This document reviews various non-neoplastic intracranial lesions that can mimic brain tumors clinically and radiologically. It presents 14 illustrative case examples categorized by etiology (infection, demyelination, vascular disease, etc.). Each case describes the patient's history and imaging findings, which initially suggested a tumor. However, pathology revealed non-neoplastic conditions like abscesses, infections, inflammatory diseases, and infarcts. The document emphasizes that while tumors are commonly considered, pathologists must be aware of non-neoplastic conditions that can also present as enhancing intracranial masses.

1. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 101
Review Article
Intracranial Lesions Mimicking Neoplasms
Clare H. Cunliffe, MD; Ingeborg Fischer, MD; David Monoky, MD; Meng Law, MD, MBBS, FRACR; Carolyn Revercomb, MD;
Susan Elrich, MD; Michael Jered Kopp, BA; David Zagzag, MD, PhD
● Context.—A broad spectrum of nonneoplastic conditions
can mimic a brain tumor, both clinically and radiologically.
In this review we consider these, taking into consideration
the following etiologic categories: infection, demyelin-
ation, vascular diseases, noninfectious inflammatory dis-
orders, and iatrogenic conditions. We give an overview of
such diseases, which represent a potential pitfall for pa-
thologists and other clinicians involved in patient care, and
present selected cases from each category.
Objective.—To illustrate the radiologic and pathologic
features of nontumoral intracranial lesions that can clini-
cally and radiologically mimic neoplasia.
Data Sources.—Case-derived material and literature re-
view.
Conclusions.—A variety of nonneoplastic lesions can
present clinically and radiologically as primary or meta-
static central nervous system tumors and result in surgical
biopsy or resection of the lesion. In such situations, the
pathologist has an important role to play in correctly de-
termining the nature of these lesions. Awareness of the en-
tities that can present in this way will assist the pathologist
in the correct diagnosis of these lesions.
(Arch Pathol Lab Med. 2009;133:101–123)
Abroad spectrum of nonneoplastic conditions can radio-
logically and clinically mimic an intracranial neo-
plasm.
In this review, we have compiled a unique series of cas-
es that presented both clinically and radiologically as in-
tracranial mass lesions. Tumor was initially considered in
each of the cases. However, pathology revealed a variety
of nonneoplastic etiologies, including demyelinating dis-
ease, vascular disease, inflammation, and infection, as well
as posttreatment effects. Although tumor is often the most
likely diagnostic consideration in a patient presenting with
a contrast-enhancing mass lesion within the brain paren-
chyma with surrounding edema and mass effect, that is
not always the case. Not uncommonly, there can be sig-
nificant overlap in the radiologic presentation between
neoplastic and nonneoplastic diseases. Both neoplastic and
nonneoplastic diseases can produce abnormal contrast en-
hancement, mass effect, and perilesional edema on both
computed tomography (CT) and magnetic resonance im-
aging (MRI). Occasionally, some of these nonneoplastic
etiologies may produce signs and symptoms mimicking
tumoral disease clinically.1
As such, these situations may
Accepted for publication July 25, 2008.
From the Department of Pathology, Division of Neuropathology (Drs
Cunliffe, Fischer, and Zagzag) and Department of Radiology, Division
of Neuroradiology (Dr Monoky), New York University Medical Center,
New York; the Departments of Radiology and Neurosurgery, Mount
Sinai Medical Center, New York, NY (Dr Law); the Office of the Chief
Medical Examiner, Washington, DC (Dr Revercomb); the Department
of Neurology, Yale University Hospital, New Haven, Conn (Dr Elrich);
and the Stern School of Business, New York University, New York (Mr
Kopp).
The authors have no relevant financial interest in the products or
companies described in this article.
Reprints: Clare H. Cunliffe, MD, Department of Pathology, Division
of Neuropathology, Mount Sinai School of Medicine, One Gustave L.
Levy Place, New York, NY 10029 (e-mail: clare@drcunliffe.com).
offer a diagnostic challenge to both the clinician and ra-
diologist, and often these patients undergo biopsy. In most
cases, the pathologist can readily differentiate between
neoplasia and nonneoplastic imitators. However, because
the benign nature of some pseudoneoplastic lesions may
not be immediately apparent on pathologic examination,
it behooves the pathologist to be aware of their existence.
The purpose of this case series is to alert pathologists,
radiologists, and other clinicians involved in the care of
neurooncologic patients to consider nonneoplastic etiolo-
gies in the differential diagnosis of both intra-axial and
extra-axial mass lesions.
Tumor-mimicking conditions from several etiologic cat-
egories are presented in tabular form, including infection
and inflammation, demyelinating disease, vascular dis-
ease, and posttreatment conditions, with accompanying il-
lustrations and discussion of the current and pertinent lit-
erature. Case examples of each condition discussed are
described in the Table.
INFECTIONS
Case Example 1: Aspergilloma
The radiologic finding of erosion of the skull base by
this mass lesion may have contributed to its interpretation
as a destructive neoplasm, with the differential diagnosis
including chondrosarcoma, metastatic lesion, osteosarco-
ma, and meningioma.
However, the histology in this case ruled out a diagnosis
of neoplasm. Based on the hematoxylin-eosin morphology
of a granulomatous process, a diagnosis of tuberculosis
came to mind. Special stains for microorganisms solved
this differential diagnostic dilemma, highlighting fungal
hyphae with the characteristic acute angle branching of
Aspergillus species. In retrospect, the history of otitis me-
dia and mastoidectomy in this patient pointed toward an
infectious process, even in the absence of predisposing
factors such as immunosuppression or diabetes. Even

2. 102 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Illustrative Case Examples With Corresponding Clinical History, Imaging Findings, Histology, and Final Pathologic
Diagnosis*
Case No. Age, y/Sex Clinical History Imaging Findings Imaging Differential Diagnoses
1 35/M Chronic otitis media s/p left mastoidec-
tomy; headaches, fever, left-sided fa-
cial numbness, diplopia, confusion
MRI: Irregularly T1 contrast enhanc-
ing, centrally hypointense left skull
base lesion involving the left maxil-
lary sinus, cavernous sinus (Figure
1, A) with erosion of left temporal
bone
Destructive neoplasm; differ-
ential diagnoses: chondro-
sarcoma, metastasis, osteo-
sarcoma, meningioma
2 37/F 10-mo H/O severe headaches, recent
onset of double vision, 14-mo H/O
amenorrhea, panhypopituitarism and
DI
MRI: 1.5-cm sellar mass extending to
suprasellar cistern adjacent to carot-
id arteries (Figure 2, A); low T1 sig-
nal intensity with thin enhancing
rim and septation (Figure 2, B)
Pituitary adenoma
3 56/F Bizarre behavior; paranoia, Klu¨ver-Bucy
syndrome
MRI: Bilateral temporal lobe lesions
(Figure 3, A and B)
Infectious process, eg, herpes
encephalitis, neoplasm
4 33/M Generalized seizures, s/p resection of
large anaplastic mixed glioma, in-
volving right frontal lobe and basal
ganglia; 2 y later, experienced 2 epi-
sodes of unconsciousness
MRI: New peripherally enhancing le-
sion of right frontal lobe (Figure 4,
A and B) with cortical extension
and perilesional edema
Recurrent tumor
5 65/F Remote H/O breast cancer s/p right to-
tal mastectomy; recent headaches
and fever
MRI: Left thalamic ring-enhancing le-
sion (Figure 5, A and B)
Favor metastatic neoplasm
over abscess
6 60/F s/p large B-cell lymphoma and CHOP
Tx; new onset seizure
MRI: 1.7-cm ring-enhancing lesion,
left parietal white matter; central
hypointensity on T1 (Figure 6, A),
hyperintense on DWI (Figure 6, B)
Necrotic lymphoma, abscess
7 35/F Bitemporal headache, left lower extrem-
ity weakness and diminished left
plantar sensation; remote PPD posi-
tive, CXR negative
MRI: 3-cm right basal ganglia periph-
erally enhancing lesion with sur-
rounding edema and midline shift
(Figure 7, A and B)
Neoplasm: primary or meta-
static
8 43/M Disorientation, word-finding difficulty,
right hemisensory impairment. HIV
positive, CD4 109, CSF protein 54
mg/dL, glucose 53 mg/dL
MRI: Right middle cerebellar pedun-
cle/hemisphere T1 hypointense, T2
hyperintense lesion (Figure 8, A and
B)
Inflammatory, demyelinating
or lymphoproliferative pro-
cess
9 62/F Progressive headaches for 1 y; CSF:
atypical lymphocytes, histiocytes, and
few eosinophils
MRI: Heterogeneous ring-enhancing
suprasellar lesion separate from pi-
tuitary and stalk, near anterior com-
municating artery (Figure 9, A and
B)
Inflammatory process, cystic
neoplasm
10 57/M s/p remote testicular cancer; 3-d H/O
bitemporal headache, confusion,
memory impairment
MRI: Bifrontal ‘‘butterfly’’ lesion, T2
hyperintense (Figure 10, A) with fo-
cal peripheral enhancement on
postcontrast T1 (Figure 10, B)
High-grade glioma
11 77/M H/O seizure disorder, hypertension
2004: New onset difficulty driving,
following directions; after biopsy,
steroid treatment with symptom
improvement
First MRI 2004: Large right frontal
contrast-enhancing mass and edema
(Figure 11, A)
2004: neoplasm
2007: Worsening speech impairment,
confusion
Second MRI 2007: Contrast-enhancing
subcortical lesion in left inferior pa-
rietal lobe (Figure 11, C)
2007: Demyelination vs neo-
plasm
12 64/M Headaches for 7 wk, nausea and vomit-
ing, 40-lb weight loss; gait ataxia
MRI: Cerebellar enhancement with
mass effect and edema (Figure 12,
A); surrounding gyriform enhance-
ment of folia on DWI (Figure 12, B)
Lhermitte-Duclos disease
13 43/F Sudden loss of right hand coordination
and difficulty driving
MRI: Left parietal lobe 2-cm white
matter–based lesion with irregular
enhancing rim and surrounding
edema (Figure 13, A and B)
High-grade glioma, lympho-
ma, metastasis, abscess
14i 38/F 18-mo H/O progressive left facial
numbness, first and second divisions
trigeminal nerve
MRI: 1.5-cm hypointense mass at left
Meckel cave, involving left trigemi-
nal ganglion (Figure 14, A)
Schwannoma vs meningioma
14ii 44/M 37-y H/O partial seizures, s/p resection
of right frontal and temporal seizure
focus; new onset increased seizure
frequency and left hemiparesis
CT: Hyperdense right frontoparietal
vertex extra-axial mass involving
calvarium (Figure 14, E)
Atypical meningioma, calvari-
al/dural metastasis

3. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 103
Extended
Surgical Procedure Histology Pathologic Diagnosis
Biopsy Granulomatous inflammation with extensive necrosis (Figure 1, B), numerous mul-
tinucleated giant cells (Figure 1, B, inset); GMS-positive septate hyphae with
acute angle branching (Figure 1, C)
Aspergilloma
Transsphenoidal hy-
pophysectomy
Nonadenomatous pituitary gland with fibrinopurulent material containing small-
to medium-sized encapsulated yeast forms (Figure 2, C), strongly PAS (Figure 2,
D) and GMS positive (Figure 2, E), weakly mucicarmine-positive capsules (Fig-
ure 2, D, inset)
Cryptococcoma
Resection of left
temporal lobe
Lymphohistiocytic perivascular infiltrate (Figure 3, C); macrophages with abundant
foamy cytoplasm (Figure 3, D); strongly PAS-positive bacilliform intracellular or-
ganisms (Figure 3, E)
Whipple disease
Resection Bacterial abscess (Figure 4, C and D). No evidence of tumor Bacterial abscess
Biopsy Intense acute inflammation with gram-positive cocci (Figure 5, C and D); Strepto-
coccus intermedius on culture
Bacterial abscess
Biopsy Neutrophilic abscess (Figure 6, D), with adjacent gliotic brain (Figure 6, C); fine,
filamentous weakly gram-positive organisms (Figure 6, E, arrow); cultures grew
Nocardia species
Nocardiosis
Stereotactic biopsy Granulomatous inflammation with rare acid-fast bacilli (Figure 7, C through E) Tuberculoma
Biopsy Bizarre, enlarged oligodendrocytes and atypical astrocytes, background histiocyte
accumulation (Figure 8, C and D); MIB1-labeled infected cells (Figure 8, E)
PML
Biopsy Gliosis, thick-walled vessels, chronic inflammation (Figure 9, C) and numerous
eosinophils (Figure 9, C, inset); eosinophilic, necrotic cystic structure with ser-
rated rim (Figure 9, D)
Cysticercosis
Resection White matter vacuolation (Figure 10, C), perivascular chronic inflammation and
gliosis (Figure 10, D); relative preservation of axons (Figure 10, E)
Tumefactive demyelination
2004: First biopsy First biopsy: demyelinating lesion (Figure 11, B) Demyelination
2007: Second biopsy Second biopsy: intense infiltrate of atypical B lymphocytes (Figure 11, D and E) Lymphoma
Resection Sharply demarcated necrosis, cerebellar cortex and white matter (Figure 12, C and
D) with ischemic neurons, microglial proliferation, and macrophage accumula-
tion (Figure 12, E)
Infarct, subacute
Resection Perivascular mixed inflammatory infiltrate (Figure 13, C and F through H), with
fibrinoid necrosis of vessel walls (Figure 13, D) highlighted by azocarmine (Fig-
ure 13, E)
Vasculitis
Resection Homogeneous eosinophilic extracellular deposits (Figure 14, B), congophilic (Fig-
ure 14, C), apple green birefringence (Figure 14, C, inset); EM: haphazard 6-␮m
fibrils (Figure 14, D)
Amyloidoma
Resection Amorphous congophilic deposits with apple green birefringence (Figure 14, F) Amyloidoma

4. 104 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Continued
Case No. Age, y/Sex Clinical History Imaging Findings Imaging Differential Diagnoses
15 33/F Recent onset of headaches MRI: Bifrontal lesion on either side of
falx, with dural extension (Figure
15, A and B)
Neurosarcoidosis, meningio-
ma, dural metastases
16 33/M H/O seizure disorder, schizophrenia,
IDDM
MRI: Multiple skull base lesions (Fig-
ure 16, A)
Meningiomas
17 62/M H/O thyroiditis, hypertension; devel-
oped vertigo, numbness left corner of
mouth, twitching left hand
MRI: Multiple enhancing lesions in
left cerebellum, corpus callosum,
cingulate gyrus, pons, thalamus, su-
prasellar region (Figure 17, A and B)
with minimal mass effect
Neoplasm: favor metastatic
18 40/M s/p remote glioma resection; 5 y later,
enlarging lesion with necrosis at site
of prior resection
MRI: Left parietal lobe lesion with pe-
ripheral enhancement on T1 (Figure
18, A), hyperintense, partially cystic
on T2 (Figure 18, B)
Recurrent tumor with cystic
change vs radiation necrosis
* s/p indicates status post; MRI, magnetic resonance imaging; GMS, Gomori methenamine silver; H/O, history of; DI, diabetes insipidus; PAS,
periodic acid–Schiff; CHOP, cyclophosphamide, adriamycin, vincristine, prednisone; Tx, treatment; DWI, diffusion weighted imaging; PPD, purified
protein derivative; CXR, chest x-ray; HIV, human immunodeficiency virus; CSF, cerebrospinal fluid; PML, progressive multifocal leukoencephalop-
athy; EM, electron microscopy; CT, computed tomography; and IDDM, insulin-dependent diabetes mellitus.
Figure 1. A, Coronal T1-weighted magnetic resonance imaging demonstrating a centrally hypointense lesion (arrow) within the left temporal
bone with irregular contrast enhancement. B, Granulomatous inflammation (hematoxylin-eosin, original magnification ϫ200). Inset, Multinucleate
giant cells (hematoxylin-eosin, original magnification ϫ400). C, Fungal hyphae with acute angle branching (Gomori methenamine silver stain,
original magnification ϫ400). Pathologic diagnosis: aspergilloma.
though most commonly occurring as an opportunistic in-
fection, aspergilloma is well described in immunocompe-
tent patients, especially in the context of local infection of
the ear or paranasal sinuses.1,2
The increase in fungal central nervous system (CNS)
disease seen by neurosurgeons and neuropathologists can
be attributed to the increasing numbers of immunocom-
promised patients, which is due to wide use of immuno-
suppressive drugs such as steroids, large elderly and di-
abetic populations, and increasing numbers of long-term
survivors of human immunodeficiency virus infection due
to antiretroviral treatment.3,4
The presentation can be very
variable, so a high index of suspicion is required in pa-
tients with a history of immunosuppression.
Intracranial fungal infection has been described follow-
ing a surgical intervention, often with fatal outcome,5
As-
pergillus species being the most commonly reported or-
ganism in these cases. Typically, cerebral aspergillosis re-
sults from hematogenous spread of the organism, or al-
ternatively by direct extension from an adjacent focus of
infection. Central nervous system Aspergillus infections
can present either as an abscess or as cerebral infarcts but
only rarely as meningitis.6
Aspergilloma may also present
as an extra-axial mass with extension into the brain pa-
renchyma. Kim et al7
described a case of extra-axial As-
pergillus flavus granuloma involving the left middle and
posterior cranial fossa, extending into the skull base and
adjacent cerebellar parenchyma. Of note, the patient was
an immunocompetent 34-year-old man with no other sig-
nificant history. Radiologically, the mass was hypointense
on T1-weighted MRI and exhibited irregular contrast en-
hancement. In the case series by Dubey et al,4
patients
with intracranial fungal granuloma most commonly pre-
sented with headache, followed by vomiting, proptosis,
and visual disturbances. Other presentations could in-
clude cranial nerve palsies and symptoms/signs of ele-
vated intracranial pressure and meningismus.8
The gran-
ulomas were most frequently seen in the frontal lobe, al-
though a classic location of aspergillomas is in a basal cra-
nial location, where it is thought to arise from an
infectious focus in the paranasal sinuses.9
In the 40 cases
described by Dubey et al,4
aspergilloma was the most fre-
quent organism found (25, 63%), followed by mucormy-
cosis (7, 18%), cryptococcoma (3), Cladosporium (3), Bipo-

5. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 105
Extended (Continued)
Surgical Procedure Histology Pathologic Diagnosis
Resection of firm,
gray mass
Hyalinized vessels surrounded by dense lymphocytic infiltrate (Figure 15, C) of pre-
dominantly B-cell type (Figure 15, D and E)
Castleman disease hyaline-
vascular type
Resection Mixed inflammatory infiltrate with admixed pale-staining histiocytes (Figure 16, B
and C)
Rosai-Dorfman disease
Biopsy Dense mixed inflammatory infiltrate (Figure 17, C) predominantly histiocytes and B
cells (Figure 17, D and E) with minor T-cell component (Figure 17, F)
Inflammatory pseudotumor
Resection Necrotic parenchyma with hemosiderin deposits and vascular channels (Figure 18,
C and D)
Radiation necrosis
Figure 2. A, Coronal T1-weighted magnetic resonance imaging (MRI) demonstrating a centrally hypointense intrasellar mass (arrow) with a thin
rim of peripheral enhancement. B, Axial T1-weighted MRI demonstrating a low signal intensity mass (arrow) within the sella with thin peripheral
enhancement and a thin enhancing septation. C, Necrotic basophilic material containing small- to medium-sized oval yeast forms (hematoxylin-
eosin, original magnification ϫ200). D, Organisms are strongly periodic acid–Schiff positive (original magnification ϫ400). Inset, Capsule of
organism is weakly mucicarmine positive (original magnification ϫ400). E, Organisms are strongly labeled by Gomori methenamine silver stain
(original magnification ϫ400). Pathologic diagnosis: cryptococcoma.
laris hawaiiensis (1), and Candida species (1). There was a
63% mortality rate in these patients, mostly due to menin-
goencephalitis.
Radiologically, fungal granulomas present as enhancing
masses.9
Adjacent to the dura, they can simulate menin-
giomas, even producing a dural tail sign.3
On CT scan,
they may be associated with paranasal sinusitis and small
areas of bony destruction.4
Their MRI appearances can
vary somewhat depending on the organism involved. As-
pergillomas tend to demonstrate intermediate signal in-
tensity surrounded by perilesional edema on T2.4
How-
ever, cryptococcomas have low T2-weighted signal inten-

6. 106 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 3. A, Axial fluid-attenuated inversion recovery magnetic resonance imaging (MRI) demonstrating bilateral hyperintense temporal lobe
lesions (arrows), left greater than right, involving cortex and subjacent white matter. B, Axial T1-weighted postcontrast MRI demonstrating bilateral
hypointense temporal lobe lesions (arrows) with peripheral enhancement and some prominent surrounding vessels. C, Perivascular lymphohistio-
cytic inflammatory infiltrate (hematoxylin-eosin, original magnification ϫ200). D, Macrophages with pale eosinophilic, foamy cytoplasm (hema-
toxylin-eosin, original magnification ϫ400). E, Brightly periodic acid-Schiff–positive intracellular organisms within macrophages (original magni-
fication ϫ400). Pathologic diagnosis: Whipple disease.
sity in contrast to the surrounding hyperintense cerebral
edema. Other fungal infections such as histoplasmosis can
also simulate brain tumors radiologically.9
Case Example 2: Pituitary Cryptococcoma
In immunosuppressed individuals, cryptococcal infec-
tions typically produce a diffuse meningitis, and infiltra-
tion of the perivascular Virchow-Robin spaces by the or-
ganism can result in the formation of small intraparen-
chymal gelatinous pseudocysts, with a minimal or absent
inflammatory response. In immunocompetent hosts, a
chronic granulomatous reaction surrounds the organisms
and there is neovascular growth around the granulomas,
producing contrast enhancement similar to that of pri-
mary or secondary brain tumors.10,11
Cryptococcomas may
be seen in individuals with a predisposition to fungal in-
fections, which may not be evident on initial inquiry, and
may require more detailed history and workup to identify
conditions such as diabetes or sarcoidosis.12
Cryptococ-
comas are most commonly found in the cerebellum, brain-
stem, basal ganglia, or temporoparietal lobes. Distinguish-
ing them from tumors and abscesses due to other organ-
isms can be challenging because there is no distinctive
radiologic feature that is unique to cryptococcomas. Typ-
ically, cryptococcal disease presents on MRI as T2 hyper-
intense cystic lesions within the bilateral basal ganglia
with variable enhancement and surrounding edema. They
also often tend to insinuate in dilated Virchow-Robin peri-
vascular spaces. Enhancing cryptococcomas often do not
show restricted diffusion on diffusion-weighted imaging
(DWI),9
low signal intensity on T1-weighted imaging, and
low9
or high intensity12
on T2 imaging, with uniform or
ring enhancement. They may also have mild surrounding
edema and focal calcification within them.12
Cryptococ-
comas may rarely involve the parasellar or pituitary re-
gion. Yu et al13
described a case of parasellar cryptococ-
coma occurring in an immunocompetent patient. The ra-
diologic features of the lesion were similar to a pituitary
adenoma, showing uniform contrast enhancement, with
low signal on T1-weighted imaging and high signal on T2
imaging. The contrast enhancement of the meninges ad-
jacent to the cryptococcoma helped in differentiating it
from an adenoma.

7. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 107
Figure 4. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrating a peripherally enhancing lesion (arrow) within
right frontal lobe, with cortical extension. B, Axial T2-weighted MRI demonstrating marked T2 hyperintense perilesional edema (arrow) typical for
a bacterial infection. C, Abscess containing dense collections of neutrophils (hematoxylin-eosin, original magnification ϫ200). D, Edge of abscess
is composed of a fibroinflammatory capsule (hematoxylin-eosin, original magnification ϫ200). Pathologic diagnosis: bacterial abscess.
Case Example 3: Whipple Disease
Whipple disease is a chronic inflammatory disorder that
involves multiple organ systems, typically the gastrointes-
tinal tract and musculoskeletal system.14
The causative
agent is a soil-borne gram-positive bacillus Tropheryma
whippelii. The classic presentation includes fever, steator-
rhea, weight loss, skin pigmentation, lymphadenopathy,
and recurrent arthritis.14,15
The walls of the intestine and
lymph nodes are found to contain accumulations of foamy
macrophages containing the characteristic periodic acid-
Schiff–positive organisms. The CNS is involved in 6% to
43% of patients with Whipple disease,15
but isolated CNS
disease is very rare, with only 14 cases described in the
literature.14,15
Radiologically, the lesions are predominantly
hyperintense on T2-weighted magnetic resonance (MR)
images and may show homogeneous or ring enhance-
ment.15
They can be surrounded by variable perilesional
edema. Generally speaking, patients presenting with pri-
mary CNS Whipple disease can be divided into 2 groups.
First, those with multiple lesions may exhibit a plethora
of neurologic symptoms and signs, including seizures,
ataxia, supranuclear vertical gaze palsy, headaches, pap-
illedema, hemiplegia, syndrome of inappropriate antidi-
uretic hormone, and fever. Interestingly, some patients
may develop oligoclonal bands in the cerebrospinal fluid
similar to those found in multiple sclerosis, cerebral lupus,
human immunodeficiency virus infection, and sarcoido-
sis.14
Those with focal mass lesions have symptoms refer-
able to the site involved. The patient described by Lohr et
al15
had an isolated frontal mass in the white matter,
which had MRI features suggestive of a low-grade glioma.
It was T2 hyperintense, was slightly hypointense on T1-
weighted images, and had subtle ring enhancement with-
out perilesional edema. As in our patient, the presentation
included behavioral changes and aggressiveness. Follow-
ing resection of the mass, the characteristic perivascular
foamy macrophages containing periodic acid-Schiff–posi-
tive, diastase-resistant rod-shaped organisms were seen.
There was marked associated gliosis.

8. 108 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 5. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrating a left thalamic ring–enhancing lesion (arrow). B,
Axial T2-weighted MRI demonstrating a well-circumscribed T2 hyperintense left thalamic lesion (arrow) with peripheral T2 hypointense rim. C,
Neutrophilic abscess with collections of basophilic organisms (hematoxylin-eosin, original magnification ϫ400). D, Organisms are gram-positive
cocci (Brown-Hopps Gram stain, original magnification ϫ1000). Pathologic diagnosis: bacterial abscess.
Other cases of solitary CNS Whipple disease have also
involved the frontoparietal regions, and in one of these,
there was associated destruction of the calvarium adjacent
to the lesion.16
In cases of multifocal disease, the lesions
have mostly occurred in the cortical or subcortical grey
matter, involving mainly the temporal lobes and thala-
mus.15
Although the clinical presentation and radiologic
findings in intracranial Whipple disease can closely mimic
those of a low-grade glioma, the histologic picture of peri-
vascular foamy histiocytes should prompt the pathologist
to look for the periodic acid-Schiff–positive intracellular
organisms and arrive at the correct diagnosis.
Case Examples 4 and 5: Bacterial Abscess
Differentiating between pyogenic brain abscesses and
centrally necrotic intra-axial tumors can often be challeng-
ing radiologically, because both commonly demonstrate
ring enhancement and perilesional edema. A helpful find-
ing on MRI examination is the presence of a hypointense
capsule on T2-weighted images, which is not usually seen
in tumors.9
Diffusion weighted imaging is a well-known
and valuable radiologic tool in these cases: brain abscesses
typically show markedly hyperintense signal changes on
DWI, whereas the appearance of high-grade gliomas
varies from slightly hyperintense to hypointense signal.17
The apparent diffusion coefficient reveals reduced values
in brain abscesses. These findings are, however, not en-
tirely specific, because a centrally reduced apparent dif-
fusion coefficient has been also reported in neoplastic le-
sions.18
Case Example 6: Nocardiosis
Brain abscess due to Nocardia species is a rare condition,
and although it can occur in patients with an intact im-

9. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 109
Figure 6. A, Axial postcontrast T1-weighted magnetic resonance imaging demonstrates a ring-enhancing lesion (arrow) within the left parietal
white matter with central hypointensity and surrounding edema. B, Axial diffusion-weighted imaging. The lesion (arrow) demonstrates hyperintensity
on diffusion imaging. C, Gliotic brain tissue with mixed inflammatory infiltrate (hematoxylin-eosin, original magnification ϫ200). D, Center of
lesion contains neutrophilic abscess (hematoxylin-eosin, original magnification ϫ200). E, Tissue Gram stain reveals fine, filamentous gram-positive
bacteria within abscess (arrow) (Brown-Hopps Gram stain, original magnification ϫ1000). Pathologic diagnosis: nocardiosis.
mune system, it is usually seen among immunocompro-
mised patients.6
It can be confused with intracranial tu-
mors radiologically.19
Ozturk et al20
described a case of
nocardial brain abscess occurring in a renal transplant re-
cipient on an immunosuppressive drug regimen. Kilincer
et al19
described a further 2 cases of nocardial brain ab-
scess, one of whom was a 39-year-old woman with sys-
temic lupus erythematosus who developed a left fronto-
parietal abscess, and the other was a 43-year-old man with
glomerulonephritis treated with corticosteroids who de-
veloped a ring-enhancing multiloculated abscess in the
left cerebellar hemisphere, with an additional 2 small su-
pratentorial lesions. Both underwent treatment with long-
term antibiotics and evacuation of the abscess. Histologi-
cally, nocardiosis appears as a necrotic lesion with acute
inflammation. The organism is weakly acid-fast with the
Fite stain, having a beaded, filamentous appearance, and
also is highlighted by the Gomori methenamine silver
stain.
Case Example 7: Tuberculoma
Intracranial tuberculomas may exhibit nodular or ring-
like enhancement on MRI similar to a primary or meta-
static brain tumor.10
When present, areas of caseation can
correlate with isointense or mixed intensity areas seen
within the mass on T1-weighted images. The surrounding
collagenous fibrosis corresponds to the slightly hyperin-
tense rim. The MRI appearance of tuberculomas varies
according to the age of the lesion. On T2-weighted im-
aging, immature tuberculomas appear as multiple small
areas of isointensity or hypointensity surrounded by hy-
perintense edema. Mature tuberculomas are heteroge-
neously hypointense or isointense throughout the lesion,
with ring enhancement seen on postcontrast T1-weighted
images. Clues to the granulomatous nature of the lesion
are its conglomerate and ring-enhancing MRI appearance.
A ‘‘targetlike’’ appearance with central calcification, peri-
lesional edema, and peripheral enhancement on CT scan
has been described, although is not always present.10
Mag-
netic resonance spectroscopy (MRS) is typically inconclu-
sive and does not help distinguish the condition from a
neoplasm. Diffusion-weighted imaging is usually hyper-
intense.9
Fortunately, if biopsy or excision is performed,
the histologic appearance of tuberculoma is characteristic,
with granulomatous inflammation, caseation, calcification,
and surrounding gliosis. If only the edge of the lesion is
biopsied, it is important for the pathologist to distinguish
this reactive gliosis from a glial neoplasm.
Case Example 8: Progressive Multifocal
Leukoencephalopathy
Typically, patients with progressive multifocal leuko-
encephalopathy (PML) present with weakness, hemiano-

10. 110 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 7. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) scan demonstrating a right basal ganglia lesion (arrow) with
irregular peripheral enhancement with midline shift and surrounding edema. B, Axial T2-weighted MRI demonstrating heterogeneous signal inten-
sity with central areas of low T2 signal and marked surrounding edema. C, Gliosis and chronic inflammation (hematoxylin-eosin, original mag-
nification ϫ200). D, Granuloma with surrounding intense chronic inflammatory infiltrate (hematoxylin-eosin, original magnification ϫ200). E, Rare
pink-stained acid-fast bacilli within the lesion (arrow) (Kinyoun acid-fast stain, original magnification ϫ1000). Pathologic diagnosis: tuberculoma.
pia or quadrantanopia, and cognitive abnormalities.21
On
imaging, PML lesions typically present as large, multifo-
cal, subcortical white matter lesions without mass effect.
They are most commonly found in the parietal lobe white
matter,22
but they can also be seen in the occipital lobe,
corpus callosum, and thalamus. Typically, PML does not
enhance, although lesions may demonstrate mild periph-
eral or scalloped areas of enhancement, often associated
with reconstitution of the patient’s immune response. In
some cases there may be low density or T2 hyperintense
cystlike areas within PML lesions.21
These may represent
areas of necrosis within the lesion. The lesions may typi-
cally show no or faint contrast enhancement. In the series
of Thurnher et al,21
a third of the patients with PML lesions
had significant mass effect with compression of the ipsi-
lateral lateral ventricle, which is in contrast to the typical
lack of mass effect described in the literature. Therefore,
necrotic white matter lesions in acquired immunodeficien-
cy syndrome patients, particularly with peripheral scal-
loping, should be considered highly suggestive of PML
rather than a necrotizing tumor, and the pathologist
should be on the alert for the accompanying histologic
appearance. On microscopic examination of the biopsy or
resection, the PML lesions exhibit demyelination and con-
tain enlarged oligodendrocytes with hyperchromatic nu-
clei, some of which may contain eosinophilic intranuclear
inclusions, and enlarged astrocytes with bizarre nuclei.23
Immunohistochemistry for the JC viral capsid protein may
also be performed as confirmation.23
Case Example 9: Neurocysticercosis
Neurocysticercosis develops when the larval form of the
tapeworm Taenia solium encysts in the brain inciting a sur-
rounding inflammatory and granulomatous response.
It is the most common cause of acquired seizures world-
wide and is increasingly seen in the United States, partic-
ularly in the immigrant community.24
Although epilepsy
is the most common presenting symptom, other manifes-
tations include severe episodic headache,25
meningitis, ob-
structive hydrocephalus if the cyst is near a ventricle or
the subarachnoid space, and cognitive problems.10,24
Ra-
diologic diagnosis is often straightforward, although the
appearance varies depending on the life cycle stage of the
parasite and the age of the lesion. The lesion can appear
as a single or multiple enhancing cysts with calcification,
the latter representing dead larvae or nodular calcified
stage.1,10
When the larvae are invading the brain, they ap-
pear as small nonenhancing edematous lesions, later form-
ing small enhancing nodules.10
As the lesions become cys-
tic and the larvae start to die, surrounding edema devel-

11. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 111
Figure 8. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) revealing hypointense, nonenhancing lesion within the right
middle cerebellar peduncle (arrow). B, Axial T2-weighted MRI demonstrating T2 hyperintense lesion within the right middle cerebellar peduncle
(arrow). C, White matter pallor with mild chronic inflammation and enlarged, hyperchromatic oligodendroglial nuclei (hematoxylin-eosin, original
magnification ϫ400). D, Enlarged, bizarre astrocytes, with collections of foamy histiocytes (hematoxylin-eosin, original magnification ϫ400). E,
Enlarged progressive multifocal leukoencephalopathy-infected cells are MIB1 (Ki-67) immunopositive (original magnification ϫ400). Pathologic
diagnosis: progressive multifocal leukoencephalopathy.
ops due to the inflammatory response to the cyst contents,
and there is ring enhancement due to the formation of
granulation tissue and a thick capsule. On DWI, the cysts
have a similar signal intensity to cerebrospinal fluid, un-
like pyogenic abscesses.9
Usually the lesions are less than
20 mm in diameter.10
A helpful finding is the identification
of a scolex (larval body) within the cyst.9
The scolex is
typically hyperintense on T1-weighted sequences.10
Soli-
tary lesions can be difficult to distinguish from a neo-
plasm owing to the surrounding edema and the cyst en-
hancement.9
It may even mimic a glioblastoma multiforme
radiologically.26
In these cases, it is helpful to correlate the findings with
other clinical data such as cerebrospinal fluid immunology
for T solium antibody titers. Pathologically, the presence of
a fibrous cystic structure with granulomatous inflamma-
tion should prompt a search for an infectious etiology. In
patients originating from endemic areas such as South
America, Africa, and Asia, a careful search for the char-
acteristic larval forms and scolices should be made.
DEMYELINATION
Case Examples 10 and 11: Demyelination
Masslike features or a so-called tumefactive appearance
of demyelinating plaques are well described in the liter-
ature. Multiple sclerosis, and other primarily demyelinat-
ing diseases, such as myelinoclastic diffuse sclerosis
(Schilder disease) and acute disseminated encephalomy-
elitis can manifest as tumefactive lesions. Differentiating
between demyelinating lesions and brain tumors, such as
gliomas, in the presence of solitary lesions can be difficult
and problematic.
As in case 10, a peripherally enhancing lesion with a
butterfly configuration occurring in a 57-year-old man
with acute onset of symptoms almost automatically trig-
gers a suspected diagnosis of glioblastoma. However, on
closer examination of the images, the incomplete ring and
peripheral contrast enhancement as seen in this case
should give rise to suspicion and perhaps prevent a pre-
mature conclusion. This condition is a ‘‘classic’’ mimic of
high-grade glioma, and recently, the characteristic horse-
shoe-shaped contrast enhancement on MRI has been de-
scribed. Additional radiologic tools, including MR perfu-
sion imaging or MRS can further aid in arriving at the
correct diagnosis, thus avoiding a surgical biopsy.27,28
Fea-
tures that favor a demyelinating lesion include a relative
lack of mass effect and vasogenic edema.10
In radiologic
parlance, the ‘‘open ring sign’’ is contrast enhancement
shaped as an open ring or a crescent in the white matter.
It is often present in large contrast-enhancing demyeli-

12. 112 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 9. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrates suprasellar heterogeneous peripherally ring-en-
hancing lesion (arrow) near the anterior communicating artery. B, Axial T2-weighted MRI demonstrates a T2 hypointense rounded suprasellar
lesion (arrow). C, Thick-walled vessel with adjacent mixed chronic inflammatory infiltrate (hematoxylin-eosin, original magnification ϫ100). Inset,
The infiltrate contains numerous eosinophils. D, Degenerated eosinophilic capsule of cysticercus, with serrated surface (hematoxylin-eosin, original
magnification ϫ200). Pathologic diagnosis: cysticercosis.
native lesions and is more likely to be associated with
these than with neoplasms or infections.29
In demyelin-
ation, the incomplete ring of enhancement may have ill-
defined margins.30
Differentiation between a solitary de-
myelinating lesion and a glioma can be very challenging
radiologically.10,30,31
Therefore, if the presentation and im-
aging findings remain inconclusive and a histologic di-
agnosis is necessary, the pathologist has to keep this con-
dition in the differential diagnosis, because erroneous di-
agnoses of high-grade glioma have been reported many
times in the medical literature, even though the distin-
guishing features are also well documented.32
When de-
myelinative lesions have a marked inflammatory compo-
nent, they may be confused with a primary CNS lympho-
ma. The more gliotic lesions are more apt to be confused
with high-grade astrocytomas, however. If one is unfa-
miliar with the characteristic appearance of Creutzfeldt
astrocytes seen in demyelination, the possibility of sub-
stantial astrocytic pleomorphism, and the occurrence of
mitotic figures in demyelinative lesions, they may be mis-
interpreted as high-grade glioma.33
VASCULAR DISORDERS
Case Example 12: Infarct
Instances in which infarcts mimic high-grade gliomas
due to contrast enhancement and mass effect are docu-
mented in the literature.34,35
To distinguish a cerebrovas-
cular accident from a neoplasm, repeat imaging studies
after a short interval or advanced techniques such as MR
perfusion may also be helpful.34,36
In most cases, diagnosis
of ischemic stroke/infarction is not problematic. The char-
acteristic clinical history of a sudden onset of neurologic
symptoms and signs, in combination with the typical ra-
diologic findings, including diffusion-restriction, T2/fluid-
attenuated inversion recovery hyperintense signal, mass
effect, and possible gyral enhancement pattern together in
a typical vascular distribution, usually leads to the correct
diagnosis.9
Confounding diagnostic features in ischemic
infarction that are more suggestive of a brain tumor in-
clude an atypical presentation, such as a slow evolution of
neurologic symptoms,10
and a poorly defined cerebral le-
sion on imaging with associated mass effect, radiologically

13. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 113
Figure 10. A, Axial T2-weighted magnetic resonance imaging (MRI) demonstrating a hyperintense bifrontal butterfly-shaped lesion (arrow) ex-
tending across the genu of the corpus callosum. B, Axial postcontrast T1-weighted MRI demonstrates peripheral enhancement surrounding the
lesion, in the form of an open ring (arrow), an imaging sign suggestive of a tumefactive demyelinating lesion. C, Extensive white matter vacuolation
with preservation of the overlying cortex (hematoxylin-eosin, original magnification ϫ40). D, Perivascular chronic inflammation with surrounding
lipid-laden macrophages and gliosis (hematoxylin-eosin, original magnification ϫ400). E, Relative preservation of axons (stained black) in areas
of demyelination (Bielschowsky stain, original magnification ϫ200). Pathologic diagnosis: tumefactive demyelinating lesion.
simulating glioma.9,10
A subacute infarction can show ir-
regular contrast enhancement and mimic high-grade gli-
oma. Some infarcts can also exhibit ring enhancement,
strongly resembling that of glioblastoma.34
An under-
standing of the cerebral arterial vasculature is essential in
arriving at a correct diagnosis.10
Diffusion weighted im-
aging is a helpful modality for distinguishing between
these 2 conditions,10
particularly when the clinical history
is obscure, and in the acute or early subacute phase of an
ischemic stroke.9
In late subacute to chronic infarctions,
however, restricted diffusion may not be evident thus
making DWI less useful in making the distinction between
tumor and an infarct.9
In this case, short-term follow-up
imaging may be necessary to document the evolution of
the lesion.10
Case Example 13: Vasculitis
The clinical presentation and imaging findings in this
case do not provide unequivocal evidence to arrive at the
correct diagnosis. The sudden focal neurologic deficit and
the ring enhancement of the deep white matter lesion
prompted the preoperative diagnosis of high-grade glio-
ma. There were no findings in the patient’s preoperative
evaluation consistent with an inflammatory process: there
were no systemic symptoms and her laboratory values in-
cluding an erythrocyte sedimentation rate and a white
blood cell count were within reference range. Indeed,
there are relatively few cases of this condition reported in
the literature, especially presenting as a solitary contrast-
enhancing mass. Further imaging studies (perfusion-
weighted MRI, angiography) may be valuable, but it has
been suggested that a stereotactic biopsy should become
the gold standard in the management of these cases, even
though the diagnostic yield is reportedly low.37,38
Behc¸et
disease has been reported to produce a solitary masslike
lesion in the hemisphere, with low attenuation on T1-
weighted MRI, and extensive hyperintensity on fluid at-
tenuated inversion recovery.39,40
However, this scenario is
very rare, as Behc¸et disease usually presents as multiple
T2 hyperintense lesions.39
Magnetic resonance spectros-
copy can be of assistance in distinguishing a vasculitic
lesion from a neoplasm. Panchal et al41
reported a case of
lymphocytic vasculitis presenting as multifocal tumorlike
lesions within the right cerebral hemisphere, which were

14. 114 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 11. A, 2004 postcontrast T1-weighted axial magnetic resonance imaging (MRI) demonstrating a right frontal heterogeneously enhancing
mass (arrow) with surrounding edema and mass effect. B, 2004 biopsy, with perivascular chronic inflammation and abundant foamy macrophages
(Luxol fast blue and hematoxylin-eosin, original magnification ϫ200). C, 2007 postcontrast T1-weighted axial MRI demonstrating a homogeneously
enhancing subcortical lesion (arrow) in the left inferior parietal lobe. D, 2007 biopsy, with monotonous lymphocytic infiltrate and numerous
apoptotic bodies (hematoxylin-eosin, original magnification ϫ200). E, 2007 biopsy, infiltrate is composed of CD20 (L26) immunopositive B cells
(original magnification ϫ200). Pathologic diagnosis: demyelinating disease and central nervous system lymphoma.
enhancing on postgadolinium T1-weighted MR, with as-
sociated massive vasogenic edema involving the whole
hemisphere. Radiologically, the lesions mimicked a mul-
tifocal glioma. However, the MRS pattern was more con-
sistent with an inflammatory process (no elevated choline
peak, marked elevation of glutamate/glutamine metabo-
lites) rather than an aggressive neoplasm. The diagnosis
was confirmed by craniotomy and excisional biopsy.
AMYLOIDOSIS
Case Examples 14i and 14ii: Amyloidoma
After the initial clinical and radiologic workup, the le-
sion in case 14i was thought to be a schwannoma of the
fifth nerve, which would fit the imaging features and pre-
sentation. A meningioma was also considered, because the
lesion showed a highly suggestive ‘‘dural tail sign’’ on
imaging. The absence of any evidence of systemic disease
associated with the deposition of amyloid in this case
made this a very difficult diagnosis.
Nonetheless, several such lesions in this location with
similar presentation and imaging findings have been re-
ported. Interestingly, the deposits were histochemically
composed of ␭ protein, as in the present case.42–44
The most frequent presentation of intracranial amyloid
is as cerebral amyloid angiopathy, or as deposits within
the senile plaques of Alzheimer disease. Amyloidoma is
seen much less frequently. Amyloid presenting clinically
and radiologically as an intracranial tumor is rare. Amy-
loid presenting as a tumorlike mass has been reported in
the cerebral hemispheres in patients ranging in age from
28 to 60 years, including the temporal45,46
and occipital
lobes,46,47
and also the cerebellopontine angle.43
Typically,
they appear as supratentorial white matter masses that are
high density on nonenhanced CT scan, with little to no
mass effect.48
They can extend up to the walls of the lateral
ventricle and have fine, irregular enhancing margins. Cen-
tral nervous system amyloid can also present as multiple
contrast-enhancing lesions in the hemispheres.49
Other locations have included the Gasserian ganglion43
manifesting clinically as trigeminal neuropathy, which
had a signal intensity similar to cortex on T1-weighted

15. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 115
Figure 12. A, Axial postcontrast T1-weight-
ed magnetic resonance imaging demonstrat-
ing abnormal gyriform enhancement involv-
ing the bilateral paramedian cerebellar hemi-
spheres, left greater than right (arrow), with
mass effect and edema. B, Axial diffusion-
weighted imaging demonstrates gyriform hy-
perintensity of the cerebellar folia (arrow),
mimicking the appearance of Lhermitte-Du-
clos disease. C, Sharply demarcated area of
cortical necrosis at right of field, extending to
underlying white matter (hematoxylin-eosin,
original magnification ϫ12). D, Eosinophilic,
demarcated area of cortical necrosis seen at
right of field (hematoxylin-eosin, original
magnification ϫ200). E, Numerous KP-1 im-
munopositive macrophages and microglia
within infarct (original magnification ϫ400).
Pathologic diagnosis: subacute infarct.
imaging, heterogeneous signal intensity on T2 imaging,
with marked uniform enhancement on postcontrast T1
imaging. The mass was thought to be a meningioma or
schwannoma preoperatively. The sella50
and choroid plex-
us are other known sites. Ragel et al47
described a 59-year-
old man with a 6-month history of confusion and head-
aches; MRI revealed a left parietooccipital lesion extend-
ing to the splenium of the corpus callosum. The mass had
MRI and MRS features of a high-grade glioma, with a
stellate hyperintense rim on T2-weighted imaging, and el-
evated choline peak on MRS. Biopsy findings were those
of amyloidoma, with amorphous congophilic deposits and
apple green birefringence. Findings not consistent with
high-grade glioma were the lack of peritumoral edema
and minimal mass effect. Another article45
described a
right temporal lobe mass in a 51-year-old woman pre-
senting with hearing loss and recurrent right-sided otitis
media. The MRI and CT findings were suspicious for gli-
oma, and stereotactic biopsy with intraoperative squash
preparation followed by routine histology and electron mi-
croscopy revealed amyloidoma.
Cerebral amyloid angiopathy can also mimic glioma ra-
diologically and clinically. Safriel et al46
reported 2 pa-
tients with MR findings suggestive of low-grade glioma.
The first case was a 49-year-old man with a tumefactive
mass in the occipitotemporal lobe without enhancement
or restricted diffusion and unremarkable spectra. Biopsy
and histopathology revealed cerebral amyloid angiopathy
with angiitis. The second case was a 71-year-old woman
with an ill-defined infiltrative nonenhancing mass, with-

16. 116 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 13. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) reveals a centrally hypointense deep left parietal lobe mass
lesion (arrow) with a thickened, irregular enhancing rim. B, Axial T2-weighted MRI demonstrates a rounded T2 hypointense left parietal lesion
(arrow) with marked surrounding edema. C, Prominent perivascular inflammatory infiltrate (hematoxylin-eosin, original magnification ϫ100). D,
Fibrinoid necrosis of vessel wall (hematoxylin-eosin, original magnification ϫ400). E, The fibrinoid necrosis is highlighted bright red by an azo-
carmine stain (original magnification ϫ400). F, Perivascular histiocytes within the infiltrate are immunopositive for CD68 (KP-1) (original magni-
fication ϫ200). G, Perivascular B cells are highlighted by the CD20 immunostain (original magnification ϫ400). H, Perivascular T cells are
highlighted by the CD3 immunostain (original magnification ϫ400). Pathologic diagnosis: vasculitis.
out restricted diffusion, within the right occipital and pa-
rietal lobes, and unremarkable MRS findings. Biopsy re-
vealed cerebral amyloid angiopathy. Cerebral amyloid an-
giopathy may also present as a mass within the brain.
Osumi et al51
describe a 59-year-old woman presenting
with a large right temporoparietal lobe mass lesion, which
was white matter based, and was nonenhancing, nonhem-
orrhagic, and low attenuation on MRI examination. A di-
agnosis of low-grade glioma was considered. Biopsy was
nondiagnostic, revealing only gliosis. Subtotal resection of
the right temporal lobe was then performed, and histology
showed congophilic vascular mural deposits of amyloid,
with diffuse white matter gliosis and edema. There was
no evidence of tumor.

17. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 117
Figure 14. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrating a mildly hypointense mass (arrow) centered at
left Meckel cave at the expected location of the trigeminal/gasserian ganglion. B, Homogeneous eosinophilic deposits are present within lesion
(hematoxylin-eosin, original magnification ϫ100). C, The deposits are stained orange-red (Congo red stain, original magnification ϫ100). Inset,
Deposits demonstrate apple green birefringence under polarized light (Congo red stain and polarized light, original magnification ϫ100). D and
inset, Electron microscopy reveals haphazard arrangement of 6-␮m fibrils, typical for amyloid. E, Axial computed tomography bone window shows
a hyperdense biconvex-shaped lesion involving the right frontoparietal calvarium causing mass effect on the right cerebral hemisphere. F, Con-
gophilic deposits have apple green birefringence (Congo red stain and polarized light, original magnification ϫ400). Pathologic diagnosis: amy-
loidoma.

18. 118 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 15. A, Axial fluid-attentuated inversion recovery magnetic resonance imaging (MRI) demonstrates increased signal intensity bifrontally on
either side of the falx (arrow). B, Axial postcontrast T1-weighted MRI shows contrast-enhancing lesion (arrow) along the falx and frontal dura
bilaterally. C, A dense lymphocytic infiltrate surrounds hyalinized central vessel (hematoxylin-eosin, original magnification ϫ400). D, The lym-
phocytic infiltrate is predominantly B cells (CD20 immunostain, original magnification ϫ400). E, There is a minor population of T cells (CD3
immunostain, original magnification ϫ400). Pathologic diagnosis: Castleman disease, hyaline-vascular type.
NONINFECTIOUS INFLAMMATORY CONDITIONS
Case Example 15: Castleman Disease
Castleman disease, also known as angiofollicular lymph
node hyperplasia, occurs in 2 forms. Most cases are the
hyaline-vascular type, as in our case, with the typical his-
tologic finding of hyalinized follicular centers with a ra-
dial penetrating vessels and prominent interfollicular cap-
illary proliferation. The plasma cell type represents only
5% to 10% of cases, and is characterized by large lym-
phoid follicles separated by sheets of mature plasma cells
and less stromal vascularization.52,53
Localized forms of the
disease are generally asymptomatic, while the generalized
form may present with fever, weight loss, anemia, poly-
neuropathy, organomegaly, and monoclonal proteinemia,
thus resembling a paraneoplastic syndrome. Intracranial
Castleman disease is very rare, with 13 cases described in
the literature, and in this locality it may mimic a neo-
plasm, in particular a meningioma. Previously described
locations include the hemisphere convexities and adjacent
to the falx. As expected with the predominantly cortical
location of the lesion, patients presented most commonly
with seizures, and focal signs such as right hand clumsi-
ness,53
left hemiparesis, and incoherent speech.52
By CT
imaging, the lesions were homogeneously enhancing with
perilesional edema.52
Some demonstrated dural enhance-
ment by MRI, mimicking a meningioma.53
Angiography
of these intracranial cases revealed no vascular blush, in
contrast to other sites where there is typically a homoge-
neous capillary blush from neovascularization.52
Although
most cases occur in adults, there is a single report in an
8-year-old girl.54
The child presented with sudden onset
of partial motor seizures and a left posterior parietal, par-
tially mineralized, contrast-enhancing meningeal mass.
The treatment of choice for localized Castleman disease
is gross total resection of the lesion, after which total and
complete recovery is the rule52,54
including resolution of
the systemic manifestations of the disorder. In summary,
although it is a rare entity in the CNS, Castleman disease
should be considered in the differential diagnosis of in-
tracranial meningeal tumors.
Case Example 16: Rosai-Dorfman Disease
Sinus histiocytosis with massive lymphadenopathy, or
Rosai-Dorfman disease, was first described in 1969.55
It
typically presents in children and young adults, and has
a mean age of onset of 20.6 years, with bilateral, painless
cervical lymphadenopathy. Some patients also have sys-
temic symptoms such as elevated sedimentation rate, fever,

19. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 119
Figure 16. A, Sagittal postcontrast T1 magnetic resonance imaging
shows a trilobed-enhancing central skull base lesion with involvement
of the sella and suprasella cistern. B, The resected lesion contains a
dense diffuse mixed inflammatory infiltrate (hematoxylin-eosin, origi-
nal magnification ϫ100). C, Within the infiltrate, there are numerous
pale-staining histiocytes and plasma cells (hematoxylin-eosin, original
magnification ϫ400). Pathologic diagnosis: Rosai-Dorfman disease.
leukocytosis, and polyclonal hypergammaglobulinemia.55
Extranodal involvement also occurs in more than 40% of
patients, particularly in the paranasal sinuses, orbit, skin,
and upper respiratory tract.56
Central nervous system in-
volvement is less common, being found in 22% of patients,
and isolated CNS disease is rarer still. Disease of the CNS
typically manifests itself in the epidural or subdural com-
partments,56
but a suprasellar location has been reported.55
Patients presenting with or developing cranial involve-
ment have a mean age of 34.9 years, with a male predom-
inance. Some of the usual presentations of intracranial dis-
ease include seizures, headache, cranial nerve deficits,
hemiparesis, and dysphasia.55
Imaging reveals single or
multiple meningeal-based masses, which are enhancing,
with variable surrounding edema, and can appear iden-
tical to a meningioma on CT and MRI scan.55,57,58
Associ-
ated lytic lesions may be seen in the skull.56
On surgical
resection, the lesion may also grossly be indistinguishable
from a meningioma, and so diagnosis will rest with his-
tology. Fortunately, differentiation of sinus histiocytosis
with massive lymphadenopathy from meningioma pre-
sents no difficulty in most cases, with the possible excep-
tion of the lymphoplasmocyte-rich variant of meningio-
ma.57
Helpful histologic features include the characteristic
pale-staining histiocytes with delicate nuclear membranes,
exhibiting emperipolesis, that is, intact lymphocytes, neu-
trophils, and plasma cells within the cytoplasm. There
may also be erythrophagocytosis and perivascular collec-
tions of plasma cells.56
Immunohistochemistry is helpful
in demonstrating the characteristic S100 protein, CD68,
and factor XIIIa–positive histiocytes, which unlike those
in Langerhans cell histiocytosis, are negative for CD1a.57
Because there are as yet only a few reports of intracra-
nial Rosai-Dorfman disease, the ideal treatment for this
condition is so far undefined. Surgery has been the treat-
ment of choice.55
Adjunctive therapy has included che-
motherapy, irradiation, and steroids. So far, no deaths
from intracranial sinus histiocytosis with massive lymph-
adenopathy have been reported, and patients who under-
went complete resections had no recurrences.55
The effec-
tiveness of steroids in this condition has been described.
McPherson et al59
reported a 53-year-old male patient with
multiple skull base lesions who underwent craniotomy for
1 lesion and experienced marked resolution of the remain-
ing lesions following corticosteroid administration.
Another systemic histiocytic disease that can involve the
CNS and produce lesions mimicking a primary brain tu-
mor is Erdheim-Chester disease.
The disease is a non–Langerhans cell histiocytosis and
usually affects middle-aged adults, producing osteoscle-
rotic and lipogranulomatous lesions of the long bones and
retroperitoneal and pulmonary fibrosis.60
When there is
neurologic involvement, it typically manifests itself as hy-
pothalamic/pituitary dysfunction.61
A solitary left tem-
poroparietal cortical lesion has been described in a pre-
viously healthy 26-year-old patient who experienced re-
cent onset of seizures.62
The lesion was solitary, well-de-
marcated and homogeneously enhancing on MRI
examination. It had minimal surrounding edema and no
mass effect. Positron emission tomography scan suggested
a low-grade neoplasm, such as astrocytoma or pleomor-
phic xanthoastrocytoma. Intraoperative squash prepara-
tions and frozen sections revealed many multinucleate
cells with a background of fibrillary astrocytes, and a di-

20. 120 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
Figure 17. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrating a homogeneously enhancing left cerebellar mass
(lower arrow) with perilesional edema and a second right pontine–enhancing nodule (upper arrow). B, Sagittal postcontrast T1-weighted MRI again
reveals the cerebellar lesion (lower arrow) with additional enhancing lesions (upper arrows) within the corpus callosum, posterior cingulate gyrus,
anterior thalamus, and suprasellar region. C, The lesion consists of a dense mixed inflammatory infiltrate (hematoxylin-eosin, original magnification
ϫ400). D, Histiocytes are present within the infiltrate (CD68 immunostain, original magnification ϫ400). E, The B-cell component of the infiltrate
is highlighted by the CD20 immunostain (original magnification ϫ400). F, Scattered rare T cells are present within the infiltrate (CD3 immunostain,
original magnification ϫ400). Pathologic diagnosis: inflammatory pseudotumor.

21. Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al 121
Figure 18. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrates a well-circumscribed mass (arrow) within the left
posterior parietooccipital region with thin peripheral enhancement. B, Axial T2-weighted MRI reveals a hyperintense partially cystic lesion (arrow)
with an internal fluid-fluid level. C, There is parenchymal necrosis with hemosiderin deposits and dilated vascular channels (hematoxylin-eosin,
original magnification ϫ200). D, Necrosis and hemosiderin deposits (hematoxylin-eosin, original magnification ϫ400). Pathologic diagnosis:
radiation necrosis.
agnosis of glial neoplasm was made. On permanent his-
tology, clusters of xanthomatous histiocytic cells were ev-
ident, many of which were multinucleate with a wreath-
like nuclear arrangement, surrounded by dense gliosis.
The histiocytic cells were KP-1 (CD68) immunopositive
and negative for CD1a and S100 (in contrast to those seen
in Rosai-Dorfman disease or Langerhans cell histiocyto-
sis).
Case Example 17: Inflammatory Pseudotumor
Inflammatory pseudotumors, also known as inflam-
matory myofibroblastic tumors, may involve any organ
system.63
In the CNS, it most commonly produces a dural-
based/meningeal mass, although it may be intraparen-
chymal or may occasionally arise from the choroid plexus,
producing a hyperdense intraventricular mass on CT im-
aging.3
Shah and McClain64
described a form of inflam-
matory pseudotumor (plasma cell granuloma) involving
the cavernous sinus and middle cranial fossa in a 14-year-
old girl. On MRI, it was seen to extend into the pterygo-
palatine and infratemporal fossae producing thickening of
the right lateral tentorium and edema of the right tem-
poral lobe. Typically, inflammatory pseudotumor is hy-
pointense on T1-weighted images and markedly hypoin-
tense on T2. Because of its polymorphous histologic ap-
pearance, ranging from hypocellular connective tissue
containing scattered mixed mononuclear inflammatory
cells to a proliferation of plump fibroblastic cells with a
prominent inflammatory component, it may potentially be
confused with a lymphoplasmacyte-rich meningioma or
even a fibroblastic meningioma. The radiologic appear-
ance of a dural-based mass may further mislead the pa-
thologist. The demographics of patients with the 2 lesions
are different, however, with most inflammatory pseudo-
tumors (73%) occurring in those younger than 40 years.10
There is a distinct male predominance,10
and most cases
in the CNS are solitary (82%). Intraparenchymal hetero-
geneously enhancing inflammatory pseudotumors may
mimic a malignant brain neoplasm.63
IATROGENIC CONDITIONS
Case Example 18: Radiation Necrosis
Distinguishing between radiation necrosis and glioma
recurrence can be difficult.65
In cases of high-grade glio-
ma, both are likely to be present at the same time, but in
these cases the challenge is to determine whether one or

22. 122 Arch Pathol Lab Med—Vol 133, January 2009 Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
the other is predominant because this may affect treat-
ment planning. Increased contrast enhancement second-
ary to irradiation may be seen within a variable time
frame after administration of radiotherapy. These changes
may be seen as soon as 2 to 4 months after the treatment
and may improve over time.9
Additionally, delayed radi-
ation necrosis should be considered when patients present
with a new enhancing lesion, particularly in the irradia-
tion field, months or years after the end of treatment.9
Ob-
viously, obtaining an accurate clinical history is important
in these cases. Diffusion weighted imaging, which shows
a spotty hypointense lesion in the irradiation field, is sug-
gestive of radiation necrosis.66
Radiation necrosis shares
some major MRI features with recurrent glioma, including
contrast enhancement, vasogenic edema, and mass effect.67
However, some additional features that may favor radia-
tion necrosis include conversion from no enhancement to
enhancement and remote new enhancement, new periven-
tricular enhancement, and ‘‘Swiss cheese’’ enhancement.68
In 1 study, MRI findings which favored recurrent tumor
included involvement of the corpus callosum with sub-
ependymal spread, corpus callosal involvement with
crossing of the midline and multifocal lesions, and the
combination of corpus callosal involvement with subep-
endymal spread and multiple lesions.65
Of note, the au-
thors found that these combinations of MRI findings rath-
er than individual features were statistically significant.
However, in many cases, the definitive diagnosis of radi-
ation necrosis versus recurrent tumor rests with surgery
and biopsy.
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