dural lesions mimicking meningiomas - unilim.fr · throughout the tumor. spindle cells in fascicles...

Dural Lesions Mimicking Meningiomas

MAHLON D. JOHNSON, MD, PHD, SUZANNE Z. POWELL, MD,PHILIP J. BOYER, MD, PHD, ROBERT J. WEIL, MD,AND PAUL L. MOOTS, MD

Recently, a number of neoplastic and nonneoplastic entities havebeen reported that radiographically and clinically mimic meningio-mas. Because these lesions occur infrequently and may resemble ameningioma during intraoperative analysis, they may not be consid-ered in the differential diagnosis. This review (and case illustrations)considers some of the newly recognized and notable lesions that canmimic meningiomas, including solitary fibrous tumors, gliosarcomas,leiomyosarcomas, hemangiopericytomas, melanocytomas, Hodgkin’sdisease, plasmacytomas, inflammatory pseudotumors, neurosarcoid-osis, plasma cell granulomas, Rosai-Dorfman disease, Castleman’sdisease, xanthomas, rheumatoid nodules, and tuberculomas. Aware-ness that these lesions involve the dura may facilitate intraoperativerecognition and, in some cases, preclude unnecessary additionalsurgery. HUM PATHOL 33:1211-1226. Copyright 2002, ElsevierScience (USA). All rights reserved.

Key words: dura, meningioma, solitary fibrous tumor, gliosar-coma, hemangiopericytoma, inflammatory pseudotumors, neurosar-coidosis, Hodgkin’s disease, plasmacytoma, plasma cell granuloma,leiomyosarcoma, rheumatoid nodules, Rosai-Dorfman disease,Castleman’s disease, xanthoma, melanocytoma.

Abbreviations: CNS, central nervous system; CT, computed to-mography; EBV, Epstein-Barr virus; EMA, epithelial membrane anti-gen; GS, gliosarcoma; HD, Hodgkin’s disease; HPC, hemangioperi-cytoma; HPF, high-power field; MRI, magnetic resonance imaging(MRI); PAS, period acid-Schiff; PGC, plasma cell granuloma; RDD,Rosai-Dorfman disease; R-S, Reed-Sternberg; SFT, solitary fibroustumor.

The occurrence of neoplastic and nonneoplasticdural-based masses that mimic meningiomas has re-ceived little attention despite several recent reports.1Because these occur infrequently, such lesions may notbe considered during intraoperative analysis. Becausetheir histologic features resemble variants of meningi-omas (Table 1), postoperative recognition may be chal-lenging as well. This review (and case illustrations)considers some of the newly recognized and notablelesions typically mistaken clinically or radiographicallyfor meningiomas. Awareness that they involve the duramay facilitate intraoperative recognition and, in somecases, prevent unnecessary additional surgery.

SOLITARY FIBROUS TUMORS

On rare occasions, solitary fibrous tumors (SFTs)may develop in the leptomeninges, where they mimic ameningioma. At least 13 cases have been reported.2-11

Typically they present in the same age group as menin-giomas (mean age, 57 years) and show a strong predi-lection for females (a 5:2 female:male ratio).2-11 Theyhave been observed at the falx, occipital and spinaldura, tentorium, and cerebellopontine angle.2-11 Othercharacteristics similar to meningioma are revealed by

computed tomography (CT) and magnetic resonanceimaging (MRI) showing a circumscribed dural-basedtumor occasionally associated with hyperostosis.2 Typi-cally these lesions enhance uniformly after administra-tion of gadolinium.2

Macroscopically, SFTs are firm, gray-white, and cir-cumscribed but not encapsulated. Reported casesrange in size from 1 to 7 cm in diameter. In 1 case, anSFT exhibited underlying invasion of the brain.

Microscopically, SFTs superficially resemble fi-brous meningiomas. However, unlike fibrous meningi-omas, SFTs usually exhibit different histologic patternsthroughout the tumor. Spindle cells in fascicles or in-dividually enveloped in collagen may dominate partsof the tumor. Other zones exhibit a capillary patternreminiscent of a hemangiopericytoma (HPC) (Fig 1).Whorls, storiform patterns, and psamomma bodies areabsent in dural lesions, although the latter have beennoted in tumors at other sites.11 The spindle cells haveelongated or round nuclei but less conspicuous nucle-oli and none of the pseudoinclusions characteristic ofmeningiomas. SFT cells, in contrast to fibrous menin-giomas, do not stain with periodic acid-Schiff (PAS). Inhypocellular areas, tumor cells encircle densely hyalin-ized capillaries (Fig 1).7,8,12 As in pulmonary tumors,capillary proliferation may be prominent and resemblean HPC in regions with numerous elongated channels.Nonetheless, in our experience capillaries tend to bemore frequently ensheathed in collagen and less com-monly branched than HPCs.6-8,12

SFTs exhibit diffuse CD34 immunoreactivity instromal spindle cells as well as endothelia in nearly allcases, in contrast to the patchy immunostaining seen in30% of HPCs and in 60% of fibrous meningiomas.Epithelial membrane antigen (EMA) and S-100 proteinimmunoreactivity are not usually seen—a feature thathelps distinguish them from fibrous meningiomas,

From the Departments of Pathology, Neurology, and Neurosur-gery, Vanderbilt Medical School and Nashville Veterans AdministrationMedical Center, Nashville, TN; Department of Pathology, Baylor Collegeof Medicine, Houston TX; and Pennsylvania State University School ofMedicine, Hershey, PA. Accepted for publication May 13, 2002.

Address correspondence and reprint requests to Mahlon John-son, MD, PhD, Department of Pathology, Vanderbilt Medical School,21st Ave. S, Nashville, TN 37232.

This is a US government work. There are no restrictions on itsuse.

0046-8177/02/3312-0011$0.00/0doi:10.1053/hupa.2002.129200

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which exhibit diffuse immunoreactivity for these anti-gens 80% of the time2-7,9,12 (Fig 2).

Case Illustration

A 57-year-old male presented with right facialweakness. MRI revealed an inhomogenous 7.5-cm massextending from the dura over the petrous bone thatcompressed the right pons and midbrain, with evidenceof erosion of the superior petrous apex and right pe-trous carotid canal (Fig 1A). Intraoperatively, the tu-mor appeared encapsulated and attached to the trigem-inal nerve. Near- total resection was achieved. Thesample consisted of multiple large, white, firm, nodularfragments of tissue measuring 7.5 � 4.0 � 1.3 cm.Microscopically, the tumor appeared unencapsulatedand populated by fascicles of elongated spindle cellsorganized in hypercellular zones. In other areas, spin-dle cells were separated by dense bands of colla-gen, which also surrounded elongated, occasionallybranched blood vessels (Fig 1B, C, and D). Also presentwere hypocellular myxoid zones with lymphocytoidcells and hyalinized blood vessels. Zones populated bydense collagen surrounding round tumor nuclei cut incross-section were also present (Fig 1C). Tumor cellsexhibited no EMA or S-100 protein immunostaining,but did exhibit extensive CD34 immunoreactivity (Fig1E).

HEMANGIOPERICYTOMAS

Representing about 0.4% of primary brain tu-mors,13 HPCs were once classified as a variant of me-ningioma. Like meningiomas, the majority of intracra-nial HPCs are supratentorial.12,13 HPCs are typicallylobular on MRI; in 2/3 of cases, this tumor has abroad-based attachment to the dura. On T1-weightedimages, HPCs appear isointense with gray matter andenhance heterogeneously after administration of gad-

olinium. They may show bony erosion but do not showthe hyperostosis or intratumoral calcification com-monly associated with meningiomas (Fig 3).14 Theirhistologic similarity to vascular meningiomas and SFTshas been reviewed in detail.12-15 In most cases, thesehighly cellular tumors are populated by sheets of cellswith ovoid or round hyperchromatic nuclei separatedby reticulin and numerous, often inconspicuous capil-laries. Mitoses are readily found. More prominent, of-ten branching capillaries produce a characteristic “stag-horn” vascular pattern, but the hyalinized vessels of ameningioma or collagen-sheathed vessels of an SFT arenot usually encountered. Fibrous areas with collagenand elongated cells, particularly in a fragmented sam-ple, may superficially resemble a fibroblastic meningi-oma, although the smaller nuclear size and absence ofnuclear inclusions argue against a diagnosis of menin-gioma. Other meningioma variants might also be sug-gested in a fragmented biopsy, but true whorls andlarge hypovascular menigothelial areas are not seen.Recognition of the numerous fine capillaries and in-creased mitotic activity usually establishes the diagnosis(Fig 2). Differentiating HPCs from SFTs and meningi-omas is critical, because their treatment and prognosisdiffer.2,12,15 A number of tumors may exhibit vascularpatterns similar to HPCs, but with dural-based tumorsthe differential diagnosis includes vascular meningio-mas, hemangioblastomas and SFTs. When the histologyis insufficient to make a diagnosis, immunohistochem-istry with antibodies to factor XIIIa, EMA, S-100 pro-tein, and CD34 may help differentiate these tu-mors.9,15,16 In contrast to SFTs, HPCs exhibit CD34immunostaining in stromal cells in only 33% of cases,and is often patchy and less intense than immunoreac-tivity in endothelial cells.2,12 Factor XIIIa immunoreac-tivity, seen in 78% of HPCs, is noted in 100% of SFTsand 65% of meningiomas. In contrast to fibroblasticmeningiomas, 80% of which exhibit EMA and S-100immunoreactivity,17 these epitopes are essentially notseen in HPCs. Vimentin immunostaining is widespreadin all 3 entities and is not diagnostic2,12 (Fig 2).

GLIOSARCOMAS

Gliosarcomas (GSs) represent 1.7% to 2.3% ofglioblastomas.18-20 Occasionally, A GS developing su-perficially in the temporal lobe may extend into theleptomeninges, eliciting a desmoplastic response thatproduces an encapsulated, firm lesion both radiograph-ically and grossly suggestive of a meningioma (Fig 4). In1 series, approximately 12% of cerebral GSs presentedas dural-based tumors.20 An extramedullary dural-basedGS of the thoracic spinal cord has also been reported.21

Intraoperatively, the firmness and circumscription ofGSs that have invaded the leptomeninges may furthersuggest a meningeal origin. In tumors with a predomi-nantely fibrosarcomal pattern, intraoperative differen-tiation between GS and a malignant fibrous meningi-oma may be challenging because both are firm andhave a prominent spindle cell component. Although

TABLE 1. Dural Lesions That Mimic Meningiomas

Primary glial and mesenchymalSolitary fibrous tumorsHemangiopericytomasGliosarcomasLeiomyosarcomasMelanocytoma

Secondary neoplasmsMetastatic carcinomasMetastatic leiomyosarcomasHodgkin’s disease

Hematopoietic neoplasmsHodgkin’s diseasePlasmacytomas

Inflammatory and histiocytosisRosai-Dorfman diseaseNeurosarcoidosisPlasma cell granulomasXanthomasCastleman’s diseaseRheumatoid nodules

InfectiousTubercculomas

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identification of an astrocytic component or sarcomaassociated with blood vessels facilitates the diagnosis ofGS, these features may not be apparent on frozen sec-tions. The true identity of the tumor is readily apparenton permanent sections demonstrating the presence ofsarcoma, usually arising from the adventitia of bloodvessels, associated with islands of malignant glioma. Anyconcern that the tumor represents a malignant menin-gioma may be dispelled with immunohistochemicalstudies demonstrating nests of glial fibrillary acidic pro-

tein (GFAP) immunoreactive anaplastic cells, factorVIII immunoreactive sarcoma around blood vessels,and lack of widespread EMA immunostaining22 (Fig 2).

Case Illustration

A 49-year-old male presented with progressive leftleg weakness. On examination, he was also found tohave homonymous hemianopsia with intact extraocularmovements and cranial nerves. He exhibited upgoing

FIGURE 1. Solitary fibrosis tumor (SFT). (A) A T1-weighted MRIimage obtained after gadolinium administration demonstrat-ing an enhancing mass attached to the dura over the petrousbone, compressing the pons and midbrain with extension intothe foramen magnum. (B) Spindle cells are separated by col-lagen. (C) In cross-sections of areas with dense collagen, tu-mor cells appear round. (D) Elongated blood vessels flankedby collagen are prominent elsewhere. (E) Spindle cells exhibitextensive, diffuse CD34 immunoreactivity. [Hematoxylin andeosin; original magnification �60 (B), �120 (C), �120 (D), �60(E).]

DURAL LESIONS MIMICKING MENINGIOMAS (Johnson et al)

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toes and decreased proprioception on the left side.Strength was 4/5 in the left leg and 5/5 in the rightextremities. MRI revealed a 4.0 � 4.0–cm mass extend-ing from the dura into the temporal lobe and a sylvianfissure compressing the posterior right frontal lobe andthe anterior horn of the right lateral ventricle (Fig 4A).The mass enhanced irregularly with gadolinium admin-istration.

Intraoperatively, the tumor was firm and wasshelled out of the sylvian fissure. Sections through themass revealed a firm, white, solid tumor without necro-sis or hemorrhage. Intraoperative smears and frozensections revealed a biphasic neoplasm populated byspindle cells with nuclear atypia and occasional mitosesflanked by collections of neoplastic astrocytes, suggest-ing a sarcomatoid glioma. Permanent sections of thetumor demonstrated large zones of spindle cell sar-coma (Fig 4B and C). In some areas, this extendedfrom blood vessels (Fig 4D and E). GFAP-immunoreac-tive neoplastic astrocytes (Fig 4E) were present in other

zones of the tumor. Tumor cells exhibited no EMAimmunoreactivity.

LEIOMYOSARCOMAS

On rare occasions, leiomyosarcomas can present asprimary intracranial tumors. These tumors arise pri-marily in males and are more commonly associatedwith human immunodeficiency virus-1 infection andimmunosuppression.23-26 However, a dural leiomyosar-coma has been reported in an immunocompetent 14-year-old female.27 Leiomyosarcomas develop as solitarymasses involving the dura of the sphenoid wing, trans-verse or cavernous sinus, or occipital or temporal lobe.A rare metastatic leiomysarcoma presenting as a men-ingioma-like mass has also been reported.28 Angiogra-phy may reveal contrast pooling, suggesting a cavern-ous hemangioma.24 MRI shows a signal intensity on T1and T2 of the gray matter25 that is enhanced with

FIGURE 2. Hemangiopericytoma (HPC). (A) A T1-weighted MRI image after gadolinium administration demonstrating enhancingmass attached to dura over the frontal lobe. (B) Cellular areas may mimic a meningothelial meningioma, but (C) fine-walledblood vessels dominate elsewhere, as demonstrated by reticulin stains. (D) Papillary architecture is also more common in HPCs butmust be differentiated from rare papillary meningiomas. (Hematoxylin and eosin; original magnification �120.)


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gadolinium administration. Histologically, these tu-mors tend to be low-grade spindle cell lesions contain-ing elongated nuclei with delicate chromatin and scat-tered mitoses (Fig 5B). As with leiomyosarcomas atother sites in immunocompromised patients with hu-man immunodeficiency virus-1, Epstein-Barr virus(EBV) ER1 mRNA and EBV nuclear antigen, or EBVlatency-associated protein, has been demonstrated intumor cells, suggesting a potential role in the patho-genesis of these neoplasms24,27 (Fig 2).

METASTATIC CARCINOMAS

Metastatic carcinoma can produce isolated durallesions mimicking a meningioma. These most com-monly result from breast cancer, adenocarcinomas,squamous cell carcinoma of the lung, and renal cellcarcinomas.29-31 Advances in chemotherapy may be al-tering the current incidence, but in the last decade,solitary metastasis to the dura in breast cancer occurredin approximately 8% of autopsied patients with this

FIGURE 3. Gliosarcoma (GS). (A) A T1-weighted MRI image ofa temporal lesion extending from the dura. (B) Spindle cellareas may resemble an atypical fibrous meningioma if nests ofneoplastic astrocytes are not identified (arrowhead and C). Insome areas, the astrocytic component may not be apparent(D) and may require GFAP immunohistochemistry (E) to identifythis element. [Hematoxylin and eosin; original magnification�60 (B and D) and �120 (C and E).]


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primary.30 Rarely, metastasis from carcinoids, adenoidcystic carcinomas, prostatic adenocarcinomas, and der-matofibrosarcomas have also produced meningioma-like masses.32-36 Typically, these tumors produce MRIimages with increased signals on T2-weighted imagesand often with an enhancing dural tail mimicking ameningioma37 (Fig 6A). Histologic features usually re-veal the metastatic nature of the tumor (Fig 6B); how-ever, lobular growth may mimic whorls or a syncytialgrowth pattern, raising the possibility of a malignantmeningioma (Fig 6C). Because metastatic carcinomasusually exhibit more intense cytokeratin and no S-100protein expression, immunohistochemical analysis gen-erally excludes meningioma17,22 (Fig 2).

Case Illustration

A 61-year-old woman presented with blurred visionand supraretro- orbital pain in her right eye. Threemonths earlier, an ophthalmologist had detected a cat-aract in her right eye. The patient had a history ofcarcinoma of the breast (stage II, N1, MO) with amastectomy and chemotherapy 8 years earlier and hadrecently completed radiotherapy and chemotherapyfor recurrent metastases to the spine.

The patient’s extraocular muscles were normal onphysical examination, but she reported pain with move-ment. Tenderness was also noted over the lumbarspine. Because of persistent symptoms, MRI was or-dered; this revealed a 4 � 1 � 1–cm extraxial mass ofthe middle cranial fossa.

Intraoperatively, the tumor was found to be at-tached to the dura and infiltrating the lateral wall of theorbit. Grossly, the tumor was tan soft tissue. Microscop-ically, the lesion appeared to be a carcinoma infiltratingthe dura, organized largely in nests. Tumor cells exhib-ited modest EMA, intense AE1/AE3, cytokeratin-7HER2/neu, and estrogen and progesterone immuno-reactivity consistent with metastatic breast carcinoma(Figs 2 and 6).

HODGKIN’S DISEASE

Hodgkin’s disease (HD) spreads hematogenouslyto the leptomeninges and dura in 0.2% to 0.5% ofpatients with stage II or III disease, producing a firm,circumscribed dural-based tumor with radiographicand intraoperative features of a meningioma.38,39

Rarely, HD may also present as a primary central ner-vous system (CNS) tumor; 3 of the 9 reported caseswere originally considered meningiomas.40-44

HD must be differentiated from lymphomas, lym-phoplasmacytic meningiomas, inflammatory pseudotu-mors, neurosarcoidosis, or infectious processes. Thepresence of Reed-Sternberg (R-S) cells with extensiveor limited membrane or cytoplasmic CD15 and CD30immunoreactivity in a lesion with polytypic T and Blymphocytes and eosinophils supports a diagnosis ofHD.45 In contrast to lymphoplasmacytic meningiomas,HD displays no identifiable meningothelial componentwith EMA immunostaining. The tumor has no granu-lomas asteroid or Schaumann bodies of neurosarcoid-osis. In contrast to Rosai-Dorfman disease, this lesionlacks a histiocytic component and emperipolesis.Plasma cell granulomas do not contain R-S cells orsignificant eosinophilic infiltrates. Like its systemiccounterpart, CNS HD exhibits EBV antigens in R-S cellsin approximately 1/2 of cases and was recently de-scribed in a case of primary CNS HD44,45 (Fig 2).

The diagnosis of primary CNS HD is predicated onthe exclusion of HD elsewhere in the body, becausemetastatic lesions are far more common.46 A thoroughstaging should include bone marrow biopsy, MRI of thechest and abdomen, and ophthalmologic examination.

Case Illustration

A 55-year-old woman presented to the emergencyroom complaining of a 1-week history of worseningheadaches and difficulty walking. She reported havinghad headaches “for years.” On MRI, T1-weighted im-

FIGURE 4. Leiomyoma and Leiomyosarcoma. (A) MRI image showing a dural-based intracranial leiomyoma mimicking ameningioma. (B) This dural leiomyosarcoma exhibits fascicular architecture, but spindle cells are without indistinct juxtanuclearvacuoles. As in (B), leiomyosarcomas are now being encountered in immunocompromised patients. (Hematoxylin and eosin;original magnification �100.)


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ages demonstrated a hypointense posterior fossa massarising from the inferior aspect of the tentorium. The2.3 � 3.2 � 3.2–cm mass was enhanced markedly aftergadolinium administration and had a dural tail (Fig 7A).

Intraoperatively, the mass was attached to the ten-torium and was firm. Frozen sections revealed an in-flammatory lesion. A gross total resection was achieved.

Microscopically, the lesion was composed of nu-merous small lymphocytes, histiocytes, scattered eosin-ophils, occasional large dysplastic cells with prominentinclusion-like nucleoli, and scarce binucleate lacunarcells (Fig 7B). The small lymphocytes were predomi-nantly UCHL-1– and CD3-immunoreactive T cells, withoccasional CD20-immunoreactive B cells. The large dys-plastic R-S cells showed strong membranous and Golgiimmunostaining with CD30 and focal staining with

CD15 (leu M-1). The R-S cells did not react with anti-bodies to EMA, UCHL-I, CD3, CD20, or S-100. Numer-ous R-S cells showed immunoreactivity for EBV latency-associated protein (Fig 7C). The small plasma cellswere polytypic in terms of IgG, IgM, IgA, and kappa andlambda light chain reactivity and were EMA immuno-reactive. There was rare S-100 protein staining in scat-tered histiocytes. Neither emperipoleses nor granulo-mas were found, and special stains revealed no bacteria,fungi, spirochetes, or acid- fast bacilli. Meningothelialcells were not seen. A diagnosis of HD, nodular scleros-ing type, was made.

Subsequent evaluation, including bone marrow bi-opsy; CT scans of the chest, abdomen and pelvis; andophthalmologic evaluation, revealed no evidence ofsystemic disease.

FIGURE 5. Metastatic carcinoma of the breast. (A) MRI show-ing a dural-based mass compressing the frontal lobe. (B andC) Carcinoma cells infiltrating the dura usually present littlediagnostic challenge but occasionally may grow in syncytia orlobules suggestive of a malignant meningioma. [Hematoxylinand eosin; original magnification �80 (B) and �250 (C).]


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Figure 6

Figure 7

Figure 8

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PLASMACYTOMAS

Plasma cell neoplasms rarely involve the CNS asdural-based lesions.47-58 Two reported cases have beenreported in older adults as masses attached to the fron-tal dura or falx.57,58 On T1-weighted images, the tumorexhibits an intermediate signal compared to that ofbrain tissue, with marked enhancement after gadolin-ium administration. On T2-weighted images, plasmacy-tomas are isointense with gray matter.57,58 Histologi-cally, they are identical to plasmacytomas elsewhere.Plasmacytomas must be differentiated from plasma cellgranulomas, which also may present as dural-based le-sions. Because plasmacytomas may contain leptomenin-ges, they must also be differentiated from lymphoplas-macytic meningiomas. Usually, their homogeneity andmonoclonal immunophenotype differentiate themfrom both granulomas and meningiomas (Figs 2 and8). Their recognition and differentiation from surgi-cally managed plasmacytic meningiomas is important,because radiation and chemotherapy after surgical re-section offer a potential cure.47-58

ROSAI-DORFMAN DISEASE

Rosai-Dorfman disease (RDD), or sinus histiocyto-sis and massive lympadenopathy, is a reactive conditiontypically associated with painless cervical lympadenopa-thy, fever, and hypergammaglobulinemia.59 Concomi-tant growth at extranodal sites such as the upper respi-ratory tract, skin, orbit, or dura has been reported.59 Atleast 6 cases of solitary dural-based RDD, mimickingmeningioma and without nodal involvement, have alsobeen described.60-64 These occur predominantly inadult males and may involve the epidural and/or sub-dural space at parasagittal, suprasellar, or cerebellarpontine angle sites.60-64 CT scans typically reveal a con-trast-enhancing hypodense tumor. Histologically, theselesions are populated by foamy histiocytes (Fig 9B) withS-100 protein, CD68, �-1-antitrypsin, and �-1-antichy-motrypsin immunoreactivity but no CD1a immuno-staining. The infiltrate also contains B and T lympho-cytes, plasma cells, and occasionally eosinophils (Fig9C). Central necrosis may be present. The hallmark of

4™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™FIGURE 6. Dural Hodgkin’s Disease. (A) A TI-weighted MRI image obtained after gadolinium administration demonstrating anenhancing mass with a dural tail arising from the inferior aspect of the tentorium cerebelli. (B) The tumor is composed of an infiltrateof lymphocytes, plasma cells, eosinophils, and R-S–like cells in fibrotic stroma. (C) R-S cell variants exhibit EBV latency-associatedprotein. [(B) PAS, original magnification �120; (C) hematoxylin, original magnification �250.]FIGURE 7. Plasmacytoma. The tumor is populated by a monomorphous population of dysplastic plasma cells without lympho-cytes or histiocytes. (Hematoxylin and eosin; original magnification �140.)FIGURE 8. Rosai-Dorfman disease. (A) An MRI image demonstrating an extra-axial lesion over the left parietal and occipital lobesthought to be a meningioma en plaque. (B) Foamy histiocytes are present in varying numbers. These histiocytes may exhibitemperipolesis. (C) Other areas of the mass contain a mixed inflammatory infiltrate of lymphocytes and plasma cells (Hematoxylinand eosin; original magnification �300.)

FIGURE 9. Neurosarcoidosis. (A) A T1-weighted MRI image demonstrating a dura-based mass mimicking a meningioma enplaque. (B) Sections reveal a granulomatous process with epithelioid histiocytes but no necrosis. Multinucleated giant cells andoccasionally Schaumann bodies are present; special stains for organisms are repeatedly negative (Hematoxylin and eosin; originalmagnification �80.)


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RDD is emperipolesis, primarily of lymphocytes, whichmay be inconspicuous (Fig 9B).

Dural RDD can be managed with surgical resectionand has a good prognosis.60-64 It must be differentiatedfrom more ominous lesions requiring aggressive ther-apy, such as Langerhans cell histiocytosis, HD, malig-nant histiocytic lymphoma, and plasma cell granuloma.In contrast to histiocytes in Langerhans cell histiocyto-sis, histiocytes in RDD are CD1a negative and lackstriking nuclear grooves and Bierbeck granules ultra-structurally. Moreover, emperipolesis is not seen inLangerhans cell histiocytosis. In contrast to HD, largeR-S–like cells immunostain for S-100 protein but arenegative for CD15, CD30, and EBV latent membraneprotein. As described later, plasma cell granulomas aretypically more fibrotic, contain histiocytes with no S-100protein immunostaining, and lack emperipolesis61,62,64

(Fig 2).

NEUROSARCOIDOSIS

Sarcoidosis involves the CNS in 5% of cases, ac-counting for approximately 5 per 1 million popula-tion.65 It usually develops in the basal leptomeningesand may involve the hypothalamus, infundibulum, orcranial nerves. Lesions seen on CT scan and operativefeatures of meningioma have been reported at thecribiform plate, sphenoid wing, optic nerve, and cere-bellar pontine angle.66-72 In rare parasagittal,68 convex-ity,69 parafalcine,70 and cerebellopontine71 examples,there has been no evidence of systemic disease, andangiotensin-converting enzyme levels were normal. Tu-mors are isointense on T1-weighted MRI images andhyperintense on T2-weighted images, with uniformenhancement after gadolinium administration65 (Fig10A). Intraoperatively, these lesions are firm, fibrousmasses attached to the dura. Histologically, pseudo-meningiomatous neurosarcoidosis is similar to sarcoid-osis elsewhere in the body, with multinucleated giantcells and epithelioid histiocytes (Fig 10B) that reactwith antibodies to MAC387 and CD68 but not withS-100 protein. Limited numbers of lymphocytes andplasma cells and extensive fibrosis are also present.Schaumann or asteroid bodies may or may not be seenin giant cells and are not specific for sarcoidosis. Al-though these are generally considered to be nonnecro-tizing lesions, focal necrosis has been reported in thecenter of granulomas in some putative cases. Specificstains for mycobacteria, fungi, and spirochetes are neg-ative (Fig 2).

PLASMA CELL GRANULOMAS

On rare occasions, plasma cell granuloma (PCG)may present as a dural-based mass clinically indistin-guishable from meningioma. In 4 cases previously re-ported and 1 case described herein, these reactive le-sions occurred primarily in adults, usually presenting asdiscrete tumors arising from the leptomeninges or

dura. MRI revealed little evidence of parenchymal in-vasion,72-74 although parenchymal involvement hasbeen described.75 Histologically, they are populated bya polytypic population of mature plasma cells, plasma-cytoid, and small nontransformed lymphocytes in abackground of variable fibrosis, fibroblasts, and en-trapped leptomeningeal cells (Fig 11B). Russell bodiesare usually present.71-74 PCGs with broad bands of fi-brosis may represent a variant sometimes described as“hyalinized”74 (Fig 11C). The reactive nature of theselesions is documented using immunohistochemistry forlight chains, IgG, IgM, and IgA, which establishes thepolyclonal nature of the process. PCGs must be differ-entiated from the other inflammatory lesions men-tioned earlier as well as from rare lymphoplasmacyticmeningiomas. Although focal EMA immunostainingmay be seen within entrapped arachnoid, PCGs lackthe focal areas of overt meningiomas and the extensiveEMA immunoreactivity common to meningiomas.17 Incontrast to RDD, histiocytes in PCG are S-100 negativeand devoid of emperipolesis. R-S cells and eosinophilsare absent71-73 (Fig 2).

Case Illustration

A 42-year-old male body shop worker was evalu-ated for unremitting headaches. He had been ondisability due to lumbar disc disease for some time.He had a history of hypertension, hypercholesterol-emia, and depression. Physical examination revealedno neurologic or ophthalmologic deficits or lymph-adenopathy.

MRI of the head demonstrated a parietal 2.5 �2.5–cm dural-based mass thought to be a meningiomaassociated with vasogenic edema of the underlyingbrain (Fig 11A). A second 1.25 � 1.25 � 0.75–cmlesion was identified at the cervical–medullary junction.MRI of the cervical spine revealed no abnormalities.

Surgery was directed at the parietal lobe lesion.Intraoperatively, the lesion was dural based, with smallsatellite lesions. This was resected without complica-tions.

Microscopically, the lesion was composed ofdura with nodules of plasma cells and lymphocytesseparated by hyalinized zones. Rare binucleateplasma cells and Russell bodies were present, butovertly dysplastic plasma cells were not found. Scat-tered histiocytes with no S-100 protein immunoreac-tivity were also present. Immunohistochemical anal-ysis revealed a polytypic plasma cell infiltrate. Nomeningioma-like histology or EMA immunoreactivitywas identified. Giant cells, foamy histiocytes, emperi-polesis, and zonal necrosis were not present (Fig 11Band C). A diagnosis of hyalinizing plasma cell gran-uloma was made.

Two years postoperatively, there has been no re-currence of the parietal lesion, the foramen magnumlesion is stable, and the patient is in good health.


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XANTHOMAS

A xanthoma or xanthogranuloma may rarelypresent as a dural-based mass mimicking a meningi-oma. This may be primary or associated with histiocy-tosis X. To date, 3 primary cases have been reported,which presented as spinal lesions in children.76-78 After

gadolinium administration, T1-weighted MRI demon-strates a homogeneously enhancing circumscribedmass. Histologically, these are encapsulated lesionspopulated by lipid-filled, CD68-positive, S-100–negativehistiocytes with small nuclei accompanied by small non-transformed lymphocytes. In contrast, Langerhans cellhistiocytosis of long duration may contain foamy histio-

FIGURE 10. Plasma cell granuloma. (A) An MRI image demon-strating a circumscribed dural-based mass over the occipitallobe. (B) Plasma cells intermingle with lymphocytes in these het-erogeneous lesions. Foamy histiocytes are not prominent. Immu-nohistochemistry demonstrates a polytypic population of plasmacells. (C) Hypocellular hyalinized areas may be present and re-semble dura. (Hematoxylin and eosin; original magnification�250.)

FIGURE 11. Rheumatoid nodules. (A) Small nodules may develop in the subrachnoid space. (B) Foamy histiocytes encircle a zoneof necrobiosis flanked by lymphocytes, plasma cells, and a rare giant cell (seen in A). [Hematoxylin and eosin; original magnifi-cation �60 (A) and �300 (B).]


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cytes, but these are S-100 protein positive and containBirbeck granules ultrastructurally77 (Fig 2).

INFLAMMATORY PSEUDOTUMORSASSOCIATED WITH SYSTEMIC DISEASE

Castleman’s disease has been associated with in-flammatory pseudotumors of the dura that resemblegiant lymph node hyperplasia associated with this dis-ease.79-82 Most cases with CNS involvement have sys-temic manifestations with lymph node hyperplasia inthe mediastium, abdomen, or neck. However, isolatedCNS Castleman’s presenting as a meningioma-like massattached to the tentorium cerebelli has recently beenreported.82 These lesions produce insidious symptomsattributable to the site of origin. MRI reveals an isoin-tense dural-based lesion that enhances uniformly withgadolinium.82 Intraoperatively, Castleman’s disease ap-pears to be a typical meningioma.82 Histologically, thislesion resembles changes seen in lymph nodes withhyperplastic follicles of mature B and T lymphocytessurrounded by a polyclonal plasmacytic infiltrate withRussell bodies. Castleman’s disease has 2 variants: thehyaline/vascular and plasmacytic types. The formermay be more common in the brain.79-82

Castleman’s disease must be differentiated from asmall-cell lymphoma, plasmacytoma, infectious process,or lymphoplasmacytic meningioma. Demonstration of

follicles with a nontransformed polytypic population oflymphocytes and plasma cells rules out the former. Theabsence of clinical evidence of infection and failure todemonstrate organisms in cultures and special stainsargues against a mycobacterium infection. No menin-geal proliferation is seen in these lesions, excluding adiagnosis of lymphoplasmacytic meningioma.

Rarely, rheumatoid arthritis is associated with thedevelopment of rheumatoid nodules that can mimicsmall meningiomas. Like their counterparts in joints,these lesions are composed of fibrous nodules with apolytypic lymphocytic infiltrate around zones of necro-sis with giant cells and epitheloid histiocytes83,84 (Figs 2and 12).

LEPTOMENINGEAL MELANOCYTICNEOPLASMS

Leptomeningeal melanocytes, present primarily inthe basal and ventral spinal leptomeninges, occasion-ally give rise to a spectrum of melanocytic neoplasmsranging from low-grade melanocytomas to malignant mel-anomas.84-86 Those that are circumscribed may be radio-graphically indistinguishable from a meningioma. Lepto-menigeal melanocytic neoplasms occur primarily inadults in the leptomeninges of the brainstem or spinalcord as solitary tumors.84-86 Grossly, they appear blackor gray, and, depending on the grade, they may com-

FIGURE 12. Melanocytoma. (A) An MRI image demonstrating acircumscribed dural-based leptomeningeal tumor at T4-T5 com-pressing the spinal cord. (B) Tumor cells grow in sheets and fasci-cles without necrosis. (C) Melanocytoma cells are primarily spin-dle cells with bland chromatin and small nucleoli but no frankanaplasia. Scattered mitoses are present. [Hematoxylin and eo-sin; original magnification �60 (A) and �300 (B).]


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press or invade the nervous system. Histologically, mostmelanocytomas are spindle cell neoplasms, althoughepithelioid cytology may dominate in some cases.85,86

Tumor cells may grow in sheets, nests, or fascicles. Theround or oval nuclei are relatively uniform, sometimeswith small nucleoli. In melanocytomas, mitotic activitymay be minimal or up to 1 per 10 high-power fields(HPFs) with a MIB-1 labeling index of 0% to 2%.86

However, an intermediate-grade variant is now recog-nized that exhibits less nesting, more diffuse growth,minimal cytologic atypia, small nucleoli, a mitotic rateof 1 to 3 per 10 HPFs, and MIB-1 labeling of 2% to4%.86 Recognition of this variant is important becauseof the reported increased risk of recurrence.86-89 Incontrast, malignant leptomeningeal melanoma exhibitscytologic anaplasia, prominent nucleoli, and oftenbrisk mitotic activity (2 to 15 per 10 HPFs), along witha MIB-1 labeling rate of 3 to 15 per 10 HPFs. Necrosismay be seen in occasional cases. Despite these features,the prognosis for malignant tumors appears to approx-imate that of uveal melanomas with less risk of metas-tasis and occasional apparent cure with complete resec-tion.90-92

Melanocytic neoplasms must be differentiatedfrom metastatic melanoma and other pigmented le-sions that occur in the leptomeninges, including therare melanotic schwannoma and its psammomatous

variant. Metastatic melanoma is usually multifocal andtypically involves the nervous system parenchyma. Epi-thelioid histology is more common; more bizarreforms, mitoses (7 to 35 per 10 HPFs), higher MIB-1labeling (17% to 38%), and necrosis are seen.86 Pig-mented schwannomas may occur intradurally at nerveroot entry zones, but most commonly occur in thedorsal leptomeninges, although ventral developmenthas been reported.93 Histologically, these tumors ex-hibit more elongated spindled nuclei and cytoplasmbut usually lack myxoid areas and Verocay bodies. Im-munohistochemical demonstration of intercellular col-lagen IV, laminin, or reticulin surrounding cells maydifferentiate these tumors from melanocytomas, whichexhibit only perifascicular deposition. Psammomatousmelanotic schwannomas are associated with 60% ofcases with Carney’s syndrome, exhibit psamomma bod-ies in more than 50% of cases, and usually occur inposterior nerve roots, skin, or the upper gastrointesti-nal tract (Fig 2).

Case Illustration

A 35-year-old woman presented with a 6-monthhistory of decreased lower extremity sensation followedby progressive weakness, greater in the right leg than inthe left leg, for 2 weeks. On the day of admission, she

FIGURE 13. Flow diagram summarizing some diagnostic considerations for dural lesions mimicking meningiomas.


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was unable to stand or walk. MRI demonstrated a 3.0 �2.0 � 1.0–cm homogeneously enhancing solid tumorventral to the spinal cord at T4-T5 with compression ofthe spinal cord (Fig 13A). The mass had an enhancingdural tail. Radiographically, the mass was thought to bea meningioma.

The patient underwent posterior resection of thetumor. Intraoperative analysis suggested a low- to inter-mediate-grade melanocytic neoplasm.

Grossly, the tumor was encapsulated, black, andsoft. Microscopically, the tumor was composed of spin-dle cells with varying amounts of pigmentationthroughout. Occasional melanophages were present.Tumor cells grew in a diffuse pattern populated byrelatively uniform cells with small round and ovoidnuclei in areas with small nucleoli, but no significantcellular atypia or bizarre forms (Fig 13B and C). Up to3 mitoses per 10 HPFs were seen focally (Fig 13D).Histology suggestive of a schwannoma or meningiomawas not seen. The MIB-1 labeling rate was approxi-mately 5%. Necrosis was not present. A diagnosis ofmelanocytoma, intermediate grade, was made.

Postoperatively, the patient was able to walk unas-sisted and experienced normal sensation in both lowerextremities.

INFECTIOUS LESIONS MIMICKINGMENINGIOMAS

Rarely, infections limited to the leptomeningesmay produce a dural-based mass that mimics a menin-gioma. In the United States, a tuberculoma from eithermycobacterium tuberculosis or mycobacterium aviumcomplex infection may produce such a lesion in animmunocompromised individual. This has recentlybeen described in a patient with systemic lupus ery-thematosus and a mycobacterium avium complex in-fection.94 Histologically, due to the leptomeningealreaction, such lesions may resemble a fibroblastic me-ningioma if the histiocytic component is not recog-nized and giant cells are lacking.94 Nonetheless, clinicalfeatures may suggest an infectious etiology in mostcases.

CONCLUSIONS

A growing number of neoplastic and nonneoplas-tic dural lesions are now recognized and have ex-panded the differential diagnosis of meningiomas.Awareness of these lesions may facilitate their recogni-tion intraoperatively and during postoperative study.

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