Meningioma Workup

  • Author: Georges Haddad, MD; Chief Editor: Tarakad S Ramachandran, MBBS, FRCP(C), FACP   more...
 
Updated: Nov 3, 2011
 

Laboratory Studies

No specific laboratory tests are used to screen for meningioma.

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Imaging Studies

  • Imaging studies are the mainstay of diagnosis. See images below for representative radiologic views of various subtypes.
  • Plain skull radiograph may reveal hyperostosis and increased vascular markings of the skull, as well as intracranial calcifications.
  • On plain head CT scans, meningiomas are usually dural-based tumors that are isoattenuating to slightly hyperattenuating.
    • They enhance homogeneously and intensely after the injection of iodinated contrast material.
    • Perilesional edema may be extensive. Hyperostosis and intratumoral calcifications may be present.
    • The tumor compresses the brain without invading it.
    • Multiple meningiomas may be difficult to differentiate from metastasis.
  • On T1- and T2-weighted MRIs, the tumors have variable signal intensity. If a meningioma is suspected, obtaining an enhanced MRI is imperative.
    • Meningiomas enhance intensely and homogeneously after injection of gadolinium gadopentetate.
    • The edema may be more apparent on MRI than on CT scanning.
    • An enhancing tail involving the dura may be apparent on MRI.
    • Cystic meningiomas may exhibit intratumoral or peritumoral cysts. The peritumoral cysts may actually represent a gliotic response and may not necessitate surgical extirpation.
  • Endovascular angiography allows the surgeon to preoperatively determine the vascularization of the tumor and its encroachment on vital vascular structures.
    • Late venous images are important to determine the patency of the involved dural sinuses.
    • Angiographic features of meningiomas include the following:
      • Supply from the external circulation
      • Mother-in-law blush (which comes early and leaves late)
      • Sunburst or radial appearance of the feeding arteries
    • Although magnetic resonance arteriography (MRA) and magnetic resonance venography (MRV) have decreased the role of classical angiography, the latter remains a powerful tool for planning surgery.
    • Angiography is still indispensable if embolization of the tumor is deemed necessary.
  • New research tools such as positron emission tomography (PET), including octreotide-PET, or magnetic resonance spectroscopy (MRS) have been used to predict in vivo the aggressiveness of meningiomas.[12] Case 1: MRI of a meningioma on plaque. Case 1: MRI of a meningioma on plaque. Case 1: Bone-window CT reveals calcification of thCase 1: Bone-window CT reveals calcification of the meningioma. Case 2: Gadolinium-enhanced MRI of a meningioma inCase 2: Gadolinium-enhanced MRI of a meningioma invading the overlying dura and bone. Compare with appearance in Case 1. Case 2: Bone-window CT scan reveals the skull invoCase 2: Bone-window CT scan reveals the skull involvement. Note the absence of tumoral calcification. Case 3: Tentorial meningioma. A, Contrast-enhancedCase 3: Tentorial meningioma. A, Contrast-enhanced CT scan shows the enhancing meningioma. Transverse T1-weighted MRIs shows isointensity of the tumor compared with the surrounding brain (B) and its homogenous enhancement (C). Coronal (D), coronal enhanced (E), and sagittal enhanced (F) T1-weighted MRIs. Posterior circulation angiograms show tumoral blush (arrow in G) and the Bernasconi-Cassinari artery (arrow in H). Case 3: Tentorial meningioma. Gadolinium-enhanced Case 3: Tentorial meningioma. Gadolinium-enhanced T1-weighted MRI immediately (A) and 2 years after surgery (B-D). Transverse images show posterior (arrow in B) and anterior (arrow in C) recurrence involving the tentorium. Sagittal images show posterior (D) and anterior (E) recurrence involving the tentorium. Lower vignette reveals complete excision of the recurrence after a second operation. Case 3: Tentorial meningioma A, Pathology showed sCase 3: Tentorial meningioma A, Pathology showed syncytial meningioma. Note hypercellularity and minimal whorling (hematoxylin-eosin, original magnification X400). B, MRI performed 4 years after the first operation reveals a recurrence over the posterior tentorium. C, Two-dimensional planning for stereotactic radiosurgery. Three recurrences lie in the plane of the tentorium on a single line. D, Three-dimensional planning for stereotactic radiosurgery. Three arcs were used to irradiate the largest recurrence. Case 4: Recurrent subcutaneous meningioma. A, PatiCase 4: Recurrent subcutaneous meningioma. A, Patient underwent surgery for a parieto-occipital meningioma in 1978. She was lost to follow-up until 1996, when this transverse T2-weighted MRI was obtained. Arrow indicates surgical bed of the resected meningioma. B, Although the initial surgical bed is tumor-free, sagittal T2-weighted MRI shows a large subcutaneous recurrence. C, Lower transverse section also shows recurrence. Note variegated appearance of the tumor. D, Transverse section at a lower level. Postoperative sagittal (E) and transverse (F, G) enhanced T1-weighted MRI shows gross total removal of the tumor. H and I, Tumoral recurrence 3 months after surgery, at the same level as in G and F, respectively. Patient received repeat surgery for subtotal removal of the tumor; a pediculated subcutaneous flap was used to close the surgical defect. After surgery, patient received conventional radiotherapy. Case 5: Bilateral olfactory meningioma invading thCase 5: Bilateral olfactory meningioma invading the facial sinuses. Coronal (A), transverse (B), and sagittal (C) gadolinium-enhanced T1-weighted MRI shows bilateral olfactory meningiomas, and the falx dividing the tumor in 2. Arrow indicates tumor invasion of the sinuses. D, Postoperative enhanced T1-weighted MRI shows that the tumor was completely removed by means of craniotomy and a transfacial approach. E, Tumor was first approached intracranially. Enhanced T1-weighted MRI reveals complete excision of the intracranial component. Arrow indicates residual in the sinuses. F, Residual was completely excised by means a transfacial approach performed with the otolaryngology team. Case 6: Subfrontal meningioma in a patient with abCase 6: Subfrontal meningioma in a patient with abnormal behavior. A, Contrast-enhanced CT scan clearly shows bilateral subfrontal meningioma. B, Transverse T1-weighted MRI of same lesion. C, Intense gadolinium enhancement of the tumor. Coronal (D) and sagittal (E) gadolinium-enhanced T1-weighted MRIs. F, Anterior circulation angiogram reveals posterior displacement of the anterior cerebral artery by tumor. G, Postoperative MRI shows complete removal of the tumor. H-I, Pathology slides (hematoxylin-eosin; original magnification X100 in H, X400 in I) show syncytial meningioma with well-identified whorls and no psammoma bodies. Case 7: Parasagittal meningioma invading the superCase 7: Parasagittal meningioma invading the superior sagittal sinus (SSS). A, Sagittal T1-weighted MRI shows a meningioma (arrow). B, T2-weighted MRI. Note midline shift and tumoral invasion of the skull (arrow). C, Transverse T2-weighted MRI. D, Angiogram shows invasion of the SSS, which remains patent. Sagittal (E, G), transverse (F) postoperative T1-weighted MRI. H, Gadolinium-enhanced postoperative T1-weighted MRI shows residual tumor, which was intentionally left to preserve patency of the SSS. I, Pathology slide (hematoxylin-eosin, original magnification X100) shows a highly vascular syncytial meningioma. This is an extra-axial tumor. Glioblastoma multifoThis is an extra-axial tumor. Glioblastoma multiforme (GBM) and astrocytoma are intraparenchymal tumors, and GBM enhances in a variegated fashion. Acoustic schwannomas are seen in the posterior fossa but not in this location. Fibrous dysplasia involves the skull but does not cause this amount of compression.
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Procedures

  • Preoperative endovascular embolization of the vascular feeders from the external circulation may be beneficial in extremely vascular meningiomas.[13]
  • If this is the case, resection should be performed shortly after embolization to decrease the likelihood of tumor revascularization.
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Histologic Findings

Meningiomas are usually globular, well-demarcated neoplasms. They have a wide dural attachment and become invaginated into the underlying brain without invading it. Their cut surface is either translucent pale or homogeneously reddish brown. It may be gritty on cutting. Some meningiomas occur as a sheetlike extension that covers the dura but does not invaginate the parenchyma; this variant is called meningioma en plaque. The last morphologic variant is the cavernous sinus meningioma that infiltrates the cavernous sinus and becomes interdigitated with its contents. The 3 most common histologic subtypes of meningiomas are the meningothelial (syncytial), transitional, and fibroblastic meningiomas. See images below for representative pathologic views of various subtypes.

Pathology slides (hematoxylin-eosin; original magnPathology slides (hematoxylin-eosin; original magnification X400 in A-B, X100 in C-D). A, Fibroblastic meningioma (arrowheads) abutting the dura (arrow). B, Psammomatous meningioma (arrow indicates psammoma body). C, Meningothelial meningioma, tumor in case 4. E, Meningioma with marked vascularity (arrowheads indicate meningioma cluster; arrow, vessel wall). Case 4: Pathology slides (hematoxylin-eosin, origiCase 4: Pathology slides (hematoxylin-eosin, original magnification X400). A, Meningioma with malignant features, as evinced by prominent nucleoli (yellow dot) and mitoses (arrows). B, Intranuclear cytoplasmic intrusion (pseudoinclusion).

Meningothelial meningiomas reveal densely packed cells that are arranged in sheets with no clearly discernible cytoplasmic borders. Although not prominent, whorls are present (calcified whorls are termed psammoma bodies). Nuclei show intranuclear vacuoles.

Fibroblastic (fibrous) meningiomas reveal sheets of interlacing spindle cells. The intercellular stroma is composed of reticulin and collagen. The transitional variety reveals features common to both the meningothelial and fibroblastic varieties; others include angiomatous, microcystic, secretory, clear cell, choroid, lymphoplasmacyte-rich, papillary, and metaplastic variants.

Meningiomas may be associated with hyperostosis.[3] The exact nature of the cause of this hyperostosis is controversial (ie, reactive versus tumoral infiltration).

Immunohistochemistry

Immunohistochemistry can help diagnose meningiomas, which are positive for epithelial membrane antigen (EMA) in 80% of cases. They stain negative for anti-Leu 7 antibodies (positive in schwannomas) and for glial fibrillary acidic protein (GFAP). Progesterone receptors can be demonstrated in the cytosol of meningiomas; the presence of other sex hormone receptors is much less consistent. Somatostatin receptors also have been demonstrated consistently in meningiomas.

Malignancy

The notion of malignancy in meningiomas is still vague.[14] Some histologic variants, such as papillary meningioma, undoubtedly carry a less favorable prognosis than other histologic types. Two features are considered clear signs of malignancy: cortical invasion by the tumor and distal metastasis. Of note, in the 2007 WHO grading scheme, brain invasion is considered a criterion for atypia.

Several stains have been used to help predict the behavior of meningiomas. These stains quantify the mitotic rate of these tumors. Bromodeoxyuridine (BudR) labeling requires an intravenous (IV) injection before tumor removal. On the other hand, immunohistologic staining for proliferating cell nuclear antigen (PCNA) can be performed on fixed specimens. Some have attempted to correlate the pathology and behavior of meningiomas to the loss of specific genetic material.

The World Health Organization classification of meningiomas is presented in Table 2.

Table. Summary of the 2007 WHO Grading Scheme for Meningiomas (Open Table in a new window)

WHO Grade Histological Subtype Histological Features
IMeningothelial, fibroblastic, transitional, angiomatous, microcystic, secretory, lymphoplasmacytic metaplastic, psammomatousDoes not fulfill criteria for grade II or III
II (Atypical)Chordoid, clear cell4 or more mitotic cells per 10 hpf and/or 3 or more of the following: increased cellularity, small cells, necrosis, prominent nucleoli, sheeting, and/or brain invasion in an otherwise Grade I tumor
III (Anaplastic)Papillary, rhabdoid[15] 20 or more mitoses per 10 hpf and/or obviously malignant cytological characteristics such that tumor cell resembles carcinoma, sarcoma, or melanoma

The expression levels of E- cadherin and beta-catenin were found to be inversely correlated with peritumoral edema, aggressiveness of meningiomas, and probability of recurrence.[16]

In a review of 21 pediatric meningiomas operated on over a period of 24 years, 24% were WHO grade II and 24% where associated with a large cystic component.[17]

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Contributor Information and Disclosures
Author

Georges Haddad, MD  Clinical Assistant Professor, Department of Medicine, Division of Vascular Surgery, American University of Beirut, Lebanon

Georges Haddad, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Ali Turkmani, MD  Staff Physician, Department of Neurosurgery, American University Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

Frederick M Vincent Sr, MD  Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Jorge C Kattah, MD  Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, and New York Academy of Sciences

Disclosure: Biogen Honoraria Consulting; Bayer Corporation Honoraria Consulting

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Tarakad S Ramachandran, MBBS, FRCP(C), FACP  Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine

Disclosure: Abbott Labs None None; Teva Marion None None; Boeringer-Ingelheim Honoraria Speaking and teaching

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors Tarafa Baghdadi, MD and Roukoz B Chamoun, MD to the development and writing of this article.

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Case 1: MRI of a meningioma on plaque.
Case 1: Bone-window CT reveals calcification of the meningioma.
Case 1: Surgical view of the tumor. The dura is opened, and the meningioma can be seen extending en plaque over the surface of the brain.
Case 1: Bone flap seen along the removed meningioma in toto.
Case 2: Gadolinium-enhanced MRI of a meningioma invading the overlying dura and bone. Compare with appearance in Case 1.
Case 2: Bone-window CT scan reveals the skull involvement. Note the absence of tumoral calcification.
Case 2: Intraoperative view shows the skull involvement.
Case 2: Bone flap was removed. Note tumoral breach of the dura. The dura and overlying skull were removed surgically. Duraplasty and cranioplasty were performed
Case 2: Surgical specimen. Complete resection was achieved.
Case 3: Tentorial meningioma. A, Contrast-enhanced CT scan shows the enhancing meningioma. Transverse T1-weighted MRIs shows isointensity of the tumor compared with the surrounding brain (B) and its homogenous enhancement (C). Coronal (D), coronal enhanced (E), and sagittal enhanced (F) T1-weighted MRIs. Posterior circulation angiograms show tumoral blush (arrow in G) and the Bernasconi-Cassinari artery (arrow in H).
Case 3: Tentorial meningioma. Gadolinium-enhanced T1-weighted MRI immediately (A) and 2 years after surgery (B-D). Transverse images show posterior (arrow in B) and anterior (arrow in C) recurrence involving the tentorium. Sagittal images show posterior (D) and anterior (E) recurrence involving the tentorium. Lower vignette reveals complete excision of the recurrence after a second operation.
Case 3: Tentorial meningioma A, Pathology showed syncytial meningioma. Note hypercellularity and minimal whorling (hematoxylin-eosin, original magnification X400). B, MRI performed 4 years after the first operation reveals a recurrence over the posterior tentorium. C, Two-dimensional planning for stereotactic radiosurgery. Three recurrences lie in the plane of the tentorium on a single line. D, Three-dimensional planning for stereotactic radiosurgery. Three arcs were used to irradiate the largest recurrence.
Case 4: Recurrent subcutaneous meningioma. A, Patient underwent surgery for a parieto-occipital meningioma in 1978. She was lost to follow-up until 1996, when this transverse T2-weighted MRI was obtained. Arrow indicates surgical bed of the resected meningioma. B, Although the initial surgical bed is tumor-free, sagittal T2-weighted MRI shows a large subcutaneous recurrence. C, Lower transverse section also shows recurrence. Note variegated appearance of the tumor. D, Transverse section at a lower level. Postoperative sagittal (E) and transverse (F, G) enhanced T1-weighted MRI shows gross total removal of the tumor. H and I, Tumoral recurrence 3 months after surgery, at the same level as in G and F, respectively. Patient received repeat surgery for subtotal removal of the tumor; a pediculated subcutaneous flap was used to close the surgical defect. After surgery, patient received conventional radiotherapy.
Case 5: Bilateral olfactory meningioma invading the facial sinuses. Coronal (A), transverse (B), and sagittal (C) gadolinium-enhanced T1-weighted MRI shows bilateral olfactory meningiomas, and the falx dividing the tumor in 2. Arrow indicates tumor invasion of the sinuses. D, Postoperative enhanced T1-weighted MRI shows that the tumor was completely removed by means of craniotomy and a transfacial approach. E, Tumor was first approached intracranially. Enhanced T1-weighted MRI reveals complete excision of the intracranial component. Arrow indicates residual in the sinuses. F, Residual was completely excised by means a transfacial approach performed with the otolaryngology team.
Case 6: Subfrontal meningioma in a patient with abnormal behavior. A, Contrast-enhanced CT scan clearly shows bilateral subfrontal meningioma. B, Transverse T1-weighted MRI of same lesion. C, Intense gadolinium enhancement of the tumor. Coronal (D) and sagittal (E) gadolinium-enhanced T1-weighted MRIs. F, Anterior circulation angiogram reveals posterior displacement of the anterior cerebral artery by tumor. G, Postoperative MRI shows complete removal of the tumor. H-I, Pathology slides (hematoxylin-eosin; original magnification X100 in H, X400 in I) show syncytial meningioma with well-identified whorls and no psammoma bodies.
Case 7: Parasagittal meningioma invading the superior sagittal sinus (SSS). A, Sagittal T1-weighted MRI shows a meningioma (arrow). B, T2-weighted MRI. Note midline shift and tumoral invasion of the skull (arrow). C, Transverse T2-weighted MRI. D, Angiogram shows invasion of the SSS, which remains patent. Sagittal (E, G), transverse (F) postoperative T1-weighted MRI. H, Gadolinium-enhanced postoperative T1-weighted MRI shows residual tumor, which was intentionally left to preserve patency of the SSS. I, Pathology slide (hematoxylin-eosin, original magnification X100) shows a highly vascular syncytial meningioma.
Pathology slides (hematoxylin-eosin; original magnification X400 in A-B, X100 in C-D). A, Fibroblastic meningioma (arrowheads) abutting the dura (arrow). B, Psammomatous meningioma (arrow indicates psammoma body). C, Meningothelial meningioma, tumor in case 4. E, Meningioma with marked vascularity (arrowheads indicate meningioma cluster; arrow, vessel wall).
Case 4: Pathology slides (hematoxylin-eosin, original magnification X400). A, Meningioma with malignant features, as evinced by prominent nucleoli (yellow dot) and mitoses (arrows). B, Intranuclear cytoplasmic intrusion (pseudoinclusion).
This is an extra-axial tumor. Glioblastoma multiforme (GBM) and astrocytoma are intraparenchymal tumors, and GBM enhances in a variegated fashion. Acoustic schwannomas are seen in the posterior fossa but not in this location. Fibrous dysplasia involves the skull but does not cause this amount of compression.
Table 1
Location Symptoms
ParasagittalMonoparesis of the contralateral leg
SubfrontalChange in mentation, apathy or disinhibited behavior, urinary incontinence
Olfactory grooveAnosmia with possible ipsilateral optic atrophy and contralateral papilledema (this triad termed Kennedy-Foster syndrome)
Cavernous sinusMultiple cranial nerve deficits (II, III, IV, V, VI), leading to decreased vision and diplopia with associated facial numbness
Occipital lobeContralateral hemianopsia
Cerebellopontine angleDecreased hearing with possible facial weakness and facial numbness
Spinal cordLocalized spinal pain, Brown-Sequard (hemispinal cord) syndrome
Optic nerveExophthalmos, monocular loss of vision or blindness, ipsilateral dilated pupil that does not react to direct light stimulation but might contract on consensual light stimulation; often, monocular optic nerve swelling with optociliary shunt vessels
Sphenoid wingSeizures; multiple cranial nerve palsies if the superior orbital fissure involved
TentorialMay protrude within supratentorial and infratentorial compartments, producing symptoms by compressing specific structures within these 2 compartments[4]
Foramen magnumParaparesis, sphincteric troubles, tongue atrophy associated with fasciculation
Table. Summary of the 2007 WHO Grading Scheme for Meningiomas
WHO Grade Histological Subtype Histological Features
IMeningothelial, fibroblastic, transitional, angiomatous, microcystic, secretory, lymphoplasmacytic metaplastic, psammomatousDoes not fulfill criteria for grade II or III
II (Atypical)Chordoid, clear cell4 or more mitotic cells per 10 hpf and/or 3 or more of the following: increased cellularity, small cells, necrosis, prominent nucleoli, sheeting, and/or brain invasion in an otherwise Grade I tumor
III (Anaplastic)Papillary, rhabdoid[15] 20 or more mitoses per 10 hpf and/or obviously malignant cytological characteristics such that tumor cell resembles carcinoma, sarcoma, or melanoma
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