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Neuroradiology: Key Differential Diagnoses and Clinical Questions equips you to make efficient, accurate diagnoses and prepare for imaging exams with hundreds of high-quality, unknown cases in neuroradiology. Drs. Juan Small and Pamela Schaefer draw upon Massachusetts General Hospital’s vast case collection to help you master the skills you need for interpreting imaging of the head, neck, brain, and spine.

  • Consult this title on your favorite e-reader with intuitive search tools and adjustable font sizes. Elsevier eBooks provide instant portable access to your entire library, no matter what device you're using or where you're located.
  • Apply systematic pattern analysis techniques to distinguish similar-looking pathological entities from one another.
  • Avoid diagnostic pitfalls by recognizing significant variations in the clinical presentation of various diseases.
  • See how diagnostic ambiguities are resolved by viewing corresponding gross pathologic and histologic images.
  • Benefit from the volume and exceptional quality of Massachusetts General Hospital’s patient case load.

Subjects

Books
Savoirs
Medicine
Rabdomiosarcoma
Derecho de autor
Vértigo (desambiguación)
Flexión
Lesión
Spinal stenosis
Artery disease
Keratocyst
Parkinson's disease
Amnesia
Spinal cord
Meningitis
Synovial cyst
Alzheimer's disease
Surgical suture
Fluid attenuated inversion recovery
Neck pain
Branchial cleft cyst
Pharmaceutical formulation
Colloid cyst
Clivus
Germinoma
Platybasia
Vindesine
Dentigerous cyst
Schwannoma
Optic nerve glioma
Hemangioblastoma
Neurodegeneration
Ranula
Encephalocele
Arachnoid cyst
Craniopharyngioma
Neurofibroma
Cerebral hemorrhage
Neurofibromatosis type II
Carotid artery stenosis
Skull fracture
Tentorium cerebelli
Agenesis of the corpus callosum
Leukodystrophy
Status epilepticus
Neuroradiology
Neuroblastoma
Progressive supranuclear palsy
Liposarcoma
Otitis externa
Epidermoid cyst
Facial nerve paralysis
Neoplasm
Peritonsillar abscess
Traumatic brain injury
Astrocytoma
Meningioma
Ependymoma
Vestibular schwannoma
Pituitary adenoma
Differential diagnosis
Ear
Demyelinating disease
Melanoma
Hypertrophy
Tuberous sclerosis
Rhabdomyosarcoma
Ewing's sarcoma
Optic Nerve
Temporal lobe
Retinoblastoma
Nasal cavity
Renal cell carcinoma
Lumbar puncture
Biopsy
Parotid gland
Lesion
Trigeminal neuralgia
Osteosarcoma
Multiple myeloma
Lipoma
Sarcoidosis
Pheochromocytoma
Saturated fat
Apparatus
Amenorrhoea
Medical imaging
Holoprosencephaly
Hydrocephalus
Cyst
Back pain
Artifact
Cholesteatoma
Hypertension
Edema
Headache
Hypothyroidism
Subluxation
Cerebral cortex
Middle ear
Adrenoleukodystrophy
X-ray computed tomography
Multiple sclerosis
Cerebellum
Hearing impairment
Dementia
Grey matter
Infection
Cranial nerve
Tuberculosis
Epileptic seizure
Optic neuritis
Neurologist
Neurology
Magnetic resonance imaging
Hyperthyroidism
Cerebrospinal fluid
Chemical element
Abscess
Fractures
Flair
Hypertension artérielle
Headache (EP)
Keith Tucker
Encéphalocèle
Gray Matter
Diverticulum
Neuraxis
Rain
Lésion
Cortisone
Fossa
Flexion
Vertigo
Ring
Maladie infectieuse
Compression
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NEURORADIOLOGY
Key Differential Diagnoses
and Clinical Questions
JUAN E. SMALL, MD
Assistant Professor of Neuroradiology, Lahey Clinic, Tufts
University School of Medicine, Burlington, Massachusetts
PAMELA W. SCHAEFER, MD
Associate Director of Neuroradiology, Clinical Director of MRI, Massachusetts General
Hospital, Associate Professor of Radiology, Harvard Medical School, Boston,
Massachusetts1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
NEURORADIOLOGY: KEY DIFFERENTIAL DIAGNOSES AND CLINICAL QUESTIONS
ISBN: 978-1-4377-1721-1
Copyright © 2013 by Saunders, an imprint of Elsevier Inc.
No part of this publication may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopying, recording, or any information storage
and retrieval system, without permission in writing from the Publisher. Details on how to
seek permission, further information about the Publisher’s permissions policies and our
arrangements with organizations such as the Copyright Clearance Center and the
Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright by
the Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional
practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and
knowledge in evaluating and using any information, methods, compounds, or
experiments described herein. In using such information or methods they should be
mindful of their own safety and the safety of others, including parties for whom they have
a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to
check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered, to verify the recommended dose or
formula, the method and duration of administration, and contraindications. It is the
responsibility of practitioners, relying on their own experience and knowledge of their
patients, to make diagnoses, to determine dosages and the best treatment for each
individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or
editors, assume any liability for any injury and/or damage to persons or property as a
matter of products liability, negligence or otherwise, or from any use or operation of any
methods, products, instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication DataSmall, Juan E.
Neuroradiology : key differential diagnoses and clinical questions / Juan E. Small, Pamela
W. Schaefer.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4377-1721-1 (hardcover : alk. paper)
I. Schaefer, Pamela W. II. Title.
[DNLM: 1. Diagnostic Techniques, Neurological–Case Reports. 2. Nervous System
Diseases–radiography–Case Reports. 3. Diagnosis, Differential–Case Reports. 4.
Neuroradiography–methods–Case Reports. WL 141]
617’.075--dc23
2012016008
Executive Content Strategist: Pamela Hetherington
Content Development Specialist: Margaret Nelson
Publishing Services Manager: Patricia Tannian
Project Manager: Carrie Stetz
Design Direction: Steven StaveDedication
This book is dedicated to my beautiful wife and best friend Kirstin.
Thank you for helping me to understand the things that really matter in
life, in ways I never could before we met. Without you, my life would be
incomplete. I love you and cherish our life together .
And to my parents, Aurora and Richard. Without your support and
unconditional love, none of my achievements would have been
possible. Thank you for encouraging me to follow my heart .
Juan E. Small
This book is dedicated to my wonderful husband, Douglas Raines, and
my beautiful daughter, Sarah Raines, who always give me
unconditional love, support, and wisdom .
Pamela W. SchaeferSection Editors
HUGH D. CURTIN, MD
Chief of Radiology
Massachusetts Eye and Ear Infirmary
Professor of Radiology
Harvard Medical School
Boston, Massachusetts
R. GILBERTO GONZALEZ, MD, PhD
Director of Neuroradiology
Massachusetts General Hospital
Professor of Radiology
Harvard Medical School
Boston, Massachusetts
HILLARY R. KELLY, MD
Neuroradiologist
Massachusetts General Hospital
Professor of Radiology
Harvard Medical School
Boston, Massachusetts
STUART R. POMERANTZ, MD
Associate Director of Neuro-CT
Neuroradiologist
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
PAMELA W. SCHAEFER, MD
Associate Director of Neuroradiology
Clinical Director of MRI
Massachusetts General Hospital
Associate Professor of Radiology
Harvard Medical School
Boston, Massachusetts
JUAN E. SMALL, MD
Assistant Professor of Neuroradiology
Lahey Clinic
Tufts University School of Medicine
Burlington, Massachusetts
TINA YOUNG-POUSSAINT, MD
Neuroradiologist
Boston Children’s Hospital
Professor of Radiology
Harvard Medical School
Boston, MassachusettsContributors
JALIL AFNAN, MD
Clinical Associate
Lahey Clinic
Tufts University School of Medicine
Burlington, Massachusetts
KENNETH S. ALLISON, MD
Instructor
Harvard Medical School
Clinical Assistant
Massachusetts General Hospital
Boston, Massachusetts
NINO BOALS, MD
Neuroradiology Fellow and Research Assistant
Massachusetts General Hospital
Boston, Massachusetts
FARGOL BOOYA, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, Massachusetts
HUI J. JENNY CHEN, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, Massachusetts
ROBERT CHEN, MD
Department of Radiology
Massachusetts General Hospital
Boston, Massachusetts
SAMI ERBAY, MD
Assistant Professor
Lahey Clinic
Tufts University School of Medicine
Burlington, Massachusetts
JOHN FAGNOU, MD
Assistant Clinical Professor
Diagnostic Imaging
University of Calgary
Calgary, Alberta, Canada
REZA FORGHANI, MD, PhD
Associate Chief
Jewish General Hospital
Assistant Professor of Radiology
McGill University
Montreal, Quebec, Canada
DANIEL THOMAS GINAT, MD
Neuroradiology FellowNeuroradiology Fellow
Harvard Medical School
Boston, Massachusetts
MAI-LAN HO, MD
Resident
Scholar’s Track
Department of Radiology
Beth Israel Deaconess Medical Center
Boston, Massachusetts
LIANGGE HSU, MD
Assistant Professor
Harvard Medical School
Staff Neuroradiologist
Brigham and Women’s Hospital
Boston, Massachusetts
SCOTT EDWARD HUNTER, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, Massachusetts
JASON MICHAEL JOHNSON, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, Massachusetts
HILLARY R. KELLY, MD
Neuroradiologist
Massachusetts General Hospital
Professor of RadiologyHarvard Medical School
Boston, Massachusetts
GIRISH KORI, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, Massachusetts
MYKOL LARVIE, MD, PhD
Instructor
Harvard Medical School
Radiologist
Massachusetts General Hospital
Boston, Massachusetts
GUL MOONIS, MD
Assistant Professor
Beth Israel Deaconess Medical Center;
Staff Radiologist
Massachusetts Eye and Ear Infirmary
Boston, Massachusetts
MICHAEL T. PREECE, MD
Department of Radiology
Massachusetts General Hospital
Boston, Massachusetts
AMMAR SARWAR, MD
Radiology FellowRadiology Fellow
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston, Massachusetts
PAMELA W. SCHAEFER, MD
Associate Director of Neuroradiology
Clinical Director of MRI
Massachusetts General Hospital
Associate Professor of Radiology
Harvard Medical School
Boston, Massachusetts
SANTOSH KUMAR SELVARAJAN, MD
Neuroradiology Fellow
Brigham and Women’s Hospital
Children’s Hospital Boston
Boston, Massachusetts
JUAN E. SMALL, MD
Assistant Professor of Neuroradiology
Lahey Clinic
Tufts University School of Medicine
Burlington, Massachusetts
HENRY S. SU, MD, PhD
Neuroradiology Fellow
Massachusetts General Hospital
Clinical Fellow
Harvard Medical School
Boston, Massachusetts
KATHARINE TANSAVATDI, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, Massachusetts
NICHOLAS A. TELISCHAK, MD
Radiology Resident
Beth Israel Deaconess Medical Center
Department of Radiology
Harvard Medical School
Boston, Massachusetts
BRIAN ZIPSER, MD
Neuroradiology Fellow
Massachusetts General Hospital
Boston, MassachusettsPreface
This book is based on the premise that one of the most powerful learning
techniques for imaging interpretation is the presentation of unknown cases.
Although primarily a case book of unknowns, the style is intentionally out of the
ordinary, with several unknown cases presented together. The choice of this format
presented several challenges, but we believe that the added value is well worth the
investment. We are convinced that side-by-side comparison and contrast of
similarappearing lesions is essential for building an invaluable visual database for imaging
interpretation. It is with the hope of increasing our diagnostic specificity that the
format of the book was chosen.
Juan E. Small, MD
Pamela W. Schaefer, MDA c k n o w l e d g m e n t s
We would like to gratefully acknowledge Lora Sickora, Pamela Hetherington, Sabina
Borza, Rebecca Gaertner, Colleen McGonigal, Carrie Stetz, and all the support staff
and illustrators at Elsevier for their help throughout this endeavor. We would also
like to acknowledge our mentors, fellows, and residents at Massachusetts General
Hospital, Brigham and Women’s Hospital, and Lahey Clinic Medical Center for their
persistent hard work and dedication to neuroradiology.How to Use This Book
Although this book does not have to be read in sequence from cover to cover, it is
essential that the cases be approached as unknowns. Attempting to interpret
several unknown cases at once can be overwhelming. To gain the most from this
text, the cases within a series should be first interpreted individually. The main
challenge is to formulate a specific differential diagnosis for each individual
unknown case. We encourage readers to then compare and contrast cases within
that series. The goal is to find the often subtle imaging characteristics that are
specific or highly suggestive of individual diagnostic considerations. The text should
be read only after this process has occurred. Each series of cases is supported by
individual diagnoses, a description of findings, and a brief discussion of the various
diagnostic considerations. Additional cases illustrate other manifestations and
considerations important for the imaging interpretation of these entities. We have
tried to highlight major teaching points and hope that you benefit as much from
reading this book as we have benefited from writing and editing it.Contents
Cover Image
Title Page
Copyright
Dedication
Section Editors
Contributors
Preface
Acknowledgments
How to Use This Book
PART 1: BRAIN AND COVERINGS
CASE 1 COMPUTED TOMOGRAPHY HYPERDENSE LESIONS
Diagnosis
Summary
Differential Diagnosis
Pearls
CASE 2 T1 HYPERINTENSE LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 3 MULTIPLE SUSCEPTIBILITY ARTIFACT LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and ComplicationsCASE 4 RING-ENHANCING LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 5 LEPTOMENINGEAL ENHANCEMENT
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 6 DURAL ENHANCEMENT
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 7 LESIONS CONTAINING FAT
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 8 EXTRAAXIAL LESIONS
Diagnosis
Summary
Spectrum of DiseaseDifferential Diagnosis of an Enhancing Dural-Based Mass
Pearls
Complications
CASE 9 BILATERAL CENTRAL GRAY MATTER ABNORMALITY
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 10 TEMPORAL LOBE LESIONS
Diagnosis
Summary
Differential Diagnosis
Pearls
Signs and Complications
CASE 11 TEMPORAL LOBE CYSTIC LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 12 CEREBELLOPONTINE ANGLE CISTERNS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 13 LATERAL VENTRICULAR LESIONS
DiagnosisSummary
Spectrum Of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 14 THIRD VENTRICULAR LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 15 FOURTH VENTRICULAR LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 16 SUPRASELLAR CYSTIC LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 17 PINEAL REGION
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
PearlsSigns and complications
CASE 18 CRANIAL NERVE LESIONS
Diagnosis
Summary
Differential Diagnosis
Pearls
Signs and Complications
CASE 19 LYTIC SKULL LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 20 SKULL FRACTURE VERSUS SUTURES
Diagnosis
Summary
Spectrum of Disease
Pearls
Signs and Complications
CASE 21 CLIVUS LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 22 HYPERDENSE CEREBELLUM
Diagnosis
Summary
Spectrum of Disease
Differential DiagnosisPearls
Signs and Complications
CASE 23 T2 HYPERINTENSE PONTINE ABNORMALITIES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 24 CEREBRAL CORTICAL NEURODEGENERATION
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Future Developments
CASE 25 CEREBRAL SUBCORTICAL NEURODEGENERATION
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Future Developments
CASE 26 EPIDERMOID VERSUS ARACHNOID CYST
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 27 CYST WITH A MURAL NODULE
DiagnosisSummary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 28 ECCHORDOSIS PHYSALIPHORA VERSUS CHORDOMA
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
PART 2: SPINE
CASE 29 ATLANTOOCCIPITAL AND ATLANTOAXIAL SEPARATION
Diagnosis
Background Summary
Differential Diagnosis
Spectrum of Disease
Complications and Treatment
Pearls
CASE 30 BASILAR INVAGINATION AND PLATYBASIA
Diagnosis
Background Summary
Spectrum of Disease
Complications and Treatment
Pearls
CASE 31 ENHANCING INTRAMEDULLARY SPINAL CORD LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
PearlsSigns and Complications
CASE 32 ENHANCING INTRAMEDULLARY CONUS LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 33 SOLITARY ENHANCING INTRADURAL, EXTRAMEDULLARY LESIONS
Diagnosis
Summary
Spectrum of Disease
Pearls
Signs and Complications
Differential Diagnosis
CASE 34 MULTIPLE ENHANCING INTRADURAL, EXTRAMEDULLARY LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 35 CYSTIC INTRADURAL EXTRAMEDULLARY LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 36 NERVE ROOT ENLARGEMENT
Diagnosis
SummarySpectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 37 POSTERIOR ELEMENT LESIONS
Diagnosis
Summary
Differential Diagnosis
Pearls
Signs and Complications
CASE 38 SACRAL MASSES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 39 DISK INFECTION VERSUS INFLAMMATORY/DEGENERATIVE
CHANGES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 40 VERTEBRAL COMPRESSION FRACTURES
Diagnosis
Summary
Differential Diagnosis
Pearls
Signs and Complications
PART 3: HEAD AND NECKCASE 41 PERIAURICULAR CYSTIC LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 42 CYSTIC LATERAL NECK MASSES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 43 INFRAHYOID NECK CYSTIC LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 44 PRESTYLOID PARAPHARYNGEAL SPACE
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 45 POSTSTYLOID PARAPHARYNGEAL SPACE
Diagnosis
Summary
Spectrum of DiseaseDifferential Diagnosis
Pearls
CASE 46 FLOOR OF MOUTH
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 47 THYROGLOSSAL DUCT ABNORMALITIES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 48 ANTERIOR SKULL BASE MASSES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 49 PETROUS APEX
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 50 EXTERNAL AUDITORY CANAL
DiagnosisSummary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 51 MIDDLE EAR
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 52 LESIONS OF THE FACIAL NERVE
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 53 LYTIC/CYSTIC MANDIBULAR LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 54 JUGULAR FORAMEN LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
PearlsSigns and Complications
CASE 55 OPTIC NERVE MASS
Diagnosis
Summary
Spectrum of Disease
Pearls
Signs and Complications
CASE 56 DILATED SUPERIOR OPHTHALMIC VEIN/ASYMMETRIC CAVERNOUS
SINUS ENHANCEMENT
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 57 LACRIMAL GLAND
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 58 NASAL CAVITY LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 59 SOLITARY PAROTID MASSES
Diagnosis
SummarySpectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 60 BILATERAL PAROTID MASSES
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 61 RETROPHARYNGEAL SPACE
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
PART 4: PEDIATRIC NEURORADIOLOGY
CASE 62 INTRAVENTRICULAR POSTERIOR FOSSA TUMORS
Diagnosis
Summary
Pearls
Spectrum of Disease
Differential Diagnosis
Signs and Complications
CASE 63 PEDIATRIC CEREBELLAR TUMORS
Diagnosis
Summary
Spectrum of Disease
Differential diagnosis
PearlsSigns and Complications
CASE 64 PEDIATRIC EXTRAAXIAL POSTERIOR FOSSA TUMORS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 65 MIDLINE POSTERIOR FOSSA EXTRAAXIAL CYSTIC LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 66 OCCIPITAL CEPHALOCELE
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 67 HOLOPROSENCEPHALY
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 68 LEUKODYSTROPHIES
Diagnosis
SummarySpectrum of Disease
Examples of Different Chronic Leukoencephalopathies
Differential Diagnoses
Pearls
Signs and Complications
CASE 69 CONGENITAL ARTERIAL ANASTOMOSIS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 70 ODONTOID: ACUTE VERSUS CHRONIC
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and Complications
CASE 71 PEDIATRIC NASOFRONTAL MASS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
CASE 72 PEDIATRIC GLOBE LESIONS
Diagnosis
Summary
Spectrum of Disease
Differential Diagnosis
Pearls
Signs and ComplicationsAbbreviations
IndexPART 1
BRAIN AND
COVERINGS1
Computed Tomography
Hyperdense Lesions
HENRY SU, MD, PHD
CASE A: A 66-year-old man presenting with sudden-onset left-sided weakness. CT,
computed tomography; CTA, CT angiogram.
CASE B: A 77-year-old man with a history of lung cancer. CT, computed tomography.CASE C: A 73-year-old man with depression, falls, and difficulty completing sentences. CT,
computed tomography; CTA, CT angiogram; FLAIR, fluid attenuated inversion recovery; gad,
gadolinium; MIPS, maximum intensity projections; PET, positron emission tomography; Susc,
susceptibility.
CASE D: A 56-year-old man with generalized tonic-clonic seizures. ADC, apparent diffusion
coefficient; CT, computed tomography; gad, gadolinium.DESCRIPTION OF FINDINGS
• Case A: A small focus of hyperdensity is present in the left middle cerebellar peduncle.
The CT angiogram demonstrates a tangle of vessels just lateral to this focus of
hemorrhage. A conventional catheter angiogram confirms the presence of an
arteriovenous malformation with arterial supply from the left anterior inferior cerebellar
artery and pontine perforators and early filling of the straight, transverse, and sigmoid
sinuses. The lesion was subsequently treated with liquid embolic material (not shown).
• Case B: A left occipital lesion demonstrates peripheral hyperdensity. There is surrounding
edema with local mass effect and effacement of the left occipital horn. After
administration of contrast, superimposed enhancement is seen along the peripheral
portions of the mass. On the coronal reformats, an additional smaller hyperdense right
cerebellar lesion with ring enhancement is noted. Given the patient’s history of lung
cancer, these findings are consistent with lung metastases.
• Case C: Small, discrete hyperdensities measuring 150 to 200 HU are consistent with
calcifications in the left occipital lobe. Surrounding parietal occipital hypodensity and
effacement of the left ventricular atrium are noted. CT angiogram maximum intensity
projection image does not demonstrate abnormal associated vessels.
Gadoliniumenhanced, T1-weighted MRI shows no associated enhancement. Marked T2/FLAIR
hyperintense signal is noted correlating with the CT hypodensity. Gradient echo imaging
shows calcific foci appearing as punctate foci of susceptibility. PET imaging demonstrates
a predominantly hypometabolic lesion. Pathologic evaluation after surgical resection
revealed an oligodendroglioma.
• Case D: A CT scan of the brain demonstrates a mass lesion centered in the left anterior
basal ganglia. There is an irregular hyperdense rim with a hypodense center. On MRI, the
rim enhances and has restricted diffusion characterized by hypointensity on the ADC
images. The findings are suggestive of a hypercellular lesion with internal necrotic or
cystic components. The patient was given a diagnosis of lymphoma, and marked
improvement of the enhancing lesion occurred after IV methotrexate was administered.DIAGNOSISDIAGNOSIS
Case A:
Intraparenchymal cerebellar hemorrhage resulting from an arteriovenous malformation
Case B:
Metastatic lung cancer
Case C:
Oligodendroglioma grade 2 (proven by pathology)
Case D:
Lymphoma
SUMMARY
The differential diagnosis of CT hyperdense lesions usually revolves around
hemorrhagic products, calcifications, or hypercellular lesions. CT attenuation value of
hyperdense lesions in the brain can be helpful in determining the etiology. Attenuation
of hyperdense hemorrhage in the brain ranges from 60 to 100 HU. Calcifications
typically have Hounsfield units in the hundreds. Care must be taken when measuring
small hyperdensities because volume averaging can underestimate the Hounsfield
units. MRI susceptibility-weighted images can also be helpful for differentiating these
entities. Intraparenchymal hemorrhage demonstrates susceptibility (low signal) with
marked enlargement or “blooming” of the hemorrhage compared with its actual size.
Calcification typically shows low signal with little to no blooming. Dense cellular
packing does not show susceptibility.
Determining the etiology of an intraparenchymal hemorrhage is important because it
will affect prognosis, treatment, and management. CT angiography is highly sensitive
and specific for identifying an underlying vascular lesion. Approximately 15% of
intraparenchymal hemorrhages result from vascular lesions such as arteriovenous
malformations and fistulae, aneurysms, dural venous sinus thrombosis, moyamoya
disease, and vasculitis. If an underlying vascular lesion is not identified, common
causes of intraparenchymal hemorrhage in elderly patients should be considered.
Hemorrhages due to anticoagulation are usually large, lobar hemorrhages, and
hypertensive hemorrhages typically are located in the deep gray nuclei, brainstem,
and cerebellum.
If anticoagulation and hypertension are not considerations, a gadolinium-enhanced
MRI with gradient echo sequences is obtained to evaluate for other causes, such as
amyloid angiopathy, underlying neoplasms, and cavernous malformations. Amyloid
angiopathy is characterized by a lobar hemorrhage with associated gray/white matter
junction microhemorrhages and/or leptomeningeal hemosiderosis on
susceptibilityweighted sequences. Neoplasms that produce intraparenchymal hemorrhage include
high-grade gliomas and metastatic tumors, such as melanoma and renal cell
carcinoma. Frequently, an underlying enhancing mass is identified after administration
of IV gadolinium. However, an underlying mass can be obscured by the hemorrhage,
and follow-up MRI is recommended if no clear cause for the parenchymal hemorrhage
is identified and neoplasm remains in the differential diagnosis. Cavernousmalformations may be the cause of acute intraparenchymal hemorrhage in young
children and young adults. They typically have a heterogenous “popcorn” appearance
with a complete hemosiderin rim on T2-weighted images and no surrounding edema.
After acute hemorrhage, there is edema and the hemosiderin rim may be obscured.
Clues to the etiology are age and associated classic cavernous malformations in other
brain locations (particularly in the familial form).
Calcifications can be either benign or associated with pathology. Intraparenchymal
calcifications are nonspecific and can be seen in a variety of etiologies, including
normal deposition in the basal ganglia, prior cerebral insult (e.g., infection,
inflammation, or ischemia), vascular abnormalities (e.g., cavernous malformations,
arteriovenous malformations, and fistulae), or neoplasms. Primary intraaxial central
nervous system neoplasms that show calcifications include astrocytomas,
oligodendrogliomas, or, rarely, glioblastomas. Case C is a grade 2 oligodendroglioma.
Low-grade oligodendrogliomas are slowly growing neoplasms typically located in a
cortical/subcortical location, most commonly in the frontal lobe. They may cause
scalloping of the adjacent calvarium. The majority demonstrate calcification and about
50% show variable enhancement. Differentiation from other neoplasms is not
definitively possible with imaging alone.
On CT, increased attenuation due to dense cellular packing usually is seen with
lymphoma and other small, round, blue-cell tumors, such as peripheral
neuroectodermal tumors and medulloblastomas, but increased density also can be
seen in glioblastomas. Lymphoma is characteristically located in the deep white matter
and deep gray nuclei. On MRI, the high cellularity is reflected by isointensity to brain
parenchyma on T2-weighted images, restricted diffusion with hyperintensity on
diffusion-weighted images, and hypointensity on ADC maps. Lymphoma typically
demonstrates avid homogenous enhancement in immunocompetent patients. In
immunocompromised patients, lymphomas may demonstrate rim enhancement with
nonenhancing regions of central necrosis. In contrast with acute hemorrhage,
lymphomas do not have susceptibility. Lymphomas usually rapidly respond to
treatment with IV methotrexate, radiation therapy, or steroids.
DIFFERENTIAL DIAGNOSIS
Acute hemorrhage
Calcification
Highly cellular neoplasms
Previous contrast
PEARLS
• Underlying etiologies for acute intraparenchymal hemorrhage should be further
assessed by CT angiogram.
• When patients with intraparenchymal hemorrhage have negative CT angiogram
findings and no history of hypertension or anticoagulation, a gadolinium-enhancedMRI with gradient echo sequences should be performed to assess for underlying
malignancy and amyloid angiopathy, respectively.
• Increased attenuation on CT examination due to dense cellular packing usually is
seen with lymphoma and other small, round, blue-cell tumors. These lesions usually
show dense, homogeneous enhancement and restricted diffusion and do not have
susceptibility.
• Attenuation of hyperdense hemorrhage in the brain typically ranges from 60 to 100
HU, whereas calcifications typically have Hounsfield units in the hundreds.
Calcifications have little to no blooming on susceptibility-weighted images, in
contrast with hemorrhage, which has marked blooming.
SUGGESTED READINGS
Dainer HM, Smirniotopoulos JG. Neuroimaging of hemorrhage and vascular malformations,
Semin Neurol. 2008;28(4):533–547.
Delgado Almondoz JE, Schaefer PW, Forero NP, et al. Diagnostic accuracy and yield of
multidetector CT angiography in the evaluation of spontaneous intraparenchymal cerebral
hemorrhage, AJNR Am J Neuroradiol. 2009;30(6):1213–1221.
Koeller KK, Rushing EJ. From the archives of the AFIP: oligodendroglioma and its variants:
radiologic-pathologic correlation, Radiographics. 2005;25(6):1669–1688.
Koeller KK, Smirniotopoulos JG, Jones RV. Primary central nervous system lymphoma:
radiologic-pathologic correlation, Radiographics. 1997;17(6):1497–1526.
Lee YY, Van Tassel P. Intracranial oligodendrogliomas: imaging findings in 35 untreated
cases, AJR Am J Roentgenol. 1989;152(2):361–369.
Morris PG, Abrey LE. Therapeutic challenges in primary CNS lymphoma, Lancet Neurol.
2009;8(6):581–592.
Osborn AG, Diagnostic neuroradiology. St Louis: Mosby; 1994.
Stadnik TW, Chaskis C, Michotte A, et al. Diffusion-weighted MR imaging of intracerebral
masses: comparison with conventional MR imaging and histologic findings, AJNR Am J
Neuroradiol. 2001;22(5):969–976.2
T1 Hyperintense Lesions
HENRY SU, MD, PHD, AND JUAN E. SMALL, MD
CASE A: A 64-year-old man with a history of amyloid angiopathy–related hemorrhages.
CASE B: A 64-year-old man with a history of renal cell carcinoma, difficulty walking, and
diplopia.CASE C: A 25-year-old man presenting after sustaining trauma.
CASE D: A 50-year-ol man presenting with a history of headaches.
CASE E: A 2-month-old male inant presenting with a giant congenital melanocytic nevus.DESCRIPTION OF FINDINGS
• Case A: An oval, nonenhancing, T1 hyperintense right parietal abnormality is evident.
Associated T2 hyperintensity and peripheral susceptibility are seen. There also is
surrounding edema. The findings are consistent with a late subacute hemorrhage in a
patient with a known history of amyloid angiopathy.
• Case B: A mass centered within the right cerebral peduncle demonstrates T1 hyperintense
foci and heterogeneous T2 hyperintense signal with surrounding edema. The postcontrast
T1-weighted image demonstrates an avidly enhancing mass consistent with a
pathologically proven hemorrhagic renal cell carcinoma metastasis.
• Case C: A large heterogeneous mass with regions of T1 hyperintensity and an associated
sinus tract is centered within the midline inferior posterior fossa. No enhancement is
identified. There are fat-fluid levels in the frontal horns of the lateral ventricles with
chemical shift artifact on the T2-weighted images as well as multiple small T1 hyperintense
foci consistent with fat within the bilateral sylvian fissures. These findings are consistent
with a ruptured dermoid cyst.
• Case D: A large, oval, well-circumscribed, T1 hyperintense, T2 hypointense, nonenhancing
intraventricular mass is noted in the region of the foramen of Monro. The location and
imaging characteristics of this lesion are consistent with a proteinaceous colloid cyst.
• Case E: There are bilateral medial temporal and right thalamic intraparenchymal as well as
scattered leptomeningeal T1 hyperntense lesions. No associated enhancement is
identified. These findings are consistent with melanocytic deposits in a patient with
neurocutaneous melanosis.DIAGNOSISDIAGNOSIS
Case A:
Late subacute hematoma in a patient with amyloid angiopathy
Case B:
Hemorrhagic metastasis (renal cell carcinoma)
Case C:
Ruptured dermoid cyst
Case D:
Colloid cyst (with proteinaceous contents)
Case E:
Neurocutaneous melanosis
SUMMARY
Intrinsic T1 hyperintensity (T1 shortening) on MRI can be due to the presence of blood
products, fat, melanin, proteinaceous material, or calcification.
Hemoglobin has different signal characteristics on MRI depending on its oxidative
state. Subacute phase methemoglobin (both intracellular and extracellular) has intrinsic
T1 hyperintense signal. Intracellular methemoglobin also demonstrates blooming on
susceptibility-weighted sequences. A history of recent trauma or anticoagulation makes
the diagnosis of T1 hyperintense intracranial hemorrhage straightforward. Patients with
a history of hypertension may have deep gray nuclei and brainstem or cerebellar T1
hyperintense subacute hemorrhages. Lobar T1 hyperintense lesions with associated
gray/white matter junction foci of susceptibility suggest amyloid angiopathy in older
patients. Furthermore, in the appropriate clinical setting, intraparenchymal T1
hyperintense lesions should raise the concern for metastatic disease. Intrinsic T1
signal can be seen in hemorrhagic metastases (e.g., renal cell, lung, thyroid). Intrinsic
T1 hyperintensity associated with metastatic melanoma may be due to either
hemorrhagic components or intrinsic T1 shortening from melanin. In many cases, an
underlying mass can be identified on contrast-enhanced sequences. If an underlying
mass is not identified, it is important to obtain follow-up imaging to rule out an
underlying enhancing lesion initially obscured by the hemorrhage. In younger patients,
T1 hyperintense hemorrhages may result from underlying vascular lesions such as
cavernous malformations (a “popcorn” appearance with complete hemosiderin rim on
gradient echo and T2-weighted sequences) or arteriovenous malformations.
Melanin-containing lesions, such as neurocutaneous melanosis, also should be
considered in the differential diagnosis of T1 shortening when the clinical setting is
appropriate. Neurocutaneous melanosis is a rare congenital phakomatosis associated
with multiple cutaneous melanocytic nevi and benign or malignant central nervous
system melanotic lesions. Its intracranial imaging characteristics are due to the
proliferation of melanocytes in the leptomeninges or parenchyma. As such, multiple T1
hyperintense lesions generally are evident. Because symptoms usually manifest by 2
to 3 years of age, a pediatric patient with cutaneous lesions and these imaging
characteristics should suggest this diagnosis despite its rarity. Hydrocephalus is seen
in two thirds of symptomatic patients due to obstruction of CSF flow.Fat-containing lesions, such as lipomas or dermoid cysts, also should be considered
in the differential diagnosis of T1 shortening. Dermoid cysts often are midline in
sellar/parasellar, frontal, and posterior fossa locations and are believed to be due to
inclusion of surface ectoderm early during embryogenesis. Twenty percent are
associated with sinus tracts. When uncomplicated, these lesions are not associated
with enhancement. Confirming the presence of fat is helpful with CT or fat-saturated
sequences on MRI. T2 signal is variable. Dermoid cyst rupture can present with
disseminated foci of intracranial T1 hyperintensity due to spillage of lipid contents into
the subarachnoid space or intraventricular compartment. Because of density
differences, lipid droplets or fat fluid levels are antidependent. Dermoid rupture can
cause chemical meningitis due to meningeal irritation from the internal contents, which
can result in leptomeningeal enhancement. Hydrocephalus may develop from blockage
of arachnoid granulations.
Protein-containing lesions also should be considered in the differential diagnosis of
T1 hyperintense lesions. The location of a protein-containing lesion is the most
important clue to diagnosis. For instance, colloid cysts, which arise from the inferior
aspect of the septum pellucidum, typically are present in the region of the foramen of
Monro. These lesions are well-circumscribed, nonenhancing cystic lesions that are
hyperintense on T1-weighted images when the protein/mucin content is relatively high.
When a well-circumscribed, homogeneous, T1 hyperintense lesion is centered in the
region of the pituitary gland, a craniopharyngioma or Rathke’s cleft cyst should be
considered.
SPECTRUM OF DISEASE
See Figure 2-1.Figure 2-1 A 56-year-old man with history of metastatic melanotic melanoma. Axial T1
precontrast image (A) demonstrates a T1 hyperintense lesion centered in the left caudate
nucleus. Postcontrast T1 image (B) also demonstrates a smaller enhancing lesion along the
medial aspect of the left parietal lobe, with surrounding edema evident on FLAIR (C). It is
difficult to determIne whether the caudate lesion enhances. Susceptibility blooming is not
associated with the intrinsically T1 hyperintense lesion; the signal characteristics could be
secondary to extracellular methemoglobin or melanin. The imaging characteristics of
metastatic melanoma may vary from patient to patient depending on whether the lesions
represent melanotic melanoma metastasis, amelanotic melanoma metastasis, or hemorrhagic
metastasis.
DIFFERENTIAL DIAGNOSIS
Hemorrhagic lesions: Hematomas, hemorrhagic infarcts, hemorrhagic infections (e.g.,
herpes simplex encephalitis), hemorrhagic neoplasms, vascular malformations, and
thrombosed aneurysms
Fatty lesions: Lipomas, dermoids, and teratomas
Melanin-containing lesions: Melanoma metastases and intraparenchmal and
leptomeningeal melanosis
Protein-containing lesions: Colloid cysts, Rathke cleft cysts, craniopharyngioma, and
atypical epidermoid
Calcified/ossified lesions or lesions with mineral accumulation: Endocrine/metabolic
disorders, calcified neoplasms, and calcifying infections
PEARLS
• An imaging interpretation error is to mistake intrinsic T1 hyperintensity for
enhancement. The imaging interpreter should closely compare T1 precontrast and T1
postcontrast sequences to avoid this pitfall.
• Side-by-side scrutiny of precontrast and postcontrast sequences is invaluable for the
identification of areas of subtle enhancement, a finding that markedly tailors the
differential diagnosis.
• Follow-up imaging in the setting of a parenchymal hemorrhage is required to rule out
an underlying enhancing vascular or neoplastic abnormality obscured by mass effect
exerted by the hematoma.
SIGNS AND COMPLICATIONS• Dermoid cyst rupture with spilling of lipid components results in a chemical meningitis
when the contents of the ruptured cyst involve the subarachnoid spaces. If spilled
lipid obstructs arachnoid granulations, hydrocephalus may develop.
• Hydrocephalus is seen in two thirds of symptomatic patients with neurocutaneous
melanosis due to obstruction of CSF flow.
SUGGESTED READINGS
Atlas SW, et al. MR imaging of intracranial metastatic melanoma, J Comput Assist Tomogr.
1987;11(4):577–582.
Cakirer S, Karaarslan E, Arslan A. Spontaneously T1-hyperintense lesions of the brain on
MRI: a pictorial review, Curr Probl Diagn Radiol. 2003;32(5):194–217.
Huisman TA. Intracranial hemorrhage: ultrasound, CT and MRI findings, Eur Radiol.
2005;15(3):434–440.
Osborn AG, Preece MT. Intracranial cysts: radiologic-pathologic correlation and imaging
approach, Radiology. 2006;239(3):650–664.
Stendel R, et al. Ruptured intracranial dermoid cysts, Surg Neurol. 2002;57(6):391–398.
Zaheer A, Ozsunar Y, Schaefer PW. Magnetic resonance imaging of cerebral hemorrhagic
stroke, Top Magn Reson Imaging. 2000;11(5):288–299.3
Multiple Susceptibility
Artifact Lesions
JUAN E. SMALL, MD
CASE A: A 48-year-old asymptomatic man with a strong family history of cerebral
microhemorrhage. GRE, gradient refocused echo.CASE B: An 87-year-old woman with a history of hyperlipidemia, hypertension, and heart
disease. GRE, gradient refocused echo.
CASE C: An 18-year-old unrestrained female driver after a motor vehicle accident. ADC,
apparent diffusion coefficient; DWI, diffusion-weighted imaging; GRE, gradient refocused
echo.CASE D: A 65-year-old woman with a history of breast cancer presenting with difficulty
walking. GRE, gradient refocused echo.
CASE E: A 64-year-old man presenting with mild cognitive impairment. GRE, gradient
refocused echo.DESCRIPTION OF FINDINGS
• Case A: Familial cavernous malformations: A patient with a familial history presents
with multiple foci of susceptibility, the largest of which (pons, left corona radiata)
demonstrate a typical “popcorn” appearance with central heterogeneity and
circumferential complete rings of hypointense signal on T2-weighted images, without
mass effect or edema.
• Case B: Hypertension: Multiple cerebral microhemorrhages involving the deep gray
nuclei, brainstem, and cerebellum in a patient with a history of hypertension. There also
are periventricular T2 hyperintensity and bilateral deep gray nuclei lacunes.
• Case C: Diffuse axonal injury: A patient with a history of trauma with
microhemorrhages involving the cerebral gray/white matter junctions, corpus callosum,
and the left middle cerebellar peduncle. There is restricted diffusion in the genu and
splenium of the corpus callosum as well as the right corona radiata.
• Case D: Hemorrhagic metastases (breast cancer): A patient with a history of
malignancy with prominent foci of susceptibility, T1 hyperintensity, associated
enhancement, and surrounding vasogenic edema.
• Case E: Amyloid angiopathy: A patient older than 60 years with multiple cerebral
microhemorrhages in a peripheral pattern (cortical/subcortical distribution) sparing the
deep white matter, basal ganglia, brainstem, and cerebellum. There is also moderate
periventricular white matter T2 hyperintensity.DIAGNOSISDIAGNOSIS
Case A:
Familial cavernous malformations
Case B:
Hypertension
Case C:
Diffuse axonal injury
Case D:
Hemorrhagic metastases (breast cancer)
Case E:
Amyloid angiopathy
SUMMARY
Cerebral microhemorrhages appear as scattered punctate foci of susceptibility on
GRE/susceptibility images. Typically, chronic microbleeds are associated with
hypertension, amyloid angiopathy, and other causes of small vessel vasculopathy.
Microhemorrhages resulting from chronic hypertension typically are located in the
deep gray nuclei, deep white matter, brainstem, and cerebellum. Approximately
56% of patients with an acute hypertensive hemorrhage have associated
microbleeds. Patients with chronic hypertension usually have periventricular white
matter FLAIR/T2 hyperintensity.
Microhemorrhages resulting from amyloid angiopathy typically occur in patients
older than 60 years, in a cortical/subcortical distribution with sparing of the deep
white matter, basal ganglia, brainstem, and cerebellum. Approximately 75% of
patients with a lobar hemorrhage resulting from amyloid angiopathy have
associated microbleeds at gray/white matter junctions. Patients with amyloid
angiopathy usually have periventricular white matter FLAIR/T2 hyperintensity and
can also have leptomeningeal hemosiderosis. Patients with the rarer inflammatory
form of amyloid angiopathy have associated vasogenic edema and leptomeningeal
enhancement.
The diagnosis of hemorrhagic metastases should be considered when additional
enhancing lesions with susceptibility and surrounding edema are seen. A study in
the literature noted that 7% of melanoma metastases were identified best on GRE
images. The most common hemorrhagic cerebral metastases are melanoma and
renal cell carcinoma. Breast carcinoma and lung carcinoma hemorrhage less
frequently but are the most common cerebral metastases and should be
considered. Thyroid carcinoma and choriocarcinoma also produce hemorrhagic
lesions, but they rarely metastasize to the brain.
Lobar or deep acute hemorrhage in young patients with additional foci of
susceptibility can suggest the diagnosis of multiple cavernous malformations,
especially if there is a classic heterogeneous lesion with a complete hemosiderin
ring and no surrounding edema. In patients with a family history of this condition, anautosomal dominant inheritance pattern is seen. It is noteworthy that these familial
lesions are not associated with developmental venous malformations.
In the setting of trauma, diffuse axonal injury should be considered.
Microhemorrhage associated with diffuse axonal injury is most often seen at
gray/white matter junctions and in the corpus callosum, subcortical and deep white
matter, and dorsolateral brainstem. In addition to punctate foci of susceptibility,
diffusion restriction may be seen at sites of diffuse axonal injury.
Lastly, any cause of vasculitis, whether infectious or inflammatory, should be
considered. In particular, septic emboli, fungal infections, and radiation and
chemotherapy changes should be considered in the appropriate clinical setting. In
addition, causes of small vessel vasculopathy, such as sickle cell disease or
cerebral autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy, should be considered.
SPECTRUM OF DISEASE
The spectrum of disease is detailed in the preceding section.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis is provided in Table 3-1.
TABLE 3-1 Young vs. Older Patient
PEARLS
Findings suggestive of hypertension include:
• “Central” predominant microhemorrhages involving the deep gray nuclei, deep
white matter, brainstem, and cerebellum
Findings suggestive of amyloid angiopathy include:
• Patients generally are older than 60 years
• A “peripheral” pattern with a cortical/subcortical distribution
• The deep white matter, basal ganglia, brainstem, and cerebellum generally are
spared
Findings suggestive of hemorrhagic metastases include:
• History of malignancy
• Enhancement associated with scattered foci of susceptibility with surroundingedema
Findings suggestive of multiple cavernous malformations include:
• History: young age and family history
• Lesions with typical popcorn appearance
SIGNS AND COMPLICATIONS
Signs and complications generally are related to acute hemorrhage and local mass
effect. Patients with amyloid angiopathy and numerous microhemorrhages may
present with dementia.
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377.
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of cerebral microbleeds and old lacunes, J Neurol Neurosurg Psychiatry.
2004;75(3):423–427.
Roob G, Schmidt R, Kapeller P, et al. MRI evidence of past cerebral microbleeds in a
healthy elderly population, Neurology. 1999;52:991–994.4
Ring-Enhancing Lesions
JUAN E. SMALL, MD
CASE A: A 39-year-old man who had a dental procedure several weeks earlier now
presenting with right leg numbness and weakness. Ax, axial; Cor, coronal; DWI,
diffusionweighted imaging.CASE B: A 37-year-old woman with a 1-month history of right-sided numbness presenting
with a 3-day history of right-sided weakness. Ax, axial; Cor, coronal; DWI, diffusion-weighted
imaging.
CASE C: A 70-year-old male smoker presenting with shortness of breath and headache of 3
weeks’ duration. Ax, axial; Cor, coronal; DWI, diffusion-weighted imaging.CASE D: A 41-year-old man with a 3-week history of recurrent sinus infections now
presenting with rapid onset of headache and confusion. Ax, axial; Cor, coronal; DWI,
diffusion-weighted imaging.
CASE E: A 36-year-old man with a history of chronic renal disease who had two kidney
transplants now presenting after a generalized seizure. Ax, axial; Cor, coronal; DWI,
diffusion-weighted imaging.DESCRIPTION OF FINDINGS
• Case A: There is a 3-cm left parietal lesion with a thin, T2 hypointense peripheral rim,
smooth enhancement, prominent surrounding edema, and central restricted diffusion. Of
note, the ring of peripheral enhancement is slightly thicker toward its cortical margin.
• Case B: There are multiple supratentorial white matter T2 hyperintense lesions. The
largest lesion in the left parietal lobe measures 2.7 cm and demonstrates a thin, smooth,
incomplete rim of enhancement. Despite the size of this lesion, a paucity of surrounding
edema and mass effect is noted. There is restricted diffusion in the periphery of the
lesion but not in the center. Lesions in the right frontal and right occipital lobe also
enhance.
• Case C: A 2.2-cm right cerebellar ring-enhancing lesion without associated restricted
diffusion is identified. Of note, there is an enhancing internal septation as well as
irregularity, nodularity, and varying thickness of the enhancing wall.
• Case D: A 5-cm, heterogeneous right occipital mass demonstrates a thick and nodular
rim of enhancement. No internal restricted diffusion is noted. However, DWI
hyperintensity associated with the enhancing rim suggests hypercellularity. Subtle
ependymal enhancement is noted along the walls of the temporal horn of the right lateral
ventricle. Marked surrounding edema and mass effect are noted.
• Case E: This patient was receiving long-term immunosuppression. There is a 1.1-cm
ring-enhancing lesion centered in the posterior left middle frontal gyrus with surrounding
edema. There is mildly restricted diffusion in the rim of the lesion but not in the center.
There is minimal surrounding linear enhancement along perivascular spaces as well as
overlying dural enhancement.DIAGNOSISDIAGNOSIS
Case A:
Abscess
Case B:
Multiple sclerosis
Case C:
Metastasis
Case D:
Glioblastoma multiforme
Case E:
Lymphoma (large B-cell lymphoma consistent with posttransplant lymphoproliferative
disorder)
SUMMARY
Several important imaging characteristics of ring-enhancing lesions often can lead to
a more specific diagnosis:
1. Multiplicity
2. Thin versus a thick/irregular rim of enhancement
3. A thicker outer margin of rim enhancement
4. An incomplete rim of enhancement
5. The presence of adjacent perivascular enhancement
6. A T2 hypointense rim
7. Central restricted diffusion
8. The degree of perilesional edema
A solitary ring-enhancing lesion is usually due to a neoplastic process, infection, or
demyelination. In decreasing order of frequency, solitary ring-enhancing lesions
represent gliomas, metastases, abscesses, or demyelinating lesions.
Multiplicity, on the other hand, in decreasing order of frequency, suggests
metastases, pyogenic abscesses, demyelinating lesions, or opportunistic infections.
In an adult patient, a heterogeneous lesion with a thick, irregular, and nodular rim of
enhancement suggests a necrotic neoplastic lesion, such as glioblastoma multiforme
or metastasis.
An abscess often presents with specific clues to the diagnosis, including
homogeneous central restricted diffusion, an often T2 hypointense peripherally
enhancing rim, considerable surrounding edema, and a thicker wall toward the
cortex/periphery. Because abscesses tend to grow away from the well-vascularized
gray matter, thinning of the medial wall is seen. Hematogenous abscesses (in the
setting of endocarditis, cardiac shunts, and pulmonary arteriovenous malformations)
are usually multiple and present at gray/white matter junctions. Perilesional edema is
usually quite prominent.
Ring enhancement associated with demyelination is often incomplete or open.
Open ring enhancement (i.e., crescentlike enhancement) greatly increases the
likelihood that the lesion represents demyelination (the likelihood ratio is five timesgreater than that of a neoplasm and 17 times greater than that of infection).
Nevertheless, because of the higher incidence of neoplasms and infection, these
entities still remain considerations with this pattern of enhancement. Further support
for this diagnosis comes in the form of multiple white matter lesions seen in a typical
distribution, such as at the callosal-septal interface, and oriented perpendicularly to
the ventricular surface.
Primary CNS lymphoma is a rare form of extranodal non-Hodgkin lymphoma.
Primary CNS lymphoma has a distinct imaging appearance because of its
hypercellularity and high nuclear/cytoplasmic ratio, as well as the disruption of the
blood-brain barrier. Masses are commonly hyperdense to isodense on computed
tomography and demonstrate dense homogeneous enhancement. On magnetic
resonance imaging, lesions are commonly hypointense to gray matter on T1-weighted
images and isointense to hyperintense on T2-weighted images, with the hypercellular
nature of these lesions resulting in DWI hyperintensity and ADC hypointensity.
Although avid homogenous enhancement is usually seen in immunocompetent
patients, imaging tends to be more variable in immunocompromised patients, and
lesions may be heterogeneously enhancing or ring enhancing. Importantly, linear
enhancement at the margins of the lesion tracking along Virchow-Robin perivascular
spaces is highly specific. Hemorrhage, calcification, and necrosis are rare prior to
treatment. In immunocompetent patients, intracranial lesions are solitary 70% of the
time, whereas in immunocompromised patients, lesions are equally likely to be
multiple versus solitary. Approximately 85% of lesions are supratentorial, with more
than 60% of intracranial lesions occuring in a periventricular location and 12% of
lesions involving the corpus callosum. The identification of a “transspatial” lesion (i.e.,
a lesion involving both the intraaxial and extraaxial space) often can be an important
clue for the diagnosis of intracranial lymphoma. Trans-spatial lesions typically have
intraparenchymal enhancement with adjacent dural enhancement.
SPECTRUM OF DISEASE
The spectrum of disease is detailed in the preceding section.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis is provided in Table 4-1.
TABLE 4-1 Solitary vs. Multiple Ring-Enhancing LesionsPEARLS
• A thick, nodular, or irregular rim of enhancement suggests a tumor.
• A lesion demonstrating homogeneous central restricted diffusion, a T2 hypointense,
smoothly enhancing rim thicker toward the brain periphery and considerable
surrounding edema, suggests an abscess.
• An incomplete rim of enhancement suggests a demyelinative lesion.
• The presence of hypointense ADC associated with the areas of enhancement, as
well as adjacent perivascular enhancement, suggests lymphoma in an
immunocompromised patient. Trans-spatial lesions also suggest lymphoma.
SIGNS AND COMPLICATIONS
Signs and complications are predominantly related to mass effect and the specific
location of the lesion.
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ringenhancing brain lesions can help to differentiate pathology, Neuroradiology.
2006;48(3):143–149.
Smirniotopoulos JG, Murphy FM, Rushing EJ, et al. Patterns of contrast enhancement in the
brain and meninges, Radiographics. 2007;27(2):525–551.5
Leptomeningeal Enhancement
JUAN E. SMALL, MD
CASE A: A 44-year-old man who had upper respiratory infection symptoms 4 weeks
earlier now presenting with severe headache, purulent otorrhea, irritability, and progressive
decline of mental status. A x, axial; C o r, coronal; S a g, sagittal.
CASE B: A 38-year-old woman with a history of diabetes insipidus and hyperprolactinemia
presenting with a complex partial seizure. A x, axial; C o r, coronal; S a g, sagittal.
CASE C: A 58-year-old woman with 5-week history of fever and headache now presenting
with increasing confusion, vomiting, and lethargy. A x, axial; C o r, coronal; S a g, sagittal.CASE D: A 2-year-old girl with a history of seizures presenting with a decline in language
function. A x, axial; C o r, coronal; S a g, sagittal.
CASE E: A 22-year-old man recently diagnosed with communicating hydrocephalus of
unknown cause now presenting with intractable headaches, lightheadedness, and
episodes of near syncope. A x, axial; C o r, coronal; S a g, sagittal.DESCRIPTION OF FINDINGS
• Case A: There is a thin, smooth pattern of leptomeningeal enhancement with left
mastoiditis evident as the source of infection.
• Case B: There is a markedly nodular pattern of leptomeningeal enhancement slightly
more prominent in the basal cisterns and the hypothalamic region. There is also
bilateral trigeminal nerve involvement. Thoracic imaging (not shown) demonstrated
mediastinal and pulmonary sarcoidosis.
• Case C: There is a thick and nodular pattern of leptomeningeal enhancement
predominantly involving the basilar cisterns.
• Case D: A thin, smooth pattern of right temporal parietal leptomeningeal enhancement
is noted. There is associated cortical atrophy, ipsilateral choroid plexus hypertrophy,
and a prominent medullary vein. A port-wine stain was seen on physical exam.
• Case E: There is very thick, smooth leptomeningeal enhancement predominantly
involving the basilar cisterns.DIAGNOSISDIAGNOSIS
Case A:
Bacterial meningitis
Case B:
Neurosarcoidosis
Case C:
Tuberculous meningitis
Case D:
Sturge-Weber syndrome
Case E:
Leptomeningeal gliomatosis
SUMMARY
The most common causes of leptomeningeal (pia/arachnoid) enhancement are
bacterial and fungal meningitis, leptomeningeal carcinomatosis, and
neurosarcoidosis. Less common etiologies include vasculitis, gliomatosis,
SturgeWeber syndrome, and moyamoya disease. Rare causes include Wegener
granulomatosis, Lyme disease, dural arteriovenous fistula, meningioangiomatosis,
and neurocutaneous melanosis. Leptomeningeal gliomatosis is very rare.
Unfortunately, most causes of leptomeningeal enhancement have similar
appearances. However, two key factors often can help narrow the differential
diagnosis. The easiest is determined first by attempting to differentiate infectious
from noninfectious entities, a prospect often aided by a suggestive clinical history or
imaging findings suggesting the source of infection. Second, the pattern of
enhancement can help tailor the differential diagnosis. Uncomplicated bacterial
meningitis typically demonstrates thin, smooth leptomeningeal enhancement.
Entities classically presenting with thick, nodular, basal predominant enhancement
include tuberculous meningitis, fungal meningitis, neurosarcoidosis, pyogenic
meningitis, and neurosyphilis. Entities with more diffuse nodular leptomeningeal
enhancement include meningeal carcinomatosis, lymphomatous meningitis, and
leukemia. Very thick, smooth, basilar leptomeningeal enhancement can suggest the
unlikely diagnosis of leptomeningeal gliomatosis in the setting of a chronic aseptic
meningitis pattern of presentation.
SPECTRUM OF DISEASE
As previously indicated, most causes of leptomeningeal enhancement can have a
similar appearance, and it is important to realize that entities that typically present
with thin/smooth, nodular, or basilar enhancement can have an atypical appearance
(for example, meningeal carcinomatosis that presents with a thin rather than a
nodular pattern of enhancement).
DIFFERENTIAL DIAGNOSISThe differential diagnosis of leptomeningeal (pia-arachnoid) enhancement can be
summarized broadly into infectious, inflammatory, vascular, neoplastic, and
traumatic etiologies (Box 5-1).
Infectious meningitis results in leptomeningeal enhancement because of the
breakdown of the blood-brain barrier. Uncomplicated bacterial meningitis usually
results in thin, smooth enhancement.
Tuberculous and fungal forms of meningitis are often basilar predominant and
confluent. In addition, fungal and tuberculous meningitis may produce thicker
nodular enhancement in contrast to the typical bacterial meningitis enhancement
pattern.
Box 5-1 Types of Differential Diagnoses
Infectious: Bacterial meningitis, viral meningitis, tuberculous meningitis, fungal
meningitis, neurosyphilis
Inflammatory: Langerhans cell histiocytosis, sarcoidosis, Wegener granulomatosis,
chemical meningitis (ruptured dermoid)
Neoplastic: Primary meningeal tumors such as meningioma, leptomeningeal
gliomatosis, melanoma, sarcoma, lymphoma; cerebrospinal fluid spread of tumor
such as medulloblastoma, germinoma, and pineoblastoma; and metastatic
carcinomatosis (breast, leukemia/lymphoma, lung, melanoma, gastrointestinal
carcinoma, genitourinary carcinoma)
Traumatic: Old subarachnoid hemorrhage, surgical scarring from a prior craniotomy,
the sequela of a lumbar puncture, or contrast leakage
Leptomeningeal carcinomatosis is typically nodular or masslike and more diffuse.
However, it is important to note that carcinomatous meningitis can appear as thin
and smooth.
Neurosarcoidosis often demonstrates a nodular pattern with basilar
predominance, and cranial nerve involvement often is present.
Sturge-Weber syndrome typically demonstrates thin, smooth leptomeningeal
enhancement associated with cortical atrophy with gyriform calcification, as well as
ipsilateral choroid plexus hypertrophy. In addition, prominent medullary and
ependymal veins can be visible.
Moyamoya disease demonstrates enhancement of multiple engorged pial and
parenchymal collateral vessels due to slow flow. The internal carotid, proximal
middle cerebral, and anterior cerebral artery flow voids are absent or small. There
frequently are associated acute and chronic hemorrhages and/or infarctions.
Meningioangiomatosis is a rare hamartomatous cortical and leptomeningeal
malformation usually appearing as a calcified cortical mass with a linear, granular,
and/or gyriform cortical and leptomeningeal enhancement pattern.
Neurocutaneous melanosis may demonstrate diffuse leptomeningeal
enhancement. This entity is associated with neurofibromatosis (particularly type 2)in more than 50% of patients.
Primary diffuse leptomeningeal gliomatosis is an exceedingly rare neoplastic
condition of meningeal glial cell infiltration without evidence of a primary
parenchymal tumor. This condition should be considered in the differential
diagnosis of chronic aseptic meningitis. Although very rare, imaging features
include a very thick, smooth, basilar predominant leptomeningeal pattern of
enhancement.
PEARLS
The following entities typically present with thin, smooth leptomeningeal
enhancement:
• Bacterial meningitis
The following entities can present with basal-predominant, nodular enhancement:
• Tuberculous meningitis
• Fungal meningitis
• Neurosarcoidosis
• Pyogenic meningitis
• Neurosyphilis
The following entities typically have more diffuse nodular leptomeningeal
enhancement:
• Meningeal carcinomatosis
• Lymphomatous meningitis
• Leukemia
SIGNS AND COMPLICATIONS
When considering infectious etiologies, look carefully for a possible source of
infection, areas of parenchymal infarction or hemmorrhage due to arterial or venous
sinus thrombosis, intracranial collections of pus, or abscesses.
SUGGESTED READINGS
Jicha GA, Glantz J, Clarke MJ, et al. Primary diffuse leptomeningeal gliomatosis, E u r
N e u r o l. 2009;62(1):16–22.
Smirniotopoulos JG, Murphy FM, Rushing EJ, et al. Patterns of contrast enhancement in
the brain and meninges, R a d i o g r a p h i c s. 2007;27(2):525–551.6
Dural Enhancement
REZA FORGHANI, MD, PHD
CASE A: A 45-year-old man with new-onset postural headache.
CASE B: A 72-year-old man, history withheld.
CASE C: A 39-year-old woman with breast cancer.