Ebook Neuroradiology - Key differential diagnoses and clinical questions: Part 1

NEURORADIOLOGY
Key Differential Diagnoses
and Clinical Questions
JUAN E. SMALL, MD, M.Sc.
Section Chief, Neuroradiology Division
Director, Neuroimaging Education
Assistant Professor of Radiology
Lahey Hospital and Medical Center
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, Massachusetts


1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
NEURORADIOLOGY: KEY DIFFERENTIAL DIAGNOSES AND CLINICAL QUESTIONS
Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

ISBN: 978-1-4377-1721-1

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Library of Congress Cataloging-in-Publication Data
Small, 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 Stave

Printed in China
Last digit is the print number:  9  8  7  6  5  4  3  2


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. Schaefer


SECTION 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
Instructor in Radiology
Harvard Medical School
Boston, Massachusetts
STUART R. POMERANTZ, MD
Associate Director of Neuro-CT
Neuroradiologist
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

vi

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, M.Sc.
Section Chief, Neuroradiology Division
Director, Neuroimaging Education
Assistant Professor of Radiology
Lahey Hospital and Medical Center
Tufts University School of Medicine
Burlington, Massachusetts
TINA YOUNG-POUSSAINT, MD
Neuroradiologist
Boston Children’s Hospital
Professor of Radiology
Harvard Medical School
Boston, Massachusetts


CONTRIBUTORS
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 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
Instructor in Radiology
Harvard 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
vii


viii

Contributors

MICHAEL T. PREECE, MD
Department of Radiology
Massachusetts General Hospital
Boston, Massachusetts
AMMAR SARWAR, MD
Radiology 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, M.Sc.
Section Chief, Neuroradiology Division
Director, Neuroimaging Education
Assistant Professor of Radiology
Lahey Hospital and Medical Center
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, Massachusetts


PREFACE
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 similar-appearing
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, MD

ix


ACKNOWLEDGMENTS
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.

xi

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

xii

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.



1

Computed Tomography
Hyperdense Lesions

HENRY SU, MD, PHD

C

B

A
2I CT

CTA

Conventional
angiogram

CASE A:  A 66-year-old man presenting with sudden-onset left-sided weakness. CT, computed tomography;
CTA, CT ­angiogram.

A

C

B
ϪI CT

I CT

D
ϪI CT

I CT

CASE B:  A 77-year-old man with a history of lung cancer. CT, computed tomography.

3


4

Brain and Coverings

A

C

B
2I CT

CTA MIPS

T1

FLAIR

Post gad

G

F

E

D

Susc

PET

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.

A

C

B
2I CT

T1

D

Post gad

E
ADC

Post gad
after treatment

CASE D:  A 56-year-old man with generalized tonic-clonic seizures. ADC, apparent diffusion coefficient; CT,

computed tomography; gad, gadolinium.


Computed Tomography Hyperdense Lesions

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. Gadolinium-enhanced, 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

5

c­ omponents. The patient was given a diagnosis of lymphoma, and marked improvement of the enhancing lesion occurred
after IV methotrexate was administered.

DIAGNOSIS
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.


6

Brain and Coverings

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 susceptibility-weighted 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. Cavernous malformations may be the cause of acute intraparenchymal hemorrhage in young children and
young adults. They typically have a hetero­
genous “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-enhanced
MRI 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.


Computed Tomography Hyperdense Lesions
SUGGESTED READINGS
Dainer HM, Smirniotopoulos JG: Neuroimaging of hemorrhage and vascular malformations, Semin Neurol
28(4):533–547, 2008.
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 30(6):1213–1221, 2009.
Koeller KK, Rushing EJ: From the archives of the AFIP: oligodendroglioma and its variants: radiologic-pathologic
correlation, Radiographics 25(6):1669–1688, 2005.

Koeller KK, Smirniotopoulos JG, Jones RV: Primary central nervous system lymphoma: radiologic-pathologic
correlation, Radiographics 17(6):1497–1526, 1997.

7

Lee YY, Van Tassel P: Intracranial oligodendrogliomas:
imaging findings in 35 untreated cases, AJR Am J Roentgenol 152(2):361–369, 1989.
Morris PG, Abrey LE: Therapeutic challenges in primary
CNS lymphoma, Lancet Neurol 8(6):581–592, 2009.
Osborn AG: Diagnostic neuroradiology, St Louis, 1994,
Mosby.
Stadnik TW, Chaskis C, Michotte A, et  al: Diffusionweighted MR imaging of intracerebral masses: comparison with conventional MR imaging and histologic
findings, AJNR Am J Neuroradiol 22(5):969–976, 2001.


2

T1 Hyperintense Lesions
HENRY SU, MD, PHD, AND JUAN E. SMALL, MD

Ax T1 C–

Ax T1 C+

Ax T2

Ax GRE

CASE A:  A 64-year-old man with a history of amyloid angiopathy–related hemorrhages.

Ax T1 C–

Ax T1 C+

Ax T2

CASE B:  A 64-year-old man with a history of renal cell carcinoma, difficulty walking, and diplopia.

9


10

Brain and Coverings

Sag T1 C–

Ax T1 C–

Ax T1 C+

Ax T1 C–

Ax T2

Ax T1 C+

CASE C:  A 25-year-old man presenting after sustaining trauma.

Sag T1 C–

Ax T1 C–

Ax T1 C+

Ax T2

CASE D:  A 50-year-ol man presenting with a history of headaches.

Ax T1 C–

Ax T1 C+

Ax T1 C–

Ax T1 C+

CASE E:  A 2-month-old male inant presenting with a giant congenital melanocytic nevus.


T1 Hyperintense Lesions

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 hem­
orrhage 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 enhanc­
ing 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 fatfluid levels in the frontal horns of the
lateral ventricles with chemical shift arti­
fact on the T2-weighted images as well
as multiple small T1 hyperintense foci
consistent with fat within the bilateral
sylvian fissures. These findings are con­
sistent with a ruptured dermoid cyst.
• CASE D: A large, oval, well-­
circumscribed, T1 hyperintense, T2
hypointense, nonenhancing intraventricu­
lar mass is noted in the region of the fora­
men of Monro. The location and imaging
characteristics of this lesion are consistent
with a proteinaceous colloid cyst.
• CASE E: There are bilateral medial tem­
poral and right thalamic intraparenchy­

mal 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.

DIAGNOSIS
Case A:  Late subacute hematoma in a patient
with amyloid angiopathy
Case B:  Hemorrhagic metastasis (renal cell
carcinoma)

11

Case C:  Ruptured dermoid cyst
Case D:  Colloid cyst (with proteinaceous con­

tents)

Case E:  Neurocutaneous melanosis

SUMMARY
Intrinsic T1 hyperintensity (T1 shortening)
on MRI can be due to the presence of blood
products, fat, melanin, proteinaceous mate­
rial, or calcification.
Hemoglobin has different signal charac­
teristics on MRI depending on its oxidative
state. Subacute phase methemoglobin (both
intracellular and extracellular) has intrinsic

T1 hyperintense signal. Intracellular meth­
emoglobin 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 hyper­
intense 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 set­
ting, intraparenchymal T1 hyperintense
lesions should raise the concern for meta­
static 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 neuro­
cutaneous melanosis, also should be con­
sidered in the differential diagnosis of T1
shortening when the clinical setting is appro­
priate. Neurocutaneous melanosis is a rare
congenital phakomatosis associated with
multiple cutaneous melanocytic nevi and
benign or malignant central nervous system


12

Brain and Coverings

melanotic lesions. Its intracranial imaging
characteristics are due to the proliferation of
melanocytes in the leptomeninges or paren­
chyma. As such, multiple T1 hyperintense
lesions generally are evident. Because symp­
toms usually manifest by 2 to 3 years of age,
a pediatric patient with cutaneous lesions
and these imaging characteristics should sug­
gest this diagnosis despite its rarity. Hydro­
cephalus 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 loca­
tions and are believed to be due to inclusion
of surface ectoderm early during embryo­
genesis. 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 intracra­
nial T1 hyperintensity due to spillage of lipid
contents into the subarachnoid space or intra­
ventricular 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

A

B

T1 hyperintense lesions. The location of a

­protein-containing lesion is the most impor­
tant clue to diagnosis. For instance, colloid
cysts, which arise from the inferior aspect of
the septum pellucidum, typically are pres­
ent in the region of the foramen of Monro.
These lesions are well-circumscribed, nonen­
hancing cystic lesions that are hyperintense
on T1-weighted images when the protein/
mucin content is relatively high. When a
well-­circumscribed, homogeneous, T1 hyper­
intense 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.

DIFFERENTIAL DIAGNOSIS
Hemorrhagic lesions: Hematomas, hemor­
rhagic infarcts, hemorrhagic infections
(e.g., herpes simplex encephalitis), hemor­
rhagic neoplasms, vascular malformations,
and thrombosed aneurysms
Fatty lesions: Lipomas, dermoids, and terato­
mas
Melanin-containing lesions: Melanoma metasta­
ses and intraparenchmal and leptomeningeal
melanosis
Protein-containing lesions: Colloid cysts,
Rathke cleft cysts, craniopharyngioma, and

atypical epidermoid

C

D

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.


T1 Hyperintense Lesions

Calcified/ossified lesions or lesions with min­
eral accumulation: Endocrine/metabolic
disorders, calcified neoplasms, and calcify­
ing 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 pit­
fall.
• Side-by-side scrutiny of precontrast and
postcontrast sequences is invaluable for the

identification of areas of subtle enhance­
ment, a finding that markedly tailors the
differential diagnosis.
• Follow-up imaging in the setting of a paren­
chymal 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 meningi­
tis when the contents of the ruptured cyst
involve the subarachnoid spaces. If spilled

13

lipid obstructs arachnoid granulations,
hydrocephalus may develop.
• Hydrocephalus is seen in two thirds of
symptomatic patients with neurocutane­
ous melanosis due to obstruction of CSF
flow.
SUGGESTED READINGS
Atlas SW, et  al: MR imaging of intracranial metastatic
melanoma, J Comput Assist Tomogr 11(4):577–582,
1987.
Cakirer S, Karaarslan E, Arslan A: Spontaneously
T1-hyperintense lesions of the brain on MRI: a pic­
torial review, Curr Probl Diagn Radiol 32(5):194–217,

2003.
Huisman TA: Intracranial hemorrhage: ultrasound, CT
and MRI findings, Eur Radiol 15(3):434–440, 2005.
Osborn AG, Preece MT: Intracranial cysts: radiologicpathologic correlation and imaging approach, Radiology 239(3):650–664, 2006.
Stendel R, et  al: Ruptured intracranial dermoid cysts,
Surg Neurol 57(6):391–398, 2002.
Zaheer A, Ozsunar Y, Schaefer PW: Magnetic resonance
imaging of cerebral hemorrhagic stroke, Top Magn
Reson Imaging 11(5):288–299, 2000.


3

Multiple Susceptibility
Artifact Lesions
JUAN E. SMALL, MD

C

B

A

GRE

GRE

D

F

E
T1

GRE

T2

T2

CASE A:  A 48-year-old asymptomatic man with a strong family history of cerebral microhemorrhage. GRE,
gradient refocused echo.

15


16

Brain and Coverings

C

B

A

GRE

GRE

D

E
GRE

GRE

F
T2

T2

CASE B:  An 87-year-old woman with a history of hyperlipidemia, hypertension, and heart disease. GRE,
gradient refocused echo.

C

B

A

GRE

GRE

D

F

E

T2

GRE

DWI

ADC

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.


Multiple Susceptibility Artifact Lesions

B

A

T1

GRE

D

C

E
GRE

T1 Post

F
T1

T1 Post

CASE D:  A 65-year-old woman with a history of breast cancer presenting with difficulty walking. GRE,
gradient refocused echo.

A

C

B
GRE

D

GRE

F

E
GRE

GRE

T2

T2

CASE E:  A 64-year-old man presenting with mild cognitive impairment. GRE, gradient refocused echo.

17


18

Brain and Coverings

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.

DIAGNOSIS
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, an autosomal dominant inheritance pattern is seen. It is noteworthy that
these familial lesions are not associated with
developmental venous malformations.