Intracranial Lesions Mimicking Neoplasms

Transcription

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, demyelination, vascular diseases, noninfectious inflammatory disorders, and iatrogenic conditions. We give an overview of
such diseases, which represent a potential pitfall for pathologists 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 clinically and radiologically mimic neoplasia.
Data Sources.—Case-derived material and literature review.
Conclusions.—A variety of nonneoplastic lesions can
present clinically and radiologically as primary or metastatic 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 determining the nature of these lesions. Awareness of the entities 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)
A
offer a diagnostic challenge to both the clinician and radiologist, 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 etiologies in the differential diagnosis of both intra-axial and
extra-axial mass lesions.
Tumor-mimicking conditions from several etiologic categories are presented in tabular form, including infection
and inflammation, demyelinating disease, vascular disease, and posttreatment conditions, with accompanying illustrations and discussion of the current and pertinent literature. Case examples of each condition discussed are
described in the Table.
broad spectrum of nonneoplastic conditions can radiologically and clinically mimic an intracranial neoplasm.
In this review, we have compiled a unique series of cases that presented both clinically and radiologically as intracranial mass lesions. Tumor was initially considered in
each of the cases. However, pathology revealed a variety
of nonneoplastic etiologies, including demyelinating disease, 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 parenchyma with surrounding edema and mass effect, that is
not always the case. Not uncommonly, there can be significant overlap in the radiologic presentation between
neoplastic and nonneoplastic diseases. Both neoplastic and
nonneoplastic diseases can produce abnormal contrast enhancement, mass effect, and perilesional edema on both
computed tomography (CT) and magnetic resonance imaging (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: [email protected]).
Arch Pathol Lab Med—Vol 133, January 2009
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, osteosarcoma, 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 media and mastoidectomy in this patient pointed toward an
infectious process, even in the absence of predisposing
factors such as immunosuppression or diabetes. Even
Intracranial Lesions Mimicking Neoplasms—Cunliffe et al
101
Illustrative Case Examples With Corresponding Clinical History, Imaging Findings, Histology, and Final Pathologic
Diagnosis*
Case No. Age, y/Sex
Clinical History
Imaging Findings
MRI: Irregularly T1 contrast enhancing, centrally hypointense left skull
base lesion involving the left maxillary sinus, cavernous sinus (Figure
1, A) with erosion of left temporal
bone
MRI: 1.5-cm sellar mass extending to
suprasellar cistern adjacent to carotid arteries (Figure 2, A); low T1 signal intensity with thin enhancing
rim and septation (Figure 2, B)
MRI: Bilateral temporal lobe lesions
(Figure 3, A and B)
Destructive neoplasm; differential diagnoses: chondrosarcoma, metastasis, osteosarcoma, meningioma
MRI: New peripherally enhancing lesion of right frontal lobe (Figure 4,
A and B) with cortical extension
and perilesional edema
Recurrent tumor
MRI: Left thalamic ring-enhancing lesion (Figure 5, A and B)
Favor metastatic neoplasm
over abscess
MRI: 1.7-cm ring-enhancing lesion,
left parietal white matter; central
hypointensity on T1 (Figure 6, A),
hyperintense on DWI (Figure 6, B)
MRI: 3-cm right basal ganglia peripherally enhancing lesion with surrounding edema and midline shift
(Figure 7, A and B)
MRI: Right middle cerebellar peduncle/hemisphere T1 hypointense, T2
hyperintense lesion (Figure 8, A and
B)
MRI: Heterogeneous ring-enhancing
suprasellar lesion separate from pituitary and stalk, near anterior communicating artery (Figure 9, A and
B)
MRI: Bifrontal ‘‘butterfly’’ lesion, T2
hyperintense (Figure 10, A) with focal peripheral enhancement on
postcontrast T1 (Figure 10, B)
First MRI 2004: Large right frontal
contrast-enhancing mass and edema
(Figure 11, A)
Necrotic lymphoma, abscess
Second MRI 2007: Contrast-enhancing
subcortical lesion in left inferior parietal lobe (Figure 11, C)
MRI: Cerebellar enhancement with
mass effect and edema (Figure 12,
A); surrounding gyriform enhancement of folia on DWI (Figure 12, B)
MRI: Left parietal lobe 2-cm white
matter–based lesion with irregular
enhancing rim and surrounding
edema (Figure 13, A and B)
MRI: 1.5-cm hypointense mass at left
Meckel cave, involving left trigeminal ganglion (Figure 14, A)
CT: Hyperdense right frontoparietal
vertex extra-axial mass involving
calvarium (Figure 14, E)
2007: Demyelination vs neoplasm
1
35/M
Chronic otitis media s/p left mastoidectomy; headaches, fever, left-sided facial numbness, diplopia, confusion
2
37/F
10-mo H/O severe headaches, recent
onset of double vision, 14-mo H/O
amenorrhea, panhypopituitarism and
DI
3
56/F
Bizarre behavior; paranoia, Klüver-Bucy
syndrome
4
33/M
5
65/F
6
60/F
Generalized seizures, s/p resection of
large anaplastic mixed glioma, involving right frontal lobe and basal
ganglia; 2 y later, experienced 2 episodes of unconsciousness
Remote H/O breast cancer s/p right total mastectomy; recent headaches
and fever
s/p large B-cell lymphoma and CHOP
Tx; new onset seizure
7
35/F
8
43/M
9
62/F
10
57/M
s/p remote testicular cancer; 3-d H/O
bitemporal headache, confusion,
memory impairment
11
77/M
H/O seizure disorder, hypertension
2004: New onset difficulty driving,
following directions; after biopsy,
steroid treatment with symptom
improvement
2007: Worsening speech impairment,
confusion
Bitemporal headache, left lower extremity weakness and diminished left
plantar sensation; remote PPD positive, CXR negative
Disorientation, word-finding difficulty,
right hemisensory impairment. HIV
positive, CD4 109, CSF protein 54
mg/dL, glucose 53 mg/dL
Progressive headaches for 1 y; CSF:
atypical lymphocytes, histiocytes, and
few eosinophils
12
64/M
Headaches for 7 wk, nausea and vomiting, 40-lb weight loss; gait ataxia
13
43/F
Sudden loss of right hand coordination
and difficulty driving
14i
38/F
14ii
44/M
18-mo H/O progressive left facial
numbness, first and second divisions
trigeminal nerve
37-y H/O partial seizures, s/p resection
of right frontal and temporal seizure
focus; new onset increased seizure
frequency and left hemiparesis
102 Arch Pathol Lab Med—Vol 133, January 2009
Imaging Differential Diagnoses
Pituitary adenoma
Infectious process, eg, herpes
encephalitis, neoplasm
Neoplasm: primary or metastatic
Inflammatory, demyelinating
or lymphoproliferative process
Inflammatory process, cystic
neoplasm
High-grade glioma
2004: neoplasm
Lhermitte-Duclos disease
High-grade glioma, lymphoma, metastasis, abscess
Schwannoma vs meningioma
Atypical meningioma, calvarial/dural metastasis
Extended
Surgical Procedure
Histology
Pathologic Diagnosis
Biopsy
Granulomatous inflammation with extensive necrosis (Figure 1, B), numerous multinucleated giant cells (Figure 1, B, inset); GMS-positive septate hyphae with
acute angle branching (Figure 1, C)
Aspergilloma
Transsphenoidal hypophysectomy
Nonadenomatous pituitary gland with fibrinopurulent material containing smallto medium-sized encapsulated yeast forms (Figure 2, C), strongly PAS (Figure 2,
D) and GMS positive (Figure 2, E), weakly mucicarmine-positive capsules (Figure 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 organisms (Figure 3, E)
Bacterial abscess (Figure 4, C and D). No evidence of tumor
Whipple disease
Biopsy
Intense acute inflammation with gram-positive cocci (Figure 5, C and D); Streptococcus 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 serrated 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 accumulation (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 (Figure 13, E)
Vasculitis
Resection
Homogeneous eosinophilic extracellular deposits (Figure 14, B), congophilic (Figure 14, C), apple green birefringence (Figure 14, C, inset); EM: haphazard 6-␮m
fibrils (Figure 14, D)
Amorphous congophilic deposits with apple green birefringence (Figure 14, F)
Amyloidoma
Resection
Resection
Bacterial abscess
Amyloidoma
103
Continued
Case No. Age, y/Sex
15
33/F
Clinical History
Imaging Findings
Imaging Differential Diagnoses
Recent onset of headaches
MRI: Bifrontal lesion on either side of
Neurosarcoidosis, meningiofalx, with dural extension (Figure
ma, dural metastases
15, A and B)
16
33/M
H/O seizure disorder, schizophrenia,
MRI: Multiple skull base lesions (FigMeningiomas
IDDM
ure 16, A)
17
62/M
H/O thyroiditis, hypertension; develMRI: Multiple enhancing lesions in
Neoplasm: favor metastatic
oped vertigo, numbness left corner of
left cerebellum, corpus callosum,
mouth, twitching left hand
cingulate gyrus, pons, thalamus, suprasellar region (Figure 17, A and B)
with minimal mass effect
18
40/M
s/p remote glioma resection; 5 y later,
MRI: Left parietal lobe lesion with peRecurrent tumor with cystic
enlarging lesion with necrosis at site
ripheral enhancement on T1 (Figure
change vs radiation necrosis
of prior resection
18, A), hyperintense, partially cystic
on T2 (Figure 18, B)
* 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 leukoencephalopathy; EM, electron microscopy; CT, computed tomography; and IDDM, insulin-dependent diabetes mellitus.
though most commonly occurring as an opportunistic infection, aspergilloma is well described in immunocompetent 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 immunocompromised patients, which is due to wide use of immunosuppressive drugs such as steroids, large elderly and diabetic 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 patients with a history of immunosuppression.
Intracranial fungal infection has been described following a surgical intervention, often with fatal outcome,5 Aspergillus species being the most commonly reported organism in these cases. Typically, cerebral aspergillosis results from hematogenous spread of the organism, or alternatively 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 parenchyma. Kim et al7 described a case of extra-axial Aspergillus 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 significant history. Radiologically, the mass was hypointense
on T1-weighted MRI and exhibited irregular contrast enhancement. In the case series by Dubey et al,4 patients
with intracranial fungal granuloma most commonly presented with headache, followed by vomiting, proptosis,
and visual disturbances. Other presentations could include cranial nerve palsies and symptoms/signs of elevated intracranial pressure and meningismus.8 The granulomas were most frequently seen in the frontal lobe, although a classic location of aspergillomas is in a basal cranial 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 frequent organism found (25, 63%), followed by mucormycosis (7, 18%), cryptococcoma (3), Cladosporium (3), Bipo-
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 ⫻200). Inset, Multinucleate
giant cells (hematoxylin-eosin, original magnification ⫻400). C, Fungal hyphae with acute angle branching (Gomori methenamine silver stain,
original magnification ⫻400). Pathologic diagnosis: aspergilloma.
Extended (Continued)
Surgical Procedure
Histology
Pathologic Diagnosis
Resection of firm,
gray mass
Hyalinized vessels surrounded by dense lymphocytic infiltrate (Figure 15, C) of predominantly B-cell type (Figure 15, D and E)
Castleman disease hyalinevascular type
Resection
Mixed inflammatory infiltrate with admixed pale-staining histiocytes (Figure 16, B
and C)
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)
Rosai-Dorfman disease
Necrotic parenchyma with hemosiderin deposits and vascular channels (Figure 18,
C and D)
Radiation necrosis
Biopsy
Resection
laris hawaiiensis (1), and Candida species (1). There was a
63% mortality rate in these patients, mostly due to meningoencephalitis.
Radiologically, fungal granulomas present as enhancing
masses.9 Adjacent to the dura, they can simulate meningiomas, even producing a dural tail sign.3 On CT scan,
Inflammatory pseudotumor
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. Aspergillomas tend to demonstrate intermediate signal intensity surrounded by perilesional edema on T2.4 However, cryptococcomas have low T2-weighted signal inten-
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 (hematoxylineosin, original magnification ⫻200). D, Organisms are strongly periodic acid–Schiff positive (original magnification ⫻400). Inset, Capsule of
organism is weakly mucicarmine positive (original magnification ⫻400). E, Organisms are strongly labeled by Gomori methenamine silver stain
(original magnification ⫻400). Pathologic diagnosis: cryptococcoma.
105
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 lymphohistiocytic inflammatory infiltrate (hematoxylin-eosin, original magnification ⫻200). D, Macrophages with pale eosinophilic, foamy cytoplasm (hematoxylin-eosin, original magnification ⫻400). E, Brightly periodic acid-Schiff–positive intracellular organisms within macrophages (original magnification ⫻400). 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 infections typically produce a diffuse meningitis, and infiltration of the perivascular Virchow-Robin spaces by the organism can result in the formation of small intraparenchymal 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 primary or secondary brain tumors.10,11 Cryptococcomas may
be seen in individuals with a predisposition to fungal infections, 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 Cryptococcomas are most commonly found in the cerebellum, brainstem, basal ganglia, or temporoparietal lobes. Distinguishing them from tumors and abscesses due to other organ106 Arch Pathol Lab Med—Vol 133, January 2009
isms can be challenging because there is no distinctive
radiologic feature that is unique to cryptococcomas. Typically, cryptococcal disease presents on MRI as T2 hyperintense cystic lesions within the bilateral basal ganglia
with variable enhancement and surrounding edema. They
also often tend to insinuate in dilated Virchow-Robin perivascular 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 Cryptococcomas may rarely involve the parasellar or pituitary region. Yu et al13 described a case of parasellar cryptococcoma occurring in an immunocompetent patient. The radiologic 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 adjacent to the cryptococcoma helped in differentiating it
from an adenoma.
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 ⫻200). D, Edge of abscess
is composed of a fibroinflammatory capsule (hematoxylin-eosin, original magnification ⫻200). Pathologic diagnosis: bacterial abscess.
Case Example 3: Whipple Disease
Whipple disease is a chronic inflammatory disorder that
involves multiple organ systems, typically the gastrointestinal tract and musculoskeletal system.14 The causative
agent is a soil-borne gram-positive bacillus Tropheryma
whippelii. The classic presentation includes fever, steatorrhea, 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 acidSchiff–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 enhancement.15 They can be surrounded by variable perilesional
edema. Generally speaking, patients presenting with primary 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, papilledema, hemiplegia, syndrome of inappropriate antidiuretic 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 sarcoidosis.14 Those with focal mass lesions have symptoms referable 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 T1weighted images, and had subtle ring enhancement without perilesional edema. As in our patient, the presentation
included behavioral changes and aggressiveness. Following resection of the mass, the characteristic perivascular
foamy macrophages containing periodic acid-Schiff–positive, diastase-resistant rod-shaped organisms were seen.
There was marked associated gliosis.
107
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 ⫻400). D, Organisms are gram-positive
cocci (Brown-Hopps Gram stain, original magnification ⫻1000). 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 thalamus.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 perivascular 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 challenging radiologically, because both commonly demonstrate
ring enhancement and perilesional edema. A helpful finding 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 entirely specific, because a centrally reduced apparent diffusion coefficient has been also reported in neoplastic lesions.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 imIntracranial Lesions Mimicking Neoplasms—Cunliffe et al
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 ⫻200). D, Center of
lesion contains neutrophilic abscess (hematoxylin-eosin, original magnification ⫻200). E, Tissue Gram stain reveals fine, filamentous gram-positive
bacteria within abscess (arrow) (Brown-Hopps Gram stain, original magnification ⫻1000). Pathologic diagnosis: nocardiosis.
mune system, it is usually seen among immunocompromised patients.6 It can be confused with intracranial tumors radiologically.19 Ozturk et al20 described a case of
nocardial brain abscess occurring in a renal transplant recipient on an immunosuppressive drug regimen. Kilincer
et al19 described a further 2 cases of nocardial brain abscess, one of whom was a 39-year-old woman with systemic lupus erythematosus who developed a left frontoparietal abscess, and the other was a 43-year-old man with
glomerulonephritis treated with corticosteroids who developed a ring-enhancing multiloculated abscess in the
left cerebellar hemisphere, with an additional 2 small supratentorial lesions. Both underwent treatment with longterm antibiotics and evacuation of the abscess. Histologically, 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 ringlike enhancement on MRI similar to a primary or metastatic 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 hyperintense rim. The MRI appearance of tuberculomas varies
according to the age of the lesion. On T2-weighted imaging, immature tuberculomas appear as multiple small
areas of isointensity or hypointensity surrounded by hyperintense edema. Mature tuberculomas are heterogeneously 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, perilesional edema, and peripheral enhancement on CT scan
has been described, although is not always present.10 Magnetic resonance spectroscopy (MRS) is typically inconclusive and does not help distinguish the condition from a
neoplasm. Diffusion-weighted imaging is usually hyperintense.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 leukoencephalopathy (PML) present with weakness, hemianoIntracranial Lesions Mimicking Neoplasms—Cunliffe et al
109
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 intensity with central areas of low T2 signal and marked surrounding edema. C, Gliosis and chronic inflammation (hematoxylin-eosin, original magnification ⫻200). D, Granuloma with surrounding intense chronic inflammatory infiltrate (hematoxylin-eosin, original magnification ⫻200). E, Rare
pink-stained acid-fast bacilli within the lesion (arrow) (Kinyoun acid-fast stain, original magnification ⫻1000). Pathologic diagnosis: tuberculoma.
pia or quadrantanopia, and cognitive abnormalities.21 On
imaging, PML lesions typically present as large, multifocal, 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 peripheral 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 typically 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 ipsilateral lateral ventricle, which is in contrast to the typical
lack of mass effect described in the literature. Therefore,
necrotic white matter lesions in acquired immunodeficiency syndrome patients, particularly with peripheral scalloping, 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 contain enlarged oligodendrocytes with hyperchromatic nu110 Arch Pathol Lab Med—Vol 133, January 2009
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 surrounding inflammatory and granulomatous response.
It is the most common cause of acquired seizures worldwide and is increasingly seen in the United States, particularly in the immigrant community.24 Although epilepsy
is the most common presenting symptom, other manifestations include severe episodic headache,25 meningitis, obstructive hydrocephalus if the cyst is near a ventricle or
the subarachnoid space, and cognitive problems.10,24 Radiologic 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 appear as small nonenhancing edematous lesions, later forming small enhancing nodules.10 As the lesions become cystic and the larvae start to die, surrounding edema develIntracranial Lesions Mimicking Neoplasms—Cunliffe et al
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 ⫻400). D, Enlarged, bizarre astrocytes, with collections of foamy histiocytes (hematoxylin-eosin, original magnification ⫻400). E,
Enlarged progressive multifocal leukoencephalopathy-infected cells are MIB1 (Ki-67) immunopositive (original magnification ⫻400). 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, unlike 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 Solitary lesions can be difficult to distinguish from a neoplasm owing to the surrounding edema and the cyst enhancement.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 inflammation 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 characteristic 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 literArch Pathol Lab Med—Vol 133, January 2009
ature. Multiple sclerosis, and other primarily demyelinating diseases, such as myelinoclastic diffuse sclerosis
(Schilder disease) and acute disseminated encephalomyelitis 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 triggers 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 premature conclusion. This condition is a ‘‘classic’’ mimic of
high-grade glioma, and recently, the characteristic horseshoe-shaped contrast enhancement on MRI has been described. Additional radiologic tools, including MR perfusion imaging or MRS can further aid in arriving at the
correct diagnosis, thus avoiding a surgical biopsy.27,28 Features 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 demyeliIntracranial Lesions Mimicking Neoplasms—Cunliffe et al
111
Figure 9. A, Axial postcontrast T1-weighted magnetic resonance imaging (MRI) demonstrates suprasellar heterogeneous peripherally ring-enhancing 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 ⫻100). Inset,
The infiltrate contains numerous eosinophils. D, Degenerated eosinophilic capsule of cysticercus, with serrated surface (hematoxylin-eosin, original
magnification ⫻200). Pathologic diagnosis: cysticercosis.
native lesions and is more likely to be associated with
these than with neoplasms or infections.29 In demyelination, the incomplete ring of enhancement may have illdefined margins.30 Differentiation between a solitary demyelinating lesion and a glioma can be very challenging
radiologically.10,30,31 Therefore, if the presentation and imaging findings remain inconclusive and a histologic diagnosis is necessary, the pathologist has to keep this condition in the differential diagnosis, because erroneous diagnoses of high-grade glioma have been reported many
times in the medical literature, even though the distinguishing features are also well documented.32 When demyelinative lesions have a marked inflammatory component, they may be confused with a primary CNS lymphoma. The more gliotic lesions are more apt to be confused
with high-grade astrocytomas, however. If one is unfamiliar with the characteristic appearance of Creutzfeldt
astrocytes seen in demyelination, the possibility of substantial astrocytic pleomorphism, and the occurrence of
mitotic figures in demyelinative lesions, they may be misinterpreted 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 documented in the literature.34,35 To distinguish a cerebrovascular 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 characteristic clinical history of a sudden onset of neurologic
symptoms and signs, in combination with the typical radiologic findings, including diffusion-restriction, T2/fluidattenuated 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 include an atypical presentation, such as a slow evolution of
neurologic symptoms,10 and a poorly defined cerebral lesion on imaging with associated mass effect, radiologically
Figure 10. A, Axial T2-weighted magnetic resonance imaging (MRI) demonstrating a hyperintense bifrontal butterfly-shaped lesion (arrow) extending 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 ⫻40). D, Perivascular chronic inflammation with surrounding
lipid-laden macrophages and gliosis (hematoxylin-eosin, original magnification ⫻400). E, Relative preservation of axons (stained black) in areas
of demyelination (Bielschowsky stain, original magnification ⫻200). Pathologic diagnosis: tumefactive demyelinating lesion.
simulating glioma.9,10 A subacute infarction can show irregular contrast enhancement and mimic high-grade glioma. Some infarcts can also exhibit ring enhancement,
strongly resembling that of glioblastoma.34 An understanding of the cerebral arterial vasculature is essential in
arriving at a correct diagnosis.10 Diffusion weighted imaging 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 glioArch Pathol Lab Med—Vol 133, January 2009
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 including 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 contrastenhancing mass. Further imaging studies (perfusionweighted 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 Behçet
disease has been reported to produce a solitary masslike
lesion in the hemisphere, with low attenuation on T1weighted MRI, and extensive hyperintensity on fluid attenuated inversion recovery.39,40 However, this scenario is
very rare, as Behçet disease usually presents as multiple
T2 hyperintense lesions.39 Magnetic resonance spectroscopy 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
113
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 ⫻200). 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 ⫻200). E, 2007 biopsy, infiltrate is composed of CD20 (L26) immunopositive B cells
(original magnification ⫻200). Pathologic diagnosis: demyelinating disease and central nervous system lymphoma.
enhancing on postgadolinium T1-weighted MR, with associated massive vasogenic edema involving the whole
hemisphere. Radiologically, the lesions mimicked a multifocal glioma. However, the MRS pattern was more consistent with an inflammatory process (no elevated choline
peak, marked elevation of glutamate/glutamine metabolites) 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 lesion in case 14i was thought to be a schwannoma of the
fifth nerve, which would fit the imaging features and presentation. 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 reported. 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. Amyloid 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. Central 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
Figure 12. A, Axial postcontrast T1-weighted magnetic resonance imaging demonstrating abnormal gyriform enhancement involving the bilateral paramedian cerebellar hemispheres, left greater than right (arrow), with
mass effect and edema. B, Axial diffusionweighted imaging demonstrates gyriform hyperintensity of the cerebellar folia (arrow),
mimicking the appearance of Lhermitte-Duclos disease. C, Sharply demarcated area of
cortical necrosis at right of field, extending to
underlying white matter (hematoxylin-eosin,
original magnification ⫻12). D, Eosinophilic,
demarcated area of cortical necrosis seen at
right of field (hematoxylin-eosin, original
magnification ⫻200). E, Numerous KP-1 immunopositive macrophages and microglia
within infarct (original magnification ⫻400).
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 plexus are other known sites. Ragel et al47 described a 59-yearold man with a 6-month history of confusion and headaches; MRI revealed a left parietooccipital lesion extending 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 elevated 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 presenting with hearing loss and recurrent right-sided otitis
media. The MRI and CT findings were suspicious for glioma, and stereotactic biopsy with intraoperative squash
preparation followed by routine histology and electron microscopy revealed amyloidoma.
Cerebral amyloid angiopathy can also mimic glioma radiologically and clinically. Safriel et al46 reported 2 patients 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, withIntracranial Lesions Mimicking Neoplasms—Cunliffe et al
115
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 ⫻100). D,
Fibrinoid necrosis of vessel wall (hematoxylin-eosin, original magnification ⫻400). E, The fibrinoid necrosis is highlighted bright red by an azocarmine stain (original magnification ⫻400). F, Perivascular histiocytes within the infiltrate are immunopositive for CD68 (KP-1) (original magnification ⫻200). G, Perivascular B cells are highlighted by the CD20 immunostain (original magnification ⫻400). H, Perivascular T cells are
highlighted by the CD3 immunostain (original magnification ⫻400). Pathologic diagnosis: vasculitis.
out restricted diffusion, within the right occipital and parietal lobes, and unremarkable MRS findings. Biopsy revealed cerebral amyloid angiopathy. Cerebral amyloid angiopathy 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, nonhem116 Arch Pathol Lab Med—Vol 133, January 2009
orrhagic, and low attenuation on MRI examination. A diagnosis 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.
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 ⫻100). C, The deposits are stained orange-red (Congo red stain, original magnification ⫻100). Inset,
Deposits demonstrate apple green birefringence under polarized light (Congo red stain and polarized light, original magnification ⫻100). 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, Congophilic deposits have apple green birefringence (Congo red stain and polarized light, original magnification ⫻400). Pathologic diagnosis: amyloidoma.
117
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 ⫻400). D, The lymphocytic infiltrate is predominantly B cells (CD20 immunostain, original magnification ⫻400). E, There is a minor population of T cells (CD3
immunostain, original magnification ⫻400). 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 histologic finding of hyalinized follicular centers with a radial penetrating vessels and prominent interfollicular capillary proliferation. The plasma cell type represents only
5% to 10% of cases, and is characterized by large lymphoid 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, polyneuropathy, 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 neoplasm, 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 clumsiness,53 left hemiparesis, and incoherent speech.52 By CT
imaging, the lesions were homogeneously enhancing with
perilesional edema.52 Some demonstrated dural enhancement 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 homogeneous 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, partially 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 intracranial 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 systemic symptoms such as elevated sedimentation rate, fever,
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, original magnification ⫻100). C, Within the infiltrate, there are numerous
pale-staining histiocytes and plasma cells (hematoxylin-eosin, original
magnification ⫻400). 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 involvement 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 compartments,56 but a suprasellar location has been reported.55
Patients presenting with or developing cranial involvement have a mean age of 34.9 years, with a male predominance. Some of the usual presentations of intracranial disease 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 identical to a meningioma on CT and MRI scan.55,57,58 Associated 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 histology. Fortunately, differentiation of sinus histiocytosis
with massive lymphadenopathy from meningioma presents no difficulty in most cases, with the possible exception of the lymphoplasmocyte-rich variant of meningioma.57
Helpful histologic features include the characteristic
pale-staining histiocytes with delicate nuclear membranes,
exhibiting emperipolesis, that is, intact lymphocytes, neutrophils, and plasma cells within the cytoplasm. There
may also be erythrophagocytosis and perivascular collections 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 intracranial Rosai-Dorfman disease, the ideal treatment for this
condition is so far undefined. Surgery has been the treatment of choice.55 Adjunctive therapy has included chemotherapy, irradiation, and steroids. So far, no deaths
from intracranial sinus histiocytosis with massive lymphadenopathy have been reported, and patients who underwent complete resections had no recurrences.55 The effectiveness 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 remaining lesions following corticosteroid administration.
Another systemic histiocytic disease that can involve the
CNS and produce lesions mimicking a primary brain tumor is Erdheim-Chester disease.
The disease is a non–Langerhans cell histiocytosis and
usually affects middle-aged adults, producing osteosclerotic and lipogranulomatous lesions of the long bones and
retroperitoneal and pulmonary fibrosis.60 When there is
neurologic involvement, it typically manifests itself as hypothalamic/pituitary dysfunction.61 A solitary left temporoparietal cortical lesion has been described in a previously healthy 26-year-old patient who experienced recent onset of seizures.62 The lesion was solitary, well-demarcated 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 pleomorphic xanthoastrocytoma. Intraoperative squash preparations and frozen sections revealed many multinucleate
cells with a background of fibrillary astrocytes, and a diIntracranial Lesions Mimicking Neoplasms—Cunliffe et al
119
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
⫻400). D, Histiocytes are present within the infiltrate (CD68 immunostain, original magnification ⫻400). E, The B-cell component of the infiltrate
is highlighted by the CD20 immunostain (original magnification ⫻400). F, Scattered rare T cells are present within the infiltrate (CD3 immunostain,
original magnification ⫻400). Pathologic diagnosis: inflammatory pseudotumor.
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 ⫻200). D, Necrosis and hemosiderin deposits (hematoxylin-eosin, original magnification ⫻400). Pathologic diagnosis:
radiation necrosis.
agnosis of glial neoplasm was made. On permanent histology, clusters of xanthomatous histiocytic cells were evident, many of which were multinucleate with a wreathlike 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 histiocytosis).
Case Example 17: Inflammatory Pseudotumor
Inflammatory pseudotumors, also known as inflammatory myofibroblastic tumors, may involve any organ
system.63 In the CNS, it most commonly produces a duralbased/meningeal mass, although it may be intraparenchymal or may occasionally arise from the choroid plexus,
producing a hyperdense intraventricular mass on CT imaging.3 Shah and McClain64 described a form of inflammatory pseudotumor (plasma cell granuloma) involving
the cavernous sinus and middle cranial fossa in a 14-yearold girl. On MRI, it was seen to extend into the pterygopalatine and infratemporal fossae producing thickening of
the right lateral tentorium and edema of the right temporal lobe. Typically, inflammatory pseudotumor is hyArch Pathol Lab Med—Vol 133, January 2009
pointense on T1-weighted images and markedly hypointense on T2. Because of its polymorphous histologic appearance, 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 appearance of a dural-based mass may further mislead the pathologist. The demographics of patients with the 2 lesions
are different, however, with most inflammatory pseudotumors (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 heterogeneously 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 glioma, both are likely to be present at the same time, but in
these cases the challenge is to determine whether one or
121
the other is predominant because this may affect treatment planning. Increased contrast enhancement secondary 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 radiation necrosis should be considered when patients present
with a new enhancing lesion, particularly in the irradiation field, months or years after the end of treatment.9 Obviously, obtaining an accurate clinical history is important
in these cases. Diffusion weighted imaging, which shows
a spotty hypointense lesion in the irradiation field, is suggestive 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 radiation necrosis include conversion from no enhancement to
enhancement and remote new enhancement, new periventricular enhancement, and ‘‘Swiss cheese’’ enhancement.68
In 1 study, MRI findings which favored recurrent tumor
included involvement of the corpus callosum with subependymal spread, corpus callosal involvement with
crossing of the midline and multifocal lesions, and the
combination of corpus callosal involvement with subependymal spread and multiple lesions.65 Of note, the authors found that these combinations of MRI findings rather than individual features were statistically significant.
However, in many cases, the definitive diagnosis of radiation necrosis versus recurrent tumor rests with surgery
and biopsy.
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Intracranial Lesions Mimicking Neoplasms

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