L
a Low torcular, effaced posterior fossa
c Common cisterns
C1l
~ • Tonsillar Ectopia o Folia orientation runs more vertically
CD
C1l
• Chiari 1 o Look for syrinx, CVJ/skull base anomalies
·C
o • Herniation Syndromes, Intracranial • Herniation Syndromes, Intracranial
C a Tonsils impacted inferiorly into FM
Cl) less Common
ro~
-C
c
• Basilar Invagination (Mimic)
a Posterior fossa CSF cisterns effaced
a Clinically associated with decreased
mental status or obtundation
ra Rare but Important
In"- • Brain Death Helpful Clues for less Common Diagnoses
"C
c:
ra • Intracranial Hypotension
a Can be spontaneous or acquired
ESSENTIAL INFORMATION o "Slumping" midbrain, flattened pons, optic
Key Differential Diagnosis Issues chiasm draped over dorsum sellae
• Cerebellar tonsils may normally lie up to 5 a Diffusely enhancing thickened dura ± SOH
mm below foramen magnum (FM) • Basilar Invagination (Mimic)
• Normal rounded tonsillar a A mimic -+ tonsils are normal
shape/configuration more important than a Primary often associated with bony
precise measurement malformations such as occipitalization of

• Normal folia course horizontally, not the atlas or Klippel-Feil; often familial
vertically a Secondary from acquired bone diseases
• Chiari 2 is not in differential diagnosis that cause "softening" & skull base
(herniated tissue is nodulus of vermis, not flattening, such as osteogenesis imperfecta,
tonsils!) osteomalacia, Paget
• Tonsillar Ectopia • Brain Death
a Zero to 4.8 mm below foramen magnum a Gyral swelling with complete central brain
a Avoid terms "Chiari A" or "Chiari 1/2" herniation -+ tonsils pushed downward
• Chiari 1 a No intracranial vascular flow
a Pointed "peg-like" cerebellar tonsils> 5 a Clinical diagnosis, legal criteria varies
mm below foramen magnum

o Absent CSF space/flow behind tonsil
Tonsillar Ectopia
I
7 Parasagiltal T2Wf MR demonslrales lOnsillar eclopia
measured at 4.7 mm. Note normal rounded
= Sagiaal nWI MR shows poinled cerebellar tonsils=
protruding through foramen magnum, effacing normal
morphology and configura lion. poslerior CSF spaces ~ _ Note relroflexed dens.
32 Foreshortened clivus, norma/4th ventricle.
lOW CEREBEllAR TONSilS
III
:l
a.
..,
[D
III
:l
(Left) Sagittal CINE phase
contrast MR demonstrates
CSF flow as black on this
diastolic image =.Lack of
-
:l
OJ
CD
posterior CSF flow E!:J is ::J
confirmed, secondary to
o..,
tonsillar impaction. (Right)
0;'
Sagittal T1WI MR shows CD
tonsillar herniation ~ as a OJ
result of a large left posterior ::J
fossa mass (not seen). Note II
III
..,
associated compression of (1)
the fourth ventricle E!:J and ::J

n
enlarged ventricles from ::r
'<
obstructive hydrocephalus 3
=. III
Intracranial Hypotension Basilar Invagination (Mimic)

shows tonsillar descent =-
obliteration of suprasellar
cistern a. as well as a
sagging and fat midbrain.
shows severe basilar
invagination secondary to
osteogenesis imperfecta with
the clivus and odontoid
nearly at right angles to each
other; margins of the
foramen magnum are
indicated =.

shows extensive bony
malformation aboullhe
foramen magnum associated
with severe type 1
Klippel-Feil syndrome, which
can mimic low cerebellar
tonsils =.
(Right) Axial
T2WI MR reveals tonsillar
herniation with bilateral
tonsils completely impacted
into the foramen magnum
=.
I
7
33
ro "CYSTIC-APPEARING" POSTERIOR FOSSA lESION
E
>-
.r:
u
c
~
Q)
DIFFERENTIAL DIAGNOSIS • Extra-axial
ro o MCM, AC, DW, neurenteric cyst, NCC,
a.. Common
c neoplasm (schwannoma)
ro
~ • Mega Cisterna Magna
(]:J • DWI, Tl C+ scans helpful additions
ro • Arachnoid Cyst
·C
• Dandy-Walker Continuum Helpful Clues for Common Diagnoses
o
C • Pilocytic Astrocytoma • Mega Cisterna Magna
2
-
ro
~
c
• Encephaloceles
• Obstructive Hydrocephalus
o Communicates freely with all CSF spaces
o Normal tegmento-vermian
• Arachnoid Cyst
angle « 5-10°)
less Common o Mass effect on vermis
• Epidermoid Cyst o ± Hydrocephalus
• Dermoid Cyst o Use FLAIR,DWI to exclude epidermoid
• Neuroglial Cyst • Dandy-Walker Continuum
• Ependymal Cyst o "Classic" Dandy-Walker malformation
• Hemangioblastoma • Cystic dilatation 4th V ~ t posterior
• Schwannoma (Cystic) fossa (PF), torcular-lambdoid inversion
• Abscess • Hypoplastic vermis
• Enlarged Perivascular Spaces • Vermian remnant rotated
Rare but Important anterosuperiorly over cyst
• Syringobulbia o Blake pouch cyst (BPC)
• Neurenteric Cyst • Embryonic BPC doesn't regress
• Atypical Teratoid-Rhabdoid Tumor • Enlarged PF, 4th V open inferiorly
• Metastases, Intracranial, Other • Vermis anatomically complete
• Neurocysticercosis • Pilocytic Astrocytoma
• Chordoma o Cystic cerebellar mass
• Congenital Muscular Dystrophy o Enhancing mural nodule
• Encephaloceles
o Isolated encephalocele: Lacks Chiari 2
ESSENTIAL INFORMATION o Chiari 3 = Chiari 2 PLUS
Key Differential Diagnosis Issues • Occipital or cervical encephalocele
• Cystic-appearing lesion exactly like CSF on containing cerebellum
all sequences? o Syndromic occipital encephalocele
o Mega cisterna magna (MCM), arachnoid • Klippel-Feil, Meckel-Gruber, etc.
cyst (AC), Dandy-Walker Continuum (DW) • Obstructive Hydrocephalus
o Trapped 4th ventricle, enlarged o Outlets obstructed- 4th ventricle t t
perivascular spaces (t PVSs), neuroglial or o Maintains "kidney bean" configuration
ependymal cyst o 3rd V, shunted lateral ventricles small
• Cystic-appearing lesion not exactly like Helpful Clues for less Common Diagnoses
CSF? • Epidermoid Cyst
o Congenital inclusion cyst (dermoid, o Cerebellopontine angle> 4th V > diploic
epidermoid, neurenteric cysts) o Frond-like, cystic (CSF-like)
o Infection such as abscess, o Doesn't suppress completely on FLAIR
neurocysticercosis (NCC) o Restricts on DWI
o eoplasm (pilocytic astrocytoma, • Dermoid Cyst
hemangioblastoma, metastasis, chordoma) o Midline "fatty" mass
• Is cyst intra- or extra-axial? • "Droplets" in CSF if ruptured
• Intra-axial • Look for dermal sinus, midline
o Trapped fourth ventricle (4th V), t PVSs vertebral/skull base anomalies
o Neoplasm (e.g., pilocytic astrocytoma),
I infection (abscess, NCC)
• Neuroglial Cyst
o CSF-like parenchymal cyst
o Inclusion cyst in 4th V (epidermoid) No enhancement, DWI restriction
7 o
34
"CYSTIC-APPEARING" POSTERIOR FOSSA LESION ,..
CJl
l:
D>
• Ependymal Cyst • Neurenteric Cyst :J
Co
o CSF-like o Slightly hyperintense extra-axial cystic
..,
OJ
o Intra- > para ventricular mass, nonenhancing D>
:J
• Hemangioblastoma o Anterior pontomedullary, CPA cisterns
o Posterior fossa mass with cyst, enhancing
mural nodule that abuts pia
o 50% infratentorial (usually off-midline)
-
:::J
.OJ.,
CO
:::J
o ± Arterial feeders, flow-voids o Intratumoral cysts, hemorrhage common
o Gross macrocysts less common
..,8"
o Look for markers of von Hippel-Lindau Qi.
(VHL) • Metastases, Intracranial, Other ..,OJ
OJ
• Visceral cysts, renal clear cell carcinoma o Myriad of non enhancing interfoliate cysts
:::J
o Adult> > older teen (unless VHL) • Low or high grade brain or spine primary II
• Check family history! • Also reported with breast primary ..,
OJ
(1)
:::J
• Schwannoma (Cystic) o Choroid plexus papilloma cysts can be ()
::T
o Vestibular schwannoma (VS) looks like "ice entirely extra-axial, nonenhancing '<
3
cream on cone" • Neurocysticercosis OJ
o Cysts can be intratumoral or VS-associated o Cyst with "dot" (scolex) inside

(arachnoid) o Subarachnoid spaces, sulcal depths most
o Solid component enhances common
• Abscess o Intraventricular cysts often isolated
o T2 hypointense rim with surrounding • 4th ventricle most common
edema • Chordoma
o Ring-enhancing o High signal T2
o DWI hyperintense, ADC hypointense o Moderate to marked enhancement unless
• Enlarged Perivascular Spaces necrotic, mucinous
o CSF-like, nonenhancing, non restricting o High attenuation foci (CT) may be occult
o Most common PF site = dentate nuclei onMR
o Less common = cerebellum, pons • Congenital Muscular Dystrophy
o Best diagnostic clues
• Severely "floppy" infant
• Syringobulbia
o May occur with either Chiari 1 or 2
• Z-shaped or cleft pons
• Multiple small CSF-like cerebellar cysts
o Cervicaljholocord syrinx common
(may be PVSsor trapped CSF from
o May extend further into brain
overmigration of neurons)
(syringocephaly)
Arachnoid Cyst
I
Sagittal T1WI MR shows a mega cisterna magna 81.
The tentorium is normally located, and the posterior
Sagittal T1WI MR shows a reuocerebellar arachnoid
cyst. There is enlargement of the posterior fossa,
7
fossa is mildly prominent. There is no mass effect upon elevation of the lent, and mild compression of Ule
the vermis. vermis.
35
ro "CYSTIC-APPEARING" POSTERIOR FOSSA LESION
E
>-
.r::::
t.l
c
~
Q)
ro
ll.
c Dandy-Walker Continuum Dandy-Walker Continuum
ro
~ (Left) Sagittal T1 WI MR
III
shows typical enlarged
ro posterior fossa, upward
'C
o rotation of the small vermian
C
Q) remnant, elevation of the
-
ro~
c
tentorium, and mass effect
upon the brainslem
"classic" Dandy-Walker
in
malformation. (Right) Sagillal

T2WI MR shows
enlargement of the inferior
4th ventricle which
communicates with an
enlarged cisterna magna in
this infant with a Blake
pouch cyst.
shows a large cystic
neoplasm of the vermis.
There is compression of the
brainstem and 4th ventricle
PJ::l by the rim-enhancing
mass. Nodular thickening E!:I
is present in the caudal
aspect of this cerebellar
"juvenile" pifocylic
astrocytoma UPA). (Right)
Axial T2WI MR shows very
high signal of the cystic
component The solid rim of
the JPA is thick Ii8 and
brighter than gray mailer.
Encephaloceles Encephaloceles
(Left) Sagillal PO FSf MR
shows a classic Chiar; 3
malformation with extension
of infratenloriallissue and
also the venous system 0::>]
into the large occipital
encephalocele. (Right) Axial
T2WI MR shows cerebellar
tissue ~ protruding into the
encephalocele sac.
I
7
36
"CYSTIC-APPEARING" POSTERIOR FOSSA LESION CIl
:><"
c:
=
III
::l
Co
...
OJ
III
::l
shows a dilated trapped 4th
ventricle in a child with a
-.....
::l
history of hydrocephalus due '<::l"0

to intraventricular
0-
hemorrhage as a premature =:!.
inFant. Note the corpus
callosum & thinned due to
'CD..."
:'"J
perivenlricular leukoma/acia.
The 3rd ventricle, unlike the
-U
'CD...:J"
4th ventricle, is normal in
size. (Rig"') Sagittal T2WI
MR in a child with mild ()
ventriculomegalyand ::r
holocord syrinx 81
'<
3
demonstrates extension of
the syrinx into the medulla
'"
=.

a small, CSF-like cyst 81
deForming the right
cerebellopontine angle.
diffusion restriction of the
lobular mass Ell confirming
the presence of an
epidermoid tumor. An
arachnoid cyst would not
restrict.
Dermoid Cyst Dermoid Cyst

shows a cystic structure [?
indenting the inferior vermis.
Note also the segmentation
anomalies of C2 81 and the
midline sagillal cleFting of
the upper cervical cord in
this child with Klippe/-Feil
anomaly. (Right) Axial OWl
MR in the same child shows
diffusion restriction 81. The
dermoid was subjacent to a
dermal sinus.
I
7
37
co "CYSTIC-APPEARING" POSTERIOR FOSSA lESION
E
>-
..c
u
c:
~
Q)
co
0...
c: Neuroglial Cyst
co
CD
shows a large CSF intensity
CO
'C cyst filling the
a pineal/quadrigeminal region.
C With the rim of brain
Q)
ro
..=c:
parenchyma stretched
around the mass, it is
intra-axial and most likely
c: represents a neuroglial cyst
<ll
.... (Right) Sagittal T1 C+ MR
eo shows a small,
1:l well-delineated CSF-filled
c:
<ll cyst SI in the inferior 4th
ventricle. Cyst displaces the
enhancing choroid plexus
IJ:11 which is draped over it.
Hemangioblastoma
teenager with von
Hippel-Lindau shows a large
tumor-associated cyst = in
the medulla. There are flow
voids e::l within the adjacent
soft tissue mass. Typical
upper cervical cord edema
SI is present. (Right)
Coronal T1 C+ MR in the
same patient shows
enhancement of the soft
tissue nodule e::l.
This is
classic hemangioblastoma
with tumor nodule, cyst wall
composed of nonneoplastic
tissue (compressed
cerebellum).
Schwannoma (Cystic) Abscess

a large cyst is associated with
an lAC/CPA mass. Note the
classic "ice cream on a
cone" Et:I enhancement,
typical for vestibulocochlear
schwannoma. Associated
cysts are uncommon. (Righi)
Axial T2WI MR shows typical
low signal intensity rim of the
abscess cavity IaI
surrounded by edema. There
is mastoiditis a the
underlying etiology of the
abscess in this child.
I
7
38
"CYSTIC-APPEARING" POSTERIOR FOSSA lESION
III
::::J
a.
OJ
....•
Enlarged Perivascular Spaces Neurenteric Cyst III
::::J
clusters of multiple tiny
hyperintense cystic areas in
dentate nuclei, basal ganglia
-.
::::J
...••
Q)
CD
E1 The cystic" lesions" are ::::J
clusters of enlarged o...••

Q)
perivascular spaces,
constituting the condition OJ
...••
called Uetat crib/e'l (French Q)
for cribriform state). It is ::::J

-U
considered a normal variant Q)
...••
and typically does not cause CD
symptoms. (RighI) Sagittal ::::J
()
T2WI MR shows a high ::r
signal cystic mass 81 that
'<
3
Q)
indents the anterior aspect of
the medulla.
Metastases, Intracranial, Other

(Left) Sagittal TI C+ MR
shows a superior 4th
ventricle mass E1 and a
large rim-enhancing
Cysts are more common
= cyst.
with posterior fossa atypical

teratoid-rhabdoid tumor than
PNET-Mf3. (Rig"') Axial
T2WI MR shows extensive
inlerfoliale cystic metastases
associated with high grade
spinal astrocytoma.
Neurocysticercosis Congenital Muscular Dystrophy

(Lefl) Sagittal TI WI MR
shows a cyst with a nodule
inside the fourth ventricle
Ncurocysticcrcosis cyst
was confirmed
pathologically. The
pro£oscolex is the viable
larva within the smooth,
thin-walled cyst. (RighI)
Axial T2WI MR shows
multiple small cystic lesions
in the dysplastic cerebellum
=. The pons is hypoplastic
with dorsal clefting ~
Hypomyelination of the
temporal lobes is present 81.
I
7
39
ro POSTERIOR FOSSA NEOPLASM, ADULT
E
>-
.c
u
c
~
Q)
DIFFERENTIAL DIAGNOSIS • Overall most common by far is
ro metastasis
a..
c Common • Hemangioblastoma most common
ro
~ • Vestibular Schwannoma
lJ)
primary
ro Less Common • Astrocytomas, most common
·C
o • Meningioma, CPA-lAC supratentorial tumors, rare in PF
C
Q)
• Metastases, CPA-lAC o Fourth ventricle
-
CO
~
c
C
• Metastasis, Parenchymal
• Subependymoma > choroid plexus
papilloma (CPP)
• Other Schwannomas • Subependymoma in inferior fourth
...
III
o Schwannoma, Trigeminal, Intracranial ventricle (obex)

al
'tl
c o Schwannoma, Facial Nerve, CPA-lAC • CPP in body/lateral recess, CPA
III
o Schwan noma, Jugular Foramen Helpful Clues for Common Diagnoses
o Schwannoma, Hypoglossal Nerve • Vestibular Schwannoma
• Subependymoma o By far most common adult posterior fossa
• Choroid Plexus Papilloma neoplasm; all others less common or rare!
Rare but Important o 90% of all CPA-lAC masses
• Astrocytomas o Looks like "ice cream on cone" (CPA-lAC)
o Glioblastoma Multiforme (GBM) o Enhances strongly
o Anaplastic Astrocytoma o ± Intra- or extra tumoral cysts
o Diffuse Astrocytoma, Low Grade Helpful Clues for Less Common Diagnoses
o Pilocytic Astrocytoma • Meningioma, CPA-lAC
• Paraganglioma, Glomus JuguJare o "Mushroom-shaped" mass caps lAC
• Dysplastic Cerebellar Gangliocytoma o Flat base towards dural surface
(Lhermitte-Duclos) o ± Hyperostosis, dural tail sign
• Medulloblastoma (Desmoplastic Variant) o 25% show lAC involvement!
• Hemangiopericytoma • Metastases, CPA-lAC
• Lymphoma o CPA metastases can arise in 4 locations
• Ecchordosis Physaliphora • Dura-arachnoid
• Rosette-Forming Glioneuronal Tumor of the • Cranial nerves (7, 8 most common)
Fourth Ventricle • Flocculus
• Cerebellar Liponeurocytoma • Choroid plexus (foramen of Luschka)
o Irregular, invasive margins
ESSENTIAL INFORMATION • Metastasis, Parenchymal
o Second only to VS as adult PF neoplasm
o Most common parenchymal PF tumor
o Rarely may be only brain metastasis!
o 95% posterior fossa (hemispheres> >
vermis> brainstem, 4th ventricle)
o < 50% of patients have VHL (look for
multiple lesions, visceral cysts, etc.)
o Imaging
• 60% non enhancing cyst + strongly
enhancing mural nodule abutting pia
• 40% solid, ± blood products
• Other Schwannomas
o Trigeminal (CN5) schwan noma
I • Upper CPA mass

• Look for "dumbbell" shape (CPA +
Meckel cave components)
7
40
POSTERIOR FOSSA NEOPLASM, ADULT ,...
C/l
c:
III
o Facial nerve (CN?) schwannoma • Rare in adults ~
a.
• CPA-lAC mass with "labyrinthine tail" • Paraganglioma, Glomus jugulare ..,III
OJ
• Look for labyrinthine segment tumor (if o Superolateral into middle ear> > CPA
o Look for "sa]t and pepper" "flow voids"
~
absent, can't distinguish from VS)
o Jugular foramen OF) schwannoma o Erosive, destructive, infiltrative
• Enhancing mass arising from JF • Dysplastic Cerebellar Gangliocytoma
• Smooth remodeling of bony margins (Lhermitte-Duclos)
• Projects cephalad into CPA cistern o Widened, irregular cerebellar folia with
o Hypog]ossal (CN12) schwannoma (rare) layered/laminated "striped" appearance
• Smooth remodeling of hypoglossal canal o May cause significant mass effect
• Look for ipsilateral tongue atrophy o Typically doesn't enhance (rarely may)
• Subependymoma • Medullob]astoma (Desmoplastic Variant)
o Middle-aged/elderly adult o "Desmoplastic" variant more common in
o Most small, asymptomatic 2nd, 3rd decades
o T2 hyperintense lobulated mass in inferior • Off-midline (lateral cerebellar
4th ventricle (obex) hemisphere) location
o May have cysts, Ca++; hemorrhage rare • Enhances; CSF spread less common
• Choroid Plexus Papilloma • Ecchordosis Physaliphora
040% of CPPs occur in 4th V, CPA o Small, gelatinous tissue mass considered
o Most common in adults ectopic notochordal remnant
o Cauliflower or frond-like excrescences o Midline of craniospinal axis from dorsum
o Intense, relatively uniform enhancement sellae to sacrococcygeal region
o Clivaljretrocliva] in posterior fossa
o Found in 2% of autopsies
• Astrocytomas
o Typically asymptomatic
o Glioblastoma Multiforme (GBM)
o Hypointense on Tl WI, hyperintense on
• Infratentorial GBMs rare
T2WI; nonenhancing
• Typically necrotic, ring-enhancing
o May involve/erode clivus, ± stalk-like
o Anaplastic Astrocytoma
connection to mass
• Also rare; infiltrative, variable
enhancement
o Diffuse Astrocytoma (Low Grade)
• Young adults
o Pilocytic Astrocytoma
Vestibular Schwannoma
I
Axial T1 C+ MR shows a large extra-axial enhancing
mass =:I displacing/rotaUng !he pons. Note !he
Axial T1 C+ MR shows a large, mushroom-shaped,
enhancing mass in the right CPA cistern. The mass
7
extension into lAC ~ and a cenfJal intratumoraf cyst has a broad base towards !he dural surface. Note dural
tail sign ES:I or reactive meningeal thickening in lAC
41
<1l
E
POSTERIOR FOSSA NEOPLASM, ADULT
>-
.s;;;:
()
c
~
Q)
<1l
D-
c Metastases, CPA-lAC Metastasis, Parenchymal
<1l
~ (Leh) Axial T2WI MR in a
co female with breast
<1l
·c carcinoma shows a lobulated
o extra-axial mass in the right
C flocculus ~ with associated
Q)
-ro
~
c
parenchymal edema ~.
Normal flocculus on left 81.
shows enhancing nodule ~
with rim-enhancing cyst [;8
This was the only lesion in a
cancer. Lesion resembles a
hemangioblastoma (HeB),
but the cyst wall in most
HCBs is nonneoplastic
(nonenhancing compressed
cerebellum).
Hemangioblastoma Schwan noma, Jugular Foramen

shows classic
tumor nodule =
hemangioblastoma with solid
abutting
pial surface of cerebellum.
Associated cyst 81 does not
enhance because wall is
compressed, nonneoplastic
cerebellum. (Right) Axial T1
C+ MR shows large, solid,
intensely enhancing,
extra-axial mass extending
into enlarged, smoothly
remodeled jugular foramen
1m. Intratumoral cysts, not
present in this case, are
common in posterior fossa
schwannomas.

shows a small, mildly
hyperintense mass m in the
inferior fourth ventricle,
found incidentally in this 43
year old male with
headache, trigeminal
neuralgia. No hydrocephalus
was idenulied. Presumed
subependymoma. (Right)
Coronal T1 C+ MR in a 43
year old female with
headaches shows a
"speckled" or "bubbly"
strongly but heterogeneously
enhancing mass in the fourth
=
I ventricle with extension
into the lateral recess 81.
7
42
POSTERIOR FOSSA NEOPLASM, ADULT
Diffuse Astrocytoma, low Grade

(Left) Axial T7 C+ MR in an
older teenager w/nausea &
vomiting shows
inhomogeneously enhancing
vermian mass I:) with cystic,
solid components.
Pre-operative diagnosis was
malignant astrocytoma.
WHO wade If tumo, was
found at biopsy, possibly
secondary to sampling as this
tumor looks nasty! (Right)
Sagittal T2WI MR in 25 year
old lema Ie with lower cranial
nerve palsies shows dorsally
exophytic pontomedullary
mass =::a. Biopsy-proven
WI 10 grade If astrocytoma.
Dysplastic Cerebellar Gangliocytoma

(lhermitte-Duclos) Medulloblastoma (Desmoplastic Variant)
shows enlarged,
dysplastic-appearing
cerebellar folia with striated,
mixed hyper-lisointense
mass in right cerebellum =::a.
(Right) Axial T2WI MR in a
26 year old male shows
inhomogeneously
cerebellum =-
hyperintense mass in lateral
Mass
enhanced heterogeneously.
Desmoplastic
medulloblastoma is most
likely etiology; were this a
child, atypical teratoid
rhabdoid tumor would be a
consideration.

a large, inhomogeneously
enhandng, destructive,
transcalvarial mass with both
intracranial ~ and
extracranial ~ components.
(RighI) Sagittal TlWI MR
shows a midline mass =
in
front of and indenting the
pons 81. Note the loss 01
cortical margin in the clivus
~ from which the mass
originates. The mass was
extremely hyperintense on
T2Wt consistent with its
notochordal remnant origin.
I
7
43
POSTERIOR FOSSA NEOPLASM, PEDIATRIC

Common • Pilocytic Astrocytoma
o Child with cystic cerebellar mass + mural
• Medulloblastoma (PNET-MB) nodule
o Solid component low density NECT, high
• Ependymoma
• Brainstem Glioma, Pediatric signal T2
Less Common o Early childhood: Solid vermis mass extends
• Ganglioglioma into, fills, &/or obstructs 4th ventricle
c:
ns • Schwannoma o Later onset: Lateral cerebellar mass
•...
aJ • Meningioma, CPA-lAC o Hypercellular: t Density on NECT, I T2
'tl
c: • Hemangioblastoma o DWI: Restricts
ns • Choroid Plexus Papilloma o 2-5% have nevoid basal cell carcinoma
Rare but Important (Gorlin) syndrome (BCCS)
• Anaplastic Astrocytoma • Typically seen with desmoplastic variant
• Atypical Teratoid-Rhabdoid Tumor • Look for jaw cysts, bifid ribs, ete.
• Choroid Plexus Carcinoma • XRT can lead to induced basal cell
• Medulloblastoma Variants carcinomas, other intracranial neoplasms
• Medulloepithelioma within irradiated field
• Dysplastic Cerebellar Gangliocytoma • Ependymoma
o Extrudes through 4th V outlet foramina
into cisterns
ESSENTIAL INFORMATION o Coarse calcifications
Key Differential Diagnosis Issues o Diffusion restriction uncommon, may
• Most common pediatric posterior fossa (PF) predict anaplastic behavior
tumors • Brainstem Glioma, Pediatric
o Medulloblastoma (PNET-MB) o Tectal plate glioma
o Astrocytomas • NECT: Increased density progresses to
• Pilocytic astrocytoma (PA) Ca++
• Infiltrating "glioma" (astrocytoma, WHO • CECT/MR: Faint or no enhancement
grade II) o Pontine glioma
o Ependymoma • Enlarged pons engulfs basilar artery
• Imaging • Enhances late in course, rarely at
o Findings on conventional MR overlap diagnosis
o Location helpful in differential diagnosis o Dorsal exophytic glioma
• Tectum, cerebellum: PA • Tumor protrudes into 4th ventricle
• Pons: Diffusely infiltrating astrocytomas • If large, may be difficult to differentiate
• Midline (vermis, fourth ventricle): from PA
PNET-MB,PA • Look for FLAIRsignal change in dorsal
• Fourth ventricle + lateral recess/CPA brainstem or peduncles
mass: Ependymoma Helpful Clues for Less Common Diagnoses
o DWI, MRS (normalized to water) • Ganglioglioma
• Can discriminate between pediatric PF o Brainstem most common PF site
tumors o Look for expansion of nucleus
• PNET-MB,atypical teratoid-rhabdoid cuneatus/gracilis
tumor (ATRT)show DWI restriction • Schwannoma
o Examine entire neuraxis in child with PF o Vestibular schwannoma (lCA/CPA) looks
tumor prior to surgery! like "ice cream on cone"
• Tl C+ essential (look for CSF spread) 01'2 hyperintensity helps differentiate from
I • History, PE (e.g., cutaneous markers) meningioma
important o Multiple in NF2
7
44
III
• Meningioma, CPA-lAC • CPA involvement more common ::::l
a.
o Broad dural base, covers lAC • Frequent metastases at diagnosis
o Variable signal, but T2 hypointensity o Both ATRT,PNET-MB show diffusion
..•
OJ
III
::::l
common restriction
o Hyperostosis, tumoral calcifications
o May have intra- or juxtatumoral cyst(s)
o Similar to CPP plus
-
:J
...
Q)
m::::l
• Hemangioblastoma • Cysts, necrosis, bleeds 8"
o Late teen or adult • CSF/ependymal/parenchymal spread
...
Qi-
o Intra-axial (cerebellum> medulla, cord) • Medulloblastoma Variants ...
Ol
• Cyst + nodule> solid o Desmoplastic medulloblastoma (MB) ~-
:J
• Solid component shows flow voids, • 5-25% of all medulloblastomas "1J
Q)
enhances avidly • 55-60% of PNET-MBs in children < 3 Y Ci3
:J
• Multiple lesions diagnostic of von • PNET-MBin older children, young adults ()
::T
Hippel-Lindau (VHL) often also desmoplastic variant '<
3
o Avidly enhancing mural nodule abuts pia • Desmoplastic subtype of MB in children Q)
o Look for visceral markers of VHL in any < 2 is major diagnostic criterion for basal
child/young adult with hemangioblastoma cell nevus syndrome (Goriin syndrome)
• Choroid Plexus Papilloma • Nodular collections of neurocytic cells
o Frond-like 4th V or CPA tumor bounded by desmoplastic zones
o Avidly enhancing • Lateral (cerebellar) location
o Hydrocephalus common o MB with extensive nodularity (MBEN)
Helpful Clues for Rare Diagnoses • Formerly called "cerebellar

neuroblastoma"
• Anaplastic Astrocytoma
• Usually occurs in infants
o Infiltrating mass involves predominantly
• Gyriform or "grape-like" appearance
white matter
o Enhancement none to sparse or patchy
• May mature - better prognosis
• Medulloepithelioma
enhancement
o Rare embryonal brain &/or ocular tumor
o Ring enhancement suggests progression to
o Inhomogeneous signal, enhancement
GBM
o Diffuse or focal hemispheric mass
o Imaging similar to PNET-MBplus
o Thick cerebellar folia with "striated"
• ATRTpatients generally younger
appearance
• Cysts, hemorrhages more common
o Evaluate for Cowden syndrome
I
Sagittal T1 C+ MR shows a typical tumor cyst with
enhancing mural nodule =_ There is hydrocephalus
and protrusion of the cerebellar tonsils ~ through the
component =
Axial T2WI MR shows increased signal of the solid
of the mass. Interstitial edema ~ is
present in the temporal lobes_
7
foramen magnum facquired Chiari 1)_
45
ro POSTERIOR FOSSA NEOPLASM, PEDIATRIC
E
>.
.c
u
c
<IJ
~
ro
0..
c Medulloblastoma (PNET-MB) Medulloblastoma (PNET-MB)
ro
~ (Left) Sagiltal T2WI MR
CD
shows a hyperintense mass
ro =:I fillingand expanding the
·C
o 4th ventricle. The tumor
C docs not extend through the
<IJ
1il
~ 4th ventricular outlet
.•... foramina. There is
c
hydrocephalus with acquired
tonsillar herniation ~.
(Rigllt) Coronal T I C+ MR
shows heterogeneous
enhancement SII of the 4th
ventricular I'N£T-MB.
(Lefl) Sagiltal T1 WI MR
shows a large tumor filling
the 4th ventricle =:I and
extruding SIIthrough the
obex into the upper spinal
canal. (RighI) Axial T2WI MR
shows a heterogeneous
tumor expanding and
extruding through the right
foramen of Luschka SII.
There are a few coarse
calcific foci ~ within the
tumor.
(Left) Sagittal T2WI MR in an

infant with a teclal plate
glioma shows marked
hydrocephalus involving the
3rd and lateral ventricles.
The corpus callosum is
stretched thin =:I. The tectal
plate [;8 is bulbous and
slightly increased in signal
intensity. The aqueduct of
Sylvius is obstructed IdJ.
(RighI) Sagiltal T2WI MR in
this child with a diffusely
infiltrating pontine glioma
shows homogeneous signal
intensity of the expanded
ponsSll.
I
7
46
Brainstem Glioma, Pediatric

(Lefl) Sagittal T1 C+ MR
the medulla 81 by a
complex mass with
inlralesional cystic areas and
avid, but heterogeneous,
enhancement in this child
with dorsal exophylic
brainstem glioma. The
inFerior 4th ventricle is
deformed by the protruding
mass. (RighI) Sagittal T2WI
MR shows marked expansion
of the medulla and upper
cervical spinal cord 81. The
inFerior 4th venuicle is
deformed ~ by the dorsally
protruding mass.
Schwannoma Schwannoma
a bulky heterogeneous right
cerebelloponline angle mass
a which crosses the
midline. There is also
extensive remodeling of the
right internal auditory canal
t=lI by this schwannoma.
(RighI) Axial T1 C+ MR in
another child shows small
bilateral vestibular
schwannomas. The right
lesion E:I assumes the
appearance of "ice cream on
a cone". Both demonstrate
intra labyrinthine extension
~.
Meningioma, CPA-lAC Meningioma, CPA-lAC

a low signal, lobular
cerebellopontine angle mass
~ with hyperostosis 81 of
the adjacent petrous apex.
There is mild rota lion of the
medulla due to mass effect.
(RighI) Coronal NECT shows
diffuse hyperostosis 81
adjacent to the meningioma
~.
I
7
47
OJ POSTERIOR FOSSA NEOPLASM, PEDIATRIC
E
>.
.r:
'-'c
~
Q)
OJ
CL
c
OJ
co shows a solid component
OJ
·C with multiple flow voids ~
o a cyst EB and edema of the
CQ) medulla and upper cervical
CO cord 81. (Right) Sagittal T7
~
••....
C
C+ MR shows the cyst 8110
better advantage than the
c prior T2WI image. Here, the
''"-
CO
cyst's contents have slightly
increased signal.
"0
c
'"

multiple Foci of abnormal
signal intensity in the
peripheral right cerebellar
hemisphere and in the
cerebellar while maller -=
adjacent 10 the lateral recess
of the 4th ventricle. (Right)
enhancement =:I Following
gadolinium administration.
The lesion adjacent to the
4th ventricle lateral recess
has ill-defined margins.
Atypical Teratoid-Rhabdoid Tumor Atypical Teratoid-Rhabdoid Tumor

shows extensive posterior
(ossa a pineal region
and intraventricular low
signal intensity masses.
MultiFocal deposits of tumor
at diagnosis are strongly
suggestive of an atypical
teratoid-rhabdoid tumor.
shows quite variable
enhancement of the
posterior Fossa~ pineal
region=, and
intraventricular B tumor
I deposits. There is marked

hydrocephalus.
7
48
POSTERIOR FOSSA NEOPLASM, PEDIATRIC en
,.-
c::
Q)
::::l
Co
..•
tIJ
Q)
Choroid Plexus Carcinoma Choroid Plexus Carcinoma
::::l
a slightly heterogeneous, but ::::l
avidly enhancing, mass ...
..."
Q)
within the right foramen of ~
Luschka =. There is an
C1l
::::l
0-
...
associated cyst 81. (Right)
Axial T2WI MR in a different
Qi.
child unde'going treatment CD
for choroid plexus carcinoma OJ
shows a large skull base ::::l
-0
metastatic deposit E.I.
...
Q)
C1l
::::l
()
::T
'<
3
Q)
Medulloepithelioma
(Left) Axial NECT in a one
day old infant shows a
dense, lobular mass filling
the posterior fossa. Foci of
increased density
superimposed in the mass
are due to hemorrhage. Note
the blood-CSF level in the
dilated infundibular recess
81. (Right) Coronal TI C+
MR in the same infant
following biopsy shows
extension into the spinal
canal [;8 Cas = in the
ventricular system follows
neurosurgical intervention.
There is extensive
ependymal seeding =.

a large nonenhancing mass
involving the left cerebellar
hemisphere. Preservation of
the cerebellar folia pallern,
or "striated cerebellum"
is characteristic for dysplastic
=-
cerebellar gangliocytoma
(Lhermitte-Duclos). This
disease has a strong
association with Cowden
syndrome. (Right) Axial
T2WI MR again shows the
=-
pattern of a "striated
cerebellum"
I
7
49
SEClilON 8
SellalJuxtasellar, Pineal Region
Pineal Region Mass, General 1-8-2
Pineal Gland Mass 1-8-6
Quadrigeminal Cistern Mass 1-8-8
Pineal + Suprasellar Lesions 1-8-10
Sella/Pituitary Normal Variants 1-8-12
Sellar/]uxtasellar Calcification 1-8-14
Enlarged Pituitary Gland 1-8-18
Intrasellar Lesion 1-8-20
Cystic Intrasellar Mass 1-8-22
Suprasellar Mass, General 1-8-24
Suprasellar Masses, Pediatric 1-8-30
Suprasellar Cystic Mass 1-8-36
Calcified Suprasellar Mass 1-8-40
Enhancing Suprasellar Mass 1-8-42
Absent/Thin Infundibular Stalk 1-8-44
Thick Infundibular Stalk 1-8-46
Hypothalamus Lesion 1-8-48

Hyperdense Suprasellar Mass 1-8-52
T1 Isointense Suprasellar Mass 1-8-54
T1 Hyperintense Suprasellar Mass 1-8-56
T1 Hypointense Suprasellar Lesion 1-8-58
c PINEAL REGION MASS, GENERAL
.Q
Ol
Q)
0:::
ro Q)
DIFFERENTIAL DIAGNOSIS Helpful Clues for less Common Diagnoses
c
a:: Common • Cavum Velum Interpositum (CVI)
..: o Axial MR/CT shows triangular-shaped CSF
.£2 • Pineal Cyst
Qi space between bodies of lateral ventricles
C/)
I1l
less Common o FLAIRsuppresses completely; no
X • Cavum Velum Interpositum (CVI) enhancement
-,::l • Meningioma
Iii o Dilatation of velum interpositum, precise
Q) • Pineocytoma etiology unknown
U)
• Arachnoid Cyst o Common in early infancy, rare in adults
C
• Tectal Plate Glioma • Meningioma
•..
III
aI • Neurocysticercosis o Avidly enhancing mass, trapped pools of

"C
C • Lipoma CSF common, focal calcification may
III
• Intracranial Hypotension represent displaced pineal
• Medial Atrial Diverticulae (Obstructive o Arise from posterior portion of the velum
Hydrocephalus) interpositum, falx, or tentorium
Rare but Important o Velum interpositum meningiomas: M = F,
• Germinoma in both pediatric & adult populations
• Epidermoid Cyst o May be symptomatic from compression of
• Dermoid Cyst quadrigeminal plate
• Vein of Galen Malformation • Pineocytoma
o Enhancing, circumscribed pineal mass
which "explodes" pineal Ca++
ESSENTIAL INFORMATION o May mimic pineal cyst or pineoblastoma
Key Differential Diagnosis Issues o May compress but does not invade
• Quadrigeminal cistern (QC) adjacent structures
o Bounded by quadrigeminal plate, o - 45% of pineal parenchymal tumors
splenium, vermis, & tentorial margin • Arachnoid Cyst
o Extends between layers of 3rd ventricle o Sharply demarcated extra-axial cyst that
tela choroidea follows CSF attenuation/signal
o Contents: Caudal internal cerebral veins ...• o Quadrigeminal arachnoid cysts (AC) are
vein of Galen, distal parts of 3rd most common infra tentorial AC
quadrigeminal artery, PCA P4 segment, & o Symptoms depend on compression of
C 9 exit brain stem, cerebellum, & aqueduct
o Synonyms: Cisterna quadrigeminalis, o Elevated ICP & sudden death have been
cistern of great cerebral vein, cisterna reported
venae magnae cerebri, Bichat canal, • Tectal Plate Glioma
cisternal quadrigeminalis, & superior o Tectal distortion or thickening by localized
cistern mass
o Tl hypointense, T2 hyperintense, ±
Helpful Clues for Common Diagnoses enhancement
• Pineal Cyst o Onset aqueductal stenosis often without
o Homogeneous fluid-filled mass above &
associated brain stem signs
clearly distinct from tectum o Reported as indolent lesions often
o 55-60% slightly T1 hyperintense to CSF;
remaining stable in size for many years
FLAIRdoesn't suppress; 60% enhance • Neurocysticercosis
(partial/complete rim, nodular) o May involve cisterns> parenchyma>
o Cystic expansion of pineal in some females
ventricles
begins in adolescence, decreases with age o Basal cistern cysts may be racemose
o Can't distinguish from pineocytoma on
o Cysts variable, typically 1 cm, range from
I basis of imaging studies alone 5-20 mm and contain a 1-4 mm scolex
8
2
PINEAL REGION MASS, GENERAL CII
"
c:
o Cystic lesion isointense to CSF,may see Helpful Clues for Rare Diagnoses
discrete, eccentric scolex
• Germinoma
• Lipoma o Pineal region mass that "engulfs" the
pineal gland
with fat attenuation/intensity o Tl/T2 iso- or hyperintense to gray matter
040-50% interhemispheric fissure (over o Strong uniform enhancement, ± CSF
corpus callosum) seeding
o Ca++ varies from none to extensive
• Epidermoid Cyst
o Fat-suppressed MR is diagnostic
o Lobulated, irregular, CSF-like mass with
• Intracranial Hypotension "fronds" insinuates cistern
o Corpus callosal descent can efface QC
o FLAIRusually doesn't completely null;
o Sagittal shows brain descent in 40-50%
diffusion yields high signal restriction
o Diffusely, intensely enhancing dura in
00.2-1.8% of all primary intracranial tumors
85% o Congenital inclusion cysts; rare malignant
o Bilateral subdural fluid collections in 15%
degeneration into squamous cell CA
• Medial Atrial Diverticulae (Obstructive • Dermoid Cyst
Hydrocephalus) o Fat appearance: Use fat suppression
o Mechanism
sequence to confirm
• Massive ventricular dilatation causes o Rupture - fat droplets in subarachnoid
stretching & dehiscence of fornix - spaces with extensive enhancement
unilateral or bilateral diverticula of possible from chemical meningitis
inferior medial atrial wall o < 0.5% of primary intracranial tumors
• Enlargement of pial pouch creates o Rare malignant degeneration into
subarachnoid cyst that may herniate squamous cell carcinoma
through incisura into QC • Vein of Galen Malformation
o Imaging o Dilated arteries feeding into large midline
• Focal dehiscence of medial atrial wall venous pouch
• Draping of medial atrial wall over free o Thin sagittal images define anatomy &
margin of tentorium with continuity of relationship to cerebral aqueduct
CSF around tentorial edge o < 1% cerebral vascular malformations at
• Contralateral internal cerebral vein any age
displaced o Neonatal> infant presentation most
• Presence of septa separating diverticulum common; rare adult presentation
from 3rd ventricle
Pineal Cyst
I
Axial FlAIR
pineal cyst
hyperintense.
= MR shows the classic finding of a presumed
that does not suppress and is moderately
Axial CrCT shows
1:11 splaying
inferolaterally Ell.
a CSF collection
the internal
Note
cerebral
the septum
between the fornices
veins & choroid
pellucidum
plexus
~ is
8
intact.
3
c PINEAL REGION MASS, GENERAL
.Q
Ol
Q)
0::
Cll
Q)
c
a::
(Left) Sagillal T2WI FS MR
shows an isoinlense mass =
wilh flow voids ~.
Visualization of a normal
pineal gland ~ & elevation
of midbrain lectum ~ helps
exclude pineal tumors from
lhe differential diagnosis.
lypical CT case of a
pineocytoma with
"exploded" pre-existing
calcificalion =.2. Also note
the typical lack of significant
mass effect.
Arachnoid Cyst Tecta I Plate Glioma

shows an arachnoid cyst
extending posteroinferiorly
from the quadrigeminal
cistern, compressing the
superior vermis inferiorly -7.
demonstrales a typical tectal
plate low grade astrocytoma
as a predominantly
homogeneous, slightly
hyperintense mass involving
the lectal plale proper EB

shows multiple cysticercosis
cysts in the quadrigeminal
cistern atrium right
lateral ventricle ~
(Courtesy E. Bravo, MO).
reveals a fat-intenSity lesion
=.2 within the quadrigeminal
cistern exerting mass effect
upon the quadrigeminal
plate (R> L). Fat suppression
(not shown) confirmed
lipoma.
I
8
4
PINEAL REGION MASS, GENERAL en
"
c:
Medial Atrial Diverticulae (Obstructive

Intracranial Hypotension Hydrocephalus)
shows cisternal effacement
by splenium = impacting
internal cerebral veins ~ &
quadrigeminal plate BI.
Note 1055 of suprasellar
cistern & dural
enhancement . (Right)
sagillal T1 WI MR shows an
atrial diverticulum ~ that -u
has protruded through the ::l
C1>
lateral ventricle medial waif OJ
under the Fornix Note ;0
the severely compressed C1>
<0
displaced 4th ventricfe BI. o·
::l
Germinoma
(Left) sagillal T1 C+ MR
shows an enhancing
germinoma !l±. Note
compression of the tectal
plate and CsF tumor
seeding BI. (Right) Axial
T2WI MR shows a T2
hyperintense lobulated mass
=
centered in ambient cistern
~
extending into suprasellar
& quadrigeminal cisterns
BI displacing the
quadrigeminal plate ~_
Dermoid Cyst Vein of Galen Malformation

(Left) Axial CECT
demonstrates a low density
ruptured dermoid in the
pineal region BI with fat
droplets in subarachnoid
spaces =. Note vemricular
shuml!:J placed for
chemical meningitis. (Right)
large well-delineated area of
signal 1055behind the 3rd
ventricle BI. Note phase
artifact from high flow I!:J &
large persistent primitive
fa/cine sinus=.
I
8
5
c PINEAL GLAND MASS
.Q
Ol
Q)
a:
ro
Q)
c
a.. Common • Teratoma
..: o 2nd most common GCT & pineal tumor
ro • Pineal Cyst
o Midline mass containing Ca++, soft tissue,
Q)
(/)
• Germinoma
ro • Pineocytoma cysts, & fat; variable enhancement
X
-
--,::l
ro
Q)
CI)
Less Common
• Teratoma
• Pineoblastoma
o Highly malignant,
tumor of pineal gland
primitive embryonal
• Pineoblastoma o Large, heterogeneous pineal mass with

t:
•..
ro Rare but Important "exploded" peripheral Ca++ &
lO
• Retinoblastoma (Trilateral) hydrocephalus
"0
t: • Germ Cell Neoplasms, Malignant NOS
ro Helpful Clues for Rare Diagnoses
:s • Diffuse Astrocytoma, Low Grade • Retinoblastoma (Trilateral)
..II:
Ul o Bilateral ocular tumors + midline
ESSENTIAL INFORMATION intracranial neuroblastic tumor

o Trilateral rare: 80% pineal, 20% suprasellar
Helpful Clues for Common Diagnoses • Germ Cell Neoplasms, Malignant NOS
• Pineal Cyst o Uncommon, highly malignant tumors:
o Homogeneous fluid-filled pineal mass Choriocarcinoma, endodermal sinus
o May see rim enhancement tumor, embryonal cell carcinoma, mixed
o Most are < 1 cm but may be up to 2 cm o Heterogeneously enhancing pineal mass
• Germinoma o Characteristic elevation of serum tumor
o Most common germ cell tumor (GCT) & markers: Choriocarcinoma, ~-hCG;
pineal tumor endodermal sinus tumor, AFP; embryonal
o Homogeneous, hyperdense mass with cell carcinoma, ~-hCG & AFP
enhancement, ± CSF seeding • Diffuse Astrocytoma, Low Grade
o Central, "engulfed" Ca++ classic o Rarely arise from pineal gland
• Pineocytoma o Pilocytic astrocytoma most common
o Demarcated round or lobular mass,
typically with Ca++
o Strong, homogeneous enhancement • Helpful to divide pineal gland masses into
o Pineal parenchymal masses
o May compress adjacent structures, but no
o Germ cell tumors
invasion
o "Other cell" tumors/lesions
Pineal Cyst Pineal Cyst
I
8 Axial FLAIR MR shows a pineal mass that does not
suppress, which is typical. Pineal cysts are very
Axial T1 C+ MR shows a pineal mass with no
enhancement, typical of a pineal cyst. If there is rim or
common, with a 1-4% prevalence at imaging. They are nodular (rare) enhancement, it may not be
most often asymptomatic. distinguishable from a pineocytoma on imaging alone.
6
PINEAL GLAND MASS
III
::::l
Q.
..,
lJl
III
Germinoma Pineocytoma
::::l
a well-defined, enhancing (j)
(1)
pinea/wmor that projects
into the posterior 3rd ~
ventricle. The patient is a '-
c
male adolescent with
x
Qi
Parinaud syndrome, typical CI>
(1)
presentation for germinoma.
OJ
(Right) Axial T1 C+ MR .""
shows a pineal mass with
peripheral & central
enhancement. Enhancement
of pineocyloma can be solid,
peripheral, or both. Imaging
of a pineocytoma may mimic
a pineal cyst or
pineoblastoma.

a heterogeneous pineal
region mass with small
hyperintense foci
representing fat =.Note
shows a cystic & solid pineal
mass with heterogeneous
enhancement. Note
Pineoblastoma is a highly
maJignanllumor with poor
survival. Spina! screening
should be performed, as up
to 45% present with spinal
dissemination.

an enhancing mass in the
pineal gland with associated
hydrocephalus in this patient
with bilateral retinoblastoma.
Trilateral disease is rare and
has a dismal prognosis.
shows a heterogeneously
enhancing mass, a mixed
malignant GCT with
embryonal carcinoma
elements. [mbryonal
carcinoma is typically part of
a mixed malignant GCT.
These types of tumors are
solid masses, often with cysts
& hemorrhage. I
8
7
c QUADRIGEMINAL CISTERN MASS
.Q
OJ
Q)
0::
ro
Q)
c
0:: Common • Cavum Velum Interpositum (CVI)
..: o Axial MR/CT shows triangular-shaped CSF
ro • Metastases
Q) space between bodies of lateral ventricles
rJ)
ro
Less Common o FLAIR suppresses completely
~
x • Cavum Velum Interpositum (CVI) • Arachnoid Cyst
--,::l • Arachnoid Cyst
ro o Sharply demarcated extra-axial cyst that
Q) • eurocysticercosis follows CSF attenuation/signal
(f)
• Ascending Transtentorial Herniation o No diffusion restriction
c:
•..
C'll
lJJ
Rare but Important • Neurocysticercosis
• Lipoma o Cystic lesion isointense to CSF, may see
'tl
c:
C'll • Epidermoid Cyst discrete, eccentric scolex
• Dermoid Cyst o Basal cistern cysts may be racemose
• Vein of Galen Malformation • Ascending Transtentorial Herniation
o Large posterior fossa mass --+ upward
herniation of vermis --+ mass effect on
ESSENTIAL INFORMATION quadrigeminal cistern ± obstructive
Key Differential Diagnosis Issues hydrocephalus
• Quadrigeminal cistern (QC) lesions are Helpful Clues for Rare Diagnoses
smaller subset of "pineal region masses" • Lipoma
o Bounded by quadrigeminal plate, o Well-delineated, lobulated, extra-axial
splenium, vermis, & tentorial margin mass with fat attenuation/intensity
o Extends between layers of tela choroidea o Ca++ varies from none to extensive
o Contents: Caudal internal cerebral veins, • Epidermoid Cyst
vein of Galen, peA (quadrigeminal or P3 o Lobulated, irregular, CSF-Iike mass
segment), posteromedial choroidal arteries, o FLAIR usually doesn't completely null;
CNIVexit diffusion yields high signal restriction
• Masses arising from QC itself (and its • Vein of Galen Malformation
contents) < < those from nearby structures o Dilated arteries feeding into large midline
Helpful Clues for Common Diagnoses venous pouch
• Metastases o Look for prominent "flow voids" and phase
o Linear &/or nodular enhancing lesions artifact
o Image entire neuraxis!
Metastases Cavum Velum Interpositum (CVI)
I
8 Sagillal T7 c+ MR shows typical leptomeningeal (pia &
arachnoid) metastases lID in the quadrigeminal cistern
Sagillal T7WI MR reveals a well-defined cavum velum
imerpasiwm isoinlense with CSF, displacing the
as well as widespread throughout the cerebellar {olia. internal cerebral veins inferiorly ~ and compressing
the quadrigeminal cistern ~.
8
QUADRIGEMINAL CISTERN MASS ,..c:
(Jl
Ql
:J
Co
.,
III
Arachnoid Cyst Neurocysticercosis Ql
:J
shows an arachnoid cyst (Jl
compressing the vermis ~
inferiorlya
quadrigeminal cistern
and extending into velum
=
widening the
OJ
c:::
c
x
inlerposilum =. (Right)
Sagittal STIR MR reveals ~
6i
(/)
Ql
multiple hyperintense CYSIS ."'
in the quadrigeminal cistern -0
= and basal subarachnoid
spaces 811.
:J
C1l
Ql
;:0
C1l
<C
o
OJ
Ascending Transtentorial Herniation lipoma

complete effacement of the
quadrigeminal cistern -=
caused by upward herniation
of the vermis through the
tentorial incisura that also
compresses the aqueduct
ED. resulting in obstructive
hydrocephalus with dilated
3rd and lateral venlricles ~.
demonstrates a fat intensity
lipoma within the
quadrigeminal cistern
displacing the vermis which
suppressed with T 1 fat
suppression (not shown).
Epidermoid Cyst Vein of Galen Malformation

(Left) Axial TI WI MR
demonstrates a lobulated
CSF-like epidermoid
within the quadrigeminal
cistern. (Right) Sagillal TI WI
MR demonstrates a
prominent flow void within
the quadrigeminal cistern
from a vein of Galen
malformation = as well as
associated fiswlae 81.
I
8
9
c PINEAL + SUPRASEllAR lESIONS
Q
OJ
Q)
a::
Cll DIFFERENTIAL DIAGNOSIS o May involve sellar & pineal regions
Q)
c • Metastases, Intracranial, Other
n.. Common o Enhancing masses at gray-white junctions
.: • Germinoma
~ o May involve pineal & suprasellar regions
Q)
rn
Cll
less Common
X • Lymphoma, Primary CNS Helpful Clues for Rare Diagnoses
--,::J • Metastases, Intracranial, Other
Co • Germ Cell Neoplasms, Malignant NOS
a; Rare but Important o Uncommon, highly malignant tumors:
(j)
c • Germ Cell Neoplasms, Malignant NOS Choriocarcinoma, endodermal sinus

III • Retinoblastoma (Quadrilateral) tumor, embryonal cell carcinoma, mixed
"-
III germ cell tumor
"C
III
o Heterogeneously enhancing masses
o Imaging cannot reliably differentiate
::J
-"(j) Key Differential Diagnosis Issues o Characteristic elevation of serum tumor
• Age may be a helpful differentiating feature markers
• Diabetes insipidus is a common presenting • Choriocarcinoma: ~-hCG; endodermal
feature of infundibular masses sinus tumor: AFP; embryonal cell
• Parinaud syndrome is a common carcinoma: ~-hCG & AFP
presentation of pineal masses • Retinoblastoma (Quadrilateral)
o Bilateral calcified ocular tumors + midline
Helpful Clues for Common Diagnoses neuroblastic tumors (pineal & suprasellar)
• Germinoma o 40% are familial & account for nearly aJl
o Most common germ cell tumor bilateral & multilateral disease
o Hug midline near 3rd ventricle: 80-90%
o Trilateral disease rare: 5-15% of familial
o Pineal region: 50-65%; suprasellar: 25-35%
lesions (80% pineal, 20% suprasellar)
o Pineal + suprasellar - 10% o Quadrilateral disease extremely rare
o Hyperdense masses on CT o Dismal prognosis, < 24 month survival
o Homogeneous enhancement
o CSF seeding common Alternative Differential Approaches
• Pineal + suprasellar lesions in a child:
Helpful Clues for less Common Diagnoses Germinoma, germ cell neoplasms,
• Lymphoma, Primary CNS retinoblastoma
o Homogeneous enhancing mass(es) along • Pineal + suprasellar lesions in an adult:
ependymal surface typical Lymphoma, metastases
Germinoma Germinoma
I
8 Sagittal T1
mass ~
C + M R shows a mildly enhancing suprasellar
& a small synchronous pineal mass 81 in this
Axial T1 C+ MR shows enhancing masses of the pineal
~ & suprasellar regions in this patient with CSF spread
patient who presented with diabetes insipidus. of germinoma. Enhancing tumor infiltrates the
10
Germinoma was proved at biopsy. ependyma of the (rontal horns =:l.
PINEAL + SUPRASELLAR LESIONS en
A
c:
Ql
:3
Co
..,
[Jl
Ql
(Left) Sagiltal TI C+ MR :3
shows an enhancing mass in
the suprasellar region that
extends into the pituitary
infundibulum SlI as well as
along the du,a of the
posterior clivus 1'1:D. Primary
lymphoma was found at
biopsy Note prominent
gland =-
enhancement of the pineal
presumed
lymphoma. (Right) Sagiltal
TI C+ MR shows resolution
of the suprasellar mass, 5
months after treatment. Note
also a normal appearance to
the pineal gland =:lI.
Germ Cell Neoplasms, Malignant NOS

(Left) Sagiltal TI C+ FS MR
shows enhancing masses in
the suprasellar & pineal
regions in a young male
patient Imaging mimics a
germinoma. Biopsy revealed
an embryonal carcinoma.
Elevation of serum markers
~-hCC & AFP is
TI WI MR shows an
enhancing pineal mass with
hydrocephalus in this patient
with bilateral retinoblastoma.
Imaging represents trilateral
disease with a pineal tumor;,
the most common location
in trilateral disease.
Retinoblastoma (Quadrilateral) Retinoblastoma (Quadrilateral)

bilateral calcified masses in
this relinoblaslOma patient
Bilateral orbital masses occur
in 25-30% of patients with
retinoblastoma. Brain
imaging is important to
search for trilateral or
quadrilateral disease. (Right)
Axial CECT shows a large
enhancing suprasellar mass
& dilatation of the temporal
horn = in this patient with
bilateral retinoblastoma. The
familial hereditary form
accounts for essentially all
multilateral disease.
I
8
1\
c: SELLA/PITUITARY NORMAL VARIANTS
.Q
OJ
OJ
a:::
ro DIFFERENTIAL DIAGNOSIS o Beware: "Macroadenoma-appearing"
OJ
c: pituitary in young males may be
0:: Common physiologic hyperplasia, not tumor!
.: • Pituitary Hyperplasia (Physiologic)
~ • Pituitary "IncidentalOIlla"
OJ
(/)
• Pituitary "lncidentaloma" o "Filling defects" in 15-20% of normal scans
ro • "Empty" Sella (ES)
X o Cystic changes common, may be transient
--,::J Less Common • "Empty" Sella (ES)
~ o Rarely (if ever) truly empty
OJ • "Bright" Pituitary Gland
(/)
• Absent Posterior Pituitary "Bright Spot" o Intrasellar CSF, pituitary gland flattened
c: against sellar floor
III • Small Sella Turcica
"-
CO • "]"-Shaped Sella o Primary ES
"C
c:
• Considered normal variant
III
Rare but Important • Usually asymptomatic, incidental
:I • Paramedian ("Kissing") Internal Carotid finding
-'"
en Arteries • 5-10% prevalence
• Peak age 40-49 years
ESSENTIAL INFORMATION o Secondary ES
• Surgery, radiation, bromocriptine
Key Differential Diagnosis Issues therapy
• Prior to evaluating sella/pituitary, essential • Sheehan syndrome (postpartum pituitary
to know patient age, gender necrosis)
o Maximum height varies with gender, age
• 6 mm children Helpful Clues for Less Common Diagnoses
• 8 mm males, postmenopausal females • "Bright" Pituitary Gland
• 10 mm young females o Neonate: Adenohypophysis large,
• 12 mm pregnant/lactating females hyperintense on T1 WI
o Size, signal! during first 6 weeks
Helpful Clues for Common Diagnoses • Absent Posterior Pituitary "Bright Spot"
• Pituitary Hyperplasia (Physiologic) o Neurohypophysis normally has short T1
o Enlarged pituitary gland
o Commonly absent in central DI
• 10-15 mm, convex upwards o Found in up to 20% of normal patients
• Enhances strongly, uniformly • Small Sella Turcica
o May be indistinguishable from o Small or shallow bony sella can be normal
macroadenoma, lymphocytic hypophysitis o Causes pituitary gland to protrude upwards
Pituitary "Incidentaloma"
I
8 Coronal T1 c+ MR in a young postpartum lactating
female shows an upwardly bulging pituitary gland =. Sagittal T1 C+ MR in asymptomaUc adult shows
nonenhancing pituitary cyst possibly a small Rathke
Physiologic hyperplasia wid, gland measured almost 12 cleft cyst Such findings are common at both imaging
mm in height (15-20% of cases) and autopsy.
12
SELLA/PITUITARY NORMAL VARIANTS en
"
l:
III
::I
Co
.,
OJ
"Bright" Pituitary Gland III
(Left) Sagittal T1 Wt MR in an ::I

asymptomatic patient shows Ul
~
a primary empty sella with
downward herniation of CSF
into the suprasellar cistern
=. The pituitary gland is
-
ro
'-
l:
X
1ii
flallened against the sellar Ul
(1)
floor 81. (Right) Sagillal
III
T1WI MR in newborn shows -~
a large, hyperintense
adenohypophysis
normal finding.
= a
II
:J
(1)
Ql
::0
(1)
(Q
o'
:J
Small Sella Turcica Small Sella Turcica

shows a small, shallow sella
turcica~. This causes the
=
normal-sized pituitary gland
to protrude superiorfy,
mimicking macroadenoma.
(Right) Coronal T1 C+ MR in
the same patient as the
previous image shows a (fat
shallow sella turcica SI,
causing upward bulging of
the pituitary gland =.
Gland
height measured 9 mm,
normal in this young woman.
Paramedian ("Kissing") Internal Carotid

Small Sella Turcica Arteries
=
shows a small, shallow sella
and pituitary 81 in a
patient with Kallmann
syndrome with
hypopituitarism. Small sella
a/so occurs as a normal
variant, indistinguishable on
imaging alone. (Right) Axial
Tf WI MR shows "flow
voids" of both cavernous
internal carotid arteries
(lCAs), which curve much
more medially than usual
=. "Kissing carotids" are
normal variants.
I
8
13
c SELLAR/JUXTASELLARCALCIFICATION
o
Ol
Q)
cr::
co
Q)
c • Physiologic Calcification, Vascular
0.. Common
a ]uxtasellar dura, vessels, not brain
• Physiologic Calcification, Vascular
• Physiologic Calcification, Dura • Atherosclerosis, Intracranial
a Some age-related ASVD Ca++ normal,
• Atherosclerosis, Intracranial
• Saccular Aneurysm physiologic
a Relationship to stenosis, stroke
• Meningioma
• Craniopharyngioma controversial
• eurocysticercosis • Thickness of Ca++ plaque does not
correlate directly with luminal stenosis
Less Common • Dense, globular Ca++ may be more
• Astrocytoma significant than mural/laminar
a Pilocytic Astrocytoma • Some authors suggest high grade of
a Diffuse Astrocytoma, Low Grade cavernous ICA Ca++ correlates with small
a Pilomyxoid Astrocytoma (not large) vessel ischemia
a Chordoid Glioma • Saccular Aneurysm
• Dermoid Cyst a Supra/juxtasellar > intracavernous
• Arteriovenous Malformation a Mural Ca++ common
Rare but Important a Can be rim, globular
• Cavernous Malformation a Aneurysm often partial/completely
• Chordoma, Clivus thrombosed

• Pituitary Macroadenoma • Meningioma
• Chondrosarcoma, Skull Base a Ca++ 20-25%
• Rathke Cleft Cyst • Diffuse or focal
• Benign Nonmeningothelial Tumors • Solid ("brain rock") or scattered
a Chondroma • Ca++ pattern highly variable
a Osteochondroma • Psammomatous ("sand-like") or
a Osteoma "sunburst" > globular> rim
a Look for dural "tail"
a Look for changes in adjacent planum
ESSENTIAL INFORMATION sphenoidale
Key Differential Diagnosis Issues a Can cause blistering, hyperostosis,
• Is patient asymptomatic? hypertrophied ethmoid or sphenoid

• Is calcification physiologic or pathologic? sinuses ("pneumosinus dilatans")
a Physiologic • Craniopharyngioma
• Vascular (age-related changes of ASVD) a In children, 90% cystic, 90% Ca++ (rim,
• Dural (petroclinoid ligament often globular)
calcified) a Adults often solid with globular Ca++
a Pathologic • Neurocysticercosis
• Look for associated mass in/around sella, a Healed racemose NCC in basal cisterns
cavernous sinus may Ca++

• Anatomic sublocation important Helpful Clues for Less Common Diagnoses
a Dura (cavernous sinus, tentorium, • AstrocytOIua
petroclinoid ligaments) calcifies but less a Pilocytic Astrocytoma
often than falx • Common in optic
a Arteries (cavernous/supraclinoid ICA) chiasm/hypothalamus/3rd ventricle (2nd
physiologic Ca++ common most common location after cerebellum)
a Pituitary, infundibulum, hypothalamus • Enhancement varies (none to striking)
almost never show physiologic Ca++ • Ca++ uncommon in supratentorial PAs!
I a Diffuse Astrocytoma, Low Grade
8
14
SELLAR/JUXTASELLAR CALCIFICATION
III
• WHO grade II may calcify but o Hypothalamus, juxtasellar lesions :l
Co
uncommon in this location uncommon ttJ
""
• No enhancement • Chordoma, Clivus III
o Pilomyxoid Astrocytoma o 35% arise in skull base :l

(f)
• Rare tumor; common location o Epicenter at sphenooccipital
-
(1)
• Hemorrhage common, Ca++ uncommon synchondrosis 1il

<-
o Chordoid Glioma o Destructive, invasive c
x
• Newly described distinct tumor entity o Often have "thumb-like" posterior tumor 5i
Ul
• Hypothalamus/anterior 3rd ventricle extension through clivus (1)
1il
mass o 50% contain ossific fragments of destroyed .""
• Ovoid, well-circumscribed bone on NECT

• Usually solid mass; may have associated o Hyperintense on T2WI
cysts (rare) • Pituitary Macroadenoma
• Hyperdense on NECT o Most common lesion in this location
• Ca++ uncommon o Only 1-2% Ca++
• Hypointense on T1-, iso- to mildly o Can be very invasive, destructive
hyperintense on T2WI • Chondrosarcoma, Skull Base
• Enhances strongly, usually uniformly o Epicenter at petro-occipital fissure
• Dermoid Cyst o 50% have chondroid calcification in tumor
o Sellar/parasellar/frontonasal region most matrix (arcs, rings)
common site o Hyperintense on T2WI
o Unilocular fat-like cyst o Enhance strongly, heterogeneously
o Look for "droplets" in sulci, cisterns o Whorls of enhancing lines within tumor
(ruptured dermoid) matrix
o 20% have capsular Ca++ • Rathke Cleft Cyst
• Arteriovenous Malformation o Only 10-15% Ca++ vs. > 90% of
o Supra/juxtasellar < hemispheres craniopharyngioma
o 25-30% Ca++ o Calcified RCC may be indistinguishable
Helpful Clues for Rare Diagnoses • Benign Nonmeningothelial Tumors

o Chondroma, osteochondroma, osteoma
o Common lesion that commonly shows
may all show Ca++ in cap or tumor matrix
o Rare cause of juxtasellar Ca++
Ca++
Physiologic Calcification, Dura Atherosclerosis, Intracranial
I
Axial bone CT shows physiologic calcification in both Axial NEeT shows prominent calcific changes in both
8
cavernous sinus wall =
cavernous internal carotid arteries as well as dura of the
petroclinoid ligaments 81.

dorsum sellae P.:iJ and both
supraclinoid internal carotid arteries 11m caused by
atheroscferosis.
15
c: SELLAR/JUXTASELLAR CALCIFICATION
o
Ol
Q)
~
ctl
Q)
c:
D..
~- Saccular Aneurysm
ctl (Left) Axial aCT shows a
Q) giant, mostly thrombosed,
Ul
ctl saccular aneurysm. Note ring
X enhancement SI of the
--,
OJ
thrombosed segment as well
ro
Qi
as globular =and rim PJ:J
calcification. (Right) Axial
(f)
CECT shows an extensive
c: plaque-like calcification
•..
nl
Cll
"0
c:
=
along the optic nerve sheath
and left anterolateral
cavernous sinus E1.
nl
OJ
-"(f)
Craniopharyngioma Neurocysticercosis
=
(Left) Axial NECT shows rim
and globular PJ:J
calcification in a mufticystic
suprasellar mass in child.
Note fluid-fluid level SI.
Most calcified suprasellar
rnasses in children are
craniopharyngiomas. (Right)
Axial NECT shows punctate
Ca++ = in the suprasellar
and ambient cisterns from
chronic racemose
cysticercosis. (Courtesy E.
Bravo, MOJ.
Pilomyxoid Astrocytoma
calcification =
hypothalamic/suprasellar
mass in 12 year old child.
Diagnosis: Pilomyxoid
variant of pi/oeytie
astrocytoma. (Right) Axial
NECT in this 48 year old
with progressive visual
decline shows hyperdense
suprasellar mass with
globular calcifications =.
papillary subtype of
craniopharyngioma.
Chordoid glioma of 3rd
I ventricle
surgery.
was found at
8
16
SElLAR/JUXTASElLAR CALCIFICATION en
~
c:
III
:J
a.
Dermoid Cyst
...
tlJ
Arteriovenous Malformation III
(Left) Axial NECT shows a :J

mass with fat-debris level E!llI (fJ
<ll
extending from the
suprasellar cistern into the
sylvian fissure. Note
calcification ~ and fat
-
III
<-
c
x
droplets in CSF = from a
ruptured dermoid. (Right)
OJ
CJ)
~
...
hyperdense =
Axial NECT shows a slightly
calcified E!llI
mass in the right medial
-1il
\J
:J
<ll
temporal lobe. CECT scans III
showed typical findings of ;0
arteriovenous malformation. <ll
to
o·
:J
Cavernous Malformation Chordoma, Clivus

very large, partially calcified
mass 6>- extending inferiorly
from the ventricles into the
hypothalamus. (Right) Axial
CECT shows destructive
lesion of central skull base
encasing both internal
carotid arteries and
containing flecks of residual
bone or calcifications ~_
Pituitary Macroadenoma Chondroma

(LeFI) Coronal CECT shows a
large, lobulated, calcified
-1>1 intra- and suprasellar
mass that encases the right
internal carotid artery [;B
Only '-2% of
macroadenomas calcify.
(Righi) Coronal CECT shows
an inlrasellar mass with
=-
dense globular calcification
typical of benign
chondroma. No stalk was
found connecting the
chondroma to parent bone.
(Courtesy L. Cromwell, MO).
I
8
17
c ENLARGED PITUITARY GLAND
.Q
Ol
<lJ
0:: o Enhances strongly, uniformly
CIl DIFFERENTIAL DIAGNOSIS
<lJ
c
• 15-20% have incidental cyst or
a.. Common nonfunctioning microadenoma
~ • Pituitary Hyperplasia (pituitary "incidentaloma")
CIl
Q)
1Il
• Pituitary Microadenoma • Variants/mimics of "enlarged pituitary"
X
CIl
• Pituitary Macroadenoma o "Pseudoenlargement" secondary to
--,
OJ
less Common unusually shallow bony sella
]1 o Medially positioned cavernous internal
<lJ • Neurosarcoid
CIJ
• Langerhans Cell Histiocytosis carotid arteries ("kissing carotids") may
C
• Lymphocytic Hypophysitis make gland appear enlarged
III
""
10 • Pituitary Macroadenoma (Mimic) Helpful Clues for Common Diagnoses
"C
c Rare but Important • Pituitary Hyperplasia
III
o Can be normal (young menstruating
OJ
• Meningioma females)
-"CIJ
o Enlarged gland ± upward bulging
• Metastases to Gland/Stalk
o May be related to end-organ failure or
• Dural A-V Fistula
• Pituicytoma neuroendocrine tumors
• Pseudotumor, Intracranial • Pituitary Microadenoma
• Lymphoma, Primary CNS o May enlarge gland
o Best identified with dynamic,
• Leukemia
contrast-enhanced MR
• Pituitary Macroadenoma
ESSENTIAL INFORMATION o Pituitary gland can't be distinguished from
Key Differential Diagnosis Issues mass
• Not all "enlarged pituitary glands" are o Enhances strongly, often heterogeneously
abnormal! Other Essential Information

o Size/height varies with gender, age • Venous congestion (intracranial
• Children = 6 mm hypotension, dAVF) can enlarge gland
• Males, postmenopausal females = 8 mm • Beware: Child or young adolescent male
• Young menstruating females = 10 mm with "pituitary adenoma" most likely has
(can bulge upwards) pituitary hyperplasia, not neoplasm!
• Pregnant, postpartum lactating females = o Evaluate for end-organ failure (e.g.,
12mm hypothyroidism)
Pituitary Hyperplasia
I
Coronal TI c+ MR in a 51 year old man shows mildly
8 Coronal TI
pituitary gland
c+
= MR shows a physiologically
in this 28 year old lactaUng woman.
enlarged
enlarged pituitary gland I:] measuring 11mm in height.
The gland measures nearly 12 mm in height. Follow-up Note faint area of slightly less enhancement ~. An 8
scan 1 year laler was normal. mm microadenoma found at surgery.
18
ENLARGED PITUITARY GLAND
Ql
::s
Q.
..,
OJ
Ql
Neurosarcoid
::s
gland =
shows enlarged pituitary
that elevates optic
chiasm SlI. Enlarged gland is
(f)
(!)
Q)
c:::
almost ;sointense with brain c
x
in this example of classic Ei
macroadenoma. (Right) C/l
Coronal Tl C+ MR shows a ~
=
Q)
diffusely enlarged pituitary .'"
gland with subtle dural -u
thickening along the floor of ~
(!)
the middle cranial fossa SlI. Q)
This proved to be ;:0

neurosarcoidosis. (!)
co
o
~
Langerhans Cell Histiocytosis

(Left) Coronal T I C+ MR
shows a uniformly enlarged,
enhancing pituitary gland SlI
with upward extension and
displacement of the optic
chiasm = in this child with
known histiocytosis. (Right)
Sagittal Tl C+ FS MR shows
enlargement of the pituitary
gland and infundibular stalk.
The lesion resolved with
corlicosteroids and
endocrine replacement.
Pituitary Macroadenoma (Mimic) Intracranial Hypotension

shows a very shallow bony
sella SlI with optic chiasm
= draped over the pituitary.
The gland measures 9 mm,
which is normal in 79 year
old women.
"Pseudo-enlarged" gland.
(Right) Sagittal TlWI MR
shows sagging midbrain.
Note upward bulging
pituitary gland with draping
gland =
of the optic chiasm over the
postural hypotension,
intractable headaches.
I
8
19
c INTRASEllAR lESION
.2
Ol
Q)
0:::
<ll
Q)
c • Pituitary Hyperplasia
0:: Common
.: o Physiologic (e.g., young menstruating or
<ll • Pituitary Hyperplasia
postpartum females)
Q)
rn • Pituitary Microadenoma
<ll o Pathologic (end-organ failure,
X::J • Empty Sella
neuroendocrine tumors, etc.)
--, less Common
co • Pituitary Microadenoma
Qi • Pituitary Macroadenoma o < 10 mm in diameter, may enlarge gland
(f)
• Rathke Cleft Cyst o 70-90% hypointense, enhance more slowly
c
....
• Craniopharyngioma than normal pituitary
'"
!O • Neurosarcoid • Empty Sella
-0
l: Rare but Important o lntrasellar CSF collection ~ pituitary gland
'" • Lymphocytic Hypophysitis flattened against sellar floor
• Intracranial Hypotension o 5-10% prevalence on MR
• "Kissing Carotid Arteries" Helpful Clues for less Common Diagnoses

• Saccular Aneurysm • Rathke Cleft Cyst
• Meningioma o T1WI: 50% hypo-, 50% hyperintense
• Metastasis to Gland/Stalk o T2WI: 70% hyper-, 30% iso-/hypointense
• Lymphoma, Primary CNS • Look for "intracystic nodule" (45-50%)
• Dural A-V Fistula • Craniopharyngioma
• CNS Siderosis o Completely intrasellar craniopharyngioma
uncommon
ESSENTIAL INFORMATION Helpful Clues for Rare Diagnoses
Key Differential Diagnosis Issues • Lymphoma, metastasis often infiltrate
adjacent structures
• Not all "enlarged pituitary glands" are
abnormal! • Venous engorgement ~ bulging gland
o Look for intracranial hypotension, dAVF
o Size/height varies with gender, age
• Pituitary "incidentaloma" (cyst, • CNS Siderosis
o "Black" pituitary gland on T2*
non functioning adenoma) in 15-20% of
o Found with iron overload states> > SAH
normal MRs
o If it doesn't enhance, cyst is a more likely
• Thalassemia
etiology than microadenoma • Hemochromatosis
Pituitary Microadenoma Rathke Cleft Cyst
I
8 =.
Coronal T2WI MR shows a hyperintense intrasellar mass
Pre-operative diagnosis was Rathke cleft cyst. An
almost entirely cystic m;croadenoma was found at
mass =
Coronal T2WI MR shows hyperintense cystic intJasellar
found incidentally on MR. This is probably a
Rathke cleft cyst or pars intermedia cyst.
surgery.
20
INTRASEllAR lESION (fl
"
c:
III
:J
C-
...
O:!
Neurosarcoid III
(Lefl) Sagittal T1 WI MR :J
shows a hyperintense (fJ
inlra~/suprase/Jar mass = ~
that displaces the pituitary ~
gland I!::ll. Totally intra sellar '-
c:
x
craniopharyngioma without
1ii
suprasellar extension is rare. (j)
(RighI) Coronal T1 C+ MR ~
m
shows a slightly enlarged
pituitary gland =
with a
thickened infundibulum
.'"
-u
::J
(1)
above ~ in a patient with m
proven neurosarcoidosis. ;:0
(1)
co
o
::J
lymphocytic Hypophysitis
shows an enlarged,
uniformly enhancing
pituitary gland =
suprasellar extension. This
with slight
was proven to be
lymphocytic hypophysitis.
(Rig"') Coronal T2WI FS MR
shows II kissing"
(paramedian) cavernous
ICAs = projecting medially
into the selJa turcica.
Cavernous ICAs normally lie
laterally within carotid sulcus
of sphenoid bone.
eNS Siderosis
shows a mass lesion diffusely
infiltrating/expanding
pituitary gland =.
Note
extension into cavernous
sinus suggesting more
aggressive pathology. (Rig"')
Coronal T2WI MR in 9 year
old with long-standing
thalassemia major shows
profoundly hypoimense
pituitary gland =
caused by
iron overload syndrome.
I
8
21
c CYSTIC INTRASELlAR MASS
Q
OJ
OJ
cr:
Iii
OJ
DIFFERENTIAL DIAGNOSIS Helpful Clues for less Common Diagnoses
c • Obstructive Hydrocephalus
0.. Common
o Anterior recesses of 3rd ventricle enlarge
• Empty Sella (ES)
• Intracranial Hypertension, Idiopathic • Herniate inferiorly into sella
• If chronic may expand, erode bony sella
less Common • Rathke Cleft Cyst
• Obstructive Hydrocephalus o Usually < 1 em; can be giant, erode sella
• Rathke Cleft Cyst o 45% have "intra cystic nodule"
• Craniopharyngioma o ± "Claw sign" (enhancing rim of pituitary
• Arachnoid Cyst (AC) around nonenhancing cyst)
• Epidermoid Cyst • Craniopharyngioma
• Neurocysticercosis Cyst o Truly intrasellar craniopharyngioma rare
Rare but Important o If no Ca++ difficult to distinguish from
• Pituitary Apoplexy Rathke cleft cyst
• Saccular Aneurysm (Thrombosed) • Arachnoid Cyst (AC)
o Truly intra sellar AC rare
o Usually extension from suprasellar AC
ESSENTIAL INFORMATION • Epidermoid Cyst
Key Differential Diagnosis Issues o Suprasellar location < off-midline
• Cystic mass originating WITHIN sella vs. • Neurocysticercosis Cyst

intra sellar extension from suprasellar lesion o Suprasellar cysts - intrasellar
• Intrasellar extension of suprasellar lesion> Helpful Clues for Rare Diagnoses
cystic intrasellar mass • Pituitary Apoplexy
Helpful Clues for Common Diagnoses o Can be life-threatening (secondary to
• Empty Sella (ES) pituitary insufficiency)
o Small crescent of compressed pituitary o Acutely may present as necrotic,
gland lines bottom of sella turcica rim-enhancing mass

o "Primary" ES considered normal variant • Saccular Aneurysm (Thrombosed)
o "Secondary" = surgery, pituitary infarction o Medially projecting from cavernous ICA
• Intracranial Hypertension, Idiopathic o If thrombosed may appear low signal

o "Pseudotumor cerebri" F> > M intensity on Tl C+ scans
o Empty sella ± dilated optic nerve sheaths,
small ventricles
Intracranial Hypertension, Idiopathic
I
8 Sagittal T1WI MR shows empty sella with herniation of
CSF through the diaphragma sellae =.lI flattening the
Axial T2WI MR shows idiopathic intracranial
hypertension (pseudolumor cerebri) with "empty sella"
pituitary gland inferiorly against the sellar floorE:l. =.lI and dilated opUc nerve sheaths 1!:i2.
22
CYSTIC INTRASEllAR MASS
III
:;,
Co
III
.,
III
:;,
shows aqueduclaf stenosis (f)
m with severe obstructive

hydrocephalus. NOle marked
enlargement of bony sella 1:1
and intrasellar herniation of
-
~
iii
'-
c
)(
iii
inferior 3rd ventricle ~ f/l
(Right) Coronal T1 WI MR ~
iii
shows an intrasellar Ralhke
clefl cyst =.
seen here as a
CSF-like mass that displaces
0"
Ihe piWitary gland inferiorly

and laterally around it.
Arachnoid Cyst (AC)

shows a CSF-like intrasellar
mass ~ Surgery disclosed
inlrasellar
craniopharyngioma with
only a small suprasellar
component. (Right) Sagiltal
T1WI MR shows an intra·
and suprasellar arachnoid
cyst 1:1. The lesion did not
restrict on OWl,
differentiating it from
epidermoid cyst.

a large epidermoid cysl
extending into the sella and
suprasellar subarachnoid
space '-=
from the
quadrigeminal and ambient
cisterns 1:1. (Right) Sagiltal
T7 C+ MR shows suprasellar
racemose NCC CYSlS
extending into sella turcica
'-=
E!ll (fattening pituitary gland
against sellar (foor ffi
I
8
23
SUPRASEllAR MASS, GENERAL
ro DIFFERENTIAL DIAGNOSIS o Thin black line (diaphragma sellae)

<IJ
c separates mass from pituitary
CL Common o "Dural tail sign"
..: • Pituitary Macroadenoma
ro • Not pathognomonic but highly
Qj • Meningioma
VJ suggestive
ro
X • Saccular Aneurysm • Signal intensity following contrast
-,:J • Craniopharyngioma usually> tumor itself
ro • Pilocytic Astrocytoma • Saccular Aneurysm
Qj
rJ) o Most arise from circle of Willis
less Common
c: o Are usually slightly eccentric, not midline
• Dilated Third Ventricle
•..
ell
o Signal intensity may be mixed
tlI • Arachnoid Cyst
"'C
c: • Neurocysticercosis • Partial/complete thrombosis common
ell
• Rathke Cleft Cyst • Complex/disturbed flow may cause spin
:J
• Neurosarcoid dephasing
-'en" • Look for phase artifact
• Germinoma o Occasionally fusiform aneurysm/ectasia of
• Dermoid Cyst basilar artery may project into suprasellar
• Lipoma cistern
Rare but Important o Most common suprasellar mass in child
• Lymphocytic Hypophysitis o Adamantinomatous subtype
• Tuber Cinereum Hamartoma o Imaging
• Epidermoid Cyst • 90% Ca++, 90% cystic
• Pituicytoma • 90% enhance (rim ± nodule)
• Diffuse Astrocytoma, Low Grade o Second peak in middle-aged adults
• Pilomyxoid Astrocytoma • Papillary subtype
• Ectopic Neurohypophysis • Solid> cystic; Ca++ uncommon
• Metastasis • Pilocytic Astrocytoma
• Lymphoma, Metastatic o Second most common suprasellar mass in
• Leukemia children (rare in adults)
• Cavernous Malformation o Hypothalamus/optic pathways
• Tuberculoma o Pilocytic > > pilomyxoid type (see below)
• Pituitary Abscess
• Dilated Third Ventricle
ESSENTIAL INFORMATION o Most common "cystic" suprasellar mass
Key Differential Diagnosis Issues o Third ventricle enlarged secondary to
• Is mass arising from pituitary or other site? obstructive hydrocephalus
• Does it mostly involve infundibular stalk? • Arachnoid Cyst
• Is patient adult or child? o Elevates, displaces third ventricle
Helpful Clues for Common Diagnoses o Suprasellar cistern, sylvian fissures
• Most common diagnoses ("big five") account common sites
for> 75% of all suprasellar masses o Variable size cysts, enhancement
• Pituitary Macroadenoma o Reactive meningeal changes may be
o Most common of all suprasellar masses =
striking (e.g., stalk thickening, vascular
suprasellar extension of macroadenoma encasement)
o Gland, mass can't be separated
• Rathke Cleft Cyst
o Cystic, hemorrhagic changes common o Look for intracystic nodule
o Mass is the pituitary gland
o Pituitary displaced by mass
I • Meningioma
o Arises from diaphragma sellae
• Neurosarcoid
o Thickened stalk may be only sign
8
24
SUPRASELLAR MASS, GENERAL C/l
~
c:
III
o Look for dural-based masses o Infiltrating mass difficult to distinguish ::J
a.
• Langerhans Cell Histiocytosis from pilocytic astrocytoma (PA)
o Thickened stalk, child with Dl • Pilomyxoid Astrocytoma ...
OJ
!!!.
• Germinoma o Rare, more aggressive PA variant ::J
o Stalk ± gland o Infant/young child with bulky H-shaped (f)
~
o Can be only site but look for pineal mass suprasellar mass 1il
c:::
• Dermoid Cyst o Often hemorrhages (PA, low grade do not) c
x
o Fat-like ± droplets (ruptured) • Metastasis iii
(f)
• Lipoma o Gland ± stalk mass in patient with known C1>
o Fatty mass stuck on hypothalamus primary ..•

0>
o Use fat-saturated Tl WI • Lymphoma, Metastatic

Helpful Clues for Rare Diagnoses o Destructive, infiltrative mass engulfs gland,
• Lymphocytic Hypophysitis stalk
o Thick, nontapering stalk ± pituitary mass • Leukemia
o Diabetes insipidus common o Gland/stalk + sinus mass clues
o Often occurs in peripartum females • Cavernous Malformation
• Tuber Cinereum Hamartoma o "Popcorn ball" mass
o Clinical presentation helpful (gelastic o Third ventricle, optic chiasm rare sites
seizures; male with precocious puberty) • Tuberculoma
o Can be "collar button" or "sessile" o TB meningitis> > frank tuberculoma in
o Between infundibulum (anteriorly), suprasellar cistern
mammillary bodies (posteriorly) o Focal mass wiring enhancement common
o Signal intensity like cortex o If caseating, mass is hypointense on T2WI
o Does not enhance o If non caseating, mass generally
• Pituicytoma hyperintense on T2WI
o Low grade (WHO I) glial neoplasm of • Pituitary Abscess
infundibulum or neurohypophysis o Very rare but potentially life-threatening
oM> F, most patients 40-60 years o May resemble pituitary apoplexy at
o Hypopituitarism, visual disturbances imaging
o Well-demarcated, homogeneously • Cystic-appearing intrasellar mass with
enhancing infundibular mass suprasellar extension
• Diffuse Astrocytoma, Low Grade • Hypodense on NECT
• Hyperintense on T2WI
• Rim-enhancing
I
=.
Sagittal T 1 C+ FS MR shows a pituitary macroadenoma
The pituitary gland cannot be seen separate from
Sagittal T7 C+ MR shows a classic suprasellar
meningioma arising from the diaphragma sellae Idl
8
U,e mass. The mass is the gland, which is diffusely which clearly separates the mass from the normal
enlarged by the tumor. =.
pituitary below Ell. Note dural "tails"
25
c SUPRASELLAR MASS, GENERAL
Q
Ol
Q)
a::
co
Q)
c
0...
Saccular Aneurysm
..:
co (Left) Sagittal T7 WI MR
Q) shows a farge, mixed signal
rn
co intensity, suprasellar mass
X =. Laminated clot of
--,
OJ
different ages gives mass an
ro "onion skin" appearance.
Q) Note residual patent lumen
(f)
81. (Right) Sagillal T7WI MR
C shows a craniopharyngioma
III
"- 81 with variable T7
ell shortening within the
"'C multilocu/aled cystic
C
III components. The pituitary
gland PJ:J:l is clearly distinct
:s
.>t:. from the mass .
en
Pilocytic Astrocytoma Dilated Third Ventricle

shows a large pi/ocytic
astrocytoma, seen here as a
lobulated inhomogeneously
enhandng suprasellar mass
=. Pituitary 81 is clearly
separate from the mass.
shows obstructive
hydrocephalus with a dilated
3rd ventricle 81. The large
anterior recesses compress
and displace the infundibular
stalk and hypothalamus
inferiorly.
=
Arachnoid Cyst Neurocysticercosis

shows a class;c suprasellar
arachnoid cyst. Note that the
CSF-Iike suprasellar mass =
elevates the 3rd ventricle
and displaces the
infundibular stalk anteriorly
81. (Right) Sagiltal T7 WI MR
in a patient with known
neurocysticercosis shows a
markedly thickened
inFundibulum e.'I as well as
multiple supra- and
intrasellar cysts =. 8asal
cistern lesions are common
in NCe.
I
8
26
SUPRASELLAR MASS, GENERAL
Rathke Cleft Cyst Neurosarcoid

(Lefl) Sagittal TI WI MR
shows a typical Rathke cle(t
cyst. Note that the
well-delineated hype,intense
sup,asellar mass I:] is clearly
distinct from the pituitary
gland below PJ:ll. (RighI)
Sagillal T1 C+ MR in a
sarcoidosis and diabetes
insipidus shows a thickened,
enhancing infundibulum =.
This was the only intracranial
finding.
(Leh) Sagillal T1 C+ MR in a
child with known
histiocytosis and diabetes
insipidus shows a strongly
enhancing mass involving
the infundibular stalk and
hypothalamus 1:]. (RighI)
Sagillal T1 C+ MR shows a
germinoma with sellar 81
and suprasellar
involvement. The
=
infundibular stalk is markedly
thickened, while the pineal
gland is normal.
(Lefl) Sagillal T1 C+ MR
shows a ruptured dermoid
cyst 81 with a large
supra/parase/Jar component.
Note multiple high signal
intensity droplets I:]
scallered throughout the
subarachnoid space. (RighI)
Sagillal T1WI MR shows a
hypothalamic lipoma
seen here as a lobulated
=-
hyperintense mass above
and behind the sella. This
was an incidental finding in
an asymptomatic patient.
I
8
27
c SUPRASELLAR MASS, GENERAL
.Q
Ol
Q)
cr:
ro
Q)
c
0:: Tuber Cinereum Hamartoma
..:
ro (Left) Sagittal T1 C+ FS MR
Q) in a 19 year old pregnant
(fl
ro woman shows a uniformly
X enhancing sellar/suprasellar
--,:J mass m. Note reactive dural
ro thickening 81. Lymphocytic
Qi hypophysitis was found at
(fJ
surgery. (Rig!Jt) Sagittal T 1 WI
m
..
C
I1l
MR shows a classic luber
cinereum hamartoma m.
The hamartoma looks like a
"t:l "collar button" of gray
c
I1l matter interposed between
the infundibulum and
mammillary bodies.

an epidermoid cyst =. The
lobulated CSF-like mass
extends into the suprasellar
!:ill and quadrigeminal 81
cisterns. (Right) Sagitlal T1
C+ MR shows a pituicytoma,
seen here as a large solid
infundibular mass !:ill with
mild mass effect on the optic
chiasm and anterior 3rd
ventricle.
Diffuse Astrocytoma, Low Grade Pilomyxoid Astrocytoma

mass =
shows a rounded enhancing
separate from
pituitary gland below Ell
displaced optic chiasm
above !:ill. Grade 11fibrillary
astrocytoma of
hypothalamus (possibly
infundibular stalk) was found
at surgery. (Right) Coronal
T2WI MR in a 21 year old
man with sudden headache
and visual problems shows a
hemorrhagic suprasellar
mass =. Initial diagnosis
was pi/oeytie astrocytoma.
I Final diagnosis was PMA.
8
28
SUPRASELLAR MASS, GENERAL en
,.-
r::
Ql
::l
Co
.,
[Jl
Metastasis Ql
::l
shows posterior pituitary en
ectopia, seen here as a !E.
hyperintense focus !:>J along !iI
c....
the upper infundibulum. r::
x
Note a small pituitary gland iii
Ell with an absent "bright en
= CD
spot". (Right) Sagittal T7 C+ Q)
MR shows a metastasis -.,
enlarging the infundibulum,
extending into the pituitary
gland ~ This was the only
intracranial manifestation of
metastatic lung carcinoma.
lymphoma, Metastatic leukemia

shows a destructive, diffusely
infiltrating mass with
signiHcant infra-, 5upra- and
relrose/Jar extension =.
Lesion enhanced strongly.
quite uniformly on T7 C+
scans (not shown) and
demonstrated "dural tail
sign" Ell. (Right) Coronal
CECT shows opacification of
sphenoid sinus Other
images (not shown)
disclosed lobulated
mucosal-based masses in the
maxillary/ethmoid sinuses.
Note rounded, thickened
infundibular stalk =.
Tuberculoma
shows suprasellar "popcorn
ball" of mixed signal intensity
~ appearing to arise within
3rd ventricle. Type 2
cavernous malformation was
diagnosed. (Right) Axial
CECT shows a tuberculoma
= in the suprasellar cistern,
seen here as a
ring-enhancing mass. Note
accompanying findings of TB
meningitis Ell. (Courtesy S.
Candy, MO).
I
8
29
c SUPRASEllAR MASSES, PEDIATRIC
.Q
Ol
Q)
0::
co DIFFERENTIAL DIAGNOSIS o Optic chiasm/hypothalamus: Pilocytic or
Q)
c pilomyxoid astrocytoma, tuber cinereum
CL Common hamartoma, lipoma
..: • Pilocytic Astrocytoma
.!!1 o Third ventricle: Hydrocephalus> >
Q)
en • Craniopharyngioma neoplasm
co • Pituitary Hyperplasia (Physiologic)
X • T1 hyperintense suprasellar mass in child?
-
....,
:J
.!!1
(jj
CI)
• Hydrocephalus
less Common
Think craniopharyngioma,
posterior pituitary ectopia
lipoma, dermoid,
• Germinoma Helpful Clues for Common Diagnoses

C
• Tuber Cinereum Hamartoma • Pilocytic Astrocytoma
...
<0
CD • Arachnoid Cyst o Most PAs occur in children 5-15 years old
"C
c • Langerhans Cell Histiocytosis o Enlarged optic nerve/chiasm/tract
co
• Pituitary Stalk Anomalies o Usually solid, iso-/hypointense on T1 WI;
:J
...:
CI)
• Teratoma hyperintense on T2WI, FLAIR
Rare but Important o Variable enhancement (none to intense)
• Lipoma o If large, bulky H-shaped mass in infant,
• Pituitary Macroadenoma may be pilomyxoid variant
• Dermoid Cyst • Craniopharyngioma
• Leukemia o 90% Ca++ (globular, rim)
• Pilomyxoid Astrocytoma 090% cystic (may have multiple)
• Saccular Aneurysm o 90% enhance (rim, nodule)
• Retinoblastoma (Trilateral) o Density/signal intensity within
• Lymphocytic Hypophysitis cysts/locules varies with content
• Lymphoma, Primary CNS • Pituitary Hyperplasia (Physiologic)
• Rathke Cleft Cyst o Up to 10 mm height, convex superior
margin in young menstruating females
o "Macroadenoma-appearing" mass in child?
ESSENTIAL INFORMATION • May be hyperplasia, not tumor
Key Differential Diagnosis Issues (especially prepubescent male)!
• Is mass extra- or intra-axial? • Hydrocephalus
• Extra-axial masses arise from o Enlarged 3rd ventricle (aqueductal
pituitary/infundibulum, meninges, vessels stenosis, obstructive hydrocephalus)
o If extra-axial mass appears to arise from o Anterior recesses protrude inferiorly
pituitary/infundibulum, determine origin o May enlarge bony sella over time
of mass as precisely as possible Helpful Clues for less Common Diagnoses
• Pituitary gland: Think physiologic • Germinoma
hyperplasia, hypophysitis, o 50-60% involve pituitary gland/stalk
macroadenoma (rare in children) o Often presents with diabetes insipidus (DI)
• Infundibular stalk: Germinoma, • Tuber Cinereum Hamartoma
histiocytosis; stalk anomalies, o Isosexual precocious puberty> gelastic
lymphoma, leukemia (rare) seizures
o Nonpituitary extra-axial masses (normal o Pedunculated ("collar button") or sessile
pituitary gland can usually be identified mass between infundibular stalk,
inferior to lesion) mamillary bodies
• Craniopharyngioma • Can be tiny (1-2 mm) or giant (3-5 em)
• Hydrocephalus • Isointense with gray matter (occasionally
• Arachnoid cyst slightly hyperintense on FLAIR)
• Saccular aneurysm • Doesn't enhance
• Intra-ax.ial masses arise from
I chiasm/hypothalamus/3rd ventricle
• Arachnoid Cyst
o 10% suprasellar
o Sharply marginated CSF-like cyst
8
30
SUPRASEllAR MASSES, PEDIATRIC
III
a Sagittal Tl- or T2WI shows 3rd ventricle • Fat suppression sequences confirm :l
C.
elevated, compressed over cyst 020% Ca++
.,
OJ
a Suppresses on FLAIR,DWI negative • Leukelnia III
:l
• Langerhans Cell Histiocytosis a Rare; look for other lesions (sinuses, dura)
(fJ
a Child usually < 2 years old • Pilomyxoid Astrocytoma CD
• May have central DI

a 10% of LCH cases involve stalk, pituitary
a Rare variant of PA
a Large, bulky suprasellar mass in infant
-
Q)
'-
c
X
iii
gland ± hypothalamus a May hemorrhage (rare in PA) Vl
• Rare: Choroid plexus, leptomeninges, • Saccular Aneurysm ~

Q)
cerebellar WM, brain parenchyma a Rare in children « 2% of all saccular -.,
II
a Look for solitary/multiple lytic skull aneurysms occur in pediatric age group) OJ
CD
lesions with "beveled edges" a When occur, often large/bizarre OJ
• Pituitary Stalk Anomalies a Thrombus common

a Posterior pituitary ectopia a Look for residual patent lumen, phase
• Short stature ± endocrine deficiencies artifact
• Posterior pituitary "bright spot" missing • Retinoblastoma (Trilateral)
• Mislocated along tuber cinereum a Third tumor in pineal or suprasellar region
• Stalk small/absent • Lymphocytic Hypophysitis

a Duplicated pituitary gland/stalk a Adolescent> child
• Endocrinologically normal a May cause DI
• ± Midline facial anomalies a Can mimic macroadenoma, pituitary
• Tuber cinereum/mamillary bodies fused apoplexy
• Teratoma • Lymphoma, Primary CNS
a Optic chiasm> pineal a Rare in children
a Ca++, cysts, soft tissue, fat a Can mimic hypophysitis, germinoma, LCH
Helpful Clues for Rare Diagnoses • Rathke Cleft Cyst
a Rare in children
• Lipoma a Cyst in/above pituitary, separate from stalk
a Fatty hypothalamic mass
a Rarely calcifies, does not enhance ("claw"
• Pituitary Macroadenoma
of enhancing pituitary tissue may
a "Figure-of-eight" pituitary mass
surround mass)
a Gland can't be separated from mass
a Intracystic nodule virtually
• Dermoid Cyst
pa thognomonic
a Fat-like mass ± droplets in CSF
I
Coronal T7 C+ MR shows chiasmatic glioma.
prechiasmaUc optic nerves are expanded
The
and
Coronal
pilocytic
T7 c+ MR shows a very large suprasellar
astrocytoma. This solid and cystic mass
8
surrounded by enhancing tumor. involves the suprasellar cistern, the chiasm, the
hypothalamus and protrudes into the 3rd ventricle.
31
c SUPRASELLAR MASSES, PEDIATRIC
.Q
OJ
Q)
a:
ro
Q)
c
a::
..:
ro (Left) Sagittal T1 WI MR
Qi shows typical cysts of
(/)
ro varying signal intensity in the
)( suprasellar cistern~ herniating
-,::J into the 3rd ventricle. There
co is enlargement of the bony
Qi sella and erosion of the
(f)
dorsum sella =:1. (Right)
C Coronal T2WI MR shows
I'll
~ calcification allhe base of
co the lesion 81.
"0
c
I'll
Germinoma
shows large pituitary gland
=:1 projecting above shallow
pituitary fossa following
prolonged shunting. Note
associated thickened
calvarium 81. (Right)
typical synchronous
suprasellar =:I, pineallaJ
masses in teen who
presented with signs of t
intracranial pressure. Note
increased signal in body of
corpus callosum at site of
hippocampal commissure
disruption c;. caused by
acute hydrocephalus.
(Leh) Sagittal T1 C+ MR in
the same patient shows
inhomogeneous
enhancement II1~LThe
suprasellar mass perches on
dorsum sella; the pineal
obstructs the aqueduct.
shows a large nonenhancing
pedunculated mass =:1
extending from tuber
cinereum between mamillary
bodies and infundibular stalk
in a child with ge/astic
seizures.
I
8
32
SUPRASELLAR MASSES, PEDIATRIC ,...
C/l
c::
CIl
::J
Q.
.,
III
Tuber Cinereum Hamartoma Arachnoid Cyst CIl
(Left) Axial FLAIR MR shows ::J
mildly increased signal (J)
(!)
intensity within the
hamarlOma =.
Unlike small
OJ
~
'-
hamartomas, which foJ/ow c
x
gray maLLersignal on T2 and 6i
FLAIR sequences, large (fl
(!)
hamarlOmas may be slightly
OJ
brighter on FLAIR and T2 0"
than gray matter. (Right) 3l
Coronal T2WI MR shows ::J
(!)
erosion of the dorsum sella, OJ
upward displacement of the ;u
hypothalamus, and extension (!)
<0
inlO the right middle cranial 0'
fossa caused by suprasellar ::J
arachnoid cyst =.
Langerhans Cell Histiocytosis Pituitary Stalk Anomalies

(Lefl) Sagittal T1 C+ MR in a
teen shows nodular
thickening of infundibular
recess ~, Additionally,
there is a tiny pars
intermedia cyst e.1. Note
upwardly convex pituitary
gland (normal physiologic
hyperplasia) =,(Right)
thickening of the tuber
cinereum {tubomammillary
fusion) = in a child with 2
pituitary glands ~ due 10
maternal genetics. Both
glands are bright on T1 WI
images in the premature
newborn.
Teratoma
(Left) SagiLLalT1 WI MR
shows bright fat with a
central focus of calcification
=. There is a soft tissue
mass ~ in the region of the
tuber cinereum in this child
who had multiple other
congenital anomalies. (Right)
Axial FLAIR MR in the same
patient shows heterogeneous
suprasellar teralOma ffi
metopic synostosis =
dehiscent tentorium Ea. A
small nodule of
perivenlricular heterotopia is
also seen in wall of right
=,
temporal horn
I
8
33
c SUPRASELLAR MASSES, PEDIATRIC
Q
OJ
Q)
cr:
ro
Q)
c
0::
..:
ro (Left) Axial T1 WI MR shows
~ a multilobed lipoma l:ll in
CO the suprasellar cistern.
"§ (Right) Sagittal T1 C+ FS MR
::::?: in the same patient shows
ro loss of signal in lipoma l:ll
-a> {ollowing fat saturation.
(/)
C
l\l
"-
CO
"C
l\l
Pituitary Macroadenoma Pituitary Macroadenoma

shows a large bilobed sellar
and suprasellar !:i12
macroadenoma in a teenager
with acromegaly. Note also
the enlarged frontal sinuses
81. (Right) Coronal T1 C+
MR shows a fairly
macroadenoma 81 that
abuts the cavernous sinus in
the same acromegaJ;c teen.
Note thickened scalp l:ll.
Pilomyxoid Astrocytoma Saccular Aneurysm

shows a large, very
hyperintense, suprasellar
pilomyxoid astrocytoma that
displaces the mesencephalon
posteriorly. (Right) Sagillal
T2WI FS MR in a newborn
shows a large, lobular,
thrombosing, suprasellar
saccular aneurysm lID.
I
8
34
SUPRASEllAR MASSES, PEDIATRIC
III
::l
Co
.,
OJ
III
::l
(Left) Axial MRA shows
obliteration of the right distal Ul
~
internal carotid artery and
faint increased signal in the
posterior ~ aspect of the
thrombosing aneurysm.
-
III
L
C
X
~
III
(Right) Coronal T2WI MR (J)
shows a large low signal ~

1il
-.,
suprasellar mass ~ that
abuts the hypothalamus. -u
Patient had ocular :J
CD
retinoblastoma. III
;0
CD
(Q
O·
:J
Retinoblastoma (Trilateral)
(Left) Coronal T1 C+ MR in
intense, uniform
enhancement. Note bilate,al
cavernous sinus invasion =.
(Right) Sagittal T1 C+ rsMR
in a pregnant teenager who
developed acute onset of
vision problems in lale 3rd
trimester shows large
enhancing mass = with
reactive dural thickening 61.
macroadenoma.
Rathke Cleft Cyst

shows thickening ~ and
subtle enhancement of the
infundibular stalk, chiasm,
and tuber cinereum. (Right)
Coronal T2WI MR shows a
well-delineated suprasellar
cyst =. The pituitary gland
and stalk are not seen, and
there was no calcification on
high resolution NECT.
I
8
35
SUPRASEllAR CYSTIC MASS
DIFFERENTIAL DIAGNOSIS • Usually longstanding, "compensated" so

no transependymal CSF
Common • Arachnoid Cyst
• Enlarged Third Ventricle o 10% of ACs suprasellar (SSAC)
o Obstructive Hydrocephalus o Sharply marginated CSF density/signal
o Aqueductal Stenosis intensity mass
• Arachnoid Cyst • Suppresses on FLAIR
• Craniopharyngioma • Does not restrict on DWI
• Neurocysticercosis (NCC) o 3rd ventricle elevated, displaced over AC
t: • Displaces temporal lobes laterally
'iij less Common
•..
aI • Displaces midbrain, pons posteriorly
• Rathke Cleft Cyst
• Infundibular stalk typically displaced
"t:
III
• Dermoid Cyst
• Epidermoid Cyst anteriorly
• Enlarged Perivascular Spaces (PVSs) • "Mickey mouse ears" on coronal = cyst +
lateral ventricles
Rare but Important
o If large, may also cause obstructive
• Pituitary Macroadenoma hydrocephalus
• Pituitary Apoplexy • Craniopharyngioma
• Astrocytoma o 90% of childhood craniopharyngiomas
o Pilocytic Astrocytoma
cystic
o Pilomyxoid Astrocytoma
• Cyst fluid hyperdense/intense to CSF
• Ependymal Cyst o 90% have some Ca++ (globular or rim)
• Saccular Aneurysm o 90% enhance (rim, nodular)
o Suprasellar cistern> > within 3rd ventricle
ESSENTIAL INFORMATION • Neurocysticercosis (NCC)
o Look for "clusters" of cysts in subarachnoid
Key Differential Diagnosis Issues cisterns ("racemose" CC)
• Where does the mass originate? o Look for cyst + scolex
o Third ventricle: Think hydrocephalus>
o FLAIRbest sequence to detect (cyst fluid
intraventricular cystic mass (ependymal doesn't suppress completely)
cyst, craniopharyngioma)
o Suprasellar cistern: Arachnoid, other Helpful Clues for less Common Diagnoses
congenital/infectious cysts • Rathke Cleft Cyst
o Pituitary gland/sella turcica: o 60% purely suprasellar or intra sellar with
Necrotic/cystic neoplasm suprasellar extension
o Brain parenchyma: Enlarged perivascular o Variable density/signal intensity
spaces, cystic/low density neoplasm • Usually t compared to CSF
• 10% calcify (curvilinear, in cyst wall)
Helpful Clues for Common Diagnoses o Look for
• Enlarged Third Ventricle • Intracystic nodule (45%)
o CSF density/signal intensity
• "Claw" of compressed, enhancing
o No enhancement (unless infection, pituitary displaced around cyst
neoplasm) • Dermoid Cyst
o Obstructive Hydrocephalus o Most common site = sellar/parasellar,
• Can be intra- or extra-ventricular frontonasal
(noncommunicating or communicating) o Fat densi ty/signal intensity
• If acute, periventricular "halo" of o 20% have capsular Ca++
transependymal CSF o Look for evidence of rupture
• "Cystic mass" = dilated 3rd ventricle • Fat droplets in subarachnoid spaces
o Aqueductal Stenosis
• Fat-fluid levels in ventricles
I • t Lateral, 3rd ventricles
• Normal 4th ventricle
• Chemical shift artifact in frequency
encoding direction
8
36
SUPRASELLAR CYSTIC MASS ,...
C/l
c
Ql
• Epidermoid Cyst o Compression/edema of hypothalamus, :l
Q.
o Rare in suprasellar cistern optic chiasm/tracts may cause III
""
o Lobulated, insinuating growth pattern hyperintensity on T2WI Ql
:l
0> 95% hypodense (similar to CSF) o Restricts on DWI
(JJ
• FLAIR,DWI best to distinguish o Markedly hypointense on ADC ~
epidermoid from AC, enlarged 3rd
ventricle
• Astrocytoma
o Pilocytic > > pilomyxoid astrocytoma
-
Q)
'x-
c
Oi
• Epidermoid doesn't suppress completely, o Most suprasellar astrocytomas are solid, en
restricts on DWI not grossly cystic ~
OJ
• Enlarged Perivascular Spaces (PVSs) • Ependymal Cyst 0""
o Usually variable-sized "clusters" o Rare; 3rd ventricle least common site

o Off-midline (basal ganglia) o Round/ovoid; CSF-like
o Round or ovoid (basal ganglia), linear • Saccular Aneurysm
(white matter) o Aneurysms may be associated with true
o Like CSF on all sequences (contain perianeurysmal cysts
interstitial fluid) • Obstructed perivascular spaces posited as
• Suppresses completely on FLAIR etiology
• Does not restrict on DWI o Partly or completely thrombosed may have
Helpful Clues for Rare Diagnoses "cystic"-appearing foci within clot

• Pituitary Macroadenoma • Rare
o Solid ± intra- or extra tumoral cysts
• Acute thrombosis can present with
panhypopituitarism, SAH
• Extratumoral cysts may be
o Imaging can mimic necrotic adenoma
trapped/enlarged PVSs or arachnoid cysts
• Hypodense center, iso-/hyperintense rim
• Cysts often hyperdense/intense
on TlWI
compared to CSF
o Solid> rim enhancement
• Look for mixed age laminated clot
• "Blooms" on GRE
• Pituitary Apoplexy
o Rare; may be life-threatening (severe
• Rim may enhance
panhypopituitarism)
o Necrotic pituitary with little/no
enhancement (may show rim)
o Hemorrhage may bloom on T2* (GRE,
SWI)
I
=-
Sagillal T2WI MR shows EVOH wilh markedly enlarged Sagillal T2WI MR shows massively enlarged 3rd SlI and
8
laleral 3rd El and 4lh I!:1\'l ventricles. A CSF
suprasellar mass caused by an enlarged 3rd venlficle
was diagnosed.
=-
laleral ventricles, an enlarged "funnel-shaped" aqueducl
=.
and a medial atrial diverticulum R> compressing
the 4th ventricle
37
c SUPRASEllAR CYSTIC MASS
o
Ol
Q)
0::
CIl
Q)
c
0..
~- Arachnoid Cyst
.!l1 (Left) Sagiltal T2WI FS MR
Q) shows a lobulated, sharply
(f)
CIl marginated, CSF-like,
X suprasellar cyst =:I extending
-,:J into the sella 8l elevating
co the 3rd ventricle ICR and
Qi causing obstruclive
(f)
hydrocephalus. (Right)
c Coronal T2WI FS MR in an 8
'..."
llJ
year old child with delayed
growth shows a hyperintense
"0 suprasellar mass =:I that
c
slightly compresses and
'" displaces the pituitary gland
SI toward the lelt.
Rathke Cleft Cyst

shows a suprasellar cystic
mass = and a moderate
compensated
hydrocephalus. Another cyst
is present in the right Meckel
cave 81 in this patient with
racemose NCe. (Right)
Sagittal T1 C+ MR shows an
intra- and suprasellar cyst
that does not enhance. Note
the displaced pituitary gland
and infundibular stalk =:I
form a "claw" around the
lesion.
Dermoid Cyst
large, mixed density
suprasellar and subfrontal
mass =:I. Low density
"droplets" that resemble fat
are seen in the adjacent
sylvian fissure E1 in this
patient with a ruptured
dermoid. (Right) Axial T2WI
MR shows an epidermoid
cyst in the suprasellar cistern,
widening the
interpeduncular fossa .:=
and extending into the
ambient and quadrigeminal
cisterns.
I
8
38
SUPRASELLAR CYSTIC MASS en
"
c:
Ql
:l
Co
..•
lJl
Ql
(Left) Sagillal TI WI MR in a
:l
1S year old with headaches (f)
CD
shows multiple CSF-like cysts
Q)
in the hypothalamus, c::
thalamus, and midbrain ~ c:
x
that bulge into the OJ
suprasellar subarachnoid Ul
space [;8 (Right) Axial TI ~

Q)
C+ MR shows 2 -~
neoplasm-associated cysts: A -u
large trapped perivascular :l
CD
space 81 caused by a Q)
pituitary macroadenoma ;0
and a small imrawmoraJ cyst CD
<0
~ within the adenoma. o·
:l
(LeFt) Axial CECT shows

pituitary apoplexy caused by
a necrotic pituitary
macroadenoma I::l. Imaging
appearance resembles a
thrombosed aneurysm.
shows a very hyperintense
suprasellar mass, almost as
bright as CSF A thin rim of
normal-looking brain borders
the mass ffi indicating its
intra-axial origin.
(Left) Sagillal STIR MR with

a close-up view shows a
large cystic lesion within the
3rd ventricle =.
The lateral
ventricles 81 are markedly
enlarged, but the 4th
ventricle ~ is normal.
shows a partially thrombosed
saccular aneurysm =. Part
of the clot is very hypodense
P!:J and is seen here as a
mass in the posterior
suprasellar cistern.
I
8
39
c
.Q CALCIFIED SUPRASELLAR MASS
OJ
OJ
0:::
ell DIFFERENTIAL DIAGNOSIS • Meningioma
OJ
C o Psammomatous (sand-like) Ca++
Cl.. Common o Solid> rim enhancement
~-
ell • Atherosclerosis, Intracranial o Middle-aged, older patients (unless NF2)
OJ
en • Craniopharyngioma • Aneurysm
ell
><::> • Meningioma o Saccular Aneurysm
-
--,
ell
OJ
(/)
• Aneurysm
o Saccular Aneurysm
o Fusiform Aneurysm, ASVD
• Calcification less common than with
fusiform aneurysm, ASVD
• Curvilinear (peripheral arcs, rings)
C
ltI Less Common pattern
~
co • Neurocysticercosis o Fusiform Aneurysm, ASVD
'0
c • Pilocytic Astrocytoma • Linear ± rim Ca++
ltI
• Dermoid Cyst • Ca++ often present in other vessels
• Pituitary Macroadenoma • Neurocysticercosis
• Tuberculosis o Nodular calcified stage
• Chondroid Tumor o Usually parenchymal> > cisternal Ca++
o Common in children, young adults
ESSENTIAL INFORMATION o Ca++ uncommon in hypothalamic PA
Key Differential Diagnosis Issues • Dermoid Cyst
• Is Ca++ curvilinear, punctate, globular, etc.? o 20% have capsular Ca++
• Does lesion enhance? o Contain lipid
o Look for evidence of rupture (fatty droplets
in subarachnoid spaces, cisterns)
• Atherosclerosis, Intracranial o No enhancement unless chemical
o Curvilinear Ca++
meningitis
o Usually bilateral
o Often multifocal Helpful Clues for Rare Diagnoses
o Older patients • Only 1-2% of macroadenomas calcify
• Craniopharyngioma • TB, healing/healed granulomatous infections
o Globular, punctate, &/or ring Ca++ cause parenchymal> > cisternal Ca++
o Younger patients (older adult tumors more • Chondromas, enchondromas arise from
often solid, Ca++ less frequent) central base of skull
Atherosclerosis, Intracranial
I
8 the suprasellar cistern =
Axial NEeT shows a fusiform, parUally calcified mass in
that represents an ectaUc~
supraclinoid, internal carotid artery with calcified
Axial NEeT shows a cystic suprasellar mass with
globular and rim calcificaUons =. Note fluid-fluid level
within one of the cysts m. This is an example of classic
atherosclerotic plaque. craniopharyngioma.
40
CALCIFIED SUPRASELLAR MASS ,...
VI
C
Ql
:J
Co
...
OJ
Ql
(Left) Axial NECT shows a :J

en
=
hyperdense suprasellar mass
with Focal calciFications
m in this patient with cfassic
CD
Q)
c::
meningioma arising from the c
X
central skull base. (Right) 1ii
Axial NECT shows a huge, (f)
well-delineated hyperdense ~
Q)
suprasellar mass with rim -""'
calciFications =. The -0
:J
diagnosis: Giant mostly
CD
thrombosed, saccular Ql
aneurysm. ;0
CD
CO
o·
:J
Fusiform Aneurysm, ASVD Neurocysticercosis

hype,dense FusiFormbasi/ar
artery aneurysm 81 and
calcified fusiform aneurysmal
ectasias of both internal
carotid arteries =. (Right)
Axial NECT shows a
suprasellar, ambient cistern
Ca++ = in this patient with
racemose Nee, multiple
cysts. (Courtesy E. Bravo,
MO).
Dermoid Cyst
with rim =
low density suprasellar mass
and globular
calciFication 81. Biopsy
disclosed pilomyxoid variant
of pi/oeytie astrocytoma.
large hypodense calciFied
suprasellar mass aD. Note fat
density droplets 81 in
subarachnoid space. This is a
ruptured dermoid cyst.
I
8
41
c ENHANCING SUPRASElLAR MASS
o
Ol
Q)
tr o Meningioma: Mass distinct from gland
Q)
C (hypointense diaphragma sellae separates
c:: Common mass above from pituitary gland below)
• Pituitary Macroadenoma • Saccular Aneurysm
• Meningioma o Coronal plane helpful in distinguishing
• Saccular Aneurysm aneurysm from normal pituitary
• Craniopharyngioma o Look for phase artifact, "flow void" on MR
• Pilocytic Astrocytoma • Craniopharyngioma
Less Common o 90% Ca++, 90% cystic, 90% enhance
..
C
III
1IJ
• Neurosarcoid
o Papillary variant (more common in adults)
may be solid, noncalcified, enhances
"tl
• Langerhans Cell Histiocytosis strongly
c
III
• Germinoma • Pilocytic Astrocytoma
• Lymphocytic Hypophysitis o More common in children
o Expands hypothalamus, optic chiasm, may
Rare but Important extend into optic nerves/tracts
• Metastasis o Variable enhancement
• Lymphoma o Pilomyxoid variant
• Leukemia • Infant> child
• Aggressive behavior
ESSENTIAL INFORMATION • Large, bulky tumor with lateral extension
to temporal lobe common
Key Differential Diagnosis Issues • Hemorrhage in 20-25%
• Effect of age on differential diagnosis
important Helpful Clues for Less Common Diagnoses
• Common lesions ("big five") account for > • Histiocytosis, germinoma in children/young
75% of all suprasellar masses adults
• Most other lesions < 1-2% each • eurosarcoid in older patients
• Differential diagnosis narrows if mass Helpful Clues for Rare Diagnoses
confined to infundibulum • Solitary metastasis to gland/stalk rare
Helpful Clues for Common Diagnoses • Lymphoma, leukemia usually with systemic
• Macroadenoma vs. Meningioma disease
o Macroadenoma: Gland can't be identified
separate from mass
I
8 Coronal T1 C + M R shows inhomogeneously enhancing
intra- and suprasellar mass =. Pituitary gland can't be
Coronal TI c+ FS MR shows suprasellar enhancing
mass 81 separated from normal pituitary gland below
found separate from and indeed IS the mass. =.
P:!.':l by thin black line of diaphragma sellae
42
ENHANCING SUPRASEllAR MASS ,..
en
c:
III
::::l
c..
..•
OJ
III

::::l
=
suprasellar enhandng mass
with prominent phase
artifact E!llI caused by large
(f)
-
C1l
Q)
basilar lip aneurysm with '-

c
><
slow intralumcnal flow. fii
(Right) Coronal T1 C+ MR in (j)
a child shows ~
Q)
intra·/supraseJlar mass. -~
Apical nonenhancing portion
is surrounded by thin
enhancing rim PJ:;}lI. Solid
portion enhances strongly
but heterogeneously =.
shows enhancing suprasellar
=
mass involving optic chiasm
hypothalamus E!llI with
pial enhancement along
inFerior fronta/lobe~.
Lesion a/so involved optic
nerve. (Right) Sagittal T1 C+
MR in child with diabetes
insipidus, known LCH,
shows thickened enhancing
pituitary stalk mass
extending into
=
hypothalamus.
in 22 year old man with
diabetes insipidus shows
hydrocephalus, enhancing
sellar/suprasellar mass.
Germinoma commonly
presents with 01;
macroadenoma oflen has
visual defects. (Right)
Coronal T1 C+ FS MR in a
19 year old pregnant woman
with acute vision problems
shows enhancing
intra-/suprasellar mass =.
macroadenoma, but the
patient's history is more
consistent with LH. I
8
43
c ABSENT/THIN INFUNDIBULAR STALK
o
OJ
aJ
0::
ro DIFFERENTIAL DIAGNOSIS • Pituitary Stalk Anomalies
aJ
C o Most common = ectopic posterior pituitary
CL less Common • Posterior pituitary "bright spot" in
• Pituitary Stalk Transection, Post-Traumatic hypothalamus
• Pituitary Stalk Transection, Post-Surgical • Stalk thin or absent
• Pituitary Stalk Anomalies • Shallow sella, small pituitary
• Septa-Optic Dysplasia (SOD) o Less common = duplicated stalk
• Holoprosencephaly • Two separate, thinned stalks present
Rare but Important • Infundibular recess of 3rd ventricle
c widened, interposed between duplicated
ro • Neurocysticercosis
•... stalks
aI • Meningitis
"'C
C
• Tuber cinereum thickened, often fused
III with mammary bodies
:J ESSENTIAL INFORMATION • Septo-Optic Dysplasia (SOD)
-"
l/) o Absent septum pellucid urn
• Is small/absent stalk congenital or acquired? o Frontal horns "pointed" inferiorly
• Clinical information extremely helpful o "Squared" or "box-like" appearance of
o History of trauma or surgery? lateral ventricles on coronal imaging
o Hypothalamic/pituitary axis dysfunction? o Small optic chiasm
o Short stature? • Holoprosencephaly
o Many people consider lobar
Helpful Clues for less Common Diagnoses holoprosencephaly = SOD
• Pituitary Stalk Transection,
Post-Traumatic Helpful Clues for Rare Diagnoses
o Usually occurs following motor vehicle • Neurocysticercosis
accident o Racemose NCC cysts in suprasellar cistern
o Can occur with closed head injury surround, stretch/thin infundibular stalk
o May occur with or without accompanying • Meningitis
basilar skull fracture o Children with group B streptococcus
• Pituitary Stalk Transection, Post-Surgical o Diencephalic infarction
o Children: Most common after o Secondary atrophy of optic chiasm,
craniopharyngioma resection pituitary stalk
o Adults: Most common after
macroadenoma resection
Pituitary Stalk Transection,

Post- Traumatic
I
8 Coronal T7WI MR in a child with remote head trauma
who subsequently developed pituitary insufficiency
SagitIBI T1 WI
hypophysectomy
MR alter lfanssphenoidal
shows very thin inlundibular stalk EI
pituitary stalkEl.
=
shows traumatic cephalocele and absenUinapparent along with secondary empty sella =.
44
ABSENT/THIN INFUNDIBULAR STALK en
,.-
c:
III
:l
a.
..•
OJ
III
Pituitary Stalk Anomalies
(Left) Sagittal TI WI MR in a :l
2 year old child with short (j)
-
(1)
stature, abnormally low bone
age shows absent
OJ
infundibular stalk a 'c:-
><
ectopic posterior pituitary 5i
bright spot ell and small rJl
(1)
pituitary gland r=J. (Right)
Coronal TlWI MR in the ..•
III
same patient as the previous

image shows absent stalk 81
and ectopic posterior
pituitary bright spot
II II in
hypothalamus =:II.
shows two small-sized
pituitary stalks =:II in this
case of duplicated pituitary
stalks. Note abnormal
configuration of posterior
pituitary 81. (Right) Coronal
T7 WI MR in the same case
as previous image shows
thinned, duplicated
in(undibular stalks 81.

shows classic SOD with thin
stalk inferiorly "pointed"
frontal horns ell and absent
septum pellucidum with
"squared off" appearance of
lateral ventricles 81. (Right)
Sagittal TI C+ MR shows
racemose NCC cysts
surrounding, stretching
infundibular stalk 81 and
extending into sella,
flattening pituitary gland
against floor =:II.
I
8
45
c THICK INFUNDIBULAR STALK
.Q
OJ
OJ
c::
OJ
OJ
c
a:: Common • Neurosarcoid
..: o Isolated stalk lesion uncommon
OJ • Neurosarcoid
o Adults> > children
OJ
(f) • Germinoma
OJ • Germinoma
X less Common
-
-,::l
~
OJ
(f)
• Meningitis
• Histiocytosis
o May be primary in stalk/hypothalamus
o Often presents with diabetes insipidus (D!)

• Lymphocytic Hypophysitis
c • Meningitis
C'Cl
.... Rare but Important o "Stalkitis" usually part of generalized
co • Metastasis (to Stalk/Pituitary)
"C pia-subarachnoid space infection
C
C'Cl • Ectopic Neurohypophysis o Isolated stalk infection rare
::l • Pituicytoma • Histiocytosis
.x • Lymphoma, Primary CNS
en o Calvarium> brain parenchyma, meninges
• Leukemia o Infundibulum/hypothalamus = most
• Transected Pituitary Stalk common CNS site
• Children> adults
ESSENTIAL INFORMATION • Absent pituitary "bright spot" common
• Stalk thick, hyperintense, enhancing
Key Differential Diagnosis Issues • Lymphocytic Hypophysitis
• Know what normal stalk looks like! o Thick, enhancing stalk ± pituitary mass
o Tapers from top (at tuber cinereum) to
bottom (pituitary gland) Helpful Clues for Rare Diagnoses
o 2 mm or less in diameter
• Metastasis, Lymphoma
o Look for other lesions, infiltration of
• "Thick" stal k
o More than 2 mm diameter
adjacent structures
o Loss of normal "top to bottom" tapering
• Pituicytoma
o Posterior pituitary "bright spot" often
• Patient age extremely important in
differential diagnosis of thick stalk absent
o Child = histiocytosis, germinoma Other Essential Information
o Adult = neurosarcoidosis, hypophysitis, • Pituitary stalk anomaly, transected stalk
metastasis, lymphoma (traumatic/post-surgical) can make stalk
appear "stubby"
Neurosarcoid Germinoma
I
8 Sagittal T I C+ MR shows a diffusely thickened, intensely
enhancing piwitary stalk = in an adult with known
Sagittal T7 C+ MR in a 13 year old girl with central 01
shows enhancing suprasellar mass = involving
sarcoidosis and diabetes insipidus. This was the only infundibulum ~ and extending into /he
inlracraniaJ lesion. hypothalamus/anterior 3rd ventricfe.
46
THICK INFUNDIBULAR STALK (fl
"
c:
III
:::l
Q.
OJ
""
III
(Left) Sagittal T I C+ MR in a
:::l
patient with (JJ
-
(I)
coccidioidomycosis
Q)
meningitis E!l:I shows diffuse L
thickening and enhancement c:
><
along the infundibular stalk lii
and hypothalamus t±. VI
(Right) Sagittal T1 C+ MR in
~
III
a child with known 0""
Langerhans cell histiocytosis J?

and central 01 shows a :J
(I)
thickened, rounded, III
enhancing infundibular stalk ;:0
=:1. This was the only (I)
<0
intracranial lesion. O·
:J
Metastasis (to Stalk/Pituitary)

(Left) Sagittal T1 C+ MR in a
middle-aged man presenting
with 01 shows thickened
infundibular/hypothalamic
enhancing mass.
granulomatous disease.
Biopsy showed LH. (Rigllt)
Sagittal T1 C+ MR in a
patient with 01 and
widespread systemic
metastases shows enhancing
mass infiltrating pituitary and
thickening infundibulum =:1.
This was the only intracranial
lesion.
child with growth failure
shows bulbous enlargement
of the infundibulum =
small pituitary gland =:1 and
absent "bright SpOI." (Right)
Sagittal T1 C+ MR in a 22
year old woman with
delayed growth,
hypopituitarism for 6 years
shows an intensely
infundibular stalk
extending into the
=
hypothalamus.
I
8
47
c HYPOTHALAMUS LESION
.Q
en
(l)
0::
Cll
(l)
c
0:: Common • Astrocytoma
~-
Cll • Pilocytic Astrocytoma o Most common primary neoplasm of
(l)
• Diffuse Astrocytoma, Low Grade hypothalamic-optic chiasm region
en
Cll o Usually low grade (pilocytic > WHO grade
X Less Common II fibrillary)
-
-,::::J
Cll
(l)
• Germinoma
o Age < 5 years
o Endocrine dysfunction in 20%
CfJ
• Neurosarcoid o Look for evidence for NFl
c
ns
•....
• Langerhans Cell Histiocytosis • 20-50% of patients with pilocytic
!Xl • Lipoma astrocytoma
'0
c • Lymphocytic Hypophysitis
ns
• Metastases Helpful Clues for Less Common Diagnoses
o Hypothalamic/Pituitary Axis Metastases • Craniopharyngioma
o Lymphoma o Second-most common suprasellar mass in
o Leukemia children
o Occurs anywhere from intrasellar to stalk
• Tuber Cinereum Hamartoma
• Ectopic Posterior Pituitary to anteroinferior 3rd ventricle
o 90% calcify, 90% have multiple cysts
Rare but Important (mixed signal intensity), 90% calcify
• Other Gliomas • Germinoma
o Chordoid Glioma o Can be primary in hypothalamus/stalk
o Pilomyxoid Astrocytoma • M = F (vs. male predominance in pineal
o Pituicytoma gland)
o Ganglioglioma o 10% "double" midline lesions (pineal &
• Demyelinating Disease hypothalamus)
o Multiple Sclerosis o DI, diencephalic syndrome, precocious
o ADEM puberty common
• Wernicke Encephalopathy o Thick enhancing stalk, 3rd floor, absent
• Cavernous Malformation posterior pituitary "bright spot"
• Neurosarcoid
ESSENTIAL INFORMATION o Adult with stalk, meningeal lesions
o Other infectious/inflammatory lesions that
can mimic sarcoid
• Wegener granulomatosis
• TB, syphilis
o Stalk/hypothalamus lesion in a child
• Lipoma
o Lipoma: Sessile T1 hyperintense lesion on
subpial surface of hypothalamus
o Osteolipoma: Rare; fat density/signal
intensity & calcification
• Lymphocytic Hypophysitis
o Peripartum female most common
o Can mimic macroadenoma
• Metastases
o Hypothalamic/Pituitary Axis Metastases
• 1-25% of systemic cancers at autopsy
I • Less common at imaging
• Breast, lung most common primary
tumors
8
48
HYPOTHALAMUS lESION en
;1r:
c:
a Lymphoma • Low grade astrocytoma

• Pituitary/stalk/hypothalamus • Enhances strongly, uniformly
uncommon site a Ganglioglioma
• Can be primary or metastatic • Very rare in hypothalamus/chiasm
a Leukemia • Young adult (mean age = 20 years)
• Often involves dura, paranasal sinuses • Demyelinating Disease
• Tuber Cinereum Hamartoma a Optic chiasm involvement> >
a Children with gelastic seizures, males with hypothalamus
isosexual precocious puberty a Enhancing, slightly enlarged optic
a Can be pedunculated or sessile nerves/chiasm seen with both MS, ADEM
a Density/signal intensity typically • Wernicke Encephalopathy ::9-
:J
isointense with cortex a Acute: Abnormal Ctl
OJ
a No Ca++, enhancement hyperintensity/enhancement of mamillary ;0
Ctl
a Sessile lesion may be difficult to bodies, inferolateral walls of 3rd ventricle, <C
o·
distinguish from hypothalamic periaqueductal gray matter :J
astrocytoma (no change on follow-up) a Chronic: Mamillary atrophy
a Note: Occurs in both alcoholics,
nonalcoholics (e.g., long-standing
• Other Gliomas
a Chordoid Glioma
parenteral nutrition)
• Floor of 3rd ventricle • Cavernous Malformation
a Hypothalamus/3rd ventricle rare location
• Hyperintense with strong, uniform
a Looks like CM elsewhere
enhancement
a Pilomyxoid Astrocytoma Other Essential Information
• Infant/young child • Child with DI, no visible lesion may have
• "H"-shaped tumor of hypothalamus; germinoma; surveillance with Tl C+ scans
extension into medial temporal lobes essential!
common
• Often large, bulky, ± hemorrhage (rare in
SELECTED REFERENCES
pilocytic astrocytoma)
]. Hamilton BE et al: Anatomic and pathologic spectrum of
• ± Hemorrhage (25% of PMAs; rare in pituitary infundibulum lesions. AJR Am J Roentgenol.
pilocytic astrocytoma) 188(3):W223-32,2007
a Pituicytoma 2. Saleem SN et al: Lesions o( the hypothalamus: MR imaging
diagnostic features. Radiographies. 27(4):1087-108, 2007
• Stalk, posterior pituitary lobe
I
Sagittal T2WI MR shows classic pilocytic astrocytoma
=:I originating from hypothalamus and optic chiasm.
Sagillal TI C+ MR shows inhomogeneously enhancing
mass in anterior 3rd venlIicle, hypothalamus =. 8
(Courtesy P.Rodriguez, MO).
49
c HYPOTHALAMUS LESION
o
en
Ql
0::
Cii
Ql
c
CL Germinoma
.:
ro (Left) Sagittal T1WI MR
Ql shows large hyperintense
(/)
ro craniopharyngioma
X originating from the 3rd
--,::J ventricle ~ and
Iii hypothalamus. Note sparing
Qj of the suprasellar cistern [;8
(/)
(Right) Sagillal T1 C+ MR in
C 13 year old boy with central
l'Cl
diabetes insipidus shows
"-
CD enhancing mass in anterior
"C 3rd ventricle/hypothalamus
c
l'Cl I:]] displacing pituitary stalk
~ anteriorly.
Neurosarcoid Langerhans Cell Histiocytosis

shows an enhancing mass
infiltrating hypothalamus I:]]
and infundibular stalk.
Patient is an adult who
presented with diabetes
insipidus. (Right) Sagittal T1
C+ MR in child with DI
shows enhancing mass =
infiltrating the hypothalamus,
tuber cinereum, infundibular
stalk, and pituitary gland.
shows enhancing mass in
anterior third ventricle,
hypothalamus 1:]]. The
pituitary stalk E!:J is slightly
thickened. (Right) Sagittal T1
=-
C+ fS MR shows pituitary
hypothalamic E!:J masses
in this patient with proven
B-cell lymphoma.
I
8
50
HYPOTHALAMUS LESION
III
::::l
Co
Tuber Cinereum Hamartoma Chordoid Glioma

-.
III
III

::::l
12 year old child with (J)
CD
gelastic seizures shows
QI
=
sessile hypothalamic mass
with cyst 81. No
enhancement was seen on
'-
c
x
0;-
T1 C+ scan. Variant cases (j)
may mimic astrocytoma. ~

OJ
(Right) Sagittal T1 WI MR in --.
this 6S year old patient ::9.
shows isoinlense ::::l
CD
hypotha/amic/3rd ventricular
=
OJ
mass displacing, ;0
compressing optic chiasm CD
(Q
!:J:I. Intense homogeneous o·
enhancement was seen on ::::l
T1 C+ slUdy.
Pilomyxoid Astrocytoma
3 year old child with NF I
and diencephalic syndrome
shows large hyperintense
hypothalamic mass bulging
into anterior 3rd ventricle
6>J. (Right) Sagillal T I C+
MR in a 22 year old woman
with hypopituitarism shows
large enhancing
hypothalamic/infundibular
stalk mass!:J:I.
Multiple Sclerosis
(Left) Sagillal fLAIR MR
shows mullifocaf
hyperintensiUes along the
callososeptal interface and in
the hemispheric white
matter, as well as optic
chiasm/hypothalamus ~
(RighI) Axial FLAIR MR in
hyperalimentation shows
hyperintensity in mammillary
bodies as well as
periaqueductal gray maller
19.
I
8
51
c HYPERDENSE SUPRASEllAR MASS
.Q
Ol
OJ
0:::
ro DIFFERENTIAL DIAGNOSIS • Saccular Aneurysm
OJ
c o Nonthrombosed aneurysms slightly
a:: Common hyperdense to brain
L
ro • Pituitary Macroadenoma o Partially/completely thrombosed
OJ
(J)
• Aneurysm aneurysms may be very hyperdense
ro o Saccular Aneurysm
X • Fusiform Aneurysm, ASVD
---,
::J o Fusiform Aneurysm, ASVD o May involve either ICA or BA
ro
• Meningioma o on aneurysmal dolichoectasia common in
OJ
(/)
Less Common older patients
C
• Craniopharyngioma o ASVD > non-ASVD (e.g., inherited
nl
•... vasculopathy, AIDS-related, etc.)
aI • Rathke Cleft Cyst
"'C
• Germinoma o ASVD often Ca++
c
nl
• Neurosarcoid • Meningioma
::l o 10% in sellar/suprasellar region
-'"
CJ)
Rare but Important o Pituitary gland separate from mass
• Parenchymal Metastases
• Primary CNS Lymphoma Helpful Clues for Less Common Diagnoses
• Pilomyxoid Astrocytoma • Craniopharyngioma
• Tuberculosis o Children: Adamantinomatous type
• Fungal Diseases • Usually cystic, Ca++
• Chordoid Glioma • Rarely hyperdense
o Adults: Papillary type more common
• Iso/slightly hyperdense
ESSENTIAL INFORMATION • Solid, rarely calcified
Key Differential Diagnosis Issues • Rathke Cleft Cyst
• Is mass from pituitary gland or other o Only 10% purely suprasellar, hyperdense
structure? • Germinoma
o Mildly hyperdense to brain
Helpful Clues for Common Diagnoses o Look for pineal mass (but can be primary
• Pituitary Macroadenoma infundibulum/3rd ventricle lesion)
o Approximately 10% hyperdense
• Cellularity, hemorrhage Alternative Differential Approaches
o Pituitary gland can't be separated from • Hyperdense suprasellar mass with Ca++
mass o Children: Craniopharyngioma
• Gland is the mass o Adults: Aneurysm, meningioma
I
8 Axial NECT in a 60 year old woman presenting in the
emergency department with severe headache shows a
Axial NECT in a patient with headache and bitemporal
hemianopsia shows a somewhat lobulated hyperdense
hyperdense mass in the suprasellar cistern !:ill. Scout suprasellar mass !:ill. CTA demonstrated partially
view (not shown) demonstrated an expanded sella. thrombosed lCA aneurysm.
52
HYPERDENSE SUPRASEllAR MASS
III
::l
Cl.
to
.,
III
(Left) Axial NECT in elderfy ::l

woman with "altered mental (fJ
staWs /I shows very large, ~
hyperdense, partially
m
c:::
calcified c
x
frontal/suprasellar mass =:I. fii
NOle acute obstructive (J)
hydrocephalus SlI. (Rig"')

~
OJ
.,
Axial NECT shows a
hyperdense suprasellar mass "U
SlI that contains punctate :::J
(1)
calcifications DJ. OJ
Craniopharyngioma was ;0
found at surgery. (1)
co
o
:::J
Germinoma
with headaches and normal
neurologic examination
shows a hyperdense
sellar/intrasellar mass =:I.
MR showed Rathke cleft cyst
with classic inlracystic
nodule. (Right) Axial NECT
in a 22 year old man with
headaches, lethargy, and
diabetes insipidus shows a
MR showed a 2nd lesion
in the pineal gland.
Tuberculosis
Extension into cavernous
sinus helps distinguish
this from many other entities
in this location. (Right) Axial
N[CT in a patient with
known tuberculosis shows
an inhomogeneously
DJ. Rim enhancement was
seen following contrast in
this patient with caseating
tuberculoma.
I
8
53
c T1 ISOINTENSE SUPRASELLARMASS
.Q
OJ
Cl)
0:::
cu DIFFERENTIAL DIAGNOSIS o No: Tuber cinereum hamartoma, RCC
Cl)
c • Few lesions remain isointense with cortex on
a:: Common all MR sequences
..: • Pituitary Macroadenoma
cu o Pituitary macroadenoma or hyperplasia
Qj • Pituitary Hyperplasia o Meningioma, tuber cinereum hamartoma
X
'"cu • Meningioma o Histiocytosis, sarcoidosis
-,:J • Pilocytic Astrocytoma
co Helpful Clues for Common Diagnoses
Cl)
(fJ
• Pituitary Macroadenoma, Hyperplasia
Less Common o Both isointense to gray matter (GM)
c
ns
•...
• Rathke Cleft Cyst • Meningioma
!Xl • Germinoma o Usually isointense on all sequences
'tl
C • Neurosarcoid o ± Ca++, enhances
ns
• Langerhans Cell Histiocytosis • Astrocytomas (pilocytic > diffusely
• Tuber Cinereum Hamartoma infiltrating)
• Lymphocytic Hypophysitis o Usually iso-/hypo- on Tl, hyperintense on
Rare but Important T2WI
• Metastasis (Pituitary &/or Stalk) o Variable enhancement (none to striking)
• Pituicytoma Helpful Clues for Less Common Diagnoses
• Rathke Cleft Cyst (depends on cyst
ESSENTIAL INFORMATION content)
o Most are hypointense
Key Differential Diagnosis Issues o 25% iso-, 10% hyperdense
• Where does lesion arise from? o Rim may enhance ("claw sign")
o Pituitary gland/sella turcica • Germinoma
(macroadenoma, hyperplasia, o Isointense on Tl-, iso/hypo on T2WI
hypophysitis, metastasis) o Enhances strongly, uniformly
o Infundibulum (germinoma, histiocytosis, • Neurosarcoid, Langerhans Cell
pituicytoma) Histiocytosis
o Brain (astrocytoma), meninges o LCH (child), sarcoid (adult) - thick,
(meningioma) enhancing stalk
• Does it enhance? • Tuber Cinereum Hamartoma
o Yes: Macroadenoma, meningioma, o > 90% isointense on Tl WI, non enhancing
aneurysm, neoplasm o May be slightly hyperintense on PD, FLAIR
I
8 Coronal TJWI MR shows a large intra- and suprasellar
mass =
elevating and compressing the optic chiasm
Sagittal T7WI MR shows an intra- and suprasellar mass
m that is isoinlensewith gray maHer. The diaphragma
m. The mass cannot be distinguished from the pituitary sellae ~ clearly separates the mass from the pituitary
gland. gland below
54
T1 ISOINTENSE SUPRASEllAR MASS (J)
"
c:
III
:J
Co
OJ
"'"
III
(Left) Axial T1WI MR shows :J

an enlarged optic chiasm c;. (f)
ell
and nerves in this patient
with neurofibromatosis type
1. (Right) Axial T1WI MR
shows a slightly
-
Q)
L
c:
><
Ci
inhomogeneous suprasellar [fl
mass I:] that is largely ~

OJ
isoinlense with adjacent ."'"
brain. -u
:J
ell
OJ
;0
ell
to
o·
:J
Tuber Cinereum Hamartoma

(Left) Coronal T1 WI MR in
21 year old woman shows a
well-delineated isoinlense
suprasellar mass I:]slightly
displacing the inlundibular
stalk to the lelt and the
pituitary gland inleriorfy. This
incidental finding is a
presumed Rathke clelt cyst.
(Right) Sagittal T1 WI MR in a
77 year old woman with
precocious puberty shows a
classic "collar button" =
lesion positioned between
the inlundibulum i/1 Iront E2
and the mamillary body
behind~.

42 year old man with
diabetes insipidus and
headache shows an
isoinlense suprasellar mass
CO> elevating and
compressing the optic
chiasm. (Rigl1t)Sagittal T IWI
MR in a patient with visual
problems and diabetes
insipidus shows an ;so;ntens€
suprasellar mass arising from
the inlundibular stalk 1:].
The lesion enhanced strongly
and uniformly. (Courtesy A
Hasso, MO).
I
8
55
c 11 HYPERINTENSE SUPRASELLAR MASS
.Q
Ol
Ql
0:::
co DIFFERENTIAL DIAGNOSIS o "Crankcase" oily content ..• Tl
Ql
C hyperintensity
a.. Common
..: Helpful Clues for Less Common Diagnoses
~ • Pituitary Macroadenoma
• Saccular Aneurysm (Thrombosed)
Ql
en • Craniopharyngioma
co o Usually eccentrically located, not directly
X Less Common suprasellar
-,::J • Saccular Aneurysm (Thrombosed)
co o Subacute/chronic mural thrombus
Qj • Rathke Cleft Cyst • Rathke Cleft Cyst
(/)
• Ectopic Neurohypophysis o May have very short Tl if high protein
C
01
•....
• Lipoma content or hemorrhage from cyst apoplexy
en • Dermoid Cyst o Look for intracystic nodule
"0
c: Rare but Important o Look for "claw" of enhancing pituitary
01
• Pituitary Apoplexy gland wrapped around cyst
• Pilomyxoid Astrocytoma • Ectopic Neurohypophysis
• Cavernous Malformation o Pituitary stalk tiny or nonexistent
• Meningioma o "Bright spot" on hypothalamus

o Does not saturate with fat suppression
• Lipoma
ESSENTIAL INFORMATION o Suppresses with fat saturation
Key Differential Diagnosis Issues • Dermoid Cyst
• Most common cause for t Tl is subacute o Fat droplets in sulci, cisterns (ruptured)
hemorrhage Helpful Clues for Rare Diagnoses
o T2* (GRE or SWI) useful • Pituitary Apoplexy
• Age helpful in common diagnoses o Subacute hemorrhage has short Tl
o Children = craniopharyngioma o Rim enhancement typical
o Adults = pituitary macroadenoma, • Pilomyxoid Astrocytoma
thrombosed aneurysm o May hemorrhage
Helpful Clues for Common Diagnoses • Cavernous Malformation
• Pituitary Macroadenoma o "Popcorn" appearance
o Hemorrhage, sometimes cystic change • Meningioma
• Craniopharyngioma o • Tl (psammomatous Ca++; hemorrhage,
o 90% Ca++, 90% cystic, 90% enhance lipomatous transformation rare)
Pituitary Macroadenoma Craniopharyngioma
I
8 Sagittal TI WI MR shows a hemorrhagic intra- and
suprasellar mass= in a patient who presented with
Coronal TlWI MR shows
hyperintense suprasellar mass ffi
a
A
homogeneously
smalle" isoinlense
pituitary apoplexy. The diagnosis was macroadenoma inCJasellarcomponent is seen BI. Craniopharyngioma
with subacute hemorrhage. with ;ntra and suprasellar components.
56
4
11 HYPERINTENSE SUPRASELLAR MASS
Q)
::::l
0-
Saccular Aneurysm (Thrombosed) Rathke Cleft Cyst

-.
tll
Q)
::::l
shows a mixed signal, mostly (J)
~
hyperintense, suprasellar
mass =. Note a "flow void"
-
III
'-
c:
-
from the anterior cerebral
x
artery SI supplying this III
largely thrombosed giant en
aneurysm. (Right) Sagittal ~
III
T1WI MR shows a presumed .-'
Rathke cleft cyst, seen here II
as a well-delineated ::::l
CD
hyperintense suprasellar III
mass ~ clearly separable ;0
from pituitary gland. This CD
(Q
was found incidentally on a c;-
standard MR scan. ::::l
Dermoid Cyst
shows a hyperintense
hypothalamic mass
absent infundibulum.
= with
Anterior pituitary ~ is
normal to slightly small in
size. Note the lack of a
"bright" neurohypophysis.
shows a mixed signaf~
primarily hyperintense mass
SI in the suprasellar and
quadrigeminal cisterns. Note
fat droplets = in
subarachnoid spaces in this
patient with ruplUred
dermoid cyst.
Cavernous Malformation Meningioma

shows a mixed iso-,
hyperintense suprasellar
mass E±I with hypointense
rim [;8 characteristic of
Zabramski type 2 cavernous
malformation. (Right) Axial
T1WI MR shows mostly
isointense suprasellar mass
with some Tl shortening ED.,
possibly caused by
psammomatous calcification,
not hemorrhage.
I
8
57
c
Q
11 HYPOINTENSE SUPRASELLAR LESION
OJ
OJ
0:: o Rim/ring (NCC, craniopharyngioma, RCC)
OJ
c Helpful Clues for Common Diagnoses
a.. Common
..: • Dilated Third Ventricle
ro • Dilated Third Ventricle
o Enlarged 3rd ventricle recesses protrude
Qi
en • Arachnoid Cyst (AC)
ro into suprasellar cistern, sella turcica
X • Neurocysticercosis (NCC)
o Behaves exactly like CSF on FLAIR, OWl
-,:J Less Common
ro • Arachnoid Cyst (AC)
OJ • Pilocytic Astrocytoma (PA) o Bows 3rd ventricle up, over cyst
(/)
• Craniopharyngioma o Suppresses on FLAIR, no restriction on
c
ro • Epidermoid Cyst OWl
"-
III • Rathke Cleft Cyst • Neurocysticercosis (NCC)
"C
r:: • Enlarged Perivascular Spaces o Cysts often show rim enhancement
III
:J
-"(/) • Pituitary Macroadenoma • Pilocytic Astrocytoma (PA)
• Saccular Aneurysm (Acutely Thrombosed) o Hyperintense to CSF on Tl WI
• Pituitary Apoplexy o Enhancement typical
• Pilomyxoid Astrocytoma • Craniopharyngioma
090% cystic, 90% Ca++, 90% enhance
o Cyst signal variable (hyper> hypointense)
• Epidermoid Cyst
Key Differential Diagnosis Issues o No suppression on FLAIR, restricts on OWl
• Tl hypointense lesion = hypointense • Rathke Cleft Cyst
compared to brain, not necessarily - CSF o Cyst fluid more often hyperintense
• Lesions CSF-like on all sequences o Look for "claw sign" of enhancing pituitary
o Enlarged 3rd ventricle, arachnoid cyst, around cyst
perivascular spaces
o Epidermoid cyst
• Lesions hypointense to brain but • Pituitary Macroadenoma
o Small intratumoral cysts common
hyperintense to CSF on Tl WI
o Extratumoral cysts (trapped perivascular
o Neoplasms
o Congenital or infectious cysts
spaces) less common
o Necrosis/apoplexy may appear cystic, show
• Enhancing hypointense lesions
o Solid (astrocytoma, adenoma) rim enhancement
Dilated Third Ventricle
I
8 Sagittal T7 WI MR shows aqueductal stenosis 81
causing marked enlargement or the third ventricle with compressing/elevaUng the 3rd ventricle=-
Sagittal T7 C+ MR shows a CSF-like suprasellar mass
deviating
herniation of anterior recesses into the suprasellar lhe inFundibulum anteriorly E1 and causing severe
cistern I!!f]. obstrucUve hydrocephalus.
58
T1 HYPOINTENSE SUPRASELLAR LESION en
"
c:
Ql
:J
a.
ro
.,
Ql
(Left) Sagittal T1 C+ MR ::l

shows multiple hypoimense (f)
CD
basal cYS15with peripheral
enhancemenl~in the
supra· and intrasellar ~
cisterns. (Right) Axial T1 WI
-'-
iil
c
X
tii
MR in child with known NFl Ul
CD
shows a lobulated
OJ
hypointense mass filling ."
the suprasellar cistern. The "U
mass enhanced strongly but :::J
CD
heterogeneously following OJ
contrast administration. :;0
CD
(Q
o·
:J

shows a mixed ;50- EI and
hypointense = suprasellar
mass in a child with chiasm
compression ~ causing
bitemporal hemianopsia.
Hypoinleflsily in this case is
caused by dense
calcification. (Right) Axial T1
C+ FS MR shows a
lobulated, CSF-Iike,
non enhancing mass
infiltrating the
quadrigeminal, ambient 1:1
and suprasellar cisterns a
Saccular Aneurysm (Acutely

Enlarged Perivascular Spaces Thrombosed)
variable-sized CSF-like cYS15
E±J in hypothalamic region.
Prominent PV5s are common
in basal ganglia, less
common in midline basal
brain structures. (Right) Axial
T1 C+ rs MR shows
nonenhancing, hypoinlense,
intra- & suprasellar mass I::]
in a female with headache &
sudden onset left CN6 palsy.
Pituitary apoplexy was
pre-operative diagnosis. An
acutely thrombosed internal
carotid artery aneurysm was
found at surgery. I
8
59
SECTION 9
Arteries
Abnormalities of Arterial Shape/Configuration 1-9-2
Fusiform Arterial Enlargement 1-9-6

Hyperattenuating ("Dense") Artery 1-9-8
Vascular Calcification(s) 1-9-10
IJl
QJ
ABNORMALITIES OF ARTERIAL SHAPE/CONFIGURATION
'C
QJ
t
« DIFFERENTIAL DIAGNOSIS o Short nonbranching -+ pseudoaneurysm,
c: blood blister-like aneurysm
...
III
Common o Long, nonbranching -+ ASVD,
lXl
"0 • Atherosclerosis, Intracranial dolichoectasia, fusiform aneurysm (ASVD,
c:
III • Dolichoectasia non-ASVD), vasculitis, vasospasm
• MR Artifacts, Flow-Related
• Atherosclerosis, Intracranial
• Fusiform Aneurysm, ASVD
o Distal basilar artery (BA),
Less Common cavernous/supra clinoid internal carotid
• Vasospasm artery (lCA) > cortical branches
• Fusiform Aneurysm/Vasculopathy, o Findings
Non-ASVD • ormal aging: Arterial Ca++, wall
• Dissection thickening
• Pseudoaneurysm • Most common: Focal stenosis, luminal
Rare but Important irregularities
• Blood Blister-like Aneurysm • Less common: Elongation/ectasia
• Vasculitis • Uncommon: Thrombosis, occlusion
o Remember: Most common cause of
• Moyamoya
"vasculitis" appearance is ASVD, not
vasculitis!
ESSENTIAL INFORMATION • Dolichoectasia
Key Differential Diagnosis Issues o Elongation, dilatation, tortuosity without
• Effect of patient age on diagnosis focal aneurysmal dilatation
o Middle-aged or elderly o BA > ICA > MCA
• Atherosclerosis (ASVD) o Slow flow may cause signal

• Dolichoectasia inhomogeneity, phase artifact
• Saccular aneurysm • MR Artifacts, Flow-Related
o Pulsation may cause spin dephasing, signal
• Fusiform aneurysm
o Child or young adult loss in adjacent CSF (especially around
• Consider inherited vasculopathy (e.g., distal basilar artery)
collagen-vascular disease like o Phase artifact propagation may distort
Ehlers-Danlos) vessel contours, propagate across imaged
• Child with fusiform vasculopathy: Check slice
HIV status o Slow flow & fully relaxed spins in entry
• Moyamoya slice(s) -+ Tl shortening may mimic
• Is there evidence for hemorrhage? thrombus
o Subarachnoid • Saccular Aneurysm
• Saccular aneurysm ± vasospasm o Round or ovoid outpouching ± "tit" or
• Blood blister-like aneurysm lobulations
• Dissection or dissecting aneurysm o Arises from major vessel bifurcation
(especially vertebrobasilar) o Variable neck (narrow, wide, broad-based)
o Parenchymal o Aneurysmal SAH common

• Moyamoya (adult) • Fusiform Aneurysm, ASVD
• Vasculitis (especially drug-related) o Long segment irregular fusiform/ovoid
• Pseudoaneurysm (especially with trauma arterial dilatation

history) o Vertebral arteries, BA > ICA, MCA
• Does lesion involve short or long segment of o Hematoma with variable aged clot
vessel, bifurcation vs. nonbranching point? common

o Short, bifurcation -+ saccular aneurysm, o Residual lumen enhances strongly
I ASVD o Variant = "giant serpentine aneurysm"
• Large, partially thrombosed mass
9
2
ABNORMALITIES OF ARTERIAL SHAPE/CONFIGURATION
• Clot of varying age o Peripheral location (distal to circle of

• No definable neck Willis)
o Often adjacent to skull base or dura
(tentorial incisura, falx)
• Vasospasm
o Etiology Helpful Clues for Rare Diagnoses
• Most common: Ruptured aneurysm ~ • Blood Blister-like Aneurysm
aSAH ~ vasospasm 5-7 days later o Broad-based hemispheric bulge
• Less common: Trauma o No definable neck
o Imaging o Contained only by adventitia/fibrous cap
• Long- or short-segment stenosis so easily ruptures
• Often multifocal o Look carefully for BBA in
• ± Cerebral ischemia/infarction "angiogram-negative" SAH
• Fusiform Aneurysm/Vasculopathy, o Most common location = supraclinoid ICA
Non-ASVD • Vasculitis
o Fusiform or ovoid dilatation in absence of o Primary arteritis of the CNS
ASVD o Secondary vasculitis
o Long, affects nonbranching vessel • Infectious
segments • Autoimmune
o Can be solitary or multifocal • Substance abuse
o Vertebral/BA > carotid • Radiation-induced
o Younger patients o Multifocal alternating stenoses, dilatations
o Inherited (e.g., Ehlers-Danlos) or acquired o Remember: Most common cause of
(viral or collagen-vascular) "vasculitic" pattern in older patient is
• Dissection ASVD!
o Can be traumatic or spontaneous
o May cause SAH
• Mimics of arterial abnormalities
o Vertebral> > internal carotid artery
o Anything with short Tl can mimic
o Look for Tl hyperintense clot around aneurysm on MRA
residual lumen
• Lipoma
o Focal dilatation ~ dissecting aneurysm
• Pituitary gland on Tl C+
• Pseudoaneurysm • ROI that includes part of adjacent vessel
o Cavitated clot lacks normal arterial wall
o Pulsation artifact
o Trauma, infection = common causes
Atherosclerosis, Intracranial Dolichoectasia
I
Anteroposterior angiography shows mulUfocal stenoses
characteristic for atherosclerosis (ASVD). ASVD is most
Axial T1WI
generalized
MR in normal 79 year old man with
arterial dolichoeclasia shows elongated.
9
common cause of this vasculitis-like pattern of €CtaUcMCA =.2 with substanUal phase arUfact SI from
alternating stenoses and dilatations. the pulsating vessel.
3
en ABNORMALITIES OF ARTERIAL SHAPE/CONFIGURATION
Q)
·C
Q)
t::
<{
c:
'"
'-
!Xl
"C (Left) Axial T2WI MR shows
c:
prominent CSF "f/ow void"
'" & around the distal basilar
artery, a common finding
with hyperdynamic but
normal arterial pulsation that
is especially common in
children. (Right) Lateral
angiography with 3D
reconstruction from selective
DSA of right internal carotid
artery shows typical
multilobulated saccular
aneurysm = arising from
junction of internal carotid,
posterior communicating
arteries.
Fusiform Aneurysm, ASVD Fusiform Aneurysm, ASVD

(Left) Sagittal MRA
reprojected from axial data
shows huge fusiform basilar
artery aneurysm in this 61
year old man with posterior
circulation TlAs. Most of the
aneurysm is filled with
thrombus~. Flow in
residual patent lumen is
present =.(Right) Lateral
angiography shows bizarre,
fusiform ectasia of middle
cerebral artery ffi extending
into M2 segment in sylvian
fissure :i8
Fusiform Aneurysm/Vasculopathy,
Vasospasm Non-ASVD
(Left) Lateral angiography
shows a saccular aneurysm
(;>J and narrowed cortical
vessels ~ indicating a
vasospasm caused by an
aneurysmal subarachnoid
hemorrhage (aSAI I). (Right)
Lateral angiography in 47
year old man with
spontaneous intracranial
hemorrhage (not shown)
shows fusiform elongation of
an MCA branch ~ Patient
later admitted to using street
drugs.
I
9
4
ABNORMALITIES OF ARTERIAL SHAPE/CONFIGURATION en
,.-
c:
Ql
:>
Q.
Fusiform Aneurysm/Vasculopathy, ..•

OJ
Ql
Non-A5VD
(Left) Axial T2WI MR in a 13 :>
yea, old child with II/VIAIOS
shows enlarged,
bizarre-appearing middle
cerebral arteries 3-. (Right)
Axial T7 C+ FS MR in a
patient with posterior
circulation ischemic
symptoms several days after
a severe deceleration injury
shows that both vertebral
arteries are markedly
enlarged by subacute clot
=. Right VA appears
completely thrombosed,
while small residual lumen is
seen on left 81.
Pseudoaneurysm Blood Blister-like Aneurysm

(Left) Axial MRA shows
traumatic pseudoaneurysm
arising from P2 segment
of posterior cerebral artery
Impaction against
tentorium during CJ 1/
probably injured PCA,
creating this gradually
enlarging pseudoaneurysm.
shows classic blood
blister-like aneurysm c7
along greater curvature of
supra clinoid internal carotid
artery. Hemispherical bulge
with broad orifice is typical
for BBAs. (Courtesy D.
Phillips, MO).
Vasculitis Moyamoya
(Left) Sagittal oblique
angiography shows classic
changes of vasculitis, with
alternating areas of stenosis
and dilatation ffi Note
pseudoaneurysm ~ a rare
complication of vasculitis.
shows tapered occlusion ~
of supra clinoid internal
carotid artery, with tangle of
"puff of smoke II
lenticulostriate :t>-
collaterals.
I
9
5
rn FUSIFORM ARTERIAL ENLARGEMENT
Q)
·C
Q)
t
<l:: o Most common manifestation of
s:: DIFFERENTIAL DIAGNOSIS
intracranial ASVD
•..
Cll
a:l Common o Vertebrobasilar > internal carotid artery

"0 • Dolichoectasia o Ectasia often extends into branches
s::
Cll • Atherosclerotic Fusiform Aneurysm • Atherosclerotic Fusiform Aneurysm
::l
..II:
• Nonaneurysmal Dissection o Thick wall ± organized thrombus
en Less Common o Variable slow flow
• Dissecting Aneurysm/Pseudoaneurysm • Nonaneurysmal Dissection
• Vasculitis o Vertebral> basilar> internal carotid artery
• Nonatherosclerotic Fusiform o Lacks changes of ASVD in other vessels
Aneurysm/V asculopath y o Can be spontaneous or traumatic
o Neurofibromatosis Type 1 Helpful Clues for Less Common Diagnoses
o Systemic Lupus Erythematosus • Dissecting Aneurysm/Pseudoaneurysm
o Ehlers-Danlos IV o Focal arterial dilatation
o Marfan Syndrome o Trauma = most common etiology
Rare but Important o Next to hard/fixed structures (bone, dura)
• Giant "Serpentine" Aneurysm • Vasculitis
• Atypical Saccular Aneurysm o Involves multiple vessels
o Alternating stenoses/dilatations
• Nonatherosclerotic Fusiform
ESSENTIAL INFORMATION Aneurysm/Vasculopathy
Key Differential Diagnosis Issues o Younger patient; history of inherited
• Ectasia = elongated/tortuous artery vasculopathy, immune disorder
• Fusiform aneurysm Helpful Clues for Rare Diagnoses
o Long segment fusiform arterial dilatation • Giant "Serpentine" Aneurysm
o Can be acute (dissecting) or chronic o Large, partially thrombosed mass
(ASVD, nonatherosclerotic vasculopathy) o Distal branches arise from aneurysm dome
Helpful Clues for Common Diagnoses o Lacks definable neck
• Dolichoectasia o ICA/MCA > vertebrobasilar artery

o Dilated/elongated arteries ± slow flow • Atypical Saccular Aneurysm
o Vessel layers intact o Arises from vessel bifurcations
o Older patients o Long "aspect ratio" - fusiform appearance
o Often multilobulated, bizarre
Dolichoectasia
I
9 Sagittal T7WI MR shows elongated basilar artery with
slow flow, thickened waif =:II. Apex of tortuous basilar
Axial T2WI MR shows an elongated, tortuous basilar
artery with thickened arterial waif ffi typical for
artery indents hypothalamus, 3rd ventricle BI. atherosclerosis-associated fusiform ectasia.
6
FUSIFORM ARTERIAL ENLARGEMENT
III
~
Q.
..•
OJ
III
(LeFt) Sagittal T7 WI MR ~
shows a large extra·axial »
;:+
mass anterior to the ro
brainstem =. Note signal ::::!.
ro
caused by slow flow, U>
laminated clot in this classic

ASVD fusiform aneurysm.
(Rig"') Axial T7 WI MR
shows an enlarged right
vertebral artery with high
signal intensity = as well as
an absent "flow void" of the
left vertebral artery PJ::I.
Dissecting Aneurysm/Pseudoaneurysm Vasculitis

(LeFt) Axial T7WI MR in a
patient with remote closed
head injury shows a
hyperintense mass ~ in the
ambient cistern with a
hypointense "slow flow" ~
seen within the mass. (Right)
Axial T2WI MR shows
strikingly enlarged middle
cerebral arteries ~ in this
chi/d with congenital
HIV/AIOS (an uncommon
but well-recognized cause of
pediatric fusiform
arteriopathy) .
Nonatherosclerotic Fusiform
Aneurysm/Vasculopathy
oblique view of the left
vertebral angiogram shows
focal elongations and
widening of the basi/ar artery
in a 6 year old child with
Ehlers-Danlos type 4. (Right)
Lateral angiography in 30
year old man with a
subarachnoid Ijemorrhage
shows an elongated,
bizarre-appearing,
multi/obulated aneurysm ~
with long "aspect ratio",
tit-like projections.
I
9
7
(j)
Q) HYPERATTENUATING ("DENSE") ARTERY
'C
Q)
t
<{
DIFFERENTIAL DIAGNOSIS • Diffuse cerebral edema makes vessels
c:
appear hyperdense ("false dense MCA
•..
III
al
Common sign")
"0
c:
• Physiologic Hyperdensity • Cerebral Ischemia-Infarction, Acute
III • Cerebral Ischemia-Infarction, Acute o Acute thrombus in affected vessel (e.g.,
Less Common true "dense MCA sign")
• Atherosclerosis, Intracranial Helpful Clues for Less Common Diagnoses
• Polycythemia • Atherosclerosis, Intracranial
• Fusiform Aneurysm (ASVD, Non-ASVD) o ASVD with microcalcifications can mimic
• Dissection "dense" MCA
• Pseudoaneurysm • Polycythemia
Rare but Important o Can be physiologic (elevated hematocrit in
• Devices and Complications newborns, high altitude, etc.)
o umerous pathologic causes
• Fusiform Aneurysm (ASVD, Non-ASVD)
ESSENTIAL INFORMATION o Vertebrobasilar > carotid circulation
Key Differential Diagnosis Issues o Thickened walls may appear hyperdense
• Presence, localization of focal neurologic o Non-ASVD: Younger; inherited
findings important vasculopathy, immune disorder
• High hematocrit/hemoconcentration can • Dissection
mimic "dense MCA sign"! o Most posterior circulation
o Compare to other intracranial vessels! o Trauma most common etiology
• Diffuse low density brain (anoxia, etc.) • Pseudoaneurysm
makes ALL vessels appear hyperdense, o Trauma most common etiology
mimics thrombus or SAH! Helpful Clues for Rare Diagnoses
Helpful Clues for Common Diagnoses • Devices and Complications
• Physiologic Hyperdensity o Coils, balloons, stents, methacrylate, etc.
o Circulating blood in arteries normally o Embolized foreign bodies, calcified
slightly hyperdense to brain atheromata can cause hyperattenuating
• Especially prominent in newborns with vessel sign
unmyelinated, hypodense brain
I
9 Axial NECT demonslIates relatively hyperdense internal
carotid arteries III] in this neonate. Note the
Axial NECT shows "false dense MCA sign" in a patient
with diffuse cerebral edema. Low density brain makes
corresponding increased density of the transverse normal MCA =:I and cerebellum SI appear
sinuses=. hyperdense.
8
HYPERATTENUATING ("DENSE") ARTERY CJl
7<:
c:
III
::J
Co
...
to
III

::J
increased density ("dot
sign") in a distal left middle
cerebral artery (MCA)
branch =.(Right) Axial
NECT shows calcified
embolus = in MCA branch
in patient with abrupt onset
right-sided weakness.

calcification in the
supraclinoid internal carotid
arteries ffi (Right) Axial
arteries 1m as well as veins
and dural sinuses m in a
patient with markedly
elevated hematocrit.
Polycythemia can mimic a
CECT scan but vessels are
usually not as dense.
Dissection Devices and Complications

(Left) Axial NECT shows high
density thrombus in the
internal carotid artery PJ:J
related to dissection of the
left ICA just above the
carotid bulb (not shown).
material =
embo/ized hyperdense
in the left MCA
in an IV drug abuser,
possibly secondary to talc
powder. Adjacent
hypodense parenchyma
is in keeping with a subacute
infarct.
I
9
9
(/)
Q) VASCULAR CALCIFICATlON(S)
·C
Q)
t::
<l:
DIFFERENTIAL DIAGNOSIS • Diabetes
o Concentric nature in contrast to eccentric
Common calcified atherosclerotic plaque
• Physiologic Calcification, Vascular • Saccular Aneurysm
• Atherosclerosis, Intracranial o Chunky or curvilinear mural calcifications
• Diabetes o May appear as hypointense rim on MR
• Saccular Aneurysm • Fusiform Aneurysm, ASVD
• Fusiform Aneurysm, ASVD o Long segment irregular fusiform dilatation
Less Common o Mural calcifications common
• Chronic Renal Failure Helpful Clues for Less Common Diagnoses
• Cavernous Malformation • Chronic Renal Failure
• Arteriovenous Malformation o Vascular calcification & arterial stiffness
• Calcified Plaque Embolus occurs due to disturbances of calcium
• Hyperparathyroidism metabolism
Rare but Important • Cavernous Malformation
• Mineralizing Microangiopathy o "Popcorn" appearance with hypointense
hemosiderin rim on T2WI MR
• Arteriovenous Malformation
ESSENTIAL INFORMATION o Calcifications in 25-30%
Key Differential Diagnosis Issues • Calcified Plaque Embolus
• Atherosclerotic, diabetic, & renal failure o Calcified cerebral emboli change in site,
calcifications are often comorbidities in the size, & attenuation with time
same patient o Not a contraindication to thrombolysis
o Subsequent hypercalcemia can lead to
• Physiologic Calcification, Vascular vascular, soft tissue, & joint calcifications
o Barely discernible mural calcifications
without narrowing Helpful Clues for Rare Diagnoses
o Unaccompanied by evidence of disease • Mineralizing Microangiopathy
o Only in medial layer; assoc. w/elastin o Deposition of calcium in small vessels of
• Atherosclerosis, Intracranial previously irradiated parenchyma
o Eccentric mural calcifications with focal o Most often occurs after combined
lumenal narrowing treatment with chemotherapy & radiation
o Mostly in intimal layer; assoc. w/collagen
Physiologic Calcification, Vascular Atherosclerosis, Intracranial
I
9 Axial NEU shows barely discernible, probable
physiologic, intracranial, vascular calcifications without
Axial NEeT shows
supracJinoid internal
eccentric calcificaUon of
carotid arteries bilaterally
the
lumenal narrowing involving bilateral internal carotid associated with lumenal narrowing.
arteries ED.
10
VASCULAR CAlCiFICATlON(S)
Diabetes Saccular Aneurysm

concentric arterial wall
calcifications of the basilar
artery ~ In the correct
clinical selling this is not a
pathognomic but a
presumptive diagnosis of
diabetes. (Right) Axial NEeT
shows chunky & curvilinear
wall calcification I:]] of a
basilar tip aneurysm. There is
also subarachnoid
hemorrhage in the basal
cisterns 81 following
rupture.
(Leh) Axial NECT shows rim

calcification of a large
fusiform basilar artery
aneurysm ~ Also note
classic atherosclerotic
eccentric internal carotid &
MCA calcifications
(Right) Axial NECT
demonstrates a calcified
cortical/subcortical mass in
the left cerebral hemisphere
I:] of a cavernous
malformation.
(Leh) Axial NECT

demonstrates an acute right
MCA stroke secondary to an
acute calcified plaque
embolism 81. (Right) Axial
NEeT shows extensive
calcifications
mineralizing
-=
of
microangiopalhy from prior

radiation therapy and
chemotherapy with
involvement of the basal
ganglia and subcortical white
maller.
I
9
11
SEClrlON 18
Dural Sinus Lesion, General 1-10-2
Enlarged Cortical Veins 1-10-8
Enlarged Deep (Medullary/Ependymal) Veins 1-10-10
Unilateral Cavernous Sinus Mass 1-10-14
Bilateral Cavernous Sinus Lesions 1-10-18
Meckel Cave Lesion 1-10-22

Hyperdense Dural Sinus 1-10-26
(/)
Q) DURAL SINUS LESION, GENERAL
(/)
::J
c:
(/)
(/) DIFFERENTIAL DIAGNOSIS • Transverse sinus (TS) most common site
::J
o o "Flow gaps" on MRV can mimic DST
c:
Q)
Common • Confirm "flow gaps" on source data
> • Arachnoid Granulations, Dural Sinuses • No "blooming" thrombus on T2*
(/)
c: • Dural Sinus Hypoplasia-Aplasia • If MRV is unclear, CTV helpful
"(jj
> • Thrombosis, Dural Sinus • Thrombosis, Dural Sinus
l: • Dural A-V Fistula o Symptoms vary with extent of thrombus,
•..'"
CO Less Common collaterals, cortical vein involvement
o NECT
l::J
l: • Meningioma
• Metastasis • Hyperdense clot in sinus
'" • Cortical/subcortical hemorrhages
• Lymphoma
• Depressed Skull Fracture (bilateral parasagittal if superior sagittal
• Intracranial Hypotension sinus or temporal lobe if vein of Labbe)
• ± Edema (vasogenic > cytotoxic)
Rare but Important o CECT shows "empty delta sign"
• Dural Venous Sinus Stenosis o MR
• Thrombophlebitis • Loss of normal "flow void"
• Polycythemia • Clot elongated, fills sinus, shows
• Hemangioma susceptibility on T2*
• Leukemia • Confirm with MRV
• Rosai-Dorfman Disease o Chronic thrombosis difficult diagnosis
• Extramedullary Hematopoiesis • Progressive recanalization &/or
• Lipoma granulation tissue forms
• Masson Vegetant Intravascular • Chronic thrombus enhances, mimicking
Hemangioendothelioma patent dural sinus
• Dura also thickens, enhances;
ESSENTIAL INFORMATION bizarre-appearing collaterals may mimic
vascular malformation
Key Differential Diagnosis Issues • May have clinical, imaging findings of
• Includes generic lesions affecting ALLdural intracranial hypertension (pseudotumor
venous sinuses cerebri)
o Cavernous sinus (CS) unique because of
• Dural A-V Fistula
contents, proximity to skull base o Most acquired; clinical manifestations vary
o Has diagnoses (e.g., perineural metastasis,
• Pulsatile tinnitus, exophthalmos
aneurysm, schwannoma) that do not affect • Less common = progressive
other sinuses encephalopathy (dementia), diffuse
• Imaging challenge: Differentiate dural sinus white matter hyperintensity from
thrombosis (DST) from stenosis, anatomic chronic venous hypertension
variants o Imaging
o CTV best
• Flow voids within wall of thrombosed
o MRV shows anatomical
dural sinus common
narrowing/occlusion • High grade lesions prone to intracranial
o T2* (GRE/SWI) shows thrombus (usually parenchymal) hemorrhage
Helpful Clues for Common Diagnoses • Small web of vessels on collapsed MRA
• Arachnoid Granulations, Dural Sinuses images may suggest diagnosis
o Can be large (> 1 cm), remodel calvarium • DSA gold standard for diagnosis
• May narrow but not occlude sinus Helpful Clues for Less Common Diagnoses
o Round/ovoid, well-circumscribed
• Meningioma
o Enhancing dural-based mass ± "tail"
I • Dural Sinus Hypoplasia-Aplasia
o Seen in up to 1/3 of normal scans
o May invade, occlude, or compress dural
sinuses
10
2
DURAL SINUS LESION, GENERAL CIl
"
c:
III
o Bony hyperostosis variable o May cause septic venous thrombosis ::l
Co
• Metastasis • Polycythemia OJ
.,
o Systemic primaries may compress or o High hematocrit - "dense" dural sinus III
::l
invade dural sinuses • Hemangioma
o Usually arise from calvarium with o Capillary/cavernous vasoformative <
C1>
::l
secondary dural involvement neoplasm CJ>
• Lymphoma o Convexity dura or venous sinus (CS most <

C1>
o Dural-based mass(es) common in common) ::J
o
c:
metastatic lymphoma o May present with mass effect or CJ>
• Depressed Skull Fracture intracranial hypertension 0-

::l
o May lacerate/compress/occlude dural sinus • Leukemia c:
CJ>
C1>
o ± Venous epidural hematoma (EDH) o Dural-based enhancing masses CJ>
o Venous EDH develops slowly, presents o May compress/invade dural sinuses

late! • Rosai-Dorfman Disease
• Intracranial Hypotension o Younger patients
o Dural venous engorgement, enhancement o Lymphadenopathy> para nasal sinus
o Slumping midbrain, tonsillar descent, disease
SDHs o Lymphadenopathy usually coexists if C S
disease is present
o Solitary/multiple dural-based enhancing
• Dural Venous Sinus Stenosis
masses
o Focal short segmental narrowing on CTV,
MRV, or DSA (venous phase)
o Dural-based enhancing masses
o May cause intractable headaches
o Dural sinus compression/invasion rare
(intracranial hypertension)
o Patients with suspected symptomatic
• Lipoma
o Fat in dural sinus rare; CS most common
venous outflow restriction, pressure
• Masson Vegetant Intravascular
gradient at venography may improve after
Hemangioendothelioma
stent
o Rare benign tumor of young patients
• Thrombophlebitis
o Papillary endothelial hyperplasia
o Complication of infection (meningitis,
o Can cause stenosis, hypertension
rhinosinusitis, or mastoiditis)
o Can mimic meningioma
o Infection spreads easily due to valveless
nature of intracranial venous system
Arachnoid Granulations, Dural Sinuses
I
Axial T2WI FS MR shows a large ovoid CSF-signal mass Axial T1 C+ FS MR in the same patient shows that the
10
=
~ in the righllranSVerse
probably represenUng
sinus with internal "flow
vein.
void" lesion E:II does not enhance and is the same signal as
CSF. Vein ~ enhances.
in an asymptomatic
This was an incidental
patient.
finding
3
rn
Q) DURAL SINUS LESION, GENERAL
rn
OJ
c
i:Ii
rn
OJ
o
c
Q) Arachnoid Granulations, Dural Sinuses
> (Left) Axial erCT shows
rn
c hypodense CST-like
Q) lobulated filling defect in the
> right transverse sinus =.
c: Note adjacent calvarial
ltl scalloping ~ (Right) Axial
"-
ell bone CT in the same patient
"C shows smooth,
c: well-delineated erosion of
ltl
the calvarium caused by
arachnoid granulation.
Arachnoid Granulations, Dural Sinuses Arachnoid Granulations, Dural Sinuses

shows a round fluid signal
cystic lesion within the
superior sagittal sinus = that
followed CSF on all
sequences. This is a variant
case because of the atypical
size and location of the
lesion. (Right) Coronal
oblique angiography shows a
large filling defect =:I in the
superior sagittal sinus caused
by giant arachnoid
granulation.
Arachnoid Granulations, Dural Sinuses Arachnoid Granulations, Dural Sinuses

(Left) Axial T2WI MR with
video inversion shows a
cluster of sharply marginated
CSF-like cysts I2J remodeling
the inner calvarium. (Right)
arachnoid granulation that
appears to communicate
directly with the adjacent
subarachnoid space via ~1
defect in its inner margin
along the inner table of the
calvarium ~. It also
contains a hypoinlense
"knuckle" of tissue E:lthat
forms an intraosseous
meningoencephalocele.
I
10
4
DURAL SINUS lESION, GENERAL en
c:
""
III
:J
Co
OJ
..,
III
(Left) Coronal MRV shows :J

no flow-relaled signal wilhin <
CD
the left transverse or sigmoid :J
sinuses on lhe MRV MIP (/)
projection. Compare to <

CD
normal dominant right
transverse = and sigmoid
~ sinuses. (Right) Coronal
:J
o
C
(/)
MRV shows flow-related en

signal within an :J
c
=.
asymmetrically smaller lefl (/)
CD
transverse sinus it is (/)
important to review the

source images before
concluding lhatlack of flow
on MIPs is genuine.
Thrombosis, Dural Sinus Thrombosis, Dural Sinus

(Left) Sagillal CTA shows
that anterior 1/3 of superior
sagittal sinus is patent E'J.
Posterior 2/3 are filled with
nonenhancing clOI =.
(Right) Axial T2' CRE MR in
II blooming" of clot in
superior sagittal sinus EB
Note extension into adjacent
cortical veins ~

(Left) Laleral MRV shows
lack of flow-relaled
enhancement in the
expected localion of lhe
superior sagittal sinus
consistent with acute
=
lhrombosis. (Right) Axial
T2WI MR shows bilateral
parenchymal foci of swelling
and high T2 signal in areas of
associated cortical venous
ischemia = in the same
patient as the prior image.
These findings are due to
associated cortical venous
occlusion.
I
10
5
'"
QJ DURAL SINUS LESION, GENERAL
'":J
C
(f)
'"
:J
o
c
QJ Dural A-V Fistula Dural A-V Fistula
> (Left) Lateral angiography
'"c
QJ
shows thrombosis at the
junction of the transverse,
> sigmoid sinus ~ with
c: retrograde filling of
ns
L.
transverse & contralaleral
1Il dural sinuses. Several
"tl enlarged lransosseous
c:
ns perforating branches from
occipital artery supply dAVF
ffi (Right) Axial T2WI MR
shows normal right "flow
void'l liB Left side is
hyperintense and contains
numerous tiny" (Jow voids"
=.:I.Dural AVF developed in
chronically occluded left
transverse sinus.
Meningioma Metastasis
densely calcified
meningioma that originated
within and mildly expands
superior sagittal sinus =.
shows dural-based metastasis
=.:I on both sides of superior
sagittal sinus, which is
invaded and thrombosed by
the tumor E!1I.
(Leh) Sagittal T1 C+ MR
shows an enhancing
dural-based mass =.:I in the
region of cisterna magna that
is encroaching into the
region of the torcular
herophili E!1I in a patient with
systemic lymphoma. (Right)
Axial NECT shows a large
acute epidural hematoma =
due to a depressed skull
fracture through the torcular
and transverse sinus (not
shown), resulting in dural
sinus laceration and
bleeding.
I
10
6
DURAL SINUS lESION, GENERAL
III
:J
C.
III
.,
III
(Left) Coronal T7 C+ MR in :J
this patient with intracranial <
(1)
hYPolensions shows :J
engorged dural venous U>
sinuses ~ thickened <

(1)
enhancing dura ~ Pituitary :J
gland (not shown) also o
C
appeared enlarged. (Right) U>
Axial MRV shows small (j)
caliber of both :J
C
transverse-sigmoid sinus U>
(1)
junctions, with focal stenosis U>
in the left transverse sinus =

in a patienl with papilledema
and headaches.
Thrombophlebitis
bilateral proptosis. The
cavernous sinuses are
enlarged with a lack of
contrast opacification due to
thrombosis PJ:ll. Mucosal
disease and fluid levels
consistent with acute
rhinosinusitis can be seen in
multiple sinuses. (Right)
Axial NECT shows
hyperdense superior sagillal
sinus ~ & cortical veins ~
and mimics CrCT in this 22
year old patient with chronic
right-to-left cardiac shunt,
hematocrit of 67.
(Left) Coronal T7 C+ MR in
this /] year old shows a
strongly enhancing
cavernous sinus lesion
left =
encasing the left internal
carotid artery a", extending
into sella and middle cranial
fossa. (Right) Sagittal T7 C+
MR in another 73 year old
with frontal 50ft tissue
swelling shows dural,
calvaria/ enhancing mass
that occludes anterior
superior sagillal sinus PlB.
Acute lymphoblastic
leukemia was found.
I
10
7
en ENLARGED CORTICAL VEINS
OJ
en
:J
c
US o Caution: Prominent veins may persist even
en DIFFERENTIAL DIAGNOSIS
:J if no residual AV shunting present
o
C
OJ
Common • Dural A-V Fistula
> • Normal o Chronic dural sinus thrombosis
en
c • Developmental Venous Anomaly (vascularized thrombus) common
.Qj
> • Arteriovenous Malformation precursor
c • Dural A-V Fistula o Cognard type ITB shows reflux into cortical
•..
ns
[JJ Less Common veins; types III-IV have direct cortical
"C • Thrombosis, Dural Sinus drainage
C
ns • Thrombosis, Cortical Venous • Hemorrhage risk t
:J
-"Vl Rare but Important Helpful Clues for Less Common Diagnoses
• Venous Varix • Thrombosis, Dural Sinus
• Vein of Galen Malformation o Thrombosis/stenosis causes increased back
• Sinus Pericranii pressure
o T2* (clot "blooms"), CECT or Tl C+ MR
("empty delta" sign) helpful
ESSENTIAL INFORMATION • Thrombosis, Cortical Venous
Key Differential Diagnosis Issues o Can occur without dural sinus occlusion
• Is there one enlarged vein or several? o Hyperdense on NECT ("cord sign")
• Are they definitely veins? Could some be o T2* most useful ("blooms")
arteries? Helpful Clues for Rare Diagnoses
• Is there evidence of thrombosis? • Venous Varix
Helpful Clues for Common Diagnoses o Usually with AVM or dAVF
• Normal o Isolated venous varices are rare

o Major anastomotic cortical veins (Trolard, • Vein of Galen Malformation
Labbe, SMCV) can be very prominent o Deep veins but cortical may t if large
• Developmental Venous Anomaly • Sinus Pericranii
o Central vein of DVA can drain cortically o Transcalvarial communication between
o "Medusa head" configuration dural venous sinus, extracranial (scalp)
• Arteriovenous Malformation veins
o Prominent cortical veins tend to be o Sometimes associated with DVA
regional, geographically related to nidus
o Look for varices, stenoses, stagnant flow
Normal Developmental Venous Anomaly
I
10 Axial Tl C+ MR shows symmetric prominenl enhancing
comcal veins, right SlI larger than lelt 1:ll1. These are
Lateral digital subtraction angiography with
rendering shows classic DVA with "hair-like" difated
3D
much larger than the other cortical veins PJ::I. medullary veins I:ll1 and large transcortical draining vein
SlI. (Courtesy P.Lasjaunias, MOJ.
8
ENLARGED CORTICAL VEINS en
,...
c:
Ql
::l
0-
[Jl
.,
Arteriovenous Malformation Dural A-V Fistula Ql

ma,kedly enlarged cortical <
veins (/I varices") =
in a ~.
::l
patient with right frontal lobe U>
arteriovenous malformation <

CD
(not shown). (RighI) Axial TI ::J
C+ FS MR in a patient with o
c:
righllransverse sinus dAVF U>
shows reflux into very en
enlarged cortical vein B. ::J
C
Note very prominent phase U>
CD
artifact=. U>
Thrombosis, Dural Sinus Thrombosis, Cortical Venous

(Lefl) Anteroposterior
angiography shows
thrombosed left transverse
sinus [~J with prominent
filling of regional cortical
veins, including vein of
Labbe EB (RighI) Axial T2*
GRE MR shows thrombosed
superior sagittal sinus ED
with blooming clot extending
into multiple enlarged
cortical veins ~.
Vein of Galen Malformation Sinus Pericranii

(Lefl) Sagillal TI WI MR
shows variant type of vein of
Galen malformation with
enlarged vein of Galen ~
straight sinus Idl and
innumerable dilated cortical
veins (RighI) Lateral
angiography shows
paramedian venous anomaly
from the sagittal sinus
involves the sagittal sinus,
calvarium, and scalp E!iilI in a
patient with sinus pericranii.
I
10
9
rJl
Q)
ENLARGED DEEP (MEDULLARY/EPENDYMAL)VEINS
rJl
:::>
c
us DIFFERENTIAL DIAGNOSIS o On Tl C+ small AVMs may appear as focal
rJl
:::>
o
"blush" & draining vein
c Common
Q)
> Helpful Clues for Less Common Diagnoses

rJl
• Arteriovenous Malformation • Sturge- Weber Syndrome
C
.Qi o Facial hemangioma ipsilateral to
> Less Common leptomeningeal (pial) angiomatosis
C
ltl
• Sturge-Weber Syndrome o Paucity of normal cortical venous drainage
•...
l:ll • Thrombosis, Deep Cerebral Venous causes chronic venous ischemia
"0
c • Thrombosis, Dural Sinus o NECT: Cortical Ca++, atrophy
ltl
• Dural A-V Fistula o CECTITl C+ MR
• Glioblastoma Multiforme • Enhancing pial angioma
• Intracranial Hypotension • Enlarged medullary veins
Rare but Important • Enlarged choroid plexus ipsilateral to
• Capillary Telangiectasia malformation common
• Blue Rubber Bleb Nevus Syndrome o FLAIRMR: "Ivy sign" of t sulcal signal
• Dural Venous Sinus Stenosis • Thrombosis, Deep Cerebral Venous

• Vein of Galen Malformation o Usually affects both internal cerebral veins
• Demyelinating Disease, NOS (ICVs) ± vein of Galen (VaG), straight

• Lymphoma, Intravascular (Angiocentric) sinus (SS)
• Encephalitis (Miscellaneous) o Initial findings may be subtle!
• Granulomatous Angiitis o NECT
• Hyperdense ICVs ± VaG, SS
• Hypodense thalami, basal ganglia, ± deep
ESSENTIAL INFORMATION white matter
Key Differential Diagnosis Issues • ± Petechial hemorrhages
• Urgent: Look for deep (i.e., internal cerebral) o CECT
vein or dural sinus occlusion! • "Empty delta sign" if clotted SS, venous
• If not venous occlusion, consider confluence
o Could the lesion be a DVA? • May see irregular "shaggy" enhancement
o Are there prominent cortical vessels as around ventricles from engorged
well? medullary veins
o Is there associated cortical abnormality? oMR
• Tl: Deep veins iso- to hyperintense
Helpful Clues for Common Diagnoses • T2: Hypointense clot may mimic "flow
• Developmental Venous Anomaly voids"
o Enlarged medullary veins • T2/FLAIR: Bilateral basal ganglia, thalami
o Drains into single dominant transcortical hyperintensities
vein • T2* (GRE/SWI): Best sequence; clots
o Empties into dural sinus or deep
"bloom"
ependymal vein • Tl C+: Deep medullary veins may
o Solitary unless blue rubber bleb nevus enlarge, enhance
syndrome o DSA
o Hemorrhage rare unless associated with
• Absent ICVs ± nonfilling of VaG, SS
cavernous malformation • Thrombosis, Dural Sinus
• Arteriovenous Malformation o Chronic superior sagittal sinus occlusion -
o Parenchymal nidus, prominent cortical
medullary, ependymal veins enlarge as
vessels collateral venous drainage
o Enlarged medullary veins less common o Can mimic blue rubber bleb nevus
o Deep (subependymal) drainage associated
syndrome
I with t hemorrhage risk • Dural A-V Fistula
o Higher Cognard grades (IlB and above)
10
10
ENLARGED DEEP (MEDULLARY/EPENDYMAL) VEINS CIl
c:
""
ll>
• Enlarged cortical> > medullary veins • Dural Venous Sinus Stenosis ::::l
Co
• Increased flow voids near or in dural a Patients often have undiagnosed source of
.,
OJ
venous sinus severe chronic recurrent headaches !!!.
a Increased collateral flow, venous
::::l
a GBM, other malignant gliomas may prominence, variable t ICP <
~.
::::l
develop necrosis, prominent • Vein of Galen Malformation Ul
neovascularity a Infant/child with dilated VOG <

<tl
a Draining deep white matter (medullary, a Enlarged ICVs, ependymal veins> > ::::l
o
ependymal) veins may become very medullary veins C
Ul
prominent • Demyelinating Disease, NOS UJ

:J
• Intracranial Hypotension a Fulminant demyelinating disease C
Ul
<tl
a Orthostatic headaches • Causes acute perivenular inflammation Ul
a Look for "sagging" floor of 3rd on sagittal, • Increased blood flow, loss of normal BBB
tonsillar herniation a MS, ADEM, acute necrotizing/hemorrhagic
a Passive dural venous congestion common; leukoencephalopathy variants
medullary/deep ependymal vein a Enhancement of deep medullary veins
enlargement less common may be very prominent
Helpful Clues for Rare Diagnoses • Lymphoma, Intravascular (Angiocentric)
a Clinical presentation
• Capillary Telangiectasia
a Large capillary telangiectasia (typically> 1
• Stroke-like symptoms
cm) may have prominent central draining • Less common: Dementia, progressive
vein mental status decline
a Intravascular tumor plugs ± extension into
a Best seen on Tl C+ scan
a Becomes hypointense on T2* (GRE/SWI)
perivascular spaces
a Punctate, linear enhancing foci
images
• Blue Rubber Bleb Nevus Syndrome • Encephalitis (Miscellaneous)
a Parenchymal T2/FLAIR abnormality ±
a Multiple cutaneous (bluish venous "blebs"),
GI hemangiomas mild-moderate enhancement
a Diverse CNS vascular malformations,
• Granulomatous Angiitis
a Enhancing foci ± mass effect
venous variants common
a May have striking deep perivenular
• Multiple DVAsclassic
• Variant: Sinus pericranii & multiple enhancement
DVAs
Developmental Venous Anomaly
I
Axial T1 C+ MR shows prominent medullary tribularies
~ of deep OVA. Prominenl septal, internal cerebral,
Ulleral 3D OSA shows a classic deep OVA. Oi/aled
medullary veins ~ drain into enlarged deep
10
subependymal roof veins 81 drained lesion. This was subependymaJ veins ~ and from there into internal
an incidenlal finding. cerebral vein 81. (Courtesy P.Ulsjaunias, MO).
11
<IJ
<1l
ENLARGED DEEP (MEDULLARY/EPENDYMAL) VEINS
<IJ
:::J
C
U5
<IJ
:::J
o
c
<1l Arteriovenous Malformation Sturge-Weber Syndrome
> (Left) Axial T I C+ MR haws
<IJ
c left parietal AVM wilh
-03 deep drainage into
> subependymal veins of
C lateral ventricle ~ NOle
•..
III
llJ
enlargement of choroid
plexus glomus secondary
"'C to increased venous
c: drainage_ (Right) Axial T1 C+
III
MR shows enhancing pial
malformation ~ Note
enlarged left thalamo-slriale
vein III prominent choroid
plexus IlI1 typical secondary
findings in Slurge-Weber
syndrome.
Thrombosis, Dural Sinus

striking linear enhancement
in deep medullary veins
secondary to venous stasis
=
caused by bilateral ICV
occlusion. (Right) Lateral
angiography shows poor
opacification of 555, with
only a few irregular, small
parasagitlal channels open
lCB Most venous drainage is
occurring through massively
enlarged medullary veins
inlO prominent
subependymal veins, ICV
~
(Left) Coronal T1 C+ MR in a
patient with chronically
thrombosed left transverse
sinus shows prominent white
matter "blushll =
with
enlarged medullary. deep
ependymal veins Ia. (Right)
Axial T1 C+ MR shows an
enhancing DVF
subslantial band of
=
wilh a
phase-encoding artifact.
There is a prominent
left-sided enhancing basal
vein •.
I
10
12
ENLARGED DEEP (MEDULLARY IEPENDYMAL) VEINS
Dl
::s
c.
..,
CD
Glioblastoma Multiforme Intracranial Hypotension Dl
::s
shows enhancing necrotic <
CD
right parieto·occipital mass ::s
a with very prominent (J)
draining veins ~. Biopsy <

CD
had dise/osed CBM. (RighI) ::s
Axial T1 C+ MR shows mild o
c
diffuse dural enhancement (J)
and prominence of the en

internal cerebral veins =. ::s
c
Venous distension is a (J)
CD
feature of decreased ICP. (J)
Demyelinating Disease, NOS

incidental finding of 12 mm
capillary telangiectasia in
deep cerebral white maller
E±. Note prominent central
vein ~ draining £0
subependymal vein of lateral
ven/rie/e. (Right) Axial T I C+
MR shows multiple enlarged,
enhancing medullary
subependymal s::I veins.
= and
Biopsy was consistent with

ADEM.
shows multiple linear
enhancing foci along deep
medullary veins and
perivascular spaces =.
Biopsy proved intravascular
lymphoma. (Right) Sagillal
T1 C+ MR shows multiple
linear enhancing foci in deep
periventricular white matter
cerebellum. This is
biopsy-proven
(Courtesy /. Pingree, MD).
I
10
13
en UNILATERAL CAVERNOUS SINUS MASS
QJ
en
:J
c
(/)
en DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
:J
o • Pituitary Macroadenoma
C Common
QJ
o Cavernous sinus invasion common with
> • Pituitary Macroadenoma
en macroadenoma
c • Meningioma
QJ o Difficult to determine unless florid
> • Schwan noma
o Mass, gland indistinguishable (gland IS
C • Metastases, Skull and Meningeal
•..
l'Cl
• Lymphoma, Metastatic, Intracranial mass)
[JJ
• Nasopharyngeal Carcinoma • Meningioma
'C
c o Diffusely infiltrates sinus, thickens dura
l'Cl
Less Common o Lateral dural wall can sometimes be
:J • Saccular Aneurysm
-"(/) identified within thickened, intensely
• Carotid-Cavernous Fistula, Traumatic enhancing CS mass
• Thrombosis, Cavernous Sinus o Look for dural "tail" along clivus,
• Dermoid Cyst tentorium
• Epidermoid Cyst o Look for other meningiomas (multiple
• Neurosarcoid meningioma syndrome)
• Pseudotumor, Intracranial • Schwannoma
• Hemangioma o Most common = trigeminal, in Meckel
Rare but Important cave
• Plexiform Neurofibroma o Typically well-marginated
• Chordoma o Usually hyperintense on T2WI

• Tuberculosis o Solitary> multiple (NF2)
• Iatrogenic • Metastases, Skull and Meningeal

o Three patterns
• Hematogenous (direct or extension from
ESSENTIAL INFORMATION skull base)
Key Differential Diagnosis Issues • Perineural along cranial nerve (usually
• Lateral dural walls of cavernous sinuses (CSs) from nasopharyngeal or sinus tumor)
should be flat or concave on axial/coronal • Direct geographic invasion (squamous
imaging cell, minor salivary gland tumors most
o Convex outer margin indicates common primaries)
abnormality • Lymphoma, Metastatic, Intracranial
o Lateral dural wall thick, easy to see; medial o Primary CS rare; usually history of disease
= thin, difficult to delineate elsewhere
• CSs are septated (not single pool of venous • Nasopharyngeal Carcinoma
blood) o Two patterns
• CSs enhance strongly but contain normal • Direct cephalad extension into central
filling "defects" (Meckel cave, cranial nerves, skull base, CS
ICA) • Perineural extension into cavernous
• If mass present, is it intrinsic or extrinsic to sinus(es) along CNV2
cavernous sinus? Helpful Clues for Less Common Diagnoses
• Where does mass originate? • Saccular Aneurysm
o Sella: Pituitary macroadenoma o Can be spontaneous, post-traumatic
o Sphenoid sinus/central skull base: (pseudoan eu rysm)
Metastasis, nasopharyngeal carcinoma o Can be patent or partially thrombosed
o Dura: Meningioma, hemangioma, o Prominent "flow void", pulsation (phase)
pseudotumor artifact
• Does it contain "flow voids"? • Carotid-Cavernous Fistula, Traumatic
o Aneurysm o Superior ophthalmic vein enlarged
I o Dural AVF o ± Basilar skull fracture
10
14
UNILATERAL CAVERNOUS SINUS MASS en
"
c:
III
o Usually at junction of vertical, horizontal Helpful Clues for Rare Diagnoses :J
Co
ICA segments
• Thrombosis, Cavernous Sinus
• Plexiform Neurofibroma ..•
tll
III
o Occurs only in NFl :J
o onenhancing thrombus, thickened o Involves cutaneous, orbital branches of
enhancing dural walls <
CNS ~-
:J
o May be secondary to sinusitis C/I
o Infiltrative, unencapsulated mass
(thrombophlebi tis) o Look for <
ct>
o Superior ophthalmic vein(s) often enlarged :J
• Scalp neurofibromas o
c:
o Proptosis common C/I
• Sphenoid wing dysplasia
• Dermoid Cyst 0.
• Chordoma :J
c:
o Typically in Meckel cave, not CS proper
o Destructive mass, midline> lateral C/I
ct>
o Fat density/signal intensity C/I
o Occasionally can originate in CS or extend
• Epidermoid Cyst asymmetrically from clivus into CS
o Typically in Meckel cave, not CS proper
o Most are very hyperintense on T2WI
• Tuberculosis
o Usually occurs as extension from CPA
o History of pu lmonary TB
lesion o Dura-arachnoid thickening from basilar
• Neurosarcoid meningitis
o Can be uni- or bilateral
• Iatrogenic
o Look for thickened infundibular stalk,
o Post-operative packing after
dural masses trans-sphenoidal macroadenoma resection
• Pseudotumor, Intracranial o Look for surgical defect in sellar floor
o Un i- > bilateral
o Caused by overpacking of defect
o Typically extends posteriorly from orbital
o May appear very bizarre
apex into CS o Fat suppression sequence helpful
o Extensive dural enhancement along
middle fossa can be present
o Occasionally can be invasive, destructive;
mimics neoplasm or aggressive infection
• Hemangioma
o True vasoformative neoplasm in CS, dura
o May mimic meningioma
I
Coronal T2WI MR shows macroadenoma thal eXlends
into the left cavernous sinus lCB displacing and
Axial TI C + FS M R shows meningioma 01 the right
cavernous sinus = with thickening along both sides of
10
encasing the cavernOUSinternal carotid artery Eli:I. The the lateral dural waif Eli:I and effacement 01 the internal
tumor laleralto the ICA I:] confirms CS invasion. archilecture comparecllo the norma"ell side!:l:.
15
en UNILATERAL CAVERNOUS SINUS MASS
QJ
en
::J
c
U5
en
::J
o
C
QJ Schwannoma Metastases, Skull and Meningeal
> (Left) Axial T I C+ MR shows
en a classic trigeminal
c
QJ schwannoma in the right
> Meckel cave 81. Compare
c with the normal left side !:l:l.
•...
'" Schwannomas are typically
/Xl hyperintense on T2WI,
"C enhancing strongly. (Right)
c
Coronal TI C+ FS MR shows
'" a unilateral cavernous sinus
::J metastasis m.
-"en
Lymphoma, Metastatic, Intracranial Nasopharyngeal Carcinoma

(Left) Axial T7 C+ FS MR in
patient with non-Ilodgkin
lymphoma who presented
with left-sided facial
weakness shows an
enhancing mass along the
maxillary division of CNS in
the cavernous sinus =-
extending into the apex of
the pterygopalatine fossa 81.
(Right) Axial TI C+ FS MR
shows nasopharyngeal
carcinoma spreading into the
=-
c/;vus
sinus/Meckel cave =
the left cavernous
and
intracavernous carotid artery
wall~
fLeft) Axial CTA in a man

with a headache, remole
history of MVA sho\Vs a
partially calcified right
cavernous carotid artery
pseudoaneurysm =:II. fRight)
Axial CECT shows prominent
orbital vessels =:II and a
markedly enlarged right
superior ophthalmic vein ~
in a patient with trauma and
right-sided proptosis. The
righl cavernous sinus is also
distended, showing
abnormal enhancement m.
I
10
16
UNILATERAL CAVERNOUS SINUS MASS en
"
c:
III
:J
Co
..•
t1J
Dermoid Cyst III
(Left) Axial TI C+ FS MR in a
:J
patient with acute sphenoid <
sinusitis shows a unilateral ~.
::J
nonenhancing clot in the Ul
cavernous ICA =-
right CS 8l a thrombosed
and early
cerebritis in the adjacent
<
CD
::J
o
c:
brain ~. (RighI) Axial TI WI Ul
MR shows a dermoid cyst in (f)
the right Meckel cave and ::J

cavernous sinus =. C
Ul
CD
Compare to the normal Ul
CSF-filled left Meckel cave

~.
Neurosarcoid
an epidermoid cyst
originating in the left Meckel
cave C. Note that the
epidermoid-filled Meckel
cave is slightly more
hyperintense than the
normal right CSF-filled left
Meckel cave ~. (Right)
Axial TI C+ FS MR shows
sarcoidosis infiltrating the
right cavernous sinus r=J and
extending along the dura of
the tenlOrium C & the
anterior middle cranial fossa
81.
(Left) Axial TI C+ MR in
woman with headache,
nausea, and vomiting shows
thickened dura along the left
cavernous sinus Ill.
SymplOms and findings
resolved quickly after IV
steroids. (Right) Axial TI C+
MR shows a clival chordoma
81 with extension into the
left cavernous sinus ~. The
right cavernous sinus,
including the Meckel cave
=.. is normal.
I
10
17
C/)
Q) BILATERAL CAVERNOUS SINUS LESIONS
C/)
::::J
C
us DIFFERENTIAL DIAGNOSIS • Variable extension into CS proper
C/)
::::J
o o Look for "dural tail" (thickening along
C
Q)
Common tentorium, middle fossa)
> • Pituitary Macroadenoma o Look for obliteration of CSFin Meckel
C/)
c • Meningioma caves
"Qj
> • Metastasis, Skull Base o May extend inferiorly along clivus
c • Lymphoma, Metastatic, Intracranial
..
'cv
1II Less Common
• Metastasis, Skull Base
o Permeative, destructive mass
"0
• Neurofibromatosis Type 2 • Hematogenous spread from extracranial
c
ltl
• Carotid-Cavernous Fistula primary common (e.g., breast)
• Thrombosis, Cavernous Sinus • Most commonly centered in central skull
• Chordoma, Clivus base (BaS), secondary extension into CS
• Plasmacytoma • May also be direct geographic extension
• Neurosarcoid from nasopharyngeal carcinoma
• Langerhans Histiocytosis, Skull Base o CS involvement can be uni-, bilateral;
symmetric or asymmetric
Rare but Important o Sagittal TI, coronal TI C+ FS scans useful
• Pseudotumor, Intracranial • Lymphoma, Metastatic, Intracranial
• Leukemia o Primary central BaS lymphoma rare
• Extramedullary Hematopoiesis o Uni- > bilateral
• Germ Cell Neoplasms o Isointense, avidly enhancing
• Erdheim-Chester Disease o Associated cranial nerve, meningeal (dural)
• Benign Nonmeningothelial Tumors lesions common
o Tumor often surrounds, encases but does
ESSENTIAL INFORMATION not occlude cavernous ICAs
o Multiple schwannomas, meningiomas
• Most common CS schwannoma =
trigeminal (Meckel cave)
• Look for meningiomas of CS, optic nerve
sheath, tentorium
o Look for bilateral vestibular schwannomas
(YS, diagnostic of NF2), evidence for prior
CPA/temporal bone surgery
• One YS + other schwan noma,
meningioma highly suggestive
• Carotid-Cavernous Fistula
o Uni- > bilateral carotid-cavernous fistulas
o Look for CS "flow voids" in addition to
ICAs
o Look for t superior ophthalmic vein(s)
(SOY)
• CTA helpful screening study
• DSAto delineate fistula site(s)
• Thrombosis, Cavernous Sinus
o Can be spontaneous, sterile, or septic
(thrombophlebitis)
• Look for infection in paranasal sinuses,
I orbits
10
18
BILATERAL CAVERNOUS SINUS LESIONS
Ql
o Nonenhancing areas within intensely Helpful Clues for Rare Diagnoses
::I
0-
enhancing CS • Pseudotumor, Intracranial ro
..•
• Lateral dural wall, CS septations o 90% of intracranial pseudotumors occur
Ql
::I
enhance, thrombus does not without orbital disease
• Look for t SOVs <
CD
o Tolosa-Hunt syndrome (painful ::I
• Chordoma, Clivus ophthalmoplegia) when CS involved en
o Destructive T2 hyperintense mass centered
• Uni- > bilateral <
CD
in clivus ::J
• Look for associated meningeal o
c
o Large lesions may invade CS thickening (can be extensive) en
• Displace but rarely occlude ICAs S[l
• Bone invasion, destruction may occur ::J
o Chondrosarcoma may mimic C
en
• Leukemia CD
• Usually unilateral, arises from o Paranasal sinus/orbit involvement typical
en
petro-occipital fissure o Bilateral CS involvement rare
• Plasmacytoma • Extramedullary Hematopoiesis
o Solitary destructive mass of central BOS
o CS involvement rare
• Centered in sphenoid sinus, clivus o Look for associated dural-based masses
• Isointense, strongly enhancing mass (calvarium, spine)
• Bi- > unilateral • Germ Cell Neoplasms
• Neurosarcoid o Rare; typically involve pituitary gland/stalk
o CS rare site
• Erdheim-Chester Disease
o Look for other lesions
o Rare non-Langerhans cell histiocytosis
• Pituitary, infundibular stalk lesion o Disseminated xanthogranulomatous
• Cranial nerve involvement infiltrative disease of unknown origin
• Dural-based masses o Adults> children
o Infiltrating CS mass(es) o Long bones> brain, CS, orbits (rare)
• Lesions enhance strongly, uniformly • Benign Nonmeningothelial Tumors
• Bone destruction rare o Benign cartilaginous tumors may arise
• Langerhans Histiocytosis, Skull Base from central BOS
o Osteolysis with sharply defined scalloped
o If large, extend intracranially into CS
margins ± soft tissue mass
o Varies from small punched out lesion to
widespread diffuse bony involvement
• May destroy almost entire BOS
o Homogeneous enhancement
I
Coronal T1 WI MR shows a large macroadenoma with
the "figure-of-eight" configuration, extension into the
Axial T1 C+ rs MR shows a strongly enhancing central
skull base mass extending laterally into both cavernous
10
suprasellar cistern and both cavernous sinuses aD. sinuses l:l1. A histologically typical meningioma was
lound at surgery.
19
(/)
Q) BILATERAL CAVERNOUS SINUS LESIONS
(/)
:J
C
(f)
(/)
:J
o
C
Q) Metastasis, Skull Base Lymphoma, Metastatic, Intracranial
> (Left) Axial T7 C+ FS MR
(/)
c shows a classic case of
"Qi nasopharyngeal carcinoma
> extending superiorly into the
c:: sphenoid sinus, clivus, and
ltl
•... cavernous sinuses =. The
m left Meckel cave is involved
"'C while the right BI is spared.
c:: (Right) Axial T7 C+ MR
ltl
shows an extensive,
destructive central skull base
mass that infiltrates the
sphenoid sinus and both
cavernous sinuses =. The
mass encases both
cavernous carotid arteries
~"
Neurofibromatosis Type 2 Carotid-Cavernous Fistula

(Leh) Coronal T 1 C+ FS MR
shows schwannomas in both
Meckel caves =. Bilateral
vagal schwannomas are also
present~. (Right) Axial
T2WI MR shows numerous
abnormal II (Jow voids II,
predominately in the left ~
but also the right =
cavernous sinuses, in this
patient with red eye,
proptosis 2 weeks following
head trauma.

bilateral cavernous sinus
thrombosis, resulting as a
complication of acute
sinusitis. Note nonenhancing
sinus=-
areas within the cavernous
thickened
=
enhancing dura of tentorium
and sphenoid wings BI.
shows a large dival
chordoma with bilateral
cavernous sinus invasion S.
I
10
20
BILATERAL CAVERNOUS SINUS LESIONS CIl
~
c:
III
::l
Co
CD
.,
Neurosarcoid III
::l
shows isointense central skull <
(1)
base mass that extends ::l
superiorly into the sella (f>
turcica and both cavernous <

(1)
sinuses (Right) Coronal ::J
T1 + FS MR shows both o
C
Meckel caves Iilled with (f>
strongly enhancing tissue m. CIl

Note that the infundibular ::J
C
stalk 81 and pituitary gland (f>
(1)
appear normal. (f>
langerhans Histiocytosis, Skull Base Pseudotumor, Intracranial

ILeft) Coronal CECT shows a
central skull base lytic lesion
with sharply defined
margins. A large 50ft tissue
component invading skull
base, both cavernous
sinuses, and nasopharynx P.:I
enhances strongly and
uniformly. (Right) Axial T1
C+ MR shows bilateral
cavernous sinus
enhancement left more
striking than right, in a
patient with left-sided cranial
neuropathies. Symptoms
resolved with the
administration of steroids.
leukemia Germ Cell Neoplasms

a leukemic mass in the right
orbit !::l infiltrating the
lacrimal gland and the
superior reclus muscle ~
Note isoinlenS€ tissue in
both cavernous sinuses ~
suggesUng extension of
leukemic infiltrate. (Right)
Coronal CECT shows an
enhancing mass infiltrating
the pituitary gland 81 and
both cavernous sinuses =.
I
10
21
en MECKEl CAVE lESION
Q)
en
:::J
c
(f)
en DIFFERENTIAL DIAGNOSIS • Acute - hyperintensity, enhancement of
:::J --- muscles of mastication
o
C
Q)
Common • Chronic - atrophy, fatty infiltration of
> • Schwannoma, Trigeminal, Intracranial muscles of mastication
en
c • Meningioma
Q) Helpful Clues for Common Diagnoses
> • Metastasis, Skull Base
• Schwannoma, Trigeminal, Intracranial
C
less Common o Variable configuration
•..
ltI
• Metastasis, CSF/Meningeal
1IJ • "Dumbbell" tumor with CPA component,
"'C
C
• Metastasis, Perineural CNV3 constriction of tumor at entrance to
ltI
• Meningitis Meckel cave, Meckel cave mass
• Neurosarcoid • May involve MC only
• Neurofibroma • ± Extracranial extension along VI, V2,
• Pseudotumor, Intracranial &/or V3
• Pituitary Macroadenoma o Unilateral unless NF2
Rare but Important o Hyperintense on T2WI, strong
• Metastasis, Perineural CNV2 enhancement on TI C+
• Trigeminal Herpetic Neuritis o May result in atrophy of muscles of
• Lipoma mastication
• Epidermoid Cyst • Meningioma
• Dermoid Cyst o Uni- > bilateral involvement
• Neurocysticercosis o Dural thickening along cavernous sinus,
• Chronic Thrombosis, Dural Sinus tentorium (dural "tail sign")
o ± Ipsilateral denervation, atrophy of
muscles of mastication
ESSENTIAL INFORMATION • Metastasis, Skull Base
---
Key Differential Diagnosis Issues o Metastases to Meckel cave can be
• Normal Meckel cave (Me) hematogenous, direct geographic

o Anatomy extension, perineural, or CSF spread
• CSF-filled, dura-arachnoid lined • Hematogenous spread to central skull
invagination into cavernous sinus (CS) base (BaS) with secondary involvement
• Contains CNS fascicles, semilunar of cavernous sinus
ganglion • Direct extension from extracranial
• Communicates directly, freely with primary (e.g., nasopharyngeal squamous
prepontine/cerebellopontine cisterns cell carcinoma) into central BaS
o Normal imaging • Uni- > bilateral involvement
• Ovoid, smooth CSF-filled cisterns on o Sagittal Tl WI helpful
axial, coronal scans resemble "open eyes" • Look for replacement of normal fatty
• Bilaterally symmetric hypointensity on clival marrow ± cortical destruction
TlWI Helpful Clues for less Common Diagnoses
• Bilaterally symmetric hyperintensity on • Metastasis, CSF/Meningeal
T2WI o Pia-arachnoid tumor spread may extend
• Abnormal Meckel cave into MCs
o "Winking" Meckel cave sign o ± Enhancement along cisternal CNS
• One MC filled with soft tissue, not CSF • Metastasis, Perineural CNV3
• One MC therefore NOT = CSF o Retrograde tumor spread along mandibular
density /intensity nerve
• Asymmetric appearance = "Winking" o Look for mass in retromolar trigone,
Meckel cave (one "eye" appears closed) masticator space
o Look for CNS motor denervation
I secondary to MC mass
o Adenoid cystic carcinoma, squamous cell
carcinoma most common
• May be only sign of subtle lesion
10
22
MECKEL CAVE LESION CJl
'"
c:
ll>
o CNV3 appears thick, enhancing ± erosion ::]
Helpful Clues for Rare Diagnoses Q.
of foramen ovale • Metastasis, Perineural CNV2 ..,
OJ
ll>
• Meningitis o Often skin carcinomas (basal, squamous ::]
o Any etiology (e.g., pyogenic, TB) cell)
o Dura-arachnoid disease can extend into
<
(1)
o Infiltrates along inferior orbital canal :J
MC o May enlarge/erode foramen rotund urn
(f)
o Look for basal cistern enhancement o Thickened, enhancing maxillary nerve

<
(1)
:J
• Neurosarcoid • Trigeminal Herpetic Neuritis .. o
C
o Pituitary gland, infundibular stalk, dural o Herpes zoster oticus > trigeminal neuntls
(f)
CJl
masses common o Edematous, enhancing CNS :J
o Can be uni- or bilateral C
• Ophthalmic division most commonly (f)
(1)
• Neurofibroma involved
(f)
o Orbit/scalp/lid plexiform in NFl

• Lipoma
o May extend posteriorly through SOF,
o MC is rare site
infiltrate VI branches - MC o Uni- > bilateral
• Pseudotumor, Intracranial • Epidermoid Cyst
o Typically originates in/around orbit
o May originate in MC or as extension from
o Extends through SOF into CS, MC
CPA epidermoid
o Variable dura-arachnoid thickening, o Does not suppress on FLAIR;restricts on
enhancement DWI
o Idiopathic invasive subtype
• Dermoid Cyst
• May erode bone, mimic aggressive o Looks like fat in MC, not CSF
infection, neoplasm o May occur with or without rupture, CSF
• Pituitary Macroadenoma fatty droplets
o Can extend into one or both CSs, MCs
o Pituitary gland generally cannot be
o Cysts in basal cisterns may extend into one
distinguished from mass or both MCs
o Gland IS mass
• Chronic Thrombosis, Dural Sinus
o Aggressive invasive type may destroy
o Chronically occluded dural sinus(es)
central skull base, clivus o Dural thickening, enhancement secondary
• Pituitary adenoma> > > > carcinoma to collateral venous drainage
• Can mimic malignant disease, so do o May involve one or both MCs
endocrine workup
I
Coronal T2WI MR shows a classic "winking Meckel
cave sign". The normal (right! Meckel cave is CSF-filled,
Coronal T7 c+ MR in the same patient shows that the
normal Meckel (right! is CSF-filled and hypointense 81
10
hyperintense 81. The left side is filled with a mass that is
hypointense and expands the Meckel cave =. =.
on this sequence. Contrast this with the enhancing mass
that fills the left Meckel cave
23
(J)
Q) MECKEL CAVE LESION
(J)
:0
C
CIJ
(J)
:0
o
C
Q)
> (Left) Coronal T1 C+ MR

(J)
c shows a meningioma in the
Q) right Meckel cave =:I. The
> left Meckel cave is filled with
C CSF E!:II as is normal. (Right)
III Axial T1 C+ MR shows a
"-
II) metastasis 10 the left petrous
"t:J apex that extends in10 the
C
III clivus and the left Meckel
cave =:I. The right Meckel
cave B is normal and
CSF-filled.
Metastasis, CSF/Meningeal
(Left) Axial T I C+ FS MR in
patient with diffuse CSF
spread of glioblastoma
multiforme shows pial
metastases covering the
cerebellum~. The tumor
has spread into the left
Meckel cave =:I. Note the
normal csr in the right
Meckel cave E!:II. (Right)
Coronal T I C+ FS MR shows
perineurallumor extension
of squamous cell carcinoma
from the masticator space
E!:IIthrough an enlarged
foramen ovate ~ into the
left cavernous sinus and
Meckel cave =:I.
Neurosarcoid
shows basilar and cisternal
meningitis = with
thickened, enhancing
meninges and extension into
the right Meckel cave ~.
(Right) Coronal T1 C+ FS
MR shows a sarcoid
infiltrating the pituitary gland
E!:II as well as both Meckel
caves =.
I
10
24
MECKEl CAVE LESION ,..c:
Ul
Ql
:J
C.
...
tll
Ql
Metastasis, Perineural CNV2
:J
an enhancing lesion in left <
cavernous sinus & Meckel ~.
:::J
cave l:ll. Thickened dura, (j)
enhancing pituitary gland, & <

CD
infundibulum (not shown) :::J
were also present. o
c:
Symptoms, findings resolved (j)
after steroids. (Right) Axial Ul

C[CT w!curved reformatted :::J
c:
(j)
image shows cheek
CD
melanoma l:ll spreading (j)
along left CNV2 from

infraorbital foramen through
inferior orbital canal !J::l &
foramen {alundum ~ into
Meckel cave B1. (Courtesy
5. van der Westhuizen, MO).

an enhancing right CNS l:ll
extending into the Meckel
cave. The left trigeminal
nerve BI and Meckel cave
appear normal. (Right) Axial
T2WI MR shows an
epidermoid in the upper
CPA cistern wrapped around
CNS, extending into the right
Meckel cave l:ll. The
epidermoid cyst is slightly
hyperintense to CSF in the
normal left Meckel cave B1.
Dermoid Cyst Chronic Thrombosis, Dural Sinus

(Left) Axial N[CT shows a
fat-I.ike lesion in the right
Meckel cave found
incidentally in a patient with
a headache after trauma. MR
discf.osed a ruptured
dermoid cyst with multiple
fat droplets in the CSF
cisterns. (RighI) Coronal TI
C+ MR in a patient with
multiple chronically
occluded venous sinuses
shows dural l:ll and Meckel
cave B engorgement
caused by collateral venous
drainage pathways.
(Courtesy M. Castillo, MO).
I
10
25
en HYPERDENSE DURAL SINUS
OJ
en
::J
c::
(f)
en DIFFERENTIAL DIAGNOSIS Helpful Clues for Common Diagnoses
::J
o • Physiologic Hyperdensity
c::
OJ
Common
> o At hematocrit of 43 (normal)
• Physiologic Hyperdensity
en
c:: • Thrombosis, Dural Sinus • Intravascular blood in arteries, veins,
OJ
• Polycythemia dural sinuses appears slightly hyperdense
> compared to normal brain
c:: • Subdural Hematoma, Acute (Mimic)
•..
t1l • At hematocrit of 70, circulating biood
lD less Common 63% denser
"0
c:: • Lymphoma, Metastatic, Intracranial o Dural sinuses appear especially dense in
t1l
• Metastases, Skull and Meningeal newborns because of
::J • Meningioma
-'" • Physiologic polycythemia at birth
(f)
Rare but Important • Unmyelinated/low density brain
• Hemangioma • Thrombosis, Dural Sinus
• Leukemia o Many causes of DST
• Extramedullary Hematopoiesis (Mimic) o Trauma
• Masson Hemangioma • May tear sinus
• ± Thrombosis
• Thin subdural hematoma can layer along
ESSENTIAL INFORMATION falx, tentorium, mimic "empty delta
Key Differential Diagnosis Issues sign" (latter seen on CECT, not NECT!)
• Evaluate density, configuration of dural o Meningitis
sinuses o Dehydration, hypovolemia
o ALLdural sinuses appear slightly • Shock, cardiac failure, other "low flow"
hyperdense compared to adjacent brain, states
CSF on NECT o Hypercoagulable states
o Margins of dural sinuses typically flat or • Antiphospholipid antibody syndrome
slightly concave • Von Willebrand disease
• Density: Is "dense dural sinus" TOO dense? • Post-anticoagulation "rebound"
o Measure dural sinus density phenomenon
o Compare to internal carotid artery (as • Postpartum
internal standard) o Hormonal
o If too dense, is it thrombosis or • Pregnancy, postpartum
polycythemia? • Oral contraceptives
• Dural sinus thrombosis (DST) > > o Hemoglobinopathies (e.g., sickle cell
polycythemia disease, thalassemia)
• Check hematocrit! o Vasculitis
• If any question, do CECT + CTV or MR + • Some vasculitides (e.g., Behc;:et)have
MRV (include GRE or SWI sequence!) propensity to cause DST
• Look for nonenhancing thrombus • Polycythemia
• Configuration: Disrupted dural sinus, o Can be physiologic
bulging dural sinus, irregular/lobulated dural • Newborn
sinus • High altitude
o Some neoplasms invade dural sinuses o Pathologic
o Usually meningioma or metastasis • Cyanotic congenital heart disease
o May appear hyperattenuating if densely • COPD
cellular o ALLvessels (arteries, veins, dural sinuses)
o May also cause dural sinus thrombosis become hyperdense in polycythemia
(e.g., meningioma in superior sagittal • t Hemoglobin protein - t dural sinus
sinus) density
I • NECT in patient with polycythemia
"looks like" a CECT
10
26
HYPERDENSE DURAL SINUS
• Do not mistake for DST (MR + MRV • Leukemia

clarifies) o Dural-based mass(es) along falx can mimic
• Subdural Hematoma, Acute (Mimic) DST
o May layer along tentorium, superior o Adjacent to, usually not within, venous
sagittal sinus ..• mimic dural thrombosis sinus <
~.
Helpful Clues for less Common Diagnoses • Extramedullary Hematopoiesis (Mimic) '"
CJ)
o Dural-based mass(es) typical adjacent to, <

• Lymphoma, Metastatic, Intracranial CD
not within, venous sinus 'c"
o
o Central skull base lymphoma may extend
diffusely • Masson Hemangioma CJ)
o Synonyms en
• Destroys bone
• Vegetant intravascular '"
c
• Infiltrates adjacent structures CJ)
CD
hemangioendothelioma CJ)
• May extend into one or both cavernous
• Intravascular papillary endothelial
sinuses
hyperplasia (IPEH)
o Hyperdense, strongly enhancing
o Found in head, neck, fingers, trunk,
• Metastases, Skull and Meningeal
occasionally viscera (liver)
o Skull metastases commonly invade
o Exuberant endothelial proliferation within
underlying dura
veins, including dural venous sinus
o If adjacent to dural venous sinus, may
o Benign; can be mistaken for angiosarcoma
extend into and compromise sinus
• Meningioma Other Essential Information
o Expands into (or, less commonly, • Foreign body can mimic DST
originates from) dural venous sinus o Retained medical devices, catheters, bone
o Grows slowly, so collateral blood flow cement, AVM glue, bullets, etc.
develops
o Sellar/parasellar/clival meningiomas
SELECTED REFERENCES
commonly involve one or both cavernous
1. Teksam Met al: Frequency and Topographic Distribution of
sinuses Brain Lesions in Pediatric Cerebral Venous Thrombosis.
AJNR Am J Neuroradiol, 2008
Helpful Clues for Rare Diagnoses 2. Healy JF et al: Polycythemia mimicking venous sinus
• Hemangioma thrombosis. AJNR Am J Neuroradioi. 23(8):1402-3, 2002
o Capillary &/or cavernous hemangiomas
may arise within dura
o Cavernous sinus common site
o May mimic meningioma
I
slighdy hyperdense =-
Coronal NECT in an asymptomaUc adult shows normal,
superior sagittal sinus falx -=
Axial NECT shows relaUvely hyperdense internal carotid
arteries in a neonate. Note that the dural venous
10
cerebri=. sinuses 81 also appear hyperdense. Low density of
unmyelinated brain accentuates this appearance.
27
(j)
Q) HYPERDENSE DURAL SINUS
(j)
:::J
C
C/)
(j)
:::J
o
C
Q) Thrombosis, Dural Sinus
> (Left) Axial NECT in a
(j)
c premature infant shows
'Qi striking hyperdensity of
> transverse sinuses II] caused
c by physiologic polycythemia
C'Cl of newborns and Jow density
"-
ell of adjacent, almost
"'C completely unmyelinated
c brain. (Right) Axial NECT
C'Cl
shows a moderately
hyperdense superior sagittal
sinus 1m (contrast with
normal mild hyperdensity).
Note subtle effacement of
the left frontal sulci E!l:I
subarachnoid hemorrhage
(later identified on FLAIR
MR).

hyperdense, expanded
straight sinus with convex
margins =. The clot extends
into the vein or Galen B
torcular Herophili PJ::I.
(Right) Axial NECT in the
same patient shows
hyperdense, expanded,
somewhat
lobulated-appearing superior
sagillal sinus ICB clot in
cortical vein ~ ("cord
sign").
(Left) Axial NECT looks like it

is a contrast-enhanced scan.
It isn't! The patient has a
markedly elevated
hematocri( which makes
dura = intracranial arteries,
veins, venous sinuses I;] all
appear hyperdense. (Right)
Axial NEeT in the same
patient shows striking
hyperdensity of superior
sagittal sinus = caused by
polycythemia (hematocrit =
70).
I
10
28
HYPERDENSE DURAL SINUS Ul
'"c:
III
::::l
a.
OJ
....•
III
(Left) Axial NECT in a patienl

::::l
with subdural hematoma <
ctl
shows mimic of thrombosed OJ
dural sinus. High densily en
blood is layered along the <
ctl
straighl sinus and falx ~ It ::::l
also mimics lhe "empty delia o
c:
sign" seen with OS!. en
which is idemified on CECT (f)
as enhancing dura ::::l

c:
surrounding nonenhancing en
ctl
clol. (Right) Axial NEeT en
shows an acute right-sided
subdural hematoma
has spread inlo
=
that
interhemispheric fissure
along lhe falx 81 and
tentorium P13.
lymphoma, Metastatic, Intracranial Metastases, Skull and Meningeal

(Left) Axial N[CT shows
bilateral hyperdense masses
in cavernous sinus = in a
lymphoma who developed
multiple cranial nerve
palsies. Note suprasellar
mass 81. MR showed
extensive skull base
infiltration~ cranial nerve
involvement. (Right) Axial
sellar/suprasellar mass
with left cavernous sinus
extension ~ NK/T-cell
lymphoma of pituitary gland
that extends into cavernous
sinus was found at surgery.
leukemia
(Left) Coronal NECT shows
hyperdense calcified mass
involving central skull base,
cavernous sinus, extending
posteriorly along clivus and
tentorium. Histologically
typical meningioma was
Axial NECT shows mulliple
hyperdense dural-based
masses over convexity,
adjacent to falx and superior
sagittal sinus.
29
PART II
Spine
Trans-Spatial
Craniovertebral Junction
Vertebral Body - Posterior Elements
Extradural
Intradural-Extramedullary
Intramedullary
SECTION 1
Trans-Spatial
Cervical, Chronic Post-Traumatic Abnormality 11-1-2
Cervical, Lower, Post-Traumatic Bony Abnormality 11-1-4
Thoracic Bony Trauma 11-1-6
Lumbar Bony Trauma 11-1-8

Scoliosis 11-1-10
Kyphosis 11-1-12
Kyphoscoliosis, Child 11-1-14
Platyspondyly, Diffuse 11-1-16
Sacral Mass, Adult 11-1-18
Sacrococcygeal Mass, Pediatric 11-1-22
Sacral Deformity 11-1-26

Acute Back Pain/Radiculopathy, Post-Operative 11-1-30
Chronic Back Pain/Radiculopathy,Post-Operative 11-1-36
Acute Upper Extremity Pain/Weakness 11-1-42
Lower Extremity Pain 11-1-48
Back Pain, Adult 11-1-52
Back Pain, Pediatric 11-1-56
co CERVICAL, CHRONIC POST-TRAUMATIC ABNORMALITY
~
Cl.
(fJ
U,
c DIFFERENTIAL DIAGNOSIS • Wide surgical decompression without fusion
co often yields unstable spine with secondary
~ Common deformity
Ql
C • Post-Traumatic • Ossification of anterior longitudinal
(fJ
C. o Accelerated Degeneration ligament (ALL)known as DISH when> 4
o Os Odontoideum adjacent levels affected
o Post-Operative Spinal Complications o May see smaller foci of ossification due to
o Kyphosis trauma, aging, or seronegative arthropathy
o Scoliosis o Look for other signs of trauma to help
o Ligament Ossification make distinction
• Trauma Mimics o Small foci of ossification ALLdistinguished
o Ossification, Anterior Longitudinal from trauma by normal configuration of
Ligament underlying vertebra
o DISH • Posterior element injuries not uncommonly
o Post-Operative Change, Normal missed acutely
o Pathologic Vertebral Fracture o Malalignment, focal degenerative disease
o Rheumatoid Arthritis, Adult signs suggest prior injury
o Juvenile Idiopathic Arthritis • Fracture nonunion sometimes difficult to
o Craniovertebral Junction Variants determine
o Klippel-Feil Spectrum o Prolonged failure of bridging callus
o OPLL • Time to healing depends on age, health,
o Achondroplasia and fracture location
less Common o Sclerosis of apposing fracture margins
• Osteomyelitis, C1-C2 • Craniocervical instability due to multiple
• Crystalline Arthropathies causes
o Gout, calcium pyrophosphate deposition o Trauma
disease, hemodialysis arthropathy o Arthritis: Rheumatoid arthritis,
seronegative, calcium pyrophosphate
deposition disease
ESSENTIAL INFORMATION o Congenital: Achondroplasia, trisomy 21
Key Differential Diagnosis Issues o Infection
• Single level &/or upper cervical degenerative • Kyphosis, scoliosis due to many causes
disease suggests prior injury o Short curve deformities suggest trauma,
infection, congenital, or tumor
Accelerated Degeneration Os Odontoideum
II
1 Sagittal oblique T2WI MR shows 2S year old man with
fXJsHraumatic disc degeneration = and uncovertebraJ
Sagittal NEeT shows nonunited dens fracture ~
odontoideum)
(os
and posHraumatic PLL ossification Ea.
arthritis. Chronic facet subluxation ~ is easily missed Pseudarthrosis in DISH -7 is a common finding and
unless oblique views are obtained. does not necessarily indicate trauma.
2
CERVICAL, CHRONIC POST-TRAUMATIC ABNORMALITY en
"tl
:J
CD
-I
~
OJ
Ossification, Anterior longitudinal :J
,
CI>
ligament en
(Left) Sagittal STIR MR
shows post-traumatic "~
OJ
kyphosis and acce/eraled
degeneralive disease. (Right)
Laleral radiograph shows
mature-appearing ossicle
fell/O be degenerative in
=-
origin, in anterior
longitudinal ligament of a 55
year old. Underlying
vertebral contour is normal,
excluding leardrop-Iype
fracture.
Post-Operative Change, Normal Rheumatoid Arthritis, Adult

(Left) Sagillal NrcT shows
normal post-operative
appearance afler C2
corpec/Omy =:I and slrul
graft E!lI placement
posleriorly. (Right) Sagillal
bone CT shows anterior
occipul-C7 subluxation !:Jl
and extensive bony erosions
~ Allhough C7-2
subluxation is more common
in rheumatoid arthrilis,
subluxation also occurs at
this level and in lower
cervical spine.
Juvenile Idiopathic Arthritis OPll

shows facet fusion at C2-3
=:I. Congenital fusion
anomalies may have same
appearance as }IA. fusions
may involve vertebral
bodies, posterior elements,
or bOlh. (Right) Sagillal bone
CT shows bulky ossification
PLL >=:> as well as ALL =:I.
Post-traumatic heterotopic
ossificalion is usually limited
to 1-2 levels in cervical
spine.
II
1
3
ro
:.::;
CERVICAL, LOWER, POST-TRAUMATIC BONY ABNORMALITY
ro
II
(f)
,
'"cro
~
DIFFERENTIAL DIAGNOSIS I I ESSENTIAL INFORMATION
f0- Common Key Differential Diagnosis Issues
al
c: • Subaxial Cervical Spine Fractures • Evaluate for post-traumatic instability with
'0. o Hyperflexion Injury, Cervical flexion/extension views
rn
o Posterior Column Injury, Cervical o Not accurate in 1st week after injury
o Burst Fracture, Cervical
o Hyperflexion-Rotation Injury, Cervical
• Signs of acute injury
o Lateral Flexion Injury, Cervical
o Malalignment, focal kyphosis, or lordosis
o Hyperextension Injury, Cervical
o Soft tissue swelling (not always present)
o Hyperextension-Rotation, Cervical
o Fracture line
o Pathologic Vertebral Fracture
• Signs of remote trauma
o Shear Injury
o Cervical deformity
• Post-Traumatic Deformity o Single level facet osteoarthritis
o Accelerated Degeneration
• MR very helpful in questions of acuity of
o Facet Arthropathy, Cervical
injury, and distinguishing trauma from
o Kyphosis
trauma mimics
o Scoliosis
o Look for bone marrow edema on fluid
• Nontraumatic Entities that Mimic Trauma sensitive sequences
o Ossification of Anterior Longitudinal
• Trauma mimics
Ligament
o Ossification of anterior longitudinal
o Metastases, Lytic Osseous
ligament: No bone donor site visible
o Rheumatoid Arthritis, Adult
o Growth disturbance in congenital and
o Juvenile Idiopathic Arthritis
childhood disorders
o Klippel-Feil Spectrum
o Infection: Vertebral end plates eroded
o Post-Operative Change, Normal
o Metastatic disease
o Facet Arthropathy, Cervical
• May see round or oval bone lesion, or
o Incomplete Fusion, Posterior Element
involvement of entire vertebral body
o Osteomyelitis, Pyogenic
• Cortex destroyed not just disrupted as in
Less Common trauma
• Spondyloarthropathy, Seronegative o Incomplete fusion shows smoothly
contoured margins, unlike trauma
II
1 Lateral radiograph shows flexion teardrop fracture
due to anterior compression, and widened interspinous
= Coronal bone CT shows isolated articular pillar fracture
I:llI of C7 due to lateral flexion injury. Although posterior
distance [;8 due to posterior distraction. column fractures may be isolated, search should be
made for associated fractures.
4
CERVICAL, LOWER, POST-TRAUMATIC BONY ABNORMALITY
Hyperflexion-Rotation Injury, Cervical

(Leh) Sagiltal bone CT shows
loss of height of C7 verlebral
body = and relropulsed
fragment ~ into canal
indicating axial load (burst)
injury. (Right) Laleral
radiograph shows focal
kyphosis indica ling flexion
injury. Grade 1
anlerofislhesis and unilateral
facel dislocation P al C5-6
indicate rotational
component of injury. C6
articular pillars are
superimposed, but pillars of
C5 and above levels are
rotated; this is a key sign of
rOlation injury.
Pathologic Vertebral Fracture

(Lefl) Sagittal bone CT shows
hyperextension injury with
small bony avulsion 81.
I'yperextension teardrop
fractures such as this are
usually smaller than Ihose
seen in hyperflexion injuries.
Note fused levels above
fracture =. (RighI) Lateral
radiograph shows severe
compression fracture of C5
81 due to multiple myeloma.
All visualized vertebrae are
oSleopenic, but no focal
lesions are visible, a
common appearance on
radiographs of diffuse spine
myeloma.
Ossification of Anterior longitudinal

ligament
(Lefl) Lateral radiograph
shows discontinuous
ligamentous ossification 1m.
Ossification is adjacent to
vertebral bodies with normal
contour, and no donor sites
are visible. (Right) Axial
N[CT shows enlarged spinal
canal and dysplastic
posterior elements. Clues lO
nonlraumatic etiology are
smooth, corticated edges of
bone defecls 81 and normal
SOfllissues.
II
1
5
ro THORACIC BONY TRAUMA
~
a.
(f)
U,
c
~
DIFFERENTIAL DIAGNOSIS I I ESSENTIAL INFORMATION
I- Common Key Differential Diagnosis Issues
al
c: • Fractures • Important to distinguish between types of
Co
II)
o Anterior Compression Fracture vertebral body fractures since treatment
o Pathologic Vertebral Fracture differs by type
o Lateral Compression Fracture • Fractures most common at thoracolumbar
o Chance Fracture junction
o Burst Fracture • When one spine fracture is seen, always look
o Facet-Lamina Fracture for others
• Nontraumatic Fracture Mimics Helpful Clues for Common Diagnoses
o Schmorl Node
• Anterior Compression Fracture
o DISH
o Never involves posterior vertebral body
o Physiologic Wedging, Vertebral Body
cortex or neural arch
o Kyphosis, Idiopathic
o Easily missed in upper T-spine on
o Scheuermann Disease
radiographs
o Limbus Vertebra/Ring Apophysis
• Chance Fracture
o Sickle Cell
o Usually extends through posterior
o Osteomyelitis, Pyogenic
vertebral body cortex, but no retropulsed
Less Common fragment
• Trauma and Post-Traumatic Abnormalities o Horizontal fracture of posterior elements
o Fracture-Dislocation, Thoracolumbar OR rupture of interspinous ligaments and
Junction facet joints
o Distraction Fx, Low Thoracic • Burst Fracture
o Kilmmell Disease o Always extends through posterior vertebral
• Nontraumatic Fracture Mimics body cortex, may have retropulsed
o Langerhans Cell Histiocytosis fragment
o Scoliosis and Kyphosis, Congenital o Vertical fracture of posterior elements also
o Renal Osteodystrophy present
o Achondroplasia • Scheuermann Disease
o Osteomyelitis, Granulomatous o 4 or more levels involved; undulating
o Cushing Disease end plates; normal anterior cortex
Anterior Compression Fracture Burst Fracture
II
1 Sagillal NECT shows T4 compression fracture ~ and
TS Chance fracture =. The degree of anlerior heighl
Sagillal bone CT shows T3 bUN fracture wilh
ret.ropulsed fragment =. Compression fractures are
loss and presence of horizontal posterior element present at T4 and T5 r.:D. Patient is skeletally immature
fracture E!2 disunguish Chance fracture. (nole ring apophyses ffi.
6
THORACIC BONY TRAUMA

right T1 0 laminar fracture PJ::l
body fracture =-
associated with vertebral
Chance
injury. Facet (ractures may
be isolated, but laminar
fractures rarely are. (Right)
Lateral radiograph shows
mild anterior wedging T12
and L 1 81. Physiologic
wedging may occur at
T11-L7 and involves both
endplates, while the anterior
vertebral body cortex is
normal,

shows thoracic kyphosis ~
without focal bony
deformity. Idiopathic
kyphosis probably originates
as a postural problem but
often becomes rigid. (Right)
Sagiltal bone CT shows 4
adjacent vertebral bodies 81
affected with anterior
wedging, undulating
endplates, and Schmor/
nodes. These findings,
especially combined with
normal anterior vertebral
body cortices, are
pathognomonic.
Fracture-Dislocation, Thoracolumbar
Junction Scoliosis and Kyphosis, Congenital
(Left) Sagiltal bone CT shows
]-column
fracture-dislocation.
~ and posterior
longitudinal ligament
= Anterior
avulsions result in
anterolisthesis of T6-7.
Posterior column disruption
is shown by spinous process
fraclure at T5 ffi laminar
fractures were also present
(not shown). (Right) Lateral
radiograph shows focal
kyphosis 81 at T10-11 due
to vertebral body fusion.
Diagnosis is readily made by
CT or MR if radiographs are
equivocal.
II
1
7
ro LUMBAR BONY TRAUMA
~
Cl.
,
(/)
C/)
c DIFFERENTIAL DIAGNOSIS o Osteomyelitis, Granulomatous
ro
~
I- Common
ell
C • Fractures ESSENTIAL INFORMATION
a. o Anterior Compression Fracture
(/) Helpful Clues for Common Diagnoses
o Burst Fracture • Anterior Compression Fracture
o Chance Fracture o Never involves posterior vertebral body
o Pathologic Vertebral Fracture cortex or neural arch
o Facet-Posterior Fracture o Unless osteoporosis, > 40% loss of height
o Transverse Process Fracture suggests Chance fracture, not compression
• Fracture Mimics, Vertebral Body • Burst Fracture
o Schmori Node o Extends through posterior vertebral body
o Physiologic Wedging cortex
o Limbus Vertebra o Usually but not always have retropulsion
o Scheuermann Disease of fragment into spinal canal
o Scoliosis and Kyphosis, Congenital o Fractures of posterior elements vertically
o Neurogenic (Charcot) Arthropathy oriented
o Sickle Cell • Chance Fracture
o Osteomyelitis, Pyogenic o Often extends through posterior cortex
o Post-Operative Spinal Complications o Always either horizontally oriented
• Fracture Mimics, Posterior Elements posterior element fracture OR widened
o Incomplete Fusion, Posterior Element interspinous distance due to interspinous
o Spondylolysis ligament rupture
o Post-Operative Change, ormal • Transverse Process Fracture
Less Common o Associated with retroperitoneal soft tissue
• Fracture and Post-Traumatic Abnormalities injury, bony and ligamentous injury in
o Lateral Compression Fracture pelvis
o Fracture-Dislocation • Physiologic Wedging
o Ktimmell Disease o May be seen at Tll-Ll levels
o Insufficiency Fracture, Pedicle o Usually affects both superior and inferior
o Apophyseal Ring Fracture endplates equally
• Fracture Mimics o No angular deformity of endplates or
o Renal Osteodystrophy anterior cortex
o Achondroplasia
Anterior Compression Fracture Burst Fracture
II
1 Sagittal bone CT shows fracture BI involving anterior
and superior cortices of vertebral body; while sparing
posterior cortex. Posterior elements are also intact
=
Sagittal bone CT shows involvement of posterior cortex
which distinguishes this injury from compression
fracture.
8
LUMBAR BONY TRAUMA
Pathologic Vertebral Fracture

(Left) Sagittal NEeT shows
anterior vertebral
compression and horizontal
fracture through posterior
elements. In contrast, a burst
fracture has vertically
oriented posterior element
fracture. (Right) Lateral
radiograph shows L3
compression fracture =.
Lytic bone lesion is not well
seen, but anterior
displacement of aorta E2
due to sort tissue rnass points
to pathologic fracture.
Schmorl Node Limbus Vertebra

shows multiple Schmorl
nodes.' Shallow, smooth,
bowl-shaped vertebral
endplate depressions [;>J.
Fractures are more angular in
appearance. (Right) Lateral
radiograph shows nonunited
ring apophysis =.Sclerotic
margins of apophysis and
subjacent vertebral body are
helpful signs to distinguish
from chip fracture.
Neurogenic (Charcot) Arthropathy Sickle Cell

shows chronic fractures with
1055 of height of L3 vertebral
body I!:iJ and absence of
anleroinferior corner of L2
E2. There is clear instability,
with widened facet joints.
Sclerosis and extensive bone
debris = are clues to
diagnosis, as is patient
history. (Right) Sagittal T2WI
MR shows central
depressions in vertebral
endplates at multiple levels,
the classic Lincoln log
II /I
appearance reflecting bone

infarcts.
II
1
9
co SCOLIOSIS
~
Cl.
CIJ,
(/)
DIFFERENTIAL DIAGNOSIS o Pneumonectomy
c
co
~ o Fibrothorax
I- Common • Tumor
Ql
c • Scoliosis, Idiopathic o Pathologic Vertebral Fracture
Q.
CIJ
• Scoliosis, Degenerative o Osteoblastoma
• Trauma o Osteoid Osteoma
o Lateral Compression Fracture, Lumbar • Congenital Syndromes with Normal
o Lateral Compression Fracture, Thoracic Segmentation
o Lateral Flexion Injury, Cervical o Connective Tissue Disorders
• Scoliosis, Neuromuscular o Neurofibromatosis Type 1
o Cerebral Palsy o Osteogenesis Imperfecta
o Muscular Dystrophy o Mucopolysaccharidoses
o Friedrich Ataxia o Fibrous Dysplasia
o Poliomyelitis o Fetal Alcohol Syndrome
o Hemiparesis/Hemiplegia o Proteus Syndrome
o Paraparesis/Paraplegia o Tethered Spinal Cord
• Scoliosis and Kyphosis, Congenital • Radiation Therapy in Childhood
o Partial Vertebral Duplication
o Failure of Vertebral Formation
o VACTERLAssociation Helpful Clues for Common Diagnoses
• Infection • Painful scoliosis: Trauma, tumor, infection
o Abscess, Paraspinal • Short-curve scoliosis: Congenital anomaly,
o Osteomyelitis, Pyogenic tumor, infection, trauma, degenerative,
o Osteomyelitis, Granulomatous post-operative
• Failed Back Surgery Syndrome • Balanced S-curve scoliosis: Idiopathic,
• Neurogenic (Charcot) Arthropathy connective tissue disorders
• Limb Length Inequality • C-curve scoliosis: Neuromuscular,
• Chest Wall Abnormality osteogenesis imperfecta
o Rib Anomaly
o Sprengel Deformity
Less Common
• Pleural or Pulmonary Abnormality
o Empyema
Scoliosis, Idiopathic
II
1 Anteroposterior radiograph shows classic, balanced,
S-shaped curve, convex to right in thoracic spine. There
Coronal T2WI MR shows asymmetric degeneraUve disc
disease, with narrowing and discogenic sclerosis E!:t on
is often minimal wedging of vertebrae on concave side left at U-4.
of scoliosis.
10
SCOLIOSIS
Trauma Scoliosis, Neuromuscular

radiograph shows lateral
compression fracture of L 7
= resulting in short-curve
scoliosis. (Right)
shows C-shaped curve SI
characteristic of
neuromuscular scoliosis.
Failure of Fusion of the
posterior elements I:] is seen
in the lumbar spine.
Rib Anomaly
radiograph shows leFt T7 7
hemivertebra IJ::]:l Fused to
T72, and right T7 I
hemivertebra Fused to T70.
(Right) Anteroposterior
radiograph shows
dextroscoliosis related to the
rib anomaly SI which has
caused separation or right
4th and 5th ribs.
Osteoid Osteoma
radiograph shows
short-curve scoliosis and
pleural thickening =
patient with focal pain.
in
Because of these Findings, CT

scan was performed and
showed osteoid osteoma.
radiograph shows extreme
scoliosis leading to
shortening of trunk in
osteogenesis imperfecta.
Multiple rib fractures are a/so
present.
II
1
11
C1l KYPHOSIS
~
C>-
,
(/)
en DIFFERENTIAL DIAGNOSIS o Osteogenesis Imperfecta
c
C1l o Neurofibromatosis Type 1
t=
Ql
Common o Achondroplasia
c: • Postural Kyphosis o Mucopolysaccharidoses
'0. • Idiopathic Kyphosis
en • Osteomyelitis, Granulomatous
• Degenerative Disc Disease
• Fracture
o Anterior Compression Fracture, Thoracic ESSENTIAL INFORMATION
o Anterior Compression Fracture, Lumbar Helpful Clues for Common Diagnoses
o Burst Fracture, Lumbar • Flexible Kyphosis: Postural, sometimes
o Hyperflexion Injury, Cervical degenerative, failed fusion
o Chance Fracture, Thoracic • Short-Curve Kyphosis: Infection, trauma,
o Chance Fracture, Lumbar Charcot arthropathy and congenital fusion
o Hangman's C2 Fracture anomalies, degenerative (sometimes
o Pathologic Vertebral Fracture adjacent to surgical fusion)
• Multiple Myeloma • Undulating Endplate: Scheuermann
• Metastases, Lytic Osseous kyphosis
• Metastases, Blastic Osseous • Cortical Break or Angular Deformity:
• Scheuermann Disease Trauma
• Failed Back Surgery Syndrome • Destruction Vertebral Endplate: Infectious
• Hardware Failure or post-infectious, neuropathic arthropathy,
Less Common severe instability
• Osteomyelitis, Pyogenic • Fused Vertebrae: Congenital, juvenile
• Seronegative Spondyloarthropathy idiopathic arthritis, infection, seronegative
• Juvenile Idiopathic Arthritis spondyloarthropathy, post-traumatic,
• Post-Operative Infection post-surgical
• Neurogenic (Charcot) Arthropathy • Multiple Wedged Vertebrae: Osteoporosis,
• Scoliosis, Neuromuscular pathologic fracture due to myeloma or
• Paraparesis/Paraplegia metastasis, Scheuermann kyphosis,
• Scoliosis and Kyphosis, Congenital osteogenesis imperfecta, achondroplasia,
o Failure of Vertebral Formation mu copo Iysaccha rid osis
o Vertebral Segmentation Failure
• Congenital Syndromes
Postural Kyphosis Degenerative Disc Disease
II
1 Lateral radiograph shows diffuse kyphosis without bony
abnormality. This is a common finding due to poor
l.iJteral radiograph
slight kyphosis
shows
at C4-5
loss of normal
I:] due to
and C5·6
lordosis and
posture and may become fixed over time. degenerative disc disease. Degenerative kyphosis is
common in both cervical and lumbar spine.
12
KYPHOSIS
Anterior Compression Fracture, Thoracic Burst Fracture, Lumbar

shows multiple compression
fraclUres = due to senile
osteoporosis in 80 year old
patient. Always consider
multiple myeloma in
differential of this
appearance. (Right) Lateral
radiograph shows dynamic
kyphosis at acute burst
fraclure = when patient
stands upright in a brace 81.
Measure deformity from 1
level above fracture to I
level below.
Chance Fracture, Lumbar Failed Back Surgery Syndrome

(Left) Sagitlal bone CT shows
kyphosis due to combination
of anterior compression =
and posterior distraction with
horizontal spinous process
fraclure 81 and widened
interspinous distance ~.
shows kyphosis =
Deformity developed
al 13-4.
post-surgery. Lucency
around pedicle screw -7 is
sign of failed fusion.
Achondroplasia Osteomyelitis, Granulomatous

(Leh) Lateral radiograph
shows anteriorly wedged
vertebral bodies, scalloped
cortices =-
posterior vertebral body
and short
pedicles characteristic of
achondroplasia. (RighI)
Sagitlal bone CT shows
characteristic hairpin-turn
kyphosis called gibbus
deformity = and extensive
spinal fusion seen in POll
disease (spinal tuberculosis).
II
1
13
ro KYPHOSCOLIOSIS, CHILD
~
D-
C/),
C/)
DIFFERENTIAL DIAGNOSIS • Syringomyelia
c
co
~ • Neurofibromatosis Type 1
I- Common • Connective Tissue Disorders
C1l
c • Traumatic • Post-Operative Spinal Complications
'0. o Burst Thoracolumbar Fracture
en • Diastematomyelia
o Lateral Compression Fracture, Lumbar
Rare but Important
o Lateral Compression Fracture, Thoracic
o Lateral Flexion Injury, Cervical
• Post-Radiation
o Chance Fracture, Thoracic
• Congenital ESSENTIAL INFORMATION
o Scoliosis and Kyphosis, Congenital
o Failure of Vertebral Formation
• MR may be useful in certain cases
o Painful scoliosis: Tumor, infection
o Atypical curve: Often have underlying
o Tethered Spinal Cord
o Caudal Regression Syndrome
bony or neural abnormalities
o Congenital scoliosis: Assess full extent of
• Scoliosis, Idiopathic
• Scheuermann Disease bony abnormalities
• Scoliosis, Neuromuscular • CT useful to characterize congenital scoliosis
• Juvenile Idiopathic Arthritis Helpful Clues for Common Diagnoses
• Kyphosis, Idiopathic • Congenital curve may progress rapidly,
• Kyphosis ormal in Infants especially if it includes unfused
Less Common hemivertebrae
• Infection • Scheuermann kyphosis presents in
o Osteomyelitis, Pyogenic adolescence, may be misdiagnosed as
o Osteomyelitis, Granulomatous
fracture
o Involves multiple levels, see Schmorl
o Prevertebral Abscess
o Post-Operative Infection nodes or undulation of end plates without
angular deformity
• Tumor
o Osteoid Osteoma
• Lumbar kyphosis normal in infants
o Lumbar lordosis develops after infant
o Osteoblastoma
o Aneurysmal Bone Cyst
begins to sit upright
o Ewing Sarcoma
o Langerhans Cell Histiocytosis
Traumatic
II
1 Sagillal bone CT shows kyphoUc deformity !l:lI in
flexion-distraction type injury. Kyphosis also seen due to
Anteroposterior bone CT 3D reformation shows left T II
hemivertebra =. Short-curve, unbalanced
burst or compression fracture. kyphoscoliosis is typical of congenital kyphoscoliosis.
14
KYPHOSCOLIOSIS, CHILD
Scheuermann Disease
(Left) COlOnaIbone CT
shows Klippe/-Feil spectrum,
with extensive fusion
anomalies of cervical spine,
with dexlroscoliosis.
Kyphosis was also present.
(Right) Sagittal bone CT
shows kyphosis due to
vertebral wedging~. Note
undulating endplates and
Schmor/ nodes at 4
contiguous levels. 7S% of
Scheuermann cases show
scoliosis.
Juvenile Idiopathic Arthritis

radiograph shows C-shaped
scoliosis typical of
neuromuscular scoliosis.
There is a/so often
persistence of infantile
kyphosis in neuromuscular
disease. (Right) Lateral
radiograph shows mild
kyphosis due to cervical
fusions~. Kyphosis due to
juvenile chronic (idiopathic)
arthritis is usually not severe.
Infection
shows infantile tuberculosis
causing kyphotic deformity,
epidural abscess =:I, and
pre vertebral abscess ~.
Spinal TB can be present
without pulmonary
abnormalities. (Right) Lateral
radiograph shows large
expansile mass =:I,
aneurysmal bone cyst in this
case, involving posterior
elements and causing
kyphotic deformity at C2- J
level.
II
1
15
Cll PlATYSPONDYlY, DIFFUSE
~
CL
(/J
U, DIFFERENTIAL DIAGNOSIS • Connective tissue disorders show scalloping
C
~
Cll of posterior vertebral body margin
I- Common o Due to dural ectasia
Ql
C • Multiple Myeloma
a. Alternative Differential Approaches
• Osteoporosis
(/)
• Uniform flattening
• Sickle Cell
o Spondyloepiphyseal dysplasia
• Scheuermann Disease
o Osteogenesis imperfecta
less Common • Anterior height loss> posterior
• Metastases, Lytic Osseous o Osteoporosis
• Osteogenesis Imperfecta o Multiple myeloma
• Mucopolysaccharidoses o Scheuermann disease
Rare but Important o Metastases, lytic osseous
• Spondyloepiphyseal Dysplasia o Osteogenesis imperfecta
• Ehlers-Danlos Syndrome • Vertebral "beak"

• Achondroplasia o Mucopolysaccharidoses
• Cushing Disease o Achondroplasia (at thoracolumbar

• Thanatophoric Dwarfism junction)
• Gaucher Disease • Limited to lumbar region
o Ehlers-Danlos syndrome
• Central loss of vertebral body height
ESSENTIAL INFORMATION o Sickle cell ("Lincoln Log" vertebrae)
Key Differential Diagnosis Issues o Cushing disease ("fish mouth" vertebrae)
• Uncommon condition irrespective of cause o Osteogenesis imperfecta ("fish mouth"
• In adults, usually due to severe osteoporosis vertebrae)
or myeloma o Gaucher disease
o Compression fractures may be so extensive • Also seen in multiple rare dwarfism
that they cause uniform flattening at all syndromes
levels o Enchondromatosis has been reported to
o More commonly, amount of vertebral involve spine
height loss varies from level to level (spond yloenchondrod ysplasia)
o Metastases uncommonly show uniform o Dysosteosclerosis
platyspondyly o Kniest dysplasia
• Dwarfisms show limb abnormalities also
Multiple Myeloma Sickle Cell
II
1 Lateral radiograph shows 1055 of vertebral body height at
almost all visualized levels, due to multiple pathologic
Sagittal T1WI MR shows abnormal low T1 marrow
signal and characteristic 1055 of vertebral body height at
fractures. Height los5 is greater anteriorly than all levels due to bone infarcts.
posteriorly.
16
PLATYSPONDYLY, DIFFUSE
Scheuermann Disease Osteogenesis Imperfecta

(Left) Laleral radiograph
shows flattened vertebral
bodies and undulating
endplates at every visualized
level. Vertebral flattening ;5
characteristically more
severe anteriorly than
posteriorly. (Right)
shows flattening of all
included vertebral bodies,
central endplate depression,
and severe osteoporosis.
Achondroplasia
fLeft) Sagittal T2WI MR
shows lIattened vertebral
bodies throughout visualized
spine and undulating
endplates. Appearance
differs from Scheuermann
disease in lack of vertebral
wedging (Righi) Sagittal
TI WI MR shows diffuse
vertebraillattening. At
thoracolumbar junction there
is additional, characteristic
anterior hypoplasia resulting
in kyphosis.
Thanatophoric Dwarfism Gaucher Disease

radiograph shows diffuse
platyspondyly
characteristic limb
=
and
shortening and deformity~.

shows extensive bony
infarcts = and" Lincoln
Log" appearance ~ that
can mimic sickle celf disease.
II
1
17
CIl SACRAL MASS, ADULT
.~
0-
,
(fJ
o Tarlov cyst is similar in etiology:
Vi
C DIFFERENTIAL DIAGNOSIS
CIl Congenital dilatation of nerve root
~ Common meningeal sleeve
CI>
c • Lytic Osseous Metastases • Tarlov cysts frequently multiple &
Q.
III
• Sacral Stress Fracture eccentrically centered over neural
• Occult Intrasacral Meningocele foramen
• Chordoma • Chordoma
• Lymphoma o Arise in midline
• Giant Cell Tumor o Most common locations: Sacrococcygeal>
• Multiple Myeloma spheno-occipital> vertebral body
• Paget Disease o Hyperintense to discs on T2WI; internal
Less Common septations, variable enhancement, often
• Anterior Sacral Meningocele amorphous intra tumoral calcium
• Aneurysmal Bone Cyst o Can have large soft tissue component
• Chondrosarcoma o Involvement of adjacent vertebral bodies

via transdiscal extension; may be epidural,
Rare but Important perivertebral, & perineural extension
• Secondary Osteosarcoma • Lymphoma
• Ewing Sarcoma o May involve epidural space with vertebral
body extension & bone erosion
ESSENTIAL INFORMATION o May be primarily osseous with bone
destruction or "ivory vertebra" appearance
Key Differential Diagnosis Issues o Appears slightly hyperdense on NECT &
• Multiplicity suggests metastases or multiple demonstrates homogeneous enhancement
myeloma • Giant Cell Tumor
• Soft tissue component with character of o Lytic expansile lesion in sacrum or a
internal matrix (e.g., chondroid matrix) can vertebral body with narrow zone of
provide diagnostic clues transition & usually non-sclerotic margins
Helpful Clues for Common Diagnoses o Although internal matrix is absent, there
• Lytic Osseous Metastases may be residual bone trabeculae
o Most often with breast, lung, kidney, o Can coexist with an ABC
thyroid, oro- & nasopharyngeal, GI tract, o Radiologically & histologically identical to
bladder, uterine, ovarian, melanoma, brown tumors, which occur in setting of
chordoma, & paraganglioma primaries hyperparathyroidism
• ExpansiJe, osteolytic lesions observed o Majority occur in 3rd to 5th decades
with kidney & thyroid mets • Multiple Myeloma
o Hypointense on Tl WI, hyperintense on o Bone scintigraphy detects only 10%; PET
T2WI & STIR; diffusely enhance imaging is sensitive for monitoring
• T1 hypointensity after therapy may be treatment response, as MM lesions are
residual tumor or fibrosis metabolically active
o Cortex, particularly posteriorly, & pedicles o Clinically, monoclonal gammopathy and
are often destroyed, while intra vertebral Bence Jones proteinuria are present
discs are usually spared • Paget Disease
• Sacral Stress Fracture o Hypointense cortex & thickened
o T1 hypointensity & T2 hyperintensity trabeculae
reflects marrow edema o Active phase: Fibrovascular marrow (Tl
• Occult Intrasacral Meningocele hypointense/T2 hyperintense)
o CSF pulsation remodels sacral canal, which o Mixed phase: Fatty marrow (hyperintense
shows smooth enlargement on T1 WI and T2WI)
II o Follows CSF signal intensity; no neural
elements are seen within cyst
• Anterior Sacral Meningocele
1
18
SACRAL MASS, ADULT
o Presacral cyst that is contiguous with o Cortical disruption & extension into soft
thecal sac, protruding through an anterior tissues
osseous defect; widened sacral canal & Helpful Clues for Rare Diagnoses
neural foramina • Secondary Osteosarcoma
o No soft tissue mass, enhancement, or o Often has an osteolytic, expansile
calcification, which are seen with appearance without periosteal reaction
sacrococcygeal teratomas • Cortical disruption may not be present
o Neurenteric cyst is within spinal canal;
• Permeative appearance with a wide zone
may be associated with dysraphism & of transition
vertebral formation anomalies • 80% have a bone matrix and 20% have a
• Aneurysmal Bone Cyst lytic appearance
o Arise in neural arch & majority (75-90%)
o Secondary osteosarcomas can occur after
extend into vertebral body radiation treatment or may be sarcomatous
o Cortical thinning & focal cortical transformation of Paget disease or other
destruction are common benign bone lesion
• More permeative bone destruction, wider • Most secondary osteosarcomas patients
zone of transition and infiltration into are older than 50 years
surrounding soft tissues with sarcomas • Insidious onset of pain, greatest at night
• Expansile remodeling of bone can result o Calcified pulmonary metastases can be
is loss of pedicle contour on AP seen
radiograph • Ewing Sarcoma
o Fluid-fluid levels can be seen with
o Permeative destructive lesions of sacrum or
telangiectatic osteogenic sarcoma as well as vertebral body; cortical perforations rather
ABC
than extensive cortical bone loss
o Majority of patients younger than 20 years o Majority before 20 years old; however,
o Renal cell carcinoma can also have a "soap
second smaller peak at age 50 years, which
bubble" expansile appearance present with spine & sacral lesions
• Chondrosarcoma o Central areas of necrosis are common
o May be isolated or secondary to
osteochond rom a/ en ch on drom a
degeneration
o 50% of these lytic destructive lesions
demonstrate a chondroid matrix with
"rings and arcs"
lytic Osseous Metastases
II
Axial NEeT shows multiple blas/ic BI and somewhat
permeative lytic lesions= throughout the sacrum and
Axial T1 WI M R shows an il/-defined T1 hypoinlense
area involving the right sacral ala ~ with haziness of
1
visualized pelvi.t;. There is no SOfllissue mass. the adjacent fat & obscuration of cortical margins.
Discrete fracture line is not identified.
19
co SACRAL MASS, ADULT
~
Cl.
(fJ,
(/)
c
co
~
I-
Occult Inlrasacral Meningocele Occult Intrasacral Meningocele
Q)
c (Left) Axial T2WI MR
Cl. demonstrates an extradural
(fJ
cyst IJ:ll of fluid signal in
caudal spinal canal. Cyst
remodels and enlarges the
spinal canal. (Right) Sagittal
TI C+ MR shows a
cyst =
flonenhancing extradural
in caudal spinal
canal. These are sacral
meningeal cysts, while dorsal
meningoceles arc true
meningoceles protruding
through dysraphism.
shows a destructive sacral
mass = that demonstrates
T I hypointensily. Mass may
extend along nerve roots and
enlarge neural foramina.
shows a destructive sacral
mass = with marked T2
hyperintensityand
septalioflS, which is
characteristic of a chordoma.
Locaf recurrence is common
(90%), and there may be
seeding along the operative
tract

epidural lymphoma that fills
the left sacral neural
foramina ~ and erodes into
adjacent bone 1J:ll. (Right)
Sagittal NECT shows massive
sacral giant cell tumor with
pelvic extension~. There is
erosion of the inFerior sacrum
=. Pathologic fractures
occur in 30%, and these
lesions are locally aggressive
with 12·50% recurrence.
II
1
20
SACRAL MASS, ADULT

innumerable small marrow
lesions = in sacrum and
iliac wings. (Right) Axial
T1WI MR shows typical
=
heterogeneous fatty signal
and thickened dark
trabeculae of Paget disease
involving the sacrum.
Anterior Sacral Meningocele Secondary Osteosarcoma

reveals a cystic presacral
mass =. Sacrum has a
scimitar shape. There is a
sma/J unrelated Tarlav cyst
81. (Right) Axial NEeT with
sofe tissue windows confirms
an aggressive, expansile
process & with multiple
areas of cortical
breakthrough. No definite
bone production by tumor is
present.
Ewing Sarcoma Ewing Sarcoma

i/f·defincd sclerosis in right
parasacral ilium a with
unilaminar periosteal
reaction. Sofllissue mass ~
is appredable on both sides
of ilium. (Right) Coronal
STIR MR demonstrates
heterogeneous high signal on
STIR and involvement of
right sacrum ~ and
adjacent portions of right
ilium. It extends along sacral
nerves a a common
pattern in sacral Ewing
sarcoma.
II
1
21
ro SACROCOCCYGEAL MASS, PEDIATRIC
~Q.
CfJ,
rJl
DIFFERENTIAL DIAGNOSIS o Sacrum and coccyx usually spared, even
C
ro when tumor spreads into spinal canal via
.=
Ql
Common sacral hiatus
c • Sacrococcygeal Teratoma o Coccyx must be resected or recurrence risk
Q.
CIl
• Presacral Abscess high
Less Common • Presacral Abscess
• Chordoma o Fever, serum inflammatory markers usually
• Neuroblastic Tumor elevated, prompting clinical consideration
• Plexiform Neurofibroma of diagnosis
• Lymphoma o Regional soft tissue inflammation, discitis,
• Chondrosarcoma epidural abscess, or vertebral osteomyelitis
• Ewing Sarcoma o Rim enhancement and diffusion
restriction on DWI MR characteristic
Rare but Important
• Rhabdomyosarcoma Helpful Clues for Less Common Diagnoses
• Osteosarcoma • Chordoma
• Dermoid and Epidermoid Tumors o Strong predilection for sacrum (50%)
• Myxopapillary Ependymoma • Other common locations include clivus

• Anterior Sacral Meningocele (35%) and vertebra (15%)
• Terminal Myelocystocele o Characteristic very high T2 signal intensity
• Enteric Cyst limits differential considerations

o No tumor matrix (in distinction to
chondrosarcoma)
ESSENTIAL INFORMATION • Osseous debris within tumor may mimic
Key Differential Diagnosis Issues matrix on CT
• Myriad pathologies produce sacrococcygeal • Neuroblastic Tumor
masses; clinical data directs differential list o Paraspinal location along sympathetic
• Fever, elevated inflammatory markers chain (neural crest derivatives)
prompt search for infection source o Benign (ganglioneuroma) -+ intermediate
• Identification of tumor matrix narrows grade (gangJioneuroblastoma) -+ highly
differential considerations malignant (neuroblastoma)
• Location and relationship of mass to o Frequently calcified, encircles vessels and
important regional structures impacts tumor regional structures
resecta bility o Important upstaging findings affecting
• Look for osseous invasion or epidural surgical management include bilaterality
extension, which may alter surgical and epidural extension
planning • MR best imaging modality for detecting
tumor extension into spinal canal
Helpful Clues for Common Diagnoses through neural foramen
• Sacrococcygeal Teratoma • Plexiform Neurofibroma
o Very heterogeneous density/signal
o Neurofibromatosis type 1
intensity, enhancement of solid tumor o Grape-like or botryform morphology with
portions characteristic distribution along nerves
o AAP grade based on proportion of external
(major or minor peripheral nerves/plexi)
and internal tumor o Hyperintense on STIR MR, T2Wl MR
• Male sex, large proportion internal • Lymphoma
tumor, older age at diagnosis portend o Protean imaging appearances
worse outcome o Often large at diagnosis; may be focal or
o Often detected on routine obstetrical
diffuse
ultrasound => elective cesarean section o Relatively low signal intensity on T2WI
II • Fetal MR valuable for confirmation of
diagnosis, AAP grading
MR ± mild diffusion restriction reflects
high tumor cellularity
1
22
SACROCOCCYGEAL MASS, PEDIATRIC
• Chondrosarcoma a Epidermoid component ~ diffusion

a Very high T2 signal intensity; may be restriction
difficult to distinguish from chordoma on • Myxopapillary Ependymoma
imaging a Very uncommon sacral and presacral
a Chondroid matrix (when present, 50%) ependymomas have been described
diagnostic a Most myxopapillary ependymomas arise
• Ewing Sarcoma near conus or filum (may be confined
a Usually older child/adolescent entirely to filum terminale)
presentation age a CSF-disseminated intradural metastases
a Aggressive or permeative bone destruction common
a Cellular signal intensity (relatively low • Anterior Sacral Meningocele
signal intensity on T2WI MR) a Cyst contiguity with thecal sac through
Helpful Clues for Rare Diagnoses enlarged neural foramen is diagnostic

a Most ASM are simple CSF signal cysts; may
• Rhabdomyosarcoma
also have lipomatous component
a Aggressive soft tissue mass with frequent
bone invasion (complex ASM)
a Rarely arises primarily in sacrum; usually
• Terminal Myelocystocele
a Spinal cord termination always low
regional extension from prostate or uterus
a Cystic dilatation of distal spinal cord
primary tumor
central canal (myelocystocele) extending
a Signal characteristics variable; frequently
through a dilated subarachnoid fluid
shows cellular characteristics with lower
collection (meningocele)
signal intensity on T2WI MR
• Enteric Cyst
• Osteosarcoma
a Fortuitous adjacent location to sacrum in
a Destructive lesion with frank bone
isolated mesenteric or intestinal
destruction and large soft tissue mass
a May arise in pre-existing lesion
duplication cyst
a Split notochord malformations
(aneurysmal bone cyst, fibrous dysplasia)
(neurenteric cysts)
a Osteoid matrix makes diagnosis
• Dermoid and Epidermoid Tumors Other Essential Information
a Consider previous lumbar puncture with • Patient age and signal characteristics on MR
nonstyletted needle, congenital dermal imaging are most helpful criteria to narrow
sinus tract pertinent differential diagnosis list
a Contains fat &/or squamous debris
Sacrococcygeal Teratoma Presacral Abscess
II
Sagittal T2WI MR shows typical case of large MP type Sagillal STIR MR shows intervertebral disc space
1
portion is predominately solid
portion E1 is more cystic.
=
2 SeT with mixed cystic and solid mass. The internal
and the external
infection at L5~57 level with extensive prevertebral T2
hyperinlensily representing presacral abscess.
23
co SACROCOCCYGEAL MASS, PEDIATRIC
~
0..
CIJ,
Cf)
c
co
t=
Q)
Chordoma
c (Left) Sagittal STIR MR
'Q. shows a well-defined,
CJ)
markedly hyperintense mass
at the S2 level involving the
central aspect o( the sacrum
extending into presacral
space and dorsally into
sacral canal. (Right) Sagittal
large presacral soft tissue
mass = with sacral vertebral
bone involvement as well as
epidural extension ~
through the neural foramina.
Plexiform Neurofibroma lymphoma

(Left) Coronal STIR MR in a
patient with NF / reveals
multilevel bilateral T2
hyperintense plexiform
neurofibromas involving the
spinal and pelvic nerves and
relevant plexuses. (RighI)
Axial TI C+ rs MR shows a
large destructive sacral mass
with avid enhancement
spreading into the dorsal soft
tissues.
Ewing Sarcoma Rhabdomyosarcoma

shows a large sacral Ewing
sarcoma with bone
destruction and extension
into the dorsa/lumbosacral
soft tissues. (Right) Sagittal
large exophytic sacral mass
engulfing lower sacral
verlebra and extending into
central spinal canal It]
through the sacral hiatus EB
II
1
24
SACROCOCCYGEAL MASS, PEDIATRIC (J)
"0
::::l
11l
-l
~
tll
::::l
en,
Osteosarcoma (j)
-0
demonstrates a destructive ~
tll
pelvic mass with multiple
enhancing areas of solid
tumor ~ as well as
fluid-filled, nonenhancing
necrotic regions =:I. (Right)
Sagittal T1 WI MR depicts a
mixed signal intensity
expansile extradural sacral
mass =:I. Additional findings
include low-lying spinal cord
and fatty filum infiltration.
Myxopapillary Ependymoma Anterior Sacral Meningocele

(Left) Sagittal T1 C+ rs MR
reveals a heterogeneous
presacral mass with osseous
destruction and spinal
extension. Conus ;5 low
lying. Exact pathological
diagnosis of this rare lesion
has been debated but shows
many features of sacral
ependymoma. (Right)
Sagittal T2WI MR
demonstrates a large CSF
signal intensity presacral cyst
that is contiguous with the
thecal sac through an
enlarged sacral foramen =:I.
Anterior Sacral Meningocele Terminal Myelocystocele

patient with caudal
regression depicts a variant
complex ASM with both cyst
and lipoma components =
extending through the sacral
foramina to produce sacral
mass. (Right) Sagittal T1WI
MR shows classic
appearance of terminal
myelocystocele, with a
low-lying tethered spinal
cord, distal hydromyelia =:I
traversing a meningocele EJ.
II
1
25
ro SACRAL DEFORMITY
~
n.
(f)
enc DIFFERENTIAL DIAGNOSIS o Bony remodeling caused by intraspinal or
ro
~ transforaminallesions can cause scalloping
t- Common or the posterior lumbar vertebra and
a> • Sacral Foraminal Mass
c sacrum, neuroforaminal widening
'Q. o Dural Dysplasia
en • Insufficiency Fracture, Sacral
o Neurofibroma o Unilateral or bilateral vertical component
• Insufficiency Fracture, Sacral through the sacral alae, possibly with a
• Sacral Traumatic Fracture horizontal component through the body
• Metastatic Disease o Subtle fracture may be hard to identify
• Ependymoma, Myxopapillary, Spinal Cord even with high-quality CT
less Common o Associated marrow edema signal most
• Dorsal Dysraphism conspicuous on fat-saturated T2WI (e.g.,
o Myelomeningocele/Myelocele STIR)
o Lipomyelomeningocele/Lipomyelocele o Increased tracer uptake on bone scan
o Terminal Myelocystocele • Sacral Traumatic Fracture
• Meningocele, Occult Intra sacral 095% occur in conjunction with other
• Meningocele, Anterior Sacral pelvic fractures
• Chordoma o Denis classification
• Teratoma, Sacrococcygeal • Zone 1: Lateral to neuroforamina
• Caudal Regression Syndrome • Zone 2: Through neuroforamina
• Zone 3: Through spinal canal
o Higher Denis zones associated with
ESSENTIAL INFORMATION increasing probability of significant
Key Differential Diagnosis Issues neurologic deficit
• Bone-algorithm CT and MR are • Metastatic Disease
complementary modalities o Renal, lung, breast, and prostate
• CT superior to assess bone cortex carcinomas are common primaries to

o Bony remodeling: Dural dysplasia, develop osseous metastases
neurofibroma, ependymoma o Sacral fracture can develop within bone
o Bone destruction: Metastases, chordoma weakened by tumor or by pelvic radiation
• MR superior to assess soft tissue contents of therapy
the sacral canal and foramina • Ependymoma, Myxopapillary, Spinal
Cord
Helpful Clues for Common Diagnoses o Most common neoplasm of the conus and
• Dural Dysplasia distal spinal canal
o Intrinsic weakness in dura
o Marked enhancement typical
o Transmission of chronic CSF pressures
o Can show signs of necrosis (heterogeneity,
leads to bony remodeling and expansion cyst formation) and hemorrhage:
of lumbosacral canal and neuroforamina Subarachnoid hemorrhage, superficial
o Contents follow CSF signal on MR and
siderosis
show no appreciable enhancement o Bony remodeling when large: Scalloping of
o Can be seen with neurofibromatosis type the margins of the spinal canal, foraminal
1, Marfan disease, homocystinuria, enlargement
Ehlers-Danlos, and ankylosing spondylitis
• Neurofibroma Helpful Clues for less Common Diagnoses
o Fusiform enlargement of nerve root(s) • Dorsal Dysraphism
o Heterogeneous enhancement o Common features: Everted elements of
o Multiple lesions typical of type 1 dorsal neural arch; tethered, dysraphic
neurofibromatosis cord
o LipomyelomeningoceJe, lipomyelocele:
II Placode adherent to fatty mass contiguous
with subcutaneous fat; intact skin
1
26
SACRAL DEFORMITY
o Myelomeningocele, myelocele: Placode o Peak incidence in 5th and 6th decades,

exposed; no overlying skin rare in children
o Lipomyelocele, myelocele: Placode lies • Teratoma, Sacrococcygeal
within spinal canal o Rare, congenital tumors arising from
o Lipomyelomeningocele, totipotential cells in the caudal cell mass
myelomeningocele: Placode and meninges o Most are large, encapsulated with mixed
protrude through spinal defect solid and cystic components
o Terminal myelocystocele: Meningeal sac o Sacral canal involved in 2%
containing tethered, hydromyelic cord o Classified by location
extends through sacral defect; intact skin • Type I: Caudal, external tumor mass
• Meningocele, Occult Intrasacral without a significant presacral
o CSF-containing meningeal cyst within the component
sacral canal; thin or imperceptible wall; no • Type II: Caudal tumor with significant
appreciable enhancement pelvic component
o Does not contain neural elements • Type III: Mainly intrapelvic, with
o Chronic CSFpulsation pressure leads to minimal external mass
expansion and bony remodeling • Type IV: Completely intrapelvic
o Often asymptomatic, may be associated (presacral)
with low back pain, radicular symptoms, • Caudal Regression Syndrome
and bladder dysfunction o Spectrum of congenital anomalies arising
• Meningocele, Anterior Sacral from maldevelopment of lower vertebral
o CSF-containing meningeal sac protruding column, cord, and pelvic viscera
into the pelvis through an enlarged sacral o Hypoplastic distal cord with truncated or
foramen or a defect in a dysplastic sacrum "blunted" terminus
o Important to determine if nerve roots o Hypoplasia or variable agenesis of the
traverse the neck of the sac for surgical lumbosacral spine
planning o Non-spine anomalies, variably present
• Chordoma • Anal atresia
o Malignant tumor arising from notochord • Bladder exstrophy, abnormalities of
remnants; 50% sacrococcygeal in location external genitalia
o Hyperintense on T2WI; usually containing • Renal aplasia or ectopia
multiple septae; calcification common in
sacral chordoma
Dural Dysplasia
II
Axial NEeT
and foramina
shows widened, remodeled sacral canal
1m due to enlarged thecal sac and nerve
root sleeves in this patient with dural dysplasia.
posterior sacrum and L5 vertebral body =
Sagittal T2WI MR shows marked seal/oping of the
with an
enlarged thecal sac in this patient with dural dysplasia
1
and neurofibromatosis type ,.
27
.~ SACRAL DEFORMITY
ro
D-
,
C/)
(/)
<::
C1l
t= Neurofibroma Insufficiency Fracture, Sacral

Ql
<:: (Left) Axial NECT shows
Q. enlarged sacral foramina ~
en due 10 multiple
neurofibromas in this patient
with NF I. Note large left
gluteal mass due 10 a
plexiform neurofibroma B.
marked osteoporosis and
disruption of the anterior
sacral cortices due to
bilaleral insufficiency
fraclures ~.
Sacral Traumatic Fracture Metastatic Disease

fraClure through the left
sacral foramina (zone It) Et
and subtle fraclure of the
right sacral ala ~. (Right)
Axial T2WI FS MR shows
presacral
rhabdomyosarcoma
engulfing and invading the
sacrum~
Ependymoma, Myxopapillary, Spinal

Cord Myelomen ingocele/ Myelocele
(Left) Sagi!!al T1 C+ MR
shows large, lobulated
hyperintense mass filling the
distal thecal sac and
expanding/remodeling the
sacrum C>. (Right) Sagittal
T2Wf MR shows open spinal
dysraphism and a CSF-filled,
hyperintense
myelomeningocele sac
containing nerve roots
inserting onto a dorsal neural
placode~.
II
1
28
SACRAL DEFORMITY
shows low-lying spinal cord
inserting directly into a
lumbosacral lipomatous
mass a extending through
a dorsal sacral defect to be
contiguous with
subcutaneous fat. Note distal
hydrosyringomyelia =.
(Right) Sagittal STIR MR
shows asymptomatic large
CSF-signal cystic mass within
the sacral canal =-
associated with marked
thinning/remodeling of the
sacral body.
Meningocele, Anterior Sacral Chordoma

shows presacral cyst 81
contiguous with thecal sac
through an enlarged sacral
foramen ~. (Right) Sagittal
T2WI MR shows large,
expansile, well-defined mass
involving sacrococcygeal
region with heterogeneously
hyperintense and fine
internal septations =.
Teratoma, Sacrococcygeal
shows a large, cauda! mass
containing soft tissue
elemen15 = and septated
cys15 81. Foci of hypointense
signal correspond to
calci{;cation or hemorrhage
radiograph shows
hypoplastic sacrum 81 and
iliac wings in this patient
with severe caudal regression
syndrome. L4 and LS
vertebrae are absent =.
II
1
29
ro ACUTE BACK PAIN/RADICUlOPATHY, POST-OPERATIVE
~
0-
(fJ,
en DIFFERENTIAL DIAGNOSIS a Scar formation within epidural space
c:
ro following lumbar surgery
t= Common a Subset of FBSS
Gl
c: • Intervertebral Disc Herniation, Recurrent a Fat suppression of Tl WI (pre- and
a. • Intervertebral Disc Herniation, Acute post-gadolinium) increases sensitivity for
I/)
o Intervertebral Disc Herniation, Cervical detecting peridural fibrosis and for
o Intervertebral Disc Herniation, Thoracic differentiating fibrosis from disc
o Intervertebral Disc Herniation, Lumbar herniation
o Intervertebral Disc Extrusion, Foraminal
• Peridural Fibrosis Helpful Clues for less Common Diagnoses
• Post-Operative Infection
less Common a Infectious sequelae following operative
• Post-Operative Infection procedures
o Abscess, Paraspinal a May manifest in one or more areas at
o Abscess, Epidural operative site including paravertebral
o Abscess, Subdural tissues and subdural or epidural spaces, but
• Post-Operative Complication frequently starts in intervertebral disc
o Hematoma space
• Hematoma, Epidural a Abscess, Paraspinal
• Hematoma, Subdural • Infection of paravertebral soft tissues
o Hardware Failure surrounding spine
o Vertebroplasty Complications • Paravertebral enhancing phlegmon or
o Bone Graft Complications peripherally enhancing liquified
Rare but Important collection
• Post-Operative Complication a Abscess, Epidural
o Brachial Plexus Traction Injury • Extradural spinal infection producing

o Infarction, Spinal Cord abscess formation
• Post-Operative Infection • Frequently spondylodiscitis extends into
o Abscess/Myelitis, Spinal Cord adjacent epidural space => enhancing
epidural phlegmon ± peripherally
enhancing fluid collection
ESSENTIAL INFORMATION • May also see isolated epidural abscess
Helpful Clues for Common Diagnoses without discitis
• Intervertebral Disc Herniation, Recurrent • Lower thoracic, lumbar> cervical, upper
o Focal extension of disc material beyond thoracic
endplate margins at previously operated a Abscess, Subdural
intervertebral disc level • Purulent pus collection developing in

o Subset of failed back surgery syndrome "potential" space between dura and
(FBSS) arachnoid
o Fat suppression of Tl WI (pre- and • Post-Operative Complication
post-gadolinium) may increase sensitivity a Hematoma, Epidural
for detecting peridural fibrosis and for • Blood extravasation into the epidural
differentiating fibrosis from disc spinal compartment
herniation • Long segmental extra-axial mass
• Intervertebral Disc Herniation, Acute encasing or displacing spinal cord or
a Localized « 50% of disc circumference) cauda equina
displacement of disc material beyond • Typically multisegmental, but Illay be
edges of vertebral ring apophyses focal when associated with focal fracture
a Unfortunate luck to present with new disc or disc extrusion
herniation after previous surgery at o Hematonla, Subdural
II another level • Accumulation of blood between dura
• Peridural Fibrosis and arachnoid
1
30
ACUTE BACKPAIN/RADICULOPATHY, POST-OPERATIVE
• Signal characteristics variable depending • Avulsion injury: Attenuated or disrupted

on age of blood products proximal roots/rami within or
o Hardware Failure immediately distal to lateral
• Mechanical breakdown, malfunction, or CSF-containing dural sac diverticulum
malposition of metallic implant devoid of neural elements ± retracted
• May present either with chronic pain or distal nerve roots, nerve "retraction ball"
calamitously with acute pain o Infarction, Spinal Cord
o Vertebroplasty Complications • Thoracic spinal cord infarction 2° arterial
• Cement extravasation into spinal canal, occlusion (radicular artery)
foramen, or vertebral venous plexus • Artery of Adamkiewicz frequently
• Pulmonary artery cement embolization implicated
• Vertebral osteomyelitis • Usually extends to involve more than
• "Bounce back" vertebral fracture one vertebral body segment
o Bone Graft Complications • Central hyperintensity on T2WI more
• Graft migration, graft displacement, or common than wedge-shaped
graft extrusion involvement of anterior 2/3 of spinal
• Abnormal alignment, position, or cord
placement of graft ± associated • Post-Operative Infection
neurologic deficit, instability, infection o Abscess/Myelitis, Spinal Cord
• Cervical> thoracic> lumbar • Spinal cord infection with necrosis
Helpful Clues for Rare Diagnoses • Spinal cord neoplasm mimic;
ring-enhancing mass within cord with
• Post-Operative Complication
appropriate clinical history of
o Brachial Plexus Traction Injury
inflammation/infection is highly
• Stretch injury or avulsion of ~ 1 cervical
suggestive
roots, brachial plexus
• Pyogenic infection most common but
• Stretch injury: Enlargement or
granulomatous infections have been
attenuation of stretched (but contiguous)
described
plexus elements
• May show positive diffusion (reduced
ADC) restriction similar to brain abscess,
but lack of diffusion restriction does not
exclude abscess
Intervertebral Disc Herniation, Intervertebral Disc Herniation,

Recurrent Recurrent
II
Sagittal T1 C+ MR in a posl-operalive
a
paUent with Axial Tl C+ FS MR in a post-operative
recurrent back pain reveals a large
patient with
post-operalive
1
=
recurrel1l back pain demonstrates
that ventrally compresses
recurrent
the thecal sac.
L4-5 IINP
recurrent disc herniation ~~L
31
Cll ACUTE BACK PAIN/RADICULOPATHY, POST-OPERATIVE
~
a.
,
(/)
en
c
~
Cll
f-
Intervertebral Disc Herniation, Cervical Intervertebral Disc Herniation, Thoracic
ell
c (Left) Axial T2* eRE MR
a. reveals a large left cervical
(/)
disc herniation producing
spinal cord deformation and
narrowing of the lefllateral
spinal canal. (RighI) Axial
T2WI MR depic15 a left
paracentral thoracic disc
herniation that produces
mild spinal cord deformation
but no significanl narrowing
of the central spinal canal.
Intervertebral Disc Herniation, Lumbar Intervertebral Disc Extrusion, Foraminal

(Lefl) Axial T2WI MR in a
patient with left leg pain
demonstrates a huge left
lateral recess disc extrusion
=:I that obliterates lhe left
lateral recess and deforms
the thecal sac. (RighI) Axial
T2WI MR reveals a huge
right Foraminal and far lateral
disc extrusion =
in a
symptomatic patient with
acute right leg pain.
Peridural Fibrosis Peridural Fibrosis

diffuse enhancement of right
lateral epidural space and
surrounding exWng root
t;econdary to peridural
fibrosis. There is extensive
enhancement of the disc
curette site =:I. (RighI) Axial
T1 C+ MR depic15 extensive
enhancing epidural fibrosis
circumferentially surrounding
the thecal sac =:I. Note
mewl susceptibility artifact
from fusion cage ~.
II
1
32
ACUTE BACK PAIN/RADICUlOPATHY, POST-OPERATIVE
Abscess, Paraspinal Abscess, Paraspinal

(LeFt) Sagiltal STIR MR aFter
L4-S posterior lumbar
interbody fusion (PUF)
shows abnormal fluid signal
intensity in L4-5 disc
interspace and posterior 50ft
tissue abscess with
fluid-debris level ffi (Right)
Axial T2WI MR following
L4-S PUF shows increased
signal intensity in dorsal soft
tissues &, abscess collection
surrounding posterior spinal
fusion hardware (metallic
susceptibility E!lI! & edema
in paraspinal muscles.
Abscess, Epidural Abscess, Epidural

(Left) Sagi!!al T7 C+ MR in a
post-operative patient with
back pain and fever
demonstrates a
well-delineated,
rim-enhancing,
post-operative epidural
abscess at the SI level
(Right) Axial T7 C+ FS MR
=.
delineates a
well-circumscribed,
abscess =
rim-enhancing epidural
producing mass
effect and displacement of
the thecal sac to the right
(LeFt) Sagi!!al T2WI MR

shows two level fusion from
CJ to C5 with metal artifact
from screws. Screw artifact
at C5 level extends to the
ventral epidural space
adjacent to the spinal cord
E1. Note congenital fusion at
C6-7. (Right) Axial T7 C+
MR following interbody
Fusion and posterior pedicle
screw fixation shows
extensive enhancement of
paraspina/ musculature
involving dorsal muscles as
we/J as psoas and multifidus
muscles=.
II
1
33
co ACUTE BACK PAIN/RADICULOPATHY, POST-OPERATIVE
~Q.
,
(f)
(/)
c
co
~
I-
Q)
Hematoma, Epidural Hematoma, Epidural
C (Left) Sagillal T7 WI MR
e- shows wide cervical
rn laminectomy defect with
intermediate signal intensity
filling the laminectomy
defect, representing epidural
hematoma; which
compresses posterior thecal
sac and spinal cord~. Note
surgical drain 81. (Right)
Sagittal TlWI MR following
L]-L5 laminectomy shows
intermediate signal mass (not
/racking CSF) filling the
laminectomy site = and
extending into dorsal
epidural space, compressing
the thecal sac.
Hematoma, Subdural Hematoma, Subdural

reveals a mildly hyperintense
subacute subdural
hematoma I:ll following
spinal surgery that dorsally
compresses the thecal sac
and spinal cord. (Right)
Sagittal T2WI MR following
vertebroplasty in a patient
with severe multilevel
degenerative disc disease
shows severe compression
deformities at T72, L1, and
moderate deformity at L2.
Note subdural I:ll and
subarachnoid blood layer PJ::l
in distal thecal sac.
Hardware Failure
(Left) Axial bone CT
following myelography with
bilateral pedicle screws in
place shows lucency
surrounding the left pedicle
screw indicating loosening
with superimposed stress
fracture through the left
pedicle and posterior
vertebral body I:ll. (Right)
Lateral radiograph in an NF I
patient with operated
scoliosis shows dramatic
presentation with acute back
pain and spinal hardware
protruding through skin.
II
1
34
ACUTE BACK PAIN/RADICULOPATHY, POST-OPERATIVE
Bone Graft Complications

(Lefl) Axial TI WI MR shows
injected low signal intensity
methacrylate within the
anterior vertebral body as
intended, as well as
extending into the left
paravertebral soft tissues =
adjacent 10 the aorta E!:I.
(RighI) Sagillal TI WI MR
depicts disccctomy and
bone graft placement at C3-4
through CS-6. There is
posterior displacement of
graft components into
ventral epidural space,
producing spinal cord
compression =.
Brachial Plexus Traction Injury Brachial Plexus Traction Injury

(Lefl) Coronal STIR MR in an
infant with right arm
paralysis following difficult
obstetrical delivery
demonstrates right C6 and
C7 nerve raal avulsion
pseudorncningoceles m.
(RighI) Axial T2' eRE MR
shows right CB and TI nerve
rool/ventral primary ramus
stretch injuries resulting in
marked nerve root
enlargement and abnormal
T2 hyperintensity.
Infarction, Spinal Cord Abscess/Myelitis, Spinal Cord

(Left) SagiHal T2WI MR in a
patient manifesting
post-operative paraplegia
following thoracoabdominal
aneurysm repair shows
abnormal T2 hyperintensity
extending from mid La distal
thoracic spinal cord =.
(RighI) SagiHal TI C+ MR
shows intramedullary
rim-enhancing spinal cord
abscess with adjacent Jow
signal intensity edema.
II
1
35
:gco CHRONIC BACK PAIN/RADICULOPATHY, POST-OPERATIVE
Q.
,
(/)
rJ)
c DIFFERENTIAL DIAGNOSIS o T1 C+ FSMR imaging increases sensitivity
co for detecting peridural fibrosis and permits
~ Common
Q)
differentiation of fibrosis from disc
c • Failed Back Surgery Syndrome herniation
Q.
(/)
• Peridural Fibrosis • Degenerative Disc Disease
• Intervertebral Disc Herniation, Recurrent o Generalized and multifactorial process
• Degenerative Disc Disease affecting discovertebral unit leading to
• Instability biomechanical/morphologic alterations
• Post-Laminectomy Spondylolisthesis o Imaging diagnosis of degenerative disc
• Accelerated Degeneration disease does not distinguish symptomatic
Less Common from asymptomatic levels
• Hardware Failure • May be asymptomatic or associated with
• Bone Graft Complications back/neck pain ± radiculopathy
• Vertebroplasty Com pJications • Instability
• Post-Operative Infection o Loss of spine motion segment stiffness,
• Scoliosis, Degenerative where applied force produces greater
displacement than normal, producing
Rare but Important
pain/deformity
• Arachnoiditis, Lumbar o Deformity increases with motion and
• Arachnoiditis Ossificans, Lumbar increases over time
o Any spinal motion segment (comprised of
ESSENTIAL INFORMATION two adjacent vertebrae, disc and
connecting spinal ligaments) may be
Key Differential Diagnosis Issues involved
• Careful clinical exam will often distinguish • Most common at post-operative levels,
radiculopathy from mechanical back pain, particularly if posterior elements
enabling a tailored differential list removed by laminectomy
• Carefully consider hardware failure or o AP translation at unstable level may vary
indolent infection in post-operative implant from few mm to entire width of vertebral
patients presenting with chronic back pain body
Helpful Clues for Common Diagnoses • Post-Laminectomy Spondylolisthesis
• Failed Back Surgery Syndrome o Loss of spine motion segment stiffness,
o Continued low back pain ± radicular pain where applied force produces greater
following lumber spinal surgery displacement than normal, producing
o Myriad etiologies manifest clinically as pain/deformity
failed back surgery syndrome (FBSS) o AP canal diameter narrows at subluxation
o Look for specific abnormal imaging level, distinguishing from spondylolysis
findings that may be addressed clinically where the AP canal diameter is increased
• Peridural Fibrosis • Accelerated Degeneration
o Scar formation within epidural space o Synonyms include spinal "transitional
following lumbar spinal surgery degenerative syndrome" and "accelerated
o Subset of FBSS segmental degeneration"
o Tl C+ FS MR imaging increases sensitivity o Degeneration of disc space/facets at level(s)
for detecting peridural fibrosis and permits adjacent to spinal fusion 2° to altered
differentiation of fibrosis from disc biomechanical forces - degenerative disc
herniation changes, disc herniation, and/or
• Intervertebral Disc Herniation, Recurrent subluxation
o Focal extension of disc material beyond o Identical changes occur at motion
endplate margins at previously operated segments above or below congenital
II intervertebral disc level
o Subset of FBSS
segmentation anomaly levels
1
36
CHRONIC BACK PAIN/RADICUlOPATHY, POST-OPERATIVE
o Look for unexpected abnormal MR

enhancement post-spinal surgery imaging
• Hardware Failure
• Scoliosis, Degenerative
o Mechanical breakdown or malfunction of
o "De novo" scoliosis
spinal fusion hardware
o Lateral spinal curvature due to
o Malposition of spinal fusion hardware
degenerative disc and facet disease
without mechanical failure of implant
o Radiculopathy secondary to foraminal
o Presentation symptoms range from
narrowing and nerve root compression
indolent with chronic pain to calamitously
o Usually seen in older patients
with acute pain
• Bone Graft Complications Helpful Clues for Rare Diagnoses
o Abnormal alignment, position, or • Arachnoiditis, Lumbar
placement of graft or hardware ± o Post-inflammatory adhesion and clumping
associated neurologic deficit, instability, of cauda equina nerve roots in thecal sac
infection o Imaging shows either absence of discrete
• Graft migration, graft displacement, or nerve roots ("empty sac") or peripheral
graft extrusion displacement of nerve roots in thecal sac
o Cervical> thoracic> lumbar • Arachnoiditis Ossificans, Lumbar
• Vertebroplasty Complications o Intradural ossification associated with
o Complication types include post-inflammatory adhesion and clumping
• Extravasation of cement into spinal of lumbar nerve roots
canal, neural foramen, or vertebral o Look for focal calcific density on CT or
venous plexus hyperintensity on TlWI and T2WI within
• Pulmonary embolization of cement lumbar nerve root aggregate
• Vertebral osteomyelitis
• "Bounce back" fracture adjacent to
vertebroplasty level
• Post-Operative Infection
o Infectious sequelae following operative
procedures
o Most frequently begins in intervertebral
disc space ~ disci tis, epidural abscess,
subdural abscess, &/or paraspinal abscess
II
SagittalT7WI MR shows large osteophyte
compressing thecal sac and prior multilevel
at U-4 Sagittal T7 C+ MR shows large recurrent
herniation compressing thecal sac E2 with thin
L4-S disc
1
laminectomies. High signal within thecal sac
residual from prior Panlopaque myelography.
=
is peripheral enhancement. Note linear enhancement
within disc due £0 disc degeneration =. 37
co CHRONIC BACK PAIN/RADICUlOPATHY, POST-OPERATIVE
~
a.
CfJ,
en
c
co
~
I-
al
C (Left) Axial TI C+ MR shows
a. a large amount of
m homogeneously enhancing
left lateral epidural fibrosis
surrounding thecal sac and
exiting root =:I. (Right) Axial
TI C+ MR demonSlrates
exuberant enhancing
epidural fibro.;is
circumferenlially surrounding
the thecal sac =:I. Note
metal artifact (rom
intervertebral fusion cages
Sli

Recurrent Recurrent
demonstrates post-operative
changes following L4 & L5
laminectomies. Absence of
enhancement helps
distinguish recurrent L4-5
disc herniation lID from
epidural scar tissue. (Right)
Axial TI C+ FS MR
demonstrates post-operative
laminectomy changes with
recurrent left L4-5
paracentral disc extrusion
=:I. Note absence of disc
fragment enhancement.

Recurrent Recurrent
shows a recurrent
intervertebral disc herniation
=:I following decompressive
laminectomy. so(t tissue
enhancement of paraspinal
muscles is common in
subacute period. (Right)
Axial TI C+ FS MR after L5
left hemilaminectomy shows
large recurrent L5-S 1 disc
extrusion/free Fragment with
variant peripheral
enhancement lID.
II
1
38
CHRONIC BACK PAIN/RADICULOPATHY, POST-OPERATIVE
Bone Graft Complications Post-Operative Infection

with right back and flank
pain and palpable mass
demonstrates protrusion of
colon and mesenteric Fat
through the large right iliac
wing bone graft harvest site
=. (Right) SagiILal T 1 C+
MR following upper lumbar
decompressive laminectomy
shows extensive mufti/evel
degenerative disc changes
and large dorsal epidural
abscess
junction.
= at lumbosacral
Post-Operative Infection Scoliosis, Degenerative

(Left) Axial T1 C+ MR in a
patient with chronic back
pain SlaWS post explantation
of spinal fusion hardware
shows enhancing muscle
changes of pyomyositis as
well as pus =and
inflammawry phlegmon in
operative bed and pedicle
screw track 7,. (Right)
shows multilevel
degenerative disc and facet
disease producing
degenerative scoliosis.
Arachnoiditis, lumbar Arachnoiditis Ossificans, lumbar

(Left) Sagittal bone CT after
myelography shows a large
soft tissue intradural filling
defect = that engulfs the
distal cauda equina =>
chronic inflammatory
pseudomass of arachnoiditis.
irregular calcification
involving the distal thecal sac
at the sacral level =.
indicating end-stage calcific
arachnoiditis (similar to
bone, less dense than
Panwpaque).
II
1
41
ro ACUTE UPPER EXTREMITY PAIN/WEAKNESS
~
Cl.
(fJ
enc DIFFERENTIAL DIAGNOSIS • Muscle, ligamentous injuries suggest
ro
~ etiology
I- Common • Cervical Fracture with Nerve Compression
Q.)
c • Intervertebral Disc Herniation o Burst Fracture, Cervical
c. o Intervertebral Disc Herniation, Cervical • Typically mid- or lower cervical spine
(fJ
o Intervertebral Disc Herniation, Traumatic • Axial compression - comminuted
• Cervical Fracture with Nerve Compression fracture extending through both
o Burst Fracture, Cervical end plates
o Hyperflexion Injury, Cervical o Hyperflexion Injury, Cervical
o Lateral Flexion Injury, Cervical • Typically mid or lower cervical spine
o Hyperflexion-Rotation Injury, Cervical • Flexion force disrupts capsular &
o Pathologic Vertebral Fracture posterior ligaments - anterior vertebral
Less Common displacement/angulation, focal kyphosis,
t space between spinous processes
• Syringomyelia
• Traumatic Dural AVFistula o Lateral Flexion Injury, Cervical
• Peripheral Neuropathy • Typically mid or lower cervical spine
o Brachial Plexus Traction Injury • Articular mass fracture ± fractures of
o Radial Neuropathy transverse and uncinate processes,
o Ulnar Neuropathy vertebral body
o Median Nerve Entrapment o Hyperflexion-Rotation Injury, Cervical
o Suprascapular erve Entrapment • Typically mid or lower cervical spine
• Infection • Traumatic disruption of cervical spine
o Abscess, Paras pinal (ligaments ± bony elements) - facet
o Abscess, Epidural subluxation, focal vertebral angulation,
o Osteomyelitis, Granulomatous rotation
o Osteomyelitis, Pyogenic o Pathologic Vertebral Fracture
• Fracture through abnormal bone
Rare but Important weakened by tumor or infection
• Idiopathic Brachial Plexus Neuritis • Search for trabecular and cortical bone
• Acute Transverse Myelitis, Idiopathic destruction, spinal cord &/or nerve root
• Secondary Acute Transverse Myelitis compression
• ADEM, Spinal Cord
• Syringomyelia
ESSENTIAL INFORMATION o Expanded spinal cord with central dilated,
Key Differential Diagnosis Issues beaded, or sacculated cystic cavity
• Careful clinical exam distinguishes • Traumatic Dural AV Fistula
radiculopathy from mechanical back pain or o AVFnidus with enlarged draining veins
myelopathy, limiting pertinent differential o Radiculopathy 2° to nerve compression by
diagnosis list enlarged epidural veins

• Peripheral Neuropathy
Helpful Clues for Common Diagnoses o Brachial Plexus Traction Injury
• Intervertebral Disc Herniation • Stretch injury or avulsion of ~ 1 cervical
o Intervertebral Disc Herniation, Cervical roots, brachial plexus elements
• Localized « 50% of disc circumference) • Denervation changes in dorsal paras pinal
displacement of disc material beyond muscles, arm and forearm muscles
edges of vertebral ring apophyses innervated by terminal peripheral nerve
• Clinical symptoms affected by level, branches
location, herniation size o Radial Neuropathy
o Intervertebral Disc Herniation, • Focal radial nerve enlargement,
II Traumatic
• Disc herniation following trauma
abnormal T2 hyperintensity
1
42
ACUTE UPPER EXTREMITY PAIN/WEAKNESS
• Characteristic entrapment locations • May produce spinal cord, nerve

include mid humeral shaft or fibrous compression
arch of Frohse o Osteomyelitis, Pyogenic
o Ulnar Neuropathy • Ill-defined abnormal vertebral marrow
• Focal ulnar nerve enlargement, abnormal signal centered at disc with loss of
T2 hyperintensity adjacent end plate definition
• Most common in cubital tunnel (elbow); • May produce spinal cord, nerve
uncommon in Guyon tunnel (wrist) or compression
brachial plexus Helpful Clues for Rare Diagnoses
o Median Nerve Entrapment
• Idiopathic Brachial Plexus Neuritis
• Focal median nerve enlargement, o Parsonage-Turner syndrome
abnormal T2 hyperintensity o Immune-mediated neuropathy of brachial
• Entrapment most common at carpal plexus
tunnel or pronator teres muscle o Smooth enlargement of brachial plexus
o Suprascapular Nerve Entrapment elements, mild diffuse nerve and muscle
• Mass impinges nerve at spinoglenoid or enhancement
suprascapular notch • Acute Transverse Myelitis, Idiopathic
• Abnormal T2 hyperintensity in o Inflammatory lesion involving both spinal
denervated muscles hemicords - bilateral motor, sensory, and
• Infection autonomic dysfunction
o Abscess, Paraspinal
o Lesion extent> 2 vertebral segments +
• Paravertebral enhancing phlegmon or eccentric enhancement
peripherally enhancing liquified pus • Secondary Acute Transverse Myelitis
collection o Inflammatory disorder of spinal cord
o Abscess, Epidural
associated with many etiologies
• Spondylodiscitis with adjacent o T2 hyperintense lesion with mild cord
enhancing epidural phlegmon ± expansion, minimal to no enhancement
peripherally enhancing fluid collection
• May extend over many vertebral o Para/postinfectious immune-mediated
segments inflammatory disorder of spinal cord white
o Osteomyelitis, Granulomatous matter
• Tuberculosis or brucellosis most o Multiple sclerosis mimic
common
II
Sagittal T2WI MR demonslIates a C4-5 cervical disc
herniation with spinal cord deformation. location
Axial T2* eRE MR shows a large left C6-7 cervical
herniation with deformation of the spinal cord
disc
1
corresponds with left arm pain. concordant with clinical localization of leh arm pain.
43
<tl ACUTE UPPER EXTREMITY PAIN/WEAKNESS
~Q.
(fJ,
(/)
C
<tl Intervertebral Disc Herniation,
~
Intervertebral Disc Herniation, Cervical Traumatic
GI
c (Left) Axial T2WI FS MR in a
'0. patient with leFtarm pain
(fJ
shows a small cervicalllNP
E!lI with abnormal
asymmetric T2
hyperintensity of the irritated
left C7 nerve root =.
(Right)
ligamentous injury with
herniated C6-7 disc 8l
disruption of anterior
longitudina/l:i4
longitudinal =-
posterior
and
interspinous ligaments P.::J.
Burst Fracture, Cervical

demonstrates a sagittally
oriented burst fracture =
through the C5 vertebral
body with extensive marrow
and soft tissue edema.
(Right) Axial bone CT reveals
a C6 burst fracture with right
facet capsular injury and
narrowing of the right C6
neural foramen.
Lateral Flexion Injury, Cervical

depicts a traumatic
hyped/exion cervical spine
injury with right C5-6 facet
perch It] and concordant
right C6 radiculopathy.
reveals isolated fracture
involving right C7 articular
pillar and transverse process
=. The fracture was much
more conspicuous on CT
(not shown) than MR.
II
1
44
ACUTE UPPER EXTREMITY PAIN/WEAKNESS VI
"C
:J
(l)
-I
Q]
:J
lateral Flexion Injury, Cervical Pathologic Vertebral Fracture '"en,
"C
facet fracture =
demonstrates a right C6-7
and
extensive sort tissue edema
~.
OJ
in patient with lateral

compression/stretch injury
and right arm pain. (Right)
Axial TI C+ FS MR shows a
pathological fracture line =
through a cervical renal cell
carcinoma lytic metastasis
with acute right arm pain.
Traumatic Dural AV Fistula

shows a large
cervicothoracic syrinx in a
symptomatic child with
Chiar; 1 malformation.
Heterogeneous signal
intensity within the syrinx
cavity reflects dynamic CST
pulsation artifact. (Right)
dilated epidural plexus flow
voids = in a patient with
healed C2 fracture
complaining of "leaky
plumbing II sound in his
head, right arm pain, and
multilevel arm weakness.
Brachial Plexus Traction Injury

demonstrates abnormal
enlargement and T2
=
hyperintensity of the right C8
and TI Ell nerve roolS
and ventral primary rami
following stretch injury.
(Right) Axial STIR MR in a
patient with radial
neuropraxic injury
("Saturday night palsy")
reveals marked abnormal
nerve T2 hyperintensity =
equal to that of regional
vessels B.
II
1
45
ro ACUTE UPPER EXTREMITY PAIN/WEAKNESS
~Q.
(fJ,
(/)
c
ctl
~
I-
(l)
Ulnar Neuropathy Median Nerve Entrapment
c (Left) Axial T2WI FS MR
reveals internal ulnar nerve
=
Q.
en architectural distortion at
cubital tunnel with
abnormally enlarged
hyperintense nerve Fascicles
and regional perineural soft
!issue edema. (Right) Axial
STIR MR depicts MR
appearance of abnormal
median nerve in the carpal
tunnel. The flexor
retinaculum is bowed
anteriorly and nerve
heterogeneous
=
in signal
is
intensity.
Suprascapular Nerve Entrapment Abscess, Epidural

fLeft) Axial T1 C+ rs
MR
rim-enhancing cyst =
producing adjacent scapular
erosion. Diffuse
enhancement of the
infraspinatus muscle
secondary to acute
denervalion is visible ~J.
(Right) Axial T 1 C+ MR with
vertebral osteomyelitis shows
pre vertebral phlegmon SI
and peripheral enhancement
of ventral epidural abscess
=
cord
de/orming the spinal
(Left) Sagillal T 1 C+ MR
(chronic coccidiomycosis)
shows destruction of C7, T1
bodies and large preverrebral
abscess = with relative
sparing of the intervertebral
discs. (RighI) Axial T1 C+
MR (chronic
coccidiomycosis) depicts a
large prevertebral abscess ~
with adjacent osseous
destruction and soft tissue
inflammation engulfing
exiting nerve roots.
II
1
46
ACUTE UPPER EXTREMITY PAIN/WEAKNESS fJl
-C
::::J
<l>
-l
~
Ql
::::J
,
(f>
(f)
(Left) Sagittal T1 C+ MR in u
an IV drug abusing patient ~
Ql
with neck pain and {ever
shows destructive changes of
C4-5 disc space with marrow
enhancement, focal
kyphosis, and epidural
phlegmon. (Right) Axial
T1WI FS MR demonstrates
extensive marrow and soft
tissue inflammalOry changes
in a patient with vertebral
pyogenic osteomyelitis and
arm pain.
(Left) Coronal oblique STIR

MR (Parsonage·Turner
syndrome) demonstrates
abnormal T2 signal
hyperintensity and
enlargement of the right
brachial plexus neural
elements =:S. (Right) Sagittal
T1 C+ MR reveals multilevel
spinal cord swelling and
abnormal intramedullary
enhancement involving both
gray and white maller.
ADEM, Spinal Cord ADEM, Spinal Cord

pediatric patient developing
right leg weakness following
a viral illness several I'veeks
previously shows multiple
patchyexpansile
intramedullary T2
hyperintense lesions. (Right)
Axial T1 C+ MR depicts a
typical case of monophasic
spine AOrM lesions with
enhancement =.
II
1
47
co LOWER EXTREMITY PAIN
ii
D-
,
C/)
rn
DIFFERENTIAL DIAGNOSIS • Protrusion: Wider than deep, limited by
c
co
~ adjacent endplates on sagittal images
I- Common • Extrusion: Deeper than wide or extends
Q)
c • Intervertebral Disc Bulge beyond either adjacent end plate on
0-
en • Intervertebral Disc Herniation sagittal images
• Stenosis, Acquired Spinal, Lumbar • Sequestration: Herniated disc not in
• Stenosis, Foraminal, Lumbar continuity with the remaining disc
• Stenosis, Congenital Spinal • Stenosis, Acquired Spinal, Lumbar
• Spondylolisthesis o Multifactorial process
• Spondylolysis o Relative lumbar canal stenosis: < 12 mm;
• Metastases absolute lumbar canal stenosis: < 10 mm
Less Common • Stenosis, Foraminal, Lumbar
• Abscess, Epidural, Paravertebral o Multifactorial process
• Hematoma, Epidural-Subdural o Loss of fat within the neural foramen on

• Ependymoma, Myxopapillary, Spinal Cord sagittal T1WI
• Neurofibroma • Stenosis, Congenital Spinal
• Schwan noma o Developmental narrowing of the lumbar
• Facet Joint Synovial Cyst canal and neural foramina due to short,
• Arachnoiditis, Lumbar squat pedicles
• Primary Bone Tumor o Otherwise mild degenerative changes in
o Multiple Myeloma disc and posterior elements can result in
o Osteoid Osteoma/Osteoblastoma symptomatic stenosis
o Osteosarcoma • Spondylolisthesis
o Chondrosarcoma o Displacement of a vertebral body relative
• Femoral Neuropathy to the inferior vertebra

• Retroperitoneal Hematoma o Direction
• Tethered Spinal Cord • Anterolisthesis

• Retrolisthesis, usually degenerative
etiology
ESSENTIAL INFORMATION • Lateral listhesis
Key Differential Diagnosis Issues o Etiology
• Majority of lower extremity pain due to • Degenerative, secondary to loss of

pathology within the extremity intervertebral disc height and laxity in
o Osteoarthritis of the hip or knee facet joints
o Meniscal pathology • Spondylolytic
o Tendinous or ligamentous injury • Traumatic
o Trauma • Spondylolysis
o Deep venous thrombosis o Defect of pars interarticularis, may be
o Infection/inflammation unilateral or bilateral
o Neoplasms of the soft tissues and bone o Classified into early, progressive, and
• Neurogenic leg pain due to impingement on terminal stages (Morita)
the distal cord or nerve roots in the spinal o Hairline fracture of early stage often
canal, neuroforamina, or retroperitoneum difficult to appreciate with CT
• Also consider vascular claudication as a • Fracture can be suggested by MR
remote source of lower extremity pain (hyperintense STIR) or SPECT (tracer
avid)
Helpful Clues for Common Diagnoses o Unilateral spondylolysis associated with
• Intervertebral Disc Bulge increased risk of contralateral pars fracture
o Diffuse (> 50% circumference) extension of
• Metastases
the disc beyond its normal margins
II • Intervertebral Disc Herniation
o Common primaries: Breast, lung, kidney,
prostate
o Classified morphologically
1
48
LOWER EXTREMITY PAIN CIl
"C
::::l
(1)
o Lesions typically multiple • Neurofibroma and Schwannoma -I

o Either lytic or sclerotic on CT, typically o Both can manifest as a transforaminal iiJ
::::l
en,
hypointense Tl/hyperintense T2 signal on ("dumbbell") mass en
-0
MR o Foraminal enlargement due to remodeling OJ
o Either epidural tumor or pathologic • Facet Joint Synovial Cyst 0;'

vertebral compression fracture can o Circumscribed, cystic lesion associated
impinge on nerve roots or the cord with a degenerative facet joint
o Can cause canal stenosis and impinge on
the ipsilateral traversing or exiting nerve
• Abscess, Epidural, Paravertebral
o Epidural fluid collection with marked
root
peripheral enhancement • Arachnoiditis, Lumbar
o Usually a post-surgical complication
o Usually in the setting of
o Clumping of nerve roots, "empty sac sign",
discitis-osteomyelitis due to pyogenic or
calcification (unusual)
mycobacterial infection
o Can also be seen with inoculation arising
• Tethered Spinal Cord
o Cord normally terminates above the L2-3
from surgery or instrumentation (e.g.,
level
epidural catheter placement)
o Causative lesions
• Hematoma, Epidural-Subdural
o MR signal of blood products varies with
• Tight filum terminale
age • Dysraphism
o Subacute hemorrhage sometimes difficult
• Diastematomyelia
to differentiate from epidural fat on both
T1 and FSET2 (another use for STIR)
• Ependymoma, Myxopapillary, Spinal
Cord
o Most common tumor of the conus
medulJaris and lumbosacral canal
o Marked enhancement typical
o Can show signs of necrosis and
hemorrhage
o Bony remodeling when large: Scalloping of
the margins of the spinal canal, foraminal
enlargement
Intervertebral Disc Bulge
II
Axial T2WI MR shows eccentric disc bulge ~ with
extraforaminal impingement on a swollen left L5 nerve
Sagittal T1WI MR shows intraforaminal disc extrusion
completely effacing the fat within the L5-S1 neural
1
root~. foramen=.
49
C'<l lOWER EXTREMITY PAIN
~
c.
(/J
en
c
~
C'<l
I-
eI)
Stenosis, Acquired Spinal, lumbar
c (Left) SagieealT2WI MR
c. shows advanced
(/J
degenerative changes with
moderate-La-severe canal
stenosis at multiple levels of
ehe lumbar spine =.
A/50
seen is hemangioma in L 1
vertebral body (Right)
moderalely severe /.5-51
foraminal stenosis =due to
endplaee osteophyte and
roslrocaudal facet
subluxation. L4-5 foramen is
narrowed by disc bulge and
facee hypertrophy. Noee
healed fracture of Ihe L4
pedicle 1J:iJ.
Spondylolisthesis
a narrowed AP diameter of
ehe lumbar canal wieh short
Ihickened pedicles =.
(Right) Laeeral myelography
sholVs bilateral L5
spondylolysis and a
pronounced L5-S I
spondylolisehesis =.There
is abrupe cue-off filling in the
caudal ehecal sac due COehe
resulting canal stenosis ~.
Spondylolysis Metastases
(Left) Sagittal T2W/ MR
shows a defece of ehe left L3
pars interarticularis 7] with
mild anterior displacement of
L3 on L4, resulting in
moderately severe narrowing
of the L3-4 neural foramen
=. (Right) Axial T7 C+ MR
shows T 12 renal cell
carcinoma metastasis with
extensive epidural
component compressing the
conus medul/aris =.
II
1
50
LOWER EXTREMITY PAl N
Abscess, Epidural, Paravertebral Hematoma, Epidural-Subdural

(Lefl) Sagittal T/ C+ MR
shows ventral epidural
abscess resulting in marked
canal stenosis at the L5 level
~. (RighI) Sagittal T2WI MR
shows dorsal epidural
hematoma from T 12-L] =-
causing severe canal stenosis
and compressing the conus
and cauda equina.

Cord Schwannoma
(Left) Sagittal T 1 C+ MR
shows a large,
mass essentially filling the
caudal thecal sac from L2
through L5 =. (RighI) Axial
T2WI MR shows right T/2-L7
lransforaminal mass, with
heterogeneously
hyperintense signal,
expanding the neural
foramen causing severe
canal stenosis and
compression of the conus
medullaris =.
Facet Joint Synovial Cyst Arachnoiditis, Lumbar

a cystic lesion in the right
lateral lumbar canal a. in
contact with a degenerated
right L4-5 facet joint,
resulting in canal stenosis
and compression of the
exiling right L5 nerve root
(not shown). (RighI) Axial
T2WI MR shows peripheral
clumping of nerve roots in
the distal thecal sac, resulting
in the "empty sac sign",
Note laminectomy at this
level.
II
1
51
ro BACK PAIN, ADULT
~
a.
CfJ,
rJ)
c DIFFERENTIAL DIAGNOSIS • Intervertebral Disc Herniation
ro
~ o Classified by morphology as protrusion,
f- Common extrusion, or sequestration
Ol
c • Intervertebral Disc Bulge • Facet Arthropathy
a. • Intervertebral Disc Herniation
en o Joint space narrowing, osteophyte
• Facet Arthropathy formation
• Intervertebral Disc Anular Tear o Often accompanied by ligamentous
• Stenosis, Acquired Spinal hypertrophy
• Spondylolysis o May be secondary to altered load bearing
• Spinal Muscle Injury in the setting of degenerative disc disease,
• Instability by which it is almost invariably
• Benign Compression Fracture accompanied
• Schmorl Node o "Blocky" facet morphology does not
Less Common necessarily represent degenerative change
• Osteomyelitis, Pyogenic • Intervertebral Disc Anular Tear
• Osteomyelitis, Granulomatous o Focal T2 hyperintensity in dorsal disc
• Metastatic Disease margin, representing disruption of the
• Insufficiency Fracture, Sacral anulus fibrosus
• Obstructive Uropathy o May enhance on post-contrast sequences
o Relatively frequent finding; majority are
Rare but Important
asymptomatic
• Ependymoma, Myxopapillary, Spinal Cord • Stenosis, Acquired Spinal
• Primary Bone Tumor o Narrowing of the spinal canal
o Multiple Myeloma
o Multifactorial
o Osteoid Osteoma/Osteoblastoma
0< 10 mm diameter of the lumbar canal is
o Osteosarcoma
absolute stenosis
o Chondrosarcoma
• Spondylolysis
• Aortic Aneurysm o Defect of pars interarticularis, may be
• Marrow Replacement Processes unilateral or bilateral
o Sickle Cell
o Classified into early, progressive, and
o Leukemia
terminal stages (Morita)
o Thalassemia
o Hairline fracture of early stage often
o Mucopolysaccharidoses
difficult to appreciate with CT; can be
suggested by MR (hyperintense STIR) or
ESSENTIAL INFORMATION SPECT (tracer avid)
o Unilateral spondylolysis associated with
Key Differential Diagnosis Issues increased risk of contralateral pars fracture
• Back pain is a major health and economic (e.g., terminal spondylolysis on one side
problem in the industrialized world with early/symptomatic spondylolysis on
• Substantial burden to the healthcare system the other)
and to the economy as a whole due to lost • Spinal Muscle Injury
productivity (disability, absenteeism) o Muscular strain, with variable degrees of
• Back pain is the most common indication edema/hemorrhage and disruption
for imaging of the spine o Best visualized on fat-saturated T2
• Most common causes of back pain are those sequences
relating to degenerative changes in the • Instability
intervertebral discs and facet joints o Greater displacement than normal for a
Helpful Clues for Common Diagnoses given force through a spinal motion
• Intervertebral Disc Bulge segment resulting in a diminished ability
II o Diffuse (> 50% circumference) extension
the disc beyond its normal margins
of of the vertebral column to protect the
spinal cord and nerve roots
1
52
BACK PAIN, ADULT
o Multifactorial o Infiltrative soft tissue signal/attenuation in

o Dynamic instability: > 3 mm motion epidural space &/or displacing normal
between flexion and extension paravertebral fat; may develop into
• Benign Compression Fracture epidural/paravertebral abscess
o Due to axial loading injury, especially • Osteomyelitis, Granulomatous
through osteoporotic bone o Infection due to tuberculosis or other
o No or minimal radial expansion of granulomatous disease (e.g., brucellosis)
vertebral circumference o Destruction of bone with relative sparing
o Horizontal fracture plane; sclerotic band of the disc
on Cl~ band-like or triangular T2 o Large psoas abscesses
hyperintensity on sagittal MR o Large prevertebral abscesses dissecting
o Anterior wedging common; posterior extensively below the anterior longitudinal
cortex usually intact and neural arch ligament
spared • Metastatic Disease
o Differentiation of benign from pathologic o Common primaries: Breast, lung, kidney,
compression fracture is often not prostate
straightforward o Lesions typically multiple
• Schmorl Node o Either lytic or sclerotic on CT, typically
o Herniation of nucleus pulposus into an hypointense T1/hyperintense '1'2signal on
adjacent vertebral body through an MR
end plate defect o Extraosseous extension may occur into the
Helpful Clues for Less Common Diagnoses epidural or paravertebral spaces

o May cause pathologic vertebral fracture
• Osteomyelitis, Pyogenic
o Early disc space destruction, with
• Insufficiency Fracture, Sacral
o Diagnosis often an unexpected finding on
hyperintense T2 signal and enhancement
MR of the lumbar spine
o Type I signal in adjacent endplate marrow
o Unilateral or bilateral vertical fractures
with enhancement on post-contrast
through the sacral ala ± horizontal fracture
sequences (MR)
through the body
o Endplate demineralization and destruction
o Linear hypointensity on '1'1WI in the
(CT)
fracture, '1'2hyperintensity appreciated
best on fat-saturated sequences (e.g., STIR)
Intervertebral Disc Herniation Facet Arthropathy
II
Axial T1WI MR shows a large extruded disc fragment in
the left antem/ate,al epidural space at the L4 leve/!:ll. facet joints at the L4·5 level =-
Axial NEeT shows severe degenerative changes in the
with joint space
1
narrowing, irregularity, and osteophyte formation.
53
ro BACK PAIN, ADULT
~
<>-
CfJ,
(/)
c
ro
~
f-
Intervertebral Disc Anular Tear
a>
c (Left) Sagittal STIR MR
Co shows focal T2
CfJ
hyperintensity in the dorsal
L5-s1 discs =
margins of the L4-s and
demonstrating presence of
anular tears. Type I
degenerative marrow change
is seen adjacent to the L4- 5
disc 81. (Right) Axial T1 WI
MR shows severe central
canal stenosis due to diffuse
disc bulging effacing the
ventral thecal sac 8l and
posterior facet degenerative
arthropathy ~ and
right-sided ligamentous
hypertrophy =.
Spinal Muscle Injury

(Left) Sagittal NECT shows
(unilatera/) L5 pars fracture
with corticated margins ffi
demonstrating presence of
terminal spondylolysis with
pseudoarthrosis. (Right)
Axial STIR MR shows
hemorrhage and edema in
the right paraspinous
musculature =.
Benign Compression Fracture

shows loss of height and
anterior wedging of the L 1
body ~ with mild canal
compromise due to
retropulsed bony elements in
this patient who suffered an
axial loading injury six
months previously. (Right)
peripherally enhancing fluid
L5-s1 disc space =-

collection replacing the
ventral
epidural and paravertebral
phlegmon, and dorsal
epidural abscess ~ in this
II intravenous drug abuser.
1
54
BACK PAIN, ADULT
Osteomyelitis, Granulomatous Metastatic Disease

pathologic marrow
epidural =
enhancement with large
and bilateral
psoas abscesses PJ:ll. (Right)
Axial T 1 C+ MR shows
vertebral melanoma
metastasis with epidural
extension -= causing severe
canal stenosis and cord
compression.
Insufficiency Fracture, Sacral Multiple Myeloma

shows cortical disruption
and hyperintense signal
=-
lhrough the second sacral
segment representing lhe
horizontal component of a
sacra! insufficiency fracture.
(Right) Sagittal T 1 WI MR
shows mulliple hypointense
vertebral lesions, some
indicated with =- in this
patient with multiple
myeloma.
Osteosarcoma Sickle Cell

lytic vertebra/lesion with
infiltrative margins and a
large extra osseous
component m arising from
Pagetic bone of the L4
vertebral body. (Right)
Coronal NECT shows
diffusely sclerotic marrow
spaces due to multiple bone
infarcts and the characteristic
central endplate
compression deformities ~
of sickle cell anemia.
II
1
55
ctl BACKPAIN, PEDIATRIC
~
Cl.
(fJ,
en DIFFERENTIAL DIAGNOSIS • Vertebral segmentation and formation
c
ctl anomalies
t=
Q)
Common • Rib fusions, pedicular bars => more likely
c • Scoliosis progressive curvature
Co a Scoliosis, Idiopathic • Trauma
en
a Scoliosis, Neuromuscular a Fracture
a Scoliosis, Congenital • Similar criteria to adults
• Trauma a Spinal Muscle Injury, Traumatic
a Fracture • MR or CT best for diagnosis
a Spinal Muscle Injury, Traumatic • T2WI FSMR or STIRMR most helpful for
• Syringomyelia diagnosis, determining extent
• Spondylolysis • Syringomyelia
• Scheuermann Disease a Chiari 1 malformation common
Less Common association in pediatric patients
• Stenosis, Congenital Spinal a Always consider traumatic, neoplastic
• Guillain-Barre Syndrome causes

• Neoplasm • Administer contrast if tumor suspected
a Leukemia or nodularity detected
a Neuroblastic Tumor • Spondylolysis
a Ewing Sarcoma a Unilateral or bilateral; may not see osseous
a Ependymoma, Myxopapillary, Spinal Cord break (stress reaction)

a Metastases, CSF Disseminated a Oblique plain radiographs, MR show
a Metastases, Hematogenous osseous defects well

a Osteoid Osteoma a Bone scintigraphy sensitive for detecting
a Langerhans Cell Histiocytosis stress reaction prior to pars fracture

• Osteomyelitis • Scheuermann Disease
a Osteomyelitis, Granulomatous a Most common in adolescent age group
a Osteomyelitis, Pyogenic a Diagnostic criteria include anterior

wedging, kyphosis, endplate irregularity
Rare but Important a May see significant kyphosis ± scoliosis
• Intervertebral Disc Herniation
• Acute Transverse Myelitis, Idiopathic Helpful Clues for Less Common Diagnoses
• Secondary Acute Transverse Myelitis • Stenosis, Congenital Spinal
a Reduced AP diameter of central spinal
canal
ESSENTIAL INFORMATION a Pedicles are short, thick, and more laterally
Key Differential Diagnosis Issues angled

• Clinical history, physical examination, and a Predisposes to symptomatic degenerative
appropriate laboratory investigations spine disease at younger age
constrains differential considerations • Guillain-Barre Syndrome
a Smooth, linear enhancement of cauda
Helpful Clues for Common Diagnoses equina and conus pia diagnostic in correct
• Scoliosis clinical context
a Scoliosis, Idiopathic
a If nodular enhancement, consider tumor
• Usually sigmoid S-shaped or granulomatous infection
• Pelvic tilt => limb-length discrepancy • Neoplasm
• No vertebral segmentation anomalies a Leukemia
a Scoliosis, Neuromuscular
• Look for "bright disc" sign (marrow
• C-shaped curvature common infiltration)
• Baclofen infusion device clue if present • Consider NHL in younger patients
II a Scoliosis, Congenital a Neuroblastic Tumor
• Often diagnosed in younger patients
1
56
BACK PAIN, PEDIATRIC
• Spinal invasion through neural foramina • Osteomyelitis

affects surgical treatment planning; MR o Osteomyelitis, Granulomatous
best for detection • May be centered at disc space; TB tends
o Ewing Sarcoma to spare disc space until late in disease
• Usually adolescent age group process
• Aggressive destructive or permeative • Look for paravertebral masses with TB
lesion, cellular MR signal characteristics o Osteomyelitis, Pyogenic
o Ependymoma, Myxopapillary, Spinal • Frequently centered in intervertebral disc
Cord space
• May present with chronic or • Abnormal marrow signal intensity,
longstanding back pain paraspinal inflammatory mass
• May have extensive intradural metastases Helpful Clues for Rare Diagnoses
at time of diagnosis • Intervertebral Disc Herniation
o Metastases, CSF Disseminated
o Diagnostic criteria identical to adults
• Consider choroid plexus, pineal region, • Acute Transverse Myelitis, Idiopathic
suprasellar, posterior fossa tumors, glial o Idiopathic inflammatory spinal cord
neoplasms, leukemia/lymphoma disorder ~ bilateral motor, sensory, and
• Most commonly seen in brain tumors autonomic dysfunction
with intimate CSF contact o Central cord lesion extends> 2 vertebral
o Metastases, Hematogenous
segments (often 3-4 segments), eccentric
• Relatively rare enhancement
• Consider neuroblastoma, lymphoma, o Thoracic> cervical cord (10%)
and tumors with bone to bone metastatic • Secondary Acute Transverse Myelitis
patterns (Ewing sarcoma, osteosarcoma) o Inflammatory disorder of spinal cord
o Osteoid Osteoma
associated with many etiologies
• Pain classically worst at night o Hyperintense lesion on T2WI with mild
• Symptoms alleviated with aspirin cord expansion without significant
o Langerhans Cell Histiocytosis
enhancement
• May mimic neoplasm symptoms, o Thoracic> cervical> conus medullaris
imaging appearance (small, round blue
cell tumor)
• Classic etiology of severe vertebra plana
• Vertebral height often makes surprising
recovery after treatment
Scoliosis, Idiopathic Scoliosis, Neuromuscular
II
Anteroposterior
patient
radiograph in a female adolescent
sho\,\ls substantialS·shaped idiopathic thoracic
Anteroposterior radiograph in a cerebral palsy patient
with spasUcity shows convex right C-shaped
1
dextrosco/iotic curvature with lumbar levoscoliosis. neuromuscular scoliosis. Note baclofen infusion system
for spasticity trealmenl.
57
<1l BACK PAIN, PEDIATRIC
~
0-
,
(f)
If)
<=
~
<1l
I-
Scoliosisr Congenital
ell
c: (Left) Coronal bone CT 3D
'0. reformats in a VACTERL
(f)
patient with convex right
spinal curvature
demonstrates multiple rib
fusions on the left, upper
thoracic block vertebra, T7
and T12 hemivertebra 8l
and T9 butterfly vertebra PJ::l.
Chiar; 1 malformation
patient shows a large
cervical syrinx. Despite
sacculated appearance, the
syrinx fluid compartments
are in contiguity and would
likely respond to a single
catheter drain.
Scheuermann Disease
(Left) Sagittal bone CT in a
pediatric patient with back
pain reveals an L5 pars
defect with minimal
anterior subluxationof L5 on
S I. (Right) Sagittal bone CT
in an adolescent patient
depicts mullilevel anterior
wedging with endplate
irregularities of Scheuermann
disease producing rounded
kyphotic thoracic deformity.
Guillain-Barre Syndrome
demonstrates marked
narrowing of lumbar spinal
canal anteroposterior
diameter. Anteroposterior
canal diameter should
normally increase rather than
decrease in lower lumbar
spine. (Right) Sagittal T1 C+
MR in a patient with
ascending paralysis
demonstrales avid smoolh,
linear enhancemenl of
venlral conus pia and cauda
equina.
II
1
58
BACK PAIN, PEDIATRIC

leukemia Cord
(Left) Sagittal STIR MR in a
newly diagnosed patient
reveals abnormal
hyperintense marrow signal
and numerous vertebral
compression fractures =.
reveals diffuse abnormal
intradural ehhancement
within thecal sac, obscuring
conus termination and cauda
equina and distorting normal
conus and cauda equina.
Metastases, CSF Disseminated

spinal surveillance imaging in
a pediatric patient with
malignant brain glial
neoplasm shows extensive
smooth and nodular
enhancing intradural drop
metastases. (Right) Axial
bone CT of the cervical spine
demonstrates a
well·circumscribed lytic
lesion in the expanded right
pedicle 1:1:1 with dense
central nidus.
Secondary Acute Transverse Myelitis

(Left) Sagittal T1 C+ fS MR
shows C3/4 disc space
height loss with fluid signal
intensity and abnormal
marrow and epidural
enhancement adjacent to
disc space indicating discitis
with osteomyelitis. No spinal
cord compression is present
associated with acute eNS
demyelination demonstrates
abnormal intramedullary T2
hyperinlensity extending to
conus level (not shown). The
areas of abnormality are
patchy rather than
contiguous. II
1
59
SIECTION 2
€:raniovertebral Junction
Cranio-Cervical Junction Acute Injury 11-2-2
CVJ Abnormality, General 11-2-4
CVJ Soft Tissue Abnormality 11-2-8

C1-C2 Instability 11-2-12
Odontoid Deformity 11-2-14
c CRANia-CERVICAL JUNCTION ACUTE INJURY
o
U
C
-,:::J DIFFERENTIAL DIAGNOSIS • CT arteriogram equally accurate and faster
CIl
~ than MR arthrogram for vertebral dissection
.0
QJ Common o Time is often of the essence in these
t
QJ
> • Trauma patients, who tend to have multiple
o o Odontoid C2 Fracture
c injuries
CIl
~ o Burst Fracture, C2
U
o Hangman's C2 Fracture
Q)
C o Jefferson C1 Fracture
• Odontoid C2 Fracture
0- o Usually low-velocity injury in elderly
en o Occipital Condyle Fracture
o Dissection, Vertebral Artery
• Jefferson CI Fracture
o If combined displacement of lateral masses
o Traumatic Disc Herniation
o Os Odontoideum
> 6.9 mm, unstable
o High likelihood of other fractures: Spine,
o Spinal Cord Injury Without Radiographic
Abnormality (SCIWORA) skull, pelvis, lower extremity
• Nontraumatic Mimics • Os Odontoideum
o Chronic, nonunited odontoid fracture
o Cran iovertebral Junction Variants
• Spinal Cord Injury Without Radiographic
Abnormality (SCIWORA)
o Occurs primarily in children
o Pseudosubluxation C2-3
o MR: Injuries to cord, ligaments,
o Torticollis
intervertebral discs, cartilaginous endplates
less Common 02/3 severe cervical injuries in children < 8
• Atlanto-Occipital Dislocation years are SCIWORA
• Atlanto-Axial Rotary Subluxation • Pseudosubluxation C2-3
o Children < 10 years old, anterolisthesis
ESSENTIAL INFORMATION may measure up to 4 mm
• MR very useful to evaluate for ligament • Atlanto-Occipital Dislocation
o High incidence cord injury
injuries
o Formerly usually fatal; now often survive
o Coronal STIRrarely performed but useful
in this region to hospital
• Coronal, sagittal reformations essential on
CT for full evaluation of injury
Odontoid C2 Fracture Burst Fracture, C2
II
2 Sagittal NCCT shows type 2 dens fracture 1::1 in an
osteoporotic patient. Soft tissue swelling is mild. These
Sagittal bone CT shows comminuted C2 body fracture
=.
with characteristic retropulsion of posterior cortex
fractures are commonly subtle on radiographs and best Additional burst fractures are commonly present
seen on lateral (not odontoid) vie\oV. elsewhere in the spine.
2
CRANia-CERVICAL JUNCTION ACUTE INJURY
Hangman's C2 Fracture Jefferson Cl Fracture

(Left) Sagittal oblique 3D CT
shows bilateral C2 pedicle
(ractures = without fracture
of vertebral body. Effendi
classification uses presence
of disruption of C2- 3 disc
and facet joints as a measure
of the severity of injury.
(Right) Axial bone CT shows
multiple fractures of C 1 ring
1:':1. Lateral displacement in
this patient indicates rupture
of transverse ligament of
dens and resultant instability.
Occipital Condyle Fracture Os Odontoideum

nondisplaced occipital
condyle fracture 1:':1 as well
as C4 articular pillar fracture
a reflecting lateral flexion
injury. (Rig"') Sagittal bone
CT shows chronic,
nonuniled dens fracture =-
so-called as odonloideum.
This may be unstable, and
flexion-extension views
should be performed.
Craniovertebral Junction Variants Craniovertebral Junction Variants

anterior and posterior cfefts
SII of C 7. Smooth, corticated
margins are signs
distinguishing this from
trauma. (Rig"') Sagittal bone
CT shows anterior arch of C I
fused 10 clivus 1:':1 and
posterior arch fused 10 C2
SII.
II
2
3
c CVJ ABNORMALITY, GENERAL
o
U
C
--,:J DIFFERENTIAL DIAGNOSIS Chondrosarcoma
o
<1l
~ Chordoma (Usually Clivus)
o
.n
Q) Common o Aneurysmal Bone Cyst
t
Q)
> • Bone Trauma • Cranial Settling, Platybasia and Basilar
.Q
c o Odontoid Fracture, C2 Invagination, Acquired
<1l
~ o Burst Fracture, C2 o Paget Disease
U
o Hangman's Fracture, C2 o Rheumatoid Arthritis, Adult
C1l
c o Jefferson Cl Fracture o Osteomalacia/Rickets
'a. o Occipital Condyle Fracture
VJ
o Os Odontoideum
Less Common
• Congenital Neural Abnormalities • Rotary Subluxation, CI-2
o Chiari 1 Malformation • Atlanto-Occipital Dislocation
o Chiari 2 Malformation
• Grisel Syndrome
• Congenital Bone and Ligament • Carotid Dissection/Pseudoaneurysm
Abnormalities
o Achondroplasia ESSENTIAL INFORMATION
o Craniovertebral Junction Variants
o Trisomy 21
• Hint: Differentiate trauma vs. bony
• Arthritis congenital variant
o Soft tissue swelling usually evident in
o Osteoarthritis
o Rheumatoid Arthritis trauma
o Cortication of bone indicates nonacute
o Spondyloarthropathy, Seronegative trauma
o Os odontoideum thought to be nonunited
o CPPD
• Soft Tissue Calcification or Ossification fracture, not congenital variant
o Calcific Tendinitis, Longus Coli
• Hint: Watch for mass adjacent to dens
o Pannus from RA: Dens eroded, no
o Spondyloarthropathy, Seronegative
o OPLL
calcification
o CPPD
o Seronegative spondyloarthropathy: Like
• Extramedullary Mass RA, plus enthesophytes, joint fusion
o Juvenile inflammatory arthropathy: Like
o Metastases
o Lymphoma
adult RA or seronegative
o Plasmacytoma spondyloarthropathy
o Pannus from Rheumatoid Arthritis • Usually involves multiple levels in
o Abscess, Epidural, Paravertebral
cervical spine
o Osteomyelitis, CI-C2 • Growth disturbance characteristic
o CPPD: Calcifications, cysts in bone
o Nasopharyngeal Carcinoma
o Infection: Usually involves disc space
o Neurofibromatosis Type 1
o Schwannoma
• Tuberculosis involves disc space later in
o Paraganglioma course of infection
o OPLL, osteoarthritis: No bony erosion
o Meningioma
o Tumor: Origin in bone, meninges or cord
• Intramedullary Mass
o Syringomyelia
• Hint: Watch for heterogeneous high signal
o Chiari 1 Malformation in bone marrow without cortical
o Chiari 2 Malformation
breakthrough
o Myeloma
o Hemangioblastoma, Spinal Cord
o Lymphoma
o Pediatric Brainstem Glioma
o Metastases
• Bone Mass
o Metastases Helpful Clues for Common Diagnoses
II o Multiple Myeloma • Types of C2 fractures
o Osteomyelitis, CI-C2 o Odontoid Fracture, C2
2
4
CVJ ABNORMALITY, GENERAL
• Type I: Obliquely oriented through tip o Instability occiput-Cl and CI-C2

• Type II: Horizontally oriented through o Unlike RA, no erosion of dens
base • Osteoarthritis
• Type Ill: Really a fracture of body; o Common at craniocervical junction
horizontally oriented, through body and o Involves synovial articulations: Facet
below base of dens joints, dens/Cl articulation
<-
o Burst Fracture, C2 o Dens and anterior arch of Cl develop c
OJ
• Axial load injury osteophytes, sclerosis best seen on CT ~

o·
• Extends through posterior cortex of o May have prominent soft tissues posterior OJ
vertebral body to dens but no erosions

o Hangman's Fracture, C2 o Facet osteoarthritis at occiput-Cl or CI-C2
• I-Iyperflexion or hyperextension, usually may develop large osteophytes, synovial
from MVA cysts
• Traumatic spondylolisthesis of C2 • Rheumatoid Arthritis
• Fracture through C2 pedicles o Calcification never present
• Usually see focal kyphosis and o Pannus heterogeneous signal intensity on
anterolisthesis at C2-C3 MR
• Effendi type I: Traumatic o Low signal intensity areas on T2Wl mimic
spondylolisthesis isolated crystals, calcification
• Effendi type II: Also disruption of C2-C3 o Almost always see erosion of dens
disc o Early erosion: Loss of subchondral bone
• Effendi type Ill: Also disruption of C2-C3 plate
facet joints o Late erosion: Pencilling of dens
o Os Odontoideum o Facet erosion: Atlanto-axial impaction
• Chronic nonunited fracture o Craniocervical disease does not occur
• Congenital Bone and Ligament without peripheral disease (hands/feet)
Abnormalities • CPPD
o May be multiple o Mimics RA on MR, but subchondral bone
o May be isolated, detected as incidental plate not eroded
finding in adulthood o Calcifications visible on CT, radiographs
o Often cause adjacent premature
degeneration
• Trisomy 21
o Spinal stenosis
Odontoid Fracture, C2 Burst Fracture, C2
II
Sagittal NECT shows type /I odontoid f,acture =. This
fracture usually occurs in elderly patients, often from a C2 =
Sagiltal NECT shows horizontal and vertical fractures of
due to axial load injury.
2
ground level fall, and may be missed on radiographs
due to oSleopenia.
5
c CVJ ABNORMALITY, GENERAL
o
nc
--,:J
ro
~
.0
OJ
t Chiari 1 Malformation Chiari 2 Malformation
OJ (Left) SagiHal T2WI MR
>
.Q shows typical peg·shaped
c
ro
~
()
Q)
tonsils =-
appearance of cerebellar
which descend to
level of CI arch. 4th
c: ventricle is normal. There is a
'0. small syrinx =.:I. (Right)
In Sagittal T2WI MR shows
characteristic Chiar; 2
features of small posterior
fossa and 4th ventricle,
medullary kink =.:I and
verminal ectopia through
foramen magnum ~.
Craniovertebral Junction Variants Trisomy 21

shows CI =.:I fused to
occiput, resulting in
dysmorphic CI·C2
articulations and dysmorphic
C2 body. Odontoid is
triangular in shape !:?:l.
(Right) SagiHal bone CT
shows OIC2 subluxation 81
without erosions. There was
no history of trauma. Marked
narrowing of spinal canal
was symptomatic.
Osteoarthritis Juvenile Idiopathic Arthritis

shows apparent mass r.:=
posterior to dens which is
osteophyte formation.
Although OA can mimic
mass on MR, diagnosis is
straightforward on CT where
bone spurs are seen. (Right)
cortical margin of odontoid
lost anteriorly due to
erosions, and 50ft tissue mass
ED is due to pannus. Cranial
settling is present, with
odontoid at level of clivus.
II
2
6
CVJ ABNORMALITY, GENERAL
()
~
OJ
::::>
Pannus from Rheumatoid Arthritis o
<
C1l
(Left) Sagittal bone CT shows ;:l.
calcifications and soft tissue C1l
0-
fullness II] at craniocervical
OJ
junction due to CPPD. CPPD
of craniocervical junction is
not uncommon in elderly
patients and may cause
instability. (Rigllt) sagitlal
STIR MR shows extensive
erosion of odontoid process
and large SOfllissue mass II]
from rheurnalOid arthritis. RA
may mimic infection or
tumor.
Osteomyelitis, C1-C2
shows epidural abscess
compressing spinal cord.
=
shows wbercular
osteomyelitis involving C2
body with extension into
pre vertebral space E!:J.
Posterior elements are also
involved =. Sparing of disc
space is characteristic of
tubercular osteomyelitis early
in its course.
Meningioma
(Left) Sagittal bone CT shows
calcified mass =
with dural
tail arising from ventral dura
at C2 providing clue to dural
origin. There is mass effect
on adjacent spinal cord.
(Rigllt) Sagittal T2WI Fs MR
shows multiple small foci =
of abnormal signal intensity
in bone marrow of C·spine,
clivus, and occiput. Note
posterior element
involvement, which is a
common MR finding with
myeloma.
II
2
7
c
CVJ SOFT TISSUE ABNORMALITY
:go
c
-,:::> • High correlation to neurologic symptoms
ro
~ with distance 9 mm or more between
.0
Q) Common Cl-2
t
Q)
> • Rheumatoid Arthritis • Retro-Odontoid Pseudotumor
.Q
c • Retro-Odontoid Pseudotumor o Increased soft tissue dorsal to odontoid
~ • Osteomyelitis, CI-C2 secondary to Cl-2 osteoarthritis
U
Ql
• Extramedullary Tumor • Low signal mass on T1 & T2 (fibrotic)
c o Metastases
.0. • May cause cervicomedullary junction
tJ) o Lymphoma compression
o Plasmacytoma o Usually seen with altered biomechanics of
o Nasopharyngeal Carcinoma lower cervical spine •• surgical/congenital
o Neurofibromatosis Type 1 fusion
o Schwannoma o Mimics appearance of RA
o Paraganglioma o Multiple other levels of degenerative disc
o Chordoma disease
o Chondrosarcoma
• Osteomyelitis, CI-C2
o Meningioma o Infection starts as septic arthritis of Cl-2
• Intramedullary Mass o Risk factors include diabetes, drug abuse,
o Syringomyelia endocarditis, immunocompromise
o Chiari 1 Malformation o Soft tissue mass and bone destruction at
o Chiari 2 Malformation Cl-2 level
o Glioma, Brainstem • Staph aureus most common organism in
o Hemangioblastoma, Spinal Cord USA
Less Common • Mycobacterium tuberculosis most
• Carotid Pseudoaneurysm/Dissection common worldwide
• Synovial Cyst o MR shows low Tl signal mass centered at
Cl-2 with variable involvement of
Rare but Important
odontoid and lateral masses at C2
• Neurenteric Cyst o May show enlarged atlanto-dental interval
o Epidural mass with thecal sac/cord
ESSENTIAL INFORMATION corn pression
o Grisel syndrome: Inflammatory,
nontraumatic subluxation of CI-C2
• Do intralesion calcifications represent following peripharyngeal infection
arc-whorl intralesional calcifications
• Extramedullary Tumor
(chondrosarcoma) or fragmented destroyed o Metastases
bone (chordoma, metastasis)?
• Multiple lesions, bone destruction,
• Does patient have known primary neoplasm systemic primary
(metastasis), myeloma (plasmacytoma), or a o Lymphoma
nasopharyngeal mass (nasopharyngeal
• Large pharyngeal mucosal space mass
carcinoma)?
with associated cervical adenopathy>
Helpful Clues for Common Diagnoses 50% of time
• Rheumatoid Arthritis • NHL 5x as common as Hodgkin disease
o Thickened & inflamed synovium called in head & neck
pannus o Nasopharyngeal Carcinoma
o ever involves spine without hands &/or • Mass centered in lateral pharyngeal
feet involvement recess of NP with deep extension &
o Odontoid erosions, ligamentous laxity cervical adenopathy
o CI-C2 instability in 33% of all RA patients • Nodal metastases present in 90% of cases
II o Neutral, flexion, and extension lateral
radiographs performed for evaluation
at presentation
2
8
CVJ SOFT TISSUE ABNORMALITY
• Multi-planar images show invasion of • Lytic mass with or without chondroid

clivus, sphenoid bone & sinus, Cl & C2 matrix, cortical disruption, and
bodies extension into soft tissues
o Neurofibromatosis Type 1 • Chondroid matrix mineralization of
• Plexiform neurofibroma => diffuse "rings and arcs" (characteristic)
enlargement of major nerve o Meningioma
trunks/branches - bulky rope-like ("bag • Foramen magnum, jugular foramen OF),
of worms") nerve expansion with upper cervical dura locations
adjacent tissue distortion • Carotid space => connection to JF above
• Look for kyphoscoliosis ± multiple nerve with JF margins showing
root tumors, plexiform neurofibroma, permeative-sclerotic or hyperostotic
dural ectasia/lateral meningocele changes on bone CT
o Schwannoma • Absence of high-velocity flow voids on
• Hypoglossal or upper cervical roots as T1 MR
site of origin • Tl C+ MR shows enhancing, JF mass
• Hypoglossal neuropathy results in Helpful Clues for Less Common Diagnoses
tongue denervation • Aneurysm/Vertebral Dissection
• Dumbbell with uniform enhancement o Multiple etiologies => dissection,
• Larger lesions may show central cystic post-traumatic, atherosclerotic, iatrogenic,
formation congenital
o Paraganglioma
• Synovial Cyst
• Multiple black dots ("pepper") in tumor o Round, central T2 hyperintense mass with
substance indicating high velocity flow low signal margin
voids from feeding arterial branches o Associated with dorsal Cl-2 articulation or
• Jugular foramen or vagal varieties may degenerated facets
present with upper cervical/skull base
level mass Helpful Clues for Rare Diagnoses
o Chordoma • Neurenteric Cyst
• Mass is hyperintense to discs on T2WI, o Intraspinal cyst + vertebral abnormalities
with multiple septa (persistent canal of Kovalevsky,
• Destructive, lytic lesion segmentation and fusion anomalies)
• May extend into disc, involve 2 or more
ad jacen t vertebrae
o Chondrosarcoma
Rheumatoid Arthritis Retro-Odontoid Pseudotumor
II
Sagittal T1WI MR shows rheumatoid arthritis involving
C1·C2 articulation with dens erosion and extensive
Sagittal T1WI MR shows CI-C2
pseudopannus =
degenerative
in patient with DISH. The odontoid
2
pannus (ormation =. There is mild compression of is not eroded, but tile ADI is t. Cord compression
medulla by pannus and obscuraUon of fat planes. occurs between degenerative pannus & posterior C 1.
9
c CVJ SOFT TISSUE ABNORMALITY
o
nc
-,::J
t1l
~
.0
Ql
t Osteomyelitis, Cl-C2 Metastases
Ql
> (Left) Sagiltal T2WI MR
.Q show large pre vertebral
c
t1l abscess spanning Cl to C4
~ lID and extension posteriorfy
U
involving interspinous region
Ql
C 81. Findings are typical for
a. T8. (Right) Axial Tl C+ FS
r/)
MR shows melaslatic lung
cancer with extensive
extracapsular nodal spread.
Post-contrast image shows
Ihe mass has ill-defined
borders with invasion of the
longus capitis muscle !'::1l and
invasion to the pharyngeal
mucosal space 81.
Metastases Lymphoma
(Left) Axial CTA shows Ihe
classic appearance of thyroid
metastasis with thin
expansiJe bony margin with
the predominalely lytic
lesion within left
facel/lamina of C3 ~.
homogeneous mass in the
relropharyngeal space,
displacing Ihe
parapharyngeal fal
anterolaterally 81 and
encircling the right internal
carotid artery
Plasmacytoma Nasopharyngeal Carcinoma

(Left) Sagiltal Tl C+ MR
shows variant MR case or
an
unusually large skull base
plasmacytoma = engulfing
the clivus and extending into
the nasopharynx and
abutting Cl-C2. (Right)
Sagiltal TlWI MR shows a
typical case of an aggressive
nasopharyngeal squamous
cell carcinoma with invasion
of Ihe skull base by direct
extension H2.
II
2
10
CVJ SOFT TISSUE ABNORMALITY en
"2.
::::l
CD
o
~
III
::::l
0·
Neurofibromatosis Type 1 Chordoma <
(Left) Axial TI C+ MR shows CD
::I.
multiple large neurofibromas CD
r:::r
within dorsal 50ft tissues and ~
III
paravertebral regions. L.
Symmetrical farge intradural C
cord =
lesions compress the cervical
at the C2 level.
(Right) Sagillal TI C+ MR
::::l
$:l-
0·
::::l
demonstrates an isointens€
expansile mass arising from
the cfivus~. Notice the
posterior indentation or
"thumbing" of the pons.
Chordoma
(Left) Sagillal T 1 C+ MR
shows large heterogeneous
signal mass in the cervical
epidural space, involving rhe
dorsal aspect of C2- 3
junction and extending
larerally, with diffuse
enhancement. (Rig"')
Coronal TI WI MR shows
typical MR case of
petro·occipital fissure skull
base chondrosarcoma =.
Carotid Pseudoaneurysm/Dissection
shows well-defined and
mass with a broad dural
margin Ea at the foramen
magnum, typical for
meningioma. There is
compression of the medulla.
(Right) Axial CTA shows the
CT features of a
pseudoaneurysm of rhe
internal carotid artery =
locared below the skull base.
II
2
11
c Cl-C2 INSTABILITY
o
nc
-,:J DIFFERENTIAL DIAGNOSIS o Transverse ligament of dens critical to
CO
~ anteroposterior stability
.c
Q) Common o Normal distance from inferior margin Cl
t
>
Q)
• Trauma arch to dens < 2 mm in adults
.Q o Jefferson Cl Fracture
c o Increased distance indicates rupture
CO
~ o Odontoid C2 Fracture transverse ligament
U
o Hyperflexion Injury, Cervical • Flexion-extension views useful
OJ
c: o Rotary Subluxation, Atlantoaxial
'Q. • May be false negative in 1st week after
CJ) o Os Odontoideum injury
o Pathologic Vertebral Fracture o Jefferson fracture unstable if combined
• Non-Traumatic lateral displacement of Cllateral masses
o Rheumatoid Arthritis, Adult relative to articular pillars of C2 " 7 mm
o Spondyloarthropathy, Seronegative • Incomplete fusion of posterior elements
Less Common does not cause instability because ligaments
• Non-Traumatic intact
o CPPD • Grisel syndrome in association with
o Osteomyelitis, CI-C2 retropharyngeal infection, primarily seen in
o Grisel Syndrome children
o Achondroplasia • Rheumatoid arthritis often also involves
o Trisomy 21 (10-20%, 1-2% Symptomatic) atlanto-axial articulations, lower cervical
o Spondyloepiphyseal Dysplasia uncovertebral and facet joints
o Mucopolysaccharidoses (MPS) o Will not be present in C-spine unless
• Mimics of Instability peripheral involvement also present
o Normal Variant o RA pannus does not calcify
o Incomplete Fusion, Posterior Element • Calcified inflammatory tissue around dens
o CraniovertebraJ Junction Variants usually due to CPPD
o Calcific Tendinitis, Longus Coli Other Essential Information
o Pseudosubluxation (Childhood) • Craniocervical junction injuries often
multilevel
ESSENTIAL INFORMATION • Os odontoideum felt to represent nonunited
dens fracture
• Imaging Evaluation of Instability
Jefferson C1 Fracture Odontoid C2 Fracture
II
2 of C1 =
Axial bone CT shows lateral dislocation
relative to C2 arUcular pillars
of lateral masses
. Combined
Sagittal NECT shows type
unstable injury seen primarily
/I odontoid fracture
in elderly paUents,
=. an
often
lateral displacement of lateral masses> 7 mm confirms after a trivial injury such as a ground level fall.
instability.
12
Cl-C2 INSTABILITY en
-C
::::s
(1)
Os Odontoideum Rheumatoid Arthritis, Adult

(Lefl) Sagillal bone CT shows
nonuniled dens fracture =..
called as odontoideum.
These are commonly
unstable and should be
evaluated with
flexion/extension views.
(RighI) Sagillal NECT shows
widening of CI-2 interval SI
due to rupture of transverse
ligament of dens caused by
pannus. Note bony erosion
ofdens=.
CPPD
fLeft) Sagillal bone CT shows
calciFications around dens
~ in this patient presenting
with instability. CPPO
crystals were seen on biopsy
at time of surgical fusion.
(RighI) Sagillal T2WI MR
shows MRSA infection
involving occiput
Prevertebral abscess =
to C2.
abscess surrounding dens =:7-

and
& narrowing spinal canal are

evident.
Craniovertebral Junction Variants

(Left) Sagillal N[CT shows
C2-] pseudosubluxation =
in a child. Posterior laminar
line from C1 to C] is normal.
C2-] anterolisthesis of < 4
mm is seen as a normal
variant in up to 40% of
children. fRighl)
shows failure of fusion of
posterior arch C 7 8l
mimicking fracture. Unlike
(racture, rnargins of defect
are smooth and corlicaled.
II
2
c ODONTOID DEFORMITY
o
13
c
--,::J DIFFERENTIAL DIAGNOSIS o CPPD
co
~ o Rarely, gout
.0
OJ Common • Hypoplasia: Odontoid short and body of C2
t
>
OJ • Trauma dysmorphic
.Q o Odontoid C2 Fracture
c Helpful Clues for Common Diagnoses
co
~ o Os Odontoideum
U • Acute Trauma: Odontoid may be displaced
• Arthritis
Q)
c o Rheumatoid Arthritis, Adult
or angled posteriorly on lateral view
a. o Often difficult to see fracture on odontoid
en o CPPD
o Seronegative Spondyloarthropathy
view, especially in osteopenic patients
• Chronic Post-Traumatic Deformity
o Os Odontoideum: Rounded ossicle
• Tumor
o Angular Deformity: Tip of odontoid
o Metastases, Lytic Osseous
o Multiple Myeloma
points posteriorly
• Craniovertebral Junction Variants • Bone Tumor: Marrow abnormality visible
on CT or MR; lytic lesions difficult to see on
Less Common radiographs due to overlying structures
• Congenital • Rheumatoid Arthritis (RA): Pannus never
o Spondyloepiphyseal Dysplasia calcifies; arthritis always present in hands or
o Hypoplastic Odontoid Process feet if seen in neck
o Klippel-Feil Spectrum • Seronegative Spondyloarthropathy
o Down Syndrome o Syndesmophytes fuse multiple vertebrae;
o Mucopolysaccharidoses erosions of odontoid may look same as RA
• Tumor • CPPD: Soft tissue mass contains calcification
o Osteochondroma • Infection: Usually unifocal; often epidural
extension
ESSENTIAL INFORMATION • Congenital Deformity: Odontoid abnormal
in shape but cortex intact; other anomalies
Key Differential Diagnosis Issues often present
• Erosion vs. hypoplasia vs. trauma
• Erosion of odontoid: Odontoid may have
pencil tip or erosion at base
• Soft tissue mass around odontoid
o Infection
o Rheumatoid arthritis
Odontoid C2 Fracture
II
2 I.2teral radiograph shows posterior displacement = of
the odontoid relative to the body of C2, indicating an
Sagittal STIR MR shows a sofl tissue mass around U,e
dens= and bony erosion of the dens 81.
odontoid fracture.
14
ODONTOID DEFORMITY
o
~
OJ
:J
Juvenile Idiopathic Arthritis a
<
C1l
(Left) Sagiltal bone CT shows ::+
chronic separation of C 1 and C1l
CT
C2 and a tapered contour of ~
OJ
the odontoid. Heterotopic
ossification 1::1 has '-
C
:J
developed between the
~
odontoid and C1. (Right) o·
Sagittal STIR MR shows a :J
treated myeloma lesion =:I
of C2, with partial collapse
of the odontoid into the
vertebral body.
Craniovertebral Junction Variants

a normal physeal scar
between
-=
the ossification
centers for the dens and for
the C2 vertebral body.
Lucency around the physeal
scar is also normal. (Right)
Lateral radiograph shows a
tapered, small odontoid
process =:I secondary to the
congenital fusion of occiput
andCl.
Down Syndrome
congenital fusion of C2 and
C3 leading to a tower-like
appearance of the odontoid
process PJ:'J. (Right) Sagiltal
bone CT shows an unusually
shaped odontoid without
erosions and the widening of
the Cl-2 interval in this
patient with symptomatic
instability related to trisomy
21.
II
2
15
SECTION 3
Vertebral Body - Posterior
Elements
Congenital Vertebral Anomalies 11-3-2
Cervical Bony Fusion 11-3-4

Flattened Vertebral Body, Solitary 11-3-6
Flattened Vertebral Body, Multiple 11-3-8
Dysmorphic Vertebral Body 11-3-10
Enlarged Vertebral Body/Posterior Element 11-3-12
Enlarged Neural Foramen 11-3-16
Vertebral Body Scalloping/Widened Canal 11-3-18
Spondylolisthesis 11-3-20
Bony Lesion, Aggressive 11-3-24
Fracture, Vertebral Body 11-3-28
Facet Abnormality, Non-traumatic 11-3-32
Fracture, Posterior Element 11-3-34
Pedicle Abnormality 11-3-36

Enlarged Vertebral Body, Soap Bubble Expansion 11-3-38
Vertebral Body Sclerosis, Focal 11-3-42
Vertebral Body Sclerosis, Diffuse 11-3-44
Vertebral Body Thickened Bony Trabeculae 11-3-46
Vertebral Body, T1 Hyperintense Signal, Diffuse 11-3-48
Vertebral Body, T1 Hyperintense Signal, Focal 11-3-50
Vertebral Body, T1 Hypointense Signal, Diffuse 11-3-52
Vertebral Body, T1 Hypointense Signal, Focal 11-3-56
l/)
c CONGENITAL VERTEBRAL ANOMALIES

Q)
E
Q)
W DIFFERENTIAL DIAGNOSIS o Post-Traumatic Deformity
~ o Osteochondroma
o
'C
Q) Common
eno • Abnormalities of Segmentation less Common
CL o Failure of Vertebral Formation
• Multiple Abnormally Formed Vertebrae
>- o Vertebral Segmentation Failure without Fusion, Congenital
'0
o o Achondroplasia
CO o Partial Vertebral Duplication
o Osteogenesis Imperfecta
~
<Il o Klippel-Feil Spectrum
.0 o Thanatophoric Dwarfism
Q) o Craniovertebral Junction Variants
1:: o Spondyloepiphyseal Dysplasia
Q) o VACTERL Association
> o Scoliosis and Kyphosis, Congenital
Q)
c: • Acquired Vertebral Body Fusion
c..
en o DISH ESSENTIAL INFORMATION
o Spondyloarthropathy, Seronegative Key Differential Diagnosis Issues
o Post-Operative Change, Normal • Must decide if single or multiple levels
• Spinal Dysraphism involved
o Incomplete Fusion, Posterior Element • Abnormalities acquired in childhood cause
o Meningocele, Dorsal Spinal growth disturbance, mimic congenital
o Myelomeningocele
anomalies
o Lipomyelomeningocele
• Extra-spinal abnormalities often helpful in
o Diastematomyelia
diagnosis
• Caudal Regression Syndrome Helpful Clues for Common Diagnoses
• Multiple Abnormally Shaped Vertebrae, • Abnormalities of segmentation may not be
Acquired visible on routine radiographs
o Scheuermann Disease o Coned-down views, CT scan, or MR useful
o Sickle Cell especially at craniocervical junction
o Juvenile Idiopathic Arthritis o Always consider, especially with atypical
o Cushing Disease scoliosis
o Osteomyelitis, Granulomatous • Short curve, unbalanced, or thoracic
o Radiation of Spine in Childhood convex left
• Single Abnormally Shaped Vertebra, • Widened spinal canal on AP radiograph sign
Acquired of dysraphism
o Limbus Vertebra
Partial Vertebral Duplication Klippel-Feil Spectrum
II
3 Coronal bone CT shows left hemivertebra =
associated rib. It causes a shorl-curve scoliosis.
lacking an Lilteral radiograph
C2-C3 involving both vertebral bodies =
shows a failure of segmentation of
and facet
joints. There is wide variability in extent of fusion in
Klippel-Feil spectrum.
2
CONGENITAL VERTEBRAL ANOMALIES
Juvenile Idiopathic Arthritis

shows small fused vertebral
bodies 81 and facet joints in
the lower cervical spine,
indistinguishable from
congenital Fusion. A wide
Cl-2 interval = is a clue to
diagnosis. (RighI) Sagittal
bone CT shows ossification
m
of the anterior longitudinal
ligament = that clearly is
beyond the margins of the
CD
3
CD
:J
vertebral bodies, en
distinguishing this entity from
fusion anomalies.
Post-Operative Change, Normal Diastematomyelia

(Left) Sagillal CECT shows
Facet joint Fusion =.
Although current fusion
techniques usually employ
hardware, older techniques
may not and may be
confused with congenital
fusion. (Right) Axial T2WI
MR shows a bone spur =
dividing the spinal canal and
a split spinal cord 81.
limbus Vertebra Osteochondroma

(Left) Sagillal NECT shows a
failure of fusion of ring
apophysis E3I that occurs in
adolescence due to
extension of disc material
between the apophysis and
the remainder of the
vertebral body. (Right) Axial
bone CT shows an
osteochondroma =
mimicking a bony septum in
the spinal canal. These
benign tumors rarely involve
the spine and are not present
at birth.
II
3
3
C
(/)
CERVICAL BONY FUSION
<1J
E
<1J
W DIFFERENTIAL DIAGNOSIS • May be associated with Sprengel
~ deformity
o
·C
<1J
Common • Often see scoliosis or kyphosis
iil • Abnormalities of Segmentation
o • Fusion due to seronegative
0...
o Failure of Vertebral Formation spondyloarthropathy
o Partial Vertebral Duplication o Normal size of vertebral bodies
o Klippel-Feil Spectrum o Intervertebral discs and facet joints fused
~ o Vertebral Segmentation Failure o Sacroiliac joints always involved with
.0
<1J • Juvenile Idiopathic Arthritis erosions often progressing to ankylosis
t
<1J • DISH o Thin syndesmophytes in ankylosing
> • Post-Traumatic Deformity
Ql spondylitis cause "bamboo spine"
c: • Spondyloarthropathy, Seronegative
c.. appearance
en • OPLL o Flowing ossification along paraspinous
• Post-Operative Change, Normal ligaments seen in psoriatic and reactive
Less Common arthritis
• Osteomyelitis, Pyogenic • Fusion due to DISH
• Osteomyelitis, Granulomatous o Flowing ossification along paraspinous
ligaments
o Patients usually older than SO years
ESSENTIAL INFORMATION o Sacroiliac joints usually normal but rarely
Helpful Clues for Common Diagnoses appear fused due to enthesophytes
• Fusion occurring congenitally or in • Surgical fusion
childhood o Older surgeries often without hardware
o Vertebral bodies small in anteroposterior Helpful Clues for Less Common Diagnoses
dimension relative to adjacent segments • Fusion due to osteomyelitis
o Juvenile idiopathic arthritis: Associated o Rare in cervical spine
with arthritis elsewhere o Vertebral body fusion usually does not
• May see cervical instability affect facet joints
• Involves vertebral bodies and facet joints o Loss of vertebral body height, loss of
o Congenital fusion: May be isolated definition of endplates
abnormality or multiple levels o Single level in pyogenic, often multiple in
• May involve vertebral body, facet joints granulomatous
or both o Often develop kyphosis
• Known as Klippel-Feil spectrum
Vertebral Segmentation Failure Juvenile Idiopathic Arthritis
II
3 Lateral radiograph shows fusion =:I of the anterior and
posterior columns of C2 and C3. Note that the vertebral
Lateral radiograph shows fusion of the C7-T2 vertebrae
9. The narrow AP dimension reflects a growth
bodies arc narrow in AP dimension, a sign of congenital disturbance from childhood fusion. The widened c/-2
or childhood fusion. 1:1] distance is a clue to }IA.
4
(Jl
CERVICAL BONY FUSION
::!.
:J
CD
<
CO
~
CO
rr
Juvenile Idiopathic Arthritis ~
Q)
(Left) Sagillal bone CT shows
an unusual fusion between CD
o
the anterior arch of the C 7 Q.
and dens PJ:ill in a patient

'<
with juvenile idiopathic -u
arthritis and c/-2
o
en
subluxation. (Right) Sagillal CD
:>.
T1 WI MR shows bulky o
anterior ossification = ~
m
confluent over 4 vertebral ro
bodies. Ossification of this 3
CO
magniwde may cause ::J
dysphagia. en
Spondyloarthropathy, Seronegative
shows thin syndesmophytes
PJ:ill along the vertebral
bodies and fusion of facet
joints =. (Right) Lateral
radiograph shows bulky
ossification of the posterior
longitudinal ligament =.
Patient has less extensive
ossification of the anterior
longitudinalligamenl.
Post-Operative Change, Normal

fusion =
shows anterior intervertebral
performed without
hardware. The normal size of
the vertebral bodies
distinguishes this from
congenital or childhood
fusion. A lack of deformity
distinguishes this from fusion
due to infection. (Right)
osteomyelitis at C6-7 =.
Osteomyelitis not
infrequently leads to
vertebral fusion.
II
3
5
~
CIl
c
FLATTENED VERTEBRAL BODY, SOLITARY
QJ
E
QJ
W DIFFERENTIAL DIAGNOSIS o Cortical destruction: Vertebral body or
neural arch
Common o "Absent pedicle" sign
• Pathologic Vertebral Fracture o Lytic or blastic lesion seen in other
o Osteoporosis vertebrae
>-
"0 o Metastases, Lytic Osseous • MR appearance often allows differentiation
o o Metastases, Blastic Osseous
CO between vertebra plana due to osteoporosis
ro
~ o Plasmacytoma and tumor
-'> o Multiple Myeloma
t
QJ a Osteoporosis: Band-like or stellate
QJ o Steroids abnormal signal, focal cortical break but
> o Langerhans Cell Histiocytosis
CI> no widespread cortical destruction
c o Giant Cell Tumor
'0. o Tumor: Cortical destruction, round or
en o Ewing Sarcoma ovoid marrow replacement, marrow
o Leukemia replacing entire vertebral body or
o Lymphoma involving neural arch
o Osteomyelitis, Pyogenic • Langerhans cell histiocytosis most likely
o Hemangioma cause in young patients
• Burst Fracture • Congenital vertebral anomalies cause
• Chance Fracture well-demarcated hypoplasia
• Failure of Vertebral Formation
less Common • Ki.immell Disease
• Ki.immell Disease a Gas in flattened vertebral body
ESSENTIAL INFORMATION • Paraspinous soft tissue mass not a helpful
Key Differential Diagnosis Issues differen tial diagnostic finding
o May be due to hematoma in
• Single vertebra plana should always raise
suspicion for underlying lytic lesion non pathologic fracture, to paraspinous
tumor, or to paraspinous abscess
• Radiographic findings suggesting that a
vertebra plana is due to tumor
o Normal bone density in remainder of spine
Osteoporosis Osteoporosis
II
3 Sagittal bone CT shows flattened, sclerotic T6 \'ertebra
81 due to subacute burst fracture, with callus
Sagittal Tl WI MR shows fracture line at LJ
surrounded by band of low signal intensity,
=
6
fracture=
formation, in elderly paUent. Mild T7 compression
is a/50 present
characteristic of acute fracture edema/hemorrhage.
rallow-up confirmed osteoporotic burst fracture.
flATTENED VERTEBRAL BODY, SOLITARY
<
<tl
;:l.
<tl
CT
Langerhans Cell Histiocytosis ~
OJ
shows pathologic L3 burst CD
o
fracture with complete Q.
vertebral marrow
'<
replacement by tumof,
cortical destruction,
exlraosseous extension
and
=-
shows vertebra plana in a= [!J
9 year old boy. Ewing <tl
sarcoma may have the same 3
appearance on imaging. <tl
:J
Ui
Burst Fracture
shows 2 vertebral bodies and
intervening disc space
involved with tumor, but
only C6 shows flattening =.
Involvement of vertebrae
with osteomyelitis lends to
be nonunifo,m. (Right)
traumatic burst fracture, with
retropulsion of posterior
vertebral body cortex 81.
Note hemangioma ~ at the
level above the fractu,e.
Failure of Vertebral Formation Ki.immell Disease

shows that the left side of L3
is markedly hypoplastic
a congenital anomaly that
=-
may be isolated or
associated with VACT£RL
syndrome. (Right) Coronal
bone CT shows flattened
vertebral body containing
gas pathognomonic for
Kiimmefl disease. Cas has
migrated from the disc space
into the nonunited fracture
with secondary
osteonecrosis.
II
3
7
C
1Il
flATTENED VERTEBRAL BODY, MULTIPLE
Q)
EQ)
w DIFFERENTIAL DIAGNOSIS oCT: Destruction of trabeculae

~ o MR: Rounded lesions underlying fractures,
o
'C
Q)
Common often elsewhere in spine as well
1ii • Traumatic Fractures
o
a..
• Myeloma, lymphoma, leukemia
• Pathologic Vertebral Fracture o Similar to metastases, but loss of pedicle
>, o Osteoporosis
-0
o
uncommonly seen on radiographs
[l) o Metastases, Lytic Osseous o MR, CT show posterior element
ro
~ o Multiple Myeloma involvement is common
.0
Q) o Metastases, Blastic Osseous o Lytic lesions in spine often difficult to see
t
Q) o Leukemia on radiographs
> o Lymphoma
Q) • Most common appearance is diffuse
c: • Sickle Cell osteopenia, fractures
enC- • Scheuermann Kyphosis o Focal, round areas of marrow replacement
less Common or diffuse marrow replacement may be
• Osteogenesis Tmperfecta seen
• Achondroplasia • Sickle cell: Vertebral height lost centrally
• Cushing Disease only ("Lincoln Log vertebrae")
• Spondyloepiphyseal Dysplasia • Scheuermann kyphosis
• Caudal Regression Syndrome o 5° wedging of at least 4 contiguous
vertebrae
Rare but Important
o Schmorl nodes & undulating vertebral
• Radiation Therapy to Spine in Childhood endplates
o Usually involves thoracic spine
Helpful Clues for Common Diagnoses • Osteogenesis Imperfecta
• Traumatic spine fractures often occur at o Severe osteopenia, thin bone cortices
multiple contiguous or noncontiguous levels o Multiple fractures varying in severity,
even in young patients including pancake vertebrae
• MR useful to look for marrow replacement o Scoliosis often present
disorder in patients with multiple fractures • Cushing Disease
• Metastases o Pronounced concavity of end plate ("fish
o Radiographs: Cortical breakthrough, loss of mouth vertebrae")
pedicle
Traumatic Fractures Osteoporosis
II
3 Sagittal STIR MR shows mulliple compression
~ due 10
fraclUres
molar vehicle accident in a 30 year old
LLlteraJ radiograph shows multiple compression fractures
~ due 10 osteoporosis. CT or MR is useful in these
patient. patients to exclude marrow replacement by tumor.
8
flATTENED VERTEBRAL BODY, MULTIPLE en
"0
::;,
(l)
<
C1l
;::l.
C1l
Metastases, Blastic Osseous .,
CJ
Q)
mulliple flallened verlebrae OJ
o
=. There is a moth-eaten Cl.
'<
appearance lhroughoullhe
verlebral bodies due 10 \J
myeloma and a single large
o
(fl
lytic lesion E2. (Right) ro.,

Coronal bone CT shows 1055 o·
.,
of heighl of mulliple
m
verlebral bodies E2 due 10 ro
blaslic metastases. Allhough 3
C1l
the bone is increased in ::;,
density, it is not structurally Ui
sound, and patients are at
increased fracture risk.

diffuse bony sclerosis and
vertebrae with variable
degrees of flallening. Cenlral
verlebral flaltening with
preserved margins =
resembles lOy "Lincoln
Logs". (Right) Sagiltal T2WI
MR shows flaltening and
wedge deformities of 5
adjacent vertebrae =.
Involvement of at least 4
vertebrae with at least 50
wedging of each verlebra,
undulating appearance of
endplales, and definable
Schmor! nodes indicate
Scheuermann kyphosis.
Osteogenesis Imperfecta
(Left) Anleroposterior
radiograph shows severe
osteoporosis. Variable
degrees of vertebral
flaltening refleCl fraclure, of
varying severity. (Right)
Coronal bone CT shows mild
verlebral flaltening and
undulating vertebral
endplates.
II
3
9
en DYSMORPHIC VERTEBRAL BODY
C
Q)
E
~ Mucopolysaccharidoses
w
~
o
·C
Q)
Common
eno • Single Vertebral Body ESSENTIAL INFORMATION
D...
o Post-Traumatic Deformity Key Differential Diagnosis Issues
>-
"0 o Schmorl ode • Single vertebrae with abnormal appearance
o o Limbus Vertebra
CO usually post-traumatic
ro
~ o Metastases, Lytic Osseous • 2 or more adjacent vertebrae with abnormal
.0
Q) • Multiple but not all Vertebral Bodies appearance usually segmentation anomaly
t
Q) o Abnormal Segmentation
> • Partial Vertebral Duplication Helpful Clues for Common Diagnoses
Q)
c: • Vertebral Segmentation Failure • Scheuermann disease causes undulating
Co
C/) • Klippel-Feil Spectrum appearance of vertebral endplates
o Scheuermann Disease • Cushing disease causes cupping deformity of
o Scoliosis
vertebral endplates
o Metastases, Lytic Osseous • Infection and neurogenic arthropathy are
centered on intervertebral disc and show
o Neurogenic (Charcot) Arthropathy
endplate erosions
o Post-Radiation Changes • Juvenile idiopathic arthritis results in
• Diffusely Abnormal Vertebral Bodies vertebral bodies that are tall relative to
o Sickle Cell anteroposterior diameter
o Osteogenesis Imperfecta • Klimmell disease distinguished by gas in
o Achondroplasia
vertebral body
• Sickle cell causes "Lincoln Log" deformity
less Common • Mucopolysaccharidoses and achondroplasia
• Single Vertebral Body cause "bullet vertebrae" with anterior portion
o Klimmell Disease of body small
o Osteochondroma • Vertebral bodies near apex of a scoliosis
o Ewing Sarcoma often mildly misshapen
o Langerhans Cell Histiocytosis • Tumors involving only part of vertebral
• Multiple Vertebral Bodies body may cause a dysmorphic appearance
o Osteomyelitis, Pyogenic due to partial collapse
o Osteomyelitis, Granulomatous
• Diffusely Abnormal Vertebral Bodies
o Thanatophoric Dwarfism
Schmorl Node Limbus Vertebra
II
3 Lateral fluoroscopy shows
extending into Schmorl node
discographic
=:I.
contrast
Schmorl nodes are
Sagittal bone CT shows well-marginated ossicle =:I at
anterior corner of vertebral body. Limbus vertebra is due
caused by disc intravasation into vertebrallxx1y. to disc herniating between vertebral body & ring
apophysis, preventing normal fusion.
10
DYSMORPHIC VERTEBRAL BODY
Vertebral Segmentation Failure Scheuermann Disease

shows congenital fusion of
occiput and C1 Ell with
resultant abnormal motion
causing a dysmorphic
appearance of C2 ~. C4
and CS are flatter than
normal, without definite
fusion anomaly. (RighI)
m
Sagiual bone CT shows mild C1l
anterior wedging and 3
C1l
irregular vertebral endplales ::J
due to multiple Schmorf en
nodes a characteristic of
Scheuermann kyphosis.
Sickle Cell
(Left) Laleral radiograph
shows fused vertebrae
with narrow AP diameter
=
due to growlh failure.
Erosion of dens ~ is a clue
to Ihe diagnosis. (Right)
Sagiual T2WI MR shows
/I Lincoln Log'I appearance
81 of almosl alf the included
vertebrae, with preserved
peripheral body height and
central flattening reflecting
bone infarcts.
Osteochondroma Osteomyelitis, Granulomatous

of C2 =
shows an osteochondroma
causing deformity
of both the C2 and C 1.
Osteochondromas of the
spine are very rare, even in
patienls with multiple
hereditary exostoses. (Right)
Sagittal bone CT shows
multiple, fused, misshapen
verlebrae and kyphosis due
to tuberculosis.
II
3
11
!!l
c:
ENLARGED VERTEBRAL BODY/POSTERIOR ElEMENT
Q)
E
Q)
w DIFFERENTIAL DIAGNOSIS • Baastrup Sign

~ o Close approx. & contact of adjacent
o
'C
Q) Common spinous process with reactive sclerosis,
Ul • Facet Arthropathy
o enlargement & flattening of apposing
a.. o Facet Arthropathy, Cervical interspinous surfaces
>-
"0 o Facet Arthropathy, Lumbar o "Kissing" spinous processes
o o Baastrup Sign
CO o Cystic degeneration of interspinous
ctl
~ • Paget Disease ligaments and posterocentral epidural cyst
.0
Q) • Aggressive Hemangioma • Paget Disease
1::
Q) • Compensatory Enlargement o Enlarged vertebra and neural arch with
> o Scoliosis
CIl diffusely coarsened & haphazard bony
c: o Spondylolysis trabecular pattern
'0.
en • Congenital Fusion • Most commonly L3 & L4
Less Common • Cortex is thickened
• Metastases, Lytic Osseous • Anterior concavity of the vertebral body
• Aneurysmal Bone Cyst is lost
• Osteoblastoma o Can cause spinal stenosis & neural
• Chordoma forami nal narrowing
o 0 epidural soft tissue component unless
Rare but Important
sarcomatous degeneration
• Fibrous Dysplasia • Aggressive Hemangioma
• Chondrosarcoma o Expanded & indistinct cortex, irregular
• Osteochondroma honeycombing pattern, & soft tissue mass
• Trabecular condensation thinner in
ESSENTIAL INFORMATION comparison to Paget disease
o Lesions commonly involve entire vertebral
Key Differential Diagnosis Issues body with extension into neural arch
• Osteoblastoma should always be considered o Typically occur between T3 & T9
in the differential diagnosis of painful o Epidural extension may cause cord
scoliosis compression
• Center of the lesion in the vertebral body vs. o Can become symptomatic with growth,
posterior element may help with the which often occurs during pregnancy
differential diagnosis • Compensatory Enlargement
Helpful Clues for Common Diagnoses o Scoliosis
• Facet Arthropathy, Cervical • Minimal structural vertebral deformities
o Capsular laxity and joint space narrowing & advanced degenerative changes
may lead to degenerative spondylolisthesis • Facet osseous overgrowth, asymmetric
o Osteoarthritis of synovial-lined disc space, & discogenic sclerosis at the
zygapophyseal joints concave aspect of the scoliosis
o Hypertrophic changes with osteophytes, • Unilateral radicular symptoms on the
normal bone mineralization, & joint space side of the concavity of the deformity
narrowing o Spondylolysis
• Facet Arthropathy, Lumbar • Defects in pars interarticularis (PI) may
o Osseous hypertrophy with articular joint be due to repetitive stress injury
space narrowing and encroachment upon • Spinal canal is elongated at the level of
neural foramen the pars defect on axial imaging
o Irritation of synovium produces synovial • Most common at LS
hyperplasia with paradoxical joint space • Sclerosis of PI, volume averaging of
widening superior facet spur, partial facetectomy,
II o Facet arthrosis syndrome with low back,
hip, and buttock pain aggravated by rest
blastic metastases may mimic
spondylolysis
3
12
• Congenital Fusion a May be associated with an aneurysmal <

ct>
a Vertebral bodies smaller than normal with bone cyst (10-15%) :4-
ct>
tapered contour at fused disc space a Painful scoliosis (50-60%) 0-
~
III
a Rudimentary disc space with reduced • Chordoma CD
height & diameter, "wasp waist" a Rare involvement of the vertebral body o
a.
a Degenerative changes at adjacent levels a Purely lytic '<
a ± Fusion of posterior elements a T2 hyperintense with multiple septations
a Variable enhancement
a Amorphous intratumoral Ca++ in 30% of
• Metastases, Lytic Osseous
vertebral lesions
a 50-70% bone destruction required for
detection on radiography Helpful Clues for Rare Diagnoses
a Lesion involves posterior cortex & pedicle • Fibrous Dysplasia
a Diffuse involvement of marrow gives the a Neural arch involvement> vertebral body
appearance of brighter disc than bone on a Spine involvement in polyostotic disease
TlWI a Mildly expansile lesion with characteristic
a Fat suppression on enhanced Tl WI helpful ground-glass matrix
to unmask lesions a Heterogeneous Tl & T2 signal and
• Aneurysmal Bone Cyst enhancement
a Arise in the neural arch with the majority • Chondrosarcoma
(75-90%) extending into the vertebral a Lytic, destructive lesion with cortical
body destruction and extension into the soft
a Expansile remodeling of bone with cortical tissues
thinning a ± Chondroid matrix (50%) of "rings & arcs"
a Fluid-fluid levels with hemorrhage • Osteochondroma
a No tumor matrix a Sessile or pedunculated osseous lesion
• Osteoblastoma contiguous with the parent vertebra
a Originate in the neural arch, often extend a Cartilaginous cap> 1.5 cm in adults
into the vertebral body concerning for malignant transformation
0> 1.5 cm (osteoid osteoma < 1.5 cm)
a Narrow zone of transition with sclerotic
rim
a Bone matrix on CT or radiograph
Facet Arthropathy
II
Axial bone
overgrowth
stenosis.
CT shows severe left unilateral
ffi
facet
causing moderately severe central interspinous ligament =
Sagittal T7WI MR shows degeneration changes of lhe
and ligamentous flavum WiU1
a poslerior epidural cySI!:;].
3
VJ
ENLARGED VERTEBRAL BODY/POSTERIOR ELEMENT
C
QJ
E
QJ
W
~
o
'C
QJ Paget Disease
U;
o (Left) Sagittal STIR MR
0..
>-
"0
o
=
shows a mildly enlarged L2
vertebral body in the AP
dimension with relatively low
CO signal. Enlargement &
ro brighter signal in the spinous
~ process 81 reflect more
.0
QJ
t fibrovascular tissue. (Right)
QJ Sagittal T2WI MR shows a T2
> hyperintense mass involving
Q)
c: a thoracic vertebral body &
'0. posterior elements, with a
(/) large amount of epidural
extension = & cord
compression =. A typical
hyperintense hemangioma is
seen the level above 81.
Scoliosis Spondylolysis
(acet osteoarthritis
asymmetric disc space
=
fLeft) Axial T2WI MR shows
narrowing, &. discogenic

sclerosis E2 at the concave
aspect of the scoliosis. Disc
bulges can be far lateral &
are better seen on the axial
views. (Right) IIxial CECT
shows myelogram of chronic
isthmic spondylolysis 1:1
resulting in the "wide canal"
sign. There is increased AP
diameler of bony canal at L5
relative to more the cephalad
levels.
Congenital Fusion Metastases, Lytic Osseous

fusion = of L I, L2, & L3
vertebral bodies. Smaller
fused vertebrae are
characteristic of congenital
fusion. Advanced
below the kyphoscoliosis
results in spinal & neural
foraminal stenosis ~.
(Rig"') Sagittal STIR MR
shows an enlarged
hyperintense upper thoracic
vertebral body lesion and
a smaller lesion in the body
below =. A heterogeneous
enlarged thyroid mass is also
II seen 81.
3
14
<
CD
;::+
CD
Aneurysmal Bone Cyst Osteoblastoma rr
~
III
large bony expansile mass OJ
o
that involves the entire 0-
posterior element ~ and

'<
body 1:1] of C2. {/uid-(fuid
levels are characteristic.
There may be minimal
enhancement (Right) Axial
T2WI MR shows a
heterogeneous mass
expanding the right lamina
E1. Scoliosis is concave on
the side of the tumor. The
mass enhanced
heterogeneously on T1 C+
scan (not shown).
Chordoma
shows diffuse marrow
replacement 811 with
enhancing epidural mass 1:1]
and severe cord compression
!:ll. T2 hyperintensity &,
heterogeneous enhancement
are typical for vertebral
chordoma. (Right) Axial
NECT shows focal expansion
of the lamina and spinous
process 811 with areas of cyst
formation &, ill-defined
calcific matrix =.
Chondrosarcoma Osteochondroma
shows a large enhancing soft
tissue mass with verlebral
body !:ll and posterior
elementlC7J involvement &,
cord compression. (Right)
Coronal T2WI rs
MR shows
a heterogeneous extradural
mass 811 with a thin T2
hyperintense cartilaginous
cap that compresses the
spinal cord against the
ventrolateral spinal eana/.
The spinal cord is deviated
anteriorly and to the left
but there's no abnormal
=
spinal cord signal.
II
3
15
en ENLARGED NEURAL FORAMEN
C
OJ
E
OJ
w DIFFERENTIAL DIAGNOSIS Circumscribed foraminal masses, often
o
~ multiple, tend to be small (1-3 cm)
o
"C
OJ
Common o Contents follow CSF, no enhancement, ±
Ui • Nerve Sheath Tumor
o opacification with myelography
CL o Schwannoma • Dural Dysplasia
o Neurofibroma o Transmission of chronic CSF pressures by
• Perineural Root Sleeve Cysts weakened dura leads to bony remodeling
~ • Dural Dysplasia and expansion of lumbosacral canal and
.n
OJ • Lytic Metastasis to Vertebral Body or Pedicle neuroforamina
t::
OJ
Less Common o Can be seen with neurofibromatosis type
>
Q) • Osteomyelitis, Granulomatous I, Marfan disease, homocystinuria,
c: Ehlers-Danlos, and ankylosing spondylitis
a. • Neuroblastic Tumor
CIl
• Post-Traumatic Pseudomeningocele • Lytic Metastasis to Vertebral Body or
• Meningocele, Lateral Pedicle
• Vertebral Artery Ectasia or Aneurysm o Destructive process with loss of cortex,
• Osteolytic Primary Bone Tumor wider zone of transition to normal bone,
o Aneurysmal Bone Cyst multiple osseous lesions
o Plasmacytoma o Renal, lung, and breast are common
primaries to develop osteolytic metastases
Rare but Important
• Hypoplastic or Absent Pedicle Helpful Clues for Less Common Diagnoses
• Osteomyelitis, Granulomatous
o Tuberculosis may present with osteolytic
ESSENTIAL INFORMATION lesion of the neural arch
Key Differential Diagnosis Issues o Also: Brucellosis, coccidioidomycosis,
• CT useful to distinguish bony remodeling blastomycosis, actinomycosis
(benign or low grade mass) from osteolysis • Neuroblastic Tumor
(aggressive neoplasm, infection) o Paravertebral mass ± transforaminal and
epidural extension
Helpful Clues for Common Diagnoses o Foraminal enlargement by remodeling or
• Nerve Sheath Tumor bony destruction
o Transforaminal "dumbbell-shaped" • Post-Traumatic Pseudomeningocele
enhancing soft tissue mass o Cystic transforaminal structure, neural
• Perineural Root Sleeve Cysts elements usually absent
Schwannoma Neurofibroma
II
3 Sagillal NECT shows an enlarged neural foramen =
with remodeled, well-corlicaled margin and severely
Axial T1 C+ MR shows an oblong, enhancing soft tissue
mass extending through and enlarging the left C4-S
thinned pedicle in this patient with a large
lfansforamina/schwannoma.
neural foramen =_ The intraspinal component causes
severe cord compression ~.
16
ENLARGED NEURAL FORAMEN
Perineural Root Sleeve Cysts Dural Dysplasia

masses =
thin-walled cystic foraminal
larger on the left,
remodeling the thoracic
neural foramina bilaterally.
(Rigllt) Lateral radiograph
shows posterior vertebral
scalloping and enlargement
of multiple neuroforamina
m
=:11 due to dural dysplasia in iil
this patient with 3
neurofibromatosis type I. CD
:J
Ui
lytic Metastasis to Vertebral Body or

Pedicle Neuroblastic Tumor
destructive renal cell
metastasis destroying
posterolateral thoracic
vertebral body, resulting in
widening of the bony
margins of the neural
foramen =:11. (Right) Sagillal
T1WI MR shows
transforaminal invasion of
the epidural space in this
patient with a paraspinal
neuroblastoma. There is
remodeling and enlargement
foramen =
of the left T12-L 1 neural
with abnormal
soft tissue also in adjacent
neuroForamina.
Post-Traumatic Pseudomeningocele Meningocele, lateral

the cyst-like fluid collection
extending through, and
chronically enlarging, the
neural (oramen -==
at the site
of a remote nerve root
avulsion. (Right) Axial NECT
shows large soft tissue
density with smooth margin
extending through an
enlarged
foramen =left thoracic
left hemithorax
neural
and filling the
in this patient
with type 1
neurofibromatosis.
II
3
17
rn
C
VERTEBRALBODY SCAllOPING/WIDENED CANAL
Q)
E
Q)
w DIFFERENTIAL DIAGNOSIS o "Waisted" appearance at the fusion due to
~ stress shielding
.g Common
Q) • Dural Dysplasia
eno • Normal Variant o Intrinsic weakness in dura, transmitted
CL
• Vertebral Segmentation Failure CSF pressure causes bony remodeling
• Dural Dysplasia o Seen with neurofibromatosis type 1,
• Intraspinal Mass Marfan disease, homocystinuria,
~
Cll o Ependymoma Ehlers-Danlos, and ankylosing spondylitis
.Q
Q) o Schwannoma • Ependymoma
t
Q) o Neurofibroma o Enhancing intramedullary or
> o Meningioma
Q) in trad ural-extramed ullary (lurn bosacral
c o Arachnoid Cyst canal) mass
'0.
In o Lipoma • Schwannonla
o Astrocytoma o Extramedullary mass, typically ventral or
o Dermoid and Epidermoid Tumors lateral to the cord or within fibers of the
less Common cauda equina
• Congenital Skeletal Disorders o Those associated with canal remodeling
o Achondroplasia typically fusiform or dumbbell in shape
o Mucopolysaccharidoses (Morquio, Hurler) • Neurofibroma
• Diastematomyelia o In this context, not reliably differentiated
• Juvenile Idiopathic Arthritis from schwannoma (see above)
• Severe, Longstanding Communicating • Meningioma
Hydrocephalus o Intradural-extramedullary enhancing mass,
• Hydrosyringomyelia with broad dural base
• Acromegaly • Arachnoid Cyst
o Circumscribed, thin-walled, nonenhancing
extramedullary mass, follows CSF
ESSENTIAL INFORMATION signal/attenuation
Helpful Clues for Common Diagnoses Helpful Clues for less Common Diagnoses
• ormal Variant • Achondroplasia
o Body slightly concave on all surfaces o Congenitally short, narrowed pedicles;
• Vertebral Segmentation Failure bullet-shaped vertebral bodies with
o Single level cervical fusion a rather posterior scalloping
common, incidental anomaly
Vertebral Segmentation Failure Dural Dysplasia
II
3 Sagittal bone CT shows developmental fusion of C3 and
C4 with "waisting" allhe level of the fusion ~
Lateral radiograph demonstrates posterior scalloping of
multiple vertebral bodies =
and enlargement of
multiple neural foramina ~ in thi5 patient with type 7
neurofibromatosis.
18
VERTEBRAL BODY SCALLOPING/WIDENED CANAL Ul
"2.
::::l
CD
<
C1>
;l.
C1>
CJ"
Schwannoma ~
llJ
(Left) Sagiltal Tl C+ MR
shows a large lobulated OJ
o
Q.
enhancing mass tilling the
'<
distal thecal sac and
expanding & remodeling the
lumbosacral canal =.
(Right) Sagittal Tl C+ MR
shows unusually extensive,
multi/eve/tumor in
m
thoracolumbar spine that ro
contains multiple areas of 3
C1>
cystic degeneration that ::::l
results in posterior vertebral Ui
scalloping =.
Arachnoid Cyst Achondroplasia

shows a large lobulated
extradural mass, tollowing
CSF signal, widening the
spinal canal by remodeling
the dorsal elements =
and
compressing the spinal cord.
shows shortened pedicles
and posterior vertebral
scalloping
Diastematomyelia Juvenile Idiopathic Arthritis

(Left) Axial T2' GRE MR
shows dysmorphic vertebral
body = with enlarged
cervical canal and a split
spinal cord ~> (Right)
tusion at multiple abnormally
slender cervical vertebral
bodies with a widened
cervical canal =.
II
3
19
c'" SPONDYlOLISTHESIS
Q)
E
Q)
w DIFFERENTIAL DIAGNOSIS • Spondylolysis ~ break in pars interarticularis

~ of vertebrae leaving two parts
o
"C
Q) Common o Anterior component of vertebral body,
eno • Pediatric Pseudosubluxation pedicle, superior facet
0..
• Dysplastic o Posterior component of inferior facet,
>. • Degenerative Disc Disease
"0 lamina, spinous process
o • Spondylolysis
CD
ro~ • Post-Treatment Instability Helpful Clues for Common Diagnoses
.0
Q) • Posterior Column Injury, Cervical • Pediatric Pseudosubluxation
t
Q)
o Normal mobility C2 on C3 in flexion
> Less Common o Seen in 40% of children at C2-3, 14% of
Q)
c:
• Osteomyelitis, Pyogenic children at C3-4 level
Co • Tuberculous Infection o Only seen with flexion
en
• Tumor o May be mistaken for ligamentous injury,
o Metastasis since 70% of cervical spine fractures in
o Lymphoma children occur from Cl to C3
o Multiple Myeloma o C2 displaced up to 3-4 mm
o Primary Bone Tumor o Age < 14 years
• Osteosarcoma o Swischuk line: Drawn from anterior aspect
• Osteoblastoma of CI-C3 spinous processes ~ normal
• Chondrosarcoma within 1 mm of anterior C2 spinous
• Rheumatoid Arthritis, Adult process
o If in doubt on plain film or CT, then MR
ESSENTIAL INFORMATION to exclude ligamentous injury

• Degenerative Disc Disease
Key Differential Diagnosis Issues o Most common at L4-5
• Spondylolisthesis ~ displacement of one o Wide canal sign not present since no
vertebral body relative to another defects in pars
o Dysplastic (congenital abnormality of o Usually grade 1 without lysis
arch) o Look for severely degenerated facets + disc
o Isthmic (fatigue or stress fractures of pars) degeneration
o Degenerative (osteoarthritic segmental o Lose of height of neural foramen with
instability of facets) stenosis as superior body slips forward
o Traumatic o Posterior retrolisthesis ~ disc degeneration
o Pathologic (local bone disease) with disc height loss, rostrocaudal
• Most common is isthmic and degenerative subluxation of facets
• Spondylolisthesis can occur with or without • Spondylolysis
spondylolysis 090% at L5-S1, bulk of remainder at L4-5
• Spondylolisthesis graded by amount of • L3 and above unusual ~ question
anterior displacement of superior body by gymnastics
25% stages o 20% may have unilateral defect in pars
o < 25% ~ grade 1, < 50 ~ grade 2, < 75% o May show contralateral compensatory
grade 3, < 100% ~ grade 4, > 100% ~ bone hypertrophy and sclerosis
spondyloptosis • Not to be mistaken for osteoid osteoma!
• Anterior displacement of vertebral body ~ o Wide canal sign present (increase in AP
"uncovering" of the posterior disc margin diameter of bony canal at lysis level
with pseudobulge deformity relative to normal levels) with bilateral
• Look for focal herniations in addition to the lysis
pseudobulge at the level of spondylolisthesis • Post-Treatment Instability
and at adjacent levels where stress is o Deformity that increases with motion and
II increased increases over time
o Dynamic slip> 3 mm in flexion/extension
3
20
SPON DYLOLISTH ESIS
o Static slip of 4.5 mm or greater Fat-suppressed post-contrast Tl images

o <
CD
o Angulation> 10-15° suggests need for useful for epidural disease and ::l-
CD
surgical intervention paravertebral/psoas extension CT
~
III
o Stabilizing anatomic structures • Tumor OJ
• Anterior longitudinal ligament (resists o Destruction of posterior elements + o
a.
hyperextension) vertebral body leads to secondary '<
• Posterior longitudinal ligament instability
• Intertransverse ligaments (connect • Rheumatoid Arthritis, Adult
neighboring transverse processes) o Subaxial anterior + posterior subluxations
• Interspinous ligaments (resists common m
hyperflexion) o Atlantoaxial subluxation in 5% of patients CD
3
• Facet capsule with cervical rheumatoid arthritis CD
:J
• Ligamentum flavum o Instability may also be present at lower Ui
• Intervertebral disc: Main stabilizer of levels of cervical spine
lumbar and thoracic spine o Spine radiographs in flexion/extension to
• Muscular attachments assess for instability
• Posterior Column Injury, Cervical o Look for Cl-2 involvement with
o Fractures of laminae, facets, or spinous retrodental pannus + subaxial
processes spondylolisthesis
o Disruption of ligaments bridging spinous
processes + laminae
SELECTED REFERENCES
o If capsular ligaments torn, facets, &/or
1. Nizard RS et al: Radiologic assessment of lumbar
laminae both fractured, rotational intervertebral instability and degenerative
instability may exist spondylolisthesis. Radiol Clin North Am. 39(1):55-71, v-vi,
o Flexion extension films or fluoroscopy to 2001
2. Brady WJ et al: ED use of flexion-extension cervical spine
assess degree of instability radiography in the evaluation of blunt trauma. Am J Emerg
Med. 17(6):504-8, 1999
Helpful Clues for Less Common Diagnoses 3. Frymoyer JW et al: Segmental instability. Rationale for
• Tuberculous Infection treatment. Spine. 10(3):280-6, 1985
o Endplate irregularity and bone destruction 4. Swischuk LE: Anterior displacement of C2 in children:
physiologic or pathologic. Radiology. 122(3):759-63, 1977
o T2 hyperintense disc, vertebral bodies 5. Cattell HS et al: Pseudosubluxation and other normal
o Look for associated epidural variations in the cervical spine in children. J Bone Joint
Surg Am. 47(7):1295-309,1965
phlegmon/ abscess
Pediatric Pseudosubluxation
II
Sagittal NECT shows slight subluxation at C2-3 =- Sagittal TI WI MR shows dysplastic spondylolisthesis in a
3
which is within normal variation. Posterior laminar fine
from Cl to C3 is normal. Normal anterior displacement
orC2 on C3 is up to 4 mm.
and trapezoid-shaped
more normal-sized L4.
LS body =-
repaired myelomeningocele patient with Chiari 2. Small
in contrast to the
21
c
(f)
SPONDYLOLISTHESIS
OJ
E
OJ
i:iJ
~
o
·C
OJ Dysplastic
t=l (Left) Sagiltal CECT shows
o
CL dysplastic form of
spondylolisthesis with slight
>-
"0 anterior subluxation L5 on 51
o
CO =:I in this 72 year old.
CO (Right) Sagittal CECT shows
~ absent pars at L5-S 7 level SlI
.0
OJ in this case of dysplastic form
t
OJ of spondylolisthesis. Contrast
> to normal pars and inFerior
Q)
facet at L4.
l::
a.
1Il
Degenerative Disc Disease

(Left) Sagiltal T 1 WI MR
shows multilevel severe
with spondylolisthesis at L4-5
=:I and retrolisthesis at L2-]
SlI. There is marked loss of
disc space height at multiple
levels. (Right) Sagittal NECT
shows spondylolisthesis and
spondylolysis at L5-S7 with a
well-defined corticated break
~ There is moderate
Foraminal stenosis at L5-51.
Spondylolysis Post- Treatment Instability

severe spondylolytic
spondylolisthesis with the
posterior margin L5 vertebral
body =:I at the same
position as the anterior
is readily apparent =
margin S 7 SlI. II pars defect
with
premature large osteophytes
and foraminal narrowing.
(Right) Lateral radiograph in
flexion shows grade 2
anterolislhesis = that
improved on extension
related to wide multilevel
laminectomies.
II
3
22
SPONDYLOLISTHESIS
Post-Treatment Instability Posterior Column Injury, Cervical

shows post-operative
spondylolisthesis following a
lumbar laminectomy L4 & 5
E1. Acute compression
fracture is present at L 1.
(Right) Coronal NECT shows
comminuted fracture of
posterior elements at C7 c::l.
m
CD
3
(l)
:J
en

shows flexion rotation injury
of the cervical spine with a
Facet fracture, vertebral
subluxation =::I, and cord
edema. There is widening of
the posterior elements at
C6-781. (Right) Sagiltal
T2WI MR shows bilateral
facet subluxation and C5-6
subluxation following
trauma, with cord
hemorrhage 81 and ALL
disruption ~.
Tumor
(Left) Sagittal N£CT shows
destruction of L5 and SI
centered at the intervertebral
disc level, with
anterolisthesis of L5 on 5 I
due to loss of disc stability
from disc space infection.
(Right) Sagiltal T1 WI MR
shows pars defect at L5-SI
E::II in this patient with
extensive bony metastatic
disease. Multiple pathologic
nodes are present lID.
II
3
23
en BONY lESION, AGGRESSIVE
C
OJ
E
OJ
LU DIFFERENTIAL DIAGNOSIS • 67% appear benign
~ • Osteomyelitis, Pyogenic
.g Common
OJ
~ o III-defined Tl hypointensity in vertebral
en • Metastases, Lytic Osseous
a marrow with loss of adjacent end plate
a.. • Metastases, Blastic Osseous delineation
>- • Lymphoma
-0 o T2/STIR hyperintense marrow
a
ro • Multiple Myeloma o Endplate osteolytic/osteosclerotic changes
ro~ • Osteomyelitis, Pyogenic on CT & vertebral collapse
.Q
OJ • Osteomyelitis, Granulomatous o Disc space narrowing & enhancement
t
OJ
less Common o ± Paraspinal/epidural infiltrative soft tissue
>
Q; • Degenerative Endplate Changes with loculated fluid (75%)
l:
.0. • Accelerated Degeneration • Osteomyelitis, Granulomatous
rn o Tuberculous spondylitis shows vertebral
• Schmorl Node
• Langerhans Cell Histiocytosis collapse & large paraspinal abscess (±
calcification)
Rare but Important
• ± Destruction of disc
• Spondyloarthropathy, Hemodialysis • Isolated posterior element involvement
• Neurogenic (Charcot) Arthropathy o Brucellar spondylitis shows anterosuperior
epiphysitis (L4) with associated sacroiliitis
ESSENTIAL INFORMATION • Intervertebral disc destruction &
relatively intact vertebrae
Key Differential Diagnosis Issues o Multiple (non)contiguous vertebrae with
• Bone destruction (tumor, infection) vs. endplate irregularity & osteolysis
remodeling, short transition zone o Enhancement of epidural soft tissue mass,
(degenerative disc disease) marrow, disc, dura, subligamentous soft
Helpful Clues for Common Diagnoses tissues
• Metastases, Lytic Osseous o Chronically shows fusion across disc space
o Lytic, permeative diffusely enhancing
lesion destroys posterior cortex & pedicle • Degenerative EndpIate Changes
o Tl hypointense/T2 hypo ~ hyperintense, o Loss of disc space height, loss of horizontal
T2 hyperintense rim surrounding nuclear cleft on T2WI, linear disc
hypointense met enhancement
• Metastases, Blastic Osseous • No bone destruction
o Sclerotic lesion destroys posterior cortex &
• Vacuum phenomenon (low Tl/T2 signal)
pedicle o Type 1: Tl hypo-!T2 hyperintense, may
o Tl/T2 hypointense with variable
show prominent enhancement
enhancement depending on degree of • Inflammatory in orgin, but association
sclerosis with lower back pain controversial
• Lymphoma • Associate with segmental instability with
o Lytic, permeative bone destruction may
good clinical outcome following fusion
cross disc spaces o Type 2: Tl/T2 hyperintense
o Tl hypointense, T2 iso-/hyperintense, &
o Type 3: Tl/T2 hypo intense, sclerosis on CT
diffuse uniform enhancement & radiographs
o ± Soft tissue mass
• Accelerated Degeneration
• Multiple Myeloma o Degenerative changes of disc space/facets
o Multifocallytic lesions with cortical at levels adjacent to surgical fusion &
disruption & extraosseous soft tissue congenital segmentation anomalies
component • Most common finding at adjacent
• Pedicle involvement is late segment is disc degeneration
II o Compression fractures with variable canal
narrowing
• No bone destruction
o Response to altered biomechanical stresses
3
24
BONY LESION, AGGRESSIVE en
~.
::l
(l)
• t Intradiscal pressure, t facet loading, & t o Low Tl signal, low to intermediate T2/STIR <
CD
mobility occur after fusion implicated in signal ;:l.
CD
causing adjacent segment disease o Progression to vertebral body collapse or <T
~
OJ
• Rate of symptomatic adjacent segment listhesis with spinal instability & cord OJ
disease t with transpedicular compression o
Cl.
instrumentation (12.2-18.5%) o Imaging simulates an infectious process '<
• Fusion with other forms of with destruction & irregular enhancement
instrumentation or with no of the endplates & narrowing of disc space
instrumentation (5.2-5.6%) o Disease correlates with duration of
• Risk factors: Instrumentation, fusion hemodialysis, although can be seen with m
length, sagittal malalignment, facet only chronic renal insufficiency CD
3
injury, age, & pre-existing degenerative • Neurogenic (Charcot) Arthropathy CD
::J
changes o Destruction of discs, end plates, & facet Cii
• Schmorl Node joints with preserved bone density

o Focal invagination of vertebral endplate by o Bone debris around vertebrae & fluid
disc material collections, which do not enhance as
• Low Tl/high T2 signal in adjacent avidly as abscess
marrow if acute o Diffuse enhancement involving discs &
• Diffuse marrow enhancement if acute, facet joints
marginal enhancement if subacute o Most often in lumbar spine, sometimes in
• Most commonly seen at the T8 through lower thoracic spine
Lllevels & always contiguous with • Involves 1-2 spinal levels
parent disc o Can be rapidly progressive destroying a
Helpful Clues for Rare Diagnoses joint in a month

o Etiologies include diabetes mellitus,
• Spondyloarthropathy, Hemodialysis
neurosyphilis, status post-traumatic
o Erosions of anterior corners of vertebral
paraplegia
body & erosions & cysts of adjacent
endplates with minimal osteophyte
formation
o Severe narrowing of disc space
o ± Soft tissue mass
o Crystal (visible calcification) & amyloid
deposition
Metastases, Lytic Osseous
II
Axial NECT shows a renal cell metastasis destroying the
right side of a thoracic vertebral body. right posterior
Sagittal NECT shows multiple blastic metastatic foci
involving lhe thoracic & lumbar vertebral bodies ffi
3
elements. & right costovertebral joint
margin shows bony expansion.
=. The ventral
25
(j)
c BONY LESION, AGGRESSIVE

Q)
E
Q)
w
'-
o
'C
Q)
(j) lymphoma
o (Left) Sagittal T1WI MR
a.. shows a soft tissue mass
>- replacing L5 vertebra with
"0 exlraosseous extension ~ &
o
CO pathologic compression
l\l fracture. (Right) Axial T1 C+
'-
.0 MR shows marrow
Q)
t replacement &
Q)
heterogeneous enhancement
> throughoullhe vertebral
Q)
body, extending into the
c
'Q. right neural arch Ell. There is
l/) extension of tumor into the
anterior paraspinous soft
tissues ~ & epidural space.
The epidural extent of the
=.
lUmor results in the "draped
curtain 1/ sign
Osteomyelitis, Pyogenic
areas of abnormal signal

Majority of the lesions are
=-
reveals mullifocal geographic
lower signal intensity than

the intervertebral discs, a
sign that these represent
tumor rather than
heterogeneous marrow.
shows C5·6 disc space
infection with disc
irregularity & increased signal
in contiguous bodies. A small
epidural abscess ~ mildly
effaces the cord. There is
extensive prevertebral edema
=.
Osteomyelitis, Granulomatous
(Left) Sagittal T2Wf FS MR
shows complete collapse of
the L2 body Ell. Adjacent
intervertebral discs are
contiguous. A focal abscess
~ protrudes posteriorly with
compression of the thecal
sac. (Right) Sagittal STIR MR
shows bone marrow edema
adjacent to endplates =-
multiple bulging discs, &
narrowing of intervertebral
discs. This pallern is
characteristic of edema
secondary either to instability
or to loss of cushioning effect
II of the intervertebral discs.
3
26
BONY LESION, AGGRESSIVE
<
CD
::l-
CD
0-
Schmorl Node
m
shows posterior solid fusion CD
o
mass from L3 10 S 1 SlI & Cl.
severe degenerative changes '<
al T1UI, U-2, & L2-] EB II
(Right) Sagillal T1 C+ fS MR
o
(fl
shows a bone bruise at level CD

...•
01 Schmorlnode. The o·
...•
band-like region of marrow
m
enhancement m m
surrounding the Schmorl 3
CD
node ~ is consistent with :J
acute injury. en

destructive lesion involving a
thoracic vertebral body &
posterior elements E:I.
Paravertebral & epidural
extension result in severe
canal narrowing !J:ll. (Right)
Sagillal T1 WI MR
demonstrates low signal in
L5 body SlI & disc space !J:ll.
Absence of T2 hyperinlensity
(not shown), disc space
enhancement, & Jack of
paravertebral infiammalOry
mass help 10 differentiate
hemodialysis
spondyloarlhropathy from
infectious spondylodiscitis.
(Left) Coronal N[CT shows

amyloid/crystal deposition
disease in patient with fang
term renal failure. There are
multiple areas boneor
erosion centered about
synovial joints =
with mild
bony expansion. (Right)
Coronal bone CT shows
extensive bony debris in the
mid-lumbar spine with
destruction of the L3 &
proliferative new bone
formation E:I. Bone mineral
density is preserved, which is
uncommon in most cases of
infection.
II
3
27
C/)
c FRACTURE,VERTEBRALBODY
Q)
E
Q)
W DIFFERENTIAL DIAGNOSIS a Chance: Anterior compression, posterior

~ distraction
o
'C
Q)
Common a Fracture/dislocation: Shear forces
Ul • Vertebral Body Only
o
CL
• Treatment of different types of fractures is
a Anterior Compression Fracture, Thoracic different, so imaging distinction is
>. a Anterior Compression Fracture, Lumbar important
"o
CO a Lateral Compression Fracture, Lumbar
• Imaging may overestimate or underestimate
~
<Il a Lateral Compression Fracture, Thoracic mechanical instability of spine
.0
Q) a Burst Fracture (Mild) • Fracture vs. fracture mimic
t
Q) a Pathologic Vertebral Fracture a History of trauma may not be available or
> a Hyperflexion Injury, Cervical
Gl reliable
c: a Hyperextension Injury, Cervical
'0. a Fractures may be single or multiple levels
en • Vertebral Body Plus Posterior Elements a May have different kinds of fractures at
a Burst Thoracolumbar Fracture different levels
a Burst Fracture, Lumbar • e.g., burst and compression at 2 different
a Burst Fracture, Cervical levels
a Pathologic Vertebral Fracture a Multiple, uniformly involved levels of
a Burst Fracture, C2
deformity usually not traumatic
a Hyperflexion Injury, Cervical
a Hyperextension Injury, Cervical Helpful Clues for Common Diagnoses
a Chance Fracture, Thoracic
• Compression Fracture
a Does not involve posterior vertebral body
a Distraction Fx, Low Thoracic
• Fracture Mimics cortex or posterior elements
a Common throughout thoracic and lumbar
a Schmorl Node
a Limbus Vertebra
spine
a Kyphosis, Idiopathic
a May involve anterior or lateral portion of
a Scheuermann Disease
vertebral body
a Sickle Cell
a Often occur at multiple levels in normal or
a Scoliosis and Kyphosis, Congenital

osteoporotic bone
a Most common type of pathologic fracture
a Neurogenic (Charcot) Arthropathy
a Osteomyelitis, Pyogenic • Burst Fracture
a Burst fracture extends through posterior
Less Common cortex of vertebral body
• Lymphoma a More severe burst fractures show vertically
• Cushing Disease oriented fractures of neural arch
• Ki.immell Disease a Most common at thoracolumbar junction
• Osteomyelitis, Granulomatous • Chance Fracture
• Congenital Syndromes a Anterior compression vertebral body
a Failure of Vertebral Formation a In conjunction with horizontally oriented
a Osteogenesis Imperfecta fracture of posterior elements OR
a Diastematomyelia ligamentous injury resulting in separation
a Achondroplasia, Mucopolysaccharidoses of adjacent spinous processes
a Mucopolysaccharidoses a Most common at thoracolumbar junction
Rare but Important • Hybrid Fractures
• Ewing Sarcoma a Some fractures have elements of both
• Apophyseal Ring Fracture burst- and chance-type injury

• Retropulsion of posterior vertebral body
cortex + separation of posterior elements
ESSENTIAL INFORMATION • Best to categorize as Chance and add
Key Differential Diagnosis Issues description of burst elements
II • Mechanism of injury • Compression or Burst Fracture due to
a Compression, burst: Axial load injuries Trauma or Osteoporosis
3
28
FRACTURE, VERTEBRAL BODY
a MR: Band-like configuration of abnormal a Smooth vertebral endplate contour,

signal multiple vertebrae
a CT: Trabeculae compressed but not a Diagnosis of exclusion
destroyed • Scheuermann Disease
• Compression or Burst Fracture due to a Undulating contour of endplates
Tumor a Discrete Schmorl nodes variably present
a Radiographic findings a 4 or more contiguous vertebral bodies with
• Focal osteopenia or osteosclerosis at least S° wedging each
• Cortical destruction • Sickle Cell
• Nonvisualization of pedicle contour on a H-shaped or "Lincoln Log" vertebrae with m
AP radiograph a helpful sign central depression and preserved margins (1)
3
a MR findings • Infection or Neuropathic Arthropathy (1)
::J
• Rounded configuration of abnormal a Endplate destroyed, irregular en
signal, or diffuse abnormal signal Helpful Clues for Less Common Diagnoses
adjacent to fracture • Kiimmell Disease
• Cortical breakthrough beyond fracture a Gas in vertebral body cleft; flattened
line is often seen vertebral body
• Additional areas of abnormal signal • Osteomyelitis, Granulomatous
without fracture helpful signs when a Multiple vertebral fusions, kyphosis
present • Congenital Vertebral Anomalies
a CT findings
a Smoothly marginated, usually involve
• Destruction of trabeculae adjacent to multiple vertebral bodies
fracture • Osteogenesis Imperfecta
• Cortical break beyond fracture line is a Severe osteopenia, scoliosis, multiple
often seen fractures of varying severity
• Additional areas of bony destruction • Achondroplasia, Mucopolysaccharidoses
without fracture helpful signs when a Bullet-shaped vertebrae
present
• Limbus Vertebra
a Ossicle anterior corner of vertebral body,
smoothly contoured & corticated
a Failure of fusion of ring apophysis
• Kyphosis, Idiopathic
Anterior Compression Fracture, Lumbar Burst Thoracolumbar Fracture
II
Lateral radiograph shows anterior compression fracture
SI in this young palient with normal bone density
Lateral radiograph shows burst fracture in a young
patient, with retropulsion of posterior vertebral body
3
Palient has chronic spondylolysis of L4. cortex~.
29
(J)
cQ)
E
Q)
w
~
a
·C
Q) Pathologic Vertebral Fracture
tl (Left) Sagiltal T2WI MR
a
Cl.. shows vertically oriented
compression fracture of L3
>-
"0
a = due to metastases from
co breast cancer. Marrow is
ro diffusely abnormal signal
~ intensity. (Rigl1t) Lateral
.0
Q)
t radiograph shows wedge
Q) deformity and "flexion
> teardrop" fragment 1::1
at
C1l CS. Widened interspinous
c:
a. distance ~ and laminar
en fracture m are evidence of
posterior distraction Force.

characteristic pattern of
cervical injury in DISH.
Hyperextension fracture ~
extends through ossified ALL
and vertebral body. In
ankylosing spondylitis,
fracture usually extends
through disc and spares
vertebral body. (Right)
Sagiltal STIR MR shows
anterior vertebral
compression =and tear of
interspinous ligaments E2
indicating flexion-distraction
(Chance) fracture.
Chance Fracture, Thoracic

(Left) Sagiltal bone CT shows
flexion-distraction injury,
with anterior compression
E1 and posterior distraction
= fractures. There is also
retropulsion r=::l of the
posterior cortex of the
vertebral body (Lypical of
burst fracture); howeve" the
preponderant patlern is that
of a Chance fracture. (Right)
Sagiltal NECT shows
fracture-dislocation at T4-S
Ell. Cord was lransected.
II
3
30
Schmorl Node Kyphosis, Idiopathic

a typical Schmorf node a a OJ
o
bowl-shaped depression in Q.
the vertebral endplate due to

'<
disc material herniating
through endplate. (Right)
marked kyphosis of the
upper thoracic spine and
multilevel degenerative disc
[!J
CD
disease m. There are no 3
congenital abnormalities, CD
::J
fractures, Scheuermann en
disease, or tumor present.
leaving idiopathic kyphosis
as the diagnosis of exclusion.
radiograph shows "butterfly
cleft=
vertebra II I'.l:m at T' I. Central
in vertebra can be
mistaken for fracture. (Right)
fracture !l:J through vertebral
body and posterior arch after
spinal fusion in this
paraplegic patient.
Neurogenic arthropathy
features fractures lhallend
nOlla heal, with resultant
abnormal motion and bony
destruction.

bony destruction at L1 and
L2 SlI due to osteomyelitis,
causing kyphosis and
hardware failure. (Right)
gas-filled cleft
posHraumatic
=
in vertebral
avascular
necrosis Kiimmell disease.
II
3
31
l/)
FACET ABNORMALITY, NON-TRAUMATIC
C
Ql
E
Ql
UJ DIFFERENTIAL DIAGNOSIS o Cartilage erosion & joint space narrowing
o Facet Synovial Cyst
Common • Extradural cystic mass extending from
• Normal Variant degenerative facet joint
o Facet Tropism • Internal high Tl/low T2 signal due to
>. • Facet Arthropathy hemorrhage or proteinaceous content &
"0
o o Facet Synovial Cyst
CO low T2 rim 2° wall calcification
ctl
~ • Tumor Destruction • Tumor Destruction
.0
Ql o Metastases, Lytic Osseous o Lytic mets: Irregular preservation of
t::
Ql o Lymphoma trabeculae & buttressing, isolated fronts of
> o Multiple Myeloma
Gl cortical bone resorption coalescing to
c: confluence
Co Less Common
rtl
• Rheumatoid Arthritis, Adult o Multiple myeloma: Sharply defined,
• Congenital Fusion spheroid lesions with smooth borders &
• Septic Facet Joint Arthritis effaced/erased trabeculae, absence of
remodeling
• Rheumatoid Arthritis, Adult
Key Differential Diagnosis Issues o Inflammatory arthritis involve synovial
• Assess vertebral abnormalities, multiplicity joints (facet & uncovertebral) w/erosions
(i.e., metastases), & soft tissue component o Cervical spine involvement in 60%
(i.e., RA pannus, epidural abscess) • C1-C2 instability in 33%; atlantoaxial
Helpful Clues for Common Diagnoses subluxation in 5%
• Normal Variant • Congenital Fusion
o Facet Tropism o Segmen tation failure of 2 or more cervical
• Asymmetry in orientation of vertebra
zygapophyseal joint surfaces up to 35% o Vertebral body narrowing at fused
• L5-S1 > L4-5 rudimentary disc space

• Stress hypertrophy of pedicle on the o ± Fusion of facets & spinous processes
more coronally oriented side • Septic Facet Joint Arthritis
• Facet Arthropathy o T2 hyperintensity and enhancement
o Osseous facet overgrowth with extends into adjacent soft tissues
encroachment upon neural foramina o ± Epidural abscess/phlegmon
Facet Tropism Facet Synovial Cyst
II
3 Axial T2WI MR shows asymmetry of the face15 and
lamina 8
Axial T2WI MRshows an extradural lesion SI extending
anleromedially into the spinal canal from a hypertrophic
facet joint !:D. Internal mixed hypoinlensily may be due
to proteinaceous material.
32
FACET ABNORMALITY, NON-TRAUMATIC en
"S!.
:::l
Cll
<
Cll
;::I.
Cll
0-
Metastases, lytic Osseous Metastases, lytic Osseous ~
Q)
shows expansile hypoinlense CD
o
lesion involving the body, a.
pedicle, and articular pillars
'<
of a mid-thoracic vertebral II
body =. The soft tissue
o
en
component extends into the CD
~
epidural space. (Right) Axial o
CTA shows a thyroid
~
m
metastasis giving thin en
expansile bony margin with 3
the predominantly lytic <tl
:::l
lesion involving the vertebral en
body and left facet/lamina of
C3 =. There is epidural
extension with cord
compression E1.
Rheumatoid Arthritis, Adult

shows multiple thoracic
bodies & articular pillar
with abnormal/ow
=
T J signal
& a large paravertebral &
epidural mass. The mass is
typical for lymphoma, given
the infiltrate nature of the
body involvement without
bone destruction & low T2
signal (not shown). (Rigl1t)
extensive erosion of the
odontoid & C2 vertebral
body ~ There is erosive
disease also at the C2-3 and
C3-4 facet joints =.
Congenital Fusion Septic Facet Joint Arthritis

Fusion of multiple facet joints
~ in the lumbar spine.
There is also partial fusion of
the intervertebral disc spaces
= and hypoplasia of the
sacrum SlI. (Right) Axial TI
C+ MR shows a large
epidural abscess with thick
enhancement~. Note a
large psoas abscess = &
extension of the inFection to
the right facet joint with
diffuse facet bone
enhancement & juxta facet
soft tissue involvement a.
II
3
33
Vl FRACTURE, POSTERIOR ELEMENT
C
OJ
E
OJ
w DIFFERENTIAL DIAGNOSIS I I ESSENTIAL INFORMATION
Common Key Differential Diagnosis Issues
• Cervical • Must distinguish between isolated posterior
o Hyperextension Injury, Cervical column injury and multicolumn injury
>,
""0
o Burst Fracture, Cervical o Isolated posterior column
o o Hangman's C2 Fracture • Due to lateral flexion or rotation, direct
CO
CIl
~ o Lateral Flexion Injury, Cervical blow, or hyperflexion
.n
OJ o Jefferson Cl Fracture • Clay shoveler's fracture a stable
t
OJ o Burst Fracture, C2 hyperflexion injury
> o Clay Shoveler's Fracture o Multiple column
ell
c: o Hyperflexion-Rotation Injury, Cervical • Due to any injury mechanism, not
Co
en o Hyperflexion Injury, Cervical necessarily unstable
• Thoracic • Non-bony involvement of middle,
o Chance Fracture, Thoracic anterior columns often best seen on MR
o Burst Thoracolumbar Fracture Helpful Clues for Common Diagnoses
o Facet-Lamina Fracture, Thoracic
• Prevertebral soft tissues of cervical spine may
• Lumbar be normal in isolated posterior element
o Burst Fracture, Lumbar
fracture
o Spondylolysis
• Burst fracture: Posterior column fracture in
o Facet-Posterior Fracture, Lumbar
vertical plane
o Transverse Process Fracture
• Flexion-distraction fracture: Posterior
o Chance Fracture, Lumbar
column fracture in horizontal plane
o Pedicle Stress Fracture
• Spondylolysis easily missed on axial images;
• All Spinal Levels use following signs
o "Double facet" sign: Spondylolysis is
Less Common anterior to facet joint
• Fracture Mimics o "Wide canal" sign: Increased AP dimension
o Metastases, Lytic Osseous of spinal canal
o Neurogenic (Charcot) Arthropathy
o Vertebral Segmentation Failure
o Hypoplastic Rib, Supernumerary Rib
Hangman's C2 Fracture
II
3 Axial bone CT shows bilateral C2 pedicle fractures
indicating hangman's-type fracture.
=:I Axial bone CT shows le{l·sided (ractures of anterior It]
and posterior 8lI ring of C7. This is a variant Jefferson
fracture.
34
FRACTURE, POSTERIOR ELEMENT en
~.
:J
(l)
<
(l)
;:l.
(1)
Burst Fracture, Lumbar cr

~
OJ
(LeFI) Axial bone CT shows
L2 burst fracture. Unlike OJ
o
Chance fracture, posterior Q.
element fractures are

'<
vertically oriented I:'] and
there is retropulsion of
posterior vertebral body
cortex ICB (RighI) Axial bone
CT shows LS spondylolysis
m
81 anterior 10 lacet joints I:'] CO
(double Facet sign). AP 3
(1)
diameter of canal is widened :J
(wide canal sign). Ui
Transverse Process Fracture

isola led Iracture ollhe L 1
superior articular process II]
with minimal displacement.
Posterior element fractures
can be isolated, but a search
should always be made lor
other Iractures. (RighI)
isolated leFt L4 laleral process
fracture =. These fractures
are often associated with
retroperitoneal and pelvic
injuries.
Chance Fracture, Lumbar Incomplete Fusion, Posterior Element

L 7 Chance fracture
(flexion-distraction) with
characteristic horizontal
Iracture 81 01posterior
elements. Vertebral body is
compressed anteriorly IJ:;J.
(RighI) Anteroposterior
radiograph shows lailure 01
lusion 01 LS lamina I:'] and
absent spinous process. This
is a very common normal
variant.
II
3
35
en PEDICLE ABNORMALITY
C
ell
E
ell
W DIFFERENTIAL DIAGNOSIS o Decreased AP dimension of spinal canal
~ and neural foramina
o
"'ell" Common • Stress Reaction
C;; • Congenitally Short Pedicles
o o Abnormal biomechanicalloading across
0..
• Stress Reaction neural arch, associated with fractures of
• Trauma the pars and pedicle, and degenerative
• Thinning/Remodeling from Intraspinal or facet disease
~ Transforaminal Mass o Sclerosis (CT) or T2/STIR hyperintensity
.0
ell o Schwannoma (MR) ± visible pedicle or pars fracture
t
ell o Neurofibroma • Thinning/Remodeling from Intraspinal or
> o Perineural Root Sleeve Cyst
ell Transforaminal Mass
c: o Arachnoid Cyst
a. o Implies chronic mass effect/slow growth
m o Dural Dysplasia o Cortical margin should be intact on
o Meningocele, Lateral thin-slice bone algorithm CT
o Ependymoma • Metastases
• Destructive Tumor o Often multiple
o Metastases, Lytic Osseous o Thin-slice bone algorithm CT useful to
o Aneurysmal Bone Cyst differentiate bony destruction from benign
Less Common bony remodeling
• Sclerotic/Bone-Forming Tumor o Purely lytic: Renal, thyroid
o Metastases, Blastic Osseous o Purely sclerotic: Prostate, carcinoid,
o Fibrous Dysplasia bladder
o Osteoid Osteoma o Mixed sclerotic &/or lytic: Lung, breast
o Osteoblastoma Helpful Clues for Less Common Diagnoses
o Osteosarcoma • Osteomyelitis, Granulomatous
• Osteomyelitis, Granulomatous o Bony destruction
• Achondroplasia o Epidural/paraspinal abscesses with
• Congenitally Absent or Hypoplastic Pedicle irregular marginal enhancement
• Congenitally Short Pedicles
o Predominately lower lumbar spine
Congenitally Short Pedicles Stress Reaction
II
3 Axial NECT shows a typical case of shari lumbar
pedicles resulung in congenital spina.l stenosis with Ule
characteristic trefoil spinal canal cross section.
within the left L4 pedicle=
Sagittal STIR MR shows abnormally hyperintense signal
in lhis 15 year old who
'aler developed a pedicle stressfracture on CT
36
PEDiClE ABNORMALITY
Schwannoma Arachnoid Cyst

shows marked thinning and OJ
o
superior displacement of an c.
'<
L I pedicle!:ll associated
with foraminal
remodeling/enlargement ~
lransforaminalschwannoma.
(Right) Axial pos/-myelogram
m
NECT shows thinning of lhe CO
pedicles l:l1 due to chronic 3
C1l
remodeling by an intraspinal :J
arachnoid cysl EJ. en
Metastases, Blastic Osseous

lumbar canal scalloping lhe
posterior vertebral body and
markedly remodeling and
thinning lhe verlebral
pedicles bilalerally l:l1.
blastic lID metastasis in the
lefl L4 pedicle due to
prostate carcinoma. Note the
permeative lytic lesions in
lhe ver/ebral body.
Osteomyelitis, Granulomatous
(Left) Sagillal T I WI MR
shows destructive process in
L2 body eXlending into
pedicle wilh abnormal
hypoinlense signal and loss
of superior cortex =.
Epidural phlegmon ex/ends
lhrough adjacenl
neuroForamina. (Right) Bone
CT (30 surface shaded
display) shows congenilal
absence of lhe righl L5
pedicle EJ. L5 spinous
process and righl pars are
fused to the L4 neural arch
EB
II
3
37
en ENLARGED VERTEBRAL BODY, SOAP BUBBLE EXPANSION
C
Q)
E
Q)
w DIFFERENTIAL DIAGNOSIS o Ovoid expansile mass originating in the

~ neural arch, often extend into the
o
·C
Q)
Common vertebral body
u; • Metastases, Lytic Osseous
o o 40% in spine
CL
o Lung Carcinoma • 40% cervical, 25% lumbar, 20% thoracic,
>-
"0 o Thyroid Carcinoma 15-20% sacrum
o o Renal Cell Carcinoma
CO o Florid edema (corona effect) suggests an
ro~ • Multiple Myeloma aggressive process, attributable to
.D
Q) • Osteoblastoma prostaglandin release by the tumor
t
Q) • Giant Cell Tumor o Peri tumoral edema enhances avidly with
> • Aneurysmal Bone Cyst
Ql gadolinium administration
c:
.0. Less Common o Usually demonstrates more discrete bone
In matrix as compared to fibrous dysplasia
• Chordoma
• Chondrosarcoma o Bone scan demonstrates avid radionuclide
uptake by the tumor
Rare but Important
• Giant Cell Tumor
• Fibrous Dysplasia o Expansile, lytic lesion with narrow zone of
• Telangiectatic Osteosarcoma transition
• Enchondroma o ± Cortical breakthrough
• Angiosarcoma o Centered in vertebral body
• Cystic Angiomatosis o Margin usually not sclerotic
o ± Residual bone trabeculae
ESSENTIAL INFORMATION • Aneurysmal Bone Cyst
o Expansile lesion may show cortical
Key Differential Diagnosis Issues breakthrough
• Zone of transition is helpful to assess o Shows a narrower zone of transition
aggressiveness o Centered in posterior elements
• Multiplicity of lesions, soft tissue o Can be associated with fibrous dysplasia
component, & vascularity of lesions can be
helpful in narrowing the differential Helpful Clues for Less Common Diagnoses
diagnosis • Chordoma
o Midline soft tissue mass with osseous
Helpful Clues for Common Diagnoses destruction
• Metastases, Lytic Osseous o T2 hyperintense mass with multiple septa
o Lung, thyroid, renal, breast,
o Can involve adjacent vertebral bodies by
oro-/nasopharyngeal carcinoma extension across disc space
• Destructive lesion involving the posterior o Arise from notochord remnants
cortex & pedicle • Chondrosarcoma
• Intervertebral discs are spared o Lytic mass ± chondroid matrix, "rings &
• Location proportionate to red marrow arcs"
(lumbar> thoracic> cervical) o Cortical disruption
• Multiple Myeloma o Extension into soft tissues
o Multifocal malignant proliferation of o Nonenhancing areas: Hyaline cartilage,
monoclonal plasma cells leads to cystic mucoid tissue, necrosis
heterogeneous Tl marrow signal o Neural arch involved more frequently than
o May be expansile, but vertebral
vertebral body
compression is more common
o Vertebral body more frequently involved Helpful Clues for Rare Diagnoses
o Pedicle involvement later than with • Fibrous Dysplasia
metastases o Well-defined, expansile, radiolucent lesion
II • Osteoblastoma o Neural arch involved more frequently than
the vertebral body
3
38
ENLARGED VERTEBRAL BODY, SOAP BUBBLE EXPANSION
o Spine involvement typically in polyostotic Coarse trabecular/honeycomb pattern is

o
disease suggestive of a vascular tumor
o Fusiform bone expansion with • Cystic Angiomatosis
"ground-glass" matrix o Lytic, well-defined, round or oval lesions
o Heterogeneous T1/T2 signal & within the medullary cavity
heterogeneous enhancement o Intact cortex & variable peripheral sclerosis
o Paraspinal soft tissue extension & vertebral o Endosteal scalloping & honeycombed or
collapse rare latticework appearance
o Prevalence of scoliosis in patients with o Discrete circular or serpentine lytic areas
polyostotic fibrous dysplasia & spinal within bone suggest vascular channels m
lesions is reported between 40% and 52% o No periosteal reaction CO
3
ctl
• Telangiectatic Osteosarcoma :::J
o Wide zone of transition with adjacent en
SELECTED REFERENCES
bone
1. Leet AI et al: Fibrous dysplasia in the spine: prevalence of
o Permeative appearance & cortical lesions and association with scoliosis. J Bone Joint Surg
disruption Am. 86-A(3):531-7, 2004
o Multiple fluid-fluid levels 2. Murphey MD et al: From the archives of the AFIP.
Musculoskeletal angiomatous lesions: radiologic-pathologic
o Soft tissue mass ± mineralization correlation. Radiographies. 15(4):893-917, 1995
• Enchondroma 3. Kumar R et al: Expansile bone lesions of the vertebra.
Radiographies. 8(4):749-69, 1988
o Expansile, homogeneous, slightly
enhancing lesion with or without
calcification
• Arise either from migration of
hyperplasitic immature spinal cartilage
outside vertebral axis
• Or from metaplasia of connective tissue
in contact with the spine or annulus
fibrosus
o Common benign cartilaginous tumour
involving the acral skeleton but extremely
rare in the vertebral column (2% of cases)
• Angiosarcoma
o Lumbar region is most commonly affected
o 33% in axial skeleton
lung Carcinoma Thyroid Carcinoma
II
=
SagillalSTfR MR shows a hyperintense lesion expanding
a
a thoracic verlebral body the articular facels &
Axial NECT shows a lytic lesion = involving the C3
body & lefl facelliamina wilh thin expansile bony
3
epidural space 1:2. margin. A soft tissue component SI in the lefl lateral
epidural space is beller seen on MR (not shown).
39
c
(/)
Q)
E
Q)
l1J
~
o
'C
Q)
Renal Cell Carcinoma Renal Cell Carcinoma
U5 (Left) Sagittal T7WI MR
o
a.. shows a large expansife mass
>.
-0
o
[IJ
of T7 & TB bodies
considerable epidural
=-
involving the ribs & right side
with
ctl extension ~. (Rig"') Axial

~ T7WI MR shows a large mass
.0
Q)
t destroying the right aspect of
Q) a mid-thoracic vertebral
> body, the right posterior
Cl> elements, and the right ribs &
c:
'0. costovertebral joint. Epidural
l/l extension causes cord
compression The ventral
margin shows bony
expansion with a "soap
bubble" pattern =:l.
Multiple Myeloma Osteoblastoma

(Left) Sagittal T7 C+ FS MR
shows [ocal tumor
involvement with
enhancement E:I with
replacement of the vertebral
& posterior element marrow
by tumor and slight spinous
process expansion~. There
is severe cord compression
at both levels. (Right) Axial
bone CT shows a
well-demarcated expansile
lesion with a narrow zone of
transition & ground-glass
matrix~. Minimal cortical
destruction with extension
into the right lateral recess is
present ~.
Osteoblastoma Giant Cell Tumor

shows extensive reactive
edema =
in the adjacent
posterior elements, vertebral
body, & sort tissues related
to an asteoblastoma. The
peritumoral edema enhances
avidly with gadolinium
administration. (Rig"') Axial
CECT shows a lytic,
vertebral body mass ~ with
posterior cortical
breakthrough. Mass extends
into the right pedicle =:l.
II
3
40
Aneurysmal Bone Cyst Chordoma

a multi/oculated mass
containing multiple
fluid-fluid levels of mixed
signal intensity, ,eflecting -u
blood products. Note
o
en
nodular enhancement of ro-
=:!.
solid componenlS & seplae o
~
between di/ated, blood-filled
m
spaces. Severe canal ro
compromise by the tumor. 3
(Right) Axial NECT shows a <1l
:J
destructive, lytic lesion with Ui
associated sofllissue
expanding lhe occipilal
condyles & skull base 81.
The anterior margin has a
scalloped appearance 1:':1.
Chordoma Chondrosarcoma
(Left) Coronal oblique S71R
MR shows a well-defined
mass involving the central
aspect of the sacrum, with
T2/STIR hyperintensily &
patchy contrast
Sagittal T7 C+ MR shows a
large, intensely enhancing
soft tissue mass with
vertebral body & posterior
element involvement ~ and
cord compression.
enhancement of septa results
in a ring & arc pattern.
Telangiectatic Osteosarcoma
{ocal expansion of the lamina
and spinous process of L2
with areas of cyst formation
1:':1
& ill-defined calcific
malrix. (Right) Axial T' C+
MR shows an aggressive
mass ~ in the L5 vertebral
body & extending into the
posterior elements, spinal
canal, paraspinous soft
tissues. Enhancement of solid
components -7 surrounds
nonenhancing, low signal
cystic areas m.
II
3
41
c
(/)
VERTEBRAL BODY SCLEROSIS, FOCAL
Q)
EQ)
w DIFFERENTIAL DIAGNOSIS a Multiple vertebral bodies typically

o involved
.'"
Q)
Common o Sclerotic (e.g., prostate, carcinoid,
1iJ • Bone Island medulloblastoma, neuroblastoma) or
o
a.. • Hemangioma mixed sclerotic and lytic (breast, lung)
>-
"0 • Degenerative Endplate Changes • Insufficiency Fracture, Pedicle
o
al • Metastases, Blastic Osseous a Reactive sclerosis of portions of the neural
ro
~ • Insufficiency Fracture, Pedicle arch associated with abnormal
-"1::
Q) • Vertebroplasty/Kyphoplasty biomechanicalloading
Q) • Compression Fracture a Can be seen with chronic fractures of the
>
Gl Less Common contralateral pedicle or pars,
c:
0- • Chronic Osteomyelitis developmentally incomplete neural arch,
m or advanced degenerative change
• Early Ankylosing Spondylitis
• Osteoid Osteoma • Compression Fracture
a Sclerosis can be seen resulting from either
trabecular impaction or from the healing
ESSENTIAL INFORMATION response
Helpful Clues for Common Diagnoses Helpful Clues for Less Common Diagnoses
• Bone Island • Chronic Osteomyelitis
a Most common cause of a focal sclerotic a Advanced destructive endplate changes,
density paravertebral soft tissue &/or fluid
a Cortical bone density with faint, a Typically more extensive involvement of
spiculated border the adjacent vertebral bodies than seen
a Normal uptake on bone scan with degenerative end plate changes
• Hemangioma • Early Ankylosing Spondylitis
a Coarse, thickened vertical trabeculations a Erosions and reactive sclerosis result in
• Degenerative Endplate Changes square vertebral bodies and "shiny corners"
a CT analog to type 3 marrow on MR • Osteoid Osteoma
a Should see advanced degenerative change a Central lytic focus with surrounding
in the adjacent disc space (reactive) bony sclerosis
a Extensive end plate sclerosis: Consider a Classic history is night pain, relieved by
chronic osteomyelitis aspirin/NSAIDs
• Metastases, Blastic Osseous
Bone Island Hemangioma
II
3 Axial bone CT shows dense, corticalbone density lesion
=:I with characteristic appearance of a bone island,
Axial bone CT shows characteristic appearance of a
benign vertebral hemangioma, with circumscribed
including spiculated or Ilbrush-like" margins and border and sparse, thickened trabeculae.
absence of destructive changes.
42
VERTEBRAL BODY SClEROSIS, FOCAL
<
CD
;:+
CD
CT
Metastases, Blastic Osseous ~
III
shows marked discogenic OJ
o
sclerosis at L2-3 EliJ in an a.
asymmetric distribution due
'<
to scoliosis and
lateral-lis thesis. (Right) Axial
NECT shows both blastic =:I
and somewhat expansile lytic
prostate carcinoma
m
metastases involving the CD
T 12 vertebral body. 3
CD
OJ
en
Insufficiency Fracture, Pedicle

developmentally incomplete
neural arch !D. Chronic
stress changes include
hypertrophy/sclerosis of the
left pedicle and stress
fracture of the left lamina EliJ.
(Right) Sagittal bone CT
shows compression fracture
of inferior 13 body ~ Note
increased sclerosis secondary
to trabecular impaction.
Remote appearing
compression fracture of L 1
and acute L5 compression
fracture also present =.
Osteoid Osteoma
shows squared configuration
of the anterior vertebral body
cortices and the
characteristic "shiny corner"
sign ~ of early ankylosing
spondylitis. fRight) Axial
bone CT shows an osteoid
osteoma in the neural arch
[;8 that contains bone matrix
and has a narrow zone of
transition. Reactive sclerosis
is present around the lesion.
II
3
43
en VERTEBRAL BODY SClEROSIS, DIFFUSE
CQ)
EQ)
i:iJ DIFFERENTIAL DIAGNOSIS o Typically involves multiple vertebral

~ bodies
.g Common
Q) o Metastases from prostate, breast, carcinoid,
Vi • Discogenic Sclerosis and urothelial primaries; in children:
o
a.. • Metastases, Blastic Osseous Neuroblastoma and medulloblastoma
>-
"0 • Chronic Discitis/Osteomyelitis • Chronic DiscitislOsteomyelitis
o • Healing Fracture
CO o Marrow sclerosis typically associated with
[I:l • Renal Osteodystrophy other findings of chronic infection
.0
Q) • Paget Disease • Advanced end plate destruction
t
Q) • Sickle Cell Disease • Paravertebral/epidural soft
>
Q) less Common tissue/phlegmon
c:
a. • Osteopetrosis • Renal Osteodystrophy
lI)
• Osteosarcoma o Osteopenia or osteosclerosis
• Myelofibrosis o May manifest with endplate sclerosis
("rugger jersey" spine)
Rare but Important
• Paget Disease
• Radiation o Patchy or diffusely sclerotic "picture frame"
• Sclerotic Myeloma vertebra due to cortical thickening
• Lymphoma o Vertebral body usually enlarged
• Hypervitaminosis A or D • Sickle Cell Disease
• Fluorosis o Medullary sclerosis due to multiple bone
infarcts
ESSENTIAL INFORMATION o Central end plate compression deformities,
causing classic "H-shaped" vertebral body
• Discogenic Sclerosis Helpful Clues for Rare Diagnoses
o Sclerotic endplate marrow, correlates to • Lymphoma
type 3 Modic changes on MR, involving o Diffuse vertebral sclerosis ("ivory vertebra")
both sides of the disc space is a rare presentation of lymphoma in the
o Endplate destruction or abnormal spine
paravertebral soft tissue should prompt
consideration of chronic osteomyelitis SELECTED REFERENCES
• Metastases, Blastic Osseous
1. Graham TS: The ivory vertebra sign. Radiology.
235(2):614-5, 2005
Discogenic Sclerosis Metastases, Blastic Osseous
II
3 Sagittal NECT shows severe disc space narrowing at
L5-SI with vacuum phenomenon and diffusely
Sagittal CECT (CT myelogram) shows an osteoblastic
metastasis (carcinoid primary) in the 13 vertebral body
increased sclerosis in the adjacent marrow spaces of L5 with 50ft tissue extension into the ventral epidural space
and the first sacral segment. causing canal stenosis.
44
VERTEBRAL BODY SClEROSIS, DIFFUSE (Jl
"0
:J
CD
<
CD
;+
CD
Chronic Discitis/Osteomyelitis cr
~
III
marked sclerosis of the L3 CO
o
and L4 bodies with extensive Cl.
endplate irregularity and
'<
bone destruction in this
patient with chronic
sequelae of pyogenic disc
space infection. (Right) Axial
CECT shows sclerotic
m
vertebral body secondary to CD
renal osteodystrophy. Note 3
CD
small nonfunctioning kidneys :J
=. Ui
Sickle Cell Disease

shows a lypical case of
vertebral Paget disease with
a diffusely sclerotic and
slighlly enlarged L3 vertebral
body 81. (Right) Coronal
NECT of this patient with
sickle cell anemia shows
diffuse vertebral sclerosis and
multiple central endplate
compression deFormities.
Osteopetrosis
shows diffuse sclerosis of the
vertebral bodies. This
appearance mixes the
features of Ilrugger jersey"
and "bone in bone"
presentations of
osteopetrosis. (Right) Sagittal
NECT shows diffusely
sclerotic thoracic vertebra
("ivory vertebra") in this
patient with lymphoma.
II
3
45
<J>
C VERTEBRAL BODY THICKENED BONY TRABECULAE
Q)
E
Q)
W DIFFERENTIAL DIAGNOSIS • Osteoporosis
~ o Marrow heterogeneity with focal islands of
o
·C
Q) Common red marrow & centers of fat
<;; • Hemangioma
o o Focal deposits of yellow marrow, esp. in
0...
• Paget Disease posterior elements, around central venous
>, • Osteoporosis
-0 channels, & adjacent to endplates
o
(l)
ro
~
.n • Fibrous Dysplasia • Fibrous Dysplasia
Q)
t • Plasmacytoma o Ground-glass matrix in mildly expanded
Q)
> Rare but Important lesion of the neural arch> vertebral body
Ql
c: • Metastases, Blastic Osseous • Plasmacytoma
Co
• Lymphoma o Originate in the vertebral body, although
en
involvement of the posterior elements not
uncommon
ESSENTIAL INFORMATION o Endplate fractures produce curvilinear low
Key Differential Diagnosis Issues signal areas &/or cortical irregularities
• Vertebral expansion in Paget disease, fibrous • Thickened cortical struts in expanded
dysplasia, plasmacytoma vertebral body, "mini brain"
• Hemangioma • Metastases, Blastic Osseous
o Corduroy pattern of thickened trabeculae o Vertebral body, esp. posterior cortex, &
& intervening fat pedicle are involved
o Aggressive lesions are characterized by o Sclerotic lesions may be discrete &
epidural extent & cord compromise nodular, mottled, or diffusely increased
o Tl/T2 hyperintense density
• Paget Disease o Hypointense on Tl WI & T2WI
o Coarsened & irregular bony trabecular o Variable enhancement depending on
pattern with cortical thickening degree of sclerosis
o Heterogeneous, predominantly • Lymphoma
hypointense on T1 & hyperintense on T2 o Bony lymphomatous involvement results
o Vertebral expansion leads to varying from hematogenous spread (95%)
degrees of spinal & neural foraminal o Diffuse, mottled pattern with reduced
stenosis signal on Tl & T2 sequences
Hemangioma
II
3 Sagittal T7WI MR shows a hyperintense L4 vertebral
lesion m without epidural expansion. hemangioma with thickened trabecula
cortex, & focal low attenuation
=
Sagittal NECT shows classic honeycomb appearance of
= intact
between trabeculae.
46
VERTEBRAL BODY THICKENED BONY TRABECULAE
<
CD
;:l.
CD
0-
Paget Disease Osteoporosis ~
OJ
(Lefl) Sagiltal TI WI MR
OJ
L2 vertebral body
enlarged
=-
demonstrates an abnormal
mildly
in AP dimension,
o
c.
'<
with slight height 1055& TI
shortening from increased
marrow fat. There is
enlargement &
heterogeneous signal in the
m
spinous process 8l ro
reflecting more fibrovascular 3
tissue content. (RighI) CD
:J
Sagiltal TlWI MR shows Vi
chronic L3 & TI 0 Iraclures
~ with laity marrow signal.
The L2 & T I 2 Iraclures are
acute with low signal
superior endplates l:i1.

shows extensive ground-glass
vertebra/lesions. There is
osseous expansion with
mixed sclerosis, lytic, &
ground-glass changes 01
the skull base, lace, spine, &
calvarium in a patient with
severe polyostotic librous
dysplasia. (RighI) Coronal
bone CT shows vertebra
plana at CS secondary to
plasmacytoma. There is a
mixed sclerotic and lytic
lesion [3>] 01 the vertebral
body.
(Lell) Sagiltal TI WI MR
shows multiple local
hypoinlenS€ areas in the
upper thoracic vertebral
bodies with epidural
extension & cord
compression 1tJ. There is a
pathologic lower thoracic
Iraclure 81 with no bony
retropulsion. (RighI) Sagiltal
NECT shows sclerotic
metastatic lesion from
lymphoma.
II
3
47
c'" VERTEBRAL BODY, 11 HYPERINTENSE SIGNAL, DIFFUSE
(!)
E
~ o More frequently seen in older patients
w
~
o • Osteoporosis
'C
(!)
Common o Decreased cellular marrow elements with
U; • Post-Irradiation Vertebral Marrow
o proportionally greater marrow fat content
0..
• Normal Variant o Osteopenia on CT or plain radiography
>-
"0 • Heterogeneous Fatty Marrow may help assist diagnosis
o
en • Osteoporosis
ro~ Helpful Clues for less Common Diagnoses
.0
less Common • Hemangiomas (Multiple)
(!)
t • Hemangiomas (Multiple) o Fatty stroma within well-delineated benign
(!)
> • Paget Disease indolent vertebral body tumors

Ql
r:: o Rarely a diagnostic dilemma
'Q. • Distinct fat signal intensity masses
en ESSENTIAL INFORMATION
within more conventional appearing
Key Differential Diagnosis Issues marrow distinguishes from diffuse
• Establish whether pattern is diffusely hyperintensity of fatty marrow involving
hyperintense marrow signal or multiple foci entirety of vertebral body marrow
of hyperintensity within more cellular • Paget Disease
marrow o Fibrovascular marrow in active phase
Helpful Clues for Common Diagnoses • Heterogeneous but predominantly
• Post-Irradiation Vertebral Marrow hypointense on Tl WI MR, hyperintense
o Diffuse hyperintense fatty marrow signal on T2WI MR
intensity within correct clinical context • Interspersed foci of fatty marrow
o Look for abrupt sharp demarcation • Post-gadolinium enhancement helps
between hyperintense fatty marrow and distinguish from diffuse fatty marrow
lower signal intensity normal marrow at o Fatty marrow in mixed phase
peripheral margin of radiation field • Hyperintense on TlWl and T2WI MR
• Normal Variant • Most often imaged in this phase
o Normal marrow complement of fat and • Involved vertebral body may be
cellular elements increased in size compared to normal
o More frequently seen in older patients adjacent vertebrae
• Heterogeneous Fatty Marrow
o Multiple patchy areas of fat signal
intensity within multiple vertebral bodies
Post-Irradiation Vertebral Marrow Post-Irradiation Vertebral Marrow
II
3 SagiNal T7 c+ MR demanslIates diffuse ve,tebral
marrow hyperintensity following craniospinal irradiaUon
Sagittal T7WI MR shows typical bright T7 hyperintensity
for CSFdisseminated aligoaslIocytoma metastases =. in the vertebral marrow at irradiated spina/levels in this
patient with breast adenocarcinoma.
48
VERTEBRAL BODY, 11 HYPERINTENSE SIGNAL, DIFFUSE CJl
"S!.
:l
ct>
<
<ll
;::I.
<ll
0-
Normal Variant Normal Variant ,
OJ
(Left) Sagittal T7 WI MR in an
elderly patient with diffuse CD
o
falty marrow and spondylitic c.
myelopathy shows diffuse
'<
marrow hyperintensity
related 10 fat content. (Right)
Sagittal T7WI MR in an older
patient with post-operative
spondylolisthesis at L4-5
m
reveals diffuse increased fally <ll
marrow signal intensity. 3
<ll
:::l
en
Heterogeneous Fatty Marrow Osteoporosis

demonstrates variant
heterogeneous fatty marrow
signal intensity in an elderly
patient with multilevel
degenerative disc disease.
shows diffusely increased
fatty marrow signal inlensity
with numerous compression
fractures at multiple levels.
Marrow signal intensity
within the fractures varies
from hypoinlense in the
acute fractures =:I to
hyperintense in a chronic
fracture~.

demonstrates one large =
and two small E!ilI fatty
stroma vertebral
hemangiomas. Diagnosis is
slightly harder because of
background mild diffuse fatty
marrow content. (Right)
Sagittal T7WI MR shows an
abnormal L2 vertebral body
=:I that is mildly enlarged in
anteroposterior dimension,
with slight height loss and T7
marrow fat.
II
3
49
rn VERTEBRAL BODY, 11 HYPERINTENSE SIGNAL, FOCAL
C
Ql
E
.!!!
w DIFFERENTIAL DIAGNOSIS o Type 2: Hyperintense on 1'1WI, isointense
~ on T2WI
o
·C
Ql
Common o Type 3: Hypointense on 1'1WI and T2WI
ii5 • Normal Variant • Focal Fatty Marrow
o
a.. • Hemangioma o Discrete focus of 1'1 hyperintensity
:>, • Degenerative Endplate Changes representing macroscopic collection of fat
u
o • Focal Fatty Marrow
co interspersed with cellular marrow elements
ro
~ • Gadolinium Enhancement o Suppresses on fat-saturated or STIR MR
~
Ql
less Common imaging
t::
Ql
• Paget Disease • Gadolinium Enhancement
> 01'1 shortening produces high 1'1 signal
Q)
c
• Metastasis, Melanoma
a.
intensity
en Rare but Important o Chemical fat saturation or STIR MR
• Vertebral Marrow Hemorrhage imaging will not abolish 1'1 shortening
(unlike fat)
Key Differential Diagnosis Issues • Paget Disease
• Use fat saturation &/or STIR MR imaging to o Enlarged vertebra and neural arch with
distinguish fat from other etiologies of 1'1 trabecular coarsening and cortical
hyperintensity thickening
• Metastasis, Melanoma
Helpful Clues for Common Diagnoses o Melanotic metastases may demonstrate 1'1
• Normal Variant hyperintensity on unenhanced 1'1WI MR
o Heterogeneous marrow signal related to
interspersed normal fat and hematopoietic Helpful Clues for Rare Diagnoses
elements in vertebral body • Vertebral Marrow Hemorrhage
• Hemangioma o Subacute blood products will demonstrate
o Benign vertebral body vascular tumor with 1'1 shortening
hyperintense 1'1 signal intensity o Consider underlying mass lesion (may be
o Usually incidental lesion identified on occult)
imaging performed for unrelated reasons
• Degenerative Endplate Changes
o Type 1: Hypointense on 1'1WI,
hyperintense on T2WI
II
3 Sagilwl T1WI MR depic15 scallered foci of marrow
hyperintensity, reflecting normal variation of vertebral
Sagillal T1WI MR reveals a hyperinlense L4 verlebral
body lesion =:I without epidural expansion. T1
marrow comfXJsition. shortening represents the fatty stromal component.
50
VERTEBRAL BODY, 11 HYPERINTENSE SIGNAL, FOCAL VI
"0
::::J
ell
<
ell
;::l.
<1l
Degenerative Endplate Changes c:r
~
Q)
reveals focal fal =.:I adjacent OJ
o
to verlebral endplales al a.
L4-5, characteristic of
'<
marrow changes. The fal
merges with adjacenl
erythropoietic marrow.
(Right) Sagillal TlWI MR
shows multilevel disc space !:!l
<1l
narrowing and disc bulges in 3
mid and lower lumbar spine. <1l
::::J
Note rally marrow adjacent en
to degeneraled endplales
8l a frequenl finding of
degenerative disc disease.
Gadolinium Enhancement
demonstrates
well-circumscribed focal
fally verlebral marrow =.:I
mimicking a vertebral
hemangioma. (Right) Sagillal
T1 C+ MR demonslrales an
enhancing L3 colon
carcinoma metastasis =
with posterior epidural
extension. Signal intensity is
similar to fat. Fat saturation
techniques are useful to
distinguish fal from
enhancement.
Paget Disease Vertebral Marrow Hemorrhage

shows an abnormal L2
vertebral body =.:I wilh
mildly enlarged
anteroposterior dimension,
mild heigh I loss, and TI
marrow fal. (Right) Axial
T1 WI MR (aneurysmal bone
cyst) shows extensive
cortical destruction around
1/2 of spinal canal and
severe canal compromise by
tumor NOle mulliloculated
mass containing mulliple
fluid-fluid levels. Mixed
signal intensity reflecls the
presence of blood products.
II
3
51
en VERTEBRAL BODY, 11 HYPOINTENSE SIGNAL, DIFFUSE
C
Q)
E
~ • Less likely to produce erroneous
w
~
o diagnosis of marrow infiltration as
'C
Q) Common radiologist gains experience using this
1ii • Hyperplastic Vertebral Marrow
o technique
0...
• Normal Variant (Technical) • Neoplasm
>- • Neoplasm o Metastases, Blastic Osseous
"o
[!J o Metastases, Blastic Osseous • Hematogenous systemic dissemination
ro
~ o Leukemia (arterial or venous via Batson plexus) >
.0
Q) o Lymphoma perineural, lymphatic, CSF spread
t::
Q) o Multiple Myeloma • Marrow initially infiltrated, trabeculae
>
Q) Less Common destroyed, then subsequently bone
c:
'Q. • HIV cortex destroyed
III
• SickJe Cell • Blastic rather than lytic presentation
• Renal Osteodystrophy occurs when bone production exceeds
bone destruction
Rare but Important o Leukemia
• Myelofibrosis • Acute or chronic, myeloid or lymphoid
• Osteopetrosis white blood cell neoplasia with spinal
• Fibrous Dysplasia involvement as component of systemic
• Extramedullary Hematopoiesis disease burden
• Single or multiple vertebral involvement
ESSENTIAL INFORMATION • Most common (classic) spinal
presentation is diffuse osteopenia with
Key Differential Diagnosis Issues multiple vertebral fractures ± lytic spine
• Determine whether there is diffusely lesions
abnormal hypointense vertebral marrow o Lymphoma
signal intensity or scattered patchy areas of • Lymphoreticular neoplasms with wide
hypointensity within multiple vertebra variety of specific diseases & cellular
• Hypointense marrow appearance by itself is differentiation
relatively nonspecific; look for ancillary • Variable imaging manifestations
clues that may permit a specific diagnosis o Multiple Myeloma
Helpful Clues for Common Diagnoses • Multifocal malignant proliferation of
• Hyperplastic Vertebral Marrow monoclonal plasma cells within bone
o Physiologic process in which fatty marrow marrow
is converted to red marrow in response to • Multifocal, diffuse, or heterogeneous Tl
systemic stress hypointensity; may be diffusely
o Intervertebral discs are hyperintense hypointense in high disease burden,
compared to vertebral marrow on Tl WI particularly if accompanied by severe
• Normal Variant (Technical) anemia
o Marrow demonstrates hypointense signal
artifactually due to MR pulse sequence
• HIV
technique o Marrow hypointensity reflects generalized
o Commonly observed when Tl FLAIR
anemia
imaging is used at higher field (2; 3T) • Need high index of suspicion to
imaging to reduce patient heating related specifically diagnose in absence of
to specific absorbed radiation (SAR) ancillary findings
o Tl FLAIRproduces lower marrow signal
• Sickle Cell
intensity in normal bone marrow o Hereditary hemoglobin abnormality
compared to that observed using spin echo resulting in anemia, deformed (sickle) red
II or fast spin echo Tl WI MR technique cells that occlude blood vessels
3
52
VERTEBRAL BODY, 11 HYPOINTENSE SIGNAL, DIFFUSE (II
~.
::l
<l>
o Classic imaging appearance: Marrow • Osteopetrosis <
CD
hypointensity with multiple H-shaped o Heterogeneous grouping of hereditary ::l.
CD
vertebral bodies osteoclast disorders Cl"
....•
OJ
o Differing disease severity depending on o Diffuse increase in bone density and
CD
hemoglobin subtype(s) and whether thickened bone cortex involving entire a
<>-
patient is homozygous or heterozygous skeleton '<
• Homozygous: HbSS (sickle cell anemia) • Fibrous Dysplasia -u
a
• Heterozygous: HbSA (sickle cell trait, o Best diagnostic clue: Mildly expansile (/)
m
asymptomatic), HbSC (less severe form) lesion with ground-glass bone matrix :J.
a
....•
o Sickle cell crisis: Acute episode of severe o Monostotic: Single bone lesion only m
bone, abdomen, chest pain • Monostotic disease usually an incidental co
3
• Renal Osteodystrophy finding CD
:J
o Bony changes attributable to chronic, o Polyostotic: Bone lesions in multiple bones Cii
end-stage renal disease • Usually presents in first or second decade
o Secondary hyperparathyroidism (HPTH), • Often associated with growth
osteomalacia, bone sclerosis, aluminum disturbances, pathological fractures
toxicity contribute to findings through abnormal weakened bone
o Best diagnostic imaging clue: "Rugger o McCune-Albright syndrome: Polyostotic
jersey" spine FD, precocious puberty, cafe-au-Iait skin
Helpful Clues for Rare Diagnoses lesions
• Myelofibrosis
o Epidural ± paravertebral proliferation of
o Very low signal intensity noted in bone
hematopoietic tissue in response to
marrow on all MR pulse sequences
profound chronic anemia
o Myelodysplastic syndromes:
o Minimally enhancing isointense thoracic
Myeloproliferative disorders that may
intra- or paraspinal soft tissue masses in
show myelofibrosis at some point in their
conjunction with diffuse marrow
evolution
hypointensity
• "Primary" form may be a precursor to
o Consider when thoracic
polycythemia vera and chronic myeloid
epidural/paraspinal isointense masses
leukemia
detected in patients with
• More commonly reflects a secondary
hemoglobinopathies or myeloproliferative
phenomenon secondary to leukemia,
disorders
lymphoma, or metastatic tumor
Normal Variant (Technical)
II
Axial T1WI MR in a chronic anemia patient shows
homogeneous hYfXJintense vertebra and iliac wing bone
Sagittal
artifactual
T1 WI MR in caudal
diffuse marrow
regression
hYfXJintensity
syndrome shows
on T1 inversion
3
marrow signal inlensil~ darker than the adjacent recovery IT1 FLAIR) pulse sequence used to limit SAR &
muscles. patient heating at 3.0 Tesla.
53
en VERTEBRAL BODY, 11 HYPOINTENSE SIGNAL, DIFFUSE
C
Q)
E
Q)
w
•...
o
'C
Q)
Metastases, Blastic Osseous Metastases, Blastic Osseous
U;
o (Lefl) Sagittal T1 WI MR
ll. demonst,ates diffuse
metastatic infiltration of bone
>-
"0 marrow manifesting low
o
CD signal intensity. There is an
CO
•... epidu,al mass at L4 =.
.0 (RighI) Sagittal T1WI MR
Q)
1: shows ma,kedly decreased
Q) signal within all ve,teb,al
> bodies and poste,io,
CIl elements, with reversal of the
c:
'0.. usual adult disc/ve,teb,al
en body ,elationship (i.e., disc is
usually da,ke, than ve,teb,al
marrow).
leukemia leukemia
(Lefl) Sagittal T1WI MR in a
patient with chronic
myelogenous leukemia
shows diffuse hypoplastic
ma"ow signal T 1 C+ MR
(not shown) showed diffuse
marrow enhancement
reveals diffuse marrow
replacement manifesting as
marrow signal intensity lower
than that of adjacent
intervertebral discs.
HIV
(Lefl) Sagittal T1WI MR
shows diffuse,
homogeneous, hypoinlense
marrow signal and multiple
vertebral compression
fractures. Severe
compression fracture is
present at L2 =. Fractures
also involve superior
endplates of L4 and L5.
(Rigilt) Sagittal T1 WI MR
demonstrates mild marrow
hypointensity in an AIDS
patient with chronic anemia
and CMV poly,adieulopathy
II
3
54
VERTEBRAL BODY, T1 HYPOINTENSE SIGNAL, DIFFUSE
<
(1)
;:l.
(1)
0-
Sickle Cell
(Left) Sagiltal Tl WI MR
m
shows diffuse hypointense OJ
a
marrow signal intensity and a.
central endplale depressions
'<
at multiple levels. Diffuse
low marrow signal indicates
hemosiderin deposition from
multiple transfusions or
myelofibrosis. (Right) Sagiltal
m
TlWI MR demonstrates low (1)
marrow signal intensity 3

(1)
within the vertebral bodies :J
and multiple endplate Ui
compression fractures.
shows homogeneous low
bone marrow signal intensity
secondary to fibrosis.
Marrow signal intensity is
lower than the intervertebral
disc signal, indicating this is
not erythropoietic marrow.
depicts typical
homogeneous, markedly
hypointense vertebral
marrow in a patient with
myelofibrosis.
Osteopetrosis
shows dense, sharply
demarcated bands of low
signal intensity due to bony
sclerosis. Note that sclerosis
and trabecular thickening are
also present centrally in the
vertebral bodies. Tl WI
would show similar low
signal intensity. (Right)
Sagiltal T I WI MR reveals
hypoinlense marrow signal
in the clivus and odontoid
process in this patient with
polyostotic fibrous dysplasia.
II
3
55
rn
C VERTEBRAL BODY, 11 HYPOINTENSE SIGNAL, FOCAL
OJ
E
OJ
l1J DIFFERENTIAL DIAGNOSIS • Bone Island
~ o Focal sclerotic lesion, markedly
.g Common
OJ hypointense on all sequences, with normal
Ul • Basivertebral Vein
o marrow signal elsewhere
a.. • Schmorl Node o CT may be useful to confirm diagnosis
>- • Bone Island
-0
o
• Hemangioma (Atypical)
[]) • Hemangioma (Atypical) o Some lipid-poor hemangiomas are
~CO • Fracture isointense or hypo intense to marrow on
.0
OJ • Surgical Material TlWI
t
OJ o Metallic Hardware o Bone algorithm CT can assess for
> o Bone Cement
OJ characteristic bony features (thickened
c:: • Osteomyelitis, Pyogenic
'Q. vertical trabeculae)
en • Osteomyelitis, Granulomatous • Fracture
• Degenerative Endplate Change (Types 1 & 3) o Fracture line often difficult to delineate on
• Metastases MR
• Multiple Myeloma o Associated marrow edema hypointense on
Less Common TlWI
• Limbus Vertebra • Osteomyelitis, Pyogenic
• Kummell Disease o Hypointense Tl marrow signal adjacent to
the level of infection
Rare but Important
• Metastases
• Vertebral Pneumatocyst o Nearly all metastases hypointense on
Tl WI, whether blastic or lytic
ESSENTIAL INFORMATION o Multiple lesions typical
• Limbus Vertebra
Helpful Clues for Diagnoses
o Unfused fragment of the ring apophysis,
• Basivertebral Vein usually anterosuperior vertebral margin
o Linear or triangular structure projecting
o Mid-lumbar most common
ventrally from the center of the posterior • KiimmelJ Disease
body o Post-traumatic osteonecrosis
• Schmorl Node o Horizontal, gas-filled intravertebral cleft is
o Hypointense Tl, variably hyperintense T2,
a characteristic finding; appears as signal
circumscribed vertebral body lesion void on MR
o In continuity with an adjacent disc space
Schmorl Node Bone Island
II
3 Sagittal T7WI MR shows circumsuibed L2 vertebral
body lesion, isointense to disc material, in contact with
Sagittal T7WI MR shows iocalsignal void within anterior
L4 body, without reactive marrow change or other
the L1-2 disc space. marrow abnormality.
56
VERTEBRAL BODY, 11 HYPOINTENSE SIGNAL, FOCAL
<
C1>
;:+
C1>
rr
~
OJ
shows L5 body lesion with OJ
o
diffusely hypointense T1 Cl.
signal I:] and extension into
'<
the ventral epidural space.
T2WI (not shown) had
typical vertical striations of
hemangioma.
Heterogeneous lesion of L 7
was also a hemangioma.
m
CD
(Right) Sagittal T1WI MR 3
shows horizontally oriented C1>
OJ
(racture extending through Ui
vertebral body ='2 and
posterior elements ~
(Chance fracture) in MVA
patient with ankylosing
spondylitis.
Metallic Hardware
shows signal void adjacent to
the C5-6 disc space,
demonstrating the presence
of an intervertebral disc
prosthesis. (Right) Sagittal
T1 WI MR shows hypointense
marrow signal in L3 and L4
!C associated with
destructive endplate changes
and epidural phlegmon ='2.
Degenerative Endplate Change (Types 1

&3) Metastases
shows hypointens€ signal in
inferior endplale marrow of
L5 ='2 associated with
advanced degenerative
changes in the L5-S7 disc
space. (RighI) Sagittal T1 WI
MR shows multiple
metastatic lesions in cervical
and thoracic vertebral bodies
='2.
II
3
57
SEClilON 4
Intervertiebral Disc - Endplatie
Disc Contour Abnormality 11-4-2
Intervertebral Disc/Endplate Irregularity 11-4-6
Vertebral Endplate Contour Abnormality 11-4-10

Intervertebral Disc, T1 Hypointense 11-4-12
Intervertebral Disc, T2 Hyperintense 11-4-14
Vertebral Endplate Signal Abnormality 11-4-16
(IJ
ro DISC CONTOUR ABNORMALITY
Ci
"0
C
W DIFFERENTIAL DIAGNOSIS o > 50% of disc circumference
u o Up to 40% of asymptomatic adults will
.'!1 Common have bulging disc
o
<1l
• Intervertebral Disc Bulge o Short radius of extension beyond disc
~
.0
(IJ
• Disc Pseudobulge margin :$ 3 mm
t • Protrusion, Intervertebral Disc
(IJ • Disc Pseudobulge
~ o Cervical o "Uncovering" of disc related to
(IJ
c o Thoracic spondylolisthesis
Cll o Lumbar o Smooth generalized extension of disc
c
c. • Extrusion, Intervertebral Disc margin without focal defect
en o Cervical • Protrusion, Intervertebral Disc
o Thoracic o Triangular focal disc abnormality with base
o Lumbar broader than apex
• Free Fragment, Intervertebral Disc o Anterior extradural mass in contiguity
o Cervical with the disc space
o Thoracic • Extrusion, Intervertebral Disc
o Lumbar o Base of herniation is narrower than
• Intervertebral Disc Extrusion, Foraminal portion extending into epidural space
• Intervertebral Disc Herniation, Recurrent o May be associated with sequestered or "free
• Peridural Fibrosis fragment"
• Osteophyte o Larger extrusion commonly show
• OPLL peripheral enhancement with granulation
• Epidural Mass tissue
o Metastasis • Intervertebral Disc Extrusion, Foraminal
o Lymphoma o Obliterated perineural fat in neural
o Epidural Abscess foramen on sagittal images
o Epidural-Subdural Hematoma o May enhance peripherally
Less Common o Contiguous to disc on parasagittal images
• Discal Cyst • Intervertebral Disc Herniation, Recurrent
• Hardware Malposition o Contiguous with intervertebral disc margin
• Meningioma (Calcified) o Central lack of enhancement, with
• Schwannoma (Foraminal) peripheral granulation tissue enhancement
• Limbus Vertebra common
o Distinguish from peridural fibrosis by
nonenhancing component, mass effect
ESSENTIAL INFORMATION • Peridural Fibrosis
Key Differential Diagnosis Issues o Scar formation within epidural space after
• Main differential point is whether or not lumbar surgery
lesion is contiguous to the intervertebral o Infiltration of epidural/perineural fat by
disc, or abutting the disc enhancing soft tissue density (intensity)
o Additional key findings include signal on o Smooth marginated soft tissue, usually
Tl, T2 images relative to nearby without mass effect
intervertebral disc; presence or absence of o Typically slightly increased in T2 signal
enhancement relative to disc herniation
o Large extrusion and protrusion should not o Homogeneously enhances
have homogeneous or intense central • Osteophyte
enhancement o Variable in MR signal due to relative
presence of bone, red marrow, or fatty
Helpful Clues for Common Diagnoses marrow
• Intervertebral Disc Bulge
II o Circumferential disc "expansion" beyond
o Often associated with disc degeneration
and disc bulge/herniation
the confines of vertebral end plates
4
2
DISC CONTOUR ABNORMALITY
o Typical "claw" configuration from adjacent o May spontaneously regress

endplates • Hardware Malposition
• OPLL o Pedicle screw position may extend into
o Flowing multilevel ossification posterior to intervertebral disc
vertebral bodies o Look for low signal of metal implant with
o Narrows AP dimension of canal and halo of high signal (spatial mismapping) o
en
produces cord compression o Precise position of screw tip requires CT ()
o May show low T1 signal (cortical bone) or • Meningioma (Calcified)

high T2 signal (fatty marrow) o Intradural-extramedullary lesion, not
o Typical "upside down T" or "bowtie" extradural
configuration on axial images o Large calcified lesion may be difficult to
• Epidural Abscess define as intradural
o Epidural mass with peripheral o Large amounts of calcification may
enhancement minimize enhancement
o Associated with findings of disc space • Schwannoma (Foramina I)
infection (endplate irregularity and o Generally not ventral to thecal sac, but
erosion, disc and body T2 hyperintensity, arise along foramen with intradural and
irregular enhancement) extradural components (dumbbell
• Epidural-Subdural Hematoma configuration)
o Acute may show isointense Tl signal, with o May be difficult to distinguish from lateral
subacute Tl hyperintense herniation
o Long segmental extra-axial mass encasing • More solid enhancement than large
or displacing cord or cauda equina herniation
o Rarely focal, as when associated with focal • May show cystic change
fracture or disc extrusion • Limbus Vertebra
o Intraosseous disc herniation at junction of
cartilaginous end plate
• Discal Cyst
o Unfused apophyseal fragment at vertebral
o Uncommon finding with degenerative disc
margin
disease
o Anterior more common and posterior
o Focal area of fluid signal intensity adjacent
o If posterior, consider limbus herniation
to intervertebral disc margin
o May reflect evolution of disc herniation
with fracture of the end plate/apophysis
with hemorrhage
Intervertebral Disc Bulge Disc Pseudobulge
II
Axial T2WI MR shows L5-57 disc bulge BI as Sagittal T1WI MR shows degeneration L5-S7 with type I
4
generalized extension
vertebrallxxiy
or the disc margin beyond the
margin, without focal deformity. aspect of disc =
endplale changes. There is "uncovering" of posterior
with thecal sac deformity. Note L4-5
retrolisthesis with uncovering of inferior disc margin ~.
3
<Il DISC CONTOUR ABNORMALITY
:ffi0-
"0
C
W
Ll
(/)
o Extrusion, Intervertebral Disc Extrusion, Intervertebral Disc

(Left) 5agillal T2WI MR
shows multiple midthoracic
disc extrusions, severely
compressing thoracic cord.
Extrusions show typical
pallern of larger componenl
in epidural space than at disc
Q)
C
base. (RighI) 5agillal T2WI
'Q. MR shows large extrusion
(Jl with free fragment al L5-5 I,
with inferior migration c=.
A
small protrusion is present at
L4-5S1. L5-51 disc is
degenerated
Intervertebral Disc Herniation,

Recurrent
(Left) 5agillal T1WI MR
shows large eXlraforaminal
extrusion -= which is
contiguous with the parent
intervertebral disc and
obscures the foramina! fat
and exiling nerve root
Compare with the normal
foramen below. (Right) Axial
T1 C+ MR shows large, right
paracentral recurrent
herniation with a small
amount of peripheral
enhancing epidural fibrosis.
The exiting root is effaced
and nol separately identified.

ill-defined soft lissue along
the course of the exiling right
L5 root l:lI due 10
post·operalive fibrosis.
(RighI) Axial T1 WI MR
shows large, well-defined
focus of very low signal
posterior to disc margin m
due 10 OPLL. There is severe
spinal cord deformalion l:lI.
II
4
4
DISC CONTOUR ABNORMALITY en
"::J
CD
Epidural Abscess
(Left) SagiLLalT2WI MR
shows destfllction of LS & S I
centered at the disc leve/,
with anlerolisthesis of L5 on o
(ii.
sac =-
S 1 and effacement of thecal
and prevertebral soft
tissue Ell. (Right) Sagillal
Cl
m
::J
T2WI MR shows a.
"2-
well-defined fluid signal OJ
intensity Ell at the site of CD
herniation on a prior study
(not shown). This may
reflect involution of a prior
hemorrhage within the disc
herniation.
(Left) SagiLLalT1 WI MR
shows linear low signal from
anterior screw ~ extending
into the ventral aspect of the
spinal canal. Note the slight
high signal halo at the screw
tip. (Right) SagiLLalT2WI MR
shows a heavily calcified
cervical meningoma seen as
lobular low signal mass ~
with broad dural margin.
Obtuse CSF margin could be
confusing for OPLL or
herniation.
limbus Vertebra limbus Vertebra

(Left) SagiLLalT2Wl MR
shows limbus herniation with
focal contour defect at the
thoracolumbar junction =.
Defining limbus avulsion or
herniation is difficult without
CT confirmation. (RighI)
Axial N[CT shows limbus
fracture 0(( of the posterior
superior margin with mild
mass effect upon thecal sac.
II
4
5
INTERVERTEBRAL DISC/ENDPlATE IRREGULARITY
DIFFERENTIAL DIAGNOSIS o Severe degenerative endplate changes may

() be associated with end plate irregularity
CIl
Common and fluid within disc giving T2
o
co • Degenerative Disc Disease hyperintensity
~
.0
Ql
• Degenerative Endplate Changes (Modic • Should not see epidural soft tissue or
t: Changes) paraspinal soft tissue
Ql
c:
Ql
• Schmorl Node o Definite overlap in MR findings between
C • Accelerated Degeneration early disc space infection and severe
Q) • Scheuermann Disease degenerative endplate changes => biopsy
c:
Co • Pyogenic Disc Space Infection required
en • Tuberculous Disc Space Infection
• Fungal Infection (Coccidiomycosis)
• Rheumatoid Arthritis • Degenerative Disc Disease/Endplate
Changes
less Common o Disc hypointense on Tl WI and T2WI
• Neurogenic (Charcot) Arthropathy o Endplates may be irregular, with Schmorl
• Ankylosing Spondylitis nodes, but margin between disc and
• Brucellosis vertebral body preserved
• Bone Infarcts o Mild post-gadolinium enhancement, often
o Sickle Cell linear along endplate margins in
o Gaucher horizontal direction
• Post-Treatment: Bone Morphogenetic o No paravertebral or epidural soft tissue to
Protein suggest infection
• Hemodialysis Spondyloarthropathy • Schmorl Node
Rare but Important o Well-defined, smoothly marginated
• Gout end plate herniation

• Spondyloepiphyseal Dysplasia o May see variable marrow signal around it,
• Ochronosis depending upon age of insult
• Acute shows t STIR, chronic shows
normal or fatty marrow halo
ESSENTIAL INFORMATION • Accelerated Degeneration
Key Differential Diagnosis Issues o Aberrant biophysical stresses from altered
• Primary consideration is infection vs. other normal spinal motion/fusion

o Classic pattern of disc space infection o Wolff law; living tissue responds to
includes chronic changes in stresses & strains

• Endplate irregularity o Increased mobility in remaining mobile
• Loss of distinction of disc margin and segments is hypothesized to cause

end plate on Tl weighted images accelerated degenerative pathologic
• Abnormal T2 signal disc hyperintensity changes
• Abnormal T2 vertebral body • Scheuermann Disease
hyperintensity o Kyphosis secondary to multiple Schmorl
• Abnormal irregular enhancement of the nodes --> vertebral body wedging

disc o Three or more wedged thoracic vertebrae
o Epidural enhancing soft tissue (phlegmon) with irregular endplates
or rim-enhancing mass (abscess) definitive o Thoracic spine pain and tenderness
findings worsened by activity in teenager, young

o Fat-suppressed T2 images &/or adult
fat-suppressed post-contrast Tl images • Pyogenic Disc Space Infection
especially useful for evaluation of o Severe endplate irregularity with loss of
paraspinal and epidural soft tissues distinction of disc from end plate
II o t T2 signal from disc, endplate, ± vertebral
body
4
6
INTERVERTEBRAL DISC/ENDPLATE IRREGULARITY
o Paravertebral and epidural soft tissue • Bone Infarcts

• Tuberculous Disc Space Infection o Sickle cell & Gaucher disease: "H-shaped"
o Endplate irregularity and osteolysis vertebral bodies
o Multiple (non)contiguous vertebrae o May see only vertebral collapse with
involved, including posterior elements Gaucher
o Migration of phlegmon underneath all • Post-Treatment: Bone Morphogenetic
with erosion of vertebral body corners Protein
o May mimic metastatic disease o Bone morphogenetic protein (rhBMP-2) m
::>
• Fungal Infection (Coccidiomycosis) bone lytic resorption defects occur at Cl.
"0
o Variable appearance from small focal body fusion sites in up to 1/3 patients 0;-
involvement ~ gross vertebral body/disc o Transforming growth factor acts as ro
destruction signaling molecule to attract mesenchymal
o Multiple bodies involved, similar to TB stem cells
• Rheumatoid Arthritis • Binds to receptors and causes stem cells
o C1-C2 instability in 33% of all RA patients to differentiate into osteoblasts with
o Facet and uncovertebral joint erosions bone formation
o Multilevel subluxations, uncommon disc • Hemodialysis Spondyloarthropathy
and adjacent vertebral body destruction o Peridiscal destructive arthritis in patient on
Helpful Clues for Less Common Diagnoses long-term hemodialysis
• Neurogenic (Charcot) Arthropathy Helpful Clues for Rare Diagnoses
o 4 of classic "S Os" related to spine: ormal • Ochronosis
density bone, destruction, disorganization, o Deposition of homogentisic acid and its
debris metabolites secondary to absence of
• Ankylosing Spondylitis homogentisic acid oxidase enzyme
o Endplate irregularity with acute o Premature degenerative disc disease with
inflammation phase, or chronic with calcified intervertebral discs
fusions and Schmorl node formation o Osteopenia and spinal ankylosis
o Irregularity with chronic fracture and Other Essential Information
pseudoarthrosis development • SED: Group of disorders (congenita, tarda)
• Brucellosis characteristic defect in epiphyses, which
o Granulomatous osteomyelitis pattern appear irregular
o May see pattern mix similar to pyogenic o Likely relate to collagen II (COL2A1 gene)
w/disc involvement, + skip lesions like TB mutations
Degenerative Endplate Changes (Modic

Degenerative Disc Disease Changes)
II
due to disc degeneravon =-
Sagitlal T2WI MR shows endplate irregularity T12-L1
and irregularity at 13-4
Sagittal T1WI MR shows multilevel severe disc
degeneration with type II endplate changes =. There is
4
from Schmorl node ~. There is multilevel severe diffuse irregularity of the endplates at these levels.
central stenosis. Note L1 hemangioma. 7
Q)
ro
Q.
u
c
W
u
(J)
o Accelerated Degeneration Scheuermann Disease

ro (Lefl) Sagiflal T2WI MR
~ shows C4-S anterior fusion
.n
Q)
t with concomitant severe disc
Q) degeneration al CS-6 =:lI
~
Q)
with loss of disc signal,
c endplate irregularity, & loss
of disc heigh/. (RighI)
Cl)
c Sagiflal bone CT shows
c. endplale irregularities and
rn vertebral wedging SI bUI no
widening of paraspinous soft
tissues. The vertebral
endplate depressions have
an undulating contour.
Tuberculous Disc Space Infection

(Lefl) Sagiflal T1 C+ MR
shows nonenhancing
necrotic bone extending into
superior LS endplale !::I &
ven1ral epidural phlegmon
=:lI. L3-4 disc space infeclion
shows irregular endplate
enhancement ~ (RighI)
Sagitwl T2WI MR shows
multifocal verlebral body
disease SI and disc
involvement with irregularity
=:lI & subligamenlous
extension.
Rheumatoid Arthritis
(Lefl) Sagiltal T2WI MR
shows minor disc
involvement at C6-7 =:lI with
extensive prevertebraf
component above and
below that disc level SI.
Note the extensive focal
body involvemenl of C7.
(RighI) Sagiltal STIR MR
shows erosive changes of C 1
and odontoid process with
peridental pannus with
effacement of thecal sac.
There is subaxial endplate
irregularity most pronounced
al C3-4 =:lI.
II
4
8
(Lefl) Coronal bone CT

shows typical appearance of
Charcot arthropathy of the
lumbar spine with
proliferative new bone
formation E!:I and lucent
pseudoarthrosis extending m
:J
transversely across all a.
columns. (RighI) Sagittal
~
Q)
T2WI MR shows a ro
pronounced oblique chronic
fracture involving the lower
thoracic spine = with the
irregular fracture site
functioning as a
pseudoarthrosis.
Post-Treatment: Bone Morphogenetic

Sickle Cell Protein
shows typical MR
appearance of vertebrae in
sickle cell disease with
H-shaped vertebrae Ell and
marrow low signal due to
hemosiderin deposition from
multiple transfusions. (RighI)
Sagittal T2Wt MR shows
multiple small "cystic"
appearing lesions with T2
hyperintensity involving the
L5 and S I bodies. Note the
smooth margins, with abrupt
transition to more normal
marrow signal, and lack of
adjacent marrow edema.
Hemodialysis Spondyloarthropathy
(Lefl) Lateral radiograph
shows destructive crystal
arthropathy at C4-5
simulating infection. There is
diffuse endplate irregularity
Ell. Soft tissue calcifications
indicate crystal deposition
J:!J. (RighI) Sagittal T2WI MR
shows a 50 year old with
epiphyseal dysplasia with
diffuse platyspondyly with
rectangular-shaped vertebral
bodies and endplate
irregularity.
II
4
9
(l)
ro VERTEBRAL ENDPLATE CONTOUR ABNORMALITY

0.
"0
C
W DIFFERENTIAL DIAGNOSIS • Limbus Vertebra: Small separate corner
(j portion of endplate, well-marginated
.!!1 Common • Fracture: Angular deformity of end plate, ±
o
co • Schmorl Node visible fracture line
~
.n
(l)
• Degenerative Endplate Changes • Scheuermann Disease: Undulating
t • Limbus Vertebra
(l) end plates 4 or more levels + kyphosis, with
c:
(l)
• Anterior Compression Fracture or without discrete Schmorl nodes
c • Lateral Compression Fracture • Osteomyelitis: Endplate erosion, vertebral
CI> • Scheuermann Disease body destruction, osteopenia or
c
Co • Osteomyelitis, Pyogenic osteosclerosis
en • Sickle Cell • Sickle Cell: Depression central portion of
Less Common endplate ("Lincoln Log")
• Neurogenic (Charcot) Arthropathy Helpful Clues for Less Common Diagnoses
• Osteomyelitis, Granulomatous • Neurogenic Arthropathy: Mimics
• Cushing Disease osteomyelitis; endplate destruction and
• Osteogenesis Imperfecta erosion, non united fracture fragments,
• Achondroplasia heterotopic ossification
• Mucopolysaccharidoses • Osteomyelitis, Granulomatous: Vertebral
• Thanatophoric Dwarfism endplate destruction and deformity, but disc
• Spondyloepiphyseal Dysplasia spaces preserved until late; may involve
multiple levels; bone fusion and kyphosis
ESSENTIAL INFORMATION • Cushing Disease: C-shaped end plate ("fish
mouth")
Key Differential Diagnosis Issues • Osteogenesis Imperfecta: Variable
• May be due to trauma, developmental or flattening and deformity due to fractures;
congenital disorders, degenerative disease or severe osteopenia
infection • Achondroplasia, Mucopolysaccharidoses:
Helpful Clues for Common Diagnoses Anterior beak deformity
• Schmorl Node: Cup-shaped defect in • Spondyloepiphyseal Dysplasia: Vertebrae
endplate flattened but taller in center than at sides
• Degenerative Changes: Osteophytes may
elongate or form hook adjacent to endplate
Degenerative Endplate Changes
II
4 Sagiltal T1WI MR shows cup-shaped deformity
endplate and normal marrow signal intensity.
= of Coronal bone CT shows advanced degenerative disc
disease, with endplate irregularities and subchondral
cysts. Endplate remodeling is partiy due to scoliosis in
this p<1lient.
10
VERTEBRAL ENDPlATE CONTOUR ABNORMALITY
Anterior Compression Fracture Scheuermann Disease

(Lcfl) Sagittal T1 WI MR
shows an L2 compression
fracture. Anterior portion of
cndplate is depressed I:] o
(f)
with cortical stepo(f. Oblique (')
fracture line ~ is
surrounded by low signal
edema. (Righi) Sagillal T1WI
MR shows undulating
vertebral endplates and mild
wedging o( 6 adjacent
vertebral bodies ~.
Although endplates are
abnormal in contour, their
signal intensity is normal.
Achondroplasia
large L3-L4 endplate erosions
=- much more severe than
seen with degenerative
disease. Sclerosis of
vertebrae adjacent to
erosions is a common finding
in vertebral osteomyelitis.
(RighI) Sagittal T1 WI MR
shows bullet-shaped
vertebrae at thoracolumbar
junction, resulting in
kyphotic deformity 1:].
De(ormity is less widespread
than in
mucopolysaccharidoses.
Mucopolysaccharidoses
flattened vertebrae with
anterior beaking
characteristic of Morquio
syndrome 1:]. (RighI)
Coronal bonc CT shows
mildly flallened vertebrae
with undulating endplatc
contours. extremity
radiographs showed
flallened epiphyscs,
corroborating diagnosis.
II
4
11
Q)
ro INTERVERTEBRAL DISC, T1 HYPOINTENSE

0.
"0
C
W DIFFERENTIAL DIAGNOSIS o May show linear low signal on all pulse
sequences with dense cortical bone
'-'
C/)
Common
(5 o Larger osteophytes may contain fatty
co • Congenital Vertebral Body Fusion marrow with t Tl signal
~
D
Q)
• Degeneration/Calcification o Claw-like appearance contiguous with
t • Degeneration/Vacuum Phenomenon
Q) end plates/ disc
~ • Osteophyte
Q) • Instrumentation/Implants
C • Instrumentation/Implants o Low signal with distortion and spatial
OJ
c less Common mismapping of signal ~ high signal
a. • Kummell Disease surrounding halo
m
• Pseudoarthrosis o Small amount of metal artifact may give
o Neurogenic (Charcot) Arthropathy significant artifact, not visible on CT/plain
o Post-Traumatic Instability films
o Post-Operative Spinal Complications • Typical following cervical discectomy
ESSENTIAL INFORMATION • Kiimmell Disease
o Nonunited vertebral body fracture
Helpful Clues for Common Diagnoses undergoes secondary necrosis and collapse
• Congenital Vertebral Body Fusion o Nitrogen accumulates in fracture cleft
o Linear small low signal disc with "wasp o Usually elderly, osteoporotic patients
waisting" of vertebral bodies o Low signal on Tl WI from gas, variable
• Degenerative Disc Disease high signal T2WI, STIRfrom body
o Calcification or vacuum phenomenon • Neurogenic (Charcot) Arthropathy
within intervertebral disc o Destructive arthropathy when pain and
o Loss of disc space height, vacuum proprioception are diminished/lost, while
phenomenon seen as low signal within joint mobility is maintained
disc on TlWI o Preserved bone density, bony debris best
o Decreased signal of intervertebral disc on seen on CT, helps distinguish from
T2WI, loss of central nucleus high signal infection
classic findings of disc degeneration o Lumbar spine, rapidly progressive, vacuum
• Osteophyte phenomenon
o Variable appearance due to type of
marrow, degree of cortical bone
Degeneration/Vacuum Phenomenon
II
4 Sagittal T2WI MR shows L1-2 congenital
mild kyphotic angular deformity:

=
fusion with
rudimentary linear low signal intervertebral disc and
Sagittal TI WI MR shows low T1 signal (rom endplates &
disc at L5-57 due to combined disc degeneration/gas &
adjacent type 111marrow change =. Note type If
endplate change L2-S and Schmor! nodes.
12
INTERVERTEBRAL DISC, T1 HYPOINTENSE
shows horizontal low signal
at LS-Sllevel due to a large
osteophyte = extending
into the inFerior neural
o
(fJ
()
foramen 8l displacing the

exiting L5 root. (Right)
Sagittal T I WI MR shows
metal artifact from Bryan
cervical disc prosthesis
made from 2 titanium alloy
=
porous coated shells. Note
low signal artifact with
spatial mismapping with
increased signal halo.
Instrumentation/I mplants Kiimmell Disease

post-operative changes
following imerbody fusion
and posterior pedicle screw
fixation with low signal from
the graft cages = and
adjacent hardware EJ.
shows severe vertebral
collapse with gas-filled
vertebral body cleft EJ and
vacuum disc phenomenon
I!:J.
Pseudoarthrosis
shows solid fusion at L4-5.
Pseudoarthrosis seen as
irregular low signal extending
through L5 disc space and
posterior elements = with
fusion above and below that
level. (Right) Sagittal T1 WI
MR shows typical MR
appearance of neuropathic
arthropathy with
anterolisthesis and sharply
demarcated endplate
erosions=.
II
4
13
Q)
roc. INTERVERTEBRAL DISC, 12 HYPERINTENSE

"0
C
W DIFFERENTIAL DIAGNOSIS o Focal increased signal in anulus on T2WI
u with low signal of parent disc
.!!1 Common o Tl C+: Focally enhancing nidus in
o
ro~ • Normal Variant posterior disc margin
..Cl
Q)
• Degenerative Disc Disease o Discography demonstrates contrast leak
t
Q)
• Vertebral Disc Anular Tear from central site of injection through
C:
Q)
• Post-Operative Change, Normal anulus
C • Post-Traumatic o Discography is more provocative test
Ql • Disc Space Infection (symptom simulation) than diagnostic
r::
Co
(/)
less Common imaging modality
• Pseudoarthrosis • Post-Operative Change, Normal
o Neurogenic (Charcot) Arthropathy o Disc intervention may lead to increased
o Seronegative Spondyloarthropathy fluid and T2 hyperintensity
o Nonspecific post-operative change
• Post-Traumatic
ESSENTIAL INFORMATION o t T2 signal suggests disc disruption
Helpful Clues for Common Diagnoses o Look for disruption of ALL, PLL
• Normal Variant • Disc Space Infection
o Central disc shows biconvex central high o Abnormal disc t T2 with abnormal
signal morphology hallmark of disc space
o Horizontal low signal extends through infection
nucleus giving bisaucer shape o 2 adjacent vertebrae involved with
o Loss of central signal with disc end plate irregularity and intervening disc
degeneration abnormality
• Degenerative Disc Disease o Paraspinal ± epidural infiltrative soft tissue
o Typical decreased signal of intervertebral ± loculated fluid collection
disc on T2WI Helpful Clues for less Common Diagnoses
o May show linear T2 hyperintensity with • Neurogenic (Charcot) Arthropathy
fluid-filled cleft in disc o Irregular disc space fluid, facet
o Uncommon discal cysts along posterior involvement, spondylolisthesis, debris,
margin disorganization
o No paravertebral or epidural mass to
suggest infection
• Vertebral Disc Anular Tear
Normal Variant Degenerative Disc Disease
II
4 Sagittal T2WI MR shows normal hyperintensity of L2-3,
L3-4 discs = with horizontal central low signal
Sagittal T2WI MR shows disc T2 hyperintensity related
=.
to degeneraUon with fluid·filled cleft This is T2
(intranuclear cleft). There is degeneration and loss of hyperintensity associated with degeneration and not
signal of L4-S, LS·Sl 81. disc space infection.
14
INTERVERTEBRAL DISC, 12 HYPERINTENSE
Degenerative Disc Disease Vertebral Disc Anular Tear

shows a well-defined fluid
signal intensity at dorsal disc
margin a. consistent with a
"discal cysl". This may
reflect involution of a prior
disc herniation hemorrhage.
m
::J
(Right) Sagittal T2WI MR a.
shows anufar tears as focal
~
Q)
hyperintensity within dorsal CD

anulus =:I. There is mild
degeneralion of L3-4 through
L5-sl with signal loss.
Vertebral Disc Anular Tear Post-Operative Change, Normal

shows linear T2
hyperintensity from ventral
anular lears al L2-] and L3-4
~. NOle type I endplale
change al L5-sl wilh
spondylolisthesis. (Right)
Sagittal STIR MR shows L4/5
pur There is fluid signal
intensity in Ihe L4/5 disc
interspace adjacenlto graft
= which can be normal.
Also large dorsal soft tissue
abnormality SI relaled to
pseudomeningocele with
hemorrhage.
Post-Traumatic
(Left) sagillal STIR MR
shows severe burst fracture
involving Ihe L1 body wilh
disc hyperinlensily =:I, with
marked posterior bony
retropulsion and severe
thecal sac compression ~.
shows T2 hyperinlensily of
intervertebral disc and
adjacent verlebral bodies
from pyogenic infection.
There is facet involvement
SI and epidural abscess =:I.
II
4
1S
<D VERTEBRALENDPLATESIGNAL ABNORMALITY
co
Cl.
-0
C
W DIFFERENTIAL DIAGNOSIS o Type III: • Tl, • T2; least common,
u approximately 1%
(J)
Common o Other signs of disc degeneration
o
co • Degenerative Endplate Changes o No associated soft tissue mass
L
.0
<D
• Schmorl Node • Schmorl Node
t • Pyogenic Osteomyelitis
<D o Intravertebral disc herniation
~ • Wedge Compression Fracture o Well-corticated margins
<D
C • Post-Treatment o May show t T2 signal if acute
Ql o Post-Operative Infection • Pyogenic Osteomyelitis
c
a. o Post-Operative Instability o Ill-defined hypointense vertebral marrow
lJ)
o Post-Operative Degenerative Endplate on Tl WI with loss of end plate definition
Changes on both sides of the disc
• Pseudoarthrosis o Paraspinal ± epidural infiltrative soft tissue
o Post-Traumatic ± loculated fluid collection
o Neurogenic (Charcot) Arthropathy • Wedge Compression Fracture
o Post-Operative o Depression of vertebral end plate, usually
• Hemangioma superior only
Less Common o t STIRsignal intensity, band-like or
• Rheumatoid Arthritis triangular configuration if acute
• Ankylosing Spondylitis Alternative Differential Approaches
• Hemodialysis Spondyloarthropathy • Bright Tl signal (fatty endplate) change vs.
Rare but Important low Tl signal
• Gout • Bright Tl signal
o Type II degenerative endplate change
o Chronic Schmorl node
ESSENTIAL INFORMATION o Chronic compression fracture
Helpful Clues for Common Diagnoses o Healed osteomyelitis (fatty marrow
• Degenerative Endplate Changes conversion)
o Type I: • Tl, t T2; present in 4% of o Hemangioma or focal fatty marrow
patients undergoing MR for disc disease • Low Tl signal
o Type II: t Tl; present in 16% of patients o Everything else!
undergoing MR for disc disease
II
4 Sagilta! T2W! MR shows degenerative type I endp!ate
changes at multiple levels as linear bands of T2
Sagittal T1 C+ FS MR is remarkable for pronounced
=.
hyperintensity adjacent to degenerated discs
type I endpJale enhancement and fine, linear
enhancement of the intervertebral disc. No endplale
16 irregularity or paravertebral mass suggests infection.
VERTEBRAL ENDPlATE SIGNAL ABNORMALITY
Schmorl Node
(Left) Sagillal TI C+ FS MR
shows inFerior endplace L 1
Schmorl node, wilh adjacent
type I degenerative endplale o
(J)
enhancement 81. (Right) ()
Sagillal T2WI MR shows

irregular T2 hyperinlensity
from the intervertebral disc
region =::Iwith epidural
phlegmon and bone
dislOrling the ventrallhecal
sac.
Wedge Compression Fracture

(Left) Sagillal STIR MR
shows horizontal band-like
appearance of multiple acule
compression fractures =-
indicating underlying benign
etiology such as trauma or
oSleopenia. (Right) Sagillal
TI WI MR show the anlerior
fusion over multiple
segments with fal signal 1::1
and irregular chronic fracture
site functioningas a
pseudoarthrosis 81.

shows palchy amorphous T2
hyperintense material
replacing intervertebral disc
and eroding adjacent
endplales =::I. (Right) Sagillal
T I WI MR shows multilevel
well-defined endplale
erosions and low Tl signal
I:D. Severa/lesions have a
"punched out" appearance,
typical for gout.
II
4
17
SECTION 5
Extradural
Epidural Mass, Spine 11-5-2
Ventral/Lateral Paraspinal Mass 11-5-8

Paraspinal Muscle Abnormality 11-5-10
Extradural Lesions, Multiple 11-5-12
Extradural Lesion, No Enhancement 11-5-14
Extradural Lesion, Solid Enhancement 11-5-16

Soft Tissue Calcification, Paraspinal 11-5-20
Extradural, Normal Marrow Signal 11-5-22
ExtraduraC Abnormal Marrow Signal 11-5-26
Extradural Lesion, T1 Hyperintense 11-5-30
Extradural Lesion, T1 Hypointense 11-5-32
Extradural Lesion, T2 Hyperintense, Tl Isointense 11-5-36
Extradural Lesion, T2 Hypointense, T1 Hypointense 11-5-40

Lumbar Soft Tissue Mass, Pediatric 11-5-42
EPIDURAL MASS, SPINE
DIFFERENTIAL DIAGNOSIS a Abnormal thickened ligamentum flavum,

may calcify
Common a Often associated with degenerative facet
• Intervertebral Disc Herniation arthropathy
• Facet Arthropathy • Epidural Lipomatosis
• Hypertrophied Ligamentum Flavum a Prominent epidural fat, can be seen with
• Epidural Lipomatosis prolonged steroid administration or
• Synovial Cyst Cushing syndrome
• Epidural Fluid Collections a Affects distal thoracic and lumbar spine
a Pseudomeningocele a Key finding is mass effect on the thecal sac
a Hematoma • "Y"shaped or trefoil configuration of
a Abscess thecal sac on axial images
• Epidural Metastatic Disease • Synovial Cyst
• Neurofibroma a Sign of facet degeneration
• Schwannoma a Circumscribed, fluid-filled structure
• Arachnoid Cyst a Adjacent/contiguous with a facet joint
• OPLL a Cyst along ventral facet may impinge on
Rare but Important thecal sac or nerve root

• Tumoral Calcinosis • Pseudomeningocele
a Epidural fluid collection
• Primary Bone Tumor
a Hemangioma a Surgical or traumatic dural defect causing a
a Plasmacytoma CSF leak

a Osteoblastoma a Margins may enhance if located within a
a Aneurysmal Bone Cyst surgical bed

a Lymphoma • Hematoma
a Leukemia a May be spontaneous or associated with
a Chordoma trauma or instrumentation

a Chondrosarcoma a Signal varies with the age of the
a Giant Cell Tumor hemorrhage
a Ewing Sarcoma a Mild or no enhancement
a Osteosarcoma • Abscess
• Extramedullary Hematopoiesis a May be associated with disc space
• Angiolipoma infection or instrumentation/inoculation

a Marked peripheral enhancement typical,
contents typically approximate fluid signal
ESSENTIAL INFORMATION on Tl/T2
Helpful Clues for Common Diagnoses • Epidural Metastatic Disease
• Intervertebral Disc Herniation a Enhancing soft tissue mass, may be
a Most common epidural mass multiple

a Virtually always ventral or ventrolateral to a Most often associated with epidural
the thecal sac extension from a vertebral metastasis

a May have thin rim of enhancement, a May also occur with transforaminal spread
especially if recurrent/post-operative from a paraspinal or posterior mediastinal
• Facet Arthropathy tumor
a Joint space narrowing, osteophyte • Neurofibroma
formation, effusion a Enhancing nodular, fusiform, or dumbbell
a Often accompanied by ligamentous mass associated with a nerve root

hypertrophy a Epidural neurofibroma typically
a May be asymmetric intraforaminal or transforaminal

II • Hypertrophied Ligamentum Flavum
5
2
o May be associated with vertebral Helpful Clues for Rare Diagnoses

scalloping, thinning/remodeling of • Tumoral Calcinosis
pedicles '. o Lobulated, calcific mass with surrounding
o Most (90%) solitary, non-syndromlC the facet joint
o May be multiple, extensive; associated o May see bone remodeling, no destruction
with plexiform neurofibromas • Hemangioma
(neurofibromatosis type 1) o Extraosseous component of an "aggressive"
• Schwannoma vertebral hemangioma more frequently
o Enhancing nodular, fusiform, or dumbbell
hypo intense on Tl WI
mass associated with a nerve root
• Lymphoma
o Most schwannoma intradural in location; o Enhancing epidural mass or epidural
epidural schwannoma typically extension from a vertebral lesion
intraforaminal or transforaminal o Spinal lymphoma may also manifest with
o Not reliably distinguished from solitary leptomeningeal or intramedullary lesions
neurofibroma
• Leukemia
• Arachnoid Cyst o Granulocytic sarcoma (chloroma)
o Thin walled, nonenhancing
• Solid mass composed of leukemic cells
o Contents follow CSF
outside of the bone marrow
o May be associated with vertebral
• In the CNS, usually epidural; distinct
scalloping, thinning/remodeling of from leukemic meningitis (subarachnoid)
pedicles • Extramedullary Hematopoiesis
• OPLL o Paravertebral and epidural lobulated
o Thickened, calcified posterior longitudinal
masses
ligament o Thoracic paraspinallocation most
o Ventral to thecal sac, may cause significant
common
canal stenosis o Associated with severe harrow hyperplasia
o Cervical involvement more frequent than due to chronic anemia
thoracic
• Angiolipoma
o Best appreciated with CT o Epidural mass with mixed fat and soft
o Most often hypo intense on Tl/T2WI
tissue components
o Center may become Tl/T2 hyperintense if
a marrow space develops within the
ossified ligament
Intervertebral Disc Herniation
II
=
Axial T2WI MR shows a sequestered disc fragment in
the left anterolateral epidural space at the L4 level
Axial T2WI MR shows bilateral facet hypertrophy =
effacing the thecal sac posterolaterally and contribuUng
5
impinging on the left L4 nerve root. to moderate canal stenosis.
3
Epidural Lipomatosis
shows severe central canal
stenosis at L4-5 due to
extensive posterior
ligamentous hypeftrophy 1:::1
effacing the thecal sac
dorsally. Note also disc
space narrowing and mild
degenerative anterolisthesis
E.:J at this level. (Right) Axial
T1WI MR shows the typical
appearance of prominent
epidural fat compressing the
thecal sac, causing a Y" or fI
trefoil appearance of the

thecal sac 1:::1.
Synovial Cyst Pseudomeningocele

a circumscribed, ring· shaped
lesion ~ arising from the
ventral aspect of the right
L4-5 lumbar facet resulting
in moderate canal stenosis.
(Right) Sagittal FSEIRshows
a large fluid collection at
L4-5 laminectomy site
extending from the epidural
space into the subcutaneous
£issues. Resulting mass effect
and small disc herniation 1:::1
significanlly effaces the
thecal sac 8>,
Abscess
shows a subdural hematoma
in the thoracic spine both
ventral 1:::1 and dorsal !:±I to
the thecal sac. (Right)
Sagittal T1 C + M R shows a
large ventral epidural
collection with enhancing
margins II] extending from
C2 into the upper thoracIc
spine, causing canal
narrowing and significant
cord compression.
II
5
4
Epidural Metastatic Disease Neurofibroma

a primary lung neoplasm
invading the chest wall and
paraspinous tissues,
extending through the neural
space =
foramen into the epidural
with mild thecal
sac effacement. (RighI) Axial
T2* GRE MR shows a
cylindricallransforaminal
mass of the cervical spine.
The intraspinal epidural
component causes severe
compression ~.
Schwan noma Arachnoid Cyst

(Lefl) Axial CrCT shows a
I'dumbbell" schwannoma
with lransforaminaJ mass and
associated bony remodeling.
The intraspinal component
has mild mass effect on the
thecal sac ffi (Righi)
circumscribed, CSF-signal
extradural mass with
widening of the canal,
containing two foci of flow
artifact=.
(Lefl) Axial bone CT shows

marked ossification of the
cervical posterior
longitudinal ligament ~
causing severe canal
stenosis. (RighI) Axial bone
CT shows tumoral calcinosis,
with an exuberant calcific
mass involving dorsal
elements of the lumbar spine
II
5
5
ro
~ EPIDURAL MASS, SPINE
:J
"0
ro
~
X
w
Q)
c: Plasmacytoma
a. (Lefl) Axial T2WI MR shows
en
an aggressive vertebral
hemangioma involving the
neural arch with marked
extension into the epidural
space contributing to severe
canal stenosis. (RighI)
Sagittal T1 WI MR shows an
upper thoracic compression
fracture with ventral epidural
extension 1:1] causing canal
stenosis and cord
compression.
Osteoblastoma Aneurysmal Bone Cyst

(Lefl) Axial T2WI MR in a
patient with a painful
scoliosis shows an expansile
mass arising from the right L2
lamina. The dorsal epidural
component mildly effaces
the poslerolalcralthecal sac
~. (RighI) Axial T2WI MR
shows a multiloculated,
expansile mass containing
multiple fluid-fluid levels
associated with the dorsal
elements.
Chondrosarcoma
shows an enhancing,
infiltrative, circumferential
epidural mass B>' with
multiple vertebral body
involvement 1:1] in this
patient with lymphoma.
(RighI) Axial T1 C+ MR
shows a large,
aggressive-looking thoracic
vertebral body mass with
peripheral enhancement and
epidural extension ~.
II
5
6
EPIDURAL MASS, SPINE en
"'C
:J
CD
m
~
~
Q)
Giant Cell Tumor Giant Cell Tumor a.

c
~
(Left) Axial CECT shows Q)
lytic, hetefOgeneously
enhancing vertebral body
mass, extending into the right
pedicle with right lateral =:I
and epidural
exlra05seOU5 extension.
mass in the cervical epidural
space, compressing the cord
at the C2-] level and
extending into the left
paravertebral region thfOugh
an enlarged left neural
foramen =:I.
Ewing Sarcoma Osteosarcoma

a thoracic vertebral body
lesion with a large
exlraosseous component
filling the left hemithorax 811
and extending into the
epidural space PJ::l. (Rigllt)
Axial T1 C+ FS MR shows a
permeative L3 lesion with
extraosseous extension into
the epidural =:I and
paravertebral 3> spaces.
shows extramedullary
hematopoiesis presenting as
a dorsal epidural soft tissue
mass =.. causing canal
stenosis and cord
compression. (Right) Sagittal
T1WI MR shows a large
dorsal epidural
heterogeneously
hyperintense mass
causing canal stenosis and
cord compression.
II
5
7
VENTRAL/LATERAL PARASPINAL MASS
DIFFERENTIAL DIAGNOSIS Testicular germ cell tumors: Nodes at level

o
of ipsilateral renal hilum
Common o Metastases
• Lymphadenopathy • Vertebral body involvement with sparing
o Lymphoma of disc space, with adjacent soft tissue
o Metastases extension
• Metastases, Vertebral Body • Aortic Aneurysm
• Aortic Aneurysm o Dilatation of the aorta (Ao) ~ l.Sx the
• Paras pinal Abscess normal diameter (S cm ascending Ao, 4 cm
• Retroperitoneal Hemorrhage arch/thoracic Ao, 3 cm distal abdominal
• Meningocele, Lateral Ao)
• Neurogenic Tumor o Always measure Ao outer-to-outer borders
o Schwannoma o Symptoms: Chest, back, or abdominal
o Neuroblastoma pain, distal embolization
o Ganglioneuroma • Paras pinal Abscess
Less Common o Look for associated disc space infection
• Extramedullary Hematopoiesis o Central necrotic foci without
• Retroperitoneal Lymphocele enhancement

• Retroperitoneal Fibrosis • Retroperitoneal Hemorrhage
• Liposarcoma, Soft Tissue o High density collection in retroperitoneal
• Fibrosarcoma, Soft Tissue space with fluid-fluid level
o Causes include anticoagulation, aneurysm,
& tumor rupture
ESSENTIAL INFORMATION • Meningocele, Lateral
Helpful Clues for Common Diagnoses o CSF signal/density meningeal protrusion
• Lymphadenopathy through neural foramen into adjacent
o Lymphatic or hematogenous spread intercostal/extrapleural space
• Testicular, ovarian cancer o Strong association with NFl
• Melanoma • Neurogenic Tumor

• Prostate, lung, breast o Schwannoma: Well-circumscribed,
o Direct extension from primary "dumbbell"-shaped, enhancing spinal mass
intra-abdominal neoplasms: Pancreas, GI centered about foramen
cancers
lymphadenopathy Metastases
II
5 Axial CEer shows a melastatic germ cell tumor as a
large confluent/ow density retroperitoneal mass 81 that
Axial T1WI MR shows a mass invading the left lateral
displaces the aorla anteriorly. foramen =.

lhoracic vertebral body, left posterior elements, & neural
Epidural extension effaces the thecal sac
but does not compress the cord.
8
VENTRAL/LATERAL PARASPINAL MASS
Aortic Aneurysm Paraspinal Abscess

retroperitoneal (ibrosis ~
surrounding an abdominal
aortic aneurysm, also called
"perianeurysmal Fibrosislr.
This is believed to result from
immunologic response to
atheromatous plaque.
brucellosis abscess = as a
well-defined, non enhancing
foci involving both psoas
muscles and the prevertebral
space.
Paraspinal Abscess Meningocele, Lateral

shows thoracic spinal TB in a
young child with kyphotic
deformity and large epidural
and paraspinal abscesses ~.
shows one appearance of
lateral meningocele
associaled with Nf I. T2
image shows dural ectasia
involving midthoracic thecal
sac ~ with right lateral
meningocele 81 projecting
into the paraspinal region.
Schwan noma Extramedullary Hematopoiesis

well-defined enhancing mass
~ within the neural
foramen with inlralumOral
cysts typical of schwannoma.
shows a lypical appearance
o( extramedullary
hematopoiesis presenting as
bilateral paraspinal masses
~. All marrow signal will be
abnormal.
II
5
9
PARASPINAl MUSClE ABNORMALITY
DIFFERENTIAL DIAGNOSIS • Pseudo meningocele

o Spinal cyst contiguous with thecal sac, not
Common lined with meninges
• Traumatic Spinal Muscle Injury o CSF-filled spinal axis cyst with supportive
• Muscle Denervation post-operative or post-traumatic ancillary
• Pseudomeningocele findings
• Paraspinal Abscess • Paraspinal Abscess
• Tumor, Benign o Paravertebral enhancing phlegmon or
o Lipoma, Soft Tissue peri pherally enhancing lig uified collection
o Hemangioma, Soft Tissue o Ill-defined infiltrative paraspinal soft tissue
o Neurofibroma o Obliterated soft tissue fascial plane
o Schwannoma o Low density or t T2 intramuscular
less Common collection
• Tumor, Malignant • Tumor, Benign
o Metastasis o Well-defined soft tissue enhancing lesion
o Fibrosarcoma, Soft Tissue o Neurofibroma, schwannoma at foramen
o Malignant Fibrous Histiocytoma Helpful Clues for less Common Diagnoses
o Neuroblastic Tumor • Tumor, Malignant
o MPNST o Enlarging, heterogeneous, soft tissue mass
• Rhabdomyolysis o Look for adjacent bone destruction
o Any patient with spontaneous
ESSENTIAL INFORMATION musculoskeletal hemorrhage should be

evaluated for underlying MFH
Helpful Clues for Common Diagnoses • Rhabdomyolysis
• Traumatic Spinal Muscle Injury o Clinical and biochemical syndrome
o Muscle T2 hyperintensity related to resulting from damage of integrity of
traumatic contusion, laceration, skeletal muscle, with release of toxic
hematoma muscle cell components into circulation
o Muscle may still be functional, even with o Elevated serum creatine kinase (CK) 5x
severe injury normal value, 100% sensitive
• Muscle Denervation o Increased T2 signal within affected skeletal
o Asymmetric muscle volume loss with fatty muscle group
replacement ~ chronic denervation
o Acute denervation may show enlargement
Traumatic Spinal Muscle Injury Traumatic Spinal Muscle Injury
II
5 Axial CECT shows a righl L3 transverse process fraclure
~ and extensive hematoma involving the right psoas
Posl-myelogram CT shows mulliple foci of calcificalion
within the dorsa! paraspinal muscles 1::1 after inlerbody
muscle and fXJ5lerior paraspinous muscles. fusion and posterior instrumentation related to operative
trauma and subsequent myositis ossificans.
10
PARASPINAL MUSCLE ABNORMALITY
Muscle Denervation Pseudo meningocele

(Left) Axial T1WI MR in
patient with Chiar; 2 shows
lumbosacral dysraphism and
repaired myelomeningocele
changes as well as striking
replacement of the
paraspinal muscles with fat,
an extreme end result of
severe chronic denervalion.
shows large dorsal soft tissue
pseudomeningocele SlI
following multilevel lumbar
laminectomy and fusion.
There are bone graft
fragments within the fluid
collection=.
Paraspinal Abscess Neurofibroma

extensive destructive
coccidiomycosis involving
the lumbar spine. Large
paravertebral
paraspinal Ee:I
=
and dorsal
abscesses are
present with vertebral body
lysis. (Right) Axial T2WI FS
MR shows a typical
appearance of large
neurofibromas in a patient
with NFl involving the upper
thoracic spine with large
exlraForaminaJ component
SlI.
Metastasis Rhabdomyolysis
renal cell metastasis
involving the right thoracic
rib with extension into the
adjacent musculature. There
is sligh I righllaleral epidural
eXlension =. (Right) Axial
hyperintensity from right
paraspinal muscles, sparing
the psoas muscle
ca,e of post-operative
= in this
rhabdomyolysis.
II
5
11
EXTRADURAL LESIONS, MUlTIPLE
DIFFERENTIAL DIAGNOSIS • Hypertrophied Ligamentum Flavum

o Similar to facet arthropathy, often at a
Common level with disc degeneration; may be a
• Multiple Disc Herniations response to altered loading or instability
• Facet Arthropathy o Posterolateral effacement of epidural fat
• Hypertrophied Ligamentum Flavum and thecal sac
• Epidural Fluid Collections • Hematoma
o Hematoma o Post-traumatic, coagulopathic, or
o Abscess post-surgical etiology
• OPLL o Signal varies with age of hemorrhage
• Epidural Metastases o Mild or no peripheral enhancement
• Plasmacytoma • Abscess
• Neurofibromatosis Type 1 o May be associated with disc space
Rare but Important infection or instrumentation/inoculation
• Extramedullary Hematopoiesis o Marked peripheral enhancement typical
• Multiple Epidural Hemangioma • OPLL
o Thickened, calcified posterior longitudinal
ligament
ESSENTIAL INFORMATION o Ventral to thecal sac, may cause significant
Helpful Clues for Common Diagnoses canal stenosis
• Multiple Disc Herniations o Cervical involvement more frequent than
o Disc herniations are most common ventral thoracic
epidural mass in the spine o Best appreciated with CT
o May have a thin rim of enhancement, • Epidural Metastases
especially if recurrent/post-operative o Enhancing soft tissue mass, may be
• Facet Arthropathy multiple
o Most often associated with disc o Most often due to epidural extension of a
degeneration at that level vertebral metastasis, primary epidural
o Thinning of articular cartilage, osteophyte metastases also occur
formation o May also occur with transforaminal spread
o Often accompanied by ligamentous from a paras pinal or posterior mediastinal
hypertrophy tumor
o "Blocky" facet morphology may be normal
variant, not degenerative
Multiple Disc Herniations
II
5 Sagittal T2WI MR shows multiple large lower thoracic
disc herniations, which efface the thecal sac and
compress the cord at multiple levels ClI.
ossified ligamentum {fayum, some labeled with
effacing the thecal saCfJOsterolaterally.
=
Sagittal T2WI MR shows multiple levels of hypertrophic,
12
EXTRADURAL lESIONS, MULTIPLE
Abscess
(Left) SagiHal TI WI MR
shows a spontaneous
epidural hematoma
presenting with two ventral
lentiform-shaped epidural
hematomas =:I effacing the
thecal sac & compressing the
spinal cord. Note the
appearance of normal dorsal
epidural fat 0:> .. (Right)
Sagittal TI C+ MR shows a
multiloculated, dorsal
epidural abscess a which
compresses cord ventrally
over a long segment.
Metal/ic artifact =:I is due 10
recently placed spinal fusion
hardware.

posterior ligament
ossification = with resulting
compression E!:1 (Right)
SagiHal T2WI MR in a patient
with metastatic thymic
carcinoma shows diffuse
vertebral metastases. In
several locations, epidural
extension = results in thecal
sac effacement, canal
stenosis, and cord
compression.
Neurofibromatosis Type 1 Extramedullary Hematopoiesis

(Leh) Sagillal TI WI MR
shows intraspinal extension
levels =-
of neurofibromas at two
causing canal
stenosis and cord
compression. (Right) SagiHal
T2WI MR shows diffusely
hypointense ,narrow and
nodular masses in the ventral
canal =
epidural space of the sacral
thalassemia.
II
5
13
EXTRADURAL LESION, NO ENHANCEMENT
DIFFERENTIAL DIAGNOSIS o Post-contrast MR should include at least 1

sequence using fat saturation
Common • Nonenhancing extradural masses can often
• Nonbony be distinguished by location
o Stenosis, Acquired Spinal, Lumbar o Sequestered disc anterior to thecal sac
o Facet Joint Synovial Cyst o Facet joint cyst adjacent to arthritic facet
o Hematoma, Epidural-Subdural joint
o Sequestered Disc Fragment o Perineural cyst in neural foramen or lateral
o Perineural Root Sleeve Cyst o Hematoma often mimics disc
o Pseudomeningocele
o Arachnoid Cyst
o Lipoma, Spinal
• Some lesions will enhance when
o Epidural Lipomatosis
acute/active but not in chronic stages
o Hematoma
o Metal Artifact
o Post-operative scar after discectomy
• Bony
o Limbus Vertebra
enhances for 12-18 months
o Schmorl node
o Schmorl Node
o Degenerative endplate changes
o Bone Island
o Acute disc sometimes shows peripheral
o Degenerative Endplate Changes (Type Ill)
o OPLL
enhancement due to inflammatory tissue
o Ossification Ligamentum Flavum • All spinal bone tumors enhance except
o Post Irradiation Vertebral Marrow osteochondroma, bone island
o Myelofibrosis
• Facet joint cyst can be followed to arthritic
facet joint
o Diastematomyelia • Pseudomeningocele vs. abscess
o Pseudomeningocele: Homogeneous fluid
Less Common with thin rim of enhancement
• Osteochondroma o Abscess: Heterogeneous fluid, thick,
• Dorsal Dermal Sinus irregular rim of enhancement
ESSENTIAL INFORMATION • Osteochondroma: Marrow continuity
Key Differential Diagnosis Issues between vertebra and exostosis
o Cartilage cap seen in childhood, tends to
• Enhancement may be difficult to see against
fatty bone marrow unless fat saturation used regress in adulthood
Stenosis, Acquired Spinal, Lumbar Facet Joint Synovial Cyst
II
5 Sagittal T2WI MR shows severe facet osteoarthritis, with
large bone spur 1:2 and associated redundancy of
Sagittal TI C + MR shows a large facet cyst 81.
Enhancement of cyst capsule, as seen here, is common.
ligamentum flavum causing spinal stenosis. Osteophyles
occasionally enhance.
14
EXTRADURAL lESION, NO ENHANCEMENT
Pseudomeningocele
(Left) sagiual T2WI MR
shows a sequestered disc 8::1
posterior to 51 vertebra.
Hematoma may have the
same appearance, probably
accounting for many cases of
"spontaneously resolving"
disc herniation. (Right)
sagiual T1 C+ MR shows a
collection =
large, nonenhancing fluid
following
spinal surgery. It can usually
be distinguished from an
abscess by smoolh walls and
a thin rim of enhancement
reflecting an adjacent
reactive change.
Degenerative Endplate Changes (Type

Epidural Lipomatosis III)
(Left) sagiu<11T2WI MR
shows extensive fat in the
spinal canal, narrowing the
thecal sac. Lipomatosis, like
all fat, shows minimal
enhancement with
gadolinium. (RighI) Sagittal
T1 WI MR shows low signal
L5-s/ disc =-
intensity adjacent to the
reflecting
reactive bony sclerosis; this
pattern wUf not enhance
with gadolinium, although
earlier phases of
degenerative change often
enhance, reflecting
hyperemia.
Osteochondroma
(Leh) Sagittal T1 C+ MR
shows a low signal intensity
throughout the spine,
nonenhancing. The vertebral
venous plexus does show
normal enhancement.
(Right) sagiual STIR MR
shows a bony projection
from the C4 vertebra =.
The continuity of bone
marrow between the
vertebral body and the
exostosis is indicative of
osteochondroma.
II
5
15
ro
~ EXTRADURAL LESION, SOLID ENHANCEMENT
:J
"0
ro
~
X DIFFERENTIAL DIAGNOSIS a Plexiform neurofibromas are
w
Q)
pathognomonic of NFl, often affect sacral
r:: Common or brachial plexus
'50 • Peridural Fibrosis
en • Schwannoma
• Metastases, Blastic Osseous a Neoplasm of Schwann cell investiture of
• Metastases, Lytic Osseous spinal and peripheral nerves
• Neurofibroma a Peripheral origin pushing adjacent axons
• Schwannoma rather than infiltration within -
• Lymphoma distinguishes from neurofibroma
• Plasmacytoma a Consider neurofibromatosis type 2 if many
Less Common tumors are identified
• Venous Vascular Malformation • Lymphoma
• Neuroblastic Tumor a Lymphoreticular neoplasms with wide
• Ewing Sarcoma variety of specific diseases & cellular
• Hemangioma differentiation
a Multiple types with protean imaging
Rare but Important
manifestations
• Langerhans Cell Histiocytosis • Plasmacytoma
• Extramedullary Hematopoiesis a Solitary monoclonal plasma cell tumor of
• Osteosarcoma bone or soft tissue
• Hemangiopericytoma a Often without specific features to
• Angiolipoma distinguish from solitary hematogenous
metastasis
Key Differential Diagnosis Issues • Venous Vascular Malformation
• Use all known clinical information as clues a Congenital transpatial vascular
to help narrow the differential possibilities malformation of venous channels present

from birth
Helpful Clues for Common Diagnoses a Mass-like, frequently enhances moderately
• Peridural Fibrosis (less than soft tissue hemangioma)
a Epidural scar formation after lumbar spinal
a No arterial vessels within lesion
surgery a Venous channels may be large; look for
a Infiltration of epidural/perineural fat by phleboliths to make specific diagnosis
enhancing soft tissue density (intensity) in • Neuroblastic Tumor
correct clinical context a Neuroblastic tumors = ganglioneuroma,
• Metastases, Blastic Osseous ganglioneuroblastoma, and neuroblastoma
a Bone production> bone destruction a Abdominal (40% adrenal, 25% paraspinal
a Destroys posterior vertebral body cortex
ganglia) > thoracic (15%) > pelvic (5%) >
first - pedicle cervical (3%); miscellaneous (12%)
a Hypointensity reflects blastic changes
a Identification of intraspinal spread has
• Metastases, Lytic Osseous important treatment and prognostic
a Bone destruction> bone production implications
a Destroys posterior vertebral body cortex
• MR is more sensitive than CT for
first - pedicle detecting intraspinal spread
a Lesions diffusely enhance (may mask
• Ewing Sarcoma
lesions if no fat suppression used) a Usually adolescents, younger adults
• Neurofibroma a Permeative cellular lytic lesion of vertebral
a Variable involvement of spinal root, neural
body or sacrum
plexus, peripheral nerve, or end organs a Involve vertebral body, ribs, ilium before
II neural arch
• Hemangioma
5
16
EXTRADURAL lESION, SOLID ENHANCEMENT
o Typical "benign" (fatty stroma) o Wide zone of transition, permeative

hemangioma hyperintense on Tl WI and appearance, cortical breakthrough, and
T2WI MR + contrast enhancement soft tissue mass
o "Aggressive" hemangioma iso- to o 80% have bone matrix visible on
hypointense on Tl WI and hyperintense radiographs and CT
on T2WI MR + avid contrast enhancement • Osteoid matrix produced directly by
• Lesion growth, bone destruction, malignant cells
vertebral collapse, absence of lesion fat, o Majority arise in posterior elements
active vascular component • Hemangiopericytoma
• Pathologic fracture or epidural extension o Hypervascular neoplasm arising from
is common - cord compression pericytes
o Avidly enhancing mass with large soft
tissue component expanding/eroding
o Abnormal histiocyte proliferation - spinal canal
granulomatous skeletal lesions • Angiolipoma
o Benign tumor with adipose and vascular
o Thoracic (54%) > lumbar (35%) > cervical
(11%)
elements
o Hyperintense mass on unenhanced Tl WI,
o Most frequent imaging appearances
enhancement on fat-suppressed Tl WI
• Vertebra plana sparing disc space
o Focal or infiltrating forms
• Destructive lesion with soft tissue
component resembling other epidural • Infiltrating more common in anterior
spinal tumors epidural space, may destroy adjacent
o Use location and patient age to suggest
bone
diagnosis • Focal more common in posterior
thoracic epidural space, no bone
o Epidural ± paravertebral proliferation of destruction
o No vascular flow voids
hematopoietic tissue rests in response to
profound chronic anemic state
o Enhancing isointense thoracic intra- or
paraspinal masses with associated diffuse
marrow hypointensity
o Mid-thoracic> cervical, lumbar
• Osteosarcoma
Peridural Fibrosis Metastases, Blastic Osseous
II
Axial T1 C+ MR demonstrates extensive enhancing
epidural fibrosis circumferenlially surrounding the thecal
Sagiltal T1 c+ MR shows abnormal enhancement of
multiple vertebral breast carcinoma metastases. CT 5
sac =.
cages 8:1.
Note metal artifact from intervertebral fusion imaging (not shown) confirmed blastic appearance.
17
EXTRADURAL LESION, SOLID ENHANCEMENT
Metastases, lytic Osseous Neurofibroma

enhancement of lytic renal
cell carcinoma metastasis
=. The diagnosis was
confirmed with bone CT (not
shown). (Right) Axial T7 C+
MR reveals a large right
lumbar epidural and
paraspinal neuroFibroma =
in a patient with confirmed
neurofibromatosis lype ,.
Schwannoma
(Left) Axial T7 C+ MR
depicts a large right
cervicothoracic
schwannoma with dumbbell
intradural and extradural
components. Note spinal
cord I:] compression.
reveals enhancing epidural
tumor extension
Ilodgkin lymphoma,
of -=
compression.
Plasmacytoma Neuroblastic Tumor

extensive enhancing epidural
tumor displacing the spinal
cord. There is also marrow
infiltration into the transverse
processes and adjacent rib.
"Drape" configuration of the
ventra/wmor extension
confirms epidural
localization. (Right) Axial T7
C+ FS MR demonstrates a
paraspinal enhancing
neuroblastoma with epidural
ipsilateral neural foramen,
displacing the dural sac.
II
5
18
EXTRADURAL lESION, SOLID ENHANCEMENT
Ewing Sarcoma Hemangioma

reveals a huge paraspinal
Ewing sarcoma that arises
from the ipsilateral posterior
rib with epidural extension,
compression. (Right) Sagiltal
T7 C+ MR depicts an
aggressive vertebral
hemangioma associated with
pathological compression
fracture, producing a large
epidural mass and thecal sac
compression.
Extramedullary Hematopoiesis
demonstrates complete
collapse of the T /2 vertebral
body (vertebra plana). The
vertebral body and the
adjacent 50ft tissues reveal
marked enhancement
following gadolinium
administralion. (Right)
Sagittal T7 C+ MR depicts an
elongated ovoid
well-circumscribed epidural
soft tissue mass with diffuse
and intense enhancement
compressing the distal
thoracic spinal cord.

a large lobulated enhancing
mass in left paravertebral soft
tissues and osseous posterior
elements El extending
along the dural margin into
the ipsilateral neural foramen
=. (Right) Sagiltal T7 C+ FS
MR demonstrates a farge
dorsal intensely enhancing
epidural mass in the upper
thoracic spine, producing
spinal cord compression.
II
5
19
SOFT TISSUE CALCIFICATION, PARASPINAL
DIFFERENTIAL DIAGNOSIS o Over time, forms cortex and internal

trabeculae
Common • In osteosarcoma, structure lacking
• Heterotopic Ossification o DISH, seronegative spondyloarthropathy:
o DISH Ossification of paraspinous ligaments
o Spinal Muscle Injury, Traumatic follows ligament contour
o Post-Operative Change, Normal o Charcot arthropathy: Combination of
o Neurogenic (Charcot) Arthropathy florid periosteal new bone and small bone
• Calcification fragments in soft tissues
o Calcific Tendinitis, Longus Coli • Usually more exuberant and
o Osteomyelitis, Granulomatous disorganized than post-traumatic
Less Common heterotopic ossification
• Heterotopic Ossification • "5 Ds" of Charcot joint: Preserved or
o Spondyloarthropathy, Seronegative increased density, bone debris,
o Osteosarcoma destruction, joint distention, joint
• Calcification dislocation
o Schwannoma • Calcification
o Polymyositis/Dermatomyositis o Calcific tendinopathy of longus coli:
o Spondyloarthropathy, Hemodialysis Linear calcification associated with longus
o Juvenile Idiopathic Arthritis coli muscle edema, often fluid collection
o Hydroxyapatite, gout, or scleroderma:
Rare but Important Amorphous or globular
• Fibrodysplasia Ossificans Progressiva (FOP) o Calcium pyrophosphate deposition
disease: Linear
ESSENTIAL INFORMATION o Granulomatous infection: Irregularly
shaped, associated with abscess
Key Differential Diagnosis Issues o Polymyositis: Fine, reticular pattern along
• Heterotopic ossification: General term fascial planes
meaning bone forming outside normal sites
o Myositis ossificans: Heterotopic Helpful Clues for Less Common Diagnoses
ossification forming in muscles • Juvenile Idiopathic Arthritis
o Causes: Trauma, surgery; paraplegia o Periosteal new bone or ligament
ossification
• Heterotopic Ossification
Heterotopic Ossification DISH
II
5 =
Coronal bone CT shows post-traumatic ossification
in paraspinous fat. Mature bone architecture anterior longitudinal ligament =.
Sagittal bone CT shows unusually bulky ossification of
This degree of
distinguishes it from osteosarcoma. ossification may cause dysphagia.
20
SOFT TISSUE CALCIFICATION, PARASPINAL
Calcific Tendinitis, Longus Coli

radiograph shows florid,
paraspinous, periosteal new
bone ~ bone sclerosis,
bone debris, disorganization,
and bone destruction, all
hallmarks of Charcot
arthropathy. (RighI) Axial
CECT shows calcification
in the longus coli muscle.
=
Muscle is Jaw attenuation
and enlarged.
Osteomyelitis, Granulomatous Spondyloarthropathy, Seronegative

vertebral body erosions and
a low attenuation
paraspinous 81 and spinal
canal mass !:;J. Note the
calcifications Itl; this
combination usually
indicates TB. (RighI)
shows slender ossification of
the paraspinou5 ligaments
=. Sacroiliac joint fusion m
is key to diagnosis.
Osteosarcoma Juvenile Idiopathic Arthritis

mass containing immature
ossification and involving
ilium, sacrum, sacroiliac
joint, and sort tissues.
Although the density of
osteosarcoma varies, its
appearance is always
aggressive. (RighI) Sagittal
bone CT shows heterotopic
ossification= related to
long-standing atlantoaxial
subluxation in jlA. Periosteal
new bone ~ is a more
common finding.
II
5
21
ell
~ EXTRADURAL, NORMAL MARROW SIGNAL
::J
""0
ell
~
X DIFFERENTIAL DIAGNOSIS o Intervertebral Disc Herniation, Lumbar
W
Gl
• Most common at L4-5, L5-S1
l: Common o Intervertebral Disc Herniation,
a. • Disc Herniation
m Foraminal
o Intervertebral Disc Herniation, Cervical • Soft tissue mass contiguous with parent
o Intervertebral Disc Herniation, Thoracic disc - extruded disc material in neural
o Intervertebral Disc Herniation, Lumbar foramen
o Intervertebral Disc Extrusion, Foraminal • Osseous Degenerative Disease
• Osseous Degenerative Disease o Intervertebral Disc Bulge
o Intervertebral Disc Bulge • Generalized circumferential disc
o Facet Mthropathy, Cervical extension beyond vertebral ring
o Facet Arthropathy, Lumbar apophyses
o Facet Joint Synovial Cyst o Facet Arthropathy, Cervical
• Infection • Osteoarthritis of synovially lined
o Abscess, Epidural apophyseal joints - facet overgrowth +
o Abscess, Paraspinal joint space narrowing
• Trauma o Facet Arthropathy, Lumbar
o Hematoma, Epidural-Subdural • Similar findings to cervical spine
o Hematoma, Spontaneous Epidural o Facet Joint Synovial Cyst
o Hematoma, Paraspinal • Extradural cystic mass communicating
• Neoplasm with facet joint + degenerative changes
o Neuroblastic Tumor disc, facet joint
o Lymphoma • Lumbar (90%) > > cervical, thoracic
o Schwan noma • Infection
o Neurofibroma o Abscess, Epidural
• Ligamentous Ossification • Extradural spinal infection with abscess
o OPLL formation ± spondylodiscitis
o DISH o Abscess, Paraspinal
o Ossification Ligamentum Flavum • Suppuration of paraspinal soft tissue
• Ligamentous Hypertrophy from direct extension or hematogenous
• Peridural Fibrosis pathogen dissemination
• Perineural Root Sleeve Cyst • Calcified psoas abscesses '* tuberculosis
Less Common • Trauma
• Epidural Lipomatosis o Hematoma, Epidural-Subdural
• Teratoma, Sacrococcygeal • Hypo-, iso-, or hyperintense depending
on blood product age
Rare but Important o Hematoma, Spontaneous Epidural
• Neurenteric Cyst • Accumulation of hemorrhage between
dura & spine without significant trauma
ESSENTIAL INFORMATION or iatrogenic procedure
o Hematoma, Paraspinal
Key Differential Diagnosis Issues • Frequently associated with vertebral
• Clinical context helps narrow differential list body fracture
Helpful Clues for Common Diagnoses • Signal intensity reflects blood product
• Disc Herniation composition, age
o Intervertebral Disc Herniation, Cervical • Neoplasm
• Localized displacement of disc material o Neuroblastic Tumor
beyond vertebral ring apophyses • Ganglioneuroma, ganglioneuroblastoma,
o Intervertebral Disc Herniation, Thoracic and neuroblastoma
II • T6 - T11 most common, rare in upper
thoracic spine
• Intraspinal spread has important
treatment and prognostic implications
5
22
EXTRADURAL, NORMAL MARROW SIGNAL
o Lymphoma o Enhancing scar formation within epidural

• Variable imaging manifestations are space after lumbar surgery
often nonspecific • Perineural Root Sleeve Cyst
o SchwannOina o Dilatation of arachnoid and dura of spinal
• Schwann cell neoplasm of peripheral posterior nerve root sheath
nervous system o Most common in lower lumbar spine and
• Consider neurofibromatosis type 2 if sacrum (Tarlov cyst)
many tumors identified Helpful Clues for Less Common Diagnoses
o Neurofibroma
• Epidural Lipomatosis
• Nerve sheath tumor of spinal root, o Excessive accumulation of intraspinal fat
neural plexus, peripheral nerve, or end (~ 7 mm) compressing thecal sac - cord
organs compression, neurologic deficits
• Plexiform neurofibroma pathognomonic o Long-term exogenous steroid
of NFl administration or excessive endogenous
• Ligamentous Ossification steroid production
o OPLL
• Teratoma, Sacrococcygeal
• Flowing multilevel ossification posterior o Large heterogeneous sacral tumor ±
to vertebral bodies calcification, cysts, hemorrhage
• "Upside down T" or "bowtie" o Rarely marrow invasion, even if adjacent
configuration on axial images soft tissue tumor or intraspinal spread
o DISH
through sacral hiatus
• Bulky flowing anterior vertebral
ossification Helpful Clues for Rare Diagnoses
• Thoracic> cervical, lumbar spine; R > > L • Neurenteric Cyst
(opposite aorta) o Intraspinal cyst lined by enteric mucosa
o Ossification Ligamentum Flavum (split notochord spectrum)
• Linear thickening and ossification of o ± Vertebral abnormalities (persistent canal
ligamentum flavum of Kovalevsky, segmentation and fusion
• Ligamentous Hypertrophy anomalies)
o Degenerative disc disease, redundancy and
thickening of ligamentum flavum - spinal
stenosis
• Peridural Fibrosis
Intervertebral Disc Herniation, Cervical Intervertebral Disc Extrusion, Foraminal
II
Sagiaal T2WI MR depicts a large rounded C5·6 disc
extrusion (base of herniation is narrower than apex
Axial T2WI MR demonstrates a large left L4-5 far lateral
disc herniation BI extending into the left neural
5
beyond the disc margin) effacing the thecal sac. foramen displacing the exiling L4 nerve root lEI.
23
C1l
~ EXTRADURAL, NORMAL MARROW SIGNAL
:J
-0
C1l
~
X
W
Ql
c: Facet Arthropalhy, Cervical Facet Arthropathy, Lumbar
C-
oo (Lefl) Axial bone CT
demonstrates severe osseous
hypertrophy and facet
degenerative changes that
distort the articular joint
surfaces. (RighI) Axial T2WI
MR reveals severe bilateral
facet degenerative changes,
with enlargement of the
facets and distortion of the
articular surfaces, narrowing
the lateral recesses.
Ligamentous thickening also
contributes to central canal
stenosis.
Facet Joint Synovial Cyst Abscess, Epidural

a large left synovial cyst 1::1
associated with severe
degenerative facet changes.
Note significant compression
of the thecal sac SI by cyst
mass effect compounded by
multifactorial spinal stenosis.
(RighI) Sagittal T I C+ MR
demonstrates a long segment
rim-enhancing lumbar
epidural abscess without
contributory discitis or
marrow signal abnormality.
Abscess, Paraspinal Hematoma, Spontaneous Epidural

(Lefl) Axial T I C+ FS MR
shO\vs abnormal paraspinaf
muscle enhancement with a
{Deal abscess = in a patient
with septic facet joint
infection. The vertebral body
and transverse process
marrow signal is normal.
(Righi) Sagittal T1 WI MR
shows a typical appearance
of a large subacute epidural
hematoma demonstrating T 1
hyperintensity 1::1. This
presentation was
spontaneous and idiopathic;
no underlying lesion was
II detected.
5
24
EXTRADURAL, NORMAL MARROW SIGNAL
Ossification ligamentum Flavum Peridural Fibrosis

(Left) Axial T IWI MR
demonstrates a small (Deus
of asymptomatic ossification
within the thoracic
IigamenlUm flavum =.1.
(Right) Axial TI C+ MR in a
post-operative patient with
pain shows diffuse
enhancement of the right
lateral epidural space and
surrounding exiting foot
secondary to peridural
fibrosis. There is extensive
enhancement of the disc
curelte site =.
Perineural Root Sleeve Cyst

reveals an incidental,
well-circumscribed,
nonenhancing, inlraspinat
CSF intensity root sleeve cyst
=.1 at the L5 level. (Right)
marked epidural lipomatosis
in a young cerebral palsy
patient. Imaging was
obtained after inability to
place an epidural catheter.
Note thick dorsal epidural fat
proliferation that
substantially narrows the
central spinal canal and
compresses the thecal sac.
Teratoma, Sacrococcygeal
reveals a heterogeneous
sacral tumor that anteriorly
displaces the reclUm and
urinary bladder. Note
absence of abnormal sacral
marrow signal and lack or
tumor extension into the
spinal canal through the
sacral hialUs. (Right) Sagittal
TI WI MR shows a large
ventral cystic mass in the
spinal canal = compressing
the ventral spinal cord in
contiguity with a second
prevertebraf enteric cyst a
with similar signal
characteristics.
II
5
25
EXTRADURAL, ABNORMAL MARROW SIGNAL
DIFFERENTIAL DIAGNOSIS • Metastases, Lytic Osseous

o Bone destruction> bone production
Common o Lesion centered in posterior cortex initially
• Vertebral Fracture with Epidural Hematoma ~ pedicle
• Osteomyelitis, Pyogenic o Usually enhances diffusely; may mask
• Metastases, Blastic Osseous lesion if fat suppression not used
• Metastases, Lytic Osseous • Osteomyelitis, Granulomatous
• Osteomyelitis, Granulomatous o Granulomatous (tuberculosis, brucellosis,
• Multiple Myeloma fungal) infection of spine + adjacent soft
• Plasmacytoma tissues
• Lymphoma • Tuberculosis: Gibbus vertebrae, relatively
• Hemangioma intact discs, large paraspinal abscesses
Less Common • Brucellosis: Anterosu perior epi physitis
• Chondrosarcoma with associated sacroiliitis
• Chordoma • Multiple Myeloma
• Osteoblastoma o Multifocal malignant bone marrow
• Aneurysmal Bone Cyst proliferation of monoclonal plasma cells
• Ewing Sarcoma o Multifocal diffuse or heterogeneous Tl
hypointensity, T2 hyperintensity, variable
Rare but Important enhancement
• Extramedullary Hematopoiesis • Plasmacytoma
• Hemangiopericytoma o Solitary monoclonal plasma cell tumor of
• Osteosarcoma bone or soft tissue
• Giant Cell Tumor o Often lacks specific features to distinguish
• Echinococcus from solitary hematogenous metastasis
• Lymphoma
ESSENTIAL INFORMATION o Lymphoreticular neoplasms with wide
variety of specific diseases, cellular
Helpful Clues for Common Diagnoses differentiation
• Vertebral Fracture with Epidural o Protean imaging manifestations often
Hematoma nonspecific
o May be seen following any cause of
• Hemangioma
vertebral fracture (traumatic, compression, o Typical "benign" (fatty stroma)
pathological) hemangioma: Hyperintense on Tl WI and
o Abnormal marrow signal reflects
T2Wl MR + contrast enhancement
combination of edema, hemorrhage o "Aggressive" hemangioma: Iso- to
o Look for fracture line to confirm diagnosis
hypointense on Tl WI, hyperintense on
• Osteomyelitis, Pyogenic T2WI + avid contrast enhancement
o Bacterial suppurative infection of • Lesion growth, bone destruction,
vertebrae, intervertebral disc vertebral collapse, absence of fat, active
o Ill-defined hypointense vertebral marrow vascular component
(TIWI), destruction of vertebral endplate • May extend epidurally ~ cord
cortex on both sides of disc compression
o Paraspinal ± epidural infiltrative soft tissue
± loculated fluid collection Helpful Clues for Less Common Diagnoses
• Metastases, Blastic Osseous • Chondrosarcoma
o Bone production> bone destruction o Primary or secondary (degeneration of
o Lesion centered in posterior cortex initially osteochondroma or enchondroma)
~ pedicle o Lytic mass ± chondroid matrix, cortical
o Hematogenous dissemination (arterial or disruption, extension into soft tissues
II venous via Batson plexus) > perineural, o Tumor cells produce chondroid matrix
lymphatic, CSF spread mineralization with "rings and arcs"
5
26
• Chordoma Hypervascular neoplasm arising from

o
o Malignant tumor arising from notochord pericytes
remnants o Avidly enhancing lesion
o Sacrococcygeal> clivus> > vertebral body expanding/eroding spinal canal, with large
o Lesion center in posterior vertebral body, soft tissue component
marked T2 hyperintensity help distinguish • Osteosarcoma
from hematogenous metastasis o Aggressive sarcoma containing matrix
• Osteoblastoma (immature, woven osteoid) produced
o Benign, well-circumscribed, expansile directly by malignant cells
lesion of neural arch with osteoid matrix o Wide zone of transition, permeative,
o Peritumoral edema may obscure lesion, cortical breakthrough, soft tissue mass
mimic malignancy or infection on MR o 80% have bone matrix visible on
• Aneurysmal Bone Cyst radiographs or CT
o Expansile neoplasm centered in neural • Giant Cell Tumor
arch containing thin-walled, blood-filled o Locally aggressive neoplasm composed of
cavities osteoclast-like giant cells
o Fluid-fluid levels 2° hemorrhage, blood o Lytic expansile lesion in vertebral body or
product sedimentation sacrum with narrow zone of transition,
• Ewing Sarcoma non-sclerotic margin
o Usually seen in adolescents, younger o Matrix absent; may have residual bone
adults trabeculae
o Permeative lytic lesion involves vertebral • Echinococcus
body, ribs before neural arch o Tapeworm infestation in endemic areas
o Multiloculated, multiseptated T2
hyperintense mass with minimal
enhancement
o Epidural ± paravertebral proliferation of
o Liver, lung most common, bone
ectopic hematopoietic tissue in response to
involvement rare
profound chronic anemia
o Minimally enhancing isointense thoracic
intra- or paraspinal masses + diffuse
cellular marrow signal
Vertebral Fracture with Epidural

Hematoma
II
Sagillal T1WI MR shows a C7 burst fracture =:I with
canal compromise caused by bolh retropulsion of the
Sagillal T1 C + M R reveals a large prevertebral
rim-enhancing abscess = extending from a C5-6 disc
5
fracture fragment and poslerior epidural hematoma 8l space infeclion E:I. There is a linear ventral epidural
compressing the spinal cord. phlegmon that extends from C4 to C6 PJ:J. 27
Q)
c: Osteomyelitis, Granulomatous
a.
C/) (Left) sagiltal T1 C+ MR
shows marrow enhancement
and palhological thoracic
vertebral fracture with
relalive preservation of the
intervertebral disc space.
There is epidural extension
with spinal cord compression
in lhis case of lab-proven TB.
(Right) sagiltal T1 C+ Fs MR
depicts multiple enhancing
vertebral metastases
producing abnormal marrow
enhancement in the cervical
and thoracic spine. There is
extensive epidural tumor
extension at T5 =.
Plasmacytoma Lymphoma
(Left) Axial T1 C+ Fs MR
shows extensive rib &
vertebral body tumor
infiltration and marrow signal
abnormality. The tumor
produces a large enhancing
epidural mass with
secondary spinal cord
compression. (Right) Axial
T1 C+ Fs MR demonstrales
extensive tumor infiltration of
a lumbar vertebra extending
into the right transverse
process and paraspinal 50ft
tissues. Characteristic
=
appearance of the "curtain
sign II
extension.
confirms epidural
Chondrosarcoma
(Left) sagiltal T1 C+ MR
reveals intense patchy
enhancement of a
destruclive vertebral mass
(path-proven
chondrosarcoma) with
severe spinal cord
compression secondary to
dorsal epidural eXlension =.
(RighI) Sagittal T7 C+ FS MR
shows a destructive
C3 vertebral tumor with
large epidural mass
compression. T2WI MR (nOI
II shown) revealed diffuse T2

hyperintensity.
5
28
Osteoblastoma Aneurysmal Bone Cyst

(Left) Axial T1 C+ MR rs
demonstrates a
heterogeneous mass EJ
expanding the left pedicle
with extensive enhancing
reactive perilumoral edema
in the adjacent posterior
elements, vertebral body,
and 50ft tissues. (Right) Axial
T1 C+ MR shows an
expansile mufti/oeulated
vertebral mass with multiple
fluid-fluid levels. Note
extensive conical
destruction, severe canal
stenosis, and enhancement
of septae between dilated,
blood-filled spaces.
Ewing Sarcoma
enhancing paravertebral
mass that extends into the
left epidural space through
the ipsilateral neural
foramen, displacing the
spinal cord. (Rig"') Sagittal
T1 C+ MR depicts a large,
lobulated enhancing mass in
dorsal 50ft tissues and dorsal
spinal osseous elements.
Note extension along dural
margin, compressing the
thecal sac and displacing
cauda equina.
shows L3 bone marrow
replacement by malignant
tumor that permeates
through the posterior cortex
into the spinal canal and
paraspinou5 50ft tissues.
There is diffuse marrow and
epidural enhancement
associated with a pathologic
fracture. (Right) Sagittal T1
C+ MR shows a large
osseous expansile mass
involving predominantly the
posterior elements, with
multiple fluid-fluid levels and
diffuse mild enhancement.
II
5
29
EXTRADURAL LESION, 11 HYPERINTENSE
DIFFERENTIAL DIAGNOSIS o Actual signal characteristics depend on

hematoma age; methemoglobin (subacute)
Common hyperintense on Tl WI
• Normal Epidural Fat o Can be clearly differentiated from epidural
• Epidural Lipomatosis fat with frequency-selective fat-suppressed
• Hematoma, Epidural-Subdural sequence
• OPLL (with Fatty Marrow) • OPLL (with Fatty Marrow)
• Extraosseous Hemangioma o Always ventral to thecal sac, mostly in
• Lipomyelomeningocele cervical spine
• Terminal Lipoma o OPLL will be most reliably defined on CT
Rare but Important • LipomyeIomeningocele
• Angiolipoma o Lumbosacral dysraphism
• Metastatic Melanoma • Everted elements of neural arch
• Caudal fatty mass, contiguous with
neural placode of a tethered, dysraphic
ESSENTIAL INFORMATION cord; disjunction protrudes through the
Helpful Clues for Common Diagnoses dysraphic defect
• Normal Epidural Fat • Skin-covered (closed spinal dysraphism)
o Usually most conspicuous dorsally in the o Often discovered in infancy, but can be
thoracic region on midline sagittal slices occult and come to attention during
o Key finding is lack of significant mass adolescence or adulthood
effect on the thecal sac • Terminal Lipoma
• Epidural Lipomatosis o Lipoma of cord terminus or filum, often
o Overabundance of epidural fat, most associated with tethered cord
commonly affecting thoracic and lumbar o Lipoma extends through caudal
spine spondyloschisis, becomes confluent with
o Resulting compression of the thecal sac subcutaneous fat
leads to a Y-shaped or trefoil cross section o Not associated with myeloschisis:
o May be associated with prolonged steroid Represents disorder of regressive
administration or with hypercortisolism differentiation rather than of primary
• Hematoma, Epidural-Subdural neurulation
II
5 Sagittal TI WI MR shows a typical case of epidural
lipomatosis in a patient taking high dose corticosteroids.
Sagittal TI WI MR shows a case of subacute
spontaneous epidural hematoma =.
Compare with
normal epidural fat dorsally I~~
30
EXTRADURAL lESION, 11 HYPERINTENSE
OPLL (with Fatty Marrow)

(Lell) Sagittal T1 WI MR
shows a large local lumbar
epidural hemorrhage,
ellacing the thecal sac and
resulting in canal stenosis.
Hyperintense T1 signal is
compatible with a subacute
chronicity. (RighI) Sagittal
T1WI MR shows
compression of an atrophic
cord by an ossilied posterior
longitudinal ligament with
areas 01 latty marrow =.
Extraosseous Hemangioma
(Lell) Sagittal T1 WI MR
shows atypical (lipid-poor)
hemangioma 01 L5 with
exlraosseous extension into
the ventral epidural space
=. A second lesion is
present at L 1 ~. (RighI)
Sagittal T1 WI MR shows
lumbosacral delect with
tethered cord = and caudal
latty mass R>J in this inlant
with IipomyeJomeningoceJe.
Terminal Lipoma
(Lell) Sagittal T1WI MR
shows a tethered cord
terminating in a fatty mass.
Overlying neural arches are
intact. (RighI) Sagittal T I WI
MR shows a large dorsal
epidural T1 hyperintense
mass with heterogeneous
signal.
II
5
31
ell
L EXTRADURAL LESION, 11 HYPOINTENSE
::J
""CJ
ell
L
X DIFFERENTIAL DIAGNOSIS • Contrast-enhanced sequences recommended

W
Cl>
for evaluation of infection, tumor, and
c: Common post-operative spine
·ii • Disc Herniation
lJ)
• Osteophyte Helpful Clues for Common Diagnoses
• Degenerated, Hypertrophic Ligamentum • Disc Herniation
Flavum o Most common ventral epidural lesion at
• Post-Operative Change, Normal level of disc space
o Epidural Gas o Extrusions extend away from disc space;
o Metal Artifact sequestered fragments will be separated

o Peridural Fibrosis from disc level
o "Vacuum disc phenomenon" (nitrogen gas)
• Facet Joint Synovial Cyst
• Epidural Fluid Collections in disc herniation can manifest as epidural
o Pseudomeningocele signal void
o Hematoma (Acute) • Peridural Fibrosis
o Epidural Abscess o Post-operative epidural scar/fibrosis in the
• Epidural Metastatic Disease surgical bed following discectomy,

laminectomy
Less Common o Peridural scar/fibrosis enhances, recurrent
• Neurofibroma disc herniation won't enhance (distinction
• Arachnoid Cyst important as it influences decision to
• Ossification of the Posterior Longitudinal re-operate in cases of failed back surgery)
Ligament (OPLL) • Facet Joint Synovial Cyst
Rare but Important o Circumscribed cystic lesion contiguous
• Extramedullary Hematopoiesis with facet joint
• Extraosseous Component of a Hemangioma o Invariably associated with degenerative
• Primary Bone Tumor facet disease
o Plasmacytoma o If marked enhancement or severe T2
o Osteoblastoma hyperintensity in adjacent marrow,
o Aneurysmal Bone Cyst consider infected facet joint
o Lymphoma/Leukemia • Pseudomeningocele
o Giant Cell Tumor o Epidural CSF collection at site of dural
o Chordoma defect (post-surgical or post-traumatic)
o Osteosarcoma • Hematoma (Acute)
o Chondrosarcoma o Lobulated collection, typically extending
o Ewing Sarcoma over multiple vertebral segments
• Tumoral Calcinosis o Oxyhemoglobin and deoxyhemoglobin
• Extradural Arteriovenous Fistula both isointense or hypointense on T1WI,
becoming hyperintense in the subacute
phase with the conversion to
ESSENTIAL INFORMATION methemoglobin
Key Differential Diagnosis Issues o No or relatively mild peripheral
• Vast majority of "extradural lesions" relate to enhancement
degeneration of intervertebral disc and o May be spontaneous, due to coagulopathy,
dorsal elements instrumentation, or trauma
• Impact of epidural mass lesion on spinal • Epidural Abscess
cord and nerve roots is best evaluated with o Lobulated collection, typically extending
MR over 1-2 vertebral segments
• CT myelography alternative in patients who o Marked peripheral enhancement (abscess);
cannot undergo MR (e.g., pacemaker, spinal epidural phlegmon may enhance more
II stimulator, etc.) homogeneousl y
5
32
EXTRADURALLESION, T1 HYPOINTENSE CJl
"'C
::::l
lD
o Associated findings: Discitis/osteomyelitis, o Paravertebral and epidural lobulated m
psoas abscess; patient typically has clinical masses; thoracic paraspinallocation most ~
~
Ql
signs of infection common n.
c
~
• Epidural Metastatic Disease o Associated with severe marrow hyperplasia Ql
o Epidural extension from bony vertebral due to chronic anemia

metastasis (renal cell, lung, lymphoma) or • Extraosseous Component of a
transforaminal extension from paraspinal Hemangioma
tumor (neuroblastoma) o Extraosseous extension of vertebral
Helpful Clues for Less Common Diagnoses hemangioma, causing epidural soft tissue
mass
• Neurofibroma
o Extraosseous component more frequently
o Can be completely extradural, can also be
intradural or transdural hypointense on Tl WI
o Circumscribed margins, foraminal
• Primary Bone Tumor
o In general, MR superior in assessing
remodeling/ en largement
epidural involvement, canal compromise,
a Rapid enlargement or pain: Consider
scope of marrow involvement, and
malignant degeneration
extension into the paraspinal soft tissues
• Arachnoid Cyst
o CT can be useful to assess matrix, zone of
a Typically dorsal to thecal sac, may extend
transition, etc.
laterally into neural foramina
a Follows CSF on all pulse sequences Alternative Differential Approaches
a Chronic CSF pressure leads to remodeling • If lesion has very low or absent signal,
and thinning of neural arch shortens differential to
• Ossification of the Posterior Longitudinal o Metal artifact
Ligament (OPLL) o Epidural gas (acute post-operative,
a Longitudinal structure in ventral epidural traumatic)
space: When large, often develops central o Gas ("vacuum disc phenomenon") in a disc
T1 hyperintensity (marrow space) herniation
a Cervical spine involvement more frequent o Ossified ligamentum flavum
than thoracic o OPLL
a Can cause significant canal compromise o Tumoral calcinosis
o Extradural arteriovenous fistula
Degenerated, Hypertrophic Ligamentum

Disc Herniation Flavum
II
Sagittal T1WI MR shows multiple disc herniations =-
the largest herniation, at C3-4, associated with cord
Axial T1WI MR through L4-5 shows advanced
degenerative facet arthropathy. Marked ligamentous
5
compression. hypertrophy is present ICB effacing the thecal sac
posterolateralfy. 33
~ EXTRADURAL LESION, T1 HYPOINTENSE
::J
"0
~
X
w
Q)
c:
unifateral mild ossification in
the ligamentum fJavum as
well-defined low signal
effacing the dorsal thecal sac
1:']. (Right) Axial T1WI MR
shows epidural fibrosis
extending from a
laminotomy defect along the
left of the thecal sac to the
ventral epidural space.
Homogeneous enhancement
is typical.
Pseudomeningocele
a circumscribed extradural
mass I:'] at the L4-5 level
closely associated with the
right facet joint. Cysts are
better evaluated on T2
images or post-contrast.
shows a large CSF collection
extending dorsally from a
laminectomy defect I:'] into
the subcutaneous tissues.
shows a large extradural
collection dorsal to the
thecal sac 1:']. Low Tl signal
was due to an acute
chronicity and was expected
to become hyperintense as
the collection aged. (Right)
Sagittal Tl WI MR shows a
ventral, epidural, mass-like
process extending cephalad
from the LJ-4 level 1:']. Key
finding is that of extensive
marrow changes ;n L3 and
L4 vertebral bodies 81.
II
5
34
EXTRADURAL LESION, 11 HYPOINTENSE
Epidural Metastatic Disease Neurofibroma

(Left) Axial Tl WI MR shows
a chest wall mass !:1:l
destroying the adjacent
thoracic vertebra = and
extending into the epidural
space EJI in this patient with
non-small cell lung
carcinoma. (Right) Axial
TlWI MR shows a
circumscribed soft tissue
mass extending through a
widened neural foramen to
abut the thecal sac.
Ossification of the Posterior longitudinal

ligament (OPll) Extramedullary Hematopoiesis
shows an extensive
ossification of the posterior
longitudinal ligament 1::1
resulting in canal stenosis
and cord compression.
shows an abnormally
hypointense marrow signal
and rounded hypointense
50ft tissue in the ventral
epidural space o( the sacral
canal = in this patient with
thalassemia.
Extraosseous Component of a
Hemangioma lymphoma/leukemia
shows a low signal mass
involving the posterior
thoracic body and dorsal
elements, with an
exlraosseous dorsal epidural
50ft tissue mass = resulting
in cord compression. (Right)
Axial Tl WI MR shows an
extensive abnormal marrow
signal due to leukemia and a
soft tissue mass in the
epidural space of the sacral
canal 1::1.
II
5
35
EXTRADURAL lESION, 12 HYPERINTENSE, 11 ISOINTENSE
DIFFERENTIAL DIAGNOSIS o Can only be differentiated from recurrent

disc herniation on post-contrast imaging
Common • Peridural fibrosis will homogeneously
• Intervertebral Disc Herniation enhance, blending into extradural fat on
• Synovial Cyst non-FS TlWI
• Peridural Fibrosis • Abscess, Epidural
• Epidural Fluid Collections o May be associated with disc space
o Abscess, Epidural infection or instrumentation/direct
o Hematoma, Epidural-Subdural (Acute) inoculation
• Epidural Metastatic Disease o Contents typically approximate fluid
• Neurofibroma signal on Tl/T2WI
• Schwannoma • Increased T1 signal (isointense) may
Rare but Important occur secondary to increased protein
• Primary Bone Tumor content
o Plasmacytoma o Marked peripheral enhancement typical
o Lymphoma on post-contrast imaging
o Chordoma • Hematoma, Epidural-Subdural (Acute)
o Chondrosarcoma o May be spontaneous or associated with
o Giant Cell Tumor trauma or instrumentation
o Ewing Sarcoma o Signal varies with the age of the
hemorrhage
• Acute hemorrhage (oxyhemoglobin) iso-
ESSENTIAL INFORMATION or mildly hypointense on Tl WI,
Helpful Clues for Common Diagnoses hyperintense on T2WI
• Intervertebral Disc Herniation o Minimal or no enhancement on
o Most common epidural lesion in adult post-contrast imaging
population • Epidural Metastatic Disease
o Intermediate-to-Iow T1 signal o Enhancing soft tissue mass, may be
o Variable T2 signal, depending on disc multiple
hydration o Most often associated with epidural
• Herniations of the protrusion and extension from a vertebral metastasis
extrusion subtypes most frequently o May also occur with transforaminal spread
hypointense relative to normal disc from a paraspinal or posterior mediastinal
• Sequestered disc fragments often of tumor
moderate-to-high T2 signal • Neurofibroma
• Synovial Cyst o Enhancing nodular, fusiform, or dumbbell
o Circumscribed, fluid-filled structure mass associated with a nerve root
o Variable iso- or hypointensity on T1 WI; o Epidural neurofibroma typically
centrally hyperintense on T2WI intraforaminal or transforaminal
o Adjacent/contiguous with a facet joint o May be associated with vertebral
o Cyst along ventral facet may impinge on scalloping, thinning/remodeling of
thecal sac or nerve root pedicles
o Seen with degenerative facet changes o Most (90%) solitary, nonsyndromic
• Peridural Fibrosis o May be multiple, extensive; associated
o Epidural scar formation following spinal with plexiform neurofibromas
surgery (neurofibromatosis type 1)
o Normal post-operative finding • Schwannoma
o Infiltrative morphology, rarely mass-like o Enhancing nodular, fusiform, or dumbbell
o Isointense T1; variable T2 signal, usually mass associated with a nerve root
II hyperintense relative to disc material
o May surround nerve root
5
36
EXTRADURAL lESION, 12 HYPERINTENSE, 11 ISOINTENSE
o Most schwannoma intradural; epidural o Heterogeneous enhancement

schwannoma typically intraforaminal or • Giant Cell Tumor
transforaminal o Lytic, expansile vertebral body lesion;
o Not reliably distinguished from solitary narrow zone of transition
neurofibroma o May extend into epidural/paraspinal
Helpful Clues for Rare Diagnoses spaces

o Heterogeneous iso- or hypointense on
• Plasmacytoma
Tl WI; heterogeneous hyperintensity on
o Solitary plasma cell tumor, osteolytic
T2WI
tumor, ± compression fracture, ±
• Areas of low-to-intermediate T2 signal
extraosseous extension
may reflect areas of high collagen
o Often indistinguishable from lytic
content and hemosiderin deposition
metastases
o Propensity to extend across sacroiliac joint
• Lymphoma
& disc space is unusual for other lesions
o Enhancing epidural mass or epidural
extension from a vertebral lesion and may simulate infection
o Often indistinguishable from metastases • Ewing Sarcoma
o Destructive tumor
o Spinal lymphoma may also manifest with
o Iso- or hypointense on Tl WI; moderate to
leptomeningeal or intramedullary lesions
hyperintense signal on T2WI
• Chordoma
o Paraspinal soft tissue mass often a feature
o Arises from notochord remnants: Midline,
osteolytic tumor of spinal Ewing sarcoma
o Sacrococcygeal location most common,
followed by clivus; vertebral lesion rather
uncommon
o May extend into epidural/paraspinal
spaces
o Heterogeneous iso- or hypointense on
T1WI; marked hyperintensity on T2WI
o Variable enhancement
• Chondrosarcoma
o Destructive tumor, chondroid matrix
o Iso- or hypointense on Tl WI; marked
hyperintensity on T2WI
Intervertebral Disc Herniation Intervertebral Disc Herniation
II
Axial T7WI MR shows sequestered disc fragment in the
=.
left anterolateral spinal canal The fragment is similar
Axial T2WI MR shows the same disc sequestration on
T2WI =1 in which it is hyperintense to both skeletal
5
in signal to skeletal muscle on T7WI. muscle and to normal disc material.
37
~ EXTRADURAL lESION, T2 HYPERINTENSE, T1 ISOINTENSE
:J
"0
ro
~
X
W
Gl
c:
an abnormal rounded mass
in Ihe righllateral spinal
canal = that is in continuity
wilh a degeneraled facel
join/. The mass has
intermediale signal on T I WI.
T2WI =-
shows the same mass on
in which Ihere is a
sharply circumscribed
margin, Ihin wall, and
hyperintense signal centrally.
Nole Ihe increased fluid
within both facel joints and a
sublfe protrusion of Ihe lefl
facet's synovial capsule

post-operative peridural
fibrosis as abnormal soft
tissue Ihat replaces the
normal (brighO epidural fal
between the anterolateral
margin of the thecal sac
and the left S 7 nerve root
=
sleeve~. (Right) Axial
T2WI MR in Ihe same patient
shows epidural fibrosis
be heterogeneously
=
to
hyperintense on FSE T2WI,

approaching Ihe intensily of
epidural fa/.
Abscess, Epidural Abscess, Epidural

shows a L]-4 disc space
infection with replaced
marrow signal in adjacent
vertebra and a ventral
epidural abscess =
hypoinlense on T1 WI. A
second dorsal epidural
collection = is a/so present.
(Right) Sagillal T2WI MR in
the same patient shows the
ventral phlegmon as
moderalely hyperinlense on
T2WI =. The full exlent of
the dorsal collection is more
apparenl ~ and approaches
CSF in hyperintensily.
II
5
38
EXTRADURAL lESION, 12 HYPERINTENSE, 11 ISOINTENSE CIl
~.
::l
CD
m
~
~
OJ
Hematoma, Epidural-Subdural (Acute) Hematoma, Epidural-Subdural (Acute) 0-
C
~
OJ
shows an acute epidural
hematoma =- isoin£ense to
lhe cord on T1WI, associaled
wilh bursl fracture of C7 81.
(Right) Sagittal STIR MR in
the same patient shows a T2
hyperintense dorsal epidural
hematoma = associated
wilh C7 burst fracture 81.
Epidural Metastatic Disease Epidural Metastatic Disease

(Left) Axial T1 WI MR in lhis
patient with metastatic lung
carcinoma shows a large
metastatic lesion to C2 with
preverlebral PJ:J:l and epidural
lID extension, isoinlense to
cord and skelelal muscle on
T IWI, effacing lhe lhecal sac
and compressing the cervical
cord 81. (Right) Axial T2'
eRE MR in the same palienl
shows lhe epidural sofllissue
=:I 10 be moderately
hyperintense on T2
weighted imaging
Neurofibroma Neurofibroma
a large lransforaminal mass,
hypointense on T I WI,
enlarging lhe lefl Lt-2 neural
foramen. The intraspinal
componenl =:I mildly effaces
lhe thecal sac. (Right) Axial
T2WI MR in lhe same palient
shows more clearly lhe
foraminal widening and
lhecal sac effacement by lhe
intraspinal component 1tJ.
Note the central
hypointensity with
surrounding T2
hyperintensity,
demonstrating the "target
sign" of a neurofibroma. II
5
39
EXTRADURAL LESION, 12 HYPOINTENSE, T1 HYPOINTENSE
DIFFERENTIAL DIAGNOSIS o If sufficiently ossified, may produce

marrow space with hyperintensity on
Common TlWI
• Intervertebral Disc Herniation o Idiopathic, probably related to
• Endplate Osteophyte hydroxyapatite or calcium pyrophosphate
• Facet Osteophyte deposition
• Ossification Ligamentum Flavum o May observe changes of DISH or OPLL
• OPLL elsewhere in spine
• Epidural Gas • OPLL
• Metal Artifact o Idiopathic condition, resulting in
Rare but Important calcification and thickening of the
• Epidural AVF posterior longitudinal ligament
o Most common in the cervical spine, can
involve upper thoracic
ESSENTIAL INFORMATION o Variable encroachment on the ventral
Helpful Clues for Common Diagnoses spinal canal
• Intervertebral Disc Herniation o If sufficiently ossified, may produce a
o Most common epidural lesion in adult marrow space with hyperintensity on
population TlWI
o Intermediate-to-Iow Tl signal • Epidural Gas
o Variable T2 signal, hyperintense signal can o Routinely seen in the acute post-operative
be seen with annular fissures and period
sequestrations o Can occur from
• Endplate Osteophyte • "Vacuum" disc phenomenon extending

o Endplate osteophyte formation commonly into disc herniation
accompanies degenerative disc disease • "Vacuum" joint phenomenon extending
o May be difficult to distinguish osteophyte into facet synovial cyst
from a disc herniation on MR; NECT can • Metal Artifact
supplement evaluation o Epidural catheters
• Ossification Ligamentum Flavum o Spinal cord stimulators

o Enlargement of ligamentum flavum o Spinal fusion hardware
causing variable posterolateral o Displaced intervertebral devices
encroachment on the thecal sac
o Best conspicuity of calcifications on NECT
Intervertebral Disc Herniation
II
5 Sagittal T1WI MR shows a large disc extrusion at L4-5.
Extruded disc material is similar in signal to the
Sagittal T2WI MR again shows large disc exlfusion that
is hypointense on T2WI.
remainder of the intervertebral disc on T I WI.
40
EXTRADURAL LESION, 12 HYPOINTENSE, 11 HYPOINTENSE
(Left) SagiLlal T IWI MR

shows severe disc space
narrowing at LS-SI with
small endplate osteophytes
=. Small disc extrusion is
present at L4-S~. (Right)
SagiLlal T2WI MR also shows
endplate osteophytes at
LS-SI =.2 and the small disc
extrusion at L4-S~.
Ossification Ligamentum Flavum Ossification Ligamentum Flavum

hypointense signal within a
thickened thoracic
ligamentum f1avum
mild posterolateral
= with
effacement of the thecal sac.

(Right) Axial T2WI MR also
shows hypoinlense signal
associated with the
thickened, ossified
ligamentum f1avum =
Metal Artifact
(Left) SagiLlal T1WI MR
shows two level fusion from
C3 to C5 with metal artifact
from screws =. Screw
artifact at C5 level extends to
the ventral epidural space
adjacent to the cord S.
Note the congenital fusion at
C6-7. (Right) SagiLlal T2WI
MR again shows metallic
artifact in epidural space at
C5S due to malpositioned
screw from anterior cervical
fusion.
II
5
41
~
OJ LUMBAR SOFT TISSUE MASS, PEDIATRIC
:J
"0
~
OJ
X DIFFERENTIAL DIAGNOSIS a Profound hypodensity on CT and Tl WI

w
Q)
hyperintensity characteristic of fat
c: Common a Use chemical fat saturation or inversion
C-
oo • Lipomyelomeningocele recovery MR techniques to confirm fat
• Myelomeningocele content
• Lipoma, Spinal • Spinal Muscle Injury, Traumatic
• Spinal Muscle Injury, Traumatic a Paraspinal muscle fiber disruption from
• Scoliosis indirect forces => abnormal muscle T2
Less Common hyperintensity and swelling
• Plexiform Neurofibroma a Most commonly from MVA; also athletic
• Ewing Sarcoma injuries, blow from falling objects, direct

• Lymphoma injury
• Venous Vascular Malformation • Scoliosis
a General term for any lateral curvature of
• Lymphatic Malformation
• Abscess, Paraspinal spine
• Dextroscoliosis: Curve convex to right
Rare but Important • Levoscoliosis: Curve convex to left
• Metastases, Lytic Osseous • Kyphoscoliosis: Scoliosis with
• Hemangiopericytoma component of kyphosis
• Meningocele, Dorsal Spinal • Rotoscoliosis: Scoliosis which includes
• Pseudomeningocele rotation of vertebrae
a Short-curve scoliosis usually has
ESSENTIAL INFORMATION underlying abnormalities; consider

congenital, neoplasm, or inflammation
• Appearance of overlying skin, pertinent Helpful Clues for Less Common Diagnoses
clinical information helps limit differential • Plexiform Neurofibroma
list a Long, bulky, multinodular nerve
enlargement is pathognomonic for NFl
Helpful Clues for Common Diagnoses a Often affects sacral or brachial plexi
• Lipomyelomeningocele • Ewing Sarcoma
a Lipomyelocele = neural placode-lipoma
a S% of all Ewing tumors in spine (sacrum>
complex contiguous with subcutaneous fat rest of spine)
through dysraphic defect, attaching to and a Usually in adolescents or younger adults
tethering spinal cord a Permeative lytic lesion of vertebral body or
a Lipomyelomeningocele = lipomyelocele +
sacrum involving vertebral body before
meningocele, enlargement of neural arch
subarachnoid space, displacement of • Contiguous spread along peripheral
neural placode outside of spinal canal nerves from spine or sacral primary, but
• Myelomeningocele may originate in soft tissues
a Posterior spinal defect lacking skin
• Lymphoma
covering => neural tissue, CSF, and a Lymphoreticular neoplasms with wide
meninges exposed to air variety of specific diseases & cellular
a Lumbosacral (44%) > thoracolumbar (32%) differentiation
> lumbar (22%) > thoracic (2%) a Multiple types demonstrate variable
a Low-lying cord on post-operative MR
imaging manifestations
imaging does not always = clinical • Venous Vascular Malformation
tethering a Congenital trans-spatial vascular
• Lipoma, Spinal malformation of venous channels present
a Arise from premature separation
from birth
II (dysjunction) of cutaneous ectoderm from
neuroectoderm during neurulation
5
42
LUMBAR SOFT TISSUE MASS, PEDIATRIC
a May be mass-like, frequently enhances a Vividly enhancing hypervascular

moderately (less than soft tissue neoplasm arising from pericytes
hemangioma) expanding/eroding spinal canal with large
a No arterial vessels within lesion, venous soft tissue component
channels may be large a Dural-based if primary, epicenter in bone if
a Look for phleboliths to make specific metastatic
diagnosis a Previously called angioblastic
• Lymphatic Malformation meningioma, but probably different
a Congenital trans-spatial vascular tumors
malformation of lymphatic channels • Meningocele, Dorsal Spinal
present from birth a Skin-covered dorsal dural sac containing
a Typically minimal to no enhancement, arachnoid, CSF protruding thorough
although septations may enhance, posterior osseous defect into subcutaneous
especially if previously inflamed tissues
a Fluid-fluid levels strongly suggest diagnosis • Always skin-covered; skin may be
a May grow rapidly if hemorrhage or dysplastic or ulcerated
concurrent viral infection a Lumbosacral junction, sacrum> > cervical,
• Abscess, Paras pinal thoracic
a Suppuration of paraspinal soft tissue from • Mild cases may show only absent
direct extension or hematogenous spinous process or localized spina bifida
dissemination of pathogens • More severe cases show multisegmental
a Identification of calcified psoas abscesses spina bifida, spinal canal enlargement
suggests tuberculous paraspinal abscess • Pseudomeningocele
a CSF-filled spinal axis cyst with supportive
post-operative or post-traumatic ancillary
• Metastases, Lytic Osseous
findings
a Osteolytic metastases of primary tumor to
a Cyst contiguous with thecal sac, not lined
spine; bone destruction exceeds bone
by meninges
production ~ lytic rather than blastic
a Fat-saturated T2WI best sequence to
a Lesion usually destroys posterior cortex,
demonstrate pseudomeningocele and
pedicle first
localize dural communication
lipomyelomeningocele
II
Sagillal T7WI MR demonsl,ales a low-lying spinal cord
inserting into a large lipomatous malformation that is
Sagillal T7WI MR shows a large unrepaired
myelomeningocele sac 1m. Neural elements are seen
5
contiguous with subcutaneous fat extending through a a
protruding into the sac which was not skin covered,
poslerior dysraphic defect confirming diagnosis of myelomeningocele.
43
<1l
~ LUMBAR SOFT TISSUE MASS, PEDIATRIC
:::J
"0
<1l
~
X
ill
Q)
c: Spinal Muscle Injury, Traumatic
enC- (Left) Sagittal T1 WI MR
demonSlrates a large
terminal lipoma adherent to
the distal spinal cord
contiguous with
subcutaneous fat in a patient
clinically presen!ing with a
palpable lumbar mass.
(RigM) Axial T2WI rsMR in
a trauma patient with back
pain and swelling reveals
characteristic diffuse soft
tissue edema in the right
paraspinal muscles and
subcutaneous tissues.
Scoliosis Plexiform Neurofibroma

(Left) Axial T2WI FS MR in a
patien! with VACTERL
demonstrates prolrusion of
the left paraspinal soft tissues
= due 10 congenital
scoliosis, explaining palpable
area of clinical concern.
Note also dysplastic right
kidney~. (RighI) Axial STIR
MR in this patient with
neurofibromalOsis type 1
reveals two palpable T2
hyperintense soft tissue
plexiform neurofibromas =.
Ewing Sarcoma lymphoma

depicts a large pelvic [wing
sarcoma with fUmor
extension into the
lumbosacral soft tissues,
producing pain and a
clinically palpable mass.
(Right) Axial T 1 C+ MR
enhancing thoracolumbar
epidural mass at the site of
palpable concern, extending
into the paraspinal muscles
and epidural space.
II
5
44
lUMBAR SOFT TISSUE MASS, PEDIATRIC
Venous Vascular Malformation lymphatic Malformation

shows homogeneous
enhancement within a
subcutaneous dorsal soft
tissue mass. The size of this
clinically palpable mass
changed with position and
onset of crying. (Right) Axial
f2WI FS MR reveals a large
abdominal 81 lymphatic
malformation with
trans-spatial extension into
the right lumbar flank soft
lissues = of this palient with
Proteus syndrome. Note
characterislic fluid-fluid level
PJ:2l.
following posterior spinal
fusion reveals a large
rim-enhancing fluid
collection = that surrounds
the hardware with marginal
inflammation in the dorsal
paraspinal soft tissues.
shows a large, lobulated,
paravertebral enhancing
mass that involves the left
dorsal elements 81. Note
extension along dural margin
into left neural foramen 1m.
Pseudomeningocele
shows mildly low-lying conus
at L2 and large skin-covered
dorsal CSF signal mass
communicating with the
=
thecal sac via a very thin,
fluid signal pedicle traversing
the posterior elements Ii8
(Right) Axial aWl MR
shows a large CSF signal
fluid collection in the dorsal
lumbar soft tissues, extending
From the right
hemilaminectomy site into
subcutaneous tissues. There
is no displacement or mass
eFFectupon the thecal sac.
II
5
45
SECTION 6
Intrad u ral- Extramed ullary
Cauda Equina Enhancement, Diffuse 11-6-2
Subarachnoid Space Narrowing 11-6-6
Intradural/Extramedullary, Leptomeningeal Enhancement 11-6-8

Intradural/Extramedullary Lesion, No Enhancement 11-6-12
Intradural/Extramedullary Lesion, Solid Enhancement 11-6-14
Intradural Lesion, Serpentine 11-6-18
Intradural/Extramedullary Lesion, Multiple 11-6-20

Intradural/Extramedullary Lesion,Ring/Peripheral Enhancement 11-6-22
Intradural/Extramedullary Lesion, T1 Hyperintense 11-6-26
Intradural/Extramedullary Lesion, T1 Hypointense 11-6-28
Intradural/Extramedullary Lesion, T1 Hypo, T2 Hypo 11-6-32
Intradural/Extramedullary Lesion, T2 Hyper, T1 Iso 11-6-34

Cauda Equina Syndrome 11-6-36
CAUDA EQUINA ENHANCEMENT, DIFFUSE
DIFFERENTIAL DIAGNOSIS a Metastatic disease may show either diffuse

smooth enhancement or more nodular
Common form
• Spinal Meningitis a Lung, breast carcinoma most common for
• CSF Disseminated Metastases systemic primaries
• Guillain-Barre Syndrome a PNET, GBM most common for CNS
• CMV Polyradiculopathy primaries
Q)
c: less Common a Look for bony metastases, retroperitoneal
c. lymphadenopathy
en • Sarcoidosis
• Arachnoiditis • Guillain-Barre Syndrome
• Lymphoma a Acute inflammatory demyelinating
• Chronic Inflammatory Demyelinating polyradiculopathy (AIDP)
Polyneuropathy (CIDP) a 1-2 cases/IOO,OOO per year
• Spinal Stenosis Compression a Monophasic demyelinating

• Disc Herniation Compression polyneuropathy related to prior infection,
• Hereditary Motor & Sensory Neuropathies esp. Campylobacter jejuni enteritis
• GB characterized by ascending limb
Rare but Important
weakness and areflexia
• Viral Radiculomyelitis
• Cranial nerve involvement in 50%
• Rabies • Back pain 30-50%
• Tick-Borne Encephalitis
• Respiratory failure
• Autonomic instability with labile BP,
ESSENTIAL INFORMATION cardiac arrhythmias
• Progression to plateau in 2 weeks
a Number of variants described
• Limited imaging differential considerations • Miller Fisher syndrome (MF) =>
include single vs. multiple root
ophthalmoplegia, ataxia, areflexia
involvement, smooth vs. nodular
• => Bickerstaff encephalitis appears closely
enhancement
related to MF with addition of alteration
a Multiple root involvement most common
of consciousness or long tract signs
and least specific for a single diagnosis
• Acute post-infectious axonal
a Single root involvement over long segment
polyradiculoneuropathy (AMSAN)
favors radiculitis secondary to disc
• Acute motor axonal neuropathy (AMAN)
herniation or stenosis
• Acute sensory ataxic neuropathy (ASAN)
a Smooth enhancement most common and
• Relapsing variants
least specific
a Treat with plasma exchange and IVlg
a Nodular enhancement much more likely
a 10% have permanent disability
with tumor or sarcoidosis
• Poor prognosis can be predicted based on
Helpful Clues for Common Diagnoses age, preceding diarrhea, and disability
• Spinal Meningitis score 2 weeks from presentation
a Shows diffuse, smooth enhancement of a Molecular mimicry => infectious agent
multiple roots and distal pial surface of sharing epitopic determinants with nerve
cord tissue incites immune response leading to
a Look for additional lesions such as nerve inflammation
subdural spinal empyema, epidural abscess a GB & variants represent autoimmune
or phlegmon disease to glycolipid structures
a Nonspecific appearance for etiology, • Campylobacter jejuni => GM1, GMlb,
whether pyogenic, granulomatous, fungal GDla, GalNac-GDla, GQlb
a Clinical history critical => LP mandatory • Haemophilus influenza => GM1, GTla
II • CSF Disseminated Metastases • Mycoplasma pneumoniae =>
Galacterocerebroside
6
2
CAUDA EQUINA ENHANCEMENT, DIFFUSE CIl
'0
::::J
CD
• Cytomegalovirus => GM2 Treatment with corticosteroids, plasma
o
o Microbial genetic polymorphism can exchange, IVIg
determine clinical presentation of human o Nerve hypertrophy of multiple roots in
autoimmune disease symmetrical fashion
• C. jejuni strain with gene cst-ll(ThrSl) o May mimic appearance of multiple
has GMI or GDla epitope => schwannomas or neurofibromas with NF2
Guillain-Barre or Nfl, respectively
• C. jejuni strain with gene cst-ll(AsnSl) • Spinal Stenosis Compression
has GQlb epitope => Miller Fisher o Typically focal, mild enhancement of
syndrome cauda equina at single level of severe
• CMV Polyradiculopathy central canal stenosis
o Infection in AIDS, impaired cell mediated o Multiple levels suggests other etiology
immunity than stenosis
o Assess for other infectious lesions => Toxo, • Disc Herniation Compression
crypto, TB, PML o Single lumbar root enhancing over long
o May progress rapidly with anesthesia and s~gment related to compression by caudal
weakness, variable amount of pain disc herniation
o Estimated 10% of AIDS patients have o Enhancement may reflect intrinsic neural
clinical deterioration related to CMV abnormality or distended radicular vein
o CMV radiculitis in 3% of autopsies of AIDS o 0 clear relationship to symptoms or
patients outcome
• Chronic Inflammatory Demyelinating SELECTED REFERENCES
Polyneuropathy (Cmp) I. Koga M et al: Campylobacter jejuni cst-II polymorph isms
o Group of disorders of peripheral nerves and association with development of Guillain-Barre
syndrome. Neurology. 69(17):1727-8; author reply 1728,
with similar clinical features
2007
o Must be distinguished from hereditary, 2. Steininger : Clinical relevance of cytomegalovirus
metabolic, and diabetic neuropathies infection in patients with disorders of the immune system.
Clin Microbiollnfec!. 13(10):953-63,2007
o Aberrant cellular and humoral immune
3. Willison HJ: Gangliosides as targets for autoimmune injury
response to peripheral nerve antigens to the nervous system. J Neurochem. 103 Suppl 1: 143-9,
o Unlike GB, CIDP is rarely preceded by 2007
4. Yuki N et al: Axonal Guillain-Barre syndrome:
infection & involved antigens are carbohydrate mimicry and pathophysiology. J Peripher
unknown Nerv Sys!. 12(4):238-49,2007
CSF Disseminated Metastases
II
rs
Sagiltal T7WI
&'
MR shows poslerior epidural abscess
wilh cauda cquina compression, L3-4 disc space
Sagillal TI WI FSMR shows multiple enhancing nodules
in distal cauda equina EJ from lung carcinoma
6
infectjon EI with body enhancement, and meningitis
= with dislal diffuse nerve rool enhancement
metastases. Marrow signal is normal. Nodular foci
indicate tumor or granulomatous disease.
3
CSF Disseminated Metastases Guillain-Barre Syndrome

(Left) SagiHal T1 C+ MR
shows glioblastoma drop
metastases as multiple
globular irregular areas of
clumped cauda equina and
distal cord 81. (RighI)
Sagittal T1 C + M R shows
rootlets =
multiple enhancing cervical
in this patient
with Cuiflain-Barre and
respiratory failure.

extensively enhancing
roots =
ventral and dorsal nerve
which spare the
distal cord. Ventral
enhancement predominating
is typical for motor variant of
Guillain-Sarre. (Right) Axial
T1 C+ fS MR shows diffuse
cauda equina enhancement
of multiple roots due to AIDS
polyradiculopathy (CMV)
=. No focal masses are
present History is critical
since appearance is
nonspecific.
shows a variant case of
spinal sarcoidosis, revealing
multiple subarachnoid
nodules =interspersed
among the cauda equina.
shows leptomeningeal root
enhancement from
disseminated intrathecal
leukemic metastasis
encircling the distal spinal
=..
cord and infiltrating the
cauda equina.
II
6
4
Chronic Inflammatory Demyelinating

Polyneuropathy (ClOP) Spinal Stenosis Compression
a typical case of spinal
chronic inflammatory
demyelinating
polyneuropathy (ClOP), with
enlargement and abnormal
intradural =
nerve enhancement of both
and extradural
!::l components. (Right)
Axial T1 C+ MR shows focal
root enhancement at site of
severe central stenosis e.
Hereditary Motor & Sensory

Disc Herniation Compression Neuropathies
single rool enhancement [;>l
due to disc herniation at L4-5
level (not shown), reflectmg
radiculitis. Engorged
radicular vein may show
similar finding. (Right)
Sagillal T1 C+ MR shows
diffusely thickening and
mildly enhancing nerves of
the cauda equina in this
patient with
Charcot-Marie-Tooth.
Viral Radiculomyelitis Tick-Borne Encephalitis

enhancement of the cord
and cauda equina =. West
Nile virus is an
arthropod-borne flavivirus
that can cause meningitis,
encephalitis, acute flaccid
paralysis, or poliomyelitis-like
syndrome. (Right) Sagittal T1
C+ MR shows rickellsial
infection (Rocky Mountain
spotted fever) with diffuse
cauda equina enhancement
=.
II
6
5
SUBARACHNOID SPACE NARROWING
DIFFERENTIAL DIAGNOSIS o Developmentally narrow canal; short,

thick pedicles
Common o Frequency: Lumbar> cervical> thoracic
• Stenosis, Acquired Spinal • Hematoma, Epidural-Subdural
• Stenosis, Congenital Spinal o May be spontaneous or associated with
• Extra-axial Mass trauma or instrumentation
o Hematoma, Epidural-Subdural o Signal varies with the age of the
Ql
c: o Abscess, Epidural hemorrhage
Co o Meningioma o Mild or no enhancement
en
o Metastasis, Epidural • Abscess, Epidural
o OPLL o May be associated with disc space
• Enlarged Cord infection or instrumentation/inoculation
o Demyelinating Disease o Marked peripheral enhancement typical
• Multiple Sclerosis, Spinal Cord (Acute) • Meningioma
• ADEM, Spinal Cord o Dural-based, circumscribed, enhancing
• Acute Transverse Myelitis, Idiopathic mass
• Neuromyelitis Optica • Multiple Sclerosis, Spinal Cord (Acute)
o Syringomyelia o Cord expansion uncommon, indicates an
o Ependymoma, Cellular, Spinal Cord acute lesion; resolves in 6-8 weeks
o Astrocytoma, Spinal Cord o Hyperintense on T2WI, variable
o Metastases, Spinal Cord enhancement
o Radiation Myelopathy o Image brain to check for supratentorial
Less Common lesion(s)
• Arachnoiditis, Lumbar • Ependymoma, Cellular, Spinal Cord
o Circumscribed, enhancing intramedullary
mass
ESSENTIAL INFORMATION o Necrosis and hemorrhage possible
Helpful Clues for Common Diagnoses • Astrocytoma, Spinal Cord
• Stenosis, Acquired Spinal o Fusiform enlargement, infiltrative margins;
o Multifactorial process involving disc no or variable enhancement
herniation and degenerative hypertrophy o Imaging cannot reliably differentiate from
of the posterior elements ependymoma

• Stenosis, Congenital Spinal o Appearance can be simulated by acute MS,
ADEM, neuromyelitis optica, myelitis
Stenosis, Acquired Spinal
II
6 Axial CECT (CT myelogram) shows almost complele Sagiltal T2WI MR shows a congenilally small cervical
=-
1055of the CSF spaces wilhin the thecal sac
protruding disc, facet arlhropathy
hypertrophy ~.
due 10
and ligamenlous
canal, with virtually complete 1055of the CSF spaces
surrounding the cord althe CJ-C5 levels.
6
SUBARACHNOID SPACE NARROWING
Hematoma, Epidural-Subdural Abscess, Epidural

a ventral, lentiform epidural
hemorrhage compressing
the thecal sac and dorsally
displacing the fibers of the
cauda equina. (Right)
Sagillal T2WI MR shows a
large ventral epidural
collection =:lI extending from
C2 into the upper thoracic
spine, effacing the CSF space
of the cervical canal and
compressing the cervical
cord. Note myelopathic
signal changes d>:.
Metastasis, Epidural
(Left) Sagillal n C+ MR
shows circumferential
enhancing epidural soft
ti.<sue=:lIthat effaces the
CSF spaces of the
mid-thoracic spine and
causes cord compression in
this patient with lymphoma.
Note prevertebral soft tissue
S> as well. (Right) Sagittal
T2WI MR shows thickened,
ossified posterior longitudinal
ligament =:lI effacing the
thecal sac and focally
compressing the cervical
cordE!lll.
Neuromyelitis Optica Astrocytoma, Spinal Cord

shows effacement of the
extramedullary CSF spaces
by a long segment of
fusiform cervical cord
enlargement. Cord
enlargement is accompanied
by diffuse T2 hyperinlensity.
shows loss of subarachnoid
spaces due to a large
heterogeneous mass
enlarging the cervical cord
and the associated syrinx 1tJ.
II
6
7
~ INTRADURAl/EXTRAMEDULLARY, LEPTOMENINGEAL ENHANCEMENT
ro
:::J
"0
Q)
DIFFERENTIAL DIAGNOSIS o Infection of spinal cord leptomeninges and
E
ro
~ subarachnoid space
;( Common o Smooth or irregular diffuse extensive
w,
ro • Guillain-Barre Syndrome meningeal enhancement or diffuse
~
:::J
"0
• Metastases, CSF Disseminated cerebral spinal fluid (CSF) enhancement
ro
~ • Meningitis, Spinal • Ependymoma, Myxopapillary, Spinal
C • Ependymoma, Myxopapillary, Spinal Cord Cord
Q)
c: • Neurofibromatosis Type I o Slow-growing glioma arising from
Co o Neurofibroma ependymal cells of filum terminale
C/)
Less Common o Enhancing cauda equina mass ±
• Neurofibromatosis Type 2 hemorrhage occurring nearly exclusively
o Schwannoma in conus, filum terminale, cauda equina
• Lymphoma • Neurofibromatosis Type 1
o Neurofibroma
• Leukemia
• Chemical Meningitis • Localized (90%), diffuse, or plexiform
(pathognomonic for NFl) neoplasms of
Rare but Important nerve sheath origin
• Sarcoidosis • Intradural/extramedullary common, may
• Arachnoiditis, Lumbar extend outside neural foramen in
• Hypertrophic Neuropathy dumbbell shape
• Anterior Radiculopathy Syndrome • Cervical> thoracic, lumbar
• ClOP
• Malignant Peripheral Nerve Sheath Tumors Helpful Clues for Less Common Diagnoses
o Schwannoma
ESSENTIAL INFORMATION • Peripheral nervous system nerve sheath
neoplasm
• Multiple in NF2; identification of other
classic lesions (vestibulocochlear or
trigeminal schwannomas) helps clinch
diagnosis
• Lymphoma
o Lymphoreticular neoplasms with wide
variety of specific diseases & cellular
differentiation
o Protean variable imaging manifestations
• Leukemia
o White blood cell neoplasia with spinal
involvement as component of systemic
disease
o Abnormal enhancement of marrow, focal
lesion, or leptomeninges on CECT and MR
o Diffuse osteopenia with multiple vertebral
fractures ± lytic spine lesions helps suggest
disease in context of intradural
enhancement
• Chemical Meningitis
o Nonspecific smooth (not nodular)
enhancement of intradural nerve roots in
correct clinical context
II o Often see some enhancement of conus pia
6
8
INTRADURAL/EXTRAMEDULLARY,LEPTOMENINGEAL ENHANCEMENT
o May persist after causative agent removed, o Avid enhancement without nodularity of
but should gradually return to normal anterior spinal cord pia and ventral
signal on follow-up studies lumbosacral nerve roots
Helpful Clues for Rare Diagnoses • CIDP
o Characterized by relapsing or progressive
• Sarcoidosis
muscle weakness ± sensory loss
o Noncaseating granulomatous disease of
o Focal or diffuse fusiform enlargement and
spine and spinal cord
abnormal T2 hyperintensity of cauda
o Protean imaging manifestations mimic
equina, nerve roots/plexi, and peripheral
multiple spinal pathologies
nerves
• Invariable presence of systemic disease
o Lumbar> cervical, brachial plexus,
helps make diagnosis and avoid biopsy
thoracic/intercostal> cranial nerve
• Arachnoiditis, Lumbar
o Both spinal nerve roots and peripheral
o Post-inflammatory adhesions + clumping
nerves (extraforaminal > intradural)
of nerve roots
o Best diagnostic clue is absence of discrete
involved
• Malignant Peripheral Nerve Sheath
nerve roots within thecal sac ("empty sac
Tumors
sign")
o Malignant tumor of neural sheath origin
• Nerves are adhesed to wall of thecal sac,
involving spinal root, neural plexus,
dural margins enhance
peripheral nerve, or end organs
o Evidence of prior lumbar surgery helps
o Large infiltrative, often hemorrhagic, soft
suggest diagnosis
tissue mass anatomically related to
• Hypertrophic Neuropathy
neurovascular bundle
o Hereditary disorder characterized by focal
o Paravertebral, rarely intraspinal
or diffuse peripheral nerve enlargement
o Fusiform peripheral nerve mass(es) ± Other Essential Information
enlarged cauda equina nerve roots • Diverse etiologies necessitate close clinical
• Anterior Radiculopathy Syndrome correlation to make a specific diagnosis
o Chemotherapy-related anterior nerve root
enhancement associated with intrathecal
methotrexate treatment
• Progressive paraparesis after intrathecal
methotrexate administration followed by
complete or partial recovery
Guillain-Barre Syndrome
II
Sagittal TI C+ MR shows diffuse smooth linear
enhancement of the conus pia and cauda equina nerve
Sagittal TI C+ MR demonstrates multiple nodular
leptomeningeal enhancing metastatic tumor deposi15
6
roots. (intracranialoligoaslrocyloma).
9
INTRADU RAL/EXTRAMEDU LLARY, LEPTOMEN ING EAL EN HANCEMENT

Cord
(Left) Axial nC+ FS MR
demonstrates smooth linear
enhancement of conus pia
and cauda equina nerve
roots. The CSF shows slightly
Ql higher signal intensity than
r::
normally expected for CSF,
Co
en suggesting proteinaceous
conten!. CSF should have
signal intensity similar to
other simple fluids on MR
imaging; variation from this
merits Further evaluation.
(Right) Sagiual T1 C+ MR
shows copious intradural
enhancing tumor filling the
distal thecal sac.
Neurofibroma Schwannoma
shows nodular enhancing
neurofibromas within the
conus leptomeninges and
the cauda equina. The
diagnosis was
neurofibromatosis type 1.
(Right) Sagiual T1 C+ MR
shows diffuse
leplOmeningeal
enhancement and
innumerable small
schwannomas in the cauda
equina. The diagnosis was
lymphoma
(Left) Sagiual T1 C+ MR
shows diffuse nodular
leptomeningeal
intrathecal dissemination of
Burkiu lymphoma. (Right)
enhancing intradural
lymphoma metastases along
the leplOmeninges,
surrounding the distal conus
and diffusely involving the
nerve roots.
II
6
10
I NTRADU RAlIEXTRAMEDU LLARY, LEPTOMEN I NGEAL EN HANCEMENT
conFirms diFFuse
leptomeningeal
enhancement from
leukemic metastasis
encircling the spinal cord
and inFiltrating the cauda
equina. (Right) Sagitlal T I
C+ MR shows diffuse
leptomeningeal
enhancement, representing
chemical meningitis in a
aneurysmal subarachnoid
hemorrhage patient. T1 WI
MR beFore contrast (not
shown) demonstrated no T1
shortening.
Sarcoidosis
shows diFFusenodular
enhancing coating of the
conus leptomeninges and
cauda equina. (Right)
diFFuseenhancement of
ventral conus pia and cauda
equina (anterior
radieulopathy syndrome).
Leptomeningeal tumor
dissemination may produce
an identical imaging
appearance to other csr
disseminated metastases.
Malignant Peripheral Nerve Sheath

Tumors
(LeFt) Sagittal T1 C+ rs
MR
demonstrates variant striking
diFFusepial and cauda
equina nerve rool
enhancement. Axial T2WI
MR images (not shown)
confirmed peripheral nerve
enlargement. (Right) Sagittal
T1 C+ MR shows a nodular
neuroFibroma along the
dorsal conus and extensive
enhancement of the distal
leptomeninges and thecal
sac From metastatic MPNST
(NFl).
II
6
INTRADURAL/EXTRAMEDULLARY LESION, NO ENHANCEMENT
DIFFERENTIAL DIAGNOSIS o CSF signal on T1WI, ~ CSF signal on T2WI

• Filum Terminale Fibrolipoma • Subarachnoid Hemorrhage
o Variable appearance depending upon clot
• CSF Flow Artifact
• Arachnoid Cyst formation, blood product age
• Conjoined Nerve Roots
Ql
Less Common o Aberrant root sleeve containing 2 nerve
C • Subarachnoid Hemorrhage roots
Co
en • Conjoined Nerve Roots • Dermoid and Epidermoid Tumors
• Dermoid and Epidermoid Tumors o Lumbosacral or cauda equina CSF signal
• Epidermoid Tumor, Acquired mass ± diffusion restriction (epidermoid)
• Meningioma (Calcified) • Epidermoid Tumor, Acquired
Rare but Important o Iatrogenically implanted epithelial
• Neurenteric Cyst elements (prior lumbar puncture with
• Arachnoiditis, Lumbar nonstyletted needle)
• ClOP • Meningioma (Calcified)
• Hypertrophic Neuropathy o Hypointense on Tl WI, T2WI;
calcifications obscure enhancement
Key Differential Diagnosis Issues o Intraspinal cyst lined by enteric mucosa ±
• Clinical correlation permits more specific vertebral anomalies
diagnosis • Arachnoiditis, Lumbar
Helpful Clues for Common Diagnoses o Post-inflammatory adhesion & clumping
• Filum Terminale Fibrolipoma of intrathecal nerve roots
o Linear fat signal in filum terminale, o May not perceive discrete nerves because
normal conus position adhesed to dural sac
• CSF Flow Artifact • CIDP
o Tl hyperintense, T2 hypointense o Focal/diffuse fusiform nerve enlargement,
com pared to CSF abnormal T2 hyperintensity
o Cannot confirm in exactly same place on • Hypertrophic Neuropathy
orthogonal imaging planes o Fusiform peripheral nerve ± cauda equina
• Arachnoid Cyst mass(es)
Filum Terminale Fibrolipoma CSF Flow Artifact
II
6 Sagittal T7WI MR demonstrates linear high signal
intensity wi!hin cauda equina, reflecting typical pallern
of ("tty infiltration by fibrolipoma.
Sagillal T7WI MR in a padent
arachnoid cYSt~
with
shows CSF flow artifact =
an epidural
in !he
thecal sac dorsal to the spinal cord, caused by altered
(Jow dynamics.
12
INTRADURAL/EXTRAMEDULLARY LESION, NO ENHANCEMENT
Arachnoid Cyst
(Left) Sagillal T7 C+ MR rs
reveals a large CSF signal
arachnoid cyst, centered in
epidural fa/, producing
dorsal mass effecl on the
dura and spinal cord. There
is no cyst wall enhancement.
(Right) Sagillal T7 C+ MR
demonslrales diffuse, slightly
increased CSF signal intensity
within the thecal sac,
reflecting proteinaceous
debris. There is no abnormal
intradural enhancement.
Conjoined Nerve Roots

(Left) Sagillal TI C+ FS MR
shows two nonenhancing
nerve roots
neural foramen.
=
in Ihe left LS
Enhancement in the
foramina above and below
the L5 level reflect
enhancement within the
dorsal rool ganglia. (Right)
Sagittal T I C+ MR sho\Vs
irregular CSF signal
architectural distortion of the
cauda equina nerve roots
without abnormal
enhancement, representing
an epidermoid that was
acquired after lumbar
puncture.
Hypertrophic Neuropathy
demonstrates a large ventral
neurenteric cyst, producing
There was no enhancement
of the cyst wall, and no
associated vertebral
anomalies were detected.
enlargement of the intradural
cauda equina nerve roots.
Imaging slices taken more
caudally (not shown) also
showed bilateral extradural
peripheral nerve
enlargement II
6
13
INTRADURAL/EXTRAMEDULLARY LESION, SOLID ENHANCEMENT
DIFFERENTIAL DIAGNOSIS • Neurofibroma

o Localized (90%), diffuse, and plexiform
Common (pathognomonic for NFl) nerve sheath
• Solid Mass neoplasms
o Schwannoma o Multilevel nerve root and paraspinal
o Meningioma tumors ~ neurofibromatosis type 1
o Neurofibroma • Ependymoma, Myxopapillary, Spinal
Ql
c: o Ependymoma, Myxopapillary, Spinal Cord Cord
"ii • Leptomeningeal o Occurs almost exclusively in conus, filum
en
o Metastases, CSF Disseminated terminale, cauda equina
o Post Chemo/Radiation Therapy Nerve o Enhancing cauda equina mass with
Enhancement hemorrhage
Less Common o Usually spans 2-4 vertebral segments; may
• Leptomeningeal fill entire lumbosacral thecal sac
o Leukemia • Metastases, CSF Disseminated
o Lymphoma o Spread of malignant tumors through the
o Guillain-Barre Syndrome subarachnoid space
o Meningitis, Spinal o Smooth/nodular enhancement distributed
o Sarcoidosis on cord surface and nerve roots
• Post Chemo/Radiation Therapy Nerve
Rare but Important
Enhancement
• Solid Mass o Nonspecific smooth (not nodular)
o Paraganglioma
enhancement of intradural nerve roots ±
o Malignant Nerve Sheath Tumors
conus pia
• Leptomeningeal o May persist after therapy completed, but
o Hypertrophic Neuropathy
should gradually return to normal signal
oCIDP
on follow-up studies
o CMV Radiculopathy
o Anterior Lumbar Radiculopathy Syndrome Helpful Clues for Less Common Diagnoses
o Metachromatic Leukodystrophy (MLD) • Leukemia
o P ET o Abnormal enhancement of leptomeninges
on CECT and MR
o Look for diffuse osteopenia, multiple
ESSENTIAL INFORMATION vertebral fractures ± lytic spine lesions to
suggest diagnosis
• Lymphoma
o Protean imaging manifestations; nodular
leptomeningeal metastases rare
• Guillain-Barre Syndrome
o Autoimmune post-infectious or
post-vaccinial acute inflammatory
demyelination of peripheral nerves, nerve
roots, cranial nerves
o Smooth pial enhancement of the cauda
equina and conus
• Meningitis, Spinal
o Infection of spinal cord leptomeninges and
subarachnoid space
o Smooth or irregular meningeal
enhancement ± CSF enhancement,
II abnormal CSF signal intensity ("dirty CSF")
• Sarcoidosis
6
14
INTRADURAl/EXTRAMEDULLARY LESION, SOLID ENHANCEMENT
o Combination of leptomeningeal and o Smooth pial enhancement of the conus,

peripheral intramedullary mass-like cauda equina
enhancement o onenhanced MR imaging is frequently
o Invariable presence of systemic disease normal - routine contrast administration
helps make diagnosis and avoid biopsy recommended in AIDS patients
Helpful Clues for Rare Diagnoses • Anterior Lumbar Radiculopathy
Syndrome
• Paraganglioma
o Chemotherapy-related anterior spinal cord
o Well-defined intradural extramedullary
pia and ventral nerve root enhancement
vascular mass with prominent flow voids,
following intrathecal methotrexate
intense enhancement
treatment
o Cauda equina > > cervical, thoracic spine
• Metachromatic Leukodystrophy (MLD)
• Malignant Nerve Sheath Tumors
o Autosomal recessive deficiency of
o Malignant nerve sheath tumor involving
lysosomal enzyme arylsulfatase A
spinal root, neural plexus, peripheral
o Nonspecific contrast enhancement of
nerve, or end organs
cauda equina nerve roots
o Large circumscribed infiltrative enhancing
o Specific diagnosis suggested by
mass ± hemorrhage
characteristic brain findings
• Hypertrophic Neuropathy
o Hereditary disorder characterized by focal • PNET
o Primary leptomeningeal origin of PNET
or diffuse peripheral nerve ± cauda equina
tumor
enlargement
o Nodular enhancement of cauda equina,
o Distal extremity atrophy ± abnormal
leptomeninges
muscle Tl hyperintensity, volume loss
(chronic denervation - fatty atrophy)
• CIDP
o Enlargement and abnormal T2
hyperintensity of nerve roots, plexi, or
peripheral nerves
o Lumbar> cervical, brachial plexus,
thoracic/ intercostal> cranial nerve
• CMV RadicuIopathy
o Immunosuppressed AIDS patients
II
Sagillal Tl c+ MR demonslrales a large homogeneous
inlradural mass Ihal fills the spinal canal and displaces
Sagittal Tl C+ FS MR reveals an intradural mass lesion
wilh avid mass enhancemenl and flallened base EE
6
the spinal cord in a paUent with path-proven suggesting dural attachment producing compression of
schwannoma. adjacent spinal cord.
15

Cord
shows a typical appearance
o( solitary intradural cauda
equina neurofibroma =.
(Right) Sagittal T' C+ MR
Ql reveals a mass within the
c: thecal sac, obscuring the
a.
rtl conus termination and cauda
equina. Note the avid
homogeneous tumor
enhancement.
Metastases, CSF Disseminated

(Lefl) Sagittal T' C+ MR
shows nodular enhancing
metastases
intracranial
=
leptomeningeal "drop"
from
oligoastrocytoma. (Right)
Sagittal T1 C+ MR
nodular cauda equina
infiltration. The cauda
equina nerve roots are
abnormally thickened with
diffuse leptomeningeal
enhancement caused by
leukemic metastasis
encircling the conus and
infiltrating the cauda equina.
shows extensive enhancing
leptomeningeal metastases in
this patient with
non-Hodgkin lymphoma.
(Rig/") Sagittal T' C+ MR
shows mild thickening and
avid enhancement of the
ventral motor roots of the
cauda equina and conus pia
=.
II
6
16
Sarcoidosis
(Lefl) Sagillal T7 C+ MR
leptomeningeal
cervical spinal cord
extending up into the
posterior fossa E±. (Rig"l)
Sagittal T I C+ MR shows
multiple enhancing
subarachnoid nodules
interspersed among the
cauda equina and studding
the conus pia.
Malignant Nerve Sheath Tumors

(Lefl) Sagittal T I C+rs MR
shows a small enhancing
intradural nodular mass
nestled within the cauda
enhancement =
equina with avid mass
typical of
paraganglioma. (Rigllt)
Sagillal T I C+ MR in a
patient wit" NFl shows a
nodular neurofibroma along
the dorsal conus and
the distal leptomeninges and
thecal sac from metastatic
malignant nerve sheath
tumor.
C1DP (MV Radiculopathy

(Lefl) Sagittal T7 C+ FS MR
demonstrates striking diffuse
pial and cauda equ;na nerve
root enhancement. Other
images (not shown)
confirmed peripheral nerve
enlargement (RighI) Sagittal
T7 C+ MR shows irregular
cauda equina nerve rool
enhancement secondary to
CMV polyradiculopathy.
Nonenhanced MR imaging
(not shown) was normal.
II
6
17
~
co
INTRADURAL LESION, SERPENTINE
:::J
"0
Q)
E DIFFERENTIAL DIAGNOSIS • GE imaging less susceptible to CSF flow
co
~ artifacts
X
UJ
Common • Turbulent flow leads to more rapid
...!.
co • CSF Flow Artifact proton dephasing with signal loss
~
:::J
"0
• Vascular Malformation, Type 1 a Repeat study with different plane of
co
~ • Vascular Malformation, Type 2
C
imaging, and GE sequences with short TE
• Redundant Roots due to Thecal Sac • Vascular Malformations
C1l
c: Compression a Most common is type 1 dural fistula
Co a Central Stenosis • Lesions are extramedullary AVFs, not
l/l
a Herniation (Uncommon) true AVMs
Less Common • Venous drainage from the DAVF results
• Tumor Feeding Vessels in increased pial vein pressure that is
a Hemangioblastoma, Spinal Cord transmitted to intrinsic cord veins
a Ependymoma, Myxopapillary, Spinal Cord • Venous hypertension from engorgement
a Paraganglioma reduces intramedullary AV pressure
a Schwannoma gradient, causing reduced tissue
• Hereditary Motor/Sensory Neuropathy perfusion & cord ischemia
• Collateral Veins/IVC Occlusion • Hallmark is T2 hyperintense cord
• Vascular Malformation, Type 3 (usually distal thoracic), intradural flow
• Vascular Malformation, Type 4 voids on cord surface, esp. dorsal
• Brain Dural A-V Fistula • Redundant Roots due to Thecal Sac
Compression
a Seen with severe central canal stenosis or,
ESSENTIAL INFORMATION much less commonly, large herniation
Helpful Clues for Common Diagnoses a Typically seen cephalad to level of severe
• CSF Flow Artifact stenosis

a Related to both time-of-flight (TOF) effects Helpful Clues for Less Common Diagnoses
and turbulent flow • Tumor Feeding Vessels
• TOF signal loss seen with SE or FSE when a Associated with vascular tumor such as
protons do not experience both initial RF ependymoma or hemangioblastoma
pulse and subsequent refocusing pulse a Look for primary enhancing soft tissue
• Increased signal loss with higher flow mass
velocity, thin slices, longer TE, imaging
perpendicular to flow
CSF Flow Artifact Vascular Malformation, Type 1
II
6 Sagillal T2WI MR shows extensive normal CSF flow
dephasing that involves the dorsal subarachnoid space =.
Sagittal T2WI MR shows typical serpentine flow voids
on dorsal aspect of thoracic cord with T2
18
= hyperintensity within distal thoracic cord (venous
hypertensive edema).
INTRADURAL LESION, SERPENTINE

Central Stenosis Cord
disc bulging =
shows severe stenosis with
producing
extensive nerve root
redundancy seen al mulliple
serpentine low signal rools of
the cauda equina within
lhecal sac 81. (Right)
intradural tumor =
Sagitlal T2WI MR shows
that has
prominent feeding serpentine
vessels 81.
Hereditary Motor/Sensory Neuropathy Collateral Veins/IVC Occlusion

(Left) Sagitlal T2WI MR
shows a case of
Charcol-Marie-Tooth with
diffuse enlargement of the
intradural cauda equina
nerve roots. The conus is
normal. (Right) Sagittal T2WI
MR shows chronic inferior
vena cava occlusion E:I with
intradural collateral venous
drainage in the lumbar spine
Vascular Malformation, Type 4 Brain Dural A-V Fistula

shows multiple prominent
flow voids within
subarachnoid space and
involving cervical cord from
lhis eXlensive AVM. (Right)
multiple flow voids on
cervical cord surface 1:1
wilh diffuse cord T2
hyperintensity. There is a
posterior fossa AV fistula
wilh intraspinal drainage 81.
II
6
19
INTRADURAL/EXTRAMEDULLARY LESION, MULTIPLE
DIFFERENTIAL DIAGNOSIS o Multiple, circumscribed extramedullary

masses associated with nerve roots, at any
Common location along the spine or cauda equina
• CSF Flow Artifact • Metastases, CSF_Disseminated
• Neurofibromatosis Type 1 o Spread from an extraspinal primary
• Neurofibromatosis Type 2 (breast, lung, lymphoma/leukemia) or
• Metastases, CSF Disseminated "drop metastases" from a CNS primary
Cl)
c: Less Common (medulloblastoma, ependymoma, GBM)
a. o Single/multiple dural- or pial-based
en • Multiple Nerve Sheath Tumors (Multiple,
Nonsyndromic) enhancing nodules; can become confluent,
o Schwannoma causing a "sugar coated" appearance
o Neurofibroma Helpful Clues for Less Common Diagnoses
• Meningiomas, Multiple • Multiple Nerve Sheath Tumors (Multiple,
• Type 1 DAVF Nonsyndromic)
• Hemangioblastoma, Spinal Cord o Most common "intradural extramedullary"
• Granulomatous Disease masses, but non-syndromic lesions are
Rare but Important usually solitary
o "Target sign", hemorrhage, degeneration all
• Cysticercosis
more common with neurofibroma than
with schwannoma
ESSENTIAL INFORMATION • Meningiomas, Multiple
Helpful Clues for Common Diagnoses o Dural-based, intensely enhancing, nearly
• Neurofibromatosis Type 1 isointense on Tl WI, variably hyperintense
o Multiple, enhancing, bulky, fusiform nerve on T2WI
root masses; may be intradural, extradural, o Multiple meningiomas can be seen with
or transdural type 2 neurofibromatosis
o Associated findings: Extraspinal plexiform Other Essential Information
neurofibromas, kyphoscoliosis, dural • Extramedullary masses (schwannomas,
ectasia meningiomas) frequently result in cord
o Suddenly enlarging or painful lesion: compression
Consider malignant degeneration
Neurofibromatosis Type 1
II
6 Sagittal T1 C+ MR shows typical case of muldple
enhancing nodules in the cauda equina in this patient
Sagittal T1 C+ MR shows muldple enhancing nodules
within fibers of tbe cauda equina in this patient with
with neurofibromatosis type 1. neurofibromatosis type 2.
20
INTRADURAL/EXTRAMEDULLARY LESION, MULTIPLE
Metastases, CSF Disseminated Metastases, CSF Disseminated

(Left) Sagittal T I C+ MR
shows typical case of drop
metastases from a pineal
germinoma, with multiple
extramedullary masses along
the surface of the conus and
fibers of the cauda equina.
(Right) Sagittal TI C+ MR
shows a bulky dural mass
compressing the
cervicomedullary junction
81 and multiple pial lesions
= in this patient with small
cell lung cancer.
Hemangioblastoma, Spinal Cord

shows T2 hyperintensity in
the cord (from venous
hypertension) and
innumerable intradural flow
voids along the exterior of
the cord in this patient with a
dural AV fistula. (Right)
Sagittal TI C+ MR shows
multiple focal enhancing
hemangioblastomas along
the dorsal cord surface
this patient with yon
= in
Hippel-Lindau. Note lesion

in the posterior fossa ~.
Cysticercosis
shows a case of
neurosarcoid, revealing
multiple enhancing
subarachnoid nodules
interspersed among the
cauda equina and along the
pia of the conus. (Right)
Sagittal CECT rCT
myelogram) shows multiple
subarachnoid filling defects,
representing cysts from
cysticercosis.
II
6
21
INTRADURAL/EXTRAMEDUllARY LESION, RING/PERIPHERAL ENHANCEMENT
DIFFERENTIAL DIAGNOSIS • Characteristic mass effect on fascicular

pattern on short axis imaging may help
Common distinguish from neurofibroma
• Arachnoid Cyst • Meningioma (Cystic or Calcified)
• Schwannoma (Cystic) o Slow growing, benign tumor originating
• Meningioma (Cystic or Calcified) from dura mater
less Common o Presence of diffuse or focal intraspinal
CI>
r:: • Neurenteric Cyst calcification helps suggest a specific
Q.
1Il • Meningitis, Spinal diagnosis
o Calcified portions may be hypo intense on
Rare but Important both T1WI MR and T2WI MR or be
• Cysticercosis relatively inconspicuous
• Arachnoiditis, Lumbar
• Arachnoiditis Ossificans, Lumbar Helpful Clues for less Common Diagnoses
• Echinococcus • Neurenteric Cyst
• Hypertrophic Neuropathy o Intraspinal cyst lined with enteric mucosa
o Abdominal or mediastinal location
• Ventral> dorsal
ESSENTIAL INFORMATION • Extramedullary (80-85%) >
Key Differential Diagnosis Issues intramedullary (10-15%)
• Using all available clinical information helps • Midline> paramedian
constrain the differential diagnosis list o Look for associated vertebral abnormalities
• Status of anatomical structures adjacent to (persistent canal of Kovalevsky,
the spinal cord may help suggest the correct segmentation, and fusion anomalies) to
diagnosis help make diagnosis
o However, not all neurenteric cysts are
Helpful Clues for Common Diagnoses associated with vertebral segmentation
• Arachnoid Cyst anomalies however
o Peripheral enhancing (faint) or
• Meningitis, Spinal
nonenhancing (more common) loculated o Infection of spinal cord leptomeninges and
extramedullary CSF intensity fluid subarachnoid space cerebrospinal fluid
collection surrounding spinal cord
o Displaces adjacent spinal cord or nerve
o Best diagnostic clue is diffuse, extensive
roots subarachnoid enhancement of meninges
o CSF signal intensity on T1WI MR, ~ CSF
and identification of CSF inflammatory
signal on T2WI MR loculations
• Reflects combination of signal alteration o Additional helpful clues (when present)
related to cyst proteinaceous content and include "dirty" CSF showing slightly
comparatively. flow related signal loss increased Tl & T2 signal intensity or
compared to CSF in thecal sac presence of fluid/debris level in terminal
o Consider FLAIRMR to accentuate signal
thecal sac
differences between cyst and CSF
(analogous to imaging brain arachnoid Helpful Clues for Rare Diagnoses
cyst) • Cysticercosis
• Schwannoma (Cystic) o CNS parasitic infection caused by pork
o Peripheral nervous system nerve sheath tapeworm (Taenia solium)
neoplasm originating from Schwann cells o Thoracic (60-75%) > cervical, lumbar
o Typically originates from dorsal rather location
than ventral spinal nerve roots o May be extraspinal (vertebral body) or
o Arises from single nerve fascicle and intraspinal (extradural, subarachnoid,
intramedullary)
II displaces other adjacent nerve fascicles
peri pherall y o Most frequently see multilocular cysts
rather than a single cyst
6
22
INTRADURAL/EXTRAMEDULLARY LESION, RING/PERIPHERAL ENHANCEMENT en
"'C
::::J
(l)
• Arachnoiditis, Lumbar a Best diagnostic clue; Identification of

;:!.
a Post-inflammatory adhesions producing multi loculated, multiseptated T2 OJ
Q.
clumping of nerve roots hyperintense vertebral body/posterior C
~
OJ
a Best diagnostic clue; Nonidentification of element mass showing minimal ,
discrete nerve roots within thecal sac enhancement m
~
~
("empty sac sign") • Hypertrophic Neuropathy OJ
3
• Nerves are adhesed to wall of thecal sac a Hereditary disorder characterized by focal CD
Q.
• Dural margins enhance or diffuse peripheral nerve enlargement C
OJ
a Evidence of prior lumbar surgery or a Fusiform peripheral nerve mass(es) ± cauda -<
residual intrathecal Pantopaque equina nerve roots
myelographic contrast helps suggest a ± Abnormal muscle Tl hyperintensity,
correct diagnosis volume loss (chronic denervation - fatty
• Arachnoiditis Ossificans, Lumbar atrophy)
a Intradural ossification associated with a Best diagnostic clue; Focal or diffuse
post-inflammatory adhesions and peripheral nerve enlargement + distal
clumping of lumbar nerve roots extremity atrophy
a Evidence of prior lumbar surgery or
residual intrathecal Pantopaque
• Using all available clinical information helps
myelographic contrast helps suggest to constrain the differential diagnosis list
correct diagnosis
• Pattern of involvement of regional spinal
a Look for focal calcific density on CT or
axis structures may also provide useful clues
hyperintensity on T1 WI and T2WI within
that can help limit diagnosis list
lumbar nerve root aggregate
• Important to assess for spinal cord
• Echinococcus compression
a Disease caused by cyst stage of
echinococcus genus tapeworm infestation
a Usually seen in patien ts living in endemic
area for echinococcus
a Liver, lung involvement are most common
a Bone involvement is rare
Arachnoid Cyst Schwan noma (Cystic)
II
Axial TI C+ FS MR shows anlerior displacement of
lower lhoracic spinal cord =:lI by a fainUy
Axial T1 C+ MR shows a wefl-circumscribed ventral
intraspinal mass compressing the spinal cord with 6
rim-enhancing posterior intraspinal fluid intensity mass
81. nonenhancing region=-
intense peripheral enhancement and a centIal cystic
23
INTRADURAL/EXTRAMEDUllARY lESION, RING/PERIPHERAL ENHANCEMENT
(Left) Sagittal T1 C+ MR in
patient with path-proven
meningioma demonstrates
an intradural mass at T3-4
Gl compression. Note avid mass
c: enhancement and small
0-
m dural taill:J suggesting
meningioma. (Right) Axial T1
C+ MR shows a heavily
hypointens€ mass =
calcified cervical dural-based
producing spinal cord E!l:I

compression. Heterogeneous
mass enhancement,
eccentricity helps distinguish
from severe focal OPLL
Neurenteric Cyst Meningitis, Spinal

demonstrates a dorsal
complex multilocular
extramedullary
heterogeneous
ring-enhancing mass 1m that
produces severe spinal cord
m compression. No
vertebral anomalies were
identified in this patient.
demonstrates smooth
abnormal enhancement of
the conus pia and cauda
equina nerve roots
(confirmed fungal
meningitis).
Meningitis, Spinal Meningitis, Spinal

shows smooth tinear
enhancement of cauda
equina nerve roots. CSF
shows slightly higher signal
intensity than normal,
indicating proteinaceous
content. (Right) Axial T1 C +
MR demonstrates diffuse
leptomeningeal
enhancement coating
cervical spinal cord. This
patient was diagnosed with
histoplasmosis and
successfully treated with
antifungal medication.
II
6
24
INTRADURAL/EXTRAMEDULLARY LESION, RING/PERIPHERAL ENHANCEMENT
Cysticercosis Cysticercosis
reveals a {ocal cystic mass
within the distal thoracic
spinal canal producing
fusiform spinal cord
expansion and
=
demonstrating mild cyst wall
Sagiual TI C+ MR shows a
cystic and solid
ring-enhancing mass that
produces severe spinal cord
compression and secondary
involvement of the upper
cervical cord.
Arachnoiditis, Lumbar Arachnoiditis Ossificans, Lumbar

depicts thickened and
clumped nerve rOOlS =
within the central aspect of
thecal sac related 10
arachnoiditis. Note prior
lamineclOmy defect,
suggesting source of
arachnoiditis. (RighI) Axial
NECT in patient with
myxopapil/ary ependymoma
(tumor not shown) shows
J;near dural calcification
Ossifying arachnoiditis is
=.
secondary to tumoral
post-hemorrhagic
inflammation.
Echinococcus Hypertrophic Neuropathy

(Left) Coronal TlWI MR
depicts multicystic
echinococcus lesions. The
large complex cystic mass
extends through the
paravertebral region into the
epidural space E2 and
compresses the thecal sac.
depicts moderate abnormal
enlargement of the intradural
cauda equina nerve roots.
There was also abnormal
enlargement of extradural
peripheral nerves in the
lower extremities (not
shown) of this patient with
Charcot-Marie-Tooth. II
6
25
INTRADURAL/EXTRAMEDULLARY LESION, 11 HYPERINTENSE
DIFFERENTIAL DIAGNOSIS o Incidental in 4-6% of autopsy subjects

o Intraspinal lipoma if larger lesion and
Common filum> 2 mm in thickness
• Metal Artifact • Lipoma
• Filum Terminale Fibrolipoma o Spinal lipoma intimately associated with
• Lipoma dorsal spinal cord (intradural) or distal
• Subdural Hematoma cord/filum insertion (terminal)
Ql
c: • Subarachnoid Hemorrhage o Hyperintense (Tl WI) intradural mass
a. • Lipomyelomeningocele o Use frequency selective fat suppression if
m
Less Common unsure of composition of hyperintense
• Dermoid and Epidermoid Tumors mass
• Melanoma Metastasis • Subarachnoid Hemorrhage
• Pantopaque o Intradural collection hyperintense on
Tl WI, predominantly hypointense on
Rare but Important T2WI or gradient-echo imaging
• Melanotic Schwan noma o Subarachnoid shows fluid-fluid level
• Melanocytoma o Subdural shows well-defined outer dural
margin, lobulated inner margin
ESSENTIAL INFORMATION • Lipomyelomeningocele
o Subcutaneous fatty mass contiguous with
Helpful Clues for Common Diagnoses neural placode/lipoma via posterior
• Metal Artifact dysraphism
o MR '* geometric distortion + signal loss o Cord always tethered
secondary to dephasing o Cutaneous stigmata (50%); hemangioma,
o Minimize with FSE, larger FOY, higher
dimple, dermal sinus, skin tag, hairy patch
bandwidth, small voxel, orientation of
frequency encode direction Helpful Clues for Less Common Diagnoses
o Minimize pedicle screw artifact by • Dermoid and Epidermoid Tumors
orienting frequency encode gradient o Epidermoid '* nonenhancing, CSF
parallel to screw long axis, using FSE signal-like intradural mass within cauda
technique equina
• Filum Terminale Fibrolipoma • Look for dermal sinus association
o Tl WI shows small linear focus of fat, with o Dermoid shows heterogeneous mass with
normal conus position and morphology mixed signal (fat)
Metal Artifact
II
6 Sagittal T1WI MR shows two level fusion from C3 to CS
with metal artifact from screws =. Screw artifact at C5
Sagittal T1WI MR shows fine linear region of T1
hyperintensity along the filum terminale due to fat 1m.
level extends to the ventral epidural space adjacent to The conus is normal in position.
thecordSl.
26
INTRADURAL/EXTRAMEDULLARY LESION, 11 HYPERINTENSE CIl
"t:l
::::J
CD
Lipoma Subdural Hematoma

shows lumbar skin dimple
= with dermal sinus tract
containing a small dermoid
t:21 The low-lying spinal
cord is affixed to a dorsal
intradural lipoma SII. (Right)
Axial T7WI MR shows Ihe
subdural location of the
hemorrhage, with an intact
curvilinear outer dural
margin and a typical
lobulated inner margin.
Dermoid and Epidermoid Tumors

shows telhered cord that
terminates into a lipomatous
mass I:lJ atlhe L4-S level,
and a dorsal bony
dysraphism. (Right) Axial
TI WI MR shows a large
dermoid tumor = with T I
hyperintensity and a
well-defined lobulated
contour.
Pantopaque Melanotic Schwannoma

(Left) A,ial T1WI MR shows
a focal high signal wilhin
distallhecal sac due 10 prior
Pantopaque myelography
m. Note changes of prior
laminectomy. (Right) Sagillal
T7 WI MR shows a varianl
case of an intradural
extramedullary schwannoma
= involving the lumbar
nerve rools wilh high signal
seen on pre-contrast T I
images due to melanin.
II
6
27
INTRADURAL/EXTRAMEDULLARYLESION, 11 HYPOINTENSE
DIFFERENTIAL DIAGNOSIS o Nonenhancing extramedullary loculated

CSF intensity collection displacing cord or
Common nerve roots
• CSF Flow Artifact o May be suggested by mass effect on cord
• Post-Operative Intrathecal Gas and nerve roots without direct wall
• Metal Artifact visualization
• Arachnoid Cyst o Partial filling of cyst may occur with CT
CI)
c: • Epidermoid myelography, with wind-sock type
a.
CJ)
• Meningioma, Calcified • Epidermoid
• Schwan noma, Cystic o Nonenhancing intradural mass similar to
• Vascular Malformation CSF intensity within cauda equina
Less Common o Should not track CSF on all pulse
• CSF Disseminated Metastases sequences, as would arachnoid cyst
• Displaced Cord with Prominent Adjacent o Should not enhance, unless complicated
CSF by infection
o Spinal Cord Herniation o If lumbar in child, look for associated
o Arachnoiditis/Adhesion dermal sinus track
o Post-Traumatic Pseudomeningocele • Meningioma, Calcified
• Arachnoiditis Ossificans o Enhancing intradural/extramedullary mass
• Cysticercosis and dural tail
• Ependymoma, Myxopapillary (Calcified) o Calcified lesions may show little
• Glioma, Exophytic enhancement, very low Tl/T2 signal

o May show target pattern with central
Rare but Important calcification, peripheral homogeneous
• eurenteric Cyst tumor enhancement
• Schwannoma, Cystic
ESSENTIAL INFORMATION o Well-circumscribed, dumbbell-shaped,
enhancing spinal mass
Helpful Clues for Common Diagnoses o May be solid, yet show Tl homogeneous
• CSF Flow Artifact hypointensity
o Linear or rounded low signal with o Tl hypointensity may also reflect cyst
ill-defined margins surrounding cord due formation
to normal CSF motion • Vascular Malformation
o Typically most prevalent in dorsal thoracic
o Serpentine flow voids with well-defined
spine margins
o Include axial GE images to minimize
o Variable pattern depending upon type
artifact and exclude vascular flow voids (fistula vs. AVM) and location (cord vs.
• Metal Artifact pial vs. transpatial)
o Geometric distortion and signal loss
o Most common is type 1, with vessels on
secondary to dephasing dorsal cord surface with cord T2
o Tl images show focal central signal loss
hyperintensity due to venous hypertension
with peripheral "halo" of t signal related to
spatial mismapping Helpful Clues for Less Common Diagnoses
o Image quality: Fast spin echo> • CSF Disseminated Metastases
conventional spin echo < gradient echo o Smooth/nodular enhancement along cord,
o Smaller voxel size, lower field strength roots is best clue
decrease artifact amount o Without contrast, leptomeningeal mets
o Appropriate geometric orientation of may show ill-defined cord & cauda with
frequency encode direction parallel to "dirty" CSF appearance
pedicle screws shows thecal sac best • Spinal Cord Herniation
II • Arachnoid Cyst o Herniation of spinal cord through defect
in dura of ventral canal
6
28
INTRADURAL/EXTRAMEDULLARY LESION, T1 HYPOINTENSE
o Focal anterior displacement of cord with o CNS parasitic infection caused by pork
expansion of dorsal subarachnoid space in tapeworm, Taenia soli urn
upper thoracic spine o Intradural cyst with evidence of similar
o Distinguish from posterior arachnoid cyst lesions in brain most helpful clue
by more abrupt cord deformity with o Parenchymal, leptomeningeal,
idiopathic herniation intraventricular, spinal form with cyst size
• Arachnoiditis/Adhesion up to 2 cm
o Focal tethering of cord to dura from prior • Exophytic Intramedullary Tumor
surgery, infection, or SAH o Solid exophytic component may mimic
o Shown by distortion of location and !D/EM lesion
morphology of cord within thecal sac o Look for contiguous extension into cord
o May be associated with arachnoid cysts, on sagittal/axial planes
superficial siderosis, cord edema o Contrast enhancement may show
• Post-Traumatic Pseudomeningocele contiguous nature of intramedullary mass
o CSF collection typically associated with
upper cervical fracture (odontoid) with • Neurenteric Cyst
ventral CSF collection and displacement of o Intraspinal cyst and vertebral
cord posteriorly abnormalities
o Multisegmental posterior displacement of o Focal osseous canal enlargement, widening
cervical cord in face of significant cervical of interpedicular distance
trauma o Complex signal transpatial mass with cord
o Distinguish from acute epidural
deformity
hemorrhage that shows isointense Tl o Smaller versions may show Tl
signal, heterogeneous T2 signal hyperintensity at Cl-2 junction
• Arachnoiditis Ossificans
o Uncommon presentation of arachnoiditis
due to prior trauma, lumbar surgery,
subarachnoid hemorrhage, myelography,
spinal anesthesia
o End-stage arachnoiditis with diffuse or
nodular low signal on all pulse sequences
involving dura and cord surface, cauda
equina
• Cysticercosis
Metal Artifact Arachnoid Cyst
II
Sagittal TI WI MR shows two level fusion from C3 to C5
with metal arUfact from screws =. Screw artifact at C5
Axial TlWI MR shows typical case of intradural
=
arachnoid cyst wilh CSF signal displacing /he cord
6
level extends to the ventral epidural space adjacent to posteriorly.
cord8l. Note congenital fusion at C6-7.
29
INTRADURAL/EXTRAMEDULLARY LESION, 11 HYPOINTENSE
Epidermoid
(Lefl) Sagiltal TI WI MR
demonstrates a hypo;ntense
intradural mass = nestled
within the cauda equina that
displaces adjacent nerve
Ql roots. (RighI) Axial TlWI MR
s:: shows epidermoid as
a.
en rounded hyperintensity
centrally within the thecal
sac, displacing roots to the
periphery.
(Lefl) Axial TI C+ MR shows

variant case or a heavily
calcified cervical meningoma
I:] displacing cord to the left
with severe cord
compression ~. (RighI)
Axial NfCT shows densely
calcHied meningioma I::]
filling the cervical thecal sac,
with displacement of the
cord to the left.
Schwannoma, Cystic Schwannoma, Cystic

(Left) Sagiltal TlWI MR
shows subtle low signal mass
caudal to the conus
medullaris, hypointense to
the cord 1:]. (RighI) Sagiltal
TI C+ MR shows ID/[M
mass with slightly
heterogeneous but intense
enhancement 1:]. Solid and
mixed solid/cystic masses
may show quite low T 1
signal.
II
6
30
INTRADURAL/EXTRAMEDULLARY LESION, 11 HYPOINTENSE
CSF Disseminated Metastases

shows multiple intradural
flow voids (rom dural fistula
with intraspinal drainage =.
(RighI) SagilLal T1WI MR
shows disseminated
leptomeningeal metastasis as
ill-defined low T1 signal,
with obscuration of the
normal cauda equina.
Arachnoiditis/Adhesion
(Lefl) Sagittal T IWI MR
shows typical case of cord
herniation demonstrating
focal cord thinning and
ventral kinking =. Primary
differential for this case is
posterior arachnoid cyst vs.
cord herniation. (RighI)
posterior displacement of the
cervical cord I:] with ventral
angulation at thoracic
junction =.due to prior
SA/-! and subsequent
arachnoiditis.
Neurenteric Cyst
patient with type I odontoid
(racture shows pronounced
CSF signal collection =
anterior to the cervical cord
with generalized posterior
cord displacement. (RighI)
mediastinal enteric cyst I:]
communicating with a
contiguous spinal canal
neurenteric cyst E:I. The
mediastinal enteric cyst
extends into the ventral
spinal canal through a patent
canal of Kovalevsky.
II
6
31
INTRADURAL/EXTRAMEDULLARYLESION, 11 HYPO, 12 HYPO
DIFFERENTIAL DIAGNOSIS • Metal Artifact

o Fast spin echo better than conventional
Common spin echo better than gradient echo
• CSF Flow Artifact o Use larger field of view
• Post-Operative Change, Normal o Appropriate geometric orientation of
• Metal Artifact frequency encode direction
• Vascular Malformation • Parallel to pedicle screws
Cl>
c • Meningioma, Calcified • Vascular Malformation
a.
l/l Less Common o Most common is type 1 dural fistula
• Ependymoma, Myxopapillary (Calcified) o Hallmark is T2 hyperintense cord (usually
• Arachnoiditis Ossificans distal thoracic), intradural flow voids
• Superficial Siderosis (especially dorsal)
• Meningioma, Calcified
o Well-defined ID/EM lesion with dural base
ESSENTIAL INFORMATION o Generally low T2 signal
Helpful Clues for Common Diagnoses o Solitary lesion, except with F2
• CSF Flow Artifact Helpful Clues for Less Common Diagnoses
o Related to both time-of-flight (TOF) effects • Ependymoma, Myxopapillary (Calcified)
and turbulent flow o Well-defined enhancing cauda equina
• Turbulent flow => more rapid dephasing mass with evidence of prior hemorrhage
with signal loss • Arachnoiditis Ossificans
• TOF signal loss seen with SE or FSEwhen o Intradural ossification associated with
protons do not experience both initial RF post-inflammatory adhesion and clumping
pulse and subsequent refocusing pulse of lumbar nerve roots
• Increased signal loss with higher flow o Low signal thickened dura and roots
velocity, thin slices, longer TE, imaging • Superficial Siderosis
perpendicular to flow o SAH (multiple etiologies) causing
• Gradient echo imaging less susceptible to hemosiderin deposition on cord, nerve
CSF flow artifacts surface
o Repeat study with different imaging plane, o Diffuse hypointensity of cord surface on
GE sequences with short TE T2WI, GE
• Post-Operative Change, Normal
o Most common will be small foci of gas
from violation of dura
CSF Flow Artifact Metal Artifact
II
6 Sagillal STIR MR shows prominent signal loss involving
the CSF throughout the cervical and upper thoracic
Axial T2 GRE MR shows Up of Baclafen delivery
catheter to the left of the upper thoracic cord =::1.
spine =::1 related to CSFpulsation and flow dephasing.
32
(Jl
INTRADURAl/EXTRAMEDULLARY LESION, 11 HYPO, 12 HYPO ~.
:J
CD

shows multiple IDIEM flow
voids = with cord
hyperintensity & expansion
from C 1-4 in this case of
posterior fossa dural fistula
~ with cervical venous
drainage. (RighI) Lateral
angiography shows
intradural draining veins E2.
This mimics the pallern of
type 1 fistula, but
hypertensive myelopathy
was caused by posterior
fossa fistula = with spinal
shunting.
Meningioma, Calcified
shows a thoracic IDIEM
mass with a central low
signal (calcification) 11Im
displacing the cord
posteriorly 81. (RighI)
broad dural-based
hypointense calcified
meningioma =producing
Arachnoiditis Ossificans
peripheral low signal
surrounding a distal thecal
sac due to thickened and
calcified dura from severe
arachnoiditis =. (Rig"')
typical case of superficial
siderosis with hypointense
deposilion along the entire
cord surface =.
II
6
33
INTRADURAL/EXTRAMEDULLARY LESION, 12 HYPER, T1 ISO
DIFFERENTIAL DIAGNOSIS o Bulky multilevel spinal nerve root tumors

in patient with NFl
Common o Rapid growth of NF suggestive of
• Schwannoma malignant transformation
• Neurofibroma o Target sign suggestive of neurofibroma ••
• Epidermoid peripheral high signal, central lower signal
• Ependymoma • Epidermoid
Cll
s:: • CSF Disseminated Metastases o Nonenhancing intradural mass similar to
Q.
l/) Less Common CSF signal on T2/Tl images
• Cysticercosis • Ependymoma
• Tuberculoma o Myxopapillary type within caudal sac may
• Sarcoidosis show near iso T1 signal, T2 hyperintensity
• Meningioma o Large fraction (20-30%) may show little
enhancement
Rare but Important
• CSF Disseminated Metastases
• Paraganglioma o Look for "dirty" CSF appearance on T1,
• Capillary Hemangioma with indistinct cauda and conus
• Neurenteric Cyst o Diffuse or nodular enhancement along
• Echinococcus cauda equina
ESSENTIAL INFORMATION • Capillary Hemangioma
Helpful Clues for Common Diagnoses o Benign tumor of endothelial cell origin
• Schwannonla o T2 hyperintense enhancing well-defined
o Well-circumscribed, dumbbell-shaped, intradural mass
enhancing spinal mass o May be indistinguishable from
o 30% of primary spine tumors meningioma or schwannoma
o 75% T2 hyperintense • Neurenteric Cyst
o Solitary unless part of inherited tumor o Intraspinal cyst and vertebral
syndrome, such as NF2 abnormalities
o Scan entire spine in asymptomatic patients o Osseous canal enlargement, widening of
with suspected neurofibromatosis type 2 interpedicular distance
• Neurofibroma o Iso- - hyperintense T1 reflecting
protein/mucin content
Schwannoma Neurofibroma
II
6 Sagillal T2WI MR shows a sharp margin of rounded
schwannoma m involving the cauda equina as a T2
Coronal STIR MR shows multiple bilateral thoracic and
lumbar nerve root neurofibromas extending through the
hyperintense mass and displacing the fOOts of cauda
34 =.
posleriorly
neural foramina into the paraspinallissues.
INTRADURAL/EXTRAMEDUllARY lESION, T2 HYPER, T1 ISO
~
--.
OJ
Epidermoid a.
c
--.OJ
T
shows a typical case of an m
intradural epidermoid tumor ~
--.
with well-defined margin and OJ
diffuse T2 hyperintensity =. 3
<ll
a.
(Right) Sagittal TlWI MR c
shows low to isoinlense Q)
signal, intradural epidermoid
masses at L2-] 81 and
-<
LS-sacrum =. There is a
dermal sinus tract extending
dorsally from the low sacral
regione=.
Epidermoid CSF Disseminated Metastases

shows a dorsal dermal sinus
~ with intradural
epidermoids involving the
cauda sac lID and near
conus 81. (Right) Sagittal
TlWI MR shows a typical
case of drop metastases from
a brain gHat neoplasm:
Abnormal slightly increased
CSF signal intensity with
poor definition of conus.
CSF Disseminated Metastases Cysticercosis

shows drop metastases from
a brain glial neoplasm as a
vague, increased signal and
obscuration of nerve roots of
cauda equina =.
(Right)
Axial T2WI MR shows cord
involvement by cysticercosis
with a well-defined rounded
lesion with T2
hyperintensity.
II
6
35
CAUDA EQUINA SYNDROME
__ D_I_FF_E_R_E_N_T_IA_L_D_I_AG_N_O_S_IS __ I I__ E_S_SE_N_T_IA_L_I_N_F_O_R_M_A_T_IO_N __

Common Key Differential Diagnosis Issues
• Stenosis, Acquired Spinal, Lumbar • Cauda equina syndrome (CES): Low back
o Intervertebral Disc Herniation, Lumbar pain, sciatica, leg weakness, saddle
o Spondylolisthesis hypoesthesia/anesthesia, urinary
• Trauma incontinence or retention, and incontinence
C1l
c: o Burst Fracture, Lumbar of bowel
Co o Sacral Fracture (Zone 3) • Substantial clinical overlap between the
l/l
o Traumatic Spondylolisthesis syndromes of the cauda equina and the
o Penetrating Injury conus medullaris
• Post-Operative Spinal Complications • Most common cause is herniation of the
• Abscess, Epidural, Paravertebral intervertebral disc
• Neoplasm • MR or CT myelography are useful modalities
o Metastases to evaluate causes of CES
o Ependymoma, Myxopapillary, Spinal Cord • Acute onset CES generally considered a
o Meningioma neurosurgical emergency, with best results if
o Arachnoid Cyst decompressed within 24-48 hours
• Hematoma, Epidural-Subdural Helpful Clues for Common Diagnoses
Less Common • Intervertebral Disc Herniation, Lumbar
• Multiple Sclerosis, Spinal Cord o CES occurs in approximately 1-2% of cases
of herniated lumbar disc
Rare but Important
o Most patients will have a long-standing
• Sarcoidosis history of back problems with or without
• Type IV AVF unilateral sciatica
• Post-Operative Spinal Complications
• Ankylosing Spondylitis
o Misplaced pedicle screw
·CIDP
o Displaced surgical device (fusion cage,
• Guillain-Barre Syndrome (Atypical
graft material, artificial disc)
Presentation)
o Epidural hematoma or abscess
o Incomplete decompression
o Retained sponge
Stenosis, Acquired Spinal, lumbar Intervertebral Disc Herniation, lumbar
II
6 Axial T2WI MR shows severe lumbar canal narrowing at
L4-5 =:I secondary to disc bulge, ligamentous
Axial T2WI MR shows huge L5-51 extrusion =
completely effacing the thecal sac at this level and
hypertrophy, and marked facet osteophyte. compressing the cauda equina.
36
CAUDA EQUINA SYNDROME en
"0
:J
lD
~
~
OJ
a.
, t, c
~
(Left) Lateral myelography OJ
=
T
shows severe L5-S I m
ij~,iI"''"
o
'I I1'0'
••
spondylolisthesis with
truncated filling of the caudal
~
~
OJ
3
,~'", '"' ," ~
thecal sac~, (RigM)
ct>
a.
c
1_,',"',,'1'
"'~~~ burst fracture of L2 with
retropulsion of a large
= -<
OJ
.•
/
t" fragment inlO the canal
1
causing severe effacement of
'.
~.~ l the thecal sac and cauda
,
"
;,
,
-~-. I
'
"
equina compression.
...;1.~'~'~)
~~.~t,~
, ~
Sacral Fracture (Zone 3) Abscess, Epidural, Paravertebral

highly comminuted sacral
fracture with vertical
fractures extending through
neural foramina = and a
transverse fracture through
S2~, (Right) Sagillal TI C+
MR shows L3-4
discilis-osleomyelilis
a large dorsal epidural
= with
abscess at Ll-] compressing

the thecal sac ~,

Cord Meningioma
shows a farge, intensely
enhancing lobulated mass
filling the distal thecal sac,
and expanding and
remodeling the sacrum 9:,.
(Right) Sagittal TI C+ MR
spinal canal =
enhancing mass in the distal
with focal
remodeling of the sacrum -7
angiomatous meningioma of
the sacral canal.
II
6
37
SECTION 7
Intramedullary
Intramedullary Mass 11-7-2
Conus Abnormality 11-7-6

Cord, Small/Atrophic 11-7-10
Intramedullary Lesions, Multiple 11-7-12
Intramedullary Lesion, Solid Enhancement 11-7-14
Intramedullary Lesion, No Enhancement 11-7-18
Intramedullary Lesion, Diffuse/Ill-defined Enhancement 11-7-20
Intramedullary Lesion, Ring/Peripheral Enhancement 11-7-24

Intramedullary Lesion, T1 Hypointense, T2 Hypointense 11-7-26
Intramedullary Lesion, T1 Hypointense 11-7-28
Intramedullary Lesion, T2 Hyperintense, T1 Isointense 11-7-30
Intramedullary Lesion, T1 Hyperintense 11-7-34
Cord Lesion, T2 Hyperintense, Ventral 11-7-38
Cord Lesion, T2 Hyperintense, Dorsal 11-7-40
Cord Lesion, T2 Hyperintense, Central 11-7-44

Myelopathy 11-7-48
INTRAMEDULLARYMASS
DIFFERENTIAL DIAGNOSIS o Typically located eccentrically, not

involving the entire cord on axial imaging;
Common relatively short in length « 2 vertebral
Q) • Demyelinating Disease bodies)
c:
c.. o Multiple Sclerosis, Spinal Cord o Enlargement of the cord is unusual
en o ADEM, Spinal Cord (6-14%)
o Acute Transverse Myelitis, Idiopathic o Multiphasic lesions: Some enhance, some
• Ependymoma, Spinal Cord don't
• Astrocytoma, Spinal Cord o 5-24% of patients with MS cord plaques
• Syringomyelia may not have supratentorial disease at
• Contusion-Hematoma, Spinal Cord presentation
Less Common • ADEM, Spinal Cord
• Hemangioblastoma, Spinal Cord o Clinical: Self-limited, monophasic
• Intramedullary Arteriovenous Malformation demyelinating illness 5-14 days following

• Infarction, Spinal Cord viral infection or vaccination
• Cavernous Malformation, Spinal Cord o Usually indistinguishable from multiple
• Metastases, Spinal Cord sclerosis on imaging
• Lymphoma • Acute Transverse Myelitis, Idiopathic
o Clinical: Acute onset myelopathy,
Rare but Important ascending or static loss of sensory and
• Sarcoidosis motor function in a bilateral and
• Cysticercosis symmetric distribution
• Schwannoma, Intramedullary o Infiltrative signal abnormality may extend
• Lipoma, Spinal above level of deficit, variable
• Ganglioglioma enhancement
• Glioblastoma Multiforme, Spinal Cord o Mild fusiform enlargement may be present
and simulate the appearance of primary
ESSENTIAL INFORMATION cord neoplasm
• Ependymoma, Spinal Cord
Key Differential Diagnosis Issues o Circumscribed, enhancing intramedullary
• MR without and with contrast is the best mass; located centrally within the cord
tool to evaluate intramedullary processes of o Can show signs of necrosis (heterogeneity,
the cord cyst formation) and hemorrhage
• Discovery of an intramedullary cord lesion (hyperintense Tl, susceptibility artifact,
typically followed by imaging of the hemosiderin "cap sign")
remainder of the neuraxis o Most common intramedullary neoplasm in
• Infiltrative cord lesion: Image brain to adults
potentially identify characteristics white • Astrocytoma, Spinal Cord
matter lesion(s) of multiple sclerosis o Fusiform enlargement, infiltrative margins,
• Discovery of intramedullary tumor typically long segment of involvement; no or
accompanied by insidious onset variable enhancement
myelopathic symptoms (months or years) o Most commonly located in the cervical
• Nearly every patient with a syrinx should be and upper thoracic cord
imaged at least once with contrast-enhanced o Uncommon/rare imaging features:
MR to exclude a cord neoplasm Hemorrhage, necrosis, caudal location,
• Hemorrhagic lesion: Think ependymoma, exophytic growth, ho]ocord involvement
hemangioblastoma, cavernoma, contusion o Cannot be reliably differentiated from
Helpful Clues for Common Diagnoses ependymoma by imaging
• Multiple Sclerosis, Spinal Cord o Second most common cord neoplasm in
II adults, most common cord neoplasm in

children (60%)
7
2
INTRAMEDULLARY MASS
• Syringomyelia o Hyperintensity on T2WI, possibly with

o Abnormal cystic cord lesion with mild expansion
surrounding gliosis; variable expansion of o Conus and variable thoracic cord
the cord; focal or extensive; typically involvement, cervical ischemia is atypical
longitudinal o Most often associated with aortic
o Secondary to chronic insult/injury pathology (dissection, thoracoabdominal
(cavitation) or to altered CSF dynamics in aortic surgery), rarely with atherosclerotic
the central canal of the cord (technically disease or embolism
termed hydromyelia, such as seen in • Cavernous Malformation, Spinal Cord
Chiari I malformation) o Variable hyperintensity on TI,
Helpful Clues for Less Common Diagnoses heterogeneously hyperintense on T2 with
• Hemangioblastoma, Spinal Cord surrounding rim of susceptibility due to
o Intensely enhancing, hypervascular prior episodes of hemorrhage that blooms
tumor(s); usually located dorsally within on gradient echo sequences
o Rare enhancement; may have some
the cord
o Multiple lesions common (check the
surrounding edema if recent bleed
posterior fossa!) • Metastases, Spinal Cord
o Most common primary is lung, followed
o Mayor may not have an associated syrinx,
which can be disproportionately large by breast
relative to the size of the actual enhancing Helpful Clues for Rare Diagnoses
tumor • Sarcoidosis
o Often with signs of prior hemorrhage o May simulate other diseases; diagnosis
o Often with prominent serpiginous usually preceded by known pulmonary or
subarachnoid flow voids due to enlarged systemic involvement
draining veins Other Essential Information
o 70-90% NOT associated wi th von
• Tumor associated syrinx (a.k.a., polar or
Hippel-Lindau
satellite cysts): Intramedullary fluid
• Intramedullary Arteriovenous collections rostral &/or caudal to the tumor,
Malformation
with nonenhancing margins
o Hyperintense T2 signal in the cord
• More rostral tumor associated with higher
o Tortuous vesselslflow voids on MR,
likelihood of syrinx formation
hypervascularity on CT angiography
• Infarction, Spinal Cord
Demyelinating Disease
II
Sagitlal T1
enhancement
in
c+
this patient
MR shows 3 foci of pathologic
=.::I due to ADEM
\vith an acute
within the cervical cord
ilJness {oJ/owing viral
=-
Sagittal T2WI MR shows complex cervical cord mass
containing foci of susceptibiHty
hemorrhage within an ependymoma.
demonstrating prior
7
prodrome.
3
2:-
rn
INTRAMEDULLARY MASS
:J
TI
Q)
E
rn
~
C
Astrocytoma, Spinal Cord
Q) (Left) Sagittal T7 C+ MR
c:
shows enhancing intra-axial
Co
(/) mass with rostral and
cauda! syrinx and satellite
lesion r=:l enlarging the
cervical cord. Note severe
syringobulbia (Right)
infiltrative lesion expanding
the mid-cervical cord. C3- S
decompressive laminectomy
has been pedormed.
Contusion-Hematoma, Spinal Cord

shows haustrated CSF-signal
mass = in the central cord
in a patient with a Chiar; 7
malformation. Hypointense
foci r=:l are due to flow
artifact. (Rig"') Sagittal STIR
MR shows heterogeneously
=
hyperintense conus lesion
representing a
hemorrhagic cord contusion,
secondary to L7 burst
fracture and traumatic
spondylolisthesis l:1.
Intramedullary Arteriovenous
Hemangioblastoma, Spinal Cord Malformation
shows a Focal enhancing
hemangioblastoma mass
expanding the cervical cord
at C4 with associated
syrinx. There is a large
cerebellar cystic mass as \Veil
156 (Righi) Sagittal T2WI MR
shows patchy hyperintensity
\Vithin the cord '5'] due to
intramedullary arteriovenous
malformation. Note dorsal
flow voids due to tortuous,
dilatated vascularity~
II
7
4
INTRAMEDUllARY MASS
Infarction, Spinal Cord Cavernous Malformation, Spinal Cord

(Left) Sagittal T2WI FSEMR
shows infiltrative
hyperintensity and mild
enlargement of the conus
medul/aris B in this patient
with lower extremity
paralysis following aortic
aneurysm repair. (Right)
slightly expansile
intramedullary lesion at the
C2-] level [i'8 with classic
mixed hyperintense
("popcorn") lesion
surrounded by a hypointense
rim.
Metastases, Spinal Cord Sarcoidosis

(Left) Sagittal T 1 C+ FS MR
show focal intramedullary
breast carcinoma metastasis
enlarging the distal cord =:I.
Note vertebral metastasis B
with mild compression
(racture. (Right) Sagittal T1
C+ MR demonstrates
extensive cord enlargement
and intramedullary
enhancement due to
sarcoidosis.
Schwan noma, Intramedullary

small, circumscribed
intramedullary enhancing
focus =- representing an
intramedullary schwannoma
(Rigl1t) Sagittal T2WI MR
shows infiltrating brainstem
and cervical cord mass with
exophytic growth into the
4th ventricle.
II
7
5
CONUS ABNORMALITY
DIFFERENTIAL DIAGNOSIS • Marked enhancement typical

• Can show signs of necrosis
Common (heterogeneity, cyst formation) and
Ql • Filum Terminale Fibrolipoma hemorrhage: Subarachnoid hemorrhage,
c:
a. • Primary Cord Neoplasm superficial siderosis
lI)
o Ependymoma, Myxopapillary, Spinal Cord • Bony remodeling when large: Vertebral
o Astrocytoma, Spinal Cord scalloping, foraminal enlargement,
o Hemangioblastoma, Spinal Cord widened and eroded pedicles
o Paraganglioma o Astrocytoma, Spinal Cord
• Demyelinating Disease • Cervical/upper thoracic most common;
• Syringomyelia rarely involves conus
• Tethered Spinal Cord o Hemangioblastoma, Spinal Cord
Less Common • Focal hyperenhancing lesion(s), often
• Cavernous Malformation, Spinal Cord with disproportionately large syrinx
• Infarction, Spinal Cord • Multiple sites of involvement in cord
• Ventriculus Terminalis and posterior fossa typical
• Often with signs of prior hemorrhage
Rare but Important
• 70-90% NOT associated with von
• Metastases, Spinal Cord Hippel-Lindau
• Arteriovenous Malformation/Fistula o Paraganglioma
• Developmental Abnormality • Virtually indistinguishable from the
o Terminal Lipoma
much more common myxopapillary
o Diastematomyelia
ependymoma
o Dorsal Dysra phism
o Infection (e.g., schistosomiasis) can
• Myelomeningocele/Myelocele simulate a conus neoplasm
• Lipomyelomeningocele/Lipomyelocele • Demyelinating Disease
• Terminal Myelocystocele o Isolated involvement of the conus with
o Caudal Regression Syndrome
multiple sclerosis probably extremely rare
o Segmental Spinal Dysgenesis
o Case reports of isolated conus involvement
• Infection with other causes of demyelination (e.g.,
o Schistosomiasis
ADEM)
o Cysticercosis
• Syringomyelia
o Tuberculoma
o Hydrosyringomyelia of the conus can
occur as an isolated finding or as a
ESSENTIAL INFORMATION component of more extensive
involvement
o Terminal syringomyelia can be seen with
tethered cord
o Tip of conus usually lies at the T12-L2 level
o Tip of conus below L2-3 is abnormal
o Associated abnormalities include thick
filum, dysraphism, vertebral anomalies,
etc.
• Cavernous Malformation, Spinal Cord
o Variable hyperintensity on Tl,
heterogeneously hyperintense on T2 with
surrounding rim of susceptibility due to
II prior episodes of hemorrhage, which
blooms on gradient echo sequences
7
6
CONUS ABNORMALITY
o Rare enhancement; may have some o Common features: Everted elements of

~
~
surrounding edema if recent bleed neural arch; tethered, dysraphic cord III
• Infarction, Spinal Cord o Lipomyelomeningocele and 1ipomyelocele: 3
CD
a.
o Hyperintensity on T2WI, possibly with Neural placode adherent to fatty mass c
mild expansion which is contiguous with subcutaneous III
o Most often associated with aortic fat; intact overlying skin -<
pathology (dissection, thoracoabdominal o Myelomeningocele and myelocele: Neural
aortic surgery), rarely with atherosclerotic placode exposed (no overlying skin)
disease or embolism o Lipomyelocele and myelocele: eural
• Ventricularis Terminalis placode lies within spinal canal
o Incidental, transient finding of childhood o Lipomyelomeningocele and
mild dilatation of the caudal terminus of myelomeningocele: eural placode and
the central canal in an otherwise normal CSF-filled meningeal sac protrude through
conus the dorsal spinal defect
o Up to 2-4 mm diameter and :s 2 cm length o Terminal myelocystocele (least common):
o No signal changes or enhancement in CSF-filled meningeal sac, containing a
adjacent parenchyma tethered cord with a terminal hydromyelic
cyst, extend through a caudal sacral defect;
intact overlying skin
• Metastases, Spinal Cord
• Schistosomiasis
o Hematogenous spread: Most common
o Intense inflammatory reaction with
primary is lung, followed by breast
ischemic necrosis due to infection by
o Drop mets: Medulloblastoma,
parasitic trematodes
ependymoma, GBM
o Cord edema and ill-defined enhancement
• Arteriovenous Malformation/Fistula
over several segments; cord enlargement
o Hyperintense T2 signal in the cord
o May simulate tumor
o Tortuous vessels/flow voids on MR,
o Thoracic cord and conus involvement
hypervascularity on CT angiography
common
• Terminal Lipoma
• Cysticercosis
o Fatty mass associated with conus
o Spinal intramedullary cysticercosis is rare;
medullaris (e.g., not a neural placode)
more common with intradural cysts
o Usually with a tethered cord; posterior
o Intramedullary disease presents with
bony dysraphism may be present
peripherally enhancing cystic lesions,
• Dorsal Dysraphism edema

Filum Terminale Fibrolipoma Cord
II
Sagiual T1WI MR shows linear hyperintensity within the
cauda equina, with normal positioning of the conus~.
Sagittal T2WI MR shows enlargement of conus
medullaris by hyperintense mass ~. Multiple
7
schwannomas seen in cauda equina in this patient with
neurofibromatosis type 2. 7
CONUS ABNORMALITY
Hemangioblastoma, Spinal Cord

Q)
(Lefl) Sagiltal T2WI MR
c:
shows enlargement of the
c.
lI) conus medullaris by an
expansile intramedullary
mass =. Decompression
laminectomy has been
performed. (RighI) Sagiual
T1 C+ MR shows large, solid,
avidly enhancing mass
involving the conus =
with
tumor syrinx superiorly ~.
Demyelinating Disease Syringomyelia

(Lefl) Sagiual T2WI MR
shows patchy hyperintensity
and expansion of the conus
medullaris = in this child
with ADEM. (RighI) Sagiltal
T2WI MR shows haustrated
syringomyelia of the distal
thoracic cord and conus in
this child with a Chiari
malformaOon.
Tethered Spinal Cord Infarction, Spinal Cord

(Lefl) Sagiltal T1 WI MR
shows a low·lying conus,
terminating at the L]-4 level
=. A thickened filum
terminale was identified on
axial imaging. (RighI) Sagiual
T2WI MR shows
hyperinlensity in the dorsal
conus with faint fusiform
enlargement = in this
patient with acute lower
extremity paralysis following
aortic aneurysm repair.
II
7
8
CONUS ABNORMALITY
Ventriculus Terminalis Metastases, Spinal Cord

shows the typical
appearance of ventriculus
lerminalis, with fusiform
enlargement of the caudal
end of the central canal =::I.
shows a rounded metastatic
lesion within the conus
medullaris =::I and rather
extensive edema throughout
the visualized cord PJ:ll.
Arteriovenous Malformation/Fistula Terminal Lipoma

shows hemorrhagic lesion of
the conus 81 (note
hemorrhagic fluid-fluid leve/)
with multiple pial flow voids
PJ:ll in this patient with a type
2 AVM. (Right) Sagittal T1 WI
MR shows a 100v-lying,
tethered cord terminating in
a small lipoma 6B

shows low-lying cord with
nellral placode adherent 10 a
caudal Fatty mass, which is
contiguous with the
subcutaneous fat through a
large dorsal lumbosacral
bony defect. The disjunction
lies within the canal
shows shortened cord with
abruplly truncated conus
medullaris 81. Note mild
hydromyelia and disordered
lower vertebral column with
diminutive, dysplastic
sacrum=.
II
7
9
CORD, SMALl/ATROPHIC
DIFFERENTIAL DIAGNOSIS • Multiple Sclerosis, Other Noncompressive

Myelopathies
Common o Diverse group of etiologies: Non-MS
Ql • Focal Cord Atrophy diagnoses include ADEM, SL£, sarcoidosis,
c:
Co o Compressive Myelopathy, Chronic HIV, syphilis, Lyme disease, and
(/)
o Multiple Sclerosis, Other Noncompressive paraneoplastic syndromes
Myelopathies • Cord Trauma, Chronic
o Cord Trauma, Chronic o Patient history usually reveals diagnosis
o Infarction, Spinal Cord, Chronic o Atrophy may be focal; in severe and
o Radiation Myelitis, Chronic proximal cases, holocord involvement may
• Diffuse Cord Atrophy be present
o Multiple Sclerosis (or Other • Infarction, Spinal Cord, Chronic
Noncompressive Myelopathy) o Uncommon due to vascular supply of cord
o Chronic, Severe Cord Trauma (e.g.,
Transection) Alternative Differential Approaches
o Severe Cerebral Atrophy
• Cervical cord typically occupies 75% of
o Infarction, Spinal Cord, Chronic
spinal canal diameter; less than 50%
o Collapsed Syrinx
generally accepted as cord atrophy
• Maximal cervical cord dimensions
Rare but Important o MR and CT myelography: 7.2 mm AP x
• Spinal Cord Herniation 13.8 mm transverse (C4-5) (Fountas)
• Spinocerebellar Ataxia (Friedreich Ataxia), o Autopsy: 0.9 mm AP x 14.9 mm transverse
Other Hereditary Paraplegia/Ataxia (C4-5) (Nordqvist)
Syndromes
• Segmental Spinal Dysgenesis
SELECTED REFERENCES
l. Fountas KN et al: Cervical spinal cord--smaller than
ESSENTIAL INFORMATION considered? Spine. 23(14): 15 13-6, 1998
2. Nordqvist L: Sagittal diameter of the spinal cord and
Helpful Clues for Common Diagnoses subarachnoid space in different age groups: a
• Compressive Myelopathy, Chronic roentgenographic post-mortem study. Acta Radiol Diagn.
5(Suppl):1-96,1964
o Chronic cord injury due to mechanical
impingement by disc herniation,
spondylolisthesis, or spinal canal mass
o Offending lesion may have been surgically
decompressed
Multiple Sclerosis, Other

Noncompressive Myelopathies
II
7 Sagittal T7WI MR shows diffuse cord atrophy from
chronic mechanical compression by marked thoracic
Sagittal STIR MR shows diffuse cord atrophy and patchy
hyperintensity in this patient with chronic multiple
OPLL=. sclerosis.
10
CORD, SMALl/ATROPHIC
~
~
Ql
3
CD
c.
C
shows diFFusecord atrophy Ql
From HIV myelopathy.
(Right) Sagittal T2WI MR in
-<
this patient status post
resection of a thoracic
ependymoma shows
tethering of an atrophic cord
dorsally into the mid-thoracic
laminectomy deFect.
Cord Trauma, Chronic Infarction, Spinal Cord, Chronic

this childhood MVA patient
shows cord atrophy, most
Focally at the TJ-4 level 81.
NOle decompression
laminectomy. Distally, small
syrinx is present =:I. (Right)
diFFusecord atrophy in this
patient with remole
post-traumatic aortic
dissection.
Spinal Cord Herniation

(LeFt) Sagittal T2WI MR
shows atrophic cervical cord
containing collapsed syrinx
=:I. Note suboccipital
craniectomy and C 1
laminectomy for
decompression of Chiari
malFormation 81. (Right)
Sagillal T2WI MR shows
anterior tethering of the cord
with enlargement of the
dorsal CSF space and Focal
AP narrowing of the cord
=:I
II
7
11
INTRAMEDULLARY LESIONS, MULTIPLE
DIFFERENTIAL DIAGNOSIS • Variable enhancement, depending on

the stage
Common o Little mass effect or edema
Q) • Multiple Sclerosis, Spinal Cord o Supratentorial involvement is typical
c:
c. • Metastases, Spinal Cord
Ul
• ADEM, Spinal Cord Helpful Clues for Less Common Diagnoses
• Hemangioblastoma, Spinal Cord
Less Common o 75% sporadic; 25% VHL-associated
• Hemangioblastoma, Spinal Cord • Ependymoma, Cellular, Spinal Cord
• Ependymoma, Cellular, Spinal Cord o Many grow centrifugally & usually cause
• Cavernous Malformation, Spinal Cord symmetric expansion of cord
Rare but Important • May help to differentiate from
• Sarcoidosis astrocytomas: More infiltrating, causing
• Cysticercosis asymmetric, lumpy cord expansion
o Multiple lesions in approximately 15-33%
ESSENTIAL INFORMATION of spontaneous cases
Key Differential Diagnosis Issues • Familial form is autosomal dominant
• Lesions in other locations such as osseous, with variable expression & more
supratentorial, & systemic can help with commonly has multiple lesions,
differential considerations occurring in as many as 73%
• Multiple Sclerosis, Spinal Cord • Sarcoidosis
o 2/3 of cord lesions in cervical cord & < 2 o Invariable presence of systemic disease
vertebral segments in length o Intramedullary lesions in cervical &
o Dorsolateral aspect of cord involving gray thoracic cord
& white matter • Cysticercosis
o Enhancement lasts 1-2 months o 5% of neurocysticercosis cases, involving
• Metastases, Spinal Cord subarachnoid space most commonly
o Typically < 1.5 em with extensive edema • Thoracic cord predilection related to
o Brain mets in 20% higher percentage blood flow
o Multifocal flame-shaped white matter
lesions
Multiple Sclerosis, Spinal Cord Metastases, Spinal Cord
II
7 Sagittal T2WI MR demonstrates mulUple hyperintense
intramedullary lesions·~ with focal cord enlargement,
Sagillal TI c+ MR shows mulliple enhancing nodules
within the cord from metastatic leukemia =.1.
There is
typical of demyelinaUon. Spinal cord & brain gray diffuse expansion of the cord.
matter involvement is common in MS.
12
INTRAMEDULLARY LESIONS, MULTIPLE
ADEM, Spinal Cord Hemangioblastoma, Spinal Cord

(Left) SagiLLalT2WI MR
demonstrates numerous
hyperintense inlramedullary
lesions within the medulla
81 & cervical spinal cord
=- characteristic of
demyelinating lesions.
Lesions typically involve both
gray & white matter
structures. (RighI) SagiLLal
TlWI MR shows 2
enhancing intramedullary
foci 1:'.2 in Ihe distal cord and
conus with associated
intraspinal cyst 81. Multiple
small tumors are seen in von
rlippel-Lindau syndrome.
Cavernous Malformation, Spinal Cord

(Lefl) SagiLLalTl C+ MR
shows 2 intramedullary
enhancing lesions in the
cervical cord 81. There is
fusiform cord enlargement &
a rostral cyst 1:'.2. (RighI)
lobulated mass in the distal
cord. The heterogeneous
signal reflects various ages of
blood by-products 81. No
edema or cord expansion is
seen. 10-30% are multiple &
more often seen with {amilial
syndrome.
Sarcoidosis
(Left) SagiLLalTl C+ MR
shows peripheral
intramedullary 1:'.2 &
leptomeningeal nodular
enhancing foci~. Central
intramedullary spread is via
perivascular spaces. (RighI)
Sagittal T2WI MR shows 2
focal intramedullary areas of
slightly decreased signal
within an extensive area of
cord edema 1:'.2. T2
hypointensity may ref/ect
calcification in degenerated
cyst wall.
II
7
13
INTRAMEDUllARY LESION, SOLID ENHANCEMENT
DIFFERENTIAL DIAGNOSIS o May have bony canal expansion

o Usually spans 2-3 vertebral segments
Common • Astrocytoma, Spinal Cord
Ql • Ependymoma, Cellular, Spinal Cord o Intramedullary enhancing, infiltrating
c:
'0. • Ependymoma, Myxopapillary, Spinal Cord mass that expands the cord
C/)
• Astrocytoma, Spinal Cord • Cervical> thoracic
• Multiple Sclerosis, Spinal Cord • Usually < 4 segments
Less Common • Multisegmental or holocord, more
• Hemangioblastoma, Spinal Cord common with pilocystic astrocytoma
• ADEM, Spinal Cord o May be associated with cyst/syrinx
• Cavernous Malformation, Spinal Cord • Multiple Sclerosis, Spinal Cord
• Neuromyelitis Optica o 10-20% cases have isolated spinal cord
• Type I DAVF involvement
o Cervical cord is most commonly affected
Rare but Important
o Dorsolateral aspect of cord
• Lymphoma o Enhancement during the acute or subacute
• Metastases, Spinal Cord state can be homogeneous, nodular, or
• Infarction, Spinal Cord ring enhancing
• Type II AVM
• Ganglioglioma Helpful Clues for Less Common Diagnoses
o Subpial intramedullary mass on dorsal
ESSENTIAL INFORMATION aspect of cord shows intense,
Key Differential Diagnosis Issues homogeneous enhancement
• Look for multiple lesions, supratentorial • ± Syrinx in > 50%
lesions, & osseous lesions in metastases, • Lesions "- 2.5 cm show serpentine flow
multiple sclerosis, ADEM, & voids
hemangioblastoma o Extensive, long segment edema
• Internal hemorrhagic products with o Hemorrhage is common
heterogeneous T1/T2 signal can be seen with • ADEM, Spinal Cord
certain lesions, such as cavernous o Multifocal spinal cord white matter lesions
malformation, ependymoma, & with little mass effect or vasogenic edema
paraganglioma o Brain typically also involved
o Enhancement depends on stage
Helpful Clues for Common Diagnoses • ± erve enhancement
• Ependymoma, Cellular, Spinal Cord • Cavernous Malformation, Spinal Cord
o Well-circumscribed, intensely enhancing o Mottled/speckled pattern due to varying
intramedullary mass causes fusiform cord stages of blood products: "Popcorn"
enlargement appearance
• Hemosiderin at cranial or caudal margin o Hemosiderin ring
"cap sign" in 20-64% of cases o ± Minimal enhancement
• Polar or intra tumoral cysts in 50-90% o No edema unless recent hemorrhage
o Associated syrinx & surrounding edema • Neuromyelitis Optica
• Ependymoma, Myxopapillary, Spinal o Idiopathic demyelinating syndrome
Cord involving the optic nerves and spinal cord
o Intensely enhancing glioma arising from o Lesions extending over 3 or more vertebral
ependymal cells of filum terminale, conus, segments on spinal cord MR
cauda equina o Distinct from "typical" MS is > 50
• May be T1 hyperintense due to mucin cells/mm3 in CSF (often
accumulation polymorphonuclear) & absent oligoclonal
II • T2 hyperintense lesion; hypointense at
margin due to hemosiderin
bands
o Normal initial brain MR
7
14
o NMO-IgG seropositivity Due to spinal occlusion: Radicular branch

o
o Associated with several systemic diseases of vertebral artery in cervical cord or aorta
including collagen vascular diseases, in thoracic & lumbar cord
autoantibody syndromes, infections, & o Thoracic cord most frequently involved as
toxin exposures it is an arterial border zone
• Type I DAVF • Type II AVM
o Cord central T2 hyperintensity + o Intramedullary glomus type arteriovenous
prominent intradural vessels on cord malformation
surface • Nidus may extend to the dorsal pial
o May show diffuse (usually faint) cord surface
enhancement o Variable enhancement of nidus, cord,
o Distal thoracic cord/conus most common vessels
location o Large cord with heterogeneous Tl/T2

signal due to blood products
o Prominent flow voids, likely draining
• Lymphoma
coronal venous plexus
o Poorly-defined mass
• Involving cervical> thoracic> lumbar • Ganglioglioma
o Young patients (4-38 years, mean = 12
o Enhancement varies from patchy to
years)
confluent & infiltrating to discrete
• Cervical> thoracic> filum
o Non-Hodgkin lymphoma (predominantly
o Long tumor length without edema
B-cel1)> Hodgkin disease
o Tumoral cyst
• Metastases, Spinal Cord
o Bone erosion and scoliosis
o Focal enhancing cord lesion with extensive
o Mixed signal intensity on T1WI & patchy
edema, out of proportion to small lesion
enhancement with cord surface
o Typically < 1.5 cm & well-circumscribed
enhancement
o Conus least commonly involved
o Hemorrhagic metastases can be seen from
thyroid and melanoma SELECTED REFERENCES
• Infarction, Spinal Cord 1. Wingerchuk DM et al: The clinical course of neuromyelitis
o Focal T2 hyperintensity & slight cord optica (Devic's syndrome). Neurology. S3(S):1107-14, 1999
2. Patel U el al: MR of spinal cord ganglioglioma. AJ RAm J
expansion Neuroradiol. 19(5):879-87, ] 998
o Patchy, ill-defined intramedullary
enhancement in subacute phase
II
Sagittal T1 C+ MR shows fusiform expansion of the
cervicothoracic cord with a large solidly enhancing
Sagittal T1 C+ MR shows diffuse central cord expansion
with solid enhancing nodule 1:':1 and cephalad cyst.
7
mass from T1-2 junction to T4 level ~ There is a small Enhancement degree and pattern is variable in cord
intra-tumoral cyst at the rostral margin =. ependymomas.
15
Astrocytoma, Spinal Cord Multiple Sclerosis, Spinal Cord

Ql (Left) Sagittal T1 C+ MR
c:
Q.
en mass involving the upper
thoracic cord, with long
segment fusiform cord
expansion. The
enhancement is fairly
homogeneous with an
irregular inferior margin C=.
shows a peripheral,
well-defined focus of cord
enhancement 81. The
multiplicity of lesions along
with lack of edema or
significant cord expansion is
typical for demyelinating
disease.
Hemangioblastoma, Spinal Cord ADEM, Spinal Cord

shows focal enhancement of
the hemangioblastoma ~
but no enhancement of the
tumor-associated cysts E:I
inferior & superior to the
tumor. Edema typically
spares the cord periphery.
(Right) Sagittal T I C+ MR
shows abnormal eccentric,
homogeneous lesion
enhancement =. Lesion
enhancement may be either
homogeneous or ring
configuration.
Cavernous Malformation, Spinal Cord Neuromyelitis Optica

shows mild enhancement of
a mostly isoinlense, slightly
expansile intramedullary
lesion at the C2-3 level =:lI.
shows fusiform expansion &
the cord a with
longitudinally extensive T2
signal abnormality> 3
vertebral segments (not
shown). Note the small
upper thoracic cord due to
prior demyelination wilh
atrophy 1!:llI.
II
7
16
INTRAMEDULLARY LESION, SOLID ENHANCEMENT
~
Ol
3
<ll
(Left) Axial T1 C+ MR shows a.
c
extensive diffuse OJ
enhanCemenllhroughoul the -<
cord substance ~ in
relapsing neuromyelitis
optica. (Right) Sagittal T1 C+
FS MR show extensive
confluent enhancement of
the distal thoracic cord.
Typical findings of cord T2
hyperintensity and intradural
vessels were also present.
Metastases, Spinal Cord Infarction, Spinal Cord

shows scattered bony
metastatic lesions =
& slight
expansion of the conus E:I
with a focal intramedullary
enhancing lesion. (Right)
intramedullary central cord
enhancement =in the
subacute phase.
Ganglioglioma
(Lefl) Sagittal T1 C+ FS MR
shows pronounced
intramedullary spiculated
enhancement B1 due to a
compact intramedullary
nidus. Multiple flow voids
P..:tJ are seen within cord,
along dorsal cervical cord
surface, and within
subarachnoid space. (Right)
infiltrating brainstem and
cervical cord mass ~ with
irregular enhancement.
Tumor extends exophytically
into the 4th ventricle
II
7
17
INTRAMEDULLARY LESION, NO ENHANCEMENT
DIFFERENTIAL DIAGNOSIS o Cord atrophy usually in late stage &

correlates with clinical disability
Common • Contusion-Hematoma, Spinal Cord
Ql • Syringomyelia o Acute: Iso-/hypointense with cord swelling
c:
c. • Multiple Sclerosis, Spinal Cord o Chronic: Focal/segmental atrophy
rJ)
• Contusion-Hematoma, Spinal Cord • Acute Transverse Myelitis, Idiopathic
• Acute Transverse Myelitis, Idiopathic o Centrally located lesion, 3-4 segments in
Less Common length
• Astrocytoma, Spinal Cord o Variable enhancement depending on age
• Ependymoma, Cellular, Spinal Cord Helpful Clues for Less Common Diagnoses
• Infarction, Spinal Cord • Astrocytoma, Spinal Cord
• ADEM, Spinal Cord o 10% of cord tumors may show no
• Cavernous Malformation, Spinal Cord enhancement
Rare but Important o Typically low grade astrocytomas (WHO
• Neurenteric Cyst grade I, II)
o Fusiform cord expansion, T2
hyperintensity
ESSENTIAL INFORMATION o Cysts uncommon in nonenhancing tumor
Key Differential Diagnosis Issues subclass
• Imaging of ADEM may be similar to • Infarction, Spinal Cord
fulminant multiple sclerosis; however, the o Early stage may have no Tl signal
former is monophasic abnormality
o ± Patchy enhancement in subacute phase
Helpful Clues for Common Diagnoses • Cavernous Malformation, Spinal Cord
• Syringomyelia o Absent or minimal enhancement
o Cystic intramedullary lesions that may be
loculated with septations Helpful Clues for Rare Diagnoses
o Enhancement suggests inflammatory or • Neurenteric Cyst
neoplastic lesion o Fluid intensity cystic lesion, typically
• Multiple Sclerosis, Spinal Cord in tra dural/ extramedullary
o Enhancement during acute/subacute phase o Segmentation & fusion anomalies
& lasts 1-2 months
• Does not reflect disease progression
Multiple Sclerosis, Spinal Cord
II
7 Sagittal T1 WI MR shows an elongated, cystic
int,amedullary lesion SI with CSF signal. This cavity is
Sagiltal T2WI rs
=.
MR shows rocal hyperintensity within
cord at C3 and C5 levels Ilomogeneous, nodular,
loculated with septaUons =. Note the cerebellar or ring enhancement occurs during the acute or
18
lonsillar ectopia =. subacute phase & lasts 1-2 months.
INTRAMEDULLARY lESION, NO ENHANCEMENT
Contusion-Hematoma, Spinal Cord Acute Transverse Myelitis, Idiopathic

shows mild cord expansion
=
and hyperintensity at C3-C4
the level of ALL & PLL
injury and posterior
subluxation =. There is
extensive preverlebral edema
eJ. (Right) Sagillal T7WI MR
shows a cervical
intramedullary lesion
spanning 5 vertebral
segments from C2-3 to C7
=. It is relatively T7
hypointense and T2
hyperintense (not shown).
Astrocytoma, Spinal Cord Infarction, Spinal Cord

(LeFt) Sagillal T7 C+ MR
shows a very large
nonenhancing spinal cord
astrocytoma =
encompassing the entire
cervical cord. (Right) Sagillal
T2WI MR shows mild cord
expansion & ventral cord
hyperintensity =.
ADEM, Spinal Cord Cavernous Malformation, Spinal Cord

hyperintensity scallered
throughout the cervical cord
with focal cord expansion
=. This is similar imaging to
fulminant multiple sclerosis,
but ADEM is typically
monophasic. (Right) Sagillal
T2WI MR shows
well-circumscribed region of
heterogeneous signal eJ
within the cord due to
varying ages of blood
products. Surrounding
hypointensity!:OJ is likely
due to a hemosiderin
Slaining. II
7
19
INTRAMEDULLARY LESION, DIFFUSE/ILL-DEFINED ENHANCEMENT
DIFFERENTIAL DIAGNOSIS • euromyelitis Optica (NMO)

o Autoimmune, inflammatory disorder
Common involving myelin of optic nerves and
Ql • Multiple Sclerosis spinal cord
r::
0- • Transverse Myelitis (ATM) o Longitudinally extensive (> 3 vertebral
W
• ADEM segments) T2 hyperintensity within cord
• Viral Myelitis o Presence of brain WM lesions does not
• Neuromyelitis Optica (NMO) exclude NMO
Less Common o May reflect autoimmune targeting of
• Type I Spinal Dural A-V Fistula Aquaporin-4 transmembrane channel
• Dural A-V Fistula (Brain) proteins
• Arterial Infarction o Respiratory failure due to extensive
• Spinal Cord Metastases cervical involvement in up to 1/3 cases
• Astrocytoma (very uncommon in MS)
o Radicular pain in 35% (uncommon in MS)
Rare but Important
o Lhermitte symptom common in MS and
• Radiation Myelopathy NMO
• Abscess/Myeli tis
• Parasitic or Bacterial Infections Helpful Clues for Less Common Diagnoses
• Type I Spinal Dural A-V Fistula
o Causes venous hypertension
ESSENTIAL INFORMATION o Intradural flow voids on cord surface from
Helpful Clues for Common Diagnoses arterialized veins
• Multiple Sclerosis o Swollen, edematous cord
o Patchy or confluent enhancement o Multisegmental T2 signal abnormality
o Cervical> thoracic o Variable enhancement
o Small focal areas of T2 signal abnormality • Arterial Infarction
o Dorsal cord at C1-2 common location o Sudden onset weakness, loss of sensation
• Transverse Myelitis (ATM) o Rapidly progressive
o Can be secondary to known cause (e.g., o Causes
MS, ADEM, cord ischemia) • Anterior spinal or radicular artery
o Can be idiopathic (unknown cause) 15% occlusion
o Thoracic> cervical • Hypotension
o Imaging normal in up to 50% o Thoracic (conus) > cervical
• ADEM o Nonspecific T2 hyper intensity ± ill-defined

o Immune-mediated, inflammatory white cord enhancement
matter disorder • Spinal Cord Metastases
• Para/post-infectious o Focal, enhancing cord lesion(s) with
• Post-immunization extensive edema
o Typically monophasic illness o Lung, breast most common primary
o Any age (more common in child, young o Rapidly progressive flaccid paraparesis
adult) o Full craniospinal imaging when focal cord
o Brain affected more than spinal cord lesion found
o Can be multifocal, patchy, or confluent o Edema out of proportion to focal small
o Check brain for multi focal white matter cord lesion suggests metastasis, even if
lesions with relatively little mass effect solitary
• Viral Myelitis • Astrocytoma
o Acute/subacute viral infection (e.g., HIV, o Enhancing infiltrating mass expanding
enteroviruses, H HSV6) cord
o Usually multisegmental o Cervical> thoracic
II o Variable enhancement from subtle to o Usually < 4 segments
profound o Occasionally asymmetric, even exophytic
7
20
INTRAMEDULLARY LESION, DIFFUSE/Ill-DEFINED ENHANCEMENT
o 80-90% low grade o Differential considerations include

o Slow onset of myelopathy o => MS
o Systemic disease
=>
• Sjogren, SLE
• Radiation Myelopathy
o => Vascular
o Spindle-shaped cord swelling with
o => Parainfectious (ADEM)
irregular, focal rind of enhancement
o => Radiation myelopathy
o Typically with doses over SO Grey (Gy)
o => Idiopa thic
o Demyelination in lateral, dorsal tracts
• Acute transverse myelitis (ATM)
o Concurrent chemotherapy may be a
o Subset of transverse myelopathy
predisposing factor, especially if
o Excludes compressive lesions
intrathecal
o Requires evidence of cord inflammation
• Parasitic or Bacterial Infections
• CSF pleocytosis or elevated IgG or MR
o Typical is well-defined, ring-enhancing
contrast-enhancement
mass within cord, with appropriate clinical
o Bilateral signs and symptoms, Clear
history of inflammation/infection
sensory level
o More uncommon ill-defined or patchy
o Progression of clinical symptoms to nadir
enhancement
between 4 hours and 21 days
o Schistosomiasis => ill-defined punctate
o Exclusion criteria for ATM
enhancement of conus
• Sarcoid
Other Essential Information • Behc;et, Sjogren, SLE
• Long (multisegmental) cord enlargement • Infectious etiologies (Lyme, HIV,
with edema, patchy enhancement favors Mycoplasma, viral)
infection/inflammation over neoplasm
• Do sagittal FLAIR or T2WI of brain in
patients with unexplained myelopathy, cord SELECTED REFERENCES
lesions! 1. Matiello M et al: Neuromyelitis optica. Curr Opin Neural.
20(3):255-60, 2007
oMS, ADEM usually have coexisting brain 2. Wingerch~lk D~ et al: Comparative immunopathogenesis
lesions of a.cute dlssemmated encephalomyelitis, neuromyelitis
optlca, and multiple sclerosis. Curr Opin Neurol.
Alternative Differential Approaches 20(3):343-50, 2007
• Acute transverse myelopathy
o Includes both inflammatory and
noninflammatory etiologies
o Excludes compressive lesions
II
Sagillal T7 c+ MR shows mulliple foci of cord
enhancement in multiple sclerosis, some well-defined =
Sagittal TI C+ FS MR shows patchy cervical cord
enhancement in this patient with acule idiopathic
7
~ and others ill-defined 81. lIansverse myelopathy No definite etiology was
established.
21
~ INTRAMEDULLARY LESION, DIFFUSE/ILL-DEFINED ENHANCEMENT
Cll
:J
-0
Q)
E
~
Cll
C
ADEM
Q)
c:
shows diffuse, patchy
a.
CIl enhancement ~ of the
uppe, and middle thoracic
spinal cord in this patient
with myelopathy following
flu-like illness. (Right) Sagittal
T7 C+ MR shows a diffusely
enlarged, swollen upper
cervical cord with ill-defined
enhancement = in this
patient with ADEM.
Myelopathy began 2 weeks
after flu-like illness.
Viral Myelitis
patient with herpes myelitis
shows extensive cord edema
and patchy enhancement
from C4 to the C7-T7 level.
=
shows minimal patchy
enhancement of the cord in
NMO, with diffuse cord
expansion. Cord
demonstrated extensive T2
abnormality (not shown) as
did the optic nerves.
Type I Spinal Dural A-V Fistula Dural A-V Fistula {Brain}

shows patchy and ill-defined
enhancement of the distal
spinal cord 8l with
scatlered prominent vessel
enhancement lie. Distal
cord showed T2
hyperintensity. (Right)
Sagillal T7 C+ FS MR shows
diffuse, patchy enhancement
SI related 10 venous
hypertensive myelopathy in
this patient with Cognard V
posterior fossa dural Avr
with intraspinal venous
drainage.
II
7
22
INTRAMEDULLARY LESION, DIFFUSE/ILL-DEFINED ENHANCEMENT
Arterial Infarction Spinal Cord Metastases

(LeFt) Sagittal T I C+rs MR
in a child with paraplegia
after minor trauma shows
mildly enlarged distal
thoracic cord ~ with diFfuse
enhancement. Exact etiology
of the infarct was never
established. (Right) Sagittal
TI C+ MR shows glioma
metastasizing from the brain
stem e1 inferiorly into cord
with multiple foci of patchy
enhancement ~.
Astrocytoma
shows large enhancing mass
with long segment fusiform
cord expansion. The
enhancement is fairly
homogeneous, with an
irregular inferior margin.
(Rigl1t) Sagittal TI C+ MR
shows infiltrating brainstem
and cervical cord mass with
patchy, irregular
enhancement =.
(LeFt) Sagittal TI C+ MR
shows case of myelopathy
fof/owing chest radiograph
for head and neck squamous
cell carcinoma. Note diffuse
patchy cord enhancement
~ with expansion and fatty
marrow replacement in the
spine. (Right) Sagittal TI C+
MR shows diffuse patchy
enhancement of the cord
and pia II] in a patient with
fever, CSF pleocytosis, and
bacteremia.
II
7
23
INTRAMEDUllARY LESION, RING/PERIPHERAL ENHANCEMENT
DIFFERENTIAL DIAGNOSIS • Ependymoma, Cellular, Spinal Cord

o Avid, sharply delineated enhancement
Common (50%)
Ql • Multiple Sclerosis, Spinal Cord o Central> eccentric location
c:
0- • Astrocytoma, Spinal Cord o Polar or intratumoral cysts (50-90%)
I/)
• Ependymoma, Cellular, Spinal Cord o Hemorrhage T1 hyperintense
• Metastases, Spinal Cord • Metastases, Spinal Cord
Rare but Important o Focal enhancing cord lesion(s) with
• Cysticercosis extensive edema
• Abscess/Myelitis, Spinal Cord o Lesions < 1.5 cm & well-circumscribed
• Epidermoid Tumor, Acquired o Hemorrhagic mets from thyroid CA,
melanoma show T2 hypointensity
• Cysticercosis
Key Differential Diagnosis Issues o Peripheral cyst enhancement
• Look for adjacent vertebral or disc o Cord pial surface enhancement &
abnormalities as a source of infection arachnoiditis
• Assess for supratentorial enhancing lesions o Adjacent acute/chronic inflammatory cell
Helpful Clues for Common Diagnoses infiltrate, "cysticercal abscess"
• Multiple Sclerosis, Spinal Cord • Abscess/Myelitis, Spinal Cord
o Enhancement may be homogeneous, o Irregular ring-enhancing intramedullary
nodular, or peripheral lesion with cord expansion
• During acute or subacute phase & lasts o ± Restricted diffusion
1-2 months o T2 hyperintensity from abscess core &
• Does not reflect disease progression surrounding edema
• Astrocytoma, Spinal Cord • Epidermoid Tumor, Acquired
o Enhancement is characteristic o Isointense to CSF/cord on T1WI;
• Mild/moderate ~ intense enhancement iso-/hyperintense to CSF on T2WI; more
• Partial ~ total hyperintense than CSF on DWI
• Infiltrating ~ well-delineated o Absent or faint peripheral enhancement
• Enhancing area is target for biopsy o Think infected cyst if prominent
o Asymmetric, can be exophytic enhancement
Multiple Sclerosis, Spinal Cord Astrocytoma, Spinal Cord
II
7 =.
Sagittal T7 C+ MR shows faint ring enhancement of
plaque at the C4-S level of the cord
Axial T7 C+ FS MR demonstrates a fusiform hypoinlense
intramedullary mass within the thoracic spinal cord with
heterogeneous rim enhancement ~.
24
INTRAMEDULLARY LESION, RING/PERIPHERAL ENHANCEMENT
~
~
Q)
Ependymoma, Cellular, Spinal Cord Metastases, Spinal Cord 3

CD
Cl.
(Left) Axial T1 C+ MR shows c:
a moderalely, Q)
helerogeneously enhanced -<
mass m that causes central
cord expansion.
Enhancemen/ degree and
pattern is variable in cord
ependymomas. (Right)
Sagiltal T1 C+ FS MR shows
focal inlramedullary
enhancement within the
distal cord & slighl expansion
of Ihe conus medullaris 81.
shows mullicysUc
parenchymal involvement of
cervical cord by
neurocysticercosis ID.. Note
both cyslic & solid
components with mild
curvilinear enhancement r..:=.
shows cord abscess with
inlernal hypoin/ensity & thick
peripheral enhancement.
Cord swelling & extensive
inlramedullary edema
mimics tumor. There are no
adjacent vertebral or disc
abnormalities to suggest
hematogenous distribution.
Abscess/Myelitis, Spinal Cord Epidermoid Tumor, Acquired

shows case of tuberculosis
producing a spinal cord
abscess. The granulomalOus
abscess demonstrates avid
ring enhancement ~ with
central low signal intensity. A
compression fracture ~ is
nOlcd. (Right) Axial T1 C+ FS
MR demonslrates a subtle
ovoid lesion = nestled
within the cauda equina,
isointense to conus. There is
sublle peripheral
enh,1ncemenl of Ihis lesion
surrounded by nerve roots.
II
7
25
INTRAMEDUllARY LESION, 11 HYPOINTENSE, 12 HYPOINTENSE
DIFFERENTIAL DIAGNOSIS o ± Cord swelling

Common o Tl & T2 heterogeneous due to blood
Ql • Instrumentation/Implants products of varying ages
c:
Co • Contusion-Hematoma, Spinal Cord o T2 hypointense rim (hemosiderin)
III
• Cavernous Malformation, Spinal Cord o No edema unless recent hemorrhage
Less Common o No prominent vascular flow voids or nidus
• Cysticercosis Helpful Clues for Less Common Diagnoses
• Type II AVM • Cysticercosis
Rare but Important o Focal cystic lesion(s) with or without
• Diastematomyelia syrinx cavity
o T2 hypointensity may be due to cyst wall
degeneration with calcification
ESSENTIAL INFORMATION o Peripheral cyst enhancement
Key Differential Diagnosis Issues • Type II AVM
• Assess for post-surgical changes o Intramedullary nidus with dorsal subpial
• Flow voids suggest vascular lesion extension
• Associated vertebral body anomalies in o Cord enlargement with heterogeneous
diastematomyelia Tl/T2 signal due to blood products & flow
voids
o Intra-/perinodal aneurysm in 40%
• Instrumentation/Implants • Subarachnoid is most common symptom
o Intrathecal & epidural catheters allow
infusion of anesthetics Helpful Clues for Rare Diagnoses
o Syringomyelia (hindbrain herniation or • Diastematomyelia
post-traumatic) treated with shunting into o Type 1 has separate dural sac & arachnoid
subarachnoid, peritoneal or pleural spaces space, more common
o Complications: Infectious/inflammatory • Iso-/hypointense spur (osseous or
process, misplacement, cord or nerve fibrous)
injury, CSF leak, & spinal hematoma o Type 2 has a single dural sac & arachnoid
• Contusion-Hematoma, Spinal Cord space
o Acute contusion is Tl iso-/ hypointense • ± Iso-/hypointense fibrous spur
o Blood products hypointense on T2 & T2* o Two hemicords with or without
GRE sequences syringohydromyelia (50%)
Instrumenta tion/I mplan ts Contusion-Hematoma, Spinal Cord
II
7 Sagillal TI WI M R shows a linear TI hypointense
catheter within the cervical syrinx cavity Ill.
Sagittal TlWI MR shows isointense/slightly hypointense
signal in the cord I:m.
rhere is isoinlense soft. tissue in
Susceptibility artifact at the entry site of the catheter is the ventral epidural space E2 representing disc
alsoseen~. extrusion &/or epidural hemorrhage.
26
CJl
INTRAMEDULLARY LESION, 11 HYPOINTENSE, 12 HYPOINTENSE "'C
::J
CD
~
~
OJ
3
Contusion-Hematoma, Spinal Cord Cavernous Malformation, Spinal Cord CD
D-
(Left) Sagittal T2WI MR C
shows severe flexion injury OJ
with subluxation of C5 more -<
than 50% over C6 body,
flexion deformity, and
widened posterior elements.
There is severe cord
compression and cord
hemorrhage~. Disruption
of the anterior longiwdinal
ligament is seen as
hyperintensity~. (Right)
well-defined focus of
predominately low signal
within the left posterior
aspect of the caudal medulla
r:i:I.
Cysticercosis Cysticercosis
shows 2 focal intramedullary
areas of slightly decreased
signal r:i:I within the
extensive area of cord edema
~ (Right) Sagillal T1WI MR
shows a focal cystic mass r:i:I
involving distel/thoracic
cord, with fusiform cord
expansion. Without the
concomitant brain
involvement, the differential
of the cord lesion would be
primarily inuamedullary
tumor.
Diastematomyelia
(Left) Coronal T2WI FS MR
shows various stages of
degradation from fluid-like
cavity in the conus lip
methemoglobin SlIO low
=-
to
signal on all pulse sequences

reflecting hemosiderin ~.
There are multiple serpentine
intradural flow voids,
particularly about the dorsal
distal cord [;>~.(Right) Axial
T2WI MR shows
marrow-filled osseous spur at
L I ~ separating dural sacs
with 2 hemicords. Focal
hydromyelia is seen in the
left hemicord r:i:I.
II
7
27
INTRAMEDULLARY LESION, 11 HYPOINTENSE
DIFFERENTIAL DIAGNOSIS • Syringomyelia

o Expanded cord with non enhancing dilated
Common or beaded cystic cavity
CIl
c:
• CSF Flow Artifact • Multiple Sclerosis, Spinal Cord
c. • Syringomyelia o Unlike supratentorial lesions, cord lesions
lf)
• Multiple Sclerosis, Spinal Cord are rarely visible as Tl hypointense
• Contusion-Hematoma, Spinal Cord • Contusion-Hematoma, Spinal Cord
• ADEM, Spinal Cord o Acute contusion appears iso-/hypointense
• Ependymoma, Cellular, Spinal Cord with cord swelling
• Astrocytoma, Spinal Cord o Hematoma later hyperintense 2 metHB 0
• Hemangioblastoma, Spinal Cord • ADEM, Spinal Cord

Less Common o Multifocal hypo intensity & slight cord
• Type II AVM swelling
• Cavernous Malformation, Spinal Cord • Ependymoma, Cellular, Spinal Cord
• Abscess/Myelitis, Spinal Cord o Iso- or slightly hypointense to spinal cord
with polar or intratumoral cysts (50-90%)
o Fusiform cord enlargement
ESSENTIAL INFORMATION • Astrocytoma, Spinal Cord
Key Differential Diagnosis Issues o Multisegmental, usually < 4 segments
• Prominent flow voids seen with type II AVM o Hypo-/isointense eccentric, infiltrative
& hemangioblastomas solid portion, indistinct margins ± syrinx
o Cystic lesions with enhancing nodule &
• CSF Flow Artifact
extensive surrounding edema
o Caused by
• Time of flight loss Helpful Clues for Less Common Diagnoses
• Flow-related enhancement • Type II AVM
• Varied turbulent flow o Enlarged cord with heterogeneous signal 2 0
velocities/directions - rapid dephasing, blood products & flow voids

signal loss, "intravoxel dephasing" • Cavernous Malformation, Spinal Cord
o Speckled "popcorn" appearance 2 varying 0
o Artifacts propagate across cord,
subarachnOid space ages of blood products
o Most common in thoracic spine • Abscess/Myelitis, Spinal Cord
o Especially common in pediatric patients o !II-defined hypointensity, expanded cord
CSF Flow Artifact
II
7 Sagittal T7 WI MR shows vague mixed hyper-,
hypoinlensily propagating across thoracic subarachnoid
Coronal TI WI MR shows dilated cysvc lesion mildly
space = and cord due 10 CSF pulsavon artifact.

expanding the cord wilh septavons PJ:ll. There may be
surrounding gliosis, myelomalacia, cord lethering,
28 edema, or arachnoidal adhesions.
INTRAMEDULLARY LESION, 11 HYPOINTENSE
~
...,
OJ
Multiple Sclerosis, Spinal Cord ADEM, Spinal Cord 3
ct>
(Left) Axial T IWI MR shows c.
c
an eccentrically located
intramedullary lesion
compatible with a
=- OJ
-<
demyelinating plaque. T1
hypointense plaques are
rarely visible. 10-20% cases
have isolated spinal cord
disease. Cord edema
resolves after 6-8 weeks, and
cord atrophy is seen in the
late stage. (RighI) Sagit/al
TI WI MR shows vague
hypointensity spanning the
cervical cord with mild
expansion D].
Astrocytoma, Spinal Cord Type II AVM

(Left) Sagit/al T1WI MR
shows a heterogeneous
hypointense intramedullary
mass expanding the cervical
cord =. (Rig/,t) Sagittal
T I WI MR shows prominent
flow voids !:ll related to an
intramedullary AVM nidus.
There is often extension to
the dorsal subpial surface.
40% of patients have
aneurysms of feeding vessels.
These findings are associated
with cutaneous angiomas,
Klippel-Trenaunay-Weber, &
Rendu-Osler-Weber
syndromes.
Cavernous Malformation, Spinal Cord Abscess/Myelitis, Spinal Cord

(Left) Sagit/al TI WI MR
lesion =
hypoinlense intramedullary
with a speckled
appearance due to blood
products of varying ages.
(Right) Sagit/al TlWI MR
shows cervical cord swelling
=-
with internal hypointensity
often seen in
inflammatory lesions.
Extensive intramedullary
edema mimics a cord tumor.
No adjacent vertebral or disc
abnormalities that suggest a
local inFectious source were
noted, implying
hematogenous distribution.
II
7
29
INTRAMEDUllARY LESION, 12 HYPERINTENSE, 11 ISOINTENSE
DIFFERENTIAL DIAGNOSIS • Targets aquaporin 4 water channel

• Secondary Acute Transverse Myelitis
Common o T2 hyperintense lesion with mild cord
Q) • Multiple Sclerosis, Spinal Cord expansion
c:
a. • Neuromyelitis Optica o No significant enhancement
C/)
• Secondary Acute Transverse Myelitis o Mild Tl hyperintensity due to petechial
• Acute Transverse Myelitis, Idiopathic hemorrhage
• Contusion-Hematoma, Spinal Cord o Etiologies: Collagen vascular disease,
• Ependymoma, Cellular, Spinal Cord infectious/post -in fectious,
• Astrocytoma, Spinal Cord post-vaccination, post-irradiation, AVM,
• Type I DAVF para neoplastic
less Common • Acute Transverse Myelitis, Idiopathic
• Hemangioblastoma, Spinal Cord o Smooth cord expansion < T2 signal
• ADEM,Spinal Cord abnormality
• Infarction, Spinal Cord o T2 hyperintensity more than 2 vertebral
• Viral Myelitis segments in length
o Central gray matter surrounded by edema,
Rare but Important
"central dot sign"
• Metastases, Spinal Cord • Contusion-Hematoma, Spinal Cord
• Abscess/Myelitis, Spinal Cord o Acute contusion: TI iso-/hypointense, T2
• Vitamin Bl2 Deficiency, Spinal Cord hyperintense with cord swelling
o Hemorrhage TI hyperintense with metHB,
ESSENTIAL INFORMATION blooming on GRE sequences
o ± Traumatic disc herniation, osseous or
Key Differential Diagnosis Issues vascular injury
• Evaluate supratentorially, including cranial • Ependymoma, Cellular, Spinal Cord
nerves o T2 hyperintense, Tl iso-/slightly
• Hemorrhagic products & flow voids can be hypointense
seen in certain lesions o Polar & intratumoral cysts (50-90%)
Helpful Clues for Common Diagnoses o Syrinx
• Multiple Sclerosis, Spinal Cord o Hemosiderin cap (20-64%)
o TI hypointensity may represent axonal o Central canal widening (20%) & posterior
loss, gliosis, white matter atrophy, & vertebral scalloping
therefore motor disability • Astrocytoma, Spinal Cord
o Cervical cord TI relaxation time may be o T2 hyperintense, solid portion TI
influenced by tissue damage upstream (i.e., iso-/hypointense
cerebral damage) o Usually < 4 segments
o Well-circumscribed T2 hyperintense o Diffuse tumor infiltration, absence of
lesions (complete demyelination) vs. hemorrhage, & intrinsic neoplastic syrinx
ill-defined (partial demyelination) cavity favor astrocytoma over
o Wedge-shaped lesions with apex directed ependymoma
centrally o Concurrent combination of intramedullary
• Neuromyelitis Optica cord tumor & nerve sheath tumor is highly
o Revised diagnostic criteria (99% sensitive, suggestive of NFl
90% specific) • Type I DAVF
o Myelitis: Longitudinally extensive cord o Flame-shaped central edema spares the
lesion, 3 or more segments in length periphery
o Optic neuritis o Low peripheral T2 signal is compatible
o Onset brain MR nondiagnostic for MS with venous hypertensive myelopathy
II o Seropositivity for neuromyelitis optica
immunoglobin G
o Cord is enlarged & TI hypointense
7
30
INTRAMEDUllARY lESION, 12 HYPERINTENSE, 11 ISOINTENSE (J)
"C
::J
11l
o Multiple small vascular flow voids are seen Enlarged cord with diffuse T2
o
;:l.
~
on the cord pial surface hyperintensity llJ
o ± Patchy cord enhancement o Rarely, syrinx or hemorrhagic products 3

<ll
(i.e., thyroid, melanoma) a.
o Most commonly at level of conus c
o Well-circumscribed < 1.5 cm enhancing llJ
Helpful Clues for less Common Diagnoses -<
lesion
o Small lesions T2 hyperintense/Tl
• Abscess/Myelitis, Spinal Cord
o Abscess core appears TI hypointense/T2
hypointense
hyperintense with surrounding edema
o Syrinx> 50%, hyperintense to CSF
o Idiopathic or hematogenous source in
o Lesions> 2.5 cm show flow voids
o ± Peritumoral edema
adults; direct extension from dysraphism
in children
o Multifocal TI hypointense/T2
• Vitamin BIZ Deficiency, Spinal Cord
o Axial T2 show "upside-down V-shaped"
hyperintense lesions with slight cord
swelling hyperintensity along dorsal columns
o Accumulation of methylmalonic acid
o Little mass effect or edema
o Concomitant brain involvement
thought to cause myelin toxicity
o Subacute combined degeneration also
• Infarction, Spinal Cord
o T2 hyperintensity involving the gray
occurs in the setting of some types of
severe anemia
matter ± adjacent white matter
o Neurologic findings may precede the
o Increased T2 signal in the adjacent anterior
anemia
vertebral body or in deep medullary
o Treatment with parenteral BI2 may
portion near end plate
o Cord enlargement in acute phase
improve symptoms, but imaging
o More common in thoracic cord because of
abnormalities may not completely resolve
arterial border zone
• Viral Myelitis SELECTED REFERENCES
o Expanded cord with TI hypo intensity & 1. Wingerchuk OM et al: Revised diagnostic criteria for
diffuse T2 hyperintensity neuromyelitis optica. Neurology. 66(10):1485-9, 2006
2. Vaithianathar L et al: Magnetic resonance imaging of the
o Long, contiguous segmental involvement
cervical spinal cord in multiple sclcrosis--a quantitative TI
o Acute myelopathy relaxation time mapping approach. J Neurol.
250(3):307-15,2003
Helpful Clues for Rare Diagnoses 3. Losseff NA et al: Tl hypointensity of the spinal cord in
• Metastases, Spinal Cord multiple sclerosis. J Neurol. 248(6):517-21, 2001
II
Sagiltal T2WI MR shows ill-defined T2 hyperintense
lesions in the cervical cord =. The lesions span the
Axial T2WI MR shows long segment of central cord T2
hyperintensity 1:1:1 & mild diffuse cord enlargement.
7
gray-white boundary & are less /han 2 vertebral Extensive cord involvement is distinct from more focal
segmen!Sin length. abnormalities typically seen wilh multiple sclerosis.
31
INTRAMEDULLARY LESION, T2 HYPERINTENSE, T1 ISOINTENSE
Secondary Acute Transverse Myelitis Acute Transverse Myelitisr Idiopathic

Ql (Left) SagiHal T2WI MR
c:
shows pattern of dural fistula
c..
en hypertensive myelopathy:
Cenlral cord hyperinlensity
EI sparing the cord
periphery. Multiple flow
voids ~ on Ihe dorsal cord
surface are distended &
arterialized veins. Fistula
itself is not visualized & is
peripherally localed in Ihe
dural rool sleeve. (Right)
Sagitlal T2WI MR shows a
long segmenl of central
edema with relative sparing
of the periphery within the
Ihoracic cord =:I.

shows neoplastic
enlargement with a solid
portion extending from C2-]
to C5-6 =:I. Hyperinlense
cysts '-= cap the rostral &
caudal ends. (Right) Sagittal
TI C+ MR demonslrales an
extensive Tl isoimense, 72
hyperintense intramedullary
lesion =:I Ihal expands the
cord & extends from pons
into thoracic cord. Septated
neoplastic syrinx m is
observed & may extend Ihe
entire length of the spinal
cord. Laminectomies are a/50
seen 8J.
Type I DAVF Hemangioblastoma, Spinal Cord

hyperintensily =
shows central cord T2
which
spares the cord periphery
due to venous hypertension.
There are multiple serpentine
intradural ffow voids from
the arterialized venous
plexus =:I. (Right) SagiHal
cervical cord expansion &
edema within Ihe cord 8:1.
There is signal heterogeneity
of Ihe tumor '-=
wilh cenlral
irregular hyperintense cyst
=:I. The edema Iypically
II spares the cord periphery.
7
32
INTRAMEDULLARY LESION, T2 HYPERINTENSE, 11 ISOINTENSE
ADEM, Spinal Cord Infarction, Spinal Cord

shows conus expansion &
decreased T llincreased T2
signal intensity
expansion & T2
=. Conus
hyperintensity can be seen

with a variety of neoplastic
or inflammatory diseases.
shows cord expansion &
hyperintensity. Only a small
part of the peripheral cord is
spared, probably with flow
from small radicular
collateral vessels. The slightly
more hypoinlense center
may represent hemorrhage.
Viral Myelitis Metastases, Spinal Cord

increased T2 signal in
swollen, edematous cord.
Contiguous segmental
involvement is most
common. In this case of
herpes zoster myelitis there is
abnormal signal extending
into the dorsal ganglion ~
shows an oval isointense
lesion with a subtle
hyperintense rim ~ in this
patient with lung cancer
metastases.
Abscess/Myelitis, Spinal Cord Vitamin 812 Deficiency, Spinal Cord

shows hyperintense epidural
mass with peripheral low
signal due to abscess =
extension into adjacent cord
&
with pyogenic myelitis. There

is adjacent cord edema m.
shows hyperintensity along
mildly enlarged posterior
cord from foramen magnum
to C7 =. T2 hyperintensity
confined to dorsal columns is
highly suggestive of this
diagnosis. Symptoms
improve with B 12 treatment,
but imaging may not
completely resolve.
II
7
33
INTRAMEDULLARY LESION, 11 HYPERINTENSE
DIFFERENTIAL DIAGNOSIS Minority of cases T1 hyperintensity due to

o
methemoglobin
Common o Enhancement is characteristic
Ql • Contusion-Hematoma, Spinal Cord • Mild => intense, partial => total,
c:
Co • Tumor Hemorrhage/Proteinaceous Cyst infiltrating => sharply delineated
CIl
o Ependymoma, Cellular, Spinal Cord o ± Cyst/syrinx (slightly hyperintense to
o Astrocytoma, Spinal Cord CSF)
o Metastases, Spinal Cord • Metastases, Spinal Cord
• Cavernous Malformation, Spinal Cord o Hemorrhagic mets, such as thyroid &
Less Common melanoma metastases
• Dermoid and Epidermoid Tumors • Growth of primary spinal melanoma if
• Lipoma slower & survival is longer
• Infection, Cryptococcoma, Tuberculoma o Focal enhancement
• Melanocytoma • Cavernous Malformation, Spinal Cord
o Speckled heterogeneous lesion with blood
Rare but Important
products of varying ages
• Intramedullary AVM
• T2 hypo intense rim 2° hemosiderin
• Minimal to no enhancement
ESSENTIAL INFORMATION o Lesions abut the pial surface
o Angiographically occult
o Clinical presentation ranges from acute
• T1 hyperintensity can be due to neurological decline 2° hemorrhage to
hemorrhage, fat, melanin
chronic progressive myelopathy due to
• Look for associated vertebral body or neural microhemorrhages & gliotic reaction to
arch abnormalities & mass effect on regional blood products
structures
• Dermoid and Epidermoid Tumors
• Contusion-Hematoma, Spinal Cord o Dermoid
o Tl hyperintensity due to methemoglobin
• Well-demarcated isodense mass ± foci of
• Early T2 hypo intensity caused by fat signal/density & calcification
deoxyhemoglobin in the local hypoxic
• Fat Tl hyperintensity is most specific for
state of the injured segment
dermoid but least common
o ± Traumatic disc herniation & vascular
• Congenital lesion presenting in young
injury
patients
o Increase in spinal cord edema during the
o Epidermoid
early period after injury & comparatively
• Hyperintense on OWl, T1 isointense to
static intramedullary hemorrhage CSF, mildly T2 hyperintense
• Ependymoma, Cellular, Spinal Cord
• Acquired or congenital, slower growing,
o Enhancing cord mass with hemorrhage
present in 3rd to 5th decade
o Fusiform cord enlargement with central o Extramedullary (60%) > intramedullary
canal widening in 20% (40%)
o Polar or intratumoral cyst (50-90%)
o Mild peripheral enhancement; however,
o More often central growth pattern
more intense enhancement if infected
o More often in the lower thoracic cord
• Lipoma
• Astrocytoma, Spinal Cord o Homogeneously T1 hyperintense
o Cord expansion
intradural nonenhancing mass
• Multisegmental, usually < 4 segments o Intradural lipoma can invaginate into the
• Holocord involvement more often with cord substance
pilocystic astrocytoma
• Weakness & sensory abnormality at
II • Can be asymmetric or exophytic lesion level
• Normal overlying skin
7
34
INTRAMEDUllARY lESION, T1 HYPERINTENSE
• ± Canal widening & dysraphism o Tl/T2 shortening by proton-proton

o Terminal lipoma can tether the cord with dipole-dipole interaction
extension through dorsal dysraphism into o Heterogeneous enhancement
subcutaneous fat o Highest concentration of melanocytes
• Tethered cord syndrome: Bowel/bladder occurs in the spinal leptomeninges in the
dysfunction, lower extremity upper cervical level
motor/sensory abnormality o Meningiomas & schwannomas may
• Cutaneous stigmata frequently seen, foot RARELYdemonstrate Tl hyper intensity
deformity, scoliosis due to melanin
• ± Syrinx Helpful Clues for Rare Diagnoses
• Infection, Cryptococcoma, Tuberculoma • Intramedullary AVM
o Tuberculoma
o Prominent vascular flow voids leading to
• Iso-/hyperintensity on Tl WI at site of & from high flow lesion
granuloma • Compact or diffuse nidus with
• Iso-/hypointense T2 rim with aneurysms (20-40%)
hyperintense center (caseous necrosis), o Heterogeneous Tl/T2 signal due to blood
surrounding hyperintense edema products
o Cryptococcus has a respiratory entry o T2 hyperintensity in the cord due to
• CNS manifestation edema, gliosis, ischemia
(meningitis/ men ingoencepha Iitis) most o Subarachnoid hemorrhage, compression,
common because CSF does not have vascular steal
anticryptococcal factors present in serum • Myelopathy (acute/progressive), pain
• Arachnoiditis ± mass lesions,
intramedullary mass lesions (abscess or
granuloma), extradural lesion SELECTED REFERENCES
• Slightly Tl hyperintense (fibrosis & ]. Leypold BG el al: The early evolution of spinal cord lesions
inflammatory cellular infiltrates), T2 on MR imaging following traumatic spinal cord injury.
AJNR Am J Neuroradiol. 29(S):1012-6, 2008
hypointense with hyperintense focus & 2. Gilltasli NZ et al: MRI findings of intramedullary spinal
surrounding hyperintense edema cryptococcoma. Diagn Interv Radiol. 13(2):64-7,2007
3. Spetzler RF et al: Modified classification of spinal cord
• Intense solid or ring-like enhancement vascular lesions. J Neurosurg. 96(2 Suppl):14S-S6, 2002
• Melanocytoma
o Primary pigmented neoplasm, involving
cord or meninges
• Can be locally invasive
Contusion-Hematoma, Spinal Cord Ependymoma, Cellular, Spinal Cord
II
Sagittal T7WI MR shows cervical kyphosis and
traumatic spondylolisthesis of C3 relalive to C4. There is
Sagittal T7WI MR shows fusiform expansion of the
cervicothoracic cord with slight heterogeneous signal
7
a burst fracture of C4 vertebral body. A large hematoma
II::)] is seen in the spinal cord.
=.
35
INTRAMEDULLARY LESION, 11 HYPERINTENSE
(l) (Left) Sagittal T7WI MR

c:
shows a lobulated
a.
(/) hyperintense intramedullary
mass expanding the distal
cord =.The T I
hyperintensity refleclS blood
produclS. (Right) Sagittal
T7 WI MR shows a
hemorrhagic spinal cord
astrocytoma. There is a
fusiform hypoinlense
intramedullary mass within
the thoracic spinal cord
extending to the conus =.
shows an expansile
intramedullary mass =.
Astrocytomas cause fusiform
cord expansion, although
they can be asymmetric or
exophytic. Methemoglobin in
a minority of cases can result
in T1 hyperintensity. (Right)
Sagillal T2WI MR in the
same patient shows the mass
m. Its superior margin ;s at
T I, and the inferior margin is
at T8 P:?:l. There may be an
associated cyst/syrinx, which
is slightly hyperintense to
CSF.
Metastases, Spinal Cord Cavernous Malformation, Spinal Cord

I
shows hypointense vertebral
body extradural metastases
81as well as a rounded
lesion in the conus =. Nigh
signal intensity likely
represents hemorrhage.
shows focal high signal
within upper cervical cord at
C 1 level from the cavernous
malformation. There is linear
high signal extending
inferiorly from a more recent
cord hemorrhage =.
II
7
36
INTRAMEDULLARY LESION, 11 HYPERINTENSE en
~.
::l
CIl
Dermoid and Epidermoid Tumors

shows a lobulaled lesion
involving lhe dislal cord and
conus medullaris. There are
patchy and curvilinear areas
of T7 hyperinlensily
representing lipid malerial.
=
shows a dorsal T7
hyperintense intradural
subpial lipoma =
with mild
spinal cord distortion.
Lipoma Infection, Cryptococcoma, Tuberculoma

a dorsal hyperintense
intradural subpial lipoma =
distorling lhe cord. Note lhe
intimate relationship of the
lipoma with dorsal spinal
cord E:I due to premature
dysjunction during neural
lUbe formation. (Right)
Sagiltal T7WI MR shows
dorsal dermal sinus tract =
with a large intradural mass
81 involving distal cord with
caudal extension.
Post·conlrasl images (not
shown) reveafenhancernenl
surrounding a cord abscess
& of a sinus tract.
Melanocytoma
shows a complex signal
intramedullary mass
involving mid-thoracic cord
wilh foci of hyperinlensity
Ell. NOle small CYSI ~ along
cephalad margin & superior
cord syrinx =.(Right)
cord hemorrhage of varying
slages of degradation,
including a fluid-like cavity in
lheconus=.
melhemoglobin 8l & low
signal reflecting hemosiderin
~. Note serpentine
intradural flow voids about
lhe dorsal distal cord~_ II
7
37
CORD LESION, 12 HYPERINTENSE, VENTRAL
DIFFERENTIAL DIAGNOSIS o T2 hyperintensity in gray matter ±

adjacent white matter, classically anterior
Common horn cells
Gl • Multiple Sclerosis, Spinal Cord o Vertebral body infarct with increased T2
C
a. • Contusion-Hematoma, Spinal Cord marrow signal in the anterior vertebral
m • Infarction, Spinal Cord body/deep medullary portion near the
• Spondylotic Myelopathy endplate
Less Common • Spondylotic Myelopathy
• Spinal Cord Herniation o Pathophysiologic factors may be static
mechanical, dynamic mechanical, & spinal
Rare but Important cord ischemia
• Viral Myelitis
• Toxin Exposure Helpful Clues for Less Common Diagnoses
• Amyotrophic Lateral Sclerosis • Spinal Cord Herniation
o Focal anterior cord displacement through a
ventral dural defect with expansion of
ESSENTIAL INFORMATION dorsal subarachnoid space
Key Differential Diagnosis Issues o Often in mid-thoracic spine with cord
• Axial T2WI: Useful to localize lesion center deformity
in relationship to spinal cord long tracts Helpful Clues for Rare Diagnoses
Helpful Clues for Common Diagnoses • Viral Myelitis
• Multiple Sclerosis, Spinal Cord o Disease of lower motor neurons that
o STIR MR is sensitive for detecting affects the gray matter of the spinal cord,
demyelinating lesions specifically ventral horns
o Ill-defined = partial demyelination; o Includes poliomyelitis
well-defined = complete demyelination • Toxin Exposure
• Contusion-Hematoma, Spinal Cord o Reported cases of T2 hyper intensity &
o Acute contusion shows T2 hyperintensity enhancement in the anterior horns &
with susceptibility artifact from blood lumbar nerve roots after heroin &
products on GRE amphetamine exposure
o STIRdetects marrow edema & ligamentous • Amyotrophic Lateral Sclerosis
injury o Earliest manifestations of ALSon imaging
• Infarction, Spinal Cord may be diffusion restriction
II
7 Axial T2WI MR reveals multiple
intramedullary demyelinating lesions
T2 hyperintense
=. =-
Sagittal T2WI MR shows intramedullary hyperintensity
a due to edema & an ovoid hypointense focus
compatible WiU1 blood products. This cord contusion is
due to a traumatic disc protrusion ~.
38
CORD LESION, 12 HYPERINTENSE, VENTRAL
Infarction, Spinal Cord Infarction, Spinal Cord

(Left) Axial T2Wf MR shows
central cord hyperintensity
Ell. (Right) Sagittal OWl MR
shows {ocal hyperintensity
within the cord due to
restricted diffusion =
very low signal from the
and
remainder of spinal soft

tissues.
Spinal Cord Herniation

shows a disc herniation at
C4-C5 that produces cord
compression and (ocal
signal =-
abnormal intramedullary T2
correlating with
clinical myelopathy. (Right)
Sagittal T2Wf MR shows
thoracic idiopathic transdural
cord herniation. There is
focal anterior displacement
of the upper thoracic cord
abulling the posterior
vertebral body margin Ell
with very sharp angulation.
Viral Myelitis Amyotrophic lateral Sclerosis

high signal intensity in the
ventral aspect of the distal
thoracic cord & conus
meduJ/aris, incfuding
involvement of the central
gray matter~. (Right) Axial
OWl MR shows restricted
diffusion = in the
corticospinal/pyramidal
tracts extending caudally
from the precentral fmotor)
gyri through the midbrain
(not shown) & into the
medulla. Patients with ALS
display fasciculations,
atrophy of extremities, &
denervation pattern on [MG.
II
7
39
CORD lESION, 12 HYPERINTENSE, DORSAL
DIFFERENTIAL DIAGNOSIS o Focal cord swelling of myelin tubes

progresses to larger areas of myelin
Common vacuolization
Q) • Multiple Sclerosis, Spinal Cord o Mild cord enlargement ± mild dorsal
c:
a. • Contusion-Hematoma, Spinal Cord column enhancement
en
less Common o Occurs in setting of some types of severe
• Subacute Combined Degeneration anemia (e.g., megaloblastic anemia)
o Copper Deficiency • Methylmalonic acid accumulation causes
o Nitrous Oxide Misuse myelin toxicity
• HIV • Neurologic findings may precede anemia
• Sarcoidosis • Treatment may improve symptoms but
• Cord Wallerian Degeneration imaging abnormalities may not
completely resolve
Rare but Important
o Copper Deficiency
• Neurosyphilis
• Spastic gait and sensory ataxia
• Etiologies include malabsorption, partial
ESSENTIAL INFORMATION gastrectomy, and hyperzincemia
• Long segment of symmetric increased T2
signal in the dorsal midline cervical and
• Intracranial periventricular, subcallosal, thoracic cord
cerebellar & brainstem lesions in MS
• Imaging findings may be reversible with
• GRE sequences helpful to evaluate for normalization of serum copper
hemorrhagic products in cord contusion o Nitrous Oxide Misuse
Helpful Clues for Common Diagnoses • May result in subacute combined
• Multiple Sclerosis, Spinal Cord degeneration with symptoms ranging
090% of cases have intracranial lesions from paresthesias to autonomic
o 10-20% cases have isolated spinal cord dysfunction
disease • Nitrous oxide inhibits the active form of
o Cervical cord is most commonly affected vitamin B12
• Acutely, central enhancement of • Toxicity is related to the patient's levels
peripheral T2 hyperintense lesion of vitamin B12
• Enhancement duration 1-2 months • Demyelination with T2 hyperintensity in
• Cord edema lasts 6-8 weeks the central posterior columns of the cord
• Dorsolateral aspect of cord involving • Pathologically usually begins in thoracic
both the white matter and adjacent gray cord
matter • Myelopathy has been reported 2-6 weeks
• Cord atrophy in late stage after nitrous oxide anesthesia
• Contusion-Hematoma, Spinal Cord • HIV
o Acute: Cord swelling & T2 hyper intensity o Most common imaging finding is atrophy
o May see hemorrhagic products within (72%)
cord, fracture, & soft tissue injury o T2 hyperintensity involving white matter
o May see traumatic disc herniation tracts laterally & symmetrically
o STIR sequence is helpful to assess marrow o May show patchy enhancement
edema and ligamentous injury o Thoracic> cervical cord
Helpful Clues for less Common Diagnoses • Rostral extension from mid to lower
• Subacute Combined Degeneration thoracic cord with disease progression
o Progressive spastic paraparesis with ataxia,
o T2 hyperintensity confined to dorsal ±
lateral columns urinary symptoms & sensory loss
o Lower cervical and upper thoracic cord
• Sarcoidosis
II o Focal or diffuse T2 hyperintensity
fusiform cord enlargement
&
7
40
CORD LESION, 12 HYPERINTENSE, DORSAL
• Myelomalacia in late stages • 3: At> 14 weeks, myelin lipid ;:;.

breakdown, gliosis, and changes in water ~
o Leptomeningeal & peripheral OJ
content and structure results in T2 3
intramedullary mass-like enhancement CD
Cl.
o Lytic spine lesions hyperintense signal C
o Male> female in spinal sarcoidosis • 4: Several years after injury, there is OJ
volume loss
-<
• Cord Wallerian Degeneration
o Post-traumatic: Increased T2 signal in o Late sequela of acute demyelinating
dorsal columns above injury level & in lesions, i.e., MS
lateral corticospinal tracts below the injury Helpful Clues for Rare Diagnoses
level • Neurosyphilis
• In lumbar or thoracic cord injury, the o a.k.a., tabes dorsalis
portion of dorsal columns that o Slowly progressive degenerative disease
undergoes wallerian degeneration is involving the posterior columns (i.e.,
smaller than in the case of a cervical demyelination) & posterior roots (i.e.,
injury inflammatory change with fibrosis) of the
• Size effect is a function of the number of spinal cord
axons damaged by the injury & o T2 hyperintensity and focal enhancement
somatotopic arrangement of ascending in the dorsal aspect of the cord
fibers in the dorsal column tracts o 3 stages: Preataxia, ataxia, & paralysis
• Corticospinal tract contains fewer axons o Onset 20-30 years after the initial infection
in distal than proximal regions; therefore
smaller in the lumbar region
o Four stages of wallerian degeneration SELECTED REFERENCES
• 1: Physical degradation of axon with 1. Pema PJ et al: Myelopathy caused by nitrous oxide toxicity.
little biochemical change in myelin AJNR Am J Neuroradiol. ] 9(S):894-6, 1998
2. Becerra JL et al: MR-pathologic comparisons of wallerian
during first 4 weeks & results in no signal degeneration in spinal cord injury. AJNR Am J Neuroradiol.
intensity abnormality 16(1):125-33, 1995
• 2: At 4-14 weeks, myelin protein
breakdown with intact myelin lipids
(high lipid-protein ratio) results in
hypointense T2 signal
Multiple Sclerosis, Spinal Cord Multiple Sclerosis, Spinal Cord
II
Axial T2WI MR shows hyperintense intramedullary Sagittal T2WI MR shows multiple T2 hyperintense foci
=. 7
are involved=
lesions with focal cord enlargement The dorsal horns
& there is local cord enlargement
The multiplicity of lesions along with the lack of
edema or significant cord expansion is typical for a
demyelinating disease.
41
CORD LESION, 12 HYPERINTENSE, DORSAL
Contusion-Hematoma, Spinal Cord Contusion-Hematoma, Spinal Cord

CIl (Left) Sagittal STIR MR
C
shows a flexion dislocation
Q.
lI) injury of T11-12 81, burst
fracture of L 1 ~ &
compression fracture of L4
=. There is conus
compression and distal cord
contusion ~. (Right) Axial
T2WI MR shows cord
compression It] and
increased signal within the
cord due to a contusion.

shows C4-S discectomy and
fusion with myelomalacia
within the cervical cord ID.
displays T2 hyperintensity
within dorsal spinal cord
with a characteristic inverted
/IV" or inverted" rabbit ears"
appearance ~.
Subacute Combined Degeneration

shows hyperintensity along a
mildly enlarged posterior
cervical cord extending from
the foramen magnum to C7
=. (Right) Sagittal T2WI MR
reveals abnormal T2
hyperintensity = posteriorly
within spinal cord from
primary HIV myelilis. These
images are used with
permission from the
American Journal of
Neuroradiology (AfNR).
II
7
42
CORD lESION, 12 HYPERINTENSE, DORSAL
HIV Sarcoidosis
hyperinlensily = within the
posterior cervical cord in a
patient with II/V
myelopathy. The pattern
may appear identical to the
findings seen from vitamin
B 7 2 deficiency. (Right)
Sagittal graphic demonstrates
multiple intramedullary
sarcoid granulomas 0 in the
brainstem and upper cervical
cord. eNS involvement is
seen in 5 % of patients with
sarcoidosis.
Sarcoidosis Sarcoidosis
shows diffuse hyperintensity
in the spinal cord,
interspersed with isointense
nodules =. There is mild
cord expansion. (Righi)
Sagittal T7 C+ MR reveals
patchy & nodular
intramedullary enhancement
=. Enhancement pattern
can vary from enhancing
dural masses to
leptomeningeal & peripheral
& mass-like intramedullary
enhancement. Enhancement
! with steroid treatment;
there is a poor correlation
with clinical response.
Cord Wallerian Degeneration Cord Wallerian Degeneration

increased signal from the
lateral aspect of the cord ~
due to waJlerian
degeneration within the
lateral corticospinal tracts.
shows increased signal from
the lateral aspect of the
cords = below level of cord
injury within the lateral
corticospinal tracts. Above
the level of injury, the dorsal
columns are involved. Below
the level of injury, the lateral
corticospinal tracts are
involved.
II
7
43
CORD lESION, 12 HYPERINTENSE, CENTRAL
DIFFERENTIAL DIAGNOSIS o Up to 33% may have isolated cord lesions

• 90% have intracranial lesions
Common o Oligoclonal bands in CSF in 90%
Q) • Syringomyelia • Acute Transverse Myelitis, Idiopathic
c:
a. • Multiple Sclerosis, Spinal Cord o Both halves of the cord result in bilateral
1Il
• Acute Transverse Myelitis, Idiopathic motor, sensory, & autonomic dysfunction
• Infarction, Spinal Cord • Defined sensory level
• Type I DAVF • CSF pleocytosis or elevated IgG index
less Common o Long cord segment involvement (> 2
• Acute Disseminated Encephalomyelitis, vertebral segments) with> 2/3 of
Spinal Cord cross-sectional area of cord
• Viral Myelitis o Central T2 hyperintensity with patchy
• Cavernous Malformation, Spinal Cord eccentric enhancement
• Astrocytoma, Spinal Cord • Infarction, Spinal Cord
• Central Spinal Cord Syndrome o Focal T2 hyperintensity in slightly
• Radiation Myelopathy expanded cord
• Gray matter, adjacent white matter, or
cross-sectional cord may be involved
ESSENTIAL INFORMATION • Classically, the anterior horn cells show
Key Differential Diagnosis Issues T2 hyperintensity
• T2 hypointensity ± susceptibility artifact on • Focal hemorrhage seen as Tl
gradient echo recalled sequences to indicate hyperintensity/T2 hypointensity
hemorrhagic products • Adjacent anterior vertebral body
• Abnormal enlarged flow voids along the infarction
surface of the cord suggest a vascular lesion o Thoracic cord most frequently involved
because of arterial border zone
Helpful Clues for Common Diagnoses o Restricted diffusion on DWI
• Syringomyelia o Acute onset of myelopathy; motor signs
o Expanded cord with dilated or beaded
predominantly
cystic cavity & surrounding
• Type I DAVF
gliosis/myelomalacia o Enlarged T2 hyperintense distal cord with
o Contrast important to exclude tumor in dilated pial veins
complex cavitary lesion • Intradural, extramedullary flow voids at
o Primary: Associated basilar invagination,
level of conus
Chiari 1 or 2 malformation o "Flame-shaped" edema spares cord
o Secondary: Seen in 25% of cord injury
periphery
• Extensive MR signal change in superior • Venous hypertension from pial vessel
spinal cord parenchyma is ancillary sign engorgement results in reduced tissue
of disease advancement in clinically perfusion & cord ischemia
progressive post-traumatic syringomyelia o 80% patients are men in 5th or 6th decade
o "Cloak-like" pain & temporary sensory loss presenting with progressive lower
with preservation of position sense, extremi ty weakness
proprioception, light touch
• Acute myelopathy due to venous
• Multiple Sclerosis, Spinal Cord thrombosis: Foix-Alajouanine syndrome
o Peripheral T2 hyperintensity with central
enhancement (acute/subacute) classic Helpful Clues for less Common Diagnoses
• < 2 vertebral segments in length • Acute Disseminated Encephalomyelitis,
• < 1/2 cross-sectional area of cord, usually Spinal Cord
dorsolateral aspect o Multifocal white matter lesions with little
• Cord atrophy mass effect or vasogenic edema
II • Cervical cord most often involved o Punctate, ring-shaped, or fluffy
o May occur in any portion of cord enhancement
7
44
o Concomitant supratentorial involvement • Central Spinal Cord Syndrome

;:!.
.,
is characteristic o Diffuse disruption axons, especially within OJ
• Cranial nerve involvement with ADEM lateral columns of cervical cord 3
CD
to help differentiate from MS (corticospinal tracts); central gray matter <>-
C
o Autoimmune process producing intact OJ
inflammatory reaction o Most common mechanism may be direct

-<
o Delay between clinical onset and compression of cord by buckling of
appearance of imaging findings ligamenta flava into an already narrowed
• Viral Myelitis spinal canal
o Either immune-mediated or direct viral o MR & pathology indicate that
invasion intramedullary hemorrhage is not a
• Echovirus, Coxsackie, CMV, necessary feature, probably uncommon
varicella-zoster, HSV,EBV,hepatitis o Predominant loss of motor function in
o Central T2 hyperintensity with variable distal muscles of the upper limbs
enhancement • Radiation Myelopathy
• Enlarged edematous cord with segmental o Fusiform cord expansion with irregular,
continuous involvement focal rind of enhancement; demyelination
• Central Tl hypointensity is higher than in lateral, dorsal tracts
CSF o Demyelination in lateral, dorsal tracts
• Cavernous Malformation, Spinal Cord o One month to years following fractionated
o Well-defined lesion with hemorrhage of radiotherapy
various ages
o Speckled signal with peripheral T2
SELECTED REFERENCES
hypointense rim (hemosiderin)
1. Jinkins JR et al: MR of parenchymal spinal cord signal
o Enhancement absent/minimal change as a sign of active advancement in clinically
o No edema, unless acute hemorrhage progressive posttraumatic syringomyelia. AJNR Am J
o 50% thoracic, 40% cervical, 10% conus Neuroradiol. 19(1):177-82, 1998
2. Quencer RM et al: Acute traumatic central cord syndrome:
• Astrocytoma, Spinal Cord MRI-pathological correlations. Neuroradiology.
o T2 hyperintense enhancing infiltrating 34(2):85-94, 1992
mass, expanding cord
o Usually < 4 segments, holocord with
pilocytic astrocytoma
• Cervical> thoracic cord
o Diffuse or partial enhancement
II
Sagittal T2WI MR shows T2 hyperintense diiataUon of
the central spinal cord, extending from the medulla
(syringobulbia) ~ to the UlOracic spine l:JlI. Chiari 1
=
Sagittal T2WI MR shows multiple hyperintense
iniiamooulfary lesions with (oc:aJ cord enlargement.
White matter & gray maller involvemenl is very
7
malformation is not identified. common.
45
Multiple Sclerosis, Spinal Cord Acute Transverse Myelitis, Idiopathic

Q) (Left) Axial T7 C+ MR shows
c:
an intramedullary lesion with
'0.
en faint ring enhancement m.
Axia/ images are useFul for
localizing the lesion in
relation to the cord's
somatotopy. (Right) Sagittal
T2WI MR demonstrates
intramedullary hyperintensity
1m extending from lower
cervical into upper thoracic
cord The signal abnormality
involves more than 2
vertebral segments in length
& more than 2/3
cross-sectional area.
Infarction, Spinal Cord Infarction, Spinal Cord

shows focal T2
I
conus ~ which shows
slight expansion. This is
spinal cord infarction after
minor trauma may be due to
fibrocartilaginous embolism.
Classically, the T2
hyperinlensily involves the
anterior horn cells. (Right)
Axial T2* eRE MR shows
central gray matter
hyperintensity =.
hyperinlensily =
shows diffuse intramedullary
in a case
of meningitis complicated by
spinal cord ischemia. Diffuse
leptomeningeal
enhancement (not shown)
extends into the posterior
fossa. (Right) Sagittal T2WI
MR shows a "flame-shaped"
hyperintensity !J:&l in the
central cord due to venous
hypertension. Note multiple
serpentine intradural flow
voids from arterialized
venous plexus II] along the
II dorsal cord surface.
7
46
CORD LESION, 12 HYPERINTENSE, CENTRAL
Acute Disseminated Encephalomyelitis,

Spinal Cord Viral Myelitis
cervicothoracic cord
expansion and central T2
hyperintensity =.
Mu/tifocal
flame-shaped white matter
lesions typically have little
mass effect or vasogenic
edema. (Right) Sagittal T2WI
MR shows fusiform
expansion of the lower
cervical and upper thoracic
cord & long segment of
diffuse hyperintensity =.
The long segment of
involvement favors direct
viral infection or post viral
demyelinating disease.
Cavernous Malformation, Spinal Cord

shows a discrete lesion
within upper cervical cord at
C1level with "popcorn'"
heterogeneous signal =.
There is peripheral
hemosiderin staining but a
lack of edema. (Right)
large spinal cord
astrocytoma encompassing
entire cervical cord =. No
normal-appearing cord
parenchyma at the level of
the tumor and the transition
between tumor and normal
cord is apparent.
Central Spinal Cord Syndrome

=
shows cord hyperintensity
& a focal disc protrusion
~ at C3-4 that severely
effaces cord. There is no
hemorrhage within the cord,
just nonspecific
hyperilltensity due to
compression & contusion.
shows diffuse cord
hyperintensityextending
inferiorly from C4 & fusiform
expansion of lower cervical
& thoracic cord. IlislOry of
radiation treatment &
marrow changes suggest
sequela of radiation.
II
7
47
MYElOPATHY
DIFFERENTIAL DIAGNOSIS o Spinal Cord Herniation

• Neoplasm and Cyst
Common o Neurenteric Cyst
<I> • Infection/Inflammation o Metastases, Spinal Cord
t:
a. o Abscess, Epidural • Vascular
w o Abscess, Subdural o Cavernous Malformation, Spinal Cord
o Multiple Sclerosis, Spinal Cord o Type II AVM
• eoplasm and Cyst o Type III AVM
o Syringomyelia • Infection/Inflammation
o Astrocytoma, Spinal Cord o Abscess/Myelitis, Spinal Cord
o Ependymoma, Cellular, Spinal Cord o Acute Transverse Myelitis, Idiopathic
o Hemangioblastoma, Spinal Cord o Secondary Acute Transverse Myelitis
• Trauma o Vitamin B12 Deficiency, Spinal Cord
o Central Spinal Cord Syndrome
o Contusion-Hematoma, Spinal Cord
o Hematoma, Epidural-Subdural ESSENTIAL INFORMATION
o Hematoma, Subdural Key Differential Diagnosis Issues
o Syrinx, Post-Traumatic • Myriad etiologies requires evaluation of
• Degenerative pertinent clinical and laboratory
o Degenerative Disc Disease information to narrow differential list
o Stenosis, Acquired Spinal, Cervical
o Kyphosis
o Spondylolisthesis • Infection/Inflammation
o OPLL o Epidural and subdural abscess =>
o Ossification Ligamentum Flavum rim-enhancing extramedullary pus ± cord

• Intervertebral Disc Herniation signal or compression
o Intervertebral Disc Herniation, Cervical • Neoplasm and Cyst
o Intervertebral Disc Herniation, Thoracic o Syringomyelia => expanded spinal cord +
o Intervertebral Disc Herniation, Traumatic central dilated, beaded, or sacculated cystic
cavity
Less Common o eoplastic syrinx => look for nodularity or
• Congenital enhancement
• TraUlna
o Stenosis, Congenital Spinal o Central spinal cord syndrome => arms>
o Scoliosis and Kyphosis, Congenital legs + bladder dysfunction, variable
• Infection/Inflammation sensory loss, high T2 cord signal
o ADEM, Spinal Cord
• Degenerative
o Viral Myelitis o OPLL, OLF => look for ligamentous
• Neoplasm and Cyst ossification with narrowing of central
o Osteochondroma spinal canal
o Pathologic Vertebral Fracture • Intervertebral Disc Herniation
o Arachnoid Cyst o Use conventional diagnostic criteria
• Vascular
o Infarction, Spinal Cord
o Type I DAVF • Congenital
o Type IV AVF o Mucopolysaccharidoses => ± dens
hypoplasia, CVJ stenosis, thickened dura at
Rare but Important foramen magnum, platyspondyly, anterior
• Congenital beaking, thoracolumbar gibbus deformity
o Spondyloepiphyseal Dysplasia o Congenital spinal stenosis => reduced AP
o Dermoid and Epidermoid Tumors
II o Osteogenesis lmperfecta
canal diameter secondary to short, squat
pedicles and laterally directed laminae
• Trauma • Infection/Inflammation
7
48
MYELOPATHY
o ADEM, spinal cord => multi focal lesions o Neurenteric cyst => intraspinal cyst lined by
(MS mimic) with minimal mass effect, enteric mucosa + vertebral segmentation
vasogenic edema abnormalities
o Viral myelitis => swollen, edematous cord o Spinal cord metastasis => focal, enhancing
with segmental contiguous T2 signal cord lesion(s) + extensive edema
abnormality • Vascular
• Neoplasm and Cyst o Cavernous malformation => locules of
o Osteochondroma => sessile or blood with fluid-fluid levels surrounded by
pedunculated osseous "cauliflower" lesion, T2 hypointense rim
marrow contiguous with parent vertebra o Type II AVM => intramedullary glomus
o Arachnoid cyst => nonenhancing type AVM (similar to brain AVM), nidus
extramedullary loculated CSF intensity may extend to dorsal subpial surface
collection displacing cord or nerve roots o Type III AVM => juvenile-type AVM
• Vascular (intramedullary, extramedullary), nidus
o Spinal cord infarction => central T2 may have extramedullary and extraspinal
hyperintensity more common than extension
wedge-shaped injury in anterior 2/3 spinal • Infection/Inflammation
cord o Spinal cord abscess/myelitis =>
Helpful Clues for Rare Diagnoses ring-enhancing mass within cord,
appropriate clinical history of
• Congenital
o Dermoid and epidermoid tumors => CSF
inflamma tion/ infection
o Acute idiopathic transverse myelitis =>
isodense/isointense lumbosacral or cauda
equina mass central cord lesion extent> 2 vertebral
o Osteogenesis imperfecta => severe
segments + eccentric enhancement
o Secondary acute transverse myelitis => T2
osteopenia & multiple fractures
hyperintense lesion with mild cord
• Trauma
o Spinal cord herniation => herniation of
expansion, minimal to no enhancement
o Vitamin BI2 deficiency => mild spinal cord
spinal cord through defect in dura of
ventral canal with expansion of dorsal enlargement, abnormal T2 hyperintensity
subarachnoid space within dorsal columns ± lateral columns
• Neoplasm and Cyst
Abscess, Epidural Abscess, Subdural
II
Sagittal TI C+ MR in a patient with meningitis shows
progression to parameningeaf inflammation and
Sagittal TI C+ FS MR demonstrates a large low signal
fluid collection= with peripheral enhancement
7
=.
epidural abscess located ventral to cord.
49
MYElOPATHY

Q)
r::
shows multiple areas of
Cl.
l/l abnormal T2 prolongation in
the brainstem and spinal
cord in a patient presenting
with myelopathy and known
MS. (Right) Sagittal T2WI
MR demonstrates a large
h%cord syrinx with
extra-axial CSF collection at
the posterior C '-C2 level in a
treated patient with Chiar; 2
malformation and congenital
craniovertebral anomalies.

depicts a very large spinal
cord astrocytoma
encompassing the entire
cervical spinal cord. No
intrinsic enhancement is
demonstrated. (Right)
Sagittal T2WI MR reveals a
typical cellular ependymoma
with central cord expansion
and mixed signal intensity
characterized by intrinsic
hypointense intramedullary
blood products.
Hemangioblastoma, Spinal Cord Central Spinal Cord Syndrome

shows a large intramedullary
hemangioblaslOma with
associated syrinx within the
upper thoracic spinal cord
and a smaller
hemangioblastoma at the
foramen of Magendie.
child following trauma
presenting clinically with
SCfWORA reveals diffuse
long segment intramedullary
high signa! intensity. Cervical
radiographs were normal.
II
7
50
MYElOPATHY CJl
't:l
:l
CD
Hematoma, Epidural-Subdural
(Left) Sagittal T2' eRE MR
demonstrates post-traumatic
cervical epidural hemorrhage
and intramedullary spinal
cord hemorrhage, leading to
cord compression secondary
to post-traumatic disc
herniation =. (Right)
SagiLtal T2WI MR confirms a
large low signal intensity
spontaneous epidural
hematoma =:I, producing
Hematoma, Subdural Syrinx, Post-Traumatic

shows a large linear,
lobulated T I hyperintense
blood collection that extends
throughout the cervical and
upper thoracic spine and
that crosses the skull base
along the clivus. (Right)
Sagittal T2WI MR
demonstrates a focal
post-traumatic syrinx = in a
patient with delayed
worsening of quadriplegia
(ascending leve/) following
skiing spinal cord injury.
Stenosis, Acquired Spinal, Cervical OPLL

reveals severe multilevel
degenerative spondylosis
compression characterized
by abnormal il1lramedullary
T2 prolongation. (Right)
Sagittal T2WI MR
demonstrates multilevel
hypointense ossification
within the posterior
longitudinal ligament
producing vel1lral spinal
cord compression with
abnormal T2 prolongation
and cord deformation.
II
7
51
MYELOPATHY
Intervertebral Disc Herniation, Cervical Intervertebral Disc Herniation, Thoracic

CIl (Left) Sagittal T2WI MR
c:
'0.. shows central disc extrusion
l/l effacing the thecal sac
causing cord compression.
Note abnormal T2
hyperintensily
(contusion/myelomalacia)
within spinal cord at C3-4.
reveals severa/large disc
extrusions that compress the
ventra/thoracic spinal cord
at multiple levels.
Intervertebral Disc Herniation,

Traumatic Mucopolysaccharidoses
shows sequelae of cervical
hyperfJexion injury with
traumatic cervical disc
herniation and ligamentous
injury with herniated C6-7
disc a disruption of
anterior longitudinalligamcnl
ligament =-
@ posterior longitudinal
and
interspinous ligaments p:jJ.
(Morquio, MPS IV) shows
odontoid hypoplasia and
thick pannus =:I producing
cervical canal stenosis and
cord compression EJ at the
craniovertebraf junction.
ADEM, Spinal Cord

shows a variant appearance
of congenital cervical spinal
stenosis that results from
short pedicles in conjunction
with congenital vertebral
anomalies, producing spinal
cord compression =:I and
abnormal cord T2
hyperintensity. (Right)
Sagillal T2WI MR
demonstrates several T2
lesions within the cervical
spinal cord in a patient with
correlative clinical history.
II
7
52
MYElOPATHY
Viral Myelitis Osteochondroma

demonstrates patchy
heterogeneous spina! cord
enhancement in a patient
with proven viral myelitis
(Varicella-Zoster). (Right)
Coronal T2WI FS MR reveals
a heterogeneous extradural
mass originating from the
right posterior spinal osseous
elements that laterally
compresses the thoracic
spinal cord.
Infarction, Spinal Cord

expansion and T2
hyperintensity of the cervical
cord extending from C3 to
C7. (Right) Sagittal T2WI MR
depicts classic central cord
T2 hyperintensity sparing the
cord periphery. Note
multiple serpentine
intradural flow voids along
the dorsal cord surface
representing the arterialized
venous plexus.

shows multiple abnormal
flow voids involving dorsal
subarachnoid space 81 and
extending into dorsal cord
surface. Tocal mixed signal
intensity = is due to high
flow aneurysm. (Right)
Sagittal T2WI MR confirms
characteristic vertebral
anomalies with severe
cranioverlebral junction
central canal stenosis
compression.
II
7
53
INDEX
A
Abscess flattened, II(3):8
brain fracture, II(3):29
cyst with nodule, 1(5):29, 30 scalloping or widened canal, II(3):18, 19
multiple enhancing lesions, 1(5):2, 4 vertebral endplate contour abnormality, 1l(4):10,
ring-enhancing lesion, solitary, 1(5):6, 8 11
cerebellar mass, 1(7):22, 25 Acidopathies, organic, 1(6):80
cystic-appearing posterior fossa lesion, 1(7):35, Acromegaly, 1(1):9, II(3):18
38 Acute necrotizing encephalopathy of childhood,
effaced sulci, focal, 1(4):17,19 1(6):93
epidural mass, 11(5):2,4. See also Epidural Acute transverse myelitis
abscess idiopathic
medulla lesion, 1(7):11, 13 acute upper extremity pain or weakness,
midbrain lesion, 1(6):100 II(1):43, 47
paraspinal. See Paraspinal abscess intramedullary lesions, no enhancement,
parenchymal lesions 1l(7):18, 19
multiple hypodense, 1(5):60, 62 intramedullary lesions, T2 hyperintense, T1
T1 hypointense, T2 hyperintense, 1(5):91, 93 isointense, II(7):30, 32
periventricular, 1(3):58, 60 intramedullary mass, II(7):2
pituitary, 1(8):25 myelopathy, II(7):49
presacral, 11(1):22,23 pediatric back pain, II(1):57
prevertebral, II(1):14 subarachnoid space narrowing, II(6):6
pyogenic, 1(7):6 T2 hyperintense cord lesions, central,
restricted diffusion, 1(5):98, 100 II(7):44, 46
ring-enhancing lesions, multiple, 1(5):12, 13-14 intramedullary lesions, diffuse/ill-defined
solitary cystic mass, 1(5):17, 19 enhancement, II(7):20, 21
spinal cord. See Spinal cord abscess secondary
subdural, 11(1):30,11(7):48,49 acute upper extremity pain or weakness,
Accelerated degeneration II(1):43
chronic back pain/radiculopathy, postoperative, intramedullary lesions, T2 hyperintense, Tl
11(1):36,39-40 isointense, II(7):30, 32
intervertebral disc end plate irregularity, II(4):6, myelopathy, 11(7):49
8 pediatric back pain, II(1):57, 59
post-traumatic, 11(1):2,4 ADEM (acute disseminating encephalomyelitis)
vertebral body, 11(3):24-25,26 basal ganglia, 1(6):70, 81
Accessory sutures, 1(1):2 cerebellar mass, 1(7):22, 25
Achondroplasia corpus callosum
bony trauma, 1l(1):6, 8 holes, 1(6):52, 53
C1-C2 instability, II(2):12 lesion without mass effect, 1(6):54
cervical abnormality, chronic post-traumatic, splenium lesion, 1(6):59, 61
1l(1):2 cranial nerve enhancement, 1(4):47
craniovertebral junction abnormalities, II(2):4 hypothalamus lesion, 1(8):49
kyphosis, II(1):12, 13 intramedullary lesions, diffuse/ill-defined
macrocephaly, 1(1):33, 37 enhancement, II(7):20, 22
pedicle abnormality, II(3):36 medulla lesion, 1(7):10, 12
platyspondyly, diffuse, 11(1):16, 17 midbrain lesion, 1(6):100, 102
vertebral anomalies, congenital, 11(3):2 multiple brain hyperintensities (T2/FLAIR),
vertebral body 1(5):70, 71
dysmorphic, 11(3):10 multiple enhancing lesions, 1(5):2, 4
INDEX
>< parenchymal lesions ependymal/subependymallesions, 1(3):9, 11
QJ
"'C multiple hypodense, 1(5):61, 63 foramen of Monro mass, 1(3):19, 21
C solitary hypodense, 1(5):57, 59 macrocephaly, 1(1):33, 37
T1 hypointense, T2 hyperintense, 1(5):90, 92 periventricular enhancing lesions, 1(3):58, 61
periventricular enhancing lesions, 1(3):58, 60 thick septum pellucidum, 1(3):16, 17
periventricular T2/FLAIR lesions, 1(3):72, 74 Alzheimer dementia
pontine lesion, 1(7):6, 8 asymmetric cerebral hemispheres, 1(6):2, 4
"pulvinar sign" (mimic), 1(6):96, 97 enlarged sulci, generalized, 1(4):8, 9
ring-enhancing lesions, multiple, 1(5):12, 14 large ventricles, 1(3):45
spinal cord thin cortex, 1(6):14-15, 18
acute upper extremity pain or weakness, Amyotrophic lateral sclerosis, 1(6):101, II(7):38, 39
II(I):43, 47 Anasarca, scalp, 1(1):4
intramedullary lesions, no enhancement, Anemia, 1(1):9. See also Sickle cell disease
II(7):18, 19 Aneurysm. See also Bone cyst, aneurysmal;
intramedullary lesions, solid enhancement, Pseudoaneurysm
II(7):14, 16 aortic, II(I):52, II(5):8, 9
intramedullary lesions, T2 hyperintense, Tl blood blister-like, 1(9):3, 5
isointense, II(7):31, 33 CPA-lAC mass, 1(4):24, 26
intramedullary lesions, Tl hypointense, dissecting, 1(4):60, 1(9):6, 7
II(7):28, 29 fusiform. See Fusiform aneurysm
intramedullary mass, II(7):2 giant serpentine, 1(9):6
multiple intramedullary lesions, II(7):12, 13 saccular. See Saccular aneurysm
myelopathy, II(7):49, 52 thrombosed, 1(5):7, 10
subarachnoid space narrowing, II(6):6 vertebral artery, II(3):16
T2 hyperintense cord lesions, central, Angiolipoma
II(7):44-45, 47 epidural mass, II(5):3, 7
thalamic lesions extradural lesions, solid enhancement, II(5):17,
bithalamic, 1(6):92, 94 19
unilateral, 1(6):90, 91 Tl hyperintense extradural lesion, II(5):30, 31
tumefactive, corpus callosum mass, 1(6):56 Angiomatosis, cystic, II(3):39. See also
white matter lesions Meningioangiomatosis
confluent, 1(6):35, 38 Angiosarcoma, II(3):39
solitary, 1(6):30, 32 Ankylosing spondylitis
Adrenoleukodystrophy, X-linked cauda equina syndrome, II(6):36
confluent white matter lesions, 1(6):34, 38 focal vertebral body sclerosis, II(3):42, 43
corpus callosum lesion without mass effect, intervertebral disc end plate irregularity, II(4):7,
1(6):54, 55 9
corpus callosum splenium lesion, 1(6):59, 61 vertebral end plate signal abnormality, II(4):16,
multiple parenchymal calcifications, 1(5):41 17
periventricular T2/FLAIR lesions, 1(3):73 Anterior horns, coarctation, 1(3):2-3, 5
Aging, brain. See Brain, normal aging Anterior radiculopathy syndrome, II(6):9, 11, 15
Aicardi-Goutieres syndrome Anticoagulation complications, 1(5):51, 54
interhemispheric fissure cysts, 1(4):21 Aortic aneurysm, II(I):52, II(5):8, 9
microcephaly, 1(1):39, 43 Apophyseal ring fracture, II(I):8, II(3):28
periventricular calcifications, 1(3):67, 71 Aqueductal stenosis
AIDS-related opportunistic infections. See macrocephaly, 1(1):32, 34
Opportunistic infections, AIDS midbrain lesion, 1(6):100, 102
Alcoholic encephalopathy suprasellar cystic mass, 1(8):36, 37
cerebellar atrophy, 1(7):18, 20 thin skull, generalized, 1(1):14
chronic, enlarged sulci, generalized, 1(4):8, 10 Arachnoid cyst
corpus callosum splenium lesion, 1(6):58, 61 cauda equina syndrome, II(6):36
large ventricles, 1(3):44, 46 cisterna magna mass, 1(4):38, 40
thin corpus callosum, 1(6):41, 44 CPA-lAC, 1(4):24, 26, 28, 29
Alexander disease epidural mass, II(5):3, 5
cerebral aqueduct/periaqueductallesion, 1(3):29, extra-axial fluid collection, CSF-like, 1(4):50, 51
31 extra-axial mass, 1(4):52, 76, 77
confluent white matter lesions, 1(6):35 extradural lesions, II(5):14, 33
II
INDEX
interhemispheric fissure cysts, 1(4):20,22 hyperattenuating, 1(9):8-9
intradural/extramedullary lesions hyperdensity, physiologic, 1(9):8
no enhancement, 11(6):12, 13 infarction, 11(7):20,23. See also Cerebral
ring/peripheral enhancement, 11(6):22,23 infarction
Tl hypo intense, 11(6):28,29 ischemia, bithalamic lesions, 1(6):92, 93
intrasellar mass, cystic, 1(8):22, 23 normal, extra-axial flow voids, 1(4):60
macrocephaly, 1(1):32, 34 shape/configuration abnormalities, 1(9):2-5
midline cyst, infratentorial, 1(7):14, 15 vascular calcifications, 1(9):10-11
myelopathy, 11(7):49 Arteriolosclerosis
pedicle abnormality, 11(3):36,37 cranial nerve enhancement, 1(4):47
pineal region mass, 1(8):2, 4 parenchymal lesions, 1(5):90,91
posterior fossa lesion, cystic-appearing, 1(7):34, periventricular T2/FLAIR lesions, 1(3):72, 73
35 pontine lesion, 1(7):6, 7
prepontine cistern mass, 1(4):33, 37 white matter lesions
quadrigeminal cistern mass, 1(8):8, 9 confluent, 1(6):34, 35
suprasellar mass solitary, 1(6):30, 32
cystic, 1(8):36, 38 Arteriovenous fistula
general, 1(8):24, 26 carotid-cavernous
pediatric, 1(8):30-31, 33 bilateral cavernous sinus lesions, 1(10):18, 20
Tl hypointense, 1(8):58 unilateral cavernous sinus mass, 1(10):14-15,
thin skull, localized, 1(1):16 16
vertebral body scalloping or widened canal, conus abnormality, 11(7):7,9
11(3):18, 19 dural. See Dural arteriovenous fistula
vestibular schwannoma with, 1(4):29, 31 epidural, 11(5):40
Arachnoid granulations extradural, 11(5):32
calvarium, 1(1):2 type IV, 11(6):36,11(7):48,53
dural sinuses, 1(4):77, 79, 1(10):2, 3-4 Arteriovenous malformation. See also
lucent skull lesions, multiple, 1(1):22,24 Developmental venous anomaly
Arachnoiditis brain cyst with nodule, 1(5):29, 31
cauda equina enhancement, diffuse, 11(6):3 cerebellar mass, 1(7):23, 26
intradural/extramedullary lesions, T1 conus abnormality, 11(7):7,9
hypointense, 11(6):29,31 cortical veins, enlarged, 1(10):8, 9
lumbar deep veins, enlarged, 1(10):10, 12
chronic back pain/radiculopathy, ependymal enhancement, 1(3):41, 43
postoperative, 11(1):37, 41 epilepsy, 1(5):118, 120
intradural/extramedullary lesions, 11(6):12, extra-axial flow voids, 1(4):60, 61
23, 25 intradural/extramedullary lesions
leptomeningeal enhancement, 11(6):9 Tl hypointense, 11(6):28,31
lower extremity pain, 11(1):49,51 Tl hypointense, T2 hypointense, 11(6):32,33
subarachnoid space narrowing, 11(6):6 intramedullary lesions, T1 hyperintense,
Arachnoiditis ossificans 11(7):35,37
chronic back pain/radiculopathy, postoperative, intramedullary mass, 11(7):3,4
11(1):37,41 medulla lesion, 1(7):10, 12
intradural/extramedullary lesions micro-AV malformations, multiple, 1(5):82, 85
ring/peripheral enhancement, 11(6):23,25 parenchymal calcification, solitary, 1(5):34-35,
Tl hypointense, 11(6):29 37
Tl hypointense, T2 hypointense, 11(6):32,33 parenchymal lesion, solitary hyperdense,
Arterial dissection 1(5):45, 47
arterial shape/configuration abnormalities, pontine lesion, 1(7):6
1(9):3,5 sellar/juxtasellar calcification, 1(8):15, 17
carotid arteries, 11(2):4,9, 11 thrombosed, 1(5):7, 10
hyperattenuating artery, 1(9):8, 9 type 1,11(6):18
nonaneurysmal, fusiform arterial enlargement, type II
1(9):6,7 intradural lesion, serpentine, 11(6):18
vertebral artery, 11(2):2 intramedullary lesion, solid enhancement,
Arteries, 1(9):2-11 11(7):15, 17
fusiform arterial enlargement, 1(9):6-7 intramedullary lesions, T1 hypointense,
11(7):28,29
iii
INDEX
)( intramedullary lesions, Tl hypointense, T2 Astrocytoma - diffuse, low grade
QJ
"'C hypointense, II(7):26, 27 bithalamic lesions, 1(6):92, 94
-C myelopathy, II(7):49
type III, II(6):18, II(7):49
cerebral aqueduct/periaqueductal lesion, 1(3):28,
30
type IV,II(6):18, 19 in children over 1 year, 1(5):112
vascular calcifications, 1(9):10 cortical hyperintensity Tl/FLAIR, 1(6):24, 26
venous effaced sulci, focal, 1(4):16, 18
extradural lesions, solid enhancement, focal cortical mass, 1(6):20, 22
II(5):16 foramen magnum mass, 1(4):42, 44
lumbar soft tissue mass, pediatric, hypothalamus lesion, 1(8):48, 49
II(5):42-43, 45 parenchymal calcification, solitary, 1(5):34, 37
vein of Galen. See Vein of Galen parenchymal lesions, 1(5):56-57, 58,90
malformation pineal gland mass, 1(8):6
vermis mass, 1(7):28-29, 30 posterior fossa, adult, 1(7):41, 43
Arthritis. See also Juvenile idiopathic arthritis; sellar/juxtasellar calcification, 1(8):14-15
Rheumatoid arthritis suprasellar mass
osteoarthritis, II(2):5, 6 enhancing, 1(8):42
septic facet joint, II(3):32, 33 general, 1(8):25, 28
Arthropathies. See also Spondyloarthropathy Tl isointense, 1(8):54, 55
crystalline, II(I):2 tecta I plate lesion, 1(6):98
facet. See Facet arthropathy thalamic lesions, unilateral, 1(6):90, 91
hemodialysis, II(I):2 thin skull, localized, 1(1):16
neurogenic. See Neurogenic arthropathy Astrocytoma - pilocytic
Astroblastoma cerebellar mass, 1(7):22, 24
"bubbly-appearing" intraventricular mass, in children over 1 year, 1(5):112, 113
1(3):37 cyst with nodule, 1(5):28, 29
in children over 1 year, 1(5):113 focal cortical mass, 1(6):21, 23
focal cortical mass, 1(6):21 fourth ventricle mass, 1(3):32, 34
Astrocytoma. See also Xanthoastrocytoma, hypothalamus lesion, 1(8):48, 49
pleomorphic infratentorial midline cyst, 1(7):14, 16
anaplastic parenchymal calcification, solitary, 1(5):34, 37
in children over 1 year, 1(5):113 parenchymal lesions, solitary hypodense,
corpus callosum mass, 1(6):56, 57 1(5):57, 59
midbrain lesion, [(6):100 pontine lesion, 1(7):6, 9
in newborn/infant, 1(5):106, 107 posterior fossa
parenchymal lesions, 1(5):56, 58, 90 adult neoplasm, 1(7):41
posterior fossa, adult, 1(7):41, 43 cystic-appearing lesion, 1(7):34, 36
posterior fossa, pediatric, 1(7):45, 48 pediatric neoplasm, 1(7):44, 45
thalamic lesion, unilateral, 1(6):90, 91 ring-enhancing lesion, solitary, 1(5):7, 11
white matter lesion, solitary, 1(6):31, 33 sellar/ juxtasellar calcification, 1(8):14
basal ganglia lesions, bilateral, 1(6):80, 82 solitary cystic mass, 1(5):17, 18
desmoplastic infantile, 1(5):107, 109 suprasellar mass
diffuse, low grade. See Astrocytoma - diffuse, calcified, 1(8):40, 41
low grade cystic, 1(8):37
diffuse fibrillary, 1(6):100, 1(7):10, 12 enhancing, 1(8):42
foramen of Monro mass, 1(3):18, 20 general, 1(8):24, 26
giant cell, sub ependymal. See Giant cell pediatric, 1(8):30, 31
astrocytoma, subependymal Tl hypointense, 1(8):58, 59
intramedullary lesions, II(7):20-21, 23 Tl isointense, 1(8):54, 55
lateral ventricle mass, 1(3):13 vermis mass, 1(7):28, 29
oligoastrocytoma, 1(6):31 Astrocytoma - pilomyxoid
pilocytic. See Astrocytoma - pilocytic in children over 1 year, 1(5):112, 114
pilomyxoid. See Astrocytoma - pilomyxoid hypothalamus lesion, 1(8):49, 51
spinal cord. See Spinal cord astrocytoma sellar/juxtasellar calcification, 1(8):15, 16
thick septum pellucidum, 1(3):16-17 suprasellar mass
vertebral body scalloping or widened canal, cystic, 1(8):37, 39
I1(3): 18 general, 1(8):25, 28
iv
INDEX
hyperdense, 1(8):52 Bone cyst, aneurysmal
pediatric, 1(8):31, 34 abnormal extradural marrow signal, 11(5):27,29
T1 hyperintense, 1(8):56 craniovertebral junction abnormalities, 11(2):4
T1 hypointense, 1(8):58 enlarged vertebral body, soap bubble expansion,
Astrocytosis, reactive 11(3):38,41
multiple brain hyperintensities (T2/FLAIR), enlarged vertebral body/posterior element,
1(5):64, 66 11(3):13, 15
solitary white matter lesion, 1(6):30, 32 epidural mass, 11(5):2,6
Ataxia, hereditary, 1(7):19, 21 extradural lesion, Tl hypointense, 11(5):32
Atherosclerosis, intracranial kyphoscoliosis, child, 11(1):14
arterial shape/configuration abnormalities, lytic skull lesion, solitary, 1(1):18
1(9):2,3 neural foramen, enlarged, 11(3):16
calcified suprasellar mass, 1(8):40 pedicle abnormality, 11(3):36
hyperattenuating artery, 1(9):8, 9 sacral mass, adult, 11(1):19
multiple brain hyperintensities (T2/FLAIR), Bone dysplasia, sclerosing, 1(1):9
1(5):64,66 Bone graft complications
sellar/juxtasellar calcification, 1(8):14, 15 acute back pain/radiculopathy, 11(1):31,35
vascular calcifications, 1(9):10 chronic back pain/radiculopathy, 11(1):37,40-41
Atlanto-occipital dislocation, 11(2):2,4 Bone island
Atrial diverticulum, medial, 1(4):21, 23 extradural lesions, no enhancement, 11(5):14
Auditory canal, internal, 1(4):24-27 focal Tl hypointense signal, vertebral body,
Axonal injury, diffuse. See Diffuse axonal injury 11(3):56
(DAI) focal vertebral body sclerosis, 11(3):42
Bone marrow
extradural
B abnormal marrow signal, 11(5):26-29
Baastrup sign, 11(3):12, 13 normal marrow signal, 11(5):22-25
Back pain fatty, 11(3):48,49, 50, 51
adult, 11(1):52-55 vertebral
pediatric, 11(1):56-59 hemorrhage, 11(3):50,51
postoperative radiculopathy hyperplastic, 11(3):52,53
acute, 11(1):30-35 post-irradiation, 11(3):48,11(5):14
chronic, 11(1):36-41 Bone morphogenetic protein, 11(4):7,9
Bacterial infections Bone tumors, primary
intramedullary lesions, 11(7):20,21 adult back pain, 11(1):52
multiple hypointense foci on T2, 1(5):80, 81 epidural mass, 11(5):2
Balloon cell dysplasia, 1(5):118, 122, 1(6):8, 10 extradural lesions, 11(5):33,37
Band heterotopia, 1(5):119, 122 lower extremity pain, 11(1):48
Basal cell carcinoma, 1(1):4, 5 Bones, worm ian, 1(1):2
Basal cell nevus syndrome, 1(2):2, 3 Brachial plexus neuritis, idiopathic, 11(1):43,47
Basal ganglia Brachial plexus traction injury
bilateral lesions, 1(6):80-83 acute back pain/radiculopathy, 11(1):31,35
calcification, 1(6):62-65 acute upper extremity pain or weakness,
T1 hyperintense, 1(6):66-69 11(1):42,45
T2 hyperintense, 1(6):70-73 Brain
Basilar invagination (mimic), 1(7):32, 33 immature, thin corpus callosum, 1(6):40, 41
Basivertebral vein, 11(3):56 injury. See also Cerebral contusion
Behfi:etdisease, 1(3):29 remote, parenchymal calcifications, 1(5):41,
Bell palsy, 1(4):47, 49 42
Benign macrocrania of infancy, 1(4):9, 11 thin corpus callosum, 1(6):41, 44
Bithalamic lesions, 1(6):92-95 neoplasms. See also specific histologic types
Blake pouch cyst, 1(4):2, 3 in children over 1 year, 1(5):112-117
Blake pouch remnant, 1(3):3, 5 epilepsy, 1(5):118
Blood-brain barrier leakage, 1(4):64-65, 67 in newborn/infant, 1(5):106-111
Blue rubber bleb nevus syndrome, 1(10):11 primary, 1(5):90-91
Bone abnormalities, congenital, 11(2):5 normal aging
Bone cement, 11(3):56 basal ganglia calcification, 1(6):62, 63
v
INDEX
>< cerebellar atrophy, 1(7):18, 19 Tl/T2 hyperintense lesions, 1(5):86-89
QJ
"'C confluent white matter lesions, 1(6):34, 35 Tl/T2 isointense lesions, 1(5):94-97
C enlarged perivascular spaces, 1(6):74, 75 tumors, pediatric
enlarged sulci, generalized, 1(4):8, 9 in children over 1 year, 1(5):112-117
extra-axial fluid collection, CSF-like, 1(4):50 in newborn/infant, 1(5):106-111
large ventricles, 1(3):44, 45 "Brain rock," 1(5):35, 38
multiple brain hyperintensities (T2/FLAIR), Brainstem
1(5):64, 65 large, 1(7):2
multiple parenchymal calcifications, 1(5):40 medulla lesion, 1(7):10
periventricular T2/FLAIRlesions, 1(3):72, 73 midbrain lesion, 1(6):100
thin cortex, 1(6):14, 15 pontine lesion, 1(7):6, 8
normal variants small, 1(7):4-5
asymmetric cerebral hemispheres, 1(6):2, 3 Brainstem glioma
corpus callosum, abnormal shape or craniovertebral junction soft tissue
configuration, 1(6):46, 47 abnormalities, II(2):9
enlarged perivascular spaces, 1(6):74 large brainstem, 1(7):2
thin corpus callosum, 1(6):40 medulla lesion, adult, 1(7):10, 12
physiologic calcification pediatric
basal ganglia, Tl hyperintense, 1(6):66, 67 in children over 1 year, 1(5):112, 114
parenchymal, 1(5):35, 38, 40 craniovertebral junction abnormalities,
Brain death II(2):4
effaced sulci, generalized, 1(4):12 exophytic, prepontine cistern mass, 1(4):32,
hyperdense CSF (mimic), 1(4):72, 73 35
low cerebellar tonsils, 1(7):32, 33 fourth ventricle mass, 1(3):32, 34
small ventricles, 1(3):48 medulla lesion, 1(7):10
Brain parenchyma, 1(5):2-123. See also in newborn/infant, 1(5):107, 111
Infratentorial brain parenchyma; Parenchymal posterior fossa neoplasm, 1(7):44, 46-47
metastases; Supratentorial brain parenchyma tecta I plate lesion, 1(6):98, 99
calcifications Brucellosis, II(4):7
multiple, 1(5):40-43 Budd-Chiari syndrome. See Chiari 2 (Budd-Chiari
physiologic, 1(5):35, 38, 40 syndrome)
solitary, 1(5):34-39 Burr holes
CSF-like lesions, 1(5):22-27 lytic skull lesion, solitary, 1(1):18, 19
cyst with nodule, 1(5):28-31 multiple lucent skull lesions, 1(1):22, 24
cystic mass, solitary, 1(5):16-21 Burst fractures
epilepsy, 1(5):118-123 cervical
fat-like lesions, 1(5):32-33 acute upper extremity pain or weakness,
hyperdense lesions II(I):42, 44
multiple, 1(5):50-55 C2, cranio-cervical junction acute injury,
solitary, 1(5):44-49 II(2):2
hypodense lesions C2, craniovertebral junction abnormalities,
multiple, 1(5):60-63 II(2):5
solitary, 1(5):56-59 C2, posterior element fracture, II(3):34
multiple brain hyperintensities (T2/FLAIR) post-traumatic bony abnormality, II(I):4, 5
common, 1(5):64-69 posterior element fracture, II(3):34
less common, 1(5):70-75 vertebral body fracture, II(3):28
rare but important, 1(5):76-79 flattened vertebral body, II(3):6, 7
multiple enhancing lesions, 1(5):2-5 lumbar
multiple hypointense foci on GRE/SWI, bony trauma, II(I):8
1(5):82-85 cauda equina syndrome, II(6):36, 37
multiple hypointense foci on T2, 1(5):80-81 kyphosis, 1I(1):12, 13
restricted diffusion, 1(5):98-101 posterior element fracture, II(3):34, 35
ring-enhancing lesions vertebral body fracture, II(3):28
multiple, 1(5):12-15 mild, vertebral body, II(3):28
solitary, 1(5):6-11 thoracic bony trauma, 1I(1):6
Tl hyperintense lesions, 1(5):102-105 thoracolumbar
Tl hypointense, T2 hyperintense lesions, posterior element fracture, II(3):34
1(5):90-93 vertebral body fracture, 1I(3):28, 29
VI
INDEX
c Carotid-cavernous fistula
bilateral cavernous sinus lesions, 1(10):18, 20
CADASIL
traumatic, unilateral cavernous sinus mass
confluent white matter lesions, 1(6):35, 37
1(10):14-15, 16 '
enlarged perivascular spaces, 1(6):74
Cauda equina enhancement, diffuse, 11(6):2-5
multiple brain hyperintensities (T2/FLAIR),
Cauda equina syndrome, 11(6):36-37
1(5):76, 77
Caudal regression syndrome
multiple hypodense parenchymal lesions,
conus abnormality, 11(7):6,9
1(5):61
flattened vertebral body, multiple, 11(3):8
periventricular T2/FLAIR lesions, 1(3):73, 75
kyphoscoliosis, child, 11(1):14
Calcific tendinitis, longus coli
sacral deformity, 11(1):27,29
CI-C2 instability, 11(2):12
vertebral anomalies, congenital, 11(3):2
craniovertebral junction abnormalities, 11(2):4
Cavernous malformation
soft tissue calcification, paraspinal, 11(5):20,21
acquired, 1(5):70, 72
Calcinosis, tumoral, 11(5):3,5, 32
basal ganglia calcification (mimic), 1(6):63
Calcium pyrophosphate deposition disease (CPPD)
"bubbly-appearing" intraventricular mass,
CI-C2 instability, 11(2):12,13
1(3):36-37, 39
chronic post-traumatic cervical abnormality,
cerebellar mass, 1(7):23, 25-26
11(1):2
congenital, 1(5):70, 72
craniovertebral junction abnormalities, 11(2):4,7
focal cortical mass, 1(6):21, 23
odontoid deformity, 11(2):14
foramen of Monro mass, 1(3):19
Callosal dysgenesis
hypothalamus lesion, 1(8):49
abnormal shape or configuration of corpus
intraventricular calcifications, 1(3):63, 65
callosum, 1(6):46, 48
extra-axial mass, CSF-Iike, 1(4):52, 53 large brainstem, 1(7):2, 3
lateral ventricle mass, 1(3):13
interhemispheric fissure cysts, 1(4):20, 22
medulla lesion, 1(7):10, 12
thin corpus callosum, 1(6):40, 43
midbrain lesion, 1(6):100, 102
Callosectomy/callosotomy, 1(6):40, 43, 46, 48
multiple hypointense foci on GRE/SWI, 1(5):82,
Calvarium fracture, 1(1):27
84-85
Canavan disease, 1(1):33, 37, 1(6):34, 38
parenchymal calcifications, 1(5):34, 36, 40
Carbon monoxide poisoning
parenchymal lesions
basal ganglia
multiple hyperdense, 1(5):50, 53
calcification, 1(6):63
solitary hyperdense, 1(5):44, 47
Tl hyperintense, 1(6):66, 68
T2 hyperintense, 1(6):70, 72
confluent white matter lesions, 1(6):35 Tl/T2 hyperintense, 1(5):86, 88
pontine lesion, 1(7):6
globus paIIidus lesions, 1(6):86, 88
sellar/juxtasellar calcification, 1(8):15, 17
multiple brain hyperintensities (T2/FLAIR),
spinal cord. See Cavernous malformation -
1(5):71, 75
spinal cord
Carcinoma
basal cell, 1(1):4, 5 suprasellar mass
general, 1(8):25, 29
choroid plexus. See Choroid plexus carcinoma
lung, 11(3):38,39
tecta I plate lesion, 1(6):98, 99
nasopharyngeal
vascular calcifications, 1(9):10, 11
craniovertebral junction abnormalities,
vermis mass, 1(7):29, 30
11(2):4
Cavernous malformation - spinal cord
craniovertebral junction soft tissue
abnormalities, 11(2):8-9, 10 conus abnormality, 11(7):6-7
unilateral cavernous sinus mass, 1(10):14, 16 intramedullary lesions
multiple, 11(7):12, 13
renal cell, 11(3):38,40
no enhancement, 11(7):18, 19
squamous cell, 1(1):4
solid enhancement, 11(7):14,16
thyroid, 11(3):38,39
Tl hyperintense, 11(7):34,36
Carcinomatosis, meningeal, 1(4):54, 55-56
Tl hypo intense, 11(7):28,29
Carotid artery
Tl hypointense, T2 hypo intense, 11(7):26,27
dissection/pseudoaneurysm, 11(2):4,9, 11
intramedullary mass, 11(7):3,5
internal, paramedian ("kissing"), 1(8):12, 13, 20,
myelopathy, 11(7):49
21
T2 hyperintense cord lesions, central, 11(7):45,
47
vii
INDEX
)( Cavernous sinuses parertchymallesions
CI.I
"'C bilateral lesions, 1(10):18-21 multiple hyperdense, 1(5):50 , 52
C thrombosis, 1(10):15,17,18-19,20 solitary hyperdense, 1(5):44, 46
unilateral mass, 1(10):14-17 Tl hyperintense, 1(5):102, 104
Cavum septi pellucidi Tl hypointense, T2 hyperintense, 1(5):91, 92
cistern and subarachnoid space normal variants, Tl/T2 hyperintense, 1(5):86, 88
1(4):2 perivascular space enhancing lesions, 1(6):76, 78
foramen of Monro mass, 1(3):18, 19 Cerebral aqueduct
thick septum pellucidum, 1(3):16 lesions, 1(3):28-31
ventricles, normal variant, 1(3):2, 4 stenosis, 1(3):28, 29
Cavum velum interpositum Cerebral atrophy, 1(3):44, II(7):1O
cistern and subarachnoid space normal variants, Cerebral contusion
1(4):2,3 asymmetric cerebral hemispheres, 1(6):2, 4
pineal region mass, 1(8):2, 3 cortical hyperintensity Tl/FLAIR, 1(6):24,25
quadrigeminal cistern mass, 1(8):8 midbrain lesion, 1(6):100, 101
Cellular ependymoma, spinal cord multiple brain hyperintensities (T2/FLAIR),
intramedullary lesions 1(5):65
multiple, II(7):12, 13 parenchymal lesions
no enhancement, II(7):18 multiple hyperdense, 1(5):50, 51
ring/peripheral enhancement, II(7):24, 25 multiple hypodense, 1(5):60, 61
solid enhancement, II(7):14, 15 solitary hyperdense, 1(5):44, 45
Tl hyperintense, II(7):34, 35-36 solitary hypodense, 1(5):56, 57
T2 hyperintense, Tl isointense, II(7):30, 32 Tl hypointense, T2 hyperintense, 1(5):90
Tl hypointense, II(7):28 Cerebral cortex. See also Cortical veins
myelopathy, II(7):48, 50 contusion, 1(4):16, 17
subarachnoid space narrowing, II(6):6 dysplasia
Central spinal cord syndrome focal cortical mass, 1(6):21, 23
myelopathy, II(7):48, 50 microcephaly, 1(1):38, 41
T2 hyperintense cord lesions, central, II(7):45, laminar necrosis, 1(5):103
47 thick, 1(6):8-13
Cephalhematoma, calcified thin, 1(6):14-19
sclerotic skull lesions, solitary, 1(1):26-27, 29 Cerebral edema
thick skull, localized, 1(1):12, 13 diffuse (mimic), 1(4):72, 73
Cephalocele traumatic
atretic, 1(1):4, 1(4):21, 23 asymmetric cerebral hemispheres, 1(6):2, 4
extra-axial fluid collection, CSF-like, 1(4):50 effaced sulci, 1(4):12, 13
lytic skull lesion, solitary, 1(1):19 multiple brain hyperintensities (T2/FLAIR),
Cerebellar tonsils, low, 1(7):32-33 1(5):65
Cerebellitis small ventricles, 1(3):48
cerebellar atrophy, 1(7):19, 21 Cerebral hemispheres, asymmetric, 1(6):2-7
cerebellar mass, 1(7):22-23, 25 Cerebral hyperperfusion syndrome
vermis mass, 1(7):29, 30 cortical enhancement, 1(6):28, 29
Cerebellopontine angle (CPA) effaced sulci, generalized, 1(4):13, 15
cystic mass, 1(4):28-31 Cerebral infarction. See also Cerebral ischemia-
mass in adults, 1(4):24-27 infarction, acute
Cerebellum chronic
atrophy, 1(7):18-21 asymmetric cerebral hemispheres, 1(6):2, 4
hemorrhage, remote, 1(7):23, 27 corpus callosum, abnormal shape or
hereditary atrophy, 1(7):19, 21 configuration, 1(6):47, 49-50
hypoplasia, 1(1):38, 42 irregular large ventricles, 1(3):54, 56
mass, 1(7):22-27 multiple brain hyperintensities (T2/FLAIR),
Cerebral amyloid disease (angiopathy) 1(5):65, 68
confluent white matter lesions, 1(6):34, 36 parenchymal lesions, 1(5):56, 58, 102
multiple brain hyperintensities (T2/FLAIR), small brainstem, 1(7):4
1(5):70, 71 thin cortex, 1(6):14, 17
multiple hypointense foci on GRE/SWI, 1(5):82, hypotensive
84 basal ganglia, 1(6):66, 68, 70
VIII
INDEX
confluent white matter lesions, 1(6):34, 36
cortical enhancement, 1(6):28, 29
extra-axial flow voids, 1(4):60, 61
intraventricular artifact, 1(3):2, 4
-
::s
Q.
cortical hyperintensity Tl/FLAIR, 1(6):24, 26 I'D
third ventricle mass, body/posterior, 1(3):26 ><
effaced sulci, generalized, 1(4):12 shunts and complications
multiple brain hyperintensities (T2/FLAIR), asymmetric lateral ventricles, 1(3):50-51, 53
1(5):65, 68 irregular large ventricles, 1(3):54, 55
putamen lesions, 1(6):84 lytic skull lesion, solitary, 1(1):18
parenchymal lesions, multiple hypodense, small ventricles, 1(3):48
1(5):60, 61 Tl hyperintense, 1(4):62-63
subacute Cervical spine
cortical enhancement, 1(6):28 accelerated degeneration, 11(1):2,4
multiple brain hyperintensities (T2/FLAIR), back pain/radiculopathy, postoperative, 11(1):30,
1(5):64-65, 68 32
parenchymal lesions, multiple hyperdense, bony fusion, 11(3):4-5
1(5):50,53 CI-C2 instability, 11(2):12-13
parenchymal lesions, solitary hypodense, chronic post-traumatic abnormality, 11(1):2-3
1(5):56,58 fracture with nerve compression, 11(1):42,44-45
parenchymal lesions, Tl/T2 hyperintense, incomplete fusion, posterior element
1(5):87, 89 CI-C2 instability mimic, 11(2):12
parenchymal lesions, Tl/T2 isointense, cranio-cervical junction acute injury, 11(2):2
1(5):95,97 post-traumatic bony abnormality, 11(1):4
pial enhancement, 1(2):16, 18 lower subaxial fractures, 11(1):4
ring-enhancing lesions, 1(5):6, 9, 13, 15 stenosis, acquired, 11(7):48,51
Cerebral ischemia-infarction, acute Chance fracture
asymmetric cerebral hemispheres, 1(6):2, 4 flattened vertebral body, solitary, 11(3):6
cerebellar mass, 1(7):22, 23 lumbar
cortical hyperintensity Tl/FLAIR, 1(6):24, 25 bony trauma, 11(1):8,9
effaced sulci, focal, 1(4):16, 17 kyphosis, 11(1):12, 13
FLAIRhyperintense CSF,1(4):65, 67 posterior element fracture, 11(3):34,35
focal cortical mass, 1(6):20, 21 thoracic
hyperattenuating artery, 1(9):8, 9 bony trauma, II(I):6
large brainstem, 1(7):2, 3 kyphoscoliosis, child, II(I):14
midbrain lesion, 1(6):100, 101 kyphosis, 11(1):12
parenchymal lesions, 1(5):56, 57, 94, 95 posterior element fracture, 11(3):34
pontine lesion, 1(7):6, 7 vertebral body fracture, 11(3):28,30
restricted diffusion, 1(5):98, 99 Charcot arthropathy. See Neurogenic arthropathy
Cerebral palsy, 11(1):10 Chemotherapy. See Radiation and chemotherapy
Cerebral venous thrombosis, deep Chest wall abnormalities, II(I):10
effaced sulci, generalized, 1(4):13, 15 Chiari 1 (Chiari-Frommel syndrome)
enlarged deep veins, 1(10):10, 12 cisterna magna mass, 1(4):38, 39
ependymal enhancement, 1(3):40-41 craniovertebral junction abnormalities, 11(2):4,
unilateral thalamic lesion, 1(6):90, 9] 6,9
Cerebritis foramen magnum mass, 1(4):42, 44
cortical enhancement, 1(6):28, 29 low cerebellar tonsils, 1(7):32-33
cortical hyperintensity Tl/FLAIR, 1(6):25 Chiari 2 (Budd-Chiari syndrome)
focal cortical mass, 1(6):20, 22 cisterna magna mass, 1(4):38, 40
multiple brain hyperintensities (T2/FLAIR), craniovertebral junction abnormalities, 11(2):4,
1(5):70, 73 6, 9
parenchymal lesions, 1(5):57, 59, 90, 93 foramen magnum mass, 1(4):42, 44
Cerebrospinal fluid (CSF). See also Flow artifacts, irregular large ventricles, 1(3):54, 56
CSF lacunar skull, 1(1):23, 25
FLAIRhyperintense, 1(4):64-67 prepontine cistern mass, 1(4):32, 34
gadolinium from blood-brain barrier leakage, tectal plate lesion, 1(6):98, 99
1(4):64-65,67 Chondroid tumor, 1(8):40
hyperdense, 1(4):72-73 Chondrosarcoma
obstructed spaces, 1(1):32, 33-34 adult back pain, II(I):52
pulsation craniovertebral junction abnormalities, 1l(Z):4,
9,11
IX
INDEX
enlarged vertebral body, soap bubble expansion, lateral ventricle mass, 1(3):12, 13
11(3):38,41 Choroid plexus papilloma
enlarged vertebral body/posterior element, asymmetric lateral ventricles, 1(3):51, 53
11(3):13, 15 "bubbly-appearing" intraventricular mass,
epidural mass, 11(5):2,6 1(3):37,39
extradural lesions, 11(5):32,37 in children over 1 year, 1(5):113, 115
extradural marrow signal, abnormal, 11(5):26,28 CPA mass, 1(4):25, 27
falx lesions, 1(2):12 foramen of Monro mass, 1(3):19
lower extremity pain, 11(1):48 fourth ventricle mass, 1(3):32, 34
sacral mass, adult, 11(1):19 intraventricular calcifications, 1(3):62, 64
sacrococcygeal mass, pediatric, 11(1):23 large ventricles, 1(3):45, 47
skull base lateral ventricle mass, 1(3):12, 14
foramen magnum masses, 1(4):43 lesion vs., 1(3):6, 7
prepontine cistern mass, 1(4):33, 36 in newborn/infant, 1(5):106, 109
sellar/juxtasellar calcification, 1(8):15 posterior fossa neoplasm, pediatric, 1(7):45
spondylolisthesis, 11(3):20 posterior fossa neoplasms, adult, 1(7):41, 42
Chordoma third ventricle mass, body/posterior, 1(3):26, 27
cavernous sinus mass, unilateral, 1(10):15, 17 third ventricle mass, general, 1(3):22, 25
clivus. See Clivus, chordoma Chronic inflammatory demyelinating
craniovertebral junction soft tissue polyneuropathy (CIDP)
abnormalities, 11(2):9, 11 cauda equina enhancement, diffuse, 11(6):3,5
enlarged vertebral body, soap bubble expansion, cauda equina syndrome, 1l(6):36
11(3):38,41 cranial nerve enhancement, 1(4):47, 49
enlarged vertebral body/posterior element, intradural/extramedullary lesions, 11(6):12, 15,
11(3):13, 15 17
epidural mass, 11(5):2 leptomeningeal enhancement, 11(6):9,11
extradural lesions, 11(5):32,37 Cisterna magna mass, 1(4):38-41. See also Mega
extradural marrow signal, abnormal, 11(5):27,28 cisterna magna
posterior fossa lesion, cystic-appearing, 1(7):35 Clay shoveler's fracture, 11(3):34
sacral deformity, 11(1):27,29 Cleidocranial dysplasia, 1(1):14, 15
sacral mass, adult, 11(1):18, 20 Clinoids, aerated, 1(1):2, 3
sacrococcygeal mass, pediatric, 11(1):22,24 Clivus
sellar/juxtasellar calcification, 1(8):15, 17 chordoma
Choriomeningitis, lymphocytic, 1(5):41, 42 bilateral cavernous sinus lesions, 1(10):19, 20
Choroid plexus craniovertebral junction abnormalities,
enlargement, 1(3):6 1l(2):4
lesions, 1(3):6-7 foramen magnum masses, 1(4):43
lipoma, 1(3):6 prepontine cistern mass, 1(4):33, 36
physiologic calcification, 1(3):62, 63 sellar/juxtasellar calcification, 1(8):15, 17
villous hypertrophy, 1(1):32, 35 nasopharyngeal tumor invading, 1(4):33, 37
xanthogranuloma, 1(5):32 neoplasms, prepontine cistern mass, 1(4):33
Choroid plexus carcinoma, 1(3):6 CMV. See Cytomegalovirus (CMV) infections
asymmetric lateral ventricles, 1(3):51 Coagulopathies, 1(5):83
"bubbly-appearing" intraventricular mass, Coats-Plus syndrome, 1(3):67, 71
1(3):37 Coccidiomycosis, 1l(4):7, 8
in children over 1 year, 1(5):113, 117 Cockayne syndrome, 1(1):39, 43
ependymal/subependymallesions, 1(3):8, 11 Collateral veins, occlusion, 11(6):18, 19
intraventricular calcifications, 1(3):63 Colloid cyst
lateral ventricle mass, 1(3):13 foramen of Monro mass, 1(3):18, 20
in newborn/infant, 1(5):107, 110 third ventricle mass, general, 1(3):22, 24
posterior fossa neoplasm, pediatric, 1(7):45, 49 Compression fractures
Choroid plexus cysts, 1(3):6 anterior
asymmetric lateral ventricles, 1(3):50, 53 lumbar, 11(1):8,12, 11(3):28, 29
"bubbly-appearing" intraventricular mass, thoracic, 11(1):6, 12, 13, 11(3):28
1(3):36,37 vertebral end plate contour abnormality,
foramen of Monro mass, 1(3):19 11(4):10, 11
intraventricular calcifications, 1(3):62, 63 benign, adult back pain, 1l(1):53, 54
x
INDEX
focal vertebral body sclerosis, 11(3):42,43
lateral
normal, 1(10):8
thrombosis =-
Q.
~
lumbar, 11(1):8,14, 11(3):28 enlarged cortical veins, 1(10):8, 9 ><
scoliosis, 11(1):10 multiple hyperdense parenchymal lesions,
thoracic, 11(1):6,14, II(3):28 1(5):50,53
vertebral endplate contour abnormality, solitary hyperdense parenchymal lesions,
11(4):10 1(5):44, 46
wedge, II(4):16, 17 solitary hypodense parenchymal lesion,
Compressive myopathy, chronic, 11(7):10 1(5):57, 59
Connatal cysts solitary white matter lesion, 1(6):31, 33
CSF-like parenchymal lesions, 1(5):23, 25 Corticobasal degeneration, 1(4):9, 11
ventricles, normal variant, 1(3):3, 5 CPPO. See Calcium pyrophosphate deposition
Connective tissue disorders disease (CPPO)
kyphoscoliosis, child, II(I):14 Cranial nerves, enhancement, 1(4):46-49
scoliosis, II(I):lO Cranio-cervical junction, acute injury, 11(2):2-3
Contrast complications Craniopharyngioma
effaced sulci, generalized, 1(4):13 in children over 1 year, 1(5):112, 115
leakage, sulcal/cisternal enhancement, 1(4):55, extra-axial mass(es), hypodense, 1(4):77, 78
57 fat-like lesions, 1(5):32, 33
Tl hyperintense CSF,1(4):62 hypothalamus lesion, 1(8):48, 50
Contrast material, 1(4):72, 73 intrasellar lesion, 1(8):20, 21
Contusion-hematoma, spinal cord intra sellar mass, cystic, 1(8):22, 23
intramedullary lesions intraventricular calcifications, 1(3):63, 65
no enhancement, II(7):18, 19 prepontine cistern mass, 1(4):33, 37
Tl hyperintense, 11(7):34,35 sellar/juxtasellar calcification, 1(8):14, 16
T2 hyperintense, Tl isointense, 11(7):30 suprasellar mass
Tl hypointense, II(7):28 calcified, 1(8):40
Tl hypointense, T2 hypointense, 11(7):26 cystic, 1(8):36, 38
intramedullary mass, 11(7):3,4 enhancing, 1(8):42, 43
myelopathy, II(7):48, 51 general, 1(8):24, 26
T2 hyperintense cord lesions hyperdense, 1(8):52, 53
dorsal, 11(7):40,42 pediatric, 1(8):30, 32
ventral, 11(7):38 Tl hyperintense, 1(8):56
Conus abnormality, 11(7):6-9 Tl hypointense, 1(8):58, 59
Convolutional markings, 1(1):2, 22, 24 third ventricle mass, 1(3):23, 25
Copper deficiency, II(7):40 Craniostenosis, 1(1):27, 29
Corpus callosum Craniovertebral junction, II(2):2-15
abnormal shape or configuration, 1(6):46-51 abnormalities, general, 11(2):4-7
dysgenesis. See Callosal dysgenesis acute injury, 1I(2):2-3
holes in, 1(6):52-53 CI-C2 instability, 11(2):12-13
lesion without mass effect, 1(6):54-55 cranio-cervical junction acute injury, 1I(2):2, 3
masses, 1(6):56-57 odontoid deformity, II(2):14-15
normal variant, 1(6):46, 47 post-traumatic cervical abnormality, chronic,
splenium lesion, 1(6):58-61 11(1):2
thin, 1(6):40-45 soft tissue abnormalities, 11(2):8-11
Cortical contusion, 1(4):16,17 variants
Cortical dysplasia CI-C2 instability, II(2):12, 13
focal congenital vertebral anomalies, 11(3):2
cortical mass, 1(6):21, 23 craniovertebral junction abnormalities,
effaced sulci, focal, 1(4):17 1I(2):4, 6
ependymal/subependymallesions, 1(3):8, 10 odontoid deformity, 11(2):14, 15
epilepsy, 1(5):118, 122 Creutzfeldt-jakob disease
Taylor type, 1(5):118, 122, 1(6):8, 10 basal ganglia
microcephaly, 1(1):38,41 bilateral lesions, 1(6):81, 83
Cortical laminar necrosis, 1(5):103 T2 hyperintense, 1(6):71, 73
Cortical veins bithalamic lesions, 1(6):93, 95
enlarged, 1(10):8-9 cortical hyperintensity Tl/FLAIR, 1(6):25
XI
INDEX
>< enlarged sulci, generalized, 1(4):9, 11 neuroglial
cu
-= large ventricles, 1(3):45 CSF-like parenchymal lesions, 1(5):23, 26
-
c "pulvinar sign," 1(6):96-97
putamen lesions, 1(6):84, 85
restricted diffusion, 1(5):99, 101
cystic-appearing posterior fossa lesion,
1(7):34, 38
solitary cystic mass, 1(5):17, 20-21
Cryptococcosis perineural root sleeve. See Perineural root sleeve
bilateral basal ganglia lesions, 1(6):81 cysts
CSF-like parenchymal lesions, 1(5):23, 26 pineal. See Pineal cyst
enlarged perivascular spaces, 1(6):74, 75 porencephalic. See Porencephalic cyst
intramedullary lesions, Tl hyperintense, Rathke cleft. See Rathke cleft cyst
11(7):35, 37 sebaceous, 1(1):4, 5
Crystalline arthropathies, 11(1):2 synovial. See Synovial cyst
CSF. See Cerebrospinal fluid (CSF) tumor-associated, 1(4):21, 23
Cushing disease Cytomegalovirus (CMV) infections
congenital vertebral anomalies, 11(3):2 congenital
flattened vertebral body, multiple, 11(3):8 asymmetric cerebral hemispheres, 1(6):2, 5
platyspondyly, diffuse, 11(1):16 basal ganglia calcification, 1(6):62, 64
thoracic bony trauma, 11(1):6 irregular large ventricles, 1(3):55, 57
vertebral body fracture, 11(3):28 periventricular calcifications, 1(3):66, 67
vertebral end plate contour abnormality, 11(4):10 polyradiculopathy, 11(6):3, 4
Cyanide poisoning, 1(6):86, 88 radiculopathy, 11(6):15, 17
Cysticercosis
conus abnormality, 11(7):7
intradural/extramedullary lesions o
multiple, 11(6):20, 21 DAI. See Diffuse axonal injury (DAI)
ring/peripheral enhancement, 11(6):22, 25 Dandy-Walker continuum
T2 hyperintense, T1 isointense, 11(6):34, 35 cisterna magna mass, 1(4):38, 40
T1 hypointense, 11(6):29 cystic-appearing posterior fossa lesion, 1(7):34,
intramedullary lesions 36
multiple, 11(7):12, 13 extra-axial fluid collection, CSF-Iike, 1(4):50, 51
ring/peripheral enhancement, 11(7):24, 25 infratentorial midline cyst, 1(7):14, 16
T1 hypointense, T2 hypointense, 11(7):26, 27 macrocephaly, 1(1):32, 35
intramedullary mass, 11(7):3 Degeneration, accelerated. See Accelerated
Cysts degeneration
arachnoid. See Arachnoid cyst Degenerative disc disease
bone. See Bone cyst, aneurysmal chronic back pain/radiculopathy, postoperative,
choroid plexus. See Choroid plexus cysts 11(1):36, 39
colloid endplate irregularity, 11(4):6, 7
foramen of Monro mass, 1(3):18, 20 kyphosis, 11(1):12
third ventricle mass, general, 1(3):22, 24 myelopathy, 11(7):48
connatal spondylolisthesis, 11(3):20, 22
CSF-like parenchymal lesions, 1(5):23, 25 T2 hyperintense disc, 11(4):14-15
ventricles, normal variant, 1(3):3, 5 T1 hypointense disc, 11(4):12
dermoid. See Dermoid cyst Dementia
discal, 11(4):3, 5 Alzheimer. See Alzheimer dementia
enteric, 11(1):23 frontotemporal. See Frontotemporal dementia
ependymal. See Ependymal cyst multi-infarct. See Multi-infarct dementia
epidermal inclusion, 1(1):4 vascular, 1(4):8, 10
epidermoid. See Epidermoid cyst with Lewy bodies, 1(4):8
germinolytic Demyelinating diseases
CSF-like parenchymal lesions, 1(5):23, 27 brain stem, large, 1(7):2, 3
ventricles, normal variant, 1(3):3, 5 conus abnormality, 11(7):6, 8
interhemispheric fissure, 1(4):20-23 deep veins, enlarged, 1(10):11, 13
leptomeningeal hypothalamus lesion, 1(8):49
extra-axial mass, CSF-like, 1(4):52 intramedullary mass, 11(7):2, 3
lytic skull lesion, solitary, 1(1):19, 21 medulla lesion, 1(7):10, 12
neurenteric. See Neurenteric cyst midbrain lesion, 1(6):100, 102
xii
INDEX
parenchymal lesions, T1 hypointense, T2 Devices and complications. See also Metal artifact
hyperintense, 1(5):90 hyperattenuating artery, 1(9):8, 9
pontine lesion, 1(7):6, 8 multiple hypointense foci on GRE/SWI, 1(5):83
subarachnoid space narrowing, 11(6):6 Diabetes mellitus
tumefactive, 1(5):6, 9, 1(7):22 cranial nerve enhancement, 1(4):47
Dermal sinus, dorsal, 11(5):14 vascular calcifications, 1(9):10, 11
Dermatomyositis, 11(5):20 Diastematomyelia
Dermoid cyst congenital vertebral anomalies, 11(3):2, 3
cavernous sinus mass, unilateral, 1(10):15, 17 conus abnormality, 11(7):6
cisterna magna mass, 1(4):39,41 extradural lesions, Il(5):14
cystic mass, solitary, 1(5):17, 20 intramedullary lesions, 11(7):26, 27
extra-axial masses, hypodense, 1(4):77, 79 kyphoscoliosis, child, 11(1):14
foramen magnum mass, 1(4):43, 45 vertebral body fracture, 11(3):28
fourth ventricle mass, 1(3):33 vertebral body scalloping or widened canal,
interhemispheric fissure cysts, 1(4):21, 23 Il(3):18, 19
lytic skull lesion, solitary, 1(1):18-19, 21 Diffuse axonal injury (DAI)
Meckel cave lesion, 1(10):23, 25 cerebral aqueduct/periaqueductallesion, 1(3):28,
midline cyst, infratentorial, 1(7): 15, 17 30
parenchyma, fat-like lesions, 1(5):32, 33 corpus callosum
pineal region mass, 1(8):3, 5 abnormal shape or configuration, 1(6):47, 50
posterior fossa lesion, cystic-appearing, 1(7):34, holes, 1(6):52
37 lesion without mass effect, 1(6):54
quadrigeminal cistern mass, 1(8):8 splenium lesion, 1(6):58, 59
ruptured large ventricles, 1(3):45
fat in sulci/cisterns/ventricles, 1(4):58, 59 midbrain lesion, 1(6):100, 101
FLAIR hyperintense CSF, 1(4):65 multiple brain hyperintensities (T2/FLAIR),
Tl hyperintense CSF, 1(4):62, 63 1(5):65, 68
Tl hyperintense parenchymal lesions, multiple hypointense foci on GRE/SWI, 1(5):82,
1(5):102 84
scalp, 1(1):4, 5, 16 parenchymal lesions
sellar/juxtasellar calcification, 1(8): 15, 17 multiple hyperdense, 1(5):50, 51
suprasellar mass multiple hypodense, 1(5):60, 62
calcified, 1(8):40, 41 Tl hypo intense, T2 hyperintense, 1(5):90
cystic, 1(8):36, 38 periventricular T2/FLAIR lesions, 1(3):72, 74
general, 1(8):25, 27 restricted diffusion, 1(5):98, 100
pediatric, 1(8):31 Dilantin, chronic use
Tl hyperintense, 1(8):56, 57 cerebellar atrophy, 1(7):18, 20
vermis mass, 1(7):29, 31 thick skull, generalized, 1(1):8, 10
Dermoid tumor Disc herniation. See Intervertebral disc herniation
intradural/extramedullary lesions, Il(6):12, 26, Discal cyst, 11(4):3, 5
27 Discitis, chronic, Il(3):44, 45
myelopathy, Il(7):49 Discogenic sclerosis, Il(3):44
sacrococcygeal mass, pediatric, 11(1):23, 24 DISH. See Skeletal hyperostosis, diffuse idiopathic
spinal cord, intramedullary lesions, 11(7):34, 37 (DISH)
vertebral body scalloping or widened canal, Dissection, arterial. See Arterial dissection
11(3):18 Distraction fracture, low thoracic, 11(1):6, Il(3):28,
Developmental venous anomaly. See also 30
Arteriovenous malformation DNET (dysembryoplastic neuroepithelial tumor)
enlarged cortical veins, 1(10):8 in children over 1 year, 1(5):112, 115
enlarged deep veins, 1(10):10, 11 cortical hyperintensity Tl/FLAIR, 1(6):25, 27
ependymal enhancement, 1(3):40, 41 cyst with nodule, 1(5):29, 31
ependymal/subependymal lesions, 1(3):8, 10 effaced sulci, focal, 1(4):16, 18
extra-axial flow voids, 1(4):60, 61 epilepsy, 1(5):119, 123
parenchymal lesions focal cortical mass, 1(6):21, 23
solitary hyperdense, 1(5):44-45, 47 solitary cystic mass, 1(5):17, 19
Tl/T2 isointense, 1(5):94, 96 solitary parenchymal calcification, 1(5):35, 39
thick cortex, 1(6):9, 12
thin skull, localized, 1(1):16, 17
XIII
INDEX
>< Dolichoectasia solitary, 1(2):4-7
ClJ
"'C arterial shape/configuration abnormalities, Dural calcifications, 1(2):2-3
-C 1(9):2, 3
fusiform arterial enlargement, 1(9):6
falx lesions, 1(2):12
physiologic, 1(2):2, 1(4):68
vertebrobasilar sellar/juxtasellar calcification, 1(8):14, 15
foramen magnum mass, 1(4):42, 43 Dural dysplasia
prepontine cistern mass, 1(4):32, 33 enlarged neural foramen, 11(3):16, 17
Down syndrome, 11(2):14, 15 pedicle abnormality, 11(3):36
Drug abuse sacral deformity, 11(1):26,27
basal ganglia vertebral body scalloping or widened canal,
bilateral lesions, 1(6):80, 83 11(3):18
T2 hyperintense, 1(6):70, 72 Dural sinuses
epilepsy, 1(5):118 arachnoid granulations, 1(4):77, 79, 1(10):2, 3-4
globus pallidus lesions, 1(6):86, 88 hyperdensity, 1(10):26-29
large ventricles, 1(3):45, 47 hypoplasia-aplasia, 1(10):2, 5
parenchymal lesions, solitary hyperdense, lesions, general, 1(10):2-7
1(5):45, 48 thrombosis
periventricular T2/FLAIR lesions, 1(3):73, 75 chronic, Meckel cave lesion, 1(10):23, 25
white matter lesions, confluent, 1(6):35 dural sinus lesion, 1(10):2, 5
Drug toxicity effaced sulci, generalized, 1(4):12-13, 15
corpus callosum splenium lesion, 1(6):58 enlarged cortical veins, 1(10):8, 9
midbrain lesion, 1(6):101 enlarged deep veins, 1(10):10, 12
multiple brain hyperintensities (T2/FLAIR), extra-axial flow voids, 1(4):60
1(5):71, 75 hyperdense extra-axial mass, 1(4):74
Dural arteriovenous fistula hyperdensity, 1(10):26, 28
brain solitary hyperdense parenchymal lesions,
intradural lesion, serpentine, 11(6):18, 19 1(5):44, 46
intramedullary lesions, 11(7):20,22 venous stenosis
cerebellar mass, 1(7):23, 26 dural sinus lesion, 1(10):3, 7
dural sinus lesion, 1(10):2, 6 enlarged deep veins, 1(10):11
enlarged cortical veins, 1(10):8, 9 Dural tail sign, 1(2):20-21
enlarged deep veins, 1(10):10-11, 12 Dural thickening, postoperative, 1(2):14
ependymal enhancement, 1(3):41, 43 Dwarfism, primordial, 1(1):14. See also
extra-axial flow voids, 1(4):60, 61 Thanatophoric dwarfism
extra-axial lesions, 1(4):69 Dyke-Davidoff-Masson syndrome
extra-axial mass, hyperdense, 1(4):74 asymmetric cerebral hemispheres, 1(6):2, 5
falx lesions, 1(2):12, 13 asymmetric lateral ventricles, 1(3):51
intrasellar lesion, 1(8):20 thick skull, localized, 1(1):12, 13
pial enhancement, 1(2):17 Dysembryoplastic neuroepithelial tumor. See DNET
pituitary gland enlargement, 1(8):18 (dysembryoplastic neuroepithelial tumor)
spinal, type 1 Dysembryoplastic neuroepithelioma, 1(4):16, 18
intradural/extramedullary lesions, multiple, Dysraphism, dorsal, 11(1):26-27, 11(7):7
11(6):20, 21
intramedullary lesion, solid enhancement,
11(7):15, 17 E
intramedullary lesions, diffuse/ill-defined Ecchordosis physaliphora
enhancement, 11(7):20,22 posterior fossa neoplasms, adult, 1(7):41, 43
intramedullary lesions, T2 hyperintense, Tl prepontine cistern mass, 1(4):33, 37
isointense, 11(7):30-31, 32 Echinococcus
myelopathy, 11(7):48, 53 abnormal extradural marrow signal, 11(5):27
T2 hyperintense cord lesions, central, intradural/extramedullary lesions, 11(6):23,25,
11(7):44,46 34
traumatic, acute upper extremity pain or Edema, scalp, 1(1):4
weakness, 11(1):42,45 Ehlers-Danlos IV, 1(9):6
vermis mass, 1(7):28, 30 Ehlers-Danlos syndrome, 11(1):16
Dural-based masses Embolism, septic
multiple, 1(2):8-11 multiple brain hyperintensities (T2/FLAIR),
1(5):71, 73
xiv
INDEX
multiple hypointense foci on GRE/SWI, 1(5):83 Encephalomalacia
Embolus, calcified asymmetric lateral ventricles, 1(3):50, 52
plaque, 1(9):10, 11 cerebellar atrophy, 1(7):18, 19-20
solitary parenchymal calcification, 1(5):35, 38 CSF-like parenchymal lesions, 1(5):22,23
Emissary veins, 1(1):2, 22, 23 large ventricles, 1(3):44
Empty sella multiple brain hyperintensities (T2/FLAIR),
cystic intrasellar mass, 1(8):22 1(5):64, 66
intrasellar lesion, 1(8):20 post-inflammatory, 1(6):2, 4
normal sella variant, 1(8):12, 13 post-ischemic, 1(5):90, 1(6):2, 3
Empyema post-traumatic, 1(5):90, 1(6):2, 4
epidural, 1(4):5, 6 solitary cystic mass, 1(5):16, 18
extra-axial thin corpus callosum, 1(6):40, 42
CSF-like fluid collection, 1(4):50, 51 thin cortex, 1(6):14, 18
effaced sulci, focal, 1(4):17 Encephalomyelitis, acute disseminating. See ADEM
falx lesions, 1(2):12, 13 (acute disseminating encephalomyelitis)
hypodense extra-axial masses, 1(4):77, 79 Encephalopathy. See also Leukoencephalopathy;
restricted diffusion, 1(5):98, 100 MELAS
scoliosis, 11(1):10 acute necrotizing, of childhood, 1(6):93
solitary dural-based mass, 1(2):4 alcoholic. See Alcoholic encephalopathy
Encephalitis. See also Herpes encephalitis Hashimoto, 1(5):76, 78
asymmetric cerebral hemispheres, 1(6):3, 5 hepatic
basal ganglia, 1(6):67, 71, 73 chronic, enlarged sulci, 1(4):9
cerebral aqueduct/periaqueductal lesion, globus pallidus lesions, 1(6):86, 88
1(3):28-29, 30 T1 hyperintense basal ganglia, 1(6):66, 68
corpus callosum splenium lesion, 1(6):58, 60 hypertensive. See Hypertensive encephalopathy
effaced sulci, generalized, 1(4):12, 14 hypoxic-ischemic. See Hypoxic-ischemic
enlarged deep veins, 1(10):11 encephalopathy (HIE)
enlarged sulci, generalized, 1(4):8 toxic/metabolic, 1(4):12, 13
HIV-related, 1(4):9, 10, 1(6):34, 37 Wernicke. See Wernicke encephalopathy
Japanese, 1(6):67 Enchondroma, 11(3):39
large brainstem, 1(7):2 Endocrine disorders, 1(6):62, 67
midbrain lesion, 1(6):100 Endolymphatic sac anomaly, 1(4):29, 31
multiple brain hyperintensities (T2/FLAIR), Enteric cyst, 11(1):23
1(5):70, 73 Ependymal cyst
panencephalitis, subacute sclerosing, 1(5):77, 79, asymmetric lateral ventricles, 1(3):51, 53
1(6):35 "bubbly-appearing" intraventricular mass,
parenchymal lesions 1(3):37
multiple hypodense, 1(5):60, 62 cystic-appearing posterior fossa lesion, 1(7):35,
solitary hypodense, 1(5):57 38
T1 hyperintense, 1(5):103, 105 foramen of Monro mass, 1(3):19, 21
T1 hypointense, T2 hyperintense, 1(5):90, 93 fourth ventricle mass, 1(3):33, 35
pontine lesion, brainstem, 1(7):7 lateral ventricle mass, 1(3):12-13, 15
Rasmussen, 1(5):77, 79 suprasellar cystic mass, 1(8):37, 39
restricted diffusion, 1(5):99, 100 third ventricle mass, body/posterior, 1(3):26
small ventricles, 1(3):48, 49 Ependymal enhancement, 1(3):40-43
thick cortex, 1(6):8, 9 Ependymal/subependymallesions, 1(3):8-11
tick-borne, 11(6):2,5 Ependymal/subependymal veins (mimic), 1(3):59
viral Ependymal veins, enlarged, 1(10):10-13
bilateral basal ganglia lesions, 1(6):81 Ependymoma
bithalamic lesions, 1(6):93 "bubbly-appearing" intraventricular mass,
focal cortical mass, 1(6):21 1(3):36,38
medulla lesion, 1(7):11 cellular, spinal cord. See Cellular ependymoma,
West Nile, 1(5):76, 78 spinal cord
white matter lesions in children over 1 year, 1(5):112, 114
confluent, 1(6):35, 37 cisterna magna mass, 1(4):38, 40
solitary, 1(6):30-31, 33 CPA mass, 1(4):25, 27
Encephalocele, 1(7):34, 36 ependymal/subependymallesions, 1(3):8
xv
INDEX
><
QJ
foramen magnum mass, 1(4):42, 44 intramedullary lesion, ring/peripheral
"'C fourth ventricle mass, 1(3):32, 33 enhancement, II(7):24, 25
C intradural/extramedullary lesions, II(6):34 intradural/extramedullary lesions
intraventricular calcifications, 1(3):62, 64 no enhancement, II(6):12
lateral ventricle mass, 1(3):13, 15 T1 hyperintense, II(6):26, 27
myxopapillary. See Myxopapillary ependymoma T2 hyperintense, T1 isointense, II(6):34, 35
pedicle abnormality, II(3):36, 37 T1 hypointense, II(6):28, 30
periventricular enhancing lesions, 1(3):58, 61 myelopathy, II(7):49
posterior fossa neoplasm, pediatric, 1(7):44, 46 sacrococcygeal mass, pediatric, II(1):23, 24
solitary parenchymal calcification, 1(5):35, spinal cord, II(7):34, 37
37-38 vertebral body scalloping or widened canal,
spinal cord, II(7):2, 3-4 II(3):18
supratentorial Epidural abscess
in newborn/infant, 1(5):106, 108 back pain/radiculopathy, postoperative, II(1):30,
solitary cystic mass, 1(5):17, 21 33
solitary hyperdense parenchymal lesions, disc contour abnormality, II(4):3, 5
1(5):45, 47 extradural lesions
vertebral body scalloping or widened canal, multiple, II(5):12, 13
II(3):18, 19 T2 hyperintense, T1 isointense, II(5):36, 38
Epidermal inclusion cyst, 1(1):4 T1 hypointense, II(5):32-33, 34
Epidermal nevus syndrome, 1(6):3, 7 myelopathy, II(7):48, 49
Epidermoid cyst normal extradural marrow signal, II(5):22, 24
cavernous sinus mass, unilateral, 1(10):15, 17 paravertebral
cisterna magna mass, 1(4):39, 41 cauda equina syndrome, II(6):36, 37
CPA-lAC, 1(4):24, 26, 28, 29 craniovertebral junction abnormalities,
extra-axial fluid collection, CSF-like (mimic), II(2):4, 7
1(4):50 lower extremity pain, II(1):49, 51
extra-axial mass subarachnoid space narrowing, II(6):6, 7
CSF-like, 1(4):52, 53 upper extremity pain or weakness, acute,
hypodense, 1(4):77, 79 II(1):43, 46
foramen magnum mass, 1(4):43, 45 Epidural fat, normal, II(5):30
fourth ventricle mass, 1(3):32, 35 Epidural gas, II(5):32, 40
infratentorial midline cyst, 1(7):14-15, 16 Epidural hematoma
interhemispheric fissure cysts, 1(4):21, 23 acute, T1 hypointense extradural lesion,
intrasellar mass, cystic, 1(8):22, 23 II(5):32, 34
intraventricular mass, "bubbly-appearing," back pain/radiculopathy, postoperative, II(1):30,
1(3):36, 39 34
lateral ventricle mass, 1(3):13 dural-based masses, 1(2):4, 5, 9, 11
lytic skull lesion, solitary, 1(1):18, 20 effaced sulci, focal, 1(4):16
Meckel cave lesion, 1(10):23, 25 epidural mass, brain, 1(4):4, 5
pineal region mass, 1(8):3, 5 extra-axial lesions, T2 hypointense, 1(4):68
posterior fossa lesion, cystic-appearing, 1(7):34, extra-axial masses, 1(4):74, 77, 79
37 extradural lesions, multiple, II(5):12, 13
prepontine cistern mass, 1(4):32, 34 lower extremity pain, II(1):49, 51
quadrigeminal cistern mass, 1(8):8, 9 spontaneous, II(5):22, 24
restricted diffusion, 1(5):98, 100 Epidural mass, spine, II(5):2-7
of scalp, 1(1): 16 Epidural-subdural hematoma
solitary cystic mass, 1(5):17, 20 cauda equina syndrome, II(6):36
suprasellar mass disc contour abnormality, II(4):3
cystic, 1(8):37, 38 extradural lesions
general, 1(8):25, 28 no enhancement, II(5):14
T1 hypointense, 1(8):58, 59 T1 hyperintense, II(5):30-31
"white," 1(5):32 T2 hyperintense, T1 isointense, II(5):36, 39
Epidermoid tumor myelopathy, II(7):48, 51
acquired normal extradural marrow signal, II(5):22
intradural/extramedullary lesions, no subarachnoid space narrowing, I1(6):6, 7
enhancement, II(6):12, 13
XVI
INDEX
Epilepsy, 1(5):118-123. See also Status epilepticus Extradural area, spine, II(5):2-45
Erdheim-Chester disease epidural mass, II(5):2-7
bilateral cavernous sinus lesions, 1(10):19 extradural lesions
dural-based masses, multiple, 1(2):8-9, 11 multiple, Il(5):12-13
dural tail sign, 1(2):20 no enhancement, II(5):14-15
falx lesions, 1(2):12 solid enhancement, II(5):16-19
Ewing sarcoma Tl hyperintense, 1I(5):30-31
back pain, pediatric, Il(1):57 T2 hyperintense, Tl isointense, II(5):36-39
epidural mass, Il(5):2, 7 Tl hypointense, II(5):32-35
extradural lesions T2 hypointense, Tl hypointense, 11(5):40-41
solid enhancement, II(5):16, 19 lumbar soft tissue mass, pediatric, II(5):42-45
T2 hyperintense, Tl isointense, II(5):37 marrow signal
Tl hypointense, II(5):32 abnormal, II(5):26-29
extradural marrow signal, abnormal, II(5):27, 29 normal, II(5):22-25
kyphoscoliosis, child, Il(1):14 paraspinal mass, ventral/lateral, 11(5):8-9
lumbar soft tissue mass, pediatric, Il(5):42, 44 paraspinal muscle abnormalities, II(5):10-11
sacral mass, adult, II(1):19, 21 soft tissue calcification, paraspinal, II(5):20-21
sacrococcygeal mass, pediatric, II(1):23, 24 Extrinsic mass effect, 1(3):50, 51
vertebral body
dysmorphic, 1I(3):10
flattened, solitary, 1I(3):6 F
fracture, II(3):28 Fabry disease, 1(5):102, 1(6):96, 97
Extra-axial flow voids, 1(4):60-61 Facet
Extra-axial lesions, T2 hypointense, 1(4):68-71 lamina fracture, thoracic, 11(1):6,7, 1I(3):34
Extra-axial masses posterior fracture, lumbar, 11(1):8,II(3):34, 35
CSF-like, 1(4):52-53 tropism, II(3):32
hyperdense, 1(4):74-75 Facet arthropathy
hypodense, 1(4):76-79 adult back pain, II(1):52, 53
Extra-axial spaces and subarachnoid cisterns, cervical
1(4):2-79 bony abnormality, post-traumatic, II(1):4
cerebellopontine angle (CPA) enlarged vertebral body/posterior element,
cystic mass, 1(4):28-31 1I(3):12, 13
mass, adult, 1(4):24-27 normal extradural marrow signal, 1I(5):22, 24
cerebrospinal fluid epidural mass, II(5):2, 3
FLAIRhyperintense, 1(4):64-67 extradural lesions, multiple, II(5):12
hyperdense, 1(4):72-73 lumbar
Tl hyperintense, 1(4):62-63 enlarged vertebral body/posterior element,
cisterna magna mass, 1(4):38-41 11(3):12,13
cranial nerve enhancement, 1(4):46-49 normal extradural marrow signal, Il(5):22, 24
epidural mass, brain, 1(4):4-7 Fahr disease
extra-axial flow voids, 1(4):60-61 basal ganglia
extra-axial fluid collection, CSF-like, 1(4):50-51 calcification, 1(6):62, 64
extra-axial lesions, T2 hypointense, 1(4):68-71 Tl hyperintense, 1(6):67, 69
extra-axial masses bithalamic lesions, 1(6):93
CSF-like, 1(4):52-53 globus palIidus lesions, 1(6):87
hyperdense, 1(4):74-75 parenchymal calcifications, multiple, 1(5):41, 43
hypodense, 1(4):76-79 parenchymal lesions, 1(5):87, 102
fat in sulci/cisterns/ventricles, 1(4):58-59 Failed back surgery syndrome
foramen magnum mass, 1(4):42-45 chronic back pain/radiculopathy, postoperative,
interhemispheric fissure cysts, 1(4):20-23 II(1):36, 37
normal variants, 1(4):2-3 kyphosis, 1I(1):12, 13
prepontine cistern mass, 1(4):32-37 scoliosis, 1I(1):1O
sulcal/cisternal enhancement, 1(4):54-57 Failure of vertebral formation
sulci, effaced cervical bony fusion, II(3):4
focal,I(4):16-19 congenital
generalized,I(4):12-15 kyphosis, II(1):10, 12
sulci, enlarged, generalized, 1(4):8-11 scoliosis, II(1):10
XVII
INDEX
>< vertebral anomalies, 11(3):2 vertebral body, 11(1):8,11(3):28
"'C
aJ kyphoscoliosis, child, 11(1):14 Friedrich ataxia, 1(7):4, II(1):10
- C vertebral body
flattened, solitary, 11(3):6,7
Frontometaphyseal dysplasia, 1(1):12
Frontotemporal dementia
fracture, 11(3):28 asymmetric cerebral hemispheres, 1(6):2, 5
Falx enlarged sulci, generalized, 1(4):8, 10
lesions, 1(2):12-13 large ventricles, 1(3):45
ossified, 1(5):32, 33 thin cortex, 1(6):15, 18
Familial tumoral calcinosis, 1(2):2 Fungal diseases
Femoral neuropathy, 11(1):48 intervertebral disc endplate irregularity, Il(4):7,
Fetal alcohol syndrome, 1(1):38, 41, 11(1):10 8
Fibro-osseous lesion, 1(2):4 multiple hypointense foci on GRE/SWl, 1(5):83,
Fibrodysplasia ossificans progressiva, 11(5):20 85
Fibrolipoma. See Filum terminale fibrolipoma multiple hypointense foci on T2, 1(5):80, 81
Fibromatosis, aggressive, 1(1):19 parenchymal lesions, Tl hyperintense, 1(5):102
Fibrosarcoma, soft tissue, 11(5):8,10 prepontine cistern mass, 1(4):33, 36
Fibrothorax, 11(1):10 ring-enhancing lesions, 1(5):7, 11, 13, 15
Fibrous dysplasia sulcal/cisternal enhancement, 1(4):55, 57
bony trabeculae, thickened, 11(3):46,47 suprasellar mass, hyperdense, 1(8):52
lytic skull lesion, solitary, 1(1):18, 21 Fusiform aneurysm
macrocephaly, 1(1):33, 37 atherosclerotic
pedicle abnormality, 11(3):36 arterial shape/configuration abnormalities,
sclerotic skull lesions, 1(1):26 , 28, 30, 31 1(9):2-3,4
scoliosis, 11(1):10 fusiform arterial enlargement, 1(9):6, 7
thick skull, 1(1):8, 10, 12, 13 vascular calcifications, 1(9):10, 11
vertebral body extra-axial flow voids, 1(4):60, 61
diffuse Tl hypointense signal, 11(3):53, 55 hyperattenuating artery, 1(9):8
enlarged, soap bubble expansion, 11(3):38-39, nonatherosclerotic
41 arterial shape/configuration abnormalities,
vertebral body/posterior element, enlarged, 1(9):3,4-5
11(3):13 fusiform arterial enlargement, 1(9):6, 7
Filum terminale fibrolipoma prepontine cistern mass, 1(4):32, 34
conus abnormality, 11(7):6,7 suprasellar mass
intradural/extramedullary lesions, 11(6):12,26 calcified, 1(8):40, 41
Fissure cysts, interhemispheric, 1(4):20-23 hyperdense, 1(8):52
Flow artifacts, CSF Fusiform arterial enlargement, 1(9):6-7
foramen of Monro mass, 1(3):18, 19
intradural/extramedullary lesions
multiple, 11(6):20 G
no enhancement, II(6):12 Gadolinium
Tl hypointense, II(6):28 blood-brain barrier leakage, FLAIRhyperintense
Tl hypointense, T2 hypointense, 11(6):32 CSF,1(4):64-65, 67
intradural lesion, serpentine, 11(6):18 focal T1 hyperintense signal, vertebral body,
intramedullary lesions, T1 hypointense, Il(7):28 II(3):50, 51
prepontine cistern mass, 1(4):32, 33 Gangliocytoma, dysplastic cerebellar
Flow voids, extra-axial, 1(4):60-61 cerebellar mass, 1(7):23, 27
Fluorosis, 1(1):9, 11(3):44 in children over 1 year, 1(5):113
Foramen magnum mass, 1(4):42-45 cortical hyperintensity Tl/FLAIR, 1(6):25, 27
Foramen of Monro mass, 1(3):18-21 posterior fossa
Foramina, asymmetric, 1(1):2, 3 adult, 1(7):41,43
Foreign bodies, scalp mass, 1(1):4 pediatric, 1(7):45, 49
Fracture-dislocation, Il(1):8 thick cortex, 1(6):9, 13
Fracture mimics vermis mass, 1(7):29, 31
cranio-cervical junction acute injury, II(2):2 Ganglioglioma
posterior elements, Il(1):4, 8 cerebellar mass, 1(7):23, 27
in children over 1 year, 1(5):112, 115
cyst with nodule, 1(5):28, 30
xviii
INDEX
cystic mass, solitary, 1(5):17, 19 in children over 1 year, 1(5):112, 115 ::s
foramen of Monro mass, 1(3):18, 20 Q.
desmoplastic infantile I'D
cyst with nodule, 1(5):29 intraventricular calcifications, 1(3):62, 65 ><
focal cortical mass, 1(6):21, 23 lateral ventricle mass, 1(3):12, 14
in newborn/infant, 1(5):106-107, 109 in newborn/infant, 1(5):106, 109
solitary cystic mass, 1(5):17, 21 Giant cell tumor
epilepsy, 1(5):119, 123 epidural mass, 11(5):2,7
focal cortical mass, 1(6):21, 23 extradural lesions, II(5):32, 37
hypothalamus lesion, 1(8):49 extradural marrow signal, abnormal, 11(5):27,29
infratentorial midline cyst, 1(7):15, 17 sacral mass, adult, II(1):18, 20
intramedullary lesion, solid enhancement, vertebral body, 11(3):6,38, 40
11(7):15,17 Giant serpentine aneurysm, 1(9):6
intramedullary mass, 11(7):3,5 Glioblastoma multiforme
parenchymal calcification, solitary, 1(5):34, 37 cerebellar mass, 1(7):23, 27
parenchymal lesion, solitary hyperdense, in children over 1 year, 1(5):113, 116
1(5):45, 48 corpus callosum, 1(6):46, 49, 56
posterior fossa, pediatric, 1(7):44, 47 cyst with nodule, 1(5):28, 30
thick cortex, 1(6):9, 12 cystic mass, solitary, 1(5):16, 18
thin skull, localized, 1(1):16, 17 enlarged deep veins, 1(10):11, 13
vermis mass, 1(7):29, 31 ependymal/subependymallesions, 1(3):8, 10
Ganglioma macrocephaly, 1(1):32, 35
effaced sulci, focal, 1(4):16, 18 midbrain lesion, 1(6):100
ring-enhancing lesion, solitary, 1(5):7, 11 multifocal, 1(5):13, 15
Ganglioneuroma, 11(5):8 multiple brain hyperintensities (T2/FLAIR),
Gaucher disease, 11(1):16,17,11(4):7 1(5):71,74
Germ cell neoplasms multiple enhancing lesions, 1(5):3, 5
cavernous sinus lesions, bilateral, 1(10):19,21 in newborn/infant, 1(5):107, 110
pineal + suprasellar lesions, 1(8):10, 11 parenchymal lesions
pineal gland mass, 1(8):6, 7 multiple hyperdense, 1(5):51, 54
Germinal matrix hemorrhage, 1(3):67, 70 multiple hypodense, 1(5):61
Germinolytic cysts solitary hyperdense, 1(5):44, 46
CSF-like parenchymal lesions, 1(5):23, 27 solitary hypodense, 1(5):56, 58
ventricles, normal variant, 1(3):3, 5 T1 hypointense, T2 hyperintense, 1(5):90
Germinoma perivascular space enhancing lesions, 1(6):76, 78
in children over 1 year, 1(5):112, 115 periventricular enhancing lesions, ](3):58, 60
ependymal/subependymallesions, 1(3):8 pial enhancement, 1(2):16, 18
foramen of Monro mass, 1(3):19, 21 posterior fossa neoplasms, adult, 1(7):41
hypothalamus lesion, 1(8):48, 50 ring-enhancing lesion, solitary, ](5):6, 8
parenchymal lesions, solitary hyperdense, spinal cord, 11(7):3
1(5):45, 48 thalamic lesion, unilateral, 1(6):90
periventricular enhancing lesions, 1(3):58, 60 thick cortex, 1(6):9, 13
pineal + suprasellar lesions, 1(8):10 vermis mass, 1(7):29, 31
pineal gland mass, 1(8):6, 7 white matter lesions
pineal region mass, 1(8):3, 5 confluent, 1(6):34, 36
suprasellar mass solitary, 1(6):30, 32
enhancing, 1(8):42, 43 Glioma
general, 1(8):25,27 brainstem, pediatric. See Brainstem glioma,
hyperdense, 1(8):52, 53 pediatric
pediatric, 1(8):30, 32 chordoid
T1 isointense, 1(8):54 hyperdense suprasellar mass, 1(8):52
thalamic lesion, unilateral, 1(6):90 hypothalamus lesion, ](8):49, 51
thick infundibular stalk, 1(8):46 sellar/juxtasellar calcification, ](8):15, 16
thick septum pellucidum, 1(3):16,17 third ventricle mass, genera], 1(3):23, 25
third ventricle mass exophytic, II(6):29
body/posterior, 1(3):26, 27 exophytic cervicomedullary, 1(7):10, 12
general, 1(3):22, 24 malignant, 1(6):28
Giant cell astrocytoma, subependymal, 1(3):8, 10 multifoca], 1(5):80, 81
XIX
INDEX
:l( optic nerve, 1(4):46, 48 cauda equina enhancement, diffuse, 11(6):2-3, 4
Q,j
"'CI optic pathway, in children over 1 year, 1(5):112, intradural/extramedullary lesions, solid
- C 114
tecta I
enhancement, 11(6):14, 16
leptomeningeal enhancement, 11(6):8, 9
cerebral aqueduct/periaqueductal lesion, pediatric back pain, 11(1):56, 58
1(3):28,29 Gyral simplification, 1(1):38, 41
midbrain lesion, 1(6):100, 103
pineal region mass, 1(8):2, 4
third ventricle mass, 1(3):23, 25 H
Gliomatosis cerebri "Hair on end," 1(1):6-7
asymmetric cerebral hemispheres, 1(6):3, 7 Hallervorden-Spatz syndrome
basal ganglia, T2 hyperintense, 1(6):71 basal ganglia calcification, 1(6):63, 65
bithalamic lesions, 1(6):92, 94 globus pallidus lesions, 1(6):87, 89
cerebral aqueduct/periaqueductallesion, 1(3):29, T1 hyperintense basal ganglia, 1(6):67, 69
31 Hangman's C2 fracture
in children over 1 year, 1(5):113 cranio-cervical junction acute injury, 11(2):2, 3
corpus callosum mass, 1(6):56, 57 craniovertebral junction abnormalities, 11(2):5
multiple brain hyperintensities (T2/FLAIR), kyphosis, 11(1):12
1(5):71,74 posterior element fracture, 11(3):34
parenchymal lesions, 1(5):90 Hardware failure
thick cortex, 1(6):9, 13 acute back pain/radiculopathy, postoperative,
white matter lesions, 1(6):31, 34, 39 11(1):31, 34
Glioneuronal tumor of fourth ventricle, rosette- chronic back pain/radiculopathy, postoperative,
forming, 1(3):33, 1(7):40 11(1):37,40
Gliosarcoma, 1(4):5, 7 kyphosis, 11(1):12
Gliosis, 1(5):64, 66 Hardware malposition, 11(4):3, 5
Globus pallidus lesions, 1(6):86-89 Hashimoto encephalopathy, 1(5):76, 78
Glutaric aciduria type 1 Heart disease, congenital, 1(1):6
macrocephaly, 1(1):33, 36 Hemangioblastoma
T2 hyperintense basal ganglia, 1(6):71, 73 cerebellar mass, 1(7):22, 24
Gout cisterna magna mass, 1(4):39, 41
chronic post-traumatic cervical abnormality, CPA cystic mass, 1(4):28, 30
11(1):2 cyst with nodule, 1(5):28, 30
intervertebral disc endplate irregularity, 11(4):7 cystic-appearing posterior fossa lesion, 1(7):35,
vertebral endplate signal abnormality, 11(4):16, 38
17 foramen magnum mass, 1(4):43, 45
Granulocyte colony-stimulation factor, 1(1):6 fourth ventricle mass, 1(3):32, 35
Granuloma, cholesterol, petrous apex, 1(5):32, 33 infratentorial midline cyst, 1(7):14, 16
Granulomatosis, lymphomatoid, 1(5):80 large brainstem, 1(7):2
Granulomatous angiitis medulla lesion, 1(7):10, 13
enlarged deep veins, 1(10):11, 13 posterior fossa
multiple brain hyperintensities (T2/FLAIR), adult, 1(7):40, 42
1(5):76, 78 pediatric, 1(7):45, 48
perivascular space enhancing lesions, 1(6):76, 79 solitary cystic mass, 1(5):17, 20
Granulomatous disease, 11(6):20, 21 vermis mass, 1(7):28, 30
Gray matter Hemangioblastoma, spinal cord
heterotopic conus abnormality, 11(7):6, 8
ependymal/subependymallesions, 1(3):8, 10 craniovertebral junction abnormalities, 11(2):4, 9
epilepsy, 1(5):118, 120 intradural/extramedullary lesions, multiple,
irregular large ventricles, 1(3):54, 56 11(6):20, 21
subcortical laminar, 1(6):15, 19 intradural lesion, serpentine, 11(6):18
Tl/T2 isointense parenchymal lesions, intramedullary lesions
1(5):95, 97 multiple, 11(7):12, 13
inborn errors of metabolism, 1(6):15, 19 solid enhancement, 11(7):14, 16
Grisel syndrome, 1I(2):4, 12 T2 hyperintense, T1 isointense, 11(7):31, 32
Guillain-Barre syndrome T1 hypointense, 11(7):28
atypical, 11(6):36 intramedullary mass, 11(7):3, 4
xx
INDEX
myelopathy, 1I(7):48, SO dural sinus, hyperdense (mimic), 1(10):27 ::::J
Hemangioendothelioma, 1(10):3 dural sinus lesion, 1(10):3 Q.
t'll
Hemangioma epidural mass ><
aggressive, 11(3):12, 14 brain, 1(4):5, 7
atypical, 11(3):56,57 spine, 11(5):3,7
calvarial, 1(2):20 extra-axial lesions, T2 hypointense, 1(4):69, 71
capillary, 1I(6):34 extra-axial mass, hyperdense, 1(4):74, 75
cavernous sinus mass, unilateral, 1(10):15 extradural lesions
dural sinus, hyperdense, 1(10):27 multiple, 11(5):12, 13
dural sinus lesion, 1(10):3, 7 solid enhancement, 11(5):17, 19
epidural, 11(5):3,6, 12 T1 hypointense, 1I(5):33, 35
extradural lesions, solid enhancement, extradural marrow signal, abnormal, 1I(5):27
1I(5):16--17,19 falx lesions, 1(2):12, 13
extradural marrow signal, abnormal, 11(5):26 paraspinal mass, ventral/lateral, 11(5):8,9
extraosseous, 1I(5):30, 31, 33, 35 thick dura or arachnoid, generalized, 1(2):14
lAC mass, 1(4):25 thick skull, generalized, 1(1):9, 11
Masson, 1(10):27 vertebral body, diffuse T1 hypointense signal,
multiple lucent skull lesions, 1(1):23, 25 11(3):53
scalp mass, 1(1):4 Hemimegalencephaly
skull asymmetric lateral ventricles, 1(3):51
"hair on end," 1(1):6, 7 epilepsy, 1(5):119, 123
lytic lesion, solitary, 1(1):18, 21 irregular large ventricles, 1(3):55, 57
sclerotic lesion, solitary, 1(1):27, 29 macrocephaly, 1(1):32
soft tissue, 1I(5):10 sporadic or familial, 1(6):3, 6
thickened bony trabeculae, 1I(3):46 thick cortex, 1(6):8-9, 11
vertebral body of tuberous sclerosis, 1(6):3, 6
diffuse T1 hyperintense signal, 11(3):48,49 Hemiparesis/hemiplegia, 1I(1):10
flattened, solitary, 11(3):6 Hemodialysis
focal sclerosis, 11(3):42 arthropathy, 11(1):2
focal T1 hyperintense signal, 11(3):50 dural calcification, 1(2):2
vertebral endplate signal abnormality, 1I(4):16 spondyloarthropathy
Hemangiopericytoma intervertebral disc end plate irregularity,
epidural mass, brain, 1(4):5, 7 11(4):7,9
extra-axial lesions, T2 hypointense, 1(4):69 vertebral endplate signal abnormality,
extra-axial mass, hyperdense, 1(4):74 1I(4):16, 17
extradural lesions, solid enhancement, 11(5):17, Hemolytic uremic syndrome, 1(6):70
19 Hemorrhage
extradural marrow signal, abnormal, 11(5):27, 29 cerebellar, remote, 1(7):23, 27
falx lesions, 1(2):12, 13 germinal matrix, 1(3):67, 70
lumbar soft tissue mass, pediatric, 1I(5):43, 45 intracranial. See Intracranial hemorrhage
posterior fossa neoplasms, adult, 1(7):40, 43 intraventricular. See Intraventricular
Hematoma. See also Contusion-hematoma, spinal hemorrhage
cord retroperitoneal, 11(5):8
epidural mass, 11(5):2,4. See also Epidural subacute (mimic), 1(4):58
hematoma subarachnoid. See Subarachnoid hemorrhage
epidural-subdural. See Epidural-subdural vertebral bone marrow, 11(3):50, 51
hematoma Hepatic encephalopathy
intracerebral. See Intracerebral hematoma chronic, enlarged sulci, 1(4):9
paraspinal, 11(5):22 globus pallidus lesions, 1(6):86, 88
retroperitoneal, 11(1):48 T1 hyperintense basal ganglia, 1(6):66, 68
subdural. See Subdural hematoma Hereditary spastic paraplegia with thin corpus
subgaleal, 1(1):4 callosum, 1(6):41
Hematopoiesis, extramedullary Herniation. See also Intervertebral disc herniation;
cavernous sinus lesions, bilateral, 1(10):19 Spinal cord herniation
dural-based masses intracranial syndromes
multiple, 1(2):8, 10 asymmetric lateral ventricles, 1(3):50, 52
solitary, 1(2):5, 7 cisterna magna mass, 1(4):38, 39
xxi
INDEX
>< low cerebellar tonsils, 1(7):32, 33 infratentorial midline cyst, 1(7):14, 16
Q,/
""Cl small ventricles, 1(3):48, 49 intrasellar mass, cystic, 1(8):22, 23
C tonsillar, 1(4):42, 43 large ventricles, 1(3):44, 45
transtentorial, ascending, 1(8):8, 9 periventricular T2/FLAIR lesions, 1(3):73, 75
Herpes encephalitis pineal region mass, 1(8):3, 5
congenital, 1(3):66, 68 posterior fossa lesion, cystic-appearing,
cortical enhancement, 1(6):28 1(7):34, 37
cortical hyperintensity Tl/FLAIR, 1(6):24, 26 suprasellar cystic mass, 1(8):36, 37
multiple brain hyperintensities (T2/FLAIR), thin cortex, 1(6):14,16-17
1(5):70, 73 thin skull, generalized, 1(1):14
parenchymal lesions, 1(5):91, 103 severe, longstanding communicating, Il(3):18
thick cortex, 1(6):8, 9 shunted, 1(1):8, 10
Herpes zoster, 1(4):47 suprasellar mass, pediatric, 1(8):30
Herpetic neuritis, trigeminal, 1(10):23, 25 Hydrosyringomyelia, 11(3):18
HIE. See Hypoxic-ischemic encephalopathy (HIE) Hygroma, subdural, 1(4):50
Hippocampal sulcus remnants, 1(5):22-23, 25 Hyperalimentation, 1(6):66, 68, 86
Histiocytoma, malignant fibrous, 11(5):10 Hyperattenuating artery, 1(9):8-9
Histiocytosis, 1(2):20, 1(8):46, 47 Hyperextension injury, cervical
HIV infections. See also Opportunistic infections, post-traumatic bony abnormality, 11(1):4,5
AIDS posterior element fracture, 11(3):34
congenital vertebral body fracture, 11(3):28,30
basal ganglia calcification, 1(6):62, 64 Hyperextension-rotation injury, cervical, Il(I):4
periventricular calcifications, 1(3):66, 69 Hyperflexion injury, cervical
Tl hyperintense basal ganglia, 1(6):67, 69 acute upper extremity pain or weakness,
diffuse Tl hypointense signal, vertebral body, 11(1):42,44
11(3):52,54 CI-C2 instability, 11(2):12
encephalitis kyphosis, 11(1):12
confluent white matter lesions, 1(6):34, 37 post-traumatic bony abnormality, 11(1):4
enlarged sulci, generalized, 1(4):9, 10 posterior element fracture, Il(3):34
T2 hyperintense cord lesions, dorsal, 11(7):40, vertebral body fracture, 11(3):28,30
42-43 Hyperflexion-rotation injury, cervical
Holoprosencephaly (HPE) acute upper extremity pain or weakness, 11(1):42
corpus callosum post-traumatic bony abnormality, 11(1):4,5
abnormal shape or configuration, 1(6):47, 51 posterior element fracture, Il(3):34
thin, 1(6):41, 45 Hyperostosis, meningioma-associated, 1(1):26, 28
dorsal cyst, 1(4):52, 53 Hyperostosis frontalis interna
infundibular stalk, absent/thin, 1(8):44 normal variants, skull, 1(1):2, 3
interhemispheric fissure cysts, 1(4):21, 23 thick skull, 1(1):8, 9, 12
irregular large ventricles, 1(3):55, 57 Hyperparathyroidism
variants, 1(6):47, 51 basal ganglia, 1(6):62, 67
Huntington disease dural calcification, 1(2):2, 3
bilateral basal ganglia lesions, 1(6):81 lucent skull lesions, multiple, 1(1):22-23, 25
enlarged sulci, generalized, 1(4):8, 11 parenchymal calcifications, multiple, 1(5):41
large ventricles, 1(3):45, 47 sclerotic skull lesions, multiple, 1(1):30, 31
putamen lesions, 1(6):84, 85 thick skull, 1(1):8-9, 11
T2 hyperintense basal ganglia, 1(6):71 thin skull, 1(1):14, 15
Hydranencephaly, 1(1):33, 36 vascular calcifications, 1(9):10
Hydration status, volume loss secondary to, 1(4):9 Hypertension, chronic, 1(5):82, 83
Hydrocephalus Hypertensive encephalopathy
macrocephaly, 1(1):32, 33-34 acute
normal pressure, 1(3):45 basal ganglia, T2 hyperintense, 1(6):71, 73
obstructive bithalamic lesions, 1(6):92, 95
asymmetric lateral ventricles, 1(3):50, 52 corpus callosum splenium lesion, 1(6):59
corpus callosum, abnormal shape or cortical enhancement, 1(6):28, 29
configuration, 1(6):47, 50 cortical hyperintensity Tl/FLAIR, 1(6):24, 26
corpus callosum, thin, 1(6):40-41, 44 effaced sulci, generalized, 1(4):13, 15
corpus callosum holes, 1(6):52, 53 multiple brain hyperintensities (T2/FLAIR),
effaced sulci, generalized, 1(4):12, 14 1(5):64,68
XXII
INDEX
parenchymal lesions, multiple hyperdense, bithalamic lesions, 1(6):92
1(5):50-51, 53 corpus callosum splenium lesion, 1(6):58, 60
parenchymal lesions, multiple hypodense, cortical hyperintensity Tl/FLAIR, 1(6):25
1(5):61, 63 effaced sulci, generalized, 1(4):12
parenchymal lesions, Tl hyperintense, enlarged sulci, generalized, 1(4):8
1(5):103 globus pallidus lesions, 1(6):86, 87
pontine lesion, 1(7):6 microcephaly, 1(1):38, 39
restricted diffusion, 1(5):99, 101 parenchymal lesions, Tl hyperintense, 1(5):103,
chronic 105
confluent white matter lesions, 1(6):34, 36 putamen lesions, 1(6):84
large ventricles, 1(3):44 small ventricles, 1(3):48, 49
multiple brain hyperintensities (T2/FLAIR), term neonate
1(5):64,67 abnormal shape or configuration of corpus
parenchymal lesions, Tl hypointense, T2 callosum, 1(6):47
hyperintense, 1(5):90, 92 bithalamic lesions, 1(6):92, 94
Hypertrophic neuropathy globus pallidus lesions, 1(6):86, 87
intradural/extramedullary lesions putamen lesions, 1(6):84, 85
no enhancement, 11(6):12, 13 Tl hyperintense basal ganglia, 1(6):66, 68
ring/peripheral enhancement, 11(6):23,25 T2 hyperintense basal ganglia, 1(6):70, 71
solid enhancement, 11(6):15 Hypoxic-ischemic injury, NOS, 1(6):62, 64
leptomeningeal enhancement, 11(6):9
Hypertrophic pachymeningitis, 1(2):12, 14, 15
Hypervitaminosis A or D, 11(3):44 I
Hypoglycemia Iatrogenic conditions, 1(10):15
basal ganglia, Tl hyperintense, 1(6):67 Inborn errors of metabolism
corpus callosum splenium lesion, 1(6):59 acute presentation, 1(3):48, 49
cortical enhancement, 1(6):28 bithalamic lesions, 1(6):93
cortical hyperintensity Tl/FLAIR, 1(6):25, 27 end-stage, 1(3):45
restricted diffusion, 1(5):99 gray matter disorders, 1(6):15, 19
Hypomelanosis of Ito, 1(6):74, 75 macrocephaly, 1(1):33
Hypomyelination "Incidentaloma," pituitary, 1(8):12
corpus callosum, abnormal shape or Infant. See a/so Prematurity; specific disorders, in
configuration, 1(6):46 newborn/infant
corpus callosum, thin, 1(6):41, 44 normal kyphosis, 11(1):14
microcephaly, 1(1):38-39, 42 normal skull, 1(1):14
thick cortex, 1(6):8, 10 small ventricles, normal, 1(3):48
white matter lesions, confluent, 1(6):34, 38 Infections
Hypoparathyroidism, 1(6):62, 67 bacterial, 1(5):80, 81, 11(7):20,21
Hypoperfusion injury, 1(6):92, 94 bilateral basal ganglia lesions, 1(6):81, 83
Hypophosphatasia, 1(1):14, 15 CMY. See Cytomegalovirus (CMV) infections
Hypophysitis, lymphocytic. See Lymphocytic congenital, 1(6):62
hypophysitis focal or multifocal, 1(7):6, 9
Hypoplastic pedicle, 11(3):16 HIY. See HIV infections; Opportunistic
Hypothalamic/pituitary axis metastasis, 1(8):48 infections, AIDS
Hypothyroidism intervertebral disc space. See Intervertebral disc
basal ganglia calcification, 1(6):62, 64 space infections
cerebellar atrophy, 1(7):19, 20 medulla lesion, 1(7):11, 13
globus pallidus lesions, 1(6):87, 89 midbrain lesion, 1(6):101
multiple parenchymal calcifications, 1(5):41, 43 Nocardia, 1(5):80, 81
Tl hyperintense basal ganglia, 1(6):67, 69 parenchymal, 1(5):60
white matter lesions, confluent, 1(6):34, 39 postoperative. See Postoperative complications,
Hypoxic-ischemic encephalopathy (HIE) infection
asymmetric cerebral hemispheres, 1(6):2-3, 5 TORCH. See TORCH infections
basal ganglia Infiltrative disorders, 1(7):7, 9, 11
bilateral lesions, 1(6):80, 82 Infratentorial brain parenchyma, 1(7):2-49
Tl hyperintense, 1(6):66, 68 brainstem
T2 hyperintense, 1(6):70, 71 large, 1(7):2-3
XXIII
INDEX
>< small, 1(7):4-5 vertebral body, focal Tl hypointense signal,
CIJ
"'t:l cerebellum II(3):56, 57
C atrophy, 1(7):18-21 disc contour abnormality, II(4):2-5
mass, 1(7):22-27 irregularity, II(4):6-9
low cerebellar tonsils, 1(7):32-33 Intervertebral disc herniation
medulla lesion, 1(7):10-13 back pain/radiculopathy
midline cyst, 1(7):14-17 adult, II(I):52, 53
pontine lesion, 1(7):6-9 pediatric, II(I):57
posterior fossa postoperative, acute, II(I):30, 32
adult neoplasms, 1(7):40-43 cervical
cystic-appearing lesion, 1(7):34-39 acute upper extremity pain or weakness,
pediatric neoplasms, 1(7):44-49 II(I):42, 43-44
vermis mass, 1(7):28-31 myelopathy, II(7):48, 52
Instrumen ta tion/implants normal extradural marrow signal, II(5):22, 23
intervertebral disc, II(4):12, 13 compression, II(6):3, 5
intramedullary lesions, II(7):26 epidural mass, II(5):2, 3
Insufficiency fracture extradural lesions
pedicle, II(I):8, II(3):42, 43 T2 hyperintense, Tl isointense, II(5):36, 37
sacral, II(I):26, 28, 53, 55 Tl hypo intense, II(5):32, 33
Interhemispheric fissure cysts, 1(4):20-23 T2 hypointense, Tl hypo intense, II(5):40
Interior vena cava occlusion, II(6):18, 19 lower extremity pain, II(I):48, 49
Intervertebral disc, II(4):2-17 lumbar, II(5):22, II(6):36
anular tear multiple extradural lesions, II(5):12
adult back pain, 11(1):52,54 recurrent
T2 hyperintense disc, II(4):14, 15 disc contour abnormality, II(4):2, 4
bulge postoperative back pain/radiculopathy,
adult back pain, II(I):52 II(I):30, 31, 36, 38
disc contour abnormality, II(4):2, 3 thoracic, II(5):22, 11(7):48
lower extremity pain, II(I):48, 49 traumatic
normal extradural marrow signal, II(5):22 acute upper extremity pain or weakness,
endplate. See Intervertebral disc end plate II(I):42, 44
extrusion cranio-cervical junction acute injury, II(2):2
disc contour abnormality, II(4):2, 4 myelopathy, 11(7):48,52
foraminal, 11(1):30,32, II(5):22, 23 Intervertebral disc space infections
free fragment, II(4):2 pyogenic, 1I(4):6-7, 8
herniation. See Intervertebral disc herniation T2 hyperintense disc, 1I(4):14, 15
instability, post-traumatic, II(4):12 tuberculous, II(4):7, 8
normal variant, II(4):14 Intracerebral hematoma
protrusion, II(4):2 hyperacute, 1(5):94, 95
pseudobulge, II(4):2, 3 parenchymal lesions
sequestered fragment, II(5):14, 15 solitary hypodense, 1(5):57, 59
T2 hyperintense, II(4):14-15 Tl hyperintense, 1(5):102, 104
Tl hypointense, II(4):12-13 Tl/T2 hyperintense, 1(5):86, 87
vertebral end plate resolving, 1(5):17,19,57,59
contour abnormality, II(4):10-11 restricted diffusion, 1(5):98
signal abnormality, II(4):16-17 subacute
Intervertebral disc endplate late, parenchymal lesions, 1(5):102, 104
degenerative changes ring-enhancing lesions, 1(5):6, 8, 13
aggressive bony lesion, II(3):24, 26 Intracranial hemorrhage
endplate contour abnormality, II(4):1O hypertensive
endplate irregularity, II(4):6, 7 cerebellar mass, 1(7):22, 23
extradural lesions, no enhancement, II(5):14, corpus callosum, abnormal shape or
15 configuration, 1(6):47, 51
signal abnormality, II(4):16 large brainstem, 1(7):2
vertebral body, focal sclerosis, II(3):42, 43 parenchymal lesions, 1(5):44, 45, 50, 52
vertebral body, focal Tl hyperintense signal, pontine lesion, 1(7):6, 8
11(3):50,51 putamen lesions, 1(6):84
xxiv
INDEX
thalamic lesion, unilateral, 1(6):90, 91 intraventricular calcification (mimic), 1(3):62
spontaneous, 1(4):16, 18 large ventricles, 1(3):44
Intracranial hypertension, idiopathic, 1(4):13, 15, lateral ventricle mass, 1(3):12, 13
1(8):22 macrocephaly, 1(1):32, 34
Intracranial hypotension T1 hyperintense CSF,1(4):62, 63
cisterna magna mass, 1(4):39, 41 Intraventricular mass, "bubbly-appearing,"
dural sinus lesion, 1(10):3, 7 1(3):36-39
enlarged deep veins, 1(10):11, 13 Intraventricular synechiae or adhesions, 1(3):51, 53
extra-axial fluid collection, CSF-like, 1(4):50, 51 Intraventricular webs or adhesions, 1(3):54-55
falx lesions, 1(2):12 Iron deficiency anemia, 1(1):6, 9
foramen magnum mass, 1(4):43 Ischemia. See also Cerebral ischemia-infarction,
idiopathic, 1(3):48, 49 acute
intrasellar lesion, 1(8):20 arterial, bithalamic lesions, 1(6):92, 93
large brainstem, 1(7):2, 3 cranial nerve enhancement, 1(4):47
low cerebellar tonsils, 1(7):32, 33 venous, 1(6):81, 92, 94
midbrain lesion, 1(6):101
pineal region mass, 1(8):3, 5
pituitary gland enlargement, 1(8):18, 19 J
prepontine cistern mass, 1(4):33, 35 Japanese encephalitis, 1(6):67
secondary, 1(3):48 Jefferson Cl fracture
small ventricles, 1(3):48, 49 CI-C2 instability, 11(2):12
thick dura or arachnoid, generalized, 1(2):14, 15 cranio-cervical junction acute injury, 11(2):2,3
Intradural-extramedullary area, spine, 11(6):2-37 craniovertebral junction abnormalities, 11(2):4
cauda equina enhancement, diffuse, 11(6):2-5 posterior element fracture, 11(3):34
intradural/extramedullary lesions Juvenile idiopathic arthritis
multiple, 11(6):20-21 cervical abnormality, chronic post-traumatic,
no enhancement, 11(6):12-13 11(1):2,3
ring/peripheral enhancement, 11(6):22-25 cervical bony fusion, 11(3):4-5
solid enhancement, 11(6):14-17 congenital vertebral anomalies, 11(3):2,3
T1 hyperintense, 11(6):26-27 craniovertebral junction abnormalities, 11(2):4,6
T2 hyperintense, T1 isointense, 11(6):34-35 dysmorphic vertebral body, 11(3):10, 11
T1 hypointense, 11(6):28-31 kyphoscoliosis, child, 11(1):14, 15
T1 hypointense, T2 hypointense, 11(6):32-33 kyphosis, 1l(1):12
intradural lesion, serpentine, 11(6):18-19 odontoid deformity, 1l(2):14, 15
leptomeningeal enhancement, 11(6):8-11 post-traumatic lower cervical bony abnormality,
subarachnoid space narrowing, 11(6):6-7 1l(1):4
Intramedullary area, spine, 11(7):2-53 soft tissue calcification, paraspinal, 11(5):20, 21
conus abnormality, 11(7):6-9 vertebral body scalloping or widened canal,
intramedullary mass, 11(7):2-5 1l(3):18, 19
lesions Juxtasellar region. See Pineal region
diffuse/ill-defined enhancement, 11(7):20-23
no enhancement, 11(7):18-19
ring/peripheral enhancement, 11(7):24-25 K
solid enhancement, 1l(7):14-17 Kaposi sarcoma, 1(1):4
T1 hyperintense, 11(7):34-37 Kernicterus
T2 hyperintense, T1 isointense, 1l(7):30-33 bithalamic lesions, 1(6):93
T1 hypointense, 11(7):28-29 globus pallidus lesions, 1(6):86-87, 89
T1 hypointense, T2 hypointense, 11(7):26-27 multiple brain hyperintensities (T2/FLAIR),
myelopathy, 11(7):48-53 1(5):77, 79
small/atrophic spinal cord, 1l(7):10-11 T1 hyperintense basal ganglia, 1(6):66, 69
Intrathecal gas, postoperative, 11(6):28 T1 hyperintense parenchymal lesions, 1(5):102
Intraventricular calcifications, 1(3):62-65 Klippel-Feil spectrum
Intraventricular hemorrhage cervical abnormality, chronic post-traumatic,
asymmetric lateral ventricles, 1(3):50, 52 11(1):2
cerebral aqueduct/periaqueductallesion, 1(3):29, cervical bony fusion, 11(3):4
31 dysmorphic vertebral body, 1l(3):10
FLAIRhyperintense CSF, 1(4):64, 66 kyphoscoliosis, child, 1l(1):14
xxv
INDEX
>< kyphosis, congenital, 11(1):10, 12 thin skull, generalized, 1(1):14, 15
CI.I
"'C lower cervical bony abnormality, post- Lambdoid defects, 1(1):23
C traumatic, 11(1):4,5 Laminar necrosis, cortical, 1(5):103
odontoid deformity, 11(2):14, 15 Langerhans cell histiocytosis (LCH)
scoliosis, congenital, 11(1):10 aggressive bony lesion, 11(3):24,27
vertebral anomalies, congenital, 11(3):2 back pain, pediatric, 11(1):57
Krabbe disease, 1(6):93,95 choroid plexus lesions, 1(3):6, 7
Ktimmel disease cranial nerve enhancement, 1(4):47
dysmorphic vertebral body, 11(3):10 dural-based masses, 1(2):5, 8, 10
flattened vertebral body, solitary, 11(3):6 ependymal enhancement, 1(3):41, 43
focal T1 hypointense signal, vertebral body, ependymal/subependymallesions, 1(3):9
11(3):56 epidural mass, brain, 1(4):5, 7
lumbar bony trauma, 11(1):8 extradural lesions, 11(5):17, 19
T1 hypointense intervertebral disc, 11(4):12, 13 flattened vertebral body, solitary, 11(3):6,7
thoracic bony trauma, 11(1):6 hypothalamus lesion, 1(8):48, 50
vertebral body fracture, 11(3):29, 31 kyphoscoliosis, child, 11(1):14
Kyphoplasty, 11(3):42 lateral ventricle mass, 1(3):13
Kyphoscoliosis, child, 11(1):14-15 medulla lesion, 1(7):11
congenital, 11(1):14-15 perivascular space enhancing lesions, 1(6):77, 79
traumatic, 11(1):14 pituitary gland enlargement, 1(8):18, 19
tumors, 11(1):14, 15 pontine lesion, 1(7):7
Kyphosis, 11(1):12-13 scalp mass, 1(1):4, 5
chronic post-traumatic cervical abnormality, skull base, 1(10):19, 21
11(1):2,3 skull lesions
congenital lytic, solitary, 1(1):18, 20
congenital vertebral anomalies, 11(3):2 multiple lucent, 1(1):22, 25
kyphoscoliosis, child, 11(1):14 suprasellar mass
lumbar bony trauma, 11(1):8 enhancing, 1(8):42, 43
myelopathy, 11(7):48 general, 1(8):25, 27
scoliosis, 11(1):10, 11 pediatric, 1(8):31, 33
thoracic bony trauma, 11(1):6,7 T1 isointense, 1(8):54
vertebral body fracture, 11(3):28,31 third ventricle mass, general, 1(3):23
idiopathic, 11(1):12 thoracic bony trauma, 11(1):6
kyphoscoliosis, child, 11(1):14 Lateral flexion injury, cervical
thoracic bony trauma, 11(1):6,7 acute upper extremity pain or weakness,
vertebral body fracture, 11(3):29,31 11(1):42,44--45
myelopathy, 11(7):48 kyphoscoliosis, child, 11(1):14
normal in infants, 11(1):14 post-traumatic bony abnormality, 11(1):4
post-traumatic lower cervical bony abnormality, posterior element fracture, 11(3):34
11(1):4 scoliosis, 11(1):10
postural, I1(1):12 Lateral ventricles, asymmetric, 1(3):2, 3
LCH. See Langerhans cell histiocytosis (LCH)
Leigh syndrome
L basal ganglia
Lacunar infarction bilateral lesions, 1(6):80
bilateral basal ganglia lesions, 1(6):80, 81 calcification, 1(6):63, 65
corpus callosum holes, 1(6):52, 53 T2 hyperintense, 1(6):71, 73
multiple brain hyperintensities (T2/FLAIR), cerebral aqueduct/periaqueductallesion, 1(3):29,
1(5):64,67 31
parenchymal lesions globus pallidus lesions, 1(6):86, 88
CSF-like, 1(5):22, 24 multiple brain hyperintensities (T2/FLAIR),
T1 hypointense, T2 hyperintense, 1(5):90 1(5):70, 72
solitary white matter lesion, 1(6):30, 31 putamen lesions, 1(6):84,85
subacute, 1(5):7 Leptomeningeal cyst, 1(1):19, 21, 1(4):52
thalamic lesion, unilateral, 1(6):90 Leukemia
Lacunar skull back pain
Chiari 2, 1(1):23, 25 adult, 11(1):52
pediatric, 11(1):56, 59
xxvi
INDEX
cavernous sinus lesions, bilateral, 1(10):19, 21 degenerated hypertrophic, Il(5):32, 33-34
in children over 1 year, 1(5):113, 117 hypertrophy, Il(5):2, 4, 12
cranial nerve enhancement, 1(4):47 ossification
dural-based masses, 1(2):5, 7, 9, 11 extradural lesions, II(5):14, 40, 41
dural sinus, hyperdense, 1(10):27, 29 myelopathy, Il(7):48
dural sinus lesions, 1(10):3, 7 normal extradural marrow signal, Il(5):23, 25
dural tail sign, 1(2):20, 21 Liliequist membrane, 1(4):2
epidural masses, 1(4):5, 7, Il(5):3 Limb length inequality, Il(I):10
extra-axial lesion, T2 hypointense, 1(4):69, 71 Limbus vertebra
extra-axial mass, hyperdense, 1(4):74, 75 disc contour abnormality, Il(4):3, 5
extradural lesion, Tl hypointense, 11(5):33,35 dysmorphic vertebral body, II(3):10
"hair on end," 1(1):6, 7 extradural lesions, no enhancement, 1I(5):14
hypothalamus lesion, 1(8):49 lumbar bony trauma, II(I):8, 9
intradural/extramedullary lesions, 1I(6):14, 16 thoracic bony trauma, II(I):6
leptomeningeal enhancemert, II(6):8, 11 vertebral anomalies, congenital, 1I(3):2, 3
multiple hypointense foci on GRE/5WI, 1(5):83 vertebral body, focal Tl hypointense signal,
parenchymal lesions II(3):56
multiple hyperdense, 1(5):51, 55 vertebral body fracture, II(3):29
solitary hyperdense, 1(5):45, 49 vertebral endplate contour abnormality, II(4):10
Tl hyperintense, 1(5):102 Lipoidal contrast (mimic), 1(4):58
periventricular enhancing lesions, 1(3):59 Lipoma
pituitary gland enlargement, 1(8):18 choroid plexus, 1(3):6
skull lesions, multiple lucent, 1(1):23 corpus callosum, abnormal shape or
sulcal/cisternal enhancement, 1(4):55 configuration, 1(6):46, 49
suprasellar mass corpus callosum mass, [(6):56, 57
enhancing, 1(8):42 CPA-lAC mass, 1(4):25, 27
general, 1(8):25, 29 dural sinus lesion, 1(10):3
pediatric, 1(8):31 extra-axial masses, hypodense, 1(4):76, 78
thick infundibular stalk, 1(8):46 fat in sulCi/cisterns/ventricles, [(4):58
vertebral body fourth ventricle mass, 1(3):33
diffuse Tl hypointense signal, 1I(3):52, 54 hypothalamus lesion, 1(8):48
flattened, Il(3):6, 8 intradural/extramedullary lesions, II(6):26, 27
Leukodystrophy intramedullary lesions, Il(7):34-35, 37
inherited, 1(5):90 Meckel cave lesion, 1(10):23
metachromatic parenchymal lesions, 1(5):32, 87
confluent white matter lesions, 1(6):34, 37 pineal region mass, 1(8):3, 4
corpus callosum lesion without mass effect, quadrigeminal cistern mass, 1(8):8, 9
1(6):54, 55 scalp mass, 1(1):4
intradural/extramedullary lesions, II(6):15 soft tissue, paraspinal muscle abnormalities,
periventricular T2IFLAIRlesions, 1(3):73 1I(5):1O
Leukoencephalopathy. See also Progressive spinal
multifocalleukoencephalopathy (PML) extradural lesions, no enhancement, Il(5):14
acute hemorrhagic, [(5):51, 55 intramedullary mass, Il(7):3
megalencephaly, 1(1):33, 36 lumbar soft tissue mass, pediatric, Il(5):42, 44
Van der Knaap, [(6):34, 38 suprasellar mass
Leukomalacia, periventricular general, 1(8):25, 27
corpus callosum pediatric, 1(8):31, 34
abnormal shape or configuration, 1(6):46, 49 Tl hyperintense, 1(8):56
lesion without mass effect, 1(6):54, 55 tectal plate lesion, 1(6):98, 99
irregular large ventricles, [(3):54, 56 terminal
multiple brain hyperintensities (T2/FLA[R), conus abnormality, 1I(7):7, 9
1(5):65, 69 TI hyperintense extradural lesion, Il(5):30,
periventricular T2/FLAIRlesions, 1(3):72, 74 31
"pulvinar sign," 1(6):96, 97 vertebral body scalloping or widened canal,
Ligament abnormalities, congenital, 1I(2):5 1I(3):18
Ligamentous hypertrophy, II(5):23 Lipomatosis
Ligamentum flavum encephalocraniocutaneous
XXVII
INDEX
>< asymmetric cerebral hemispheres, 1(6):3, 7 multiple enhancing lesions, 1(5):3
Q,j
"C fat in sulci/cisterns/ventricles, 1(4):58, 59 parenchymal lesions, multiple hypodense,
-C fat-like lesions, 1(5):32
fourth ventricle mass, 1(3):33, 35
1(5):61
periventricular enhancing lesions, 1(3):58, 61
epidural periventricular T2/FLAIR lesions, 1(3):72, 75
epidural mass, 11(5):2,4 pial enhancement, 1(2):17, 19
extradural lesion, 11(5):14, 15,30 ring-enhancing lesions, multiple, 1(5):13, 15
normal extradural marrow signal, 11(5):23,25 Lymphadenopathies, 11(5):8
Lipomyelomeningocele/lipomyelocele Lymphatic malformation, 11(5):43,45
conus abnormality, 11(7):7,9 Lymphocele, retroperitoneal, 11(5):8
extradural lesion, 11(5):30,31 Lymphocytic hypophysitis
intradural/extramedullary lesion, 11(6):26,27 dural tail sign, 1(2):20, 21
lumbar soft tissue mass, pediatric, 11(5):42,43 hypothalamus lesion, 1(8):48, 50
sacral deformity, 11(1):26-27, 29 intrasellar lesion, 1(8):20, 21
vertebral anomalies, congenital, 11(3):2 pituitary gland enlargement, 1(8):18,19
Liponeurocytoma, cerebellar, 1(7):40 suprasella r mass
Liposarcoma, soft tissue, 11(5):8 enhancing, 1(8):42, 43
Lissencephaly type 1 general, 1(8):25, 28
epilepsy, 1(5):119 pediatric, 1(8):31, 35
thick cortex, 1(6):9, 12 T1 isointense, 1(8):54, 55
Lithium intoxication, 1(7):18 thick infundibular stalk, 1(8):46, 47
Longitudinal ligament ossification Lymphoma. See also Lymphoma, primary CNS
anterior, 11(1):2,3 aggressive bony lesion, 11(3):24,26
posterior cauda equina enhancement, diffuse, 11(6):3,4
cervical abnormality, chronic post-traumatic, cranial nerve enhancement, 1(4):47, 49
11(1):2,3 dural sinus lesion, 1(10):3, 6
cervical bony fusion, 11(3):4,5 epidural
craniovertebral junction abnormalities, brain mass, 1(4):4, 6
11(2):4 disc contour abnormality, 11(4):2
disc contour abnormality, 11(4):3,4 spinal mass, 11(5):3,6
epidural mass, 11(5):3,5 extradural lesions
extradural lesions, multiple, 11(5):12,13 solid enhancement, 11(5):16,18
extradural lesions, no enhancement, 11(5):14 T2 hyperintense, Tl isointense, 11(5):37
extradural lesions, T1 hypo intense, 11(5):33, T1 hypointense, 11(5):33, 35
35 extradural marrow signal, 11(5):23,26, 28
extradural lesions, T2 hypointense, Tl extramedullary, 11(2):4,8, 10
hypointense, 11(5):40 facet abnormality, non-traumatic, 11(3):32,33
myelopathy, 11(7):48,51 hypothalamus lesion, 1(8):49, 50
normal extradural marrow signal, 11(5):23 intradural/extramedullary lesions, 11(6):14,16
subarachnoid space narrowing, 11(6):6,7 intramedullary lesion or mass, 11(7):3,15
with fatty marrow, 11(5):30,31 intravascular (angiocentric)
Longus coli. See Calcific tendinitis, longus coli confluent white matter lesions, 1(6):34, 39
Lower extremity pain, 11(1):48-51 enlarged deep veins, 1(10):11, 13
Lumbar spine multiple brain hyperintensities (T2/FLAIR),
acute back pain/radiculopathy, postoperative, 1(5):76-77, 79
11(1):30,32 multiple enhancing lesions, 1(5):3, 5
bony trauma, 11(1):8-9 multiple hypodense parenchymal lesions,
lateral compression fracture, 11(1):10 1(5):61
soft tissue mass, pediatric, 11(5):42-45 perivascular space enhancing lesions, 1(6):76,
Lung abnormalities, 11(1):10 78
Lung carcinoma, 11(3):38,39 leptomeningeal enhancement, 11(6):8,10
Lyme disease lumbar soft tissue mass, pediatric, 11(5):42,44
corpus callosum lesion without mass effect, metastatic, intracranial
1(6):54 cavernous sinus lesions, bilateral, 1(10):18, 20
cranial nerve enhancement, 1(4):47, 49 cavernous sinus mass, unilateral, 1(10):14, 16
multiple brain hyperintensities (T2/FLAIR), dural-based mass, 1(2):4, 6, 8, 10
1(5):76, 78 dural tail sign, 1(2):20
xxviii
INDEX
extra-axial lesions, T2 hypointense, Magnetic resonance imaging artifacts. See MR
1(4):68-69,71 artifacts
extra-axial mass, hyperdense, 1(4):74 Malformations, congenital, 1(5):23, 27
hyperdense dural sinus, 1(10):27, 29 Manganese toxicity, 1(6):80, 82
lucent skull lesions, multiple, 1(1):23 Maple syrup urine disease
medulla lesion, 1(7):10 confluent white matter lesions, 1(6):34, 39
suprasellar mass, general, 1(8):25, 29 globus pallidus lesions, 1(6):87
thick dura or arachnoid, generalized, 1(2):14 pontine lesion, 1(7):7
paraspinal mass, ventral/lateral, 11(5):8 Marchiafava-Bignami disease, 1(6):47, 51, 52, 53
parenchymal, 1(5):80 Marfan syndrome, 1(9):6
pontine lesion, 1(7):6 Marrow. See Bone marrow
posterior fossa neoplasms, adult, 1(7):40 Mass effect, extrinsic, 1(3):50, 51
sacral mass, adult, 11(1):18,20 Massa intermedia
sacrococcygeal mass, pediatric, 11(1):22,24 normal, 1(3):22, 23
scalp mass, 1(1):4 prominent (Chiari 2), 1(3):22, 24, 26, 27
spondylolisthesis, 11(3):20 Masson hemangioma, 1(10):27
suprasellar mass, enhancing, 1(8):42 Meckel cave lesion, 1(10):22-25
thickened bony trabeculae, 11(3):46,47 Medial atrial diverticula. See Hydrocephalus,
vertebral body obstructive
diffuse sclerosis, 11(3):44,45 Median nerve entrapment, 11(1):43,46
diffuse Tl hypointense signal, 11(3):52 Medulla lesions, 1(7):10-13
flattened, multiple, 11(3):8 Medullary infarct
fracture, 11(3):28 lateral, 1(7):10, 11
Lymphoma, primary CNS medial, 1(7):10-11, 13
basal ganglia lesions, bilateral, 1(6):80, 82 Medullary veins, enlarged, 1(10):10-13
bithalamic lesions, 1(6):92, 95 Medulloblastoma
corpus callosum, 1(6):46, 49, 56 PNET-MB
ependymal enhancement, 1(3):40, 43 cerebellar mass, 1(7):22, 24
ependymal/subependymal lesions, 1(3):8, 11 in children over 1 year, 1(5):112, 114
intrasellar lesion, 1(8):20, 21 ependymal/subependymallesions, 1(3):8
lateral ventricle mass, 1(3):13, 15 fourth ventricle mass, 1(3):32, 33
multiple brain hyperintensities (T2/FLAIR), intraventricular calcifications, 1(3):63, 65
1(5):65, 69 in newborn/infant, 1(5):106, 108
multiple enhancing lesions, 1(5):3, 4 parenchymal lesion, solitary hyperdense,
parenchymal lesions 1(5):45, 47
multiple hyperdense, 1(5):51, 54 posterior fossa neoplasm, pediatric, 1(7):44,
solitary hyperdense, 1(5):45, 48 46
Tl/T2 hyperintense, 1(5):87, 89 vermis mass, 1(7):28, 29
Tl/T2 isointense, 1(5):95, 96 variants, 1(7):41, 43, 45
periventricular enhancing lesions, 1(3):58, 60 Medulloepithelioma
pineal + suprasellar lesions, 1(8):10, 11 in newborn/infant, 1(5):107, 111
pituitary gland enlargement, 1(8):18 posterior fossa neoplasm, pediatric, 1(7):45, 49
restricted diffusion, 1(5):99, 100 Mega cisterna magna
ring-enhancing lesions, 1(5):6, 9, 12, 15 cistern and subarachnoid space normal variants,
suprasellar mass 1(4):2-3
hyperdense, 1(8):52, 53 extra-axial fluid collection, CSF-like, 1(4):50, 51
pediatric, 1(8):31, 35 infratentorial midline cyst, 1(7):14, 15
thick infundibular stalk, 1(8):46 posterior fossa lesion, cystic-appearing, 1(7):34,
thick septum pellucidum, 1(3):16, 17 35
third ventricle mass, general, 1(3):23 thin skull, localized, 1(1):16, 17
white matter lesions, confluent, 1(6):34, 39 Megalencephaly
large ventricles, 1(3):45, 47
macrocephaly, 1(1):33, 36
M with dilated perivascular spaces, 1(6):74, 75
Macrocephaly, 1(1):32-37 Melanocytoma
Macrocrania intradural/extramedullary lesions, Tl
benign familial, 1(1):32, 33 hyperintense, 11(6):26
of infancy, benign, 1(4):9, 11
xxix
INDEX
intramedullary lesions, T1 hyperintense, pial enhancement, 1(2):17, 19
II(7):35, 37 sulcal/cisternal enhancement, 1(4):55, 57
meningeal,I(5):102 thick cortex, 1(6):9, 13
Melanoma Meningioma
metastases atypical and malignant
extradural lesion, T1 hyperintense, II(5):30 dural tail sign, 1(2):20
intradural/extramedullary lesions, T1 epidural mass, brain, 1(4):5,7
hyperintense, II(6):26 solitary dural-based mass, 1(2):4, 6
parenchymal lesions, T1 hyperintense, calcified
1(5):102, 105 disc contour abnormality, II(4):3, 5
vertebral body, focal T1 hyperintense signal, intradural/extramedullary lesions, no
II(3):50 enhancement, II(6):12
parenchymal lesions intradural/extramedullary lesions, ring/
solitary hyperdense, 1(5):45, 48 peripheral enhancement, II(6):22, 24
Tl hyperintense, 1(5):102, 105 intradural/extramedullary lesions, T1
Melanosis, neurocutaneous, 1(2):4, 1(4):55, 57 hypointense, II(6):28, 30
MELAS intradural/extramedullary lesions, T1
acute, cortical hyperintensity Tl/FLAIR, 1(6):25 hypo intense, T2 hypointense, II(6):32,
asymmetric cerebral hemispheres, 1(6):3, 6 33
basal ganglia suprasellar mass, 1(8):40, 41
bilateral lesions, 1(6):80 cauda equina syndrome, II(6):36, 37
calcification, 1(6):62, 64 cavernous sinus lesions or mass, 1(10):14, 15, 18,
T2 hyperintense, 1(6):71 19
cortical enhancement, 1(6):28 in children over 1 year, 1(5):113
parenchymal calcifications, multiple, 1(5):41, 43 choroid plexus, 1(3):6, 7
Melorheostosis, 1(1):8, 30 cisterna magna mass, 1(4):38, 40
Meningeal metastases. See also Skull metastases CPA-lAC mass
in children over 1 year, 1(5):113,117 adult, 1(4):24, 25, 1(7):40
dural-based masses, 1(2):4, 6, 8, 9 pediatric, 1(7):45, 47
dural tail sign, 1(2):20 craniovertebral junction abnormalities, 11(2):4,
effaced sulci, focal, 1(4):16, 19 7,9,11
effaced sulci, generalized, 1(4):12, 14 cystic
falx lesions, 1(2):12 intradural/extramedullary lesions, 11(6):22,
FLAIRhyperintense CSF, 1(4):64, 67 24
hyperde.nse CSF,1(4):72 solitary cystic mass, 1(5):16, 20
hyperdense dural sinus, 1(10):27, 29 dural-based masses, 1(2):4, 5, 8, 9
hyperdense extra-axial mass, 1(4):74, 75 dural calcification, 1(2):2, 3
pial enhancement, 1(2):16, 17-18 dural sinus, hyperdense, 1(10):27, 29
prepontine cistern mass, 1(4):32, 34 dural sinus lesion, 1(10):2-3, 6
T2 hypointense extra-axial lesions, 1(4):68, 70 dural tail sign, 1(2):20
thick dura or arachnoid, generalized, 1(2):14 effaced sulci, focal, 1(4):16, 18
unilateral cavernous sinus mass, 1(10):14, 16 epidural mass, brain, [(4):4, 5
Meninges, 1(2):2-21 extra-axial lesion or mass
dural-based mass hyperdense, 1(4):74, 75
multiple, 1(2):8-11 T2 hypointense, [(4):68, 70
solitary, 1(2):4-7 falx lesions, 1(2):12, 13
dural calcifications, 1(2):2-3 foramen magnum mass, 1(4):42, 44
dural tail sign, 1(2):20-21 intradural/extramedullary lesions
falx lesions, 1(2):12-13 multiple, II(6):20
pial enhancement, 1(2):16-19 solid enhancement, 11(6):14,15
thick dura or arachnoid, generalized, 1(2):14-15 T2 hyperintense, T1 isointense, II(6):34
Meningioangiomatosis intraosseous, 1(1):27, 29
effaced sulci, focal, 1(4):17, 19 intrasellar lesion, 1(8):20
parenchymal calcification, 1(5):35, 39 intraventricular calcifications, [(3):62, 64
parenchymal lesions, solitary hyperdense, lateral ventricle, 1(3):12, 14, 51
1(5):45, 49 lipomatous, 1(4):58, 59, 1(5):32
perivascular space enhancing lesions, 1(6):77, 79 Meckel cave lesion, 1(10):22, 24
xxx
INDEX
parenchymal lesions, Tl/T2 isointense, 1(5):94,
96
enlarged neural foramen, 11(3):16, 17
pedicle abnormality, II(3):36 =-
Q..
~
pineal region mass, 1(8):2, 4 ventral/lateral paraspinal mass, 11(5):8,9 ><
pituitary gland enlargement, 1(8):18 occult intrasacral, II(I):18, 20, 27, 29
prepontine cistern mass, 1(4):32, 34 MERRF(myoclonus epilepsy with ragged red
restricted diffusion, 1(5):99 fibers), 1(6):71, 73
sellar/juxtasellar calcification, 1(8):14, 16 Mesial temporal sclerosis, 1(5):118, 119
subarachnoid space narrowing, II(6):6 Metabolic disorders
suprasellar mass bilateral basal ganglia lesions, 1(6):81
enhancing, 1(8):42 inherited
general, 1(8):24, 25 confluent white matter lesions, 1(6):35, 37
hyperdense, 1(8):52, 53 thin corpus callosum, 1(6):41, 45
Tl hyperintense, 1(8):56, 57 Metal artifact
Tl isointense, 1(8):54 extradural lesions
thick dura or arachnoid, generalized, 1(2):14, 15 no enhancement, II(5):14
thick skull, localized, 1(1):12 Tl hypointense, II(5):32
thin skull, localized, 1(1):16, 17 T2 hypointense, Tl hypointense, 11(5):40,41
vertebral body scalloping or widened canal, intradural/extramedullary lesions
11(3):18 Tl hyperintense, II(6):26
Meningitis Tl hypointense, II(6):28, 29
carcinomatous, 1(4):62 Tl hypointense, T2 hypointense, 11(6):32
chemical, II(6):8-9, 11 vertebral body, focal Tl hypointense signal,
complications, 1(3):45, 46 11(3):56,57
CSF Metastases
FLAIRhyperintense, 1(4):64, 66 adult back pain, II(I):53, 55
hyperdense, 1(4):72, 73 cauda equina syndrome, 11(6):36
Tl hyperintense, 1(4):62, 63 choroidal, 1(3):26, 27
dural calcification, 1(2):2 cisterna magna mass, 1(4):38-39, 40
infundibular stalk, 1(8):44, 46, 47 CPA-lAC mass, 1(4):24, 26, 1(7):40, 42
large ventricles, 1(3):44, 46 cranial nerve enhancement, 1(4):46, 47
lymphomatous, 1(4):54, 56 CSF disseminated
Meckel cave lesion, 1(10):23, 24 cauda equina enhancement, diffuse, II(6):2,
microcephaly, 1(1):38, 40 3-4
perivascular space enhancing lesions, 1(6):76, 77 intradural/extramedullary lesions, multiple,
pial enhancement, 1(2):16, 17 11(6):20,21
small ventricles, 1(3):48 intradural/extramedullary lesions, solid
spinal enhancement, II(6):14, 16
cauda equina enhancement, diffuse, 11(6):2,3 intradural/extramedullary lesions, T2
intradural/extramedullary lesions, ring/ hyperintense, Tl isointense, II(6):34, 35
peripheral enhancement, II(6):22, 24 intradural/extramedullary lesions, Tl
intradural/extramedullary lesions, solid hypointense, 11(6):28,31
enhancement, 11(6):14,17 leptomeningeal enhancement, II(6):8, 9
leptomeningeal enhancement, 11(6):8,10 pediatric back pain, II(I):57, 59
sulcal/cisternal enhancement, 1(4):54, 55 CSF/meningeal, 1(10):22, 24
sulci diffuse sclerotic, 1(1):8, 10
effaced, 1(4):12, 14, 17 dural, 1(4):4, 6
enlarged,I(4):8 dural sinus lesion, 1(10):3, 6
thick dura or arachnoid, generalized, 1(2):14, 15 ependymal/subependymallesions,I(3):8
tuberculosis, 1(4):54, 56 epidural
Meningocele disc contour abnormality, II(4):2
anterior sacral epidural mass, spinal, II(5):2, 5
sacral deformity, 11(1):27,29 extradural lesions, multiple, 11(5):12, 13
sacral mass, adult, II(I):18-19, 21 extradural lesions, T2 hyperintense, Tl
sacrococcygeal mass, pediatric, 11(1):23,24 isointense, 11(5):36,39
dorsal spinal, II(3):2, 11(5):43,45 extradural lesions, Tl hypo intense, II(5):33,
extra-axial fluid collection, CSF-like, 1(4):50 35
lateral subarachnoid space narrowing, 11(6):6,7
XXXI
INDEX
>< extramedullary, II(2):4, 8, 10 Midline anomaly, 1(1):38, 42
aJ hematogenous, II(I):57
"'C Mineral deposition, 1(5):102, 103
-C hypothalamic/pituitary
intracranial
axis, 1(8):48 Mineralization, 1(6):80, 82
Mitochondrial disorders
cystic-appearing posterior fossa lesion, bithalamic lesions, 1(6):93
1(7):35, 39 encephalopathies, 1(6):81
foramen magnum mass, 1(4):42 medulla lesion, 1(7):11
irregular large ventricles, 1(3):54, 57 midbrain cytopathy, 1(6):101, 103
pineal + suprasellar lesions, 1(8):10 pontine lesion, 1(7):7
intraventricular Morphogenetic protein, bone, II(4):7, 9
choroid plexus lesions, 1(3):6, 7 Motor neuropathies, hereditary
foramen of Monro mass, 1(3):18, 20 cauda equina enhancement, diffuse, II(6):2, 5
fourth ventricle mass, 1(3):32-33 intradural lesion, serpentine, II(6):18, 19
lateral ventricle mass, 1(3):12, 14 Moyamoya
thick septum pellucidum, 1(3):16, 17 arterial shape/configuration abnormalities,
lower extremity pain, 11(1):48-49, 50 1(9):3,5
melanoma. See Melanoma, metastases FLAIRhyperintense CSF,1(4):65
meningeal. See Meningeal metastases perivascular space enhancing lesions (mimic),
midbrain lesion, 1(6):100, 102 1(6):77, 79
osseous. See Osseous metastases, blastic; Osseous pial enhancement, 1(2):16, 19
metastases, lytic MR artifacts
osteoblastic, 1(1):12, 13 flow-related
paraspinal muscle abnormalities, II(5):1O, 11 arterial shape/configuration abnormalities,
parenchymal. See Parenchymal metastases 1(9):2,4
perineural CNV2, 1(10):23, 25 cistern and subarachnoid space normal
perineural CNV3, 1(10):22-23, 24 variants, 1(4):2, 3
perivascular space enhancing lesions, 1(6):76 FLAIRhyperintense CSF,1(4):64, 66
pituitary T1 hyperintense CSF,1(4):62
intrasellar lesion, 1(8):20 Tl hyperintense parenchymal lesions,
pituitary gland enlargement, 1(8):18 1(5):102, 104
Tl isointense suprasellar mass, 1(8):54 T2 hypointense extra-axial lesions, 1(4):68,
pontine lesion, 1(7):6 69
quadrigeminal cistern mass, 1(8):8 third ventricle mass, general, 1(3):22, 23
sacral deformity, 11(1):26, 28 magnetic susceptibility
skull base. See a/so Skull metastases FLAIRhyperintense CSF,1(4):64, 66
bilateral cavernous sinus lesions, 1(10):18, 20 T1 hyperintense CSF,1(4):62
Meckel cave lesion, 1(10):22, 24 T2 hypo intense extra-axial lesions, 1(4):68,
spondylolisthesis, II(3):20 69
to stalk/pituitary, 1(8):46, 47 patient-related, 1(4):64, 66
suprasellar mass, 1(8):25, 29, 42 Mucopolysaccharidoses
vermis mass, 1(7):28, 30 adult back pain, II(I):52
vertebral body CI-C2 instability, II(2):12
focal T1 hypointense signal, II(3):56, 57 craniovertebral junction abnormalities, II(2):4
ventral/lateral paraspinal mass, II(5):8 CSF-Iike parenchymal lesions, 1(5):23, 26
white matter lesion, solitary, 1(6):30, 32 kyphosis, 11(1):12
Methanol toxicity, 1(6):84, 85 macrocephaly, 1(1):33, 37
Methylmalonic acidemia, 1(6):87, 89 multiple brain hyperintensities (T2/FLAIR),
Micro-arteriovenous malformations, multiple, 1(5):64, 67
1(5):82, 85 myelopathy, II(7):48, 52
Microangiopathy odontoid deformity, 11(2):14
mineralizing, 1(5):83, 1(9):10, 11 perivascular spaces, enlarged, 1(6):74, 75
thrombotic, 1(5):51, 55, 102 periventricular T2/FLAIR lesions, 1(3):73
Microcephaly, 1(1):38-42 platyspondyly, diffuse, 11(1):16
thick skull, generalized, 1(1):8, 10 scoliosis, 11(1):10
thin cortex, 1(6):15, 19 vertebral anomalies, congenital, 11(3):2
Microlissencephaly, 1(1):39, 43 vertebral body
Midbrain lesions, 1(6):100-103 dysmorphic, II(3):10
XXXII
INDEX
fracture, II(3):29 periventricular enhancing lesions, 1(3):58, 59
scalloping or widened canal, 1l(3):18 periventricular T2/FLAIR lesions, 1(3):72, 74
vertebral endplate contour abnormality, II(4):1O, pontine lesion, 1(7):6, 8
11 restricted diffusion, 1(5):99, 101
Multi-infarct dementia ring-enhancing lesions, multiple, 1(5):12, 14
asymmetric cerebral hemispheres, 1(6):2, 5 small brainstem, 1(7):4, 5
confluent white matter lesions, 1(6):34, 36 spinal cord
large ventricles, 1(3):45, 47 cauda equina syndrome, II(6):36
thin cortex, 1(6):15, 18 intramedullary lesions, multiple, 11(7):12
Multiple myeloma intramedullary lesions, no enhancement,
adult back pain, Il(I):53, 55 II(7):18
aggressive bony lesion, II(3):24, 26 intramedullary lesions, ring/peripheral
craniovertebral junction abnormalities, Il(2):4, 7 enhancement, II(7):24
extradural marrow signal, abnormal, II(5):26, 28 intramedullary lesions, solid enhancement,
facet abnormality, non-traumatic, II(3):32 II(7):14, 16
kyphosis, Il(I): 12 intramedullary lesions, T2 hyperintense, Tl
lower extremity pain, 11(1):48 isointense, II(7):30, 31
odontoid deformity, II(2):14, 15 intramedullary lesions, Tl hypointense,
platyspondyly, diffuse, II(I):16 11(7):28,29
sacral mass, adult, II(I):18, 21 intramedullary mass, Il(7):2
spondylolisthesis, II(3):20 myelopathy, II(7):48, 50
vertebral body small/atrophic, II(7):1O, 11
diffuse Tl hypointense signal, II(3):52, 54 T2 hyperintense cord lesions, central,
enlarged, soap bubble expansion, II(3):38, 40 11(7):44, 45-46
flattened, II(3):6, 8, 9 T2 hyperintense cord lesions, dorsal, II(7):40,
focal Tl hypointense signal, II(3):56 41
Multiple sclerosis T2 hyperintense cord lesions, ventral, II(7):38
bithalamic lesions, 1(6):92 thalamic lesion, unilateral, 1(6):90
cerebellar mass, 1(7):22, 25 thin cortex, 1(6):14, 18
cerebral aqueduct/periaqueductallesion, 1(3):28, tumefactive, 1(6):56, 57
30 white matter lesions
corpus callosum confluent, 1(6):34, 36
abnormal shape or configuration, 1(6):47, 50 solitary, 1(6):30, 32
holes, 1(6):52 Multiple system atrophy
lesion without mass effect, 1(6):54 cerebellar atrophy, 1(7):19, 21
splenium lesion, 1(6):58, 59 enlarged sulci, generalized, 1(4):9
thin, 1(6):40, 42 pontine lesion, 1(7):7, 9
cranial nerve enhancement, 1(4):46, 48 putamen lesions, 1(6):84
cystic mass, solitary, 1(5):17, 19 small brainstem, 1(7):4, 5
enlarged sulci, generalized, 1(4):9, 11 Muscle de nervation, II(5):1O, 11
ependymal enhancement, 1(3):40, 41 Muscular dystrophy
ependymal/subependymallesions, 1(3):8, 10 congenital
hypothalamus lesion, 1(8):49, 51 cystic-appearing posterior fossa lesion,
intramedullary lesions, II(7):20, 21 1(7):35, 39
large ventricles, 1(3):44, 46 small brainstem, 1(7):4
medulla lesion, 1(7):10, 12 thick cortex, 1(6):9, 12
midbrain lesion, 1(6):100, 102 scoliosis, II(I):10
multiple brain hyperintensities (T2/FLAIR), Myelin vacuolization, 1(5):64, 67
1(5):65, 68-69 Myelination, normal, 1(5):64, 66
multiple enhancing lesions, 1(5):2, 3 Myelitis. See also Acute transverse myelitis; Spinal
parenchymal lesions cord myelitis
CSF-like, 1(5):22, 24 radiation-induced, II(7):10
hypodense, 1(5):57, 59, 60 viral
Tl hyperintense, 1(5):102, 104 intramedullary lesions, diffuse/ill-defined
Tl hypointense, T2 hyperintense, 1(5):90, 92 enhancement, 11(7):20, 22
Tl/T2 hyperintense, 1(5):86, 88 intramedullary lesions, T2 hyperintense, Tl
isointense, 11(7):31, 33
XXXIII
INDEX
>C myelopathy, II(7):49, 53 corpus callosum splenium lesion, 1(6):58, 61
GJ
"'Cl T2 hyperintense cord lesions, central, midbrain lesions, 1(6):100, 103
-C Il(7):45, 47
T2 hyperintense cord lesions, ventral,
II(7):38, 39
pontine lesion, malignant, 1(7):6, 9
posterior fossa, adult, 1(7):40-43
primary CNS, 1(4):16
Myelocystocele, terminal "pulvinar sign" (mimic), 1(6):96, 97
conus abnormality, Il(7):7 with CSF seeding, 1(3):40, 42
sacral deformity, 1I(1):26-27 Nerve roots, conjoined, II(6):12, 13
sacrococcygeal mass, pediatric, 1I(1):23, 24 Nerve sheath tumors
Myelofibrosis malignant, intradural/extramedullary, II(6):15,
diffuse T1 hypointense signal, vertebral body, 17
1I(3):53, 55 malignant peripheral
diffuse vertebral body sclerosis, II(3):44 leptomeningeal enhancement, 11(6):9,11
extradural lesions, no enhancement, Il(5):14, 15 paras pinal muscle abnormalities, II(5):10
Myeloma multiple nonsyndromic, II(6):20
multiple dural-based masses, 1(2):9, 11 Neural foramen, enlarged, II(3):16-17
multiple lucent skull lesions, 1(1):22, 25 Neurenteric cyst
sclerotic, Il(3):44 cisterna magna mass, 1(4):39, 41
Myelomeningocele/myelocele CPA mass, 1(4):25, 29, 31
congenital vertebral anomalies, II(3):2 craniovertebral junction soft tissue
conus abnormality, II(7):7 abnormalities, II(2):9
lumbar soft tissue mass, pediatric, II(5):42, 43 cystic mass, solitary, 1(5):17, 21
sacral deformity, II(I):26-27, 28 extra-axial mass, 1(4):52, 53, 77
Myelopathy, 1I(7):48-53. See also Radiation injuries extradural marrow signal, normal, 1l(5):23, 25
and necrosis, myelopathy foramen magnum mass, 1(4):43, 45
Myoclonus epilepsy with ragged red fibers infratentorial midline cyst, 1(7):15, 17
(MERRF),1(6):71, 73 intradural/extramedullary lesions
Myxoma, metastatic atrial, 1(5):83 no enhancement, II(6):12, 13
Myxopapillaryependymoma ring/peripheral enhancement, II(6):22, 24
calcified, II(6):29, 32 T2 hyperintense, T1 isointense, II(6):34
sacrococcygeal mass, pediatric, II(I):23, 24 T1 hypointense, II(6):29, 31
spinal cord intramedullary lesions, no enhancement,
adult back pain, II(I):52 II(7):18
cauda equina syndrome, II(6):36, 37 myelopathy, II(7):49
conus abnormality, II(7):6, 7 posterior fossa lesion, cystic-appearing, 1(7):35,
intradural/extramedullary lesions, solid 39
enhancement, Il(6):14, 16 prepontine cistern mass, 1(4):33, 37
intradural lesion, serpentine, II(6):18, 19 Neuritis, post-viral, 1(4):47
intramedullary lesion, solid enhancement, Neuroblastic tumor
II(7):14 enlarged neural foramen, II(3):16, 17
leptomeningeal enhancement, II(6):8, 10 extradural lesions, solid enhancement, II(5):16,
lower extremity pain, II(I):49, 51 18
pediatric back pain, II(I):57, 59 normal extradural marrow signal, II(5):22
sacral deformity, II(I):26, 28 paraspinal muscle abnormalities, 11(5):10
pediatric back pain, II(I):56-57
sacrococcygeal mass, pediatric, II(I):22, 24
N Neuroblastoma
Nasopharyngeal carcinoma metastatic
craniovertebral junction abnormalities, II(2):4, in children over 1 year, 1(5):113, 117
8-9,10 "hair on end," 1(1):6, 7
invading clivus, 1(4):33, 37 solitary dural-based mass, 1(2):5, 7
unilateral cavernous sinus mass, 1(10):14, 16 ventral/lateral paraspinal mass, 11(5):8
NBIA (neurodegeneration with brain iron Neurocutaneous melanosis
accumulation), 1(6):87, 89 in children over 1 year, 1(5):112
Neoplasms. See also specific histologic types and in newborn/infant, 1(5):107, 111
locations perivascular space enhancing lesions, 1(6):77, 79
bilateral basal ganglia lesions, 1(6):80 pial enhancement, 1(2):17, 19
clival, 1(4):33
XXXIV
INDEX
T1 hyperintense parenchymal lesions, 1(5):102 intraventricular calcifications, 1(3):63, 65
Neurocysticercosis intraventricular mass, "bubbly-appearing,"
basal ganglia calcification, 1(6):62, 63 1(3):36,38
cerebral aqueduct/periaqueductallesion, 1(3):28, lateral ventricle mass, 1(3):12, 14
30 Neurodegeneration with brain iron accumulation
cyst with nodule, 1(5):28, 29 (NBIA), 1(6):87, 89
cystic mass Neuroectodermal tumor, primitive. See PNET
CPA, 1(4):28, 30 (primitive neuroectodermal tumor)
solitary, 1(5):16, 18 Neuroepithelial tumor, dysembryoplastic. See
effaced sulci, fotal, 1(4):16 DNET (dysembryoplastic neuroepithelial
extra-axial mass tumor)
CSF-like, 1(4):52, 53 Neurofibroma
hypodense, 1(4):76, 78 epidural mass, 11(5):2-3, 5
foramen of Monro mass, 1(3):18, 20 extradural lesions
fourth ventricle mass, 1(3):32, 34 solid enhancement, 11(5):16, 18
infratentorial midline cyst, 1(7):14, 16 T2 hyperintense, T1 isointense, 11(5):36,39
infundibular stalk, absent/thin, 1(8):44, 45 T1 hypointense, 11(5):33, 35
interhemispheric fissure cysts, 1(4):20, 22 extradural marrow signal, normal, 11(5):23
intrasellar mass, cystic, 1(8):22, 23 intradural/extramedullary lesions
intraventricular calcifications, 1(3):62, 64 multiple, 11(6):20
intraventricular mass, "bubbly-appearing," solid enhancement, 11(6):14, 16
1(3):36,38 T2 hyperintense, Tl isointense, 11(6):34
lateral ventricle, asymmetric, 1(3):51 leptomeningeal enhancement, 11(6):8,10
lateral ventricle mass, 1(3):12, 14 lower extremity pain, 11(1):49
Meckel cave lesion, 1(10):23 Meckel cave lesion, 1(10):23
multiple brain hyperintensities (T2/FLAIR), neural foramen, enlarged, 11(3):16
1(5):71, 73 paraspinal muscle abnormalities, 11(5):10, 11
multiple enhancing lesions, 1(5):2, 4 pedicle abnormality, 11(3):36
multiple hypointense foci on GRE/SWI, plexiform
1(5):82-83, 85 cranial nerve enhancement, 1(4):46, 48
parenchymal calcifications lumbar soft tissue mass, pediatric, 11(5):42,44
multiple, 1(5):40, 41 sacrococcygeal mass, pediatric, 11(1):22,24
solitary, 1(5):34, 35 unilateral cavernous sinus mass, 1(10):15
parenchymal lesions sacral deformity, 11(1):26,28
CSF-like, 1(5):22, 24 scalp, 1(1):16
T1 hypointense, T2 hyperintense, 1(5):90 vertebral body scalloping or widened canal,
periventricular calcifications, 1(3):66-67, 69 11(3):18
pineal region mass, 1(8):2-3, 4 Neurofibromatosis type 1 (Nfl)
posterior fossa lesion, cystic-appearing, 1(7):35, basal ganglia
39 bilateral lesions, 1(6):80, 82
prepontine cistern mass, 1(4):32-33, 35 T1 hyperintense, 1(6):66, 67
quadrigeminal cistern mass, 1(8):8, 9 T2 hyperintense, 1(6):70, 72
ring-enhancing lesions, 1(5):6, 9, 12, 14 cranial nerve enhancement, 1(4):46
sellar/juxtasellar calcification, 1(8):14, 16 craniovertebral junction abnormalities, 11(2):4,
sulcal/cisternal enhancement, 1(4):54, 56 9,11
suprasellar mass extradural lesions, multiple, 11(5):12, 13
calcified, 1(8):40, 41 fusiform arterial enlargement, 1(9):6
cystic, 1(8):36, 38 globus pallidus lesions, 1(6):86, 88
general, 1(8):24, 26 intradural/extramedullary lesions, multiple,
T1 hypointense, 1(8):58, 59 11(6):20
third ventricle mass kyphoscoliosis, child, 11(1):14
body/posterior, 1(3):26, 27 kyphosis, 11(1):12
general, 1(3):22, 24 leptomeningeal enhancement, 11(6):8
Neurocytoma, central lucent skull lesions, multiple, 1(1):23
in children over 1 year, 1(5):113 macrocephaly, 1(1):32, 36
foramen of Monro mass, 1(3):18-19, 21 multiple brain hyperintensities (T2/FLAIR),
fourth ventricle mass, 1(3):33 1(5):64, 66
xxxv
INDEX
>< parenchymal lesions cauda equina enhancement, diffuse, I1(6):2, 5
QJ
"'C Tl hyperintense, 1(5):102, 105 intradural lesion, serpentine, II(6):18, 19
-C Tl hypointense, T2 hyperintense, 1(5):91, 93
Tl/T2 hyperintense, 1(5):87
peripheral, 11(1):42-43, 45-46
radial, 11(1):42-43, 45
pontine lesion, 1(7):7 ulnar, I1(1):43, 46
scalp mass, 1(1):4, 5 Neurosarcoid
scoliosis, I1(I): 10 cavernous sinus mass or lesions
septum pellucidum, thick, 1(3):16, 17 bilateral, 1(10):19, 21
tectal plate lesion, 1(6):98, 99 unilateral, 1(10):15, 17
thalamic lesion, unilateral, 1(6):90, 91 cranial nerve enhancement, 1(4):47, 49
Neurofibromatosis type 2 (NF2) dural-based masses, 1(2):4, 6, 8, 10
cavernous sinus lesions, bilateral, 1(10):18, 20 dural tail sign, 1(2):20, 21
in children over 1 year, 1(5):113, 116 effaced sulci, generalized, 1(4):12
choroid plexus lesions, 1(3):6 ependymal enhancement, 1(3):41, 43
CPA-lAC mass, 1(4):24, 26 ependymal/subependymallesions, 1(3):9
cranial nerve enhancement, 1(4):46, 48 epidural mass, brain, 1(4):4-5, 6
dural-based masses, multiple, 1(2):8, 10 extra-axial lesions or mass, 1(4):69, 71, 74
intradural/extramedullary lesions, multiple, falx lesions, 1(2):12, 13
I1(6):20 hypothalamus lesion, 1(8):48, 50
intraventricular calcifications, 1(3):62, 64 intrasellar lesion, 1(8):20, 21
leptomeningeal enhancement, I1(6):8 lateral ventricle mass, ](3):12, 15
Neurogenic arthropathy lucent skull lesions, multiple, 1(1):23
aggressive bony lesion, I1(3):25, 27 Mecke] cave lesion, 1(10):23, 24
intervertebral disc medulla lesion, 1(7):11
endplate irregularity, I1(4):7, 9 mu]tiple brain hyperintensities (T2/FLAIR),
T2 hyperintense, I1(4):14 1(5):76, 78
Tl hypo intense, I1(4):12, 13 mu]tiple enhancing lesions, 1(5):3, 5
kyphosis, I1(1):12 multiple hypointense foci on T2, 1(5):80, 81
lumbar bony trauma, I1(1):8, 9 parenchymal lesions
posterior element fracture, I1(3):34 multiple hyperdense, ](5):51, 55
scoliosis, I1(1):1O solitary hyperdense, 1(5):45, 49
soft tissue calcification, paraspinal, II(5):20, 21 Tl hypointense, T2 hyperintense, 1(5):90
vertebral body, dysmorphic, I1(3):10 Tl/T2 isointense, 1(5):95
vertebral body fracture, II(3):28, 31 perivascular space enhancing lesions, 1(6):76, 77
vertebral end plate abnormalities, II(4):1O, 16 pial enhancement, 1(2):16, 18
Neuroglia] cyst pituitary gland enlargement, 1(8):18, 19
CSF-Iike parenchyma] lesions, 1(5):23, 26 pontine lesion, 1(7):7
cystic-appearing posterior fossa lesion, ](7):34, prepontine cistern mass, 1(4):33, 36
38 sulcal/cisternal enhancement, 1(4):54, 56
solitary cystic mass, 1(5):17, 20-21 suprasellar mass
Neurohypophysis, ectopic enhancing, 1(8):42, 43
suprasellar mass genera], 1(8):24-25, 27
general, 1(8):24, 29 hyperdense, 1(8):52
Tl hyperintense, 1(8):56, 57 Tl isointense, 1(8):54
thick infundibular stalk, 1(8):46, 47 thick dura or arachnoid, generalized, 1(2):14, 15
Neuromyelitis optica thick infundibular stalk, 1(8):46
intramedullary lesions third ventricle mass, general, 1(3):22, 24
diffuse/ill-defined enhancement, II(7):20, 22 Neurosarcoidosis, 1(1):19, 1(6):81
solid enhancement, II(7):14-15, 16-17 Neurosyphilis, 1(4):5, I1(7):41
T2 hyperintense, Tl isointense, I1(7):30, 31 Nitrous oxide misuse, 11(7):40
subarachnoid space narrowing, I1(6):6, 7 Nocardia infections, 1(5):80, 81
Neuropathies Nonmeningothelial tumors
CIDP. See Chronic inflammatory demyelinating benign
polyneuropathy (CIDP) cavernous sinus lesions, bilateral, 1(10):19
femora], I1(1):48 dural-based mass, solitary, 1(2):5, 6
hypertrophic. See Hypertrophic neuropathy dural calcification, 1(2):2, 3
motor and sensory, hereditary sellar/juxtasellar calcification, 1(8):15
INDEX
malignant cranio-cervical junction acute injury, 11(2):2, 3
hyperdense extra-axial mass, 1(4):74 craniovertebral junction abnormalities, II(2):5
solitary dural-based mass, 1(2):5, 7 odontoid deformity, 11(2):14
Nutrition status, 1(4):9 Osmotic demyelination syndrome
basal ganglia, 1(6):71, 72, 81, 83
bithalamic lesions, 1(6):93
o cortical enhancement, 1(6):28
Occipital bones, squamous, 1(1):16 large brainstem, 1(7):2, 3
Occipital condyle fracture, II(2):2, 3, 4 multiple brain hyperintensities (T2/FLAlR),
Ochronosis, II(4):7 1(5):71,74-75
Odontoid C2 fracture parenchymal lesions, multiple hypodense,
CI-C2 instability, II(2):12 1(5):61
cranio-cervical junction acute injury, 11(2):2 pontine lesion, 1(7):6, 9
craniovertebral junction abnormalities, II(2):4-5 putamen lesions, 1(6):84, 85
odontoid deformity, II(2):14 restricted diffusion, 1(5):99, 101
Odontoid deformity, II(2):14-15 white matter lesion, solitary, 1(6):31, 33
Odontoid process, hypoplastic, 11(2):14, 15 Osseous metaplasia, 1(2):2, 3, 12
Oligoastrocytoma, 1(6):31 Osseous metastases, blastic
Oligodendroglioma abnormal extradural marrow signal, II(5):26
anaplastic, 1(5):45, 48, 1(6):24-25 aggressive bony lesion, II(3):24, 25
cerebellar mass, 1(7):23, 27 extradural lesions, solid enhancement, 11(5):16,
in children over 1 year, 1(5):112 17
corpus callosum mass, 1(6):56, 57 kyphosis, 11(1):12
cortical hyperintensity Tl/FLAIR, 1(6):24, 27 pedicle abnormality, 11(3):36, 37
effaced sulci, focal, 1(4):16, 18 thickened bony trabeculae, 11(3):46, 47
focal cortical mass, 1(6):20, 22 vertebral body
parenchymal calcification, solitary, 1(5):34, 36 diffuse sclerosis, 11(3):44
parenchymal lesions, 1(5):56, 58,90 diffuse Tl hypointense signal, 11(3):52, 54
thin skull, localized, 1(1):16, 17 flattened, II(3):6, 8, 9
white matter lesion, solitary, 1(6):31, 33 focal sclerosis, 11(3):42, 43
Olivary degeneration, hypertrophic Osseous metastases, lytic
large brainstem, 1(7):2, 3 abnormal extradural marrow signal, II(5):26
medulla lesion, 1(7):11, 13 aggressive bony lesion, II(3):24, 25
Olivopontocerebellar degeneration cervical bony abnormality, post-traumatic,
multiple brain hyperintensities (T2/FLAIR), 11(1):4
1(5):77,79 extradural lesions, solid enhancement, II(5):16,
small brainstem, 1(7):4, 5 18
Opportunistic infections, AIDS. See also HIV facet abnormality, non-traumatic, II(3):32, 33
infections kyphosis, 11(1):12
cranial nerve enhancement, 1(4):47, 49 lumbar soft tissue mass, pediatric, 11(5):43
cyst with nodule, 1(5):29, 31 odontoid deformity, 1I(2):14
ependymal enhancement, 1(3):40, 42 pedicle abnormality, II(3):36
ependymal/subependymallesions, 1(3):9 platyspondyly, diffuse, 1I(1):16
multiple brain hyperintensities (T2/FLAIR), posterior element
1(5):71,74 enlarged, II(3):13, 14
multiple enhancing lesions, 1(5):2, 4 fracture, II(3):34
multiple hypodense parenchymal lesions, sacral mass, adult, 11(1):18, 19
1(5):60-61, 62 vertebral body
multiple parenchymal calcifications, 1(5):41 dysmorphic, II(3): 10
ring-enhancing lesions, multiple, 1(5):12, 14 enlarged, II(3):13, 14, 38
sulcal/cisternal enhancement, 1(4):55 flattened, II(3):6, 7, 8
Optic nerve glioma, 1(4):46, 48 to vertebral body or pedicle, II(3):16, 17
Optic nerve sheath, enlarged, 1(4):2, 3 Ossification
Optic neuritis, 1(4):46 heterotopic, II(5):20
Os odontoideum ligamentum flavum
C1-C2 instability, 11(2):12, 13 extradural lesions, no enhancement, II(5):14
cervical abnormality, chronic post-traumatic, myelopathy, II(7):48
11(1):2
INDEX
normal extradural marrow signal, 11(5):23, 25 sellar/juxtasellar calcification, 1(8): 14
T2 hypointense, Tl hypointense extradural Osteomalacia, lI(2):4
lesion, 11(5):40, 41 Osteomyelitis
longitudinal ligament. See Longitudinal CI-C2
ligament ossification cervical abnormality, chronic post-traumatic,
Osteoarthritis, lI(2):5, 6 lI(I):2
Osteoblastoma craniovertebral junction abnormalities,
abnormal extradural marrow signal, lI(5):27, 29 11(2):4, 7, 8, 10
back pain, adult, 11(1):52 instability, lI(2):12
enlarged vertebral body, soap bubble expansion, chronic
11(3):38, 40 diffuse vertebral body sclerosis, lI(3):44, 45
enlarged vertebral body/posterior element, focal vertebral body sclerosis, lI(3):42
lI(3): 13, 15 thick skull, localized, 1(1):12
epidural mass, lI(5):2, 6 granulomatous
extradural lesion, T1 hypo intense, lI(5):32 abnormal extradural marrow signal, 11(5):26,
kyphoscoliosis, child, lI(I):14 28
lower extremity pain, lI(I):48 acute upper extremity pain or weakness,
pedicle abnormality, lI(3):36 11(1):43, 46
scoliosis, lI(I):10 adult back pain, 11(1):53, 55
spondylolisthesis, 11(3):20 aggressive bony lesion, lI(3):24, 26
Osteochondroma cervical bony fusion, lI(3):4
congenital vertebral anomalies, lI(3):2, 3 congenital vertebral anomalies, lI(3):2
dysmorphic vertebral body, lI(3):10, 11 kyphoscoliosis, child, lI(I):14, 15
enlarged vertebral body/posterior element, kyphosis, lI(1):12, 13
lI(3): 13, 15 neural foramen, enlarged, 11(3):16
extradural lesions, no enhancement, 11(5):14, 15 pediatric back pain, lI(I):57
myelopathy, 11(7):49, 53 pedicle abnormality, lI(3):36, 37
odontoid deformity, lI(2):14 soft tissue calcification, paraspinal, lI(5):20,
sellar/juxtasellar calcification, 1(8):14 21
thick skull, localized, 1(1): 12 thoracic bony trauma, 11(1):6
Osteodystrophy, renal vertebral body, dysmorphic, lI(3):10, 11
lumbar bony trauma, lI(I):8 vertebral body, focal Tl hypo intense signal,
thoracic bony trauma, lI(I):6 11(3):56
vertebral body, diffuse Tl hypointense signal, vertebral body fracture, lI(3):29
lI(3):53 vertebral end plate contour abnormality,
vertebral body sclerosis, diffuse, lI(3):44, 45 lI(4):10
Osteogenesis imperfecta lytic skull lesion, solitary, 1(1):19, 21
kyphosis, lI(I): 12 pyogenic
platyspondyly, diffuse, lI(I): 16, 17 abnormal extradural marrow signal, lI(5):26,
scoliosis, lI(I): 10, 11 27
thin skull, generalized, 1(1):14, 15 acute upper extremity pain or weakness,
vertebral anomalies, congenital, lI(3):2 lI(I):43, 47
vertebral body adult back pain, 11(1):53, 54
dysmorphic, lI(3): 10 aggressive bony lesion, 11(3):24, 26
flattened, lI(3):8, 9 cervical bony abnormality, post-traumatic
fracture, lI(3):29 lower, lI(I):4
vertebral endplate contour abnormality, lI(4):1O cervical bony fusion, lI(3):4, 5
Osteoid osteoma kyphoscoliosis, child, lI(I):14, 15
adult back pain, lI(I):52 kyphosis, lI(I): 12
kyphoscoliosis, child, lI(I):14 lumbar bony trauma, lI(I):8
lower extremity pain, lI(I):48 pediatric back pain, lI(I):57, 59
pediatric back pain, lI(1):57, 59 scoliosis, lI(I):10
pedicle abnormality, 11(3):36 spondylolisthesis, lI(3):21, 23
scoliosis, lI(I): 10, 11 vertebral body, dysmorphic, lI(3):10
vertebral body sclerosis, focal, lI(3):42, 43 vertebral body, flattened, 11(3):6, 7
Osteoma vertebral body, focal Tl hypointense signal,
sclerotic skull lesions, 1(1):26 , 28, 30, 31 11(3):56, 57
INDEX
vertebral body fracture, I1(3):28, 31 sacral mass, adult, 11(1):18,21
vertebral endplate contour abnormality, sclerotic skull lesions, 1(1):26 , 28, 30, 31
11(4):10 thick skull, 1(1):8, 10, 12, 13
vertebral end plate signal abnormality, thickened bony trabeculae, I1(3):46, 47
I1(4):16, 17 thin skull, localized, 1(1):16, 17
skull, 1(1):23, 26, 29 vertebral body
Osteopathia striata, 1(1):12, 30 diffuse sclerosis, I1(3):44, 45
Osteopetrosis diffuse T1 hyperintense signal, 11(3):48,49
"hair on end," 1(1):6 enlarged, I1(3):12, 14
thick skull, generalized, 1(1):9, 11 focal T1 hyperintense signal, 11(3):50,51
thick skull, localized, 1(1):12 Panencephalitis, subacute sclerosing, 1(5):77, 79,
vertebral body, diffuse Tl hypointense signal, 1(6):35
I1(3):53, 55 Pantopaque
vertebral body sclerosis, diffuse, 11(3):44,45 extra-axial lesions, T2 hypointense, 1(4):69
Osteophytes fat-like lesions, 1(5):32
disc contour abnormality, 11(4):2-3 intradural/extramedullary lesions, T1
endplate, I1(5):40, 41 hyperintense, 11(6):26,27
extradural lesion, Tl hypointense, 11(5):32 T1 hyperintense CSF,1(4):62
facet, I1(5):40 Pantothenate kinase associated neurodegeneration
intervertebral disc, T1 hypointense, I1(4):12, 13 (PKAN),1(6):81
Osteopoikilosis, 1(1):30 Papilloma, choroid plexus. See Choroid plexus
Osteoporosis papilloma
lucent skull lesions, multiple, 1(1):22, 25 Paraganglioma
platyspondyly, diffuse, 11(1):16 conus abnormality, 11(7):6
thickened bony trabeculae, I1(3):46, 47 craniovertebral junction abnormalities, 11(2):4,9
vertebral body glomus jugulare, 1(7):41
diffuse T1 hyperintense signal, I1(3):48, 49 intradural/extramedullary lesions, I1(6):15, 17,
flattened, 11(3):6,8 34
Osteoradionecrosis, 1(1):23 intradural lesion, serpentine, I1(6):18
Osteosarcoma Paraneoplastic syndromes
abnormal extradural marrow signal, 11(5):27,29 bithalamic lesions, 1(6):93, 95
adult back pain, 11(1):53,55 cerebellar atrophy, 1(7):18, 20
diffuse vertebral body sclerosis, 11(3):44 multiple brain hyperintensities (T2/FLAIR),
epidural mass, 11(5):2,7 1(5):76, 79
extradural lesions, 11(5):17,32 Paraparesis/paraplegia, I1(1):10, 12
lower extremity pain, 11(1):48 Parasites
pedicle abnormality, 11(3):36 basal ganglia calcification, 1(6):63
sacrococcygeal mass, pediatric, I1(1):23, 24 cyst with nodule, 1(5):29, 31
secondary, I1(1):19, 21 cystic mass, solitary, 1(5):17, 21
soft tissue calcification, paraspinal, I1(5):20, 21 intramedullary lesions, 11(7):21
spondylolisthesis, I1(3):20 intraventricular mass, "bubbly-appearing,"
telangiectatic, 11(3):39,41 1(3):36
thick skull, localized, 1(1):12 multiple brain hyperintensities (T2/FLAIR),
1(5):71, 73
multiple enhancing lesions, 1(5):3, 5
p parenchymal calcification, 1(5):35, 38
Pachygyria-polymicrogyria parenchymal lesions
asymmetric cerebral hemispheres, 1(6):3, 6 CSF-Iike, 1(5):23, 26
epilepsy, 1(5):118-119, 122 multiple hyperdense, 1(5):51, 55
focal cortical mass, 1(6):21, 23 ring-enhancing lesions, 1(5):7, 11, 13, 15
thick cortex, 1(6):8, 11 Paraspinal abscess
Pachymeningitis, hypertrophic, 1(2):12, 14, 15, acute back pain/radiculopathy, postoperative,
1(4):69 11(1):30,32
Paget disease acute upper extremity pain or weakness, 11(1):43
craniovertebral junction abnormalities, 11(2):4 lumbar soft tissue mass, pediatric, I1(5):43, 45
lytic skull lesion, solitary, 1(1):18, 20 normal extradural marrow signal, 11(5):22,24
posterior element, enlarged, I1(3):12, 14 paraspinal muscle abnormalities, 11(5):10,11
XXXIX
INDEX
>< scoliosis, II(I):10 Perineural root sleeve cysts
CIJ
"'C ventral/lateral paraspinal mass, II(5):8, 9 extradural, normal marrow signal, II(5):23, 25
C Paraspinal hematoma, II(5):22 extradural lesions, no enhancement, 11(5):14
Paraspinal mass, ventral/lateral, II(5):8-9 neural foramen, enlarged, 11(3):16, 17
Paraspinal muscle abnormalities, II(5):10-11 pedicle abnormality, 11(3):36
Parenchymal metastases Peripheral neuropathy, 11(1):42-43, 45-46
cerebellar mass, 1(7):22, 24 Perisylvian dysplasia, 1(5):118, 120
cerebral aqueduct/periaqueductallesion, 1(3):29 Perivascular space enhancing lesions, 1(6):76-79
in children over 1 year, 1(5):113 Perivascular spaces, enlarged, 1(6):74-75
cortical mass, focal, 1(6):20, 21 basal ganglia, bilateral lesions, 1(6):80, 81
cyst with nodule, 1(5):28, 30 cerebellar mass, 1(7):22, 24
cystic mass, solitary, 1(5):16, 18 cerebral aqueduct/periaqueductallesion, 1(3):28,
large brainstem, 1(7):2 30
multiple brain hyperintensities (T2/FLAIR), corpus callosum
1(5):65, 69 holes, 1(6):52, 53
multiple enhancing lesions, 1(5):2, 3 lesion without mass effect, 1(6):54, 55
multiple hypointense foci on GRE/SWI, 1(5):82, mass, 1(6):56, 57
84 splenium lesion, 1(6):59
multiple hypo intense foci on T2, 1(5):80 cystic mass, solitary, 1(5):16, 17
parenchymal calcifications, 1(5):35, 39, 41, 42 infratentorial midline cyst, 1(7):15, 17
parenchymal lesions midbrain lesion, 1(6):100, 102
multiple hyperdense, 1(5):50, 52 multiple brain hyper intensities (T2/FLAIR),
multiple hypodense, 1(5):60, 62 1(5):64,67
solitary hyperdense, 1(5):44, 46 parenchymal lesions
solitary hypodense, 1(5):56 CSF-like, 1(5):22, 23
Tl hyperintense, 1(5):102, 104 Tl hypointense, T2 hyperintense, 1(5):90, 91
Tl hypointense, T2 hyperintense, 1(5):91, 92 posterior fossa lesion, cystic-appearing, 1(7):35,
Tl/T2 hyperintense, 1(5):87, 89 39
Tl/T2 isointense, 1(5):94-95,96 suprasellar mass
periventricular enhancing lesions, 1(3):58, 61 cystic, 1(8):37, 39
periventricular T2/FLAIR lesions, 1(3):72, 74 Tl hypointense, 1(8):58, 59
posterior fossa neoplasms, adult, 1(7):40, 42 white matter lesions, 1(6):30, 31, 34, 39
ring-enhancing lesions, 1(5):6, 7, 12, 13 Periventricular abscess, 1(3):58, 60
sulci, focal effaced, 1(4):16, 19 Periventricular calcifications, 1(3):66-71
suprasellar mass, hyperdense, 1(8):52 Periventricular enhancing lesions, 1(3):58-61
Parietal foramina, 1(1):22, 24 Periventricular T2/FLAIR lesions, 1(3):72-75
Parietal thinning, 1(1):2, 3, 16 Petro us apex
Parkinson disease asymmetric marrow
enlarged sulci, generalized, 1(4):9 fat-like lesions, 1(5):32, 33
midbrain lesion, 1(6):101 skull normal variants, 1(1):2, 3
putamen lesions, 1(6):84 cholesterol granuloma, 1(5):32, 33
Pediatric back pain, II(I):56-59 Phenytoin, chronic use
Pedicles cerebellar atrophy, 1(7):18, 20
abnormalities, 11(3):36-37 thick skull, generalized, 1(1):8, 10
absent or hypoplastic, II(3):16, 36, 37 Pial enhancement, 1(2):16-19
congenitally short, II(3):36 Pineal cyst
stress fracture, posterior element, II(3):34 extra-axial mass
Peridural fibrosis CSF-like, 1(4):52, 53
back pain/radiculopathy, postoperative hypodense, 1(4):76, 78
acute, II(I):30, 32 interhemispheric fissure cysts, 1(4):20,21
chronic, II(I):36, 38 pineal gland mass, 1(8):6
disc contour abnormality, II(4):2, 4 pineal region mass, 1(8):2, 3
extradural lesions Pineal gland mass, 1(8):6-7
solid enhancement, II(5):16, 17 Pineal region, 1(8):2-59
T2 hyperintense, Tl isointense, II(5):36, 38 hypothalamus lesion, 1(8):48-51
Tl hypo intense, II(5):32, 34 infundibular stalk, 1(8):44-45, 46-47
normal extradural marrow signal, II(5):23, 25 intrasellar lesion, 1(8):20-21
xl
INDEX
intrasellar mass, cystic, 1(8):22-23 cystic, 1(8):37, 39
pineal + suprasellar lesions, 1(8):10-11 enhancing, 1(8):42
pineal gland mass, 1(8):6-7 general, 1(8):24, 25
pineal region mass, 1(8):2-5 hyperdense, 1(8):52
pituitary gland, enlarged, 1(8):18-19 pediatric, 1(8):31, 34
quadrigeminal cistern mass, 1(8):8-9 T1 hyperintense, 1(8):56
sella/pituitary normal variants, 1(8):12-13 T1 hypo intense, 1(8):58
sellar/juxtasellar calcification, 1(8):14-17 T1 isointense, 1(8):54
suprasellar masses Pituitary metastases
calcified, 1(8):40-41 intrasellar lesion, 1(8):20
cystic, 1(8):36-39 pituitary gland enlargement, 1(8):18
enhancing, 1(8):42-43 Tl isointense suprasellar mass, 1(8):54
general, 1(8):24-29 Pituitary microadenoma
hyperdense, 1(8):52-53 dural tail sign, 1(2):20, 21
pediatric, 1(8):30-35 intrasellar lesion, 1(8):20
T1 hyperintense, 1(8):56-57 pituitary gland enlargement, 1(8):18
T1 hypointense, 1(8):58-59 sellar/juxtasellar calcification, 1(8):15, 17
T1 isointense, 1(8):54-55 third ventricle mass, general, 1(3):23, 25
Pineoblastoma Pituitary stalk
in children over 1 year, 1(5):113, 116 anomalies
in newborn/infant, 1(5):107, 111 absent/thin infundibular stalk, 1(8):44, 45
pineal gland mass, 1(8):6, 7 suprasellar mass, pediatric, 1(8):31, 33
Pineocytoma, 1(8):2, 4, 6, 7 transection, 1(8):44, 46
Pituicytoma PKAN (pantothenate kinase associated
hypothalamus lesion, 1(8):49, 51 neurodegeneration),I(6):81
pituitary gland enlargement, 1(8):18 Plagiocephaly, 1(6):3, 6
suprasellar mass, 1(8):25, 28, 54, 55 Plasmacytoma, II(5):32
thick infundibular stalk, 1(8):46, 47 abnormal extradural marrow signal, II(5):26, 28
Pituitary abscess, 1(8):25 cavernous sinus lesions, bilateral, 1(10):19, 21
Pituitary apoplexy craniovertebral junction abnormalities, 11(2):4,
intrasellar mass, cystic, 1(8):22 8,10
suprasellar mass dural-based mass, 1(2):5
cystic, 1(8):37, 39 epidural mass, 1(4):5, 6, II(5):2, 6
T1 hyperintense, 1(8):56 extradural lesions
T1 hypointense, 1(8):58 multiple, II(5): 12
Pituitary bright spot, 1(8):12 solid enhancement, II(5):16, 18
Pituitary gland. See also Pineal region T2 hyperintense, T1 isointense, II(5):37
"bright," 1(8):12, 13 lytic skull lesion, 1(1):18, 20
ectopic, 1(8):49 neural foramen, enlarged, 11(3):16
enlarged, 1(8):18-19 skull base, 1(4):33, 36
normal variants, 1(8):12-13 thickened bony trabeculae, II(3):46, 47
Pituitary hyperplasia vertebral body, flattened, II(3):6
intrasellar lesion, 1(8):20 Platyspondyly, diffuse, II(1):16-17
physiologic, 1(8):12, 30, 32 Plexitis, choroid plexus, 1(3):6, 7
pituitary gland enlargement, 1(8):18, 19 PNET (primitive neuroectodermal tumor). See also
suprasellar mass, 1(8):54 Medulloblastoma, PNET-MB
Pituitary macroadenoma intradural/extramedullary lesions, II(6):15
cavernous sinus mass or lesions, 1(10):14, 15, 18, midbrain lesion, 1(6):100
19 supratentorial, pediatric, 1(5):106,113,116
giant invasive, 1(4):43 Pneumatocyst, vertebral, II(3):56
intrasellar lesion, 1(8):20 Pneumocephalus
Meckel cave lesion, 1(10):23 extra-axial mass or lesions
mimics, 1(8):18, 19 hypodense, 1(4):76, 78
pituitary gland enlargement, 1(8):18, 19 T2 hypointense, 1(4):68, 70
prepontine cistern mass, 1(4):32, 35 multiple hypointense foci on GRE/SWI, 1(5):82,
suprasellar mass 84
calcified, 1(8):40 Pneumonectomy, II(l):10
xli
INDEX
Poliomyelitis, 11(1):10 cauda equina syndrome, 11(6):36
Polycythemia cervical abnormality, chronic post-traumatic,
dural sinus, hyperdense, 1(10):26-27, 28 11(1):2
dural sinus lesion, 1(10):3, 7 kyphoscoliosis, child, 11(1):14
hyperattenuating artery, 1(9):8, 9 lumbar bony trauma, 11(1):8
Polymicrogyria. See Pachygyria-polymicrogyria T1 hypointense disc, 11(4):12
Polymyositis, II(5):20 vertebral endplate signal abnormality, 11(4):16
Polyneuropathy, chronic inflammatory Postoperative state
demyelinating. See Chronic inflammatory corpus callosum holes, 1(6):52
demyelinating polyneuropathy (ClOP) epidural fluid, effusion, fat, or air, 1(4):76, 78
Pontine lesion, 1(7):6-9 normal change
Pontocerebellar hypoplasia, 1(7):4 cervical abnormality, chronic post-traumatic,
Porencephalic cyst 11(1):2,3
CSF-like parenchymal lesions, 1(5):22, 24 cervical bony fusion, 11(3):4,5
irregular large ventricles, 1(3):54, 56 congenital vertebral anomalies, 11(3):2,3
solitary cystic mass, 1(5):16, 18 extradural lesion, Tl hypo intense, 11(5):32
Post-radiation changes. See Radiation injuries and intradural/extramedullary lesions, 11(6):32
necrosis; Radiation therapy lower cervical bony abnormality, post-
Post-surgical state. See Postoperative state traumatic, 11(1):4
Post-transplant lymphoproliferative disorder, lumbar bony trauma, 11(1):8
1(5):80 soft tissue calcification, paraspinal, 11(5):20
Post-traumatic deformity T2 hyperintense disc, 11(4):14, 15
cervical bony fusion, 11(3):4 Prematurity
congenital vertebral anomalies, 11(3):2 small brainstem, 1(7):4
dysmorphic vertebral body, 11(3):10 thin corpus callosum, 1(6):40, 43
Post-traumatic state, 11(4):14, 15, 16 thin cortex, 1(6):14, 16
Posterior column injury, cervical, 11(1):4,11(3):21, Prepontine cistern mass, 1(4):32-37
23 Presacral abscess, 11(1):22,23
Posterior elements, spine Prevertebral abscess, 11(1):14
enlarged, 11(3):12-15 Primitive neuroectodermal tumor. See PNET
fractures, 11(3):34-35 (primitive neuroectodermal tumor)
incomplete fusion Primordial dwarfism, 1(1):14
CI-C2 instability mimic, 11(2):12 Progeroid syndromes, 1(1):39, 43
congenital vertebral anomalies, 11(3):2 Progressive multifocalleukoencephalopathy (PML)
cranio-cervical junction acute injury, 11(2):2 confluent white matter lesions, 1(6):34
fracture mimic, 11(1):4,8 corpus callosum lesion without mass effect,
post-traumatic bony abnormality, 11(1):4 1(6):54, 55
posterior element fracture, 11(3):34, 35 corpus callosum splenium lesion, 1(6):59, 61
lumbar bony trauma (fracture mimic), 11(1):8 medulla lesion, 1(7):11, 13
Posterior fossa midbrain lesion, 1(6):101, 103
adult neoplasms, 1(7):40-43 multiple brain hyperintensities (T2/FLAIR),
cystic-appearing lesion, 1(7):34-39 1(5):71, 74
pediatric neoplasms, 1(7):44-49 pontine lesion, 1(7):6
Posterior reversible encephalopathy syndrome Progressive supranuclear palsy
(PRES),1(6):81. See also Hypertensive midbrain lesion, 1(6):101
encephalopathy, acute small brainstem, 1(7):4, 5
Postoperative complications tecta I plate lesion, 1(6):98, 99
infection Proteus syndrome, 1(6):3, 7, 11(1):10
acute back pain/radiculopathy, postoperative, Pseudo-thick cortex. See Hypomyelination
11(1):30,31, 33, 35 Pseudo-TORCH
chronic back pain/radiculopathy, microcephaly, 1(1):39, 43
postoperative, 11(1):37,41 multiple parenchymal calcifications, 1(5):41, 43
kyphoscoliosis, child, 11(1):14 periventricular calcifications, 1(3):67, 71
kyphosis, 11(1):12 Pseudoaneurysm
spinal arterial shape/configuration abnormalities,
acute back pain/radiculopathy, postoperative, 1(9):3,5
11(1):30-31, 33-35 dissecting, 1(9):6, 7
xlii
INDEX
extra-axial flow voids, 1(4):60
hyperattenuating artery, 1(9):8
configuration, 1(6):47, 50
enlarged sulci, generalized, 1(4):9, 11 =..,-
Q.
Pseudoarthrosis large ventricles, 1(3):44-45, 46 ><

T2 hyperintense disc, 11(4):14 multiple brain hyperintensities (T2/FLAIR),
T1 hypointense intervertebral disc, 11(4):12, 13 1(5):65, 69
vertebral endplate signal abnormality, 11(4):16 multiple hypointense foci on GRE/SWI, 1(5):83
Pseudo hypoparathyroidism nerve, post-procedure, 11(6):14
basal ganglia calcification, 1(6):62 parenchymal calcifications, 1(5):41, 43
dural calcification, 1(2):2 parenchymal lesions, 1(5):90
multiple parenchymal calcifications, 1(5):40 periventricular calcifications, 1(3):67, 70-71
T1 hyperintense basal ganglia, 1(6):67 periventricular T2/FLAIR lesions, 1(3):72, 74
Pseudomeningocele ring-enhancing lesions, multiple, 1(5):13, 15
epidural mass, 11(5):2,4 Radiation injuries and necrosis
extradural lesions, 11(5):14, 15,32,34 diffuse vertebral body sclerosis, 11(3):44
lumbar soft tissue mass, pediatric, 11(5):43,45 dysmorphic vertebral body, 11(3):10
paraspinal muscle abnormalities, 11(5):10, 11 myelopathy
post-traumatic intramedullary lesions, diffuse/ill-defined
enlarged neural foramen, 11(3):16, 17 enhancement, 11(7):21,23
intradural/extramedullary lesions, 11(6):29, subarachnoid space narrowing, 11(6):6
31 T2 hyperintense cord lesions, central,
Pseudoneoplasm, calcifying, 1(2):4 11(7):45,47
Pseudopseudohypoparathyroidism, 1(6):67 pontine lesion, 1(7):7
Pseudosubluxation ring-enhancing lesion, solitary, 1(5):6
C2-3, 11(2):2 Radiation therapy
pediatric kyphoscoliosis, child, 11(1):14
C1-C2 instability, 11(2):12 post-procedure changes, 11(3):10
spondylolysis, 11(3):20,21 spinal, in childhood
Pseudotumor congenital vertebral anomalies, 11(3):2
intracranial flattened vertebral body, multiple, 11(3):8
bilateral cavernous sinus lesions, 1(10):19, 21 scoliosis, 11(1):10
CPA mass, 1(4):25, 27 Radiculomyelitis, viral, 11(6):2,5
Meckel cave lesion, 1(10):23, 25 Radiculopathy
pituitary gland enlargement, 1(8):18 anterior radiculopathy syndrome, 11(6):9,II, 15
solitary dural-based mass, 1(2):5, 7 back pain, postoperative
thick dura or arachnoid, generalized, 1(2):14 acute, 11(1):30-35
unilateral cavernous sinus mass, 1(10):15, 17 chronic, 11(1):36-41
retro-odontoid, 11(2):8,9 cytomegalovirus- related
"Pulvinar sign," 1(6):96-97 cauda equina enhancement, diffuse, 11(6):3,4
Putamen lesions, 1(6):84-85 intradural/extramedullary lesions, solid
Pycnodystosis, 1(1):8 enhancement, 11(6):15, 17
Pyogenic abscess, 1(7):6 Rasmussen encephalitis, 1(5):77, 79
Rathke cleft cyst
extra-axial mass, 1(4):77, 79
Q intrasellar lesion, 1(8):20
Quadrigeminal cistern mass, 1(8):8 intrasellar mass, cystic, 1(8):22, 23
Quadrigeminal plate lesions, 1(6):98-99 sellar/juxtasellar calcification, 1(8):15
suprasellar mass
cystic, 1(8):36, 38
R general, 1(8):24, 27
Rabies, [[(6):2 hyperdense, 1(8):52, 53
Radial neuropathy, 11(1):42-43, 45 pediatric, 1(8):31, 35
Radiation and chemotherapy. See also Radiation T1 hyperintense, 1(8):56, 57
therapy T1 hypointense, 1(8):58
basal ganglia calcification, 1(6):63, 65 T1 isointense, 1(8):54, 55
cerebellar atrophy, 1(7):18, 20 Renal cell carcinoma, 11(3):38,40
confluent white matter lesions, 1(6):34, 37 Renal failure, chronic
corpus callosum, abnormal shape or FLAIRhyperintense CSF,1(4):65, 67
xliii
INDEX
>< hyperdense CSF,1(4):72 sellar/juxtasellar calcification, 1(8):14, 16
Q,j
"'C vascular calcifications, 1(9):10 suprasellar mass
C Retinoblastoma calcified, 1(8):40, 41
quadrilateral, 1(8):10, 11 cystic, 1(8):37, 39
trilateral enhancing, 1(8):42, 43
pineal gland mass, 1(8):6, 7 general, 1(8):24, 26
suprasellar mass, pediatric, 1(8):31, 35 hyperdense, 1(8):52
Retroperitoneal hematoma, 11(1):48 pediatric, 1(8):31, 34-35
Rhabdomyolysis, 11(5):10, 11 thrombosed
Rhabdomyosarcoma, 11(1):23,24 acute, 1(8):58, 59
Rheumatoid arthritis intra sellar mass, cystic, 1(8):22
CI-C2 instability, 11(2):12, 13 suprasellar mass, 1(8):56, 57
cervical abnormality, chronic post-traumatic, vascular calcifications, 1(9):10, 11
11(1):2,3 Sacral deformity, 11(1):26-29
craniovertebral junction abnormalities, 11(2):5, Sacral foraminal mass, 11(1):26
8, 9 Sacral fractures
facet abnormality, non-traumatic, 11(3):32,33 traumatic, 11(1):26,28
intervertebral disc endplate irregularity, 11(4):7, zone 3, 11(6):36, 37
8 Sacral mass, adult, 11(1):18-21
lower cervical bony abnormality, post- Sarcoidosis
traumatic, 11(1):4 cauda equina enhancement, diffuse, 11(6):3,4
odontoid deformity, 11(2):14 cauda equina syndrome, 11(6):36
pannus from, 11(2):5,7 cord lesions, dorsal, 11(7):40-41, 43
spondylolisthesis, 11(3):21 CPA-lAC mass, 1(4):25, 26
vertebral endplate signal abnormality, 11(4):16 intradural/extramedullary lesions, 11(6):14-15,
Rhombencephalosynapsis (mimics), 1(7):29, 31 17,34
Rib anomalies intramedullary lesions, 11(7):12, 13
hypoplastic or supernumerary rib, 11(3):34 intramedullary mass, 11(7):3,5
scoliosis, 11(1):10, 11 leptomeningeal enhancement, 11(6):9,11
Rickets Sarcoma
craniovertebral junction abnormalities, 11(2):4 primary CNS, pediatric, 1(5):112
multiple hypodense parenchymal lesions, scalp mass, 1(1):4
1(5):61, 63 Scalp and skull, 1(1):2-43. See also Skull base; Skull
thin skull, generalized, 1(1):14 metastases
Rosai-Dorfman disease "hair on end," 1(1):6-7
dural sinus lesion, 1(10):3 lacunar skull
dural tail sign, 1(2):20 Chiari 2, 1(1):23, 25
epidural mass, brain, 1(4):5 thin skull, generalized, 1(1):14, 15
falx lesions, 1(2):12 macrocephaly, 1(1):32-37
multiple dural-based masses, 1(2):9, 11 microcephaly, 1(1):38-42
solitary dural-based mass, 1(2):5, 7 scalp mass or lesions, 1(1):4-5, 16
Rotary subluxation, atlanto-axial sclerotic skull lesions
CI-C2, 11(2):4,12 multiple, 1(1):30-31
cranio-cervical junction acute injury, 11(2):2 solitary, 1(1):26-29
Rubella, congenital, 1(3):66, 69 skull, normal variants, 1(1):2-3
lytic skull lesion, solitary, 1(1):18, 19
multiple lucent skull lesions, 1(1):22
s thick skull, generalized, 1(1):8, 9
Saccular aneurysm thin skull, localized, 1(1):16
arterial shape/configuration abnormalities, skull lesions
1(9):2, 4 lucent, multiple, 1(1):22-25
atypical, 1(9):6, 7 lytic, solitary, 1(1):18-21
cavernous sinus mass, unilateral, 1(10):14, 16 thick skull
extra-axial flow voids, 1(4):60, 61 generalized, 1(1):8-11
extra-axial lesions, 1(4):68, 71 localized, 1(1):12-13
intrasellar lesion, 1(8):20 thin skull
parenchymal calcification, 1(5):35, 39 generalized,I(I):14-15
localized,I(I):16-17
xliv
INDEX
Scheuermann disease
congenital vertebral anomalies, II(3):2
intradural/extramedullary
multiple, II(6):20
lesions
=
C.
I'D
dysmorphic vertebral body, II(3):10, 11 solid enhancement, II(6):14, 15 ><
intervertebral disc end plate irregularity, II(4):6, T2 hyperintense, T1 isointense, II(6):34
8 intradural lesion, serpentine, II(6):18
kyphoscoliosis, child, 11(1):14,IS intramedullary mass, II(7):3, 5
kyphosis, 11(1):12,II(3):8, 9 intraparenchymal, 1(5):29, 31
lumbar bony trauma, II(1):8 jugular foramen
pediatric back pain, II(1):S6, S8 CPA mass, adult, 1(4):25, 27
platyspondyly, diffuse, II(l): 16, 17 intramural CPA cystic mass, 1(4):29, 31
thoracic bony trauma, 1T(1):6,7 posterior fossa, adult, 1(7):41, 42
vertebral body fracture, II(3):29 leptomeningeal enhancement, II(6):8, 10
vertebral endplate contour abnormality, II(4):1O, lower extremity pain, II(1):49, 51
11 melanotic, 11(6):26,27
Schistosomiasis, II(7):7 paraspinal muscle abnormalities, II(5):10
Schizencephaly pedicle abnormality, II(3):36, 37
asymmetric cerebral hemispheres, 1(6):3, 7 posterior fossa, pediatric, 1(7):44, 47
epilepsy, 1(5):118, 121 prepontine cistern mass, 1(4):33, 37
irregular large ventricles, 1(3):55, 57 soft tissue calcification, paraspinal, II(5):20
Schmorl node trigeminal, intracranial, [(7):40, 1(10):22, 23
adult back pain, 1T(1):53 ventra[/Iateral paraspinal mass, 11(5):8,9
aggressive bony lesion, II(3):25, 27 vertebral body scalloping or widened canal,
dysmorphic vertebral body, II(3):10 11(3):18,19
extradural lesions, no enhancement, 11(5):14 vestibular
focal T1 hypointense signal, vertebral body, CPA-lAC mass, [(4):24, 25
II(3):56 posterior fossa neoplasms, adult, 1(7):40, 41
intervertebral disc endplate irregularity, II(4):6 with arachnoid cyst, CPA cystic mass, [(4):29,
lumbar bony trauma, II(1):8, 9 31
thoracic bony trauma, II(1):6 with intramural CPA cysts, 1(4):28, 30
vertebral body fracture, II(3):28, 31 Scleroderma, linear (coup de Sabre), 1(1):16
vertebral endplate contour abnormality, II(4):1O Scoliosis, 11(1):10-11
vertebral endplate signal abnormality, II(4):16, cervical abnormality, chronic post-traumatic,
17 II(1):2
Schwan noma congenital, II(l):lO, 11
cavernous sinus mass, unilateral, 1(10):14, 16 congenital vertebral anomalies, II(3):2
in children over 1 year, 1(5):113 kyphoscoliosis, child, II(1):14
craniovertebral junction abnormalities, II(2):4, 9 kyphosis, II(l): 12
cystic lumbar bony trauma, II(1):8
cystic-appearing posterior fossa lesion, myelopathy, 1T(7):48
1(7):35,38 pediatric back pain, II(1):56, 58
extra-axial mass, CSF-Iike, 1(4):52 thoracic bony trauma, II(1):6, 7
intradural/extramedullary lesions, II(6):22, vertebral body fracture, II(3):28, 31
23,28,30 degenerative, II(1):10, 37, 41
solitary cystic mass, 1(5):17, 21 dysmorphic vertebral body, II(3):10
dural tail sign, 1(2):20, 21 idiopathic, II(l):lO
enlarged neural foramen, II(3):16 kyphoscoliosis, child, II(1):14
epidural mass, II(5):3, 5 pediatric back pain, II(1):56, 57
extra-axial mass or lesions, 1(4):68, 70, 76 lower cervical bony abnormality, post-
extradural lesions, II(5):16, 18, 36-37 traumatic, II(1):4
extradural marrow signal, normal, II(5):23 lumbar soft tissue mass, pediatric, II(5):42, 44
facial nerve, CPA-lAC, 1(4):25,27 neuromuscular, 11(1):10,11
cystic mass, 1(4):29, 31 kyphoscoliosis, child, II(1):14, 15
posterior fossa, adult, 1(7):41 kyphosis, II(l): 12
foramen magnum mass, 1(4):42, 44 pediatric back pain, 11(1):56,57
foraminal, II(4):3 traumatic, 11(1):10,11
hypoglossal nerve, 1(7):41 vertebral body/posterior element, enlarged,
11(3):12,14
xlv
INDEX
Sebaceous cyst, 1(1):4, 5 normal extradural marrow signal, 11(5):23
Sella turcica. See also Pineal region soft tissue calcification, paraspinal, 11(5):20
cystic intrasellar mass, 1(8):22-23 thoracic bony trauma, 11(1):6
empty sella Skull. See Scalp and skull
cystic intrasellar mass, 1(8):22 Skull base
intrasellar lesion, 1(8):20 chondrosarcoma, 1(4):33, 36, 43
normal variant, 1(8):12, 13 metastases, 1(10):18, 20, 22, 24
intrasellar lesion, 1(8):20-21 plasmacytoma, 1(4):33, 36
J-shaped, 1(8):12 Skull fracture, depressed, 1(10):3, 6
normal variants, 1(8):12-13 Skull metastases. See also Meningeal metastases
small, 1(8):12, 13 "hair on end," 1(1):6
Sellar/juxta sellar calcification, 1(8):14-17 lytic skull lesion, solitary, 1(1):18, 20
Sensory neuropathies, hereditary multiple lucent skull lesions, 1(1):22, 24
cauda equina enhancement, diffuse, 11(6):2,5 scalp mass, 1(1):4, 5
intradural lesion, serpentine, 11(6):18, 19 sclerotic skull lesions, 1(1):26 , 27, 30
Septic emboli, 1(5):71, 73, 83 Solitary fibrous tumor, meningeal, 1(2):12
Septic facet joint arthritis, 11(3):32, 33 Solvent inhalation, 1(6):93
Septo-optic dysplasia Spherocytosis, hereditary, 1(1):6
absent/thin infundibular stalk, 1(8):44, 45 Spinal cord. See also Spinal cord terms below; specific
epilepsy, 1(5):118, 121 disorders, spinal cord
Septum pellucidum, thick, 1(3):16-17 adhesions, 11(6):29, 31
Shear injury, 11(1):4 cavernous malformation. See Cavernous
Sickle cell disease malformation - spinal cord
adult back pain, 11(1):53,55 injuries, 11(2):2,11(7):10, 11
"hair on end," 1(1):6,76 primary neoplasms, 11(7):6
intervertebral disc endplate irregularity, 11(4):7, small/atrophic, 11(7):10-11
9 T2 hyperintense lesions
lumbar bony trauma, 11(1):8,9 central, 11(7):44-47
multiple brain hyperintensities (T2/FLAIR), dorsal, 11(7):40-43
1(5):70,72 ventral, 11(7):38-39
platyspondyly, diffuse, 11(1):16 tethered
thick skull, generalized, 1(1):8, 11 cauda equina syndrome, 11(6):36
thoracic bony trauma, 11(1):6 conus abnormality, 11(7):6,8
vertebral anomalies, congenital, 11(3):2 kyphoscoliosis, child, 11(1):14
vertebral body lower extremity pain, 11(1):49
diffuse sclerosis, 11(3):44,45 scoliosis, 11(1):10
diffuse T1 hypointense signal, 11(3):52-53, 55 Spinal cord abscess
dysmorphic, 11(3):10, 11 acute back pain/radiculopathy, postoperative,
flattened, 11(3):8,9 11(1):31,35
fracture, 11(3):29 intramedullary lesions
vertebral endplate contour abnormality, 11(4):10 diffuse/ill-defined enhancement, 11(7):20,23
Siderosis ring/peripheral enhancement, 11(7):24,25
CNS, 1(8):20, 21 T2 hyperintense, T1 isointense, 11(7):31,33
superficial T1 hypointense, 11(7):28,29
effaced sulci, focal, 1(4):17 myelopathy, 11(7):49
hyperdense CSF,1(4):72 Spinal cord astrocytoma
intradural/extramedullary lesions, 11(6):32, conus abnormality, 11(7):6,8
33 intramedullary lesions
Sinus pericranii no enhancement, 11(7):18, 19
enlarged cortical veins, 1(10):8, 9 ring/peripheral enhancement, 11(7):24
lytic skull lesion, solitary, 1(1):19, 21 solid enhancement, 11(7):14, 16
scalp mass, 1(1):4 T1 hyperintense, 11(7):34, 36
Skeletal hyperostosis, diffuse idiopathic (DISH) T2 hyperintense, T1 isointense, 11(7):30,32
cervical bony fusion, 11(3):4,5 T1 hypointense, 11(7):28, 29
chronic post-traumatic cervical abnormality, intramedullary mass, 11(7):2,4
11(1):2 myelopathy, 11(7):48,50
congenital vertebral anomalies, 11(3):2 subarachnoid space narrowing, 11(6):6,7
xlvi
INDEX
T2 hyperintense cord lesions, central, 11(7):45,
47
cervical
chronic post-traumatic abnormality, 1I(1):2-3
-=
Q.
Spinal cord herniation

intradural/extramedullary lesions, Tl
lower, post-traumatic bony abnormality,
11(1):4-5
"><
hypointense, 11(6):28-29, 31 kyphoscoliosis, child, 1I(1):14-15
intradural lesion, serpentine, 11(6):18 kyphosis, 11(1):12-13
myelopathy, 11(7):49 lower extremity pain, 1I(1):48-51
small/atrophic spinal cord, 11(7):10, 11 lumbar bony trauma, II(I):8-9
T2 hyperintense cord lesions, ventral, 11(7):38, platyspondyly, diffuse, II(I):16-17
39 sacral deformity, 1I(1):26-29
Spinal cord infarction sacral mass, adult, II(I):18-21
acute back pain/radiculopathy, postoperative, sacrococcygeal mass, pediatric, 11(1):22-25
11(1):31, 35 scoliosis, II(I):IO-11
chronic, small/atrophic spinal cord, 11(7):10, 11 thoracic bony trauma, 11(1):6-7
conus abnormality, 11(7):7, 8 upper extremity pain or weakness, acute,
intramedullary lesions II(I):42-47
no enhancement, 11(7):18, 19 Spinal dysgenesis, segmental, 11(7):6, 10
solid enhancement, 11(7):15, 17 Spinal dysraphism, II(3):2
T2 hyperintense, T1 isointense, 11(7):31, 33 Spinal fractures, II(I):56
intramedullary mass, 1I(7):3, 5 Spinal injuries, penetrating, 11(6):36
myelopathy, 1I(7):49, 53 Spinal instability
T2 hyperintense cord lesions, central, 1I(7):44, adult back pain, 11(1):52-53
46 chronic back pain/radiculopathy, postoperative,
T2 hyperintense cord lesions, ventral, 11(7):38, 11(1):36
39 post-treatment, II(3):20-21, 22-23
Spinal cord metastases Spinal muscle injury
conus abnormality, 11(7):7, 9 adult back pain, II(I):52, 54
intramedullary lesions traumatic
diffuse/ill-defined enhancement, 11(7):20, 23 lumbar soft tissue mass, pediatric, II(5):42, 44
multiple, 1I(7):12 paraspinal muscle abnormalities, 11(5):10
ring/peripheral enhancement, 11(7):24, 25 pediatric back pain, 11(1):56
solid enhancement, 1I(7):15, 17 soft tissue calcification, paraspinal, 11(5):20
T1 hyperintense, 11(7):34, 36 Spinal stenosis
T2 hyperintense, T1 isointense, 11(7):31, 33 acquired
intramedullary mass, 11(7):3, 5 adult back pain, II(I):52, 54
myelopathy, 11(7):49 cervical, II(7):48, 51
subarachnoid space narrowing, 11(6):6 subarachnoid space narrowing, 11(6):6
Spinal cord myelitis acquired, lumbar
acute back pain/radiculopathy, postoperative, cauda equina syndrome, 11(6):36
11(1):31, 35 extradural lesions, 1I(5):14
intramedullary lesions lower extremity pain, 11(1):48, SO
diffuse/ill-defined enhancement, 11(7):20, 23 central, 11(6):18, 19
ring/peripheral enhancement, 1I(7):24, 25 compression, 1I(6):3, 5
T2 hyperintense, T1 isointense, 11(7):31, 33 congenital
T1 hypointense, 11(7):28, 29 lower extremity pain, 1I(1):48, SO
myelopathy, 11(7):49 myelopathy, 11(7):48, 52
Spinal cord syndrome, central pediatric back pain, 1I(1):56, 58
myelopathy, 11(7):48, SO subarachnoid space narrowing, 11(6):6
T2 hyperintense cord lesions, central, 1I(7):4S, foraminal, lumbar, 11(1):48, SO
47 Spinocerebellar ataxia, 1(7):4, II(7): 10
Spinal disorders, trans-spatial, 11(1):2-59 Spondylitis, ankylosing. See Ankylosing spondylitis
back pain Spondyloarthropathy
adult, 11(1):52-55 hemodialysis
pediatric, 11(1):56-59 aggressive bony lesion, 11(3):25, 27
back pain/radiculopathy, postoperative soft tissue calcification, paraspinal, 11(5):20
acute, 11(1):30-35 vertebral endplate signal abnormality,
chronic, 1I(1):36-41 11(4):16, 17
INDEX
><
QJ
hemodialysis-related, 11(4):7, 9 Striatonigral degeneration, 1(7):4, 5
"C seronegative Sturge-Weber syndrome
-
C C1-C2 instability, 11(2):12
cervical bony fusion, 11(3):4,5
asymmetric cerebral hemispheres, 1(6):3, 6
choroid plexus lesions, 1(3):6, 7
congenital vertebral anomalies, 11(3):2,3 enlarged deep veins, 1(10):10, 12
craniovertebral junction abnormalities, ependymal enhancement, 1(3):40
11(2):4 epilepsy, 1(5):119, 123
kyphosis, 11(1):12 multiple parenchymal calcifications, 1(5):41, 42
odontoid deformity, 11(2):14 pial enhancement, 1(2):16, 18
post-traumatic lower cervical bony sulcal/Cisternal enhancement, 1(4):54, 57
abnormality, 11(1):4 Subacute combined degeneration, 1I(7):40, 42
soft tissue calcification, paraspinal, 11(5):20, Subarachnoid cisterns. See Extra-axial spaces and
21 subarachnoid cisterns
T2 hyperintense disc, 11(4):14 Subarachnoid hemorrhage
Spondyloepiphyseal dysplasia aneurysmal
C1-C2 instability, 11(2):12 effaced sulci, generalized, 1(4):12, 14
congenital vertebral anomalies, 11(3):2 hyperdense CSF,1(4):72
flattened vertebral body, multiple, 11(3):8,9 sulcal/cisternal enhancement, 1(4):55
intervertebral disc endplate irregularity, 11(4):7, FLAIRhyperintense CSF,1(4):64, 65
9 intradural/extramedullary lesions, 11(6):12, 13,
myelopathy, 11(7):48, 53 26
odontoid deformity, 11(2):14 large ventricles, 1(3):44, 46
platyspondyly, diffuse, 11(1):16, 17 nonaneurysmal perimesencephalic, 1(4):72, 73
vertebral endplate contour abnormality, 11(4):10, Tl hyperintense CSF,1(4):62, 63
11 traumatic, 1(4):72
Spondylolisthesis, 11(3):20-23 Subarachnoid space narrowing, 11(6):6-7
cauda equina syndrome, 11(6):36, 37 Subarachnoid spaces, enlarged
dysplastic, 11(3):20, 21-22 benign, 1(4):9, 11
lower extremity pain, 11(1):48, 50 cistern and subarachnoid space normal variants,
myelopathy, 11(7):48 1(4):2, 3
post-laminectomy, 11(1):36, 39 extra-axial fluid collection, CSF-Iike, 1(4):50
traumatic, 11(6):36 macrocephaly, 1(1):32, 35
Spondylolysis Subdural abscess, 11(1):30, 11(7):48, 49
adult back pain, 11(1):52, 54 Subdural effusion, 1(4):50
enlarged vertebral body/posterior element, Subdural hematoma
11(3):12, 14 acute
lower extremity pain, 11(1):48, 50 falx lesions, 1(2):12
lumbar bony trauma, 11(1):8 hyperdense dural sinus (mimic), 1(10):27, 29
pediatric back pain, II(1):56, 58 hyperdense extra-axial mass, 1(4):74
posterior element fracture, 11(3):34, 35 acute back pain/radiculopathy, postoperative,
spondylolisthesis, 11(3):20, 22 TI(1):30-31,43
Spondylotic myelopathy, 11(7):38, 39 chronic
Sprengel deformity, 11(1):10 calcified, 1(1):9, 11, 12, 13
Squamous bones, 1(1):16 dural calcification, 1(2):2, 3
Squamous cell carcinoma, 1(1):4 extra-axial fluid collection, CSF-Iike, 1(4):50,
Status epilepticus 51
corpus callosum splenium lesion, 1(6):58, 60 hypodense extra-axial masses, 1(4):76, 77
cortical enhancement, 1(6):28, 29 macrocephaly, 1(1):32, 35
cortical hyperintensity Tl/FLAIR, 1(6):24, 26 multiple dural-based masses, 1(2):8, 10
effaced sulci, generalized, 1(4):13, 15 thick dura or arachnoid, generalized, 1(2):14,
epilepsy, 1(5):119, 123 15
"pulvinar sign," 1(6):96 effaced sulci, focal, 1(4):16
restricted diffusion, 1(5):99, 101 intradural/extramedullary lesions, T1
Steroids, 1(4):9, 11(3):6 hyperintense, TI(6):26, 27
Streak artifact, 1(4):72, 73 lower extremity pain, 1I(1):49, 51
Stress fracture, sacral, 11(1):18, 19 mixed, 1(4):68, 71
Stress reactions, 11(3):36 myelopathy, 11(7):48, 51
subacute, 1(4):12, 14
INDEX
Subdural hygroma, 1(4):50 Surgical defects
Subependymallesions, 1(3):8-11 asymmetric lateral ventricles, 1(3):50, 52
Subependymal veins (mimic), 1(3):59 calvarial, 1(1):18, 22, 24
Subependymoma irregular large ventricles, 1(3):54, 55
"bubbly-appearing" intraventricular mass, Susac syndrome
1(3):36,38 corpus callosum holes, 1(6):52, 53
cisterna magna mass, 1(4):39,41 corpus callosum lesion without mass effect,
foramen magnum mass, 1(4):42, 45 1(6):54, 55
foramen of Monro mass, 1(3):18, 21 multiple brain hyperintensities (T2/FLAIR),
fourth ventricle mass, 1(3):32, 34 1(5):71, 75
intraventricular calcifications, 1(3):63, 65 multiple enhancing lesions, 1(5):3, 5
lateral ventricle mass, 1(3): 12, 15 parenchymal lesions, 1(5):90, 92
posterior fossa neoplasms, adult, 1(7):41, 42 periventricular enhancing lesions, 1(3):58, 61
Subgaleal hematoma, 1(1):4 periventricular T2/FLAIR lesions, 1(3):73, 75
Sulcal/cisternal enhancement, 1(4):54-57 thin corpus callosum, 1(6):41, 44
Sulci Sutures, accessory, 1(1):2
effaced, focal, 1(4):16-19 Synovial cyst
enlarged, generalized, 1(4):8-11 craniovertebral junction soft tissue
Suprapineal recess, dilated, 1(3):26 abnormalities, 11(2):9
Suprascapular nerve entrapment, 11(1):43, 46 epidural mass, 11(5):2, 4
Suprasellar mass extradural lesions, 11(5):36, 38
calcified, 1(8):40-41 facet joint
cystic, 1(8):36-39 extradural lesions, no enhancement, 11(5):14
enhancing, 1(8):42-43 lower extremity pain, I1(1):49, 51
general, 1(8):24-29 non-traumatic facet abnormality, 11(3):32
pediatric, 1(8):30-35 normal extradural marrow signal, 11(5):22, 24
Supratentorial brain parenchyma, 1(6):2-103 TI hypointense extradural lesion, 11(5):32, 34
asymmetric cerebral hemispheres, 1(6):2-7 Syphilis, acquired, 1(1):23
basal ganglia Syringobulbia
bilateral lesions, 1(6):80-83 cystic-appearing posterior fossa lesion, 1(7):35,
calcification, 1(6):62-65 37
TI hyperintense, 1(6):66-69 large brainstem, 1(7):2
T2 hyperintense, 1(6):70-73 medulla lesion, 1(7):11, 13
bithalamic lesions, 1(6):92-95 Syringomyelia
corpus callosum acute upper extremity pain or weakness,
abnormal shape or configuration, 1(6):46-51 11(1):42, 45
holes in, 1(6):52-53 conus abnormality, 11(7):6, 8
lesion without mass effect, 1(6):54-55 craniovertebral junction abnormalities, I1(2):4, 9
masses, 1(6):56-57 foramen magnum mass, 1(4):43, 45
splenium lesion, 1(6):58-61 intramedullary mass or lesions, I1(7):3, 18, 28
thin, 1(6):40-45 kyphoscoliosis, child, 11(1):14
cortical enhancement, 1(6):28-29 myelopathy, 11(7):48, 50
cortical hyperintensity TI/FLAIR, 1(6):24-27 pediatric back pain, 11(1):56, 58
focal cortical mass, 1(6):20-23 subarachnoid space narrowing, 11(6):6
globus pallidus lesions, 1(6):86-89 T2 hyperintense cord lesions, central, 11(7):44,
midbrain lesion, 1(6):100-103 45
perivascular space enhancing lesions, 1(6):76-79 Syrinx
perivascular spaces, enlarged, 1(6):74-75 collapsed, 11(7):10, 11
"pulvinar sign," 1(6):96-97 post-traumatic, I1(7):48, 51
putamen lesions, 1(6):84-85 Systemic lupus erythematosus
tecta I (quadrigeminal plate) lesion, 1(6):98-99 basal ganglia, T2 hyperintense, 1(6):70, 72
thick cortex, 1(6):8-13 corpus callosum splenium lesion, 1(6):59
thin cortex, 1(6):14-19 fusiform arterial enlargement, 1(9):6
unilateral thalamic lesion, 1(6):90-91 multiple hypodense parenchymal lesions,
white matter lesions (5):61, 63
confluent, 1(6):34-39
solitary, 1(6):30-33
xlix
INDEX
><
QJ T compression fractures
"'C Taylor cortical dysplasia, 1(5):118, 122,1(6):8, 10 anterior, 11(1):6,12, 13, 11(3):28
C
Tectal plate lesions, 1(6):98-99 lateral, 11(1):6,10, 14, 11(3):28
Telangiectasia disc herniation, 11(5):22,11(7):48
ataxia, 1(7):19 distraction fracture, low, 11(1):6,11(3):28,30
capillary Thoracolumbar junction fracture-dislocation
enlarged deep veins, 1(10):11, 13 11(1):6,7 '
parenchymal lesions, 1(5):94, 96 Thrombocolumbar fracture, burst, 11(1):14
pontine lesion, 1(7):6 Thrombolysis complications, 1(5):51, 55
radiation-induced, 1(5):83, 85 Thrombophlebitis, 1(10):3, 7
Temporal bone, squamous, 1(1):16 Thrombosis. See also Cerebral venous thrombosis
deep ,
Tendinitis. See Calcific tendinitis, longus coli
Teratoid-rhabdoid tumor, atypical cortical veins
in children over 1 year, 1(5):113, 117 effaced sulci, focal, 1(4):17, 19
fourth ventricle mass, 1(3):33, 35 hyperdense extra-axial mass, 1(4):74
in newborn/infant, 1(5):107, 110 multiple brain hyperintensities (T2/FLAIR),
posterior fossa lesion, cystic-appearing, 1(7):35, 1(5):70, 72
39 deep venous, 1(5):70, 72
posterior fossa neoplasm, pediatric, 1(7):45, 48 dural sinus
vermis mass, 1(7):29, 31 effaced sulci, generalized, 1(4):12-13, 15
Teratoma extra-axial flow voids, 1(4):60
fat in sulci/cisterns/ventricles, 1(4):58, 59 hyperdense extra-axial mass, 1(4):74, 75
lateral ventricle mass, 1(3):13, 15 microangiopathies, 1(5):51, 55, 102
macrocephaly, 1(1):32, 35 Thyroid carcinoma, 11(3):38,39
parenchyma, fat-like lesions, 1(5):32, 33 Tonsillar ectopia, 1(7):32
pediatric Tonsillar herniation, acquired, 1(4):42, 43
in children over 1 year, 1(5):113, 116 TORCH infections. See also Pseudo-TORCH
in newborn/infant, 1(5):106, 108 ependymal/subependymallesions, 1(3):9, 11
suprasellar mass, 1(8):31, 33 intraventricular calcification (mimic), 1(3):63
pineal gland mass, 1(8):6, 7 microcephaly, 1(1):38, 40
sacrococcygeal parenchymal calcifications, 1(5):35, 39, 41, 42
normal extradural marrow signal, 11(5):23,25 periventricular calcification, 1(3):66
sacral deformity, 11(1):27, 29 periventricular T2/FLAIR lesions, 1(3):73
sacrococcygeal mass, pediatric, 11(1):22,23 Torticollis, 11(2):2
Thalamic infarct, 1(6):96, 97 Toxic exposure
Thalamic lesions basal ganglia lesions, bilateral, 1(6):80, 83
bithalamic, 1(6):92-95 bithalamic lesions, 1(6):93
unilateral, 1(6):90-91 cord lesions, ventral, 11(7):38
Thalassemia epilepsy, 1(5):118
adult back pain, 11(1):52 Toxoplasmosis
"hair on end," 1(1):6 acquired
thick skull, generalized, 1(1):9, 11 basal ganglia calcification, 1(6):62-63, 65
Thanatophoric dwarfism multiple hypointense foci on T2, 1(5):80, 81
dysmorphic vertebral body, 11(3):10 periventricular enhancing lesions, 1(3):58, 60
platyspondyly, diffuse, 11(1):16, 17 ring-enhancing lesion, solitary, 1(5):6
vertebral anomalies, congenital, 11(3):2 basal ganglia lesions, bilateral, 1(6):81
vertebral endplate contour abnormality, 11(4):10 congenital, 1(3):66, 68
Third ventricle cyst with nodule, 1(5):29, 31
body/posterior mass, 1(3):26-27 Transient metabolic derangement, 1(6):58, 60
dilated, 1(8):24, 26, 58 Transtentorial herniation, ascending, 1(8):8, 9
enlarged, 1(8):36 Transverse process fractures, 11(1):8,11(3):34,35
mass, general, 1(3):22-25 Trauma
Thoracic spine. See also Chance fracture, thoracic bilateral basal ganglia lesions, 1(6):80, 82
acute back pain/radiculopathy, postoperative, cervical abnormality, chronic post-traumatic
11(1):30,32 (mimics), 11(1):2
bony trauma, 11(1):6-7 enlarged sulci, generalized, 1(4):9, 10
microcephaly, non accidental, 1(1):38, 40
INDEX
pedicle abnormality, II(3):36 ependymal/subependymallesions, 1(3):8, 9
post-traumatic deformity epilepsy, 1(5):118, 121
cervical bony fusion, II(3):4 foramen of Monro mass, 1(3):18, 20
congenital vertebral anomalies, 1I(3):2 intraventricular calcifications, 1(3):62, 64
dysmorphic vertebral body, II(3):10 irregular large ventricles, 1(3):54, 56
post-traumatic state, II(4):14, 15, 16 macrocephaly, 1(1):32, 36
Trisomy 21, II(2):5, 6, 12 multiple brain hyperintensities (T2/FLAIR),
Tuber cinereum hamartoma [(5):71, 75
hypothalamus lesion, 1(8):49, 51 parenchymal calcifications, [(5):40-41, 42
parenchymal lesions, 1(5):95, 97 parenchymal lesions
suprasellar mass multiple hyperdense, [(5):51, 54
general, 1(8):25, 28 multiple hypodense, 1(5):61, 63
pediatric, 1(8):30, 32-33 solitary hyperdense, [(5):45, 49
Tl isointense, 1(8):54, 55 Tl hyperintense, 1(5):102-103, 105
third ventricle mass, 1(3):23, 25 Tl hypointense, T2 hyperintense, 1(5):91, 93
Tuberculoma Tl/T2 isointense, 1(5):95, 97
acquired, 1(5):7, 10 periventricular calcifications, 1(3):66, 69
conus abnormality, II(7):6 Tuberous sclerosis hemimegalencephaly, 1(6):3, 6
epidural mass, 1(4):5, 6 Tumor-associated cysts, nonneoplastic, 1(6):74, 75
intradural/extramedullary lesions, II(6):34 Tumoral calcinosis, familial, 1(2):2
intramedullary lesions, II(7):35
medulla lesion, 1(7):11, 13
multiple hypointense foci on GRE/SWI, 1(5):83 U
parenchymal lesions Ulnar neuropathy, 11(1):43,46
multiple hyperdense, 1(5):51, 54 Upper extremity pain or weakness, acute, 11(1):42-
solitary hyperdense, 1(5):45, 49 47
solitary hypodense, 1(5):57 Uropathy, obstructive, II(I):52
pontine lesion, 1(7):6
suprasellar mass, 1(8):25, 29
Tuberculosis V
basal ganglia calcification, 1(6):63 VACTERL,11(1):10,11(3):2
cavernous sinus mass, unilateral, 1(10):15 Vascular calcifications, 1(9):10-11
cerebellar mass, 1(7):23, 26 mimics, 1(6):63, 65
dural-based masses, 1(2):4, 6, 9, 11 physiologic, 1(8):14,1(9):10
dural tail sign, 1(2):20, 21 Vascular dementia, 1(4):8, 10
ependymal enhancement, 1(3):40, 43 Vascular grooves, 1(1):2
extra-axial mass, hyperdense, 1(4):74 Vascular lesions, pontine, 1(7):6, 8
lytic skull lesion, 1(1):18 Vascular malformation. See Arteriovenous
meningitis, 1(4):54, 56 malformation
multiple enhancing lesions, 1(5):2-3, 4 Vasculitis
multiple hypointense foci on T2, 1(5):80, 81 arterial shape/configuration abnormalities,
parenchymal calcifications, 1(5):34, 36, 40, 41 1(9):3,5
parenchymal lesions, 1(5):61, 62 basal ganglia, 1(6):70
perivascular space enhancing lesions, 1(6):76, 78 bithalamic lesions, 1(6):92-93
periventricular calcifications, 1(3):67, 70 corpus callosum lesion without mass effect,
prepontine cistern mass, 1(4):33, 35 1(6):54
ring-enhancing lesions, 1(5):12, 14 cortical enhancement, 1(6):28, 29
spondylolisthesis, II(3):21 cortical hyperintensity Tl/FLAIR, 1(6):24, 26
suprasellar mass ependymal enhancement, 1(3):41, 43
calcified, 1(8):40 ependymal/subependymallesions, 1(3):9, 11
hyperdense, 1(8):52, 53 fusiform arterial enlargement, 1(9):6, 7
Tuberous sclerosis complex infectious, 1(6):70, 72
basal ganglia calcification (mimic), 1(6):63, 65 medulla lesion, 1(7):10
cortex, thick, 1(6):8, 10 midbrain lesion, 1(6):101
cortical hyperintensity Tl/FLAIR, 1(6):25, 27 multiple brain hyperintensities (T2/FLAIR),
cortical mass, focal, [(6):20-21, 22 1(5):70, 72
effaced sulci, focal, [(4):17 multiple enhancing lesions, 1(5):3, 5
Ii
INDEX
><
CI.I
multiple hypointense foci on GRE/SWI, 1(5):83, large ventricles, 1(3):44-47
"'C 85 lateral ventricles
-C parenchymal lesions
multiple hypodense, 1(5):61, 63
asymmetric, 1(3):50-53
irregular, 1(3):54-57
T1 hypointense, T2 hyperintense, 1(5):91, 93 mass in, 1(3):12-15
perivascular space enhancing lesions, 1(6):76, 78 normal variant, 1(3):50, 51
periventricular enhancing lesions, 1(3):58, 61 normal variants, 1(3):2-5, 48
periventricular T2/FLAIRlesions, 1(3):72-73, 75 periventricular enhancing lesions, 1(3):58-61
pial enhancement, 1(2):16, 18 periventricular T2/FLAIRlesions, 1(3):72-75
pontine lesion, 1(7):7 septum pellucidum, thick, 1(3):16-17
Vasospasm, 1(9):3, 4 small ventricles, 1(3):48-49
Vein of Galen malformation third ventricle mass
enlarged cortical veins, 1(10):8, 9 body/posterior, 1(3):26-27
enlarged deep veins, 1(10):11 general, 1(3):22-25
extra-axial flow voids, 1(4):60 Ventriculitis
pineal region mass, 1(8):3, 5 choroid plexus, 1(3):6, 7
quadrigeminal cistern mass, 1(8):8, 9 chronic, 1(3):67, 70
Veins and venous sinuses, 1(10):2-29 ependymal enhancement, 1(3):40, 42
cavernous sinus lesions, bilateral, 1(10):18-21 ependymallsubependymallesions, 1(3):8-9, 11
cavernous sinus mass, unilateral, 1(10):14-17 FLAIRhyperintense CSF,1(4):64, 67
cortical veins, enlarged, 1(10):8-9 hyperdense CSF,1(4):72
deep veins, enlarged, 1(10):10-13 lateral ventricles, asymmetric, 1(3):50, 53
dural sinus, hyperdense, 1(10):26-29 T1 hyperintense CSF,1(4):62, 63
dural sinus lesions, 1(10):2-7 Ventriculus terminalis, !I(7):7, 9
Meckel cave lesion, 1(10):22-25 Vermian hypoplasia, congenital
normal,I(4):60 cerebellar atrophy (mimic), 1(7):19, 21
Vena cava (IVe) occlusion, !I(6):18, 19 infratentorial midline cyst, 1(7):15, 17
Venolymphatic malformations, 1(1):4 Vermis mass, 1(7):28-31
Venous anomaly, developmental. See Vertebral artery, !I(2):2, !I(3):16
Developmental venous anomaly Vertebral body, !I(3):2-57
Venous congestion, subependymal, 1(3):40 accelerated degeneration, !I(3):24-25, 26
Venous infarction, 1(6):20, 22, 81 bony lesions, aggressive, !I(3):24-27
Venous ischemia, 1(6):81, 92, 94 cervical bony fusion, !I(3):4-5
Venous lakes, 1(1):2, 22, 23 congenital anomalies, !I(3):2-3
Venous thrombosis, 1(6):92, 94. See also Cortical dysmorphic, !I(3):1O-11
veins, thrombosis enlarged
Venous varix soap bubble expansion, !I(3):38-41
enlarged cortical veins, 1(10):8 vertebral body or posterior element, !I(3):12-
extra-axial flow voids, 1(4):60 15
isolated,I(4):74 facet abnormality, non-traumatic, !I(3):32-33
Ventricles and periventricular regions, 1(3):2-75 facet synovial cyst, !I(3):32
calcifications failure of formation. See Failure of vertebral
intraventricular, 1(3):62-65 formation
periventricular, 1(3):66-71 flattened
cerebral aqueduct/periaqueductallesion, multiple, !I(3):8-9
1(3):28-31 solitary, !I(3):6-7
choroid plexus lesions, 1(3):6-7 fractures
ependymal enhancement, 1(3):40-43 posterior element, !I(3):34-35
ependymal/subependymallesions, 1(3):8-11 vertebral body, !I(3):28-31
foramen of Monro mass, 1(3):18-21 fusion, congenital
fourth ventricle enlarged vertebral body/posterior element,
masses, 1(3):32-35 !I(3):13, 14
open inferior (Blake pouch remnant), 1(3):3, facet abnormality, non-traumatic, !I(3):32, 33
5 Tl hypointense intervertebral disc, !I(4):12
"trapped," 1(3):33, 35 hypoplastic or absent pedicle, !I(3):16
intraventricular mass, "bubbly-appearing," neural foramen, enlarged, !I(3):16-17
1(3):36-39
Iii
INDEX
normal variants Vertebral segmentation failure
diffuse T1 hyperintense signal, 11(3):48,49 cervical bony fusion, 11(3):4
diffuse T1 hypointense signal, 11(3):52,53 congenital scoliosis or kyphosis, 11(1):12
facet tropism, 11(3):32 congenital vertebral anomalies, 11(3):2
focal T1 hyperintense signal, 11(3):50 dysmorphic vertebral body, 11(3):10, 11
scalloping or widened canal, 11(3):18 posterior element fracture, 11(3):34
pedicle abnormality, 11(3):36-37 vertebral body scalloping or widened canal,
physiologic wedging, 11(1):6,7, 8 11(3):18
scalloping or widened canal, 11(3):18-19 Vertebrobasilar dolichoectasia
sclerosis foramen of Monro mass, 1(3):19, 21
diffuse, 11(3):44-45 third ventricle mass (mimic), 1(3):22, 24
focal, 11(3):42-43 Vertebrobasilar insufficiency, chronic, 1(7):18
spondylolisthesis, 1T(3):20-23 Vertebroplasty
T1 hyperintense signal focal vertebral body sclerosis, 11(3):42
diffuse, 11(3):48-49 postoperative back pain/radiculopathy, 11(1):31,
focal, 11(3):50-51 35,37
T1 hypointense signal Vitamin B12 deficiency, spinal cord, 11(7):31,33, 49
diffuse, 11(3):51-55
focal, 11(3):56-57
thickened bony trabeculae, 11(3):46-47 w
tumors, 11(3):21,23 Wallerian degeneration
Vertebral body sclerosis medulla lesion, 1(7):10, 12
diffuse, 11(3):44-45 midbrain lesion, 1(6):100, 102
focal, 11(3):42-43 pontine lesion, 1(7):6
Vertebral duplication, partial small brainstem, 1(7):4
cervical bony fusion, 11(3):4 spinal cord, 11(7):41,43
congenital scoliosis or kyphosis, 11(1):10 Wedge compression fracture, 11(4):16, 17
congenital vertebral anomalies, 11(3):2 Wegener granulomatosis, brain
dysmorphic vertebral body, 11(3):10 multiple brain hyperintensities (T2/FLAIR),
extradural lesions, no enhancement, 11(5):14 1(5):76
kyphoscoliosis, child, 11(1):14 perivascular space enhancing lesions, 1(6):77, 79
Vertebral endplate contour abnormality, 11(4):10- pial enhancement, 1(2):17
11 Wernicke encephalopathy
Vertebral fractures. See also Fracture mimics bithalamic lesions, 1(6):93, 95
cervical abnormality, chronic post-traumatic, cerebral aqueduct/periaqueductallesion, 1(3):29,
11(1):2 31
craniovertebral junction abnormalities, 11(2):4-5 hypothalamus lesion, 1(8):49, 51
focal T1 hypointense signal, 11(3):56, 57 midbrain lesion, 1(6):101, 103
healing, 11(3):44 restricted diffusion, 1(5):99
pathologic West Nile encephalitis, 1(5):76, 78
acute upper extremity pain or weakness, Whipple disease, 1(7):7
11(1):42,45 White matter
C1-C2 instability, 11(2):12 confluent lesions, 1(6):34-39
cranio-cervical junction acute injury, 11(2):2 decreased volume, 1(6):46
flattened vertebral body, 11(3):6,8 disease with lactate, 1(6):59
kyphosis, 11(1):12 injury of prematurity, 1(6):40, 43
lower cervical bony abnormality, post- solitary lesions, 1(6):30-33
traumatic, 11(1):4,5 Wilson disease
lumbar bony trauma, 11(1):8,9 basal ganglia
myelopathy, 11(7):48 bilateral lesions, 1(6):81, 83
posterior element fracture, 11(3):34 T1 hyperintense, 1(6):66, 69
scoliosis, 11(1):10 T2 hyperintense, 1(6):71
thoracic bony trauma, II(1):6 bithalamic lesions, 1(6):93
vertebral body, 11(3):28,30 cerebral aqueduct/periaqueductallesion, 1(3):29,
posterior element, 11(3):34-35 31
traumatic, 11(3):8 globus pallidus lesions, 1(6):87
vertebral body, 11(3):28-31 Wormian bones, 1(1):2, 3
with epidural hematoma, 11(5):26,27
liii
INDEX
><
Q,j X
""C
Xanthoastrocytoma, pleomorphic
C
in children over 1 year, 1(5):113, 116
cortical hyperintensity Tl/FLA1R, 1(6):25, 27
cyst with nodule, 1(5):28, 30
effaced sulci, focal, 1(4):16, 19
epilepsy, 1(5):119, 123
focal cortical mass, 1(6):20, 22
infratentorial midline cyst, 1(7):15
solitary cystic mass, 1(5):17, 20
Xanthogranuloma
choroid plexus, 1(4):58, 59, 1(5):32
third ventricle mass, body/posterior, 1(3):26, 27
Z
Zellweger syndrome, 1(6):34, 38
liv

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ii

Anne G. Osborn, MD, FACR Kevin R. Moore, MD

Gregory L. Katzman, MD, MBA

Composition by Amirsys, Inc., Salt Lake City, Utah

Printed in Canada by Friesens, Altona, Manitoba, Canada

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Library of Congress Cataloging-in-Publication Data

Our EXPERTddx series is designed to help radiologists reach reliable-indeed, expert-conclusions.

Anne G. Osborn, MD, FACR

Medical Text Editing

Art Direction and Design

Thin Skull, Generalized

Multiple Lucent Skull Lesions 1·1·22

Clinically Based Differentials Lateral Ventricle Mass 1-3·12

Third Ventricle Mass, General 1·3·22

Third Ventricle Mass, Body/Posterior 1-3·26

Cerebral Aqueduct/Periaqueductal Lesion 1·3·28

Asymmetric Lateral Ventricles 1-3-50 Modality-Specific Imaging Findings

Periventricular Enhancing Lesions 1-3-58 T1 Hyperintense CSF 1-4-62

Anatomically Based Differentials Generic Imaging Patterns

Enlarged Sulci, Generalized 1-4-8 Ring-Enhancing Lesion, Multiple 1-5-12

Effaced Sulci, Focal 1-4-16 CSF-like Parenchymal Lesion(s) 1-5-22

Interhemispheric Fissure Cysts 1-4-20 Cyst with Nodule 1-5-28

Cystic CPA Mass 1-4-28

Midbrain Lesion 1-6-100

Supratentorial Brain Parenchyma

Tl Isointense Suprasellar Mass 1-8-54

Posterior Fossa Neoplasm, Pediatric 1-7-44 Arteries

Anatomically Based Differentials

Pineal + Suprasellar Lesions 1-8-10

SeliarIJuxtaseliar Calcification 1-8-14

lntrasellar Lesion 1-8-20 Enlarged Cortical Veins 1-10-8

Cystic Intrasellar Mass 1-8-22 Enlarged Deep (Medullary/Ependymal) Veins 1-10-10

Suprasellar Mass, General 1-8-24 Unilateral Cavernous Sinus Mass 1-10-14

Suprasellar Masses, Pediatric 1-8-30 Bilateral Cavernous Sinus Lesions 1-10-18

Suprasellar Cystic Mass 1-8-36 Meckel Cave Lesion 1-10-22

Calcified Suprasellar Mass 1-8-40

Fracture, Posterior Element 11-3-34

Pedicle Abnormality 11-3-36

Intervertebral Disc - Endplate

Generic Imaging Patterns

Generic Imaging Patterns

Extradural Lesion, No Enhancement 11-5-14 Intradural/Extramedullary Lesion, T1 11-6-26

Clinically Based Differentials

Generic Imaging Patterns

Intramedullary Lesion, Solid Enhancement 11-7-14

Intramedullary Lesion, Diffuse/Ill-defined 11-7-20

Modality-Specific Imaging Findings

Intramedullary Lesion, T1 Hyperintense 11-7-34

Generic Imaging Patterns

Clinically Based Differentials

Arachnoid Granulations, Calvarium Emissary Veins

Parietal Thinning Asymmetric Marrow, Petrous Apex

Hyperostosis Frontalis Interna Wormian Bones

• Metastases, Skull • Lipoma

Subgaleal Hematoma Lipoma

(Left) Axial NECT shows a ::l

Dermoid Cyst Basal Cell Carcinoma

Neurofibromatosis Type 1 Langerhans Cell Histiocytosis

• Iron Deficiency Anemia o Dural/scalp involvement common

• Cyanotic Congenital Heart Disease o Often known primary malignancy

Rare but Important Helpful Clues for Less Common Diagnoses

• Red marrow hyperplasia neutropenia