Meningioma 

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

Background

Meningioma, the term coined by Harvey Cushing, refers to a set of tumors that arise contiguously to the meninges.

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Pathophysiology

Meningiomas may occur intracranially or within the spinal canal. They are thought to arise from arachnoidal cap cells, which reside in the arachnoid layer covering the surface of the brain. See the images below.

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.

Meningiomas commonly are found at the surface of the brain, either over the convexity or at the skull base. In rare cases, meningiomas occur in an intraventricular or intraosseous location. The problem of classifying meningioma is that arachnoidal cells may express both mesenchymal and epithelial characteristics. Other mesodermal structures also may give rise to similar tumors (eg, hemangiopericytomas or sarcomas). The classification of all of these tumors together is controversial. The current trend is to separate unequivocal meningiomas from other less well-defined neoplasms. Undoubtedly, advances in molecular biology will allow scientists to determine the exact genomic aberration responsible for each specific neoplasm.

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Epidemiology

Frequency

United States

The annual incidence of symptomatic meningiomas is approximately 2 cases per 100,000 individuals. Meningiomas account for approximately 20% of all primary intracranial neoplasms. However, the true prevalence is likely higher than this because autopsy studies reveal that 2.3% of individuals have undiagnosed asymptomatic meningiomas. Meningiomas are multiple in 5-40% of cases, particularly when they associated with neurofibromatosis type 2 (NF2). Familial meningiomas are rare unless associated with NF2.[1]

International

The frequency of meningiomas in Africa is nearly 30% of all primary intracranial tumors.

Mortality/Morbidity

Mortality and morbidity rates for meningiomas are difficult to assess. Some meningiomas are discovered fortuitously when CT or MRI is done to assess for unrelated diseases or conditions. Therefore, some patients die with meningioma and not from it. Estimates of the 5-year survival usually range from 73-94%.

A systematic review of the literature regarding the clinical behavior of small, untreated meningiomas suggests that most meningiomas 2.5 cm or less in diameter do not proceed to cause symptoms in the 5 years following their discovery. Patients with tumors 2.5-3 cm in initial size went on to develop new or worsened symptoms 17% of the time. Those that do cause symptoms can usually be predicted with close radiographic follow-up.[2]

Meningiomas usually grow slowly, and they may produce severe morbidity before causing death.

Factors that may be predictive of a high postoperative morbidity rate include patient-related factors (eg, advanced age, comorbid states such as diabetes or coronary artery disease, preoperative neurological status), tumor factors (eg, location, size, consistency, vascularity, vascular or neural involvement), previous surgery, or previous radiation therapy.

Race

Meningiomas are more prevalent in Africa than in North America or Europe. In Los Angeles County, meningioma is reported more commonly in African Americans than in others.

Sex

Meningiomas afflict women more often than men. The male-to-female ratio ranges from 1:1.4 to 1:2.8.

  • The female preponderance may be less pronounced in the black population than in other groups.
  • Meningiomas are equally distributed between boys and girls.

Age

The incidence increases with age. Ages and corresponding incidence rates reported from 2002 are as follows:

  • Age 0-19 years - 0.12
  • Age 20-34 years - 0.74
  • Age 35-44 years - 2.62
  • Age 45-54 years - 4.89
  • Age 55-64 years - 7.89
  • Age 65-74 years - 12.79
  • Age 75-84 years - 17.04
  • Age 85 years and older - 18.86
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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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