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

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: 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.

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]
The frequency of meningiomas in Africa is nearly 30% of all primary intracranial tumors. [2]


as evinced by focal weakness. location. vascular or neural involvement). Some meningiomas are discovered fortuitously when CT or MRI is done to assess for unrelated diseases or conditions. Those that do cause symptoms can usually be predicted with close radiographic follow-up. Compression of the underlying brain can give rise to focal or more generalized cerebral dysfunction. Meningiomas are equally distributed between boys and girls. comorbid states such as diabetes or coronary artery disease. size.89 Age 55-64 years .[3] Meningiomas usually grow slowly. Conversely. New-onset seizures in adults justify neuroimaging (eg.12.0. [5] The signs and symptoms secondary to meningiomas may appear or become exacerbated during pregnancy but usually abate or improve in the postpartum period. apathy. Symptoms and Signs Associated with Meningiomas in Specific Locations . some patients die with meningioma and not from it. preoperative neurological status). compressing the brain or the cranial nerves.89 Age 65-74 years . advanced age. A systematic review of the literature regarding the clinical behavior of small. they may occur with other conditions or lesions. tumor factors (eg.    Irritation: By irritating the underlying cortex.74 Age 35-44 years .4. Estimates of the 5-year survival usually range from 73-94%. The male-to-female ratio ranges from 1:1.04 Age 85 years and older .18. Patients with tumors 2. Stereotypic symptoms: Meningiomas in specific locations may give rise to the stereotyped symptoms listed in the Table.17. MRI) to exclude the possibility of an intracranial neoplasm.7.Mortality and morbidity rates for meningiomas are difficult to assess. previous surgery.8. untreated meningiomas suggests that most meningiomas 2. meningioma is reported more commonly in African Americans than in others.2. They may cause symptoms by irritating the underlying cortex. Age The incidence increases with age. In Los Angeles County. Race Meningiomas are more prevalent in Africa than in North America or Europe. or inducing vascular injuries to the brain.62 Age 45-54 years . vascularity. These stereotypical symptoms are not pathognomonic of meningiomas in these locations. Therefore. consistency.5 cm or less in diameter do not proceed to cause symptoms in the 5 years following their discovery. or previous radiation therapy. Compression: Localized or nonspecific headaches are common. meningiomas in these locations may remain asymptomatic or produce other unlisted symptoms.4 to 1:2. dysphasia.0. Table. Ages and corresponding incidence rates reported from 2002 are as follows:         Age 0-19 years . meningiomas can cause seizures.   The female preponderance may be less pronounced in the black population than in other groups.86 History Meningiomas produce their symptoms by several mechanisms. and they may produce severe morbidity before causing death.12 Age 20-34 years . and/or somnolence. Factors that may be predictive of a high postoperative morbidity rate include patient-related factors (eg. Sex Meningiomas afflict women more often than men. producing hyperostosis[4] and/or invading the overlying soft tissues.79 Age 75-84 years .5-3 cm in initial size went on to develop new or worsened symptoms 17% of the time.

sphincteric troubles. Miscellaneous Intraventricular meningiomas may present with obstructive hydrocephalus. producing symptoms by compressing specific structures within these 2 compartments [6] Foramen magnum Paraparesis. Meningiomas in the vicinity of the sella turcica may produce panhypopituitarism.  Involvement of the cranial nerves may lead to anosmia.[7] Physical The physical findings mirror the aforementioned symptoms and include signs due to raised intracranial pressure. ultimately. often. possibly presenting either as transient ischemic attack (TIA)–like episodes or as stroke. facial paresis. urinary incontinence Olfactory groove Anosmia with possible ipsilateral optic atrophy and contralateral papilledema (this triad termed Kennedy-Foster syndrome) Cavernous sinus Multiple cranial nerve deficits (II. decreased facial sensation. and hemiatrophy of the tongue. tongue atrophy associated with fasciculation Vascular: This presentation. and presence of the Babinski sign. right-left disorientation. although rare. decreased hearing. VI). and finger agnosia. diplopia. positive Hoffman sign. Meningiomas of the skull base may narrow and even occlude important cerebral arteries. decreased mentation and. . Rarely. monocular optic nerve swelling with optociliary shunt vessels Sphenoid wing Seizures.  Compression of the underlying parenchyma may give rise to pyramidal signs that are exemplified by pronator drift. optic atrophy. namely Castleman syndrome. ipsilateral dilated pupil that does not react to direct light stimulation but might contract on consensual light stimulation. to brain herniation. compression of the underlying parenchyma. deviation of the uvula.  Raised intracranial pressure leads to papilledema. visual field defects. Parietal-lobe syndrome may occur if the parietal lobes are compressed. involvement of cranial nerves.(Open Table in a new window)   o o o o Location Symptoms Parasagittal Monoparesis of the contralateral leg Subfrontal Change in mentation. IV. Meningiomas that compress the visual pathways produce various visual field defects. Brown-Sequard (hemispinal cord) syndrome Optic nerve Exophthalmos. apathy or disinhibited behavior. multiple cranial nerve palsies if the superior orbital fissure involved Tentorial May protrude within supratentorial and infratentorial compartments. o Compression of the dominant (usually left) parietal lobe may give rise to Gerstmann syndrome: agraphia. acalculia. should be considered. depending on their location. hyperreflexia. leading to decreased vision and diplopia with associated facial numbness Occipital lobe Contralateral hemianopsia Cerebellopontine angle Decreased hearing with possible facial weakness and facial numbness Spinal cord Localized spinal pain. V. chordoid meningiomas can present with hematologic disturbances. III. and involvement of bone and subcutaneous tissues by the meningioma. monocular loss of vision or blindness.

Of interest. all published studies have relatively small sample sizes and a short period of follow-up.  Spinal meningiomas may give rise to a Brown-Sequard syndrome (ie. o Causes                     Trauma and viruses have been investigated as possible causative agents for development of meningiomas. and androgen receptors on some of these tumors. ultimately. increased expression of cyclooxygenase 2 and ornithine decarboxylase. Meningiomas can also be associated with different genetic syndromes. High-dose cranial irradiation may induce meningiomas after a short latency period. At present. posttraumatic insult) resulting in the upregulation of COX-2 has been investigated in the tumorogenesis of meningiomas. Up to 60% of sporadic meningiomas were found to harbor NF2 mutations. Other cytogenetic alterations are chromosomal loss of 1p. However. 6q. Genetic causes have been implicated in the development of meningiomas. The invasive potential of meningioma cells seems to be reflected by a balance between the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs). an oncofetal RNA-binding protein. The best-characterized and most common genetic alteration is the loss of the NF2 gene (NF2) on chromosome 22q[9] . The most consistent chromosomal abnormality isolated in meningiomas is on the long arm of chromosome 22. Patients subjected to low-dose irradiation for tinea capitis may develop multiple meningiomas decades later in the field of irradiation. the role of radiation in the genesis of meningiomas has been shown. The following events were found to be associated with higher grades of meningiomas: loss of the tumor suppressor in lung cancer-1 gene (TSLC-1). Progression to anaplastic meningioma has been associated with involvement of chromosomal site 17q. namely Gorlin[10] and Rubinstein-Taybi syndromes[11] . loss of progesterone receptors. Monosomy of chromosome 7 is a rare cytogenetic change. IMP3. Whether cell phone use increases the risk of meningiomas (and of brain tumors in general) remains of great interest. contralateral decreased pain sensation. the available data do not support such an association. shortened time to recurrence. and 14q. including increased incidence in women versus men and the presence of estrogen.Compression of the nondominant (usually right) parietal lobe leads to tactile and visual extinction and neglect of the contralateral side. sphincteric weakness and. [12] Several findings suggest an association between hormones and the risk for meningiomas. The role of inflammation (eg. However. [13] Differential Diagnoses      Brainstem Gliomas Cavernous Sinus Syndromes Complex Partial Seizures Craniopharyngioma Frontal Lobe Syndromes . [8] On the other hand. NF2 encodes a tumor suppressor known as merlin (or schwannomin). Loss of chromosome 10 is associated with increased tumor grade. however. decrease in position sense). 3p. it is frequently reported in radiation-induced meningiomas. o Compression of the occipital lobes leads to a congruent homonymous hemianopsia. has been identified as a potential biomarker in patients who have a high risk of recurrent meningioma. progesterone. ipsilateral weakness. However. the exact nature of this relationship and its implication on the management of meningiomas remain under investigation. the meningioma locus is close to but probably different from the gene responsible for NF2. no definitive proof has yet been found. complete quadriparesis or paraparesis. especially with the recent tremendous increase in the use of these devices worldwide. and shortened survival.

Hyperostosis and intratumoral calcifications may be present.  An enhancing tail involving the dura may be apparent on MRI.  Meningiomas enhance intensely and homogeneously after injection of gadolinium gadopentetate. Imaging Studies Imaging studies are the mainstay of diagnosis. See images below for representative radiologic views of various subtypes. meningiomas are usually dural-based tumors that are isoattenuating to slightly hyperattenuating. the tumors have variable signal intensity.  The edema may be more apparent on MRI than on CT scanning. On T1. Type 2 Oligodendroglioma Persistent Idiopathic Facial Pain Pituitary Tumors Primary CNS Lymphoma Laboratory Studies No specific laboratory tests are used to screen for meningioma. New research tools such as positron emission tomography (PET). . If a meningioma is suspected.[14] See the images below. The peritumoral cysts may actually represent a gliotic response and may not necessitate surgical extirpation.and T2-weighted MRIs.        Glioblastoma Multiforme Low-Grade Astrocytoma Neurofibromatosis. On plain head CT scans. 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. Cystic meningiomas may exhibit intratumoral or peritumoral cysts. Angiography is still indispensable if embolization of the tumor is deemed necessary. Late venous images are important to determine the patency of the involved dural sinuses. including octreotide-PET. Perilesional edema may be extensive.   They enhance homogeneously and intensely after the injection of iodinated contrast material. the latter remains a powerful tool for planning surgery. Endovascular angiography allows the surgeon to preoperatively determine the vascularization of the tumor and its encroachment on vital vascular structures. or magnetic resonance spectroscopy (MRS) have been used to predict in vivo the aggressiveness of meningiomas.  Multiple meningiomas may be difficult to differentiate from metastasis. obtaining an enhanced MRI is imperative. Type 1 Neurofibromatosis. as well as intracranial calcifications.  The tumor compresses the brain without invading it. Plain skull radiograph may reveal hyperostosis and increased vascular markings of the skull.

a pediculated subcutaneous flap was used to close the surgical defect. when this transverse T2-weighted MRI was obtained. D. G) enhanced T1-weighted MRI shows gross total removal of the tumor. B. A. Posterior circulation angiograms show tumoral blush (arrow in G) and the Bernasconi-Cassinari artery (arrow in H). Postoperative sagittal (E) and transverse (F. H and I. C. A. Pathology showed syncytial meningioma. C. Contrast-enhanced CT scan shows the enhancing meningioma. Three recurrences lie in the plane of the tentorium on a single line. Case 3: Tentorial meningioma A. Note the absence of tumoral calcification. Transverse T1-weighted MRIs shows isointensity of the tumor compared with the surrounding brain (B) and its homogenous enhancement (C). D. Note hypercellularity and minimal whorling (hematoxylin-eosin. Case 4: Recurrent subcutaneous meningioma. She was lost to follow-up until 1996. Three arcs were used to irradiate the largest recurrence. After surgery. original magnification X400). Compare with appearance in Case 1. Although the initial surgical bed is tumor-free. Transverse section at a lower level. Transverse images show posterior (arrow in B) and anterior (arrow in C) recurrence involving the tentorium. Case 1: Bone-window CT reveals calcification of the meningioma.Case 1: MRI of a meningioma on plaque. sagittal T2-weighted MRI shows a large subcutaneous recurrence. Tumoral recurrence 3 months after surgery. and the . at the same level as in G and F. Sagittal images show posterior (D) and anterior (E) recurrence involving the tentorium. respectively. Case 5: Bilateral olfactory meningioma invading the facial sinuses. Case 3: Tentorial meningioma. Case 2: Gadolinium-enhanced MRI of a meningioma invading the overlying dura and bone. transverse (B). Patient underwent surgery for a parieto- occipital meningioma in 1978. and sagittal (C) gadolinium-enhanced T1-weighted MRI shows bilateral olfactory meningiomas. B. Patient received repeat surgery for subtotal removal of the tumor. Gadolinium-enhanced T1-weighted MRI immediately (A) and 2 years after surgery (B-D). Lower vignette reveals complete excision of the recurrence after a second operation. MRI performed 4 years after the first operation reveals a recurrence over the posterior tentorium. Lower transverse section also shows recurrence. Arrow indicates surgical bed of the resected meningioma. Coronal (A). Coronal (D). Two-dimensional planning for stereotactic radiosurgery. Note variegated appearance of the tumor. coronal enhanced (E). and sagittal enhanced (F) T1-weighted MRIs. Case 2: Bone-window CT scan reveals the skull involvement. patient received conventional radiotherapy. Case 3: Tentorial meningioma. Three-dimensional planning for stereotactic radiosurgery.

Fibrous dysplasia involves the skull but does not cause this amount of compression. transitional. Immunohistochemistry . Postoperative enhanced T1-weighted MRI shows that the tumor was completely removed by means of craniotomy and a transfacial approach. Tumor was first approached intracranially. It may be gritty on cutting. A. Histologic Findings Meningiomas are usually globular.falx dividing the tumor in 2. this variant is called meningioma en plaque. resection should be performed shortly after embolization to decrease the likelihood of tumor revascularization. Sagittal (E. C. G. secretory. X100 in C-D). B. papillary. Residual was completely excised by means a transfacial approach performed with the otolaryngology team. H-I. original magnification X400). choroid. Their cut surface is either translucent pale or homogeneously reddish brown. F. original magnification X100) shows a highly vascular syncytial meningioma. C. D. which was intentionally left to preserve patency of the SSS. as evinced by prominent nucleoli (yellow dot) and mitoses (arrows). B. Fibroblastic (fibrous) meningiomas reveal sheets of interlacing spindle cells. The last morphologic variant is the cavernous sinus meningioma that infiltrates the cavernous sinus and becomes interdigitated with its contents. Anterior circulation angiogram reveals posterior displacement of the anterior cerebral artery by tumor. H. original magnification X400 in A-B. D. Sagittal T1-weighted MRI shows a meningioma (arrow). A. and GBM enhances in a variegated fashion. Meningiomas may be associated with hyperostosis. They have a wide dural attachment and become invaginated into the underlying brain without invading it. See images below for representative pathologic views of various subtypes. Nuclei show intranuclear vacuoles. arrow. Although not prominent. Postoperative MRI shows complete removal of the tumor. Pathology slides (hematoxylin-eosin. and metaplastic variants. X400 in I) show syncytial meningioma with well-identified whorls and no psammoma bodies. Transverse T2-weighted MRI.[16] clear cell. Coronal (D) and sagittal (E) gadolinium-enhanced T1-weighted MRIs. microcystic. transverse (F) postoperative T1weighted MRI. B. B. Acoustic schwannomas are seen in the posterior fossa but not in this location. The intercellular stroma is composed of reticulin and collagen. Angiogram shows invasion of the SSS. Case 4: Pathology slides (hematoxylin-eosin. reactive versus tumoral infiltration). Meningioma with marked vascularity (arrowheads indicate meningioma cluster. Note midline shift and tumoral invasion of the skull (arrow). lymphoplasmacyte-rich. Pathology slide (hematoxylin-eosin. which remains patent. original magnification X100 in H. Meningothelial meningioma. and fibroblastic meningiomas. E. others include angiomatous. vessel wall). Contrast- enhanced CT scan clearly shows bilateral subfrontal meningioma. C.[4] The exact nature of the cause of this hyperostosis is controversial (ie. Enhanced T1-weighted MRI reveals complete excision of the intracranial component. The transitional variety reveals features common to both the meningothelial and fibroblastic varieties.[15] If this is the case. Arrow indicates tumor invasion of the sinuses. I. tumor in case 4. Case 7: Parasagittal meningioma invading the superior sagittal sinus (SSS). F. Some meningiomas occur as a sheetlike extension that covers the dura but does not invaginate the parenchyma. Gadolinium-enhanced postoperative T1-weighted MRI shows residual tumor. Fibroblastic meningioma (arrowheads) abutting the dura (arrow). Pathology slides (hematoxylin-eosin. Transverse T1-weighted MRI of same lesion. E. Procedures Preoperative endovascular embolization of the vascular feeders from the external circulation may be beneficial in extremely vascular meningiomas. T2-weighted MRI. Psammomatous meningioma (arrow indicates psammoma body). Arrow indicates residual in the sinuses. Glioblastoma multiforme (GBM) and astrocytoma are intraparenchymal tumors. Meningioma with malignant features. G). This is an extra-axial tumor. Intense gadolinium enhancement of the tumor. The 3 most common histologic subtypes of meningiomas are the meningothelial (syncytial). Meningothelial meningiomas reveal densely packed cells that are arranged in sheets with no clearly discernible cytoplasmic borders. A. A. well-demarcated neoplasms. Case 6: Subfrontal meningioma in a patient with abnormal behavior. Intranuclear cytoplasmic intrusion (pseudoinclusion). whorls are present (calcified whorls are termed psammoma bodies).

clear cell 4 or more mitotic cells per 10 hpf and/or 3 or more of the following: increased cellularity. Bromodeoxyuridine (BudR) labeling requires an intravenous (IV) injection before tumor removal. fibroblastic. [19] Two features are considered clear signs of malignancy: cortical invasion by the tumor and distal metastasis. [22] Medical Care         Medical care for meningiomas has been disappointing. On the other hand. and hydroxyurea (ribonucleotide reductase inhibitor). Of note. and probability of recurrence. Several stains have been used to help predict the behavior of meningiomas. sheeting. transitional.Immunohistochemistry can help diagnose meningiomas. Some have attempted to correlate the pathology and behavior of meningiomas to the loss of specific genetic material. [23] The use of corticosteroids preoperatively and postoperatively has significantly decreased the mortality and morbidity rates associated with surgical resection. rhabdoid[20] 20 or more mitoses per 10 hpf and/or obviously malignant cytological characteristics such that tumor cell resembles carcinoma. lymphoplasmacytic metaplastic. psammomatous Does not fulfill criteria for grade II or III II (Atypical) Chordoid. microcystic. secretory. They stain negative for anti-Leu 7 antibodies (positive in schwannomas) and for glial fibrillary acidic protein (GFAP). The last 3 drugs also showed disappointing results. necrosis. such as papillary meningioma. brain invasion is considered a criterion for atypia. or melanoma The expression levels of E. The current experience with chemotherapy is disappointing. and interferon-alpha. A recently published prospective phase 2 study of irinotecan (CPT-11) also failed to demonstrate any efficacy. [21] In a review of 21 pediatric meningiomas operated on over a period of 24 years. Summary of the 2007 WHO Grading Scheme for Meningiomas (Open Table in a new window) WHO Grade Histological Subtype Histological Features I Meningothelial. This modality of treatment is reserved for malignant cases after failure of surgery and radiotherapy to control the disease. in the 2007 WHO grading scheme. The World Health Organization classification of meningiomas is presented in Table 2. The combination of interferon alpha and 5-fluorouracil synergistically reduces meningioma cell proliferation in culture and warrants further investigation. RU-486 (synthetic antiprogestin). 24% were WHO grade II and 24% where associated with a large cystic component. and/or brain invasion in an otherwise Grade I tumor III (Anaplastic) Papillary. It is restricted either to perioperative drugs or to medications that are used after all other means of treatment have failed. Antiepileptic drugs should be started preoperatively in supratentorial surgery and continued postoperatively for no less than 3 months. which are positive for epithelial membrane antigen (EMA) in 80% of cases. which had no effect against recurrent meningiomas in a phase 2 study[24] . The main drugs studied include temozolomide. sarcoma. prominent nucleoli. the presence of other sex hormone receptors is much less consistent. small cells.[8] . Somatostatin receptors also have been demonstrated consistently in meningiomas. immunohistologic staining for proliferating cell nuclear antigen (PCNA) can be performed on fixed specimens. Progesterone receptors can be demonstrated in the cytosol of meningiomas. These stains quantify the mitotic rate of these tumors.[18] Some histologic variants. aggressiveness of meningiomas. angiomatous.cadherin and beta-catenin were found to be inversely correlated with peritumoral edema. Some studies have shown a possible role of COX-2 inhibitors in the treatment of recurrent meningiomas. [17] Malignancy The notion of malignancy in meningiomas is still vague. undoubtedly carry a less favorable prognosis than other histologic types. Table.

It has been advocated as an effective management strategy for small meningiomas and for meningiomas involving the skull base or the cavernous sinus. Dural tails that are apparent on MRI are best removed. If feasible. The surgeon also can use commercially available dural substitutes. always start by coagulating the arterial feeders to the meningioma. Approximately 40% of 273 meningiomas (in 244 patients) grew within a 4-year period. This was actually more likely to occur with significant. 30] In general the ideal treatment of a benign meningioma is surgical resection if possible. Lack of calcification. and the meningioma can be seen extending en plaque over the surface of the brain. Make a provision for harvesting a suitable dural substitute (pericranium or fascia lata). Convexity meningioma . convexity. the long-term follow up after radiosurgery was reported. The main caveat was tumor size. all involved or hyperostotic bone should be removed. See the images below. age younger than 60 years and tumor size larger than 25 mm (diameter) were also associated with a greater risk.          The role of targeted chemotherapy to block the tumorogenic pathways of meningiomas at specific sites is being extensively investigated. these results have not been confirmed in randomized trials. FAS inhibitor (cerulein) decreased meningioma cell survival in vitro. Radiotherapy is mainly used as adjuvant therapy for incompletely resected. In a recently published series. Oya et al reported on the natural history of meningiomas. or parasagittal. It is used primarily to prevent tumor progression. The dura and overlying skull were removed surgically. Surgical strategies for managing meningiomas in specific locations are discussed in the sections that follow. The study found GKR to be effective. [25] Molecules to block specific growth factors or enzymes are being developed. and peritumoral edema were predictors of growth in follow up. It can also be used as primary treatment in some cases (optic nerve meningiomas[28] and some unresectable tumors). high-grade and/or recurrent tumors. Note tumoral breach of the dura. The dura involved by the tumor as well as a dural rim that is free from tumor should be resected (duraplasty is performed).[29. Case 1: Bone flap seen along the removed meningioma in toto. Atypical meningioma (WHO grade II) and anaplastic meningioma (WHO grade III) showed increased fatty acid synthase (FAS) expression. Hasegawa et al treated 46 patients with gamma knife radiation (GKR) as the initial treatment modality. Complete resection was achieved. [26] Although most meningiomas grow slowly and have a low mitotic rate. even though some may not be involved with the tumor. Surgical Care The constant principles in meningioma resection are the following: If possible. In addition. The dura is opened.[32. baseline peritumoral edema. 33] It is mainly used for small (< 3 cm in diameter) residual or recurrent lesions when surgery is considered to carry a significantly high risk of morbidity. GKR may be selected over surgery in patients with significant medical comorbidities. clinical benefit has been reported in many case series with either tumor regression or stasis after radiotherapy. Case 1: Surgical view of the tumor. [31] The lesions were falcine. however. Large tumors had the possibility of severe postirradiation edema. Case 2: Bone flap was removed. Duraplasty and cranioplasty were performed Case 2: Surgical specimen. increased FAS expression in human meningiomas represents a novel therapeutic target for the treatment of unresectable or malignant meningiomas. hyperintensity in T2 MRI. Stereotactic radiosurgery has been shown to provide excellent local tumor control with minimal toxicity. Thus. a tumor control rate of 94% was found after an average of 103 months.[27]The prospect of benign meningioma growth is an important factor to consider in their proper management. Case 2: Intraoperative view shows the skull involvement.

Perform dural grafting. The diagnostic test of choice is still endovascular angiography with late venous images to look for a possible delayed filling of the involved portion of the SSS. and the posterior third. . The dural blood vessels should be coagulated before opening the dura to decrease tumor vascularity. To allow adequate visualization. the decision of whether to sacrifice it depends on the involved segment. Coagulate the surface of the tumor. Parasagittal meningiomas These tumors may arise from the convexity and involve the superior sagittal sinus (SSS) by medial extension. Unless the tumor is small and can be removed in 1 piece. separating the tumor from the brain may be difficult. Every attempt should be made to preserve at least one of the olfactory nerves. Some surgeons resect a partially involved sinus and reconstruct it later (either with a vein or prosthetic graft). This layer may not be complete at the depth of the tumor. If the sinus is occluded gradually by the tumor. the middle third. these tumors are best approached through a low craniotomy. then core it and invaginate the outer layer to allow further circumferential dissection. A unilateral approach is usually sufficient. sacrificed at times. This is achieved by removing the supraorbital rim. If the SSS is completely obliterated by tumor. the best strategy for excising convexity meningiomas is to find the arachnoidal plane and dissect it gently.Opening the scalp and skull may be bloody because of the hypertrophy of blood vessels originating from the external circulation. By entering the frontal sinus and removing the orbital rim. The former subgroup is easier to treat surgically because of its superficial location. MRV is not yet sensitive enough to confirm unequivocally the complete occlusion of the SSS. The foremost consideration in surgically treating parasagittal meningiomas is to decide what to do with the SSS. The midline burr hole should be placed just above the frontonasal suture. Placing patties circumferentially around the tumor allows quick identification of this crucial plane at a later time. If the SSS is only partially involved. the venous drainage will be diverted over time through parasagittal veins. Usually the tumor is separated from underlying brain parenchyma by an arachnoid layer. In this author's experience. The surgeon should be careful not to injure the veins that run anteriorly and posteriorly to the tumor. the falx should be sectioned after ligating the most anterior aspect of the SSS. The author's opinion is that explaining to the patient that some tumor was left behind that may need further resection at a later date is better than taking undue risk of neurological deficit by obliterating more of the SSS. or they may arise from the falx and involve the SSS by upward extension. a low approach is provided. These veins may provide crucial collateral circulation for the venous drainage of the cerebrum and should be preserved at all costs. In this location. The anterior third of the SSS can usually be sacrificed with impunity. thus appearing subcutaneously. the SSS is never sacrificed beyond the anterior third. it can be ligated safely and excised. never ligated. Olfactory groove and tuberculum sellae meningiomas To avoid undue retraction of the frontal lobes. The tumor may breach the sanctity of the dura and the bone.

Note that the usual relationship between the optic nerves and the carotid arteries might not hold true owing to displacement of these vital structures by tumor. which arises from the cavernous portion of the carotid artery and runs posteriorly to supply the tentorium. Studying the preoperative angiogram is imperative in cases of torcular meningiomas to delineate the patency of the different sinuses and the available collateral circulation. These should be coagulated thoroughly before one attempts to remove the tumor. the anterior cranial fossa. . This relationship is lost in cerebellopontine angle meningiomas. Cerebellopontine angle meningiomas In acoustic neuromas. Meningiomas involving the cavernous sinus The issue of meningiomas involving the cavernous sinus is currently an area of intense interest in neurosurgery. Tentorial and torcular meningiomas Tentorial meningiomas may be supplied by a multitude of vessels that arise from the tentorial leaf. No one doubts that. The following opinion is a personal reflection on the matter. the interface of the tumor and the petrous bone should be followed. Care should be taken to identify and preserve both optic nerves. The debate centers on 2 points: when to operate and how aggressive the resection should be. the middle cranial fossa. Tentorial meningiomas often grow in both the infratentorial and supratentorial compartments and should be approached accordingly.These tumors receive their blood supply through various sources: the ethmoidal branches of the ophthalmic arteries. and diverging views may be found in the literature. These tumors often invade the ethmoid sinuses and. A partial cerebellar resection may be necessary to avoid undue retraction of the brain. Removing these tumors completely is often impossible because of partial involvement of the venous sinuses. Medial tumors may extend within the cavernous sinus. To do so. A major supply may be the Bernasconi-Cassinari artery. branches from the middle meningeal artery. the surgeon should first diminish its blood supply by coagulating its supplying arteries from the dura. the sphenoid sinus. and the anterior clinoid. A definite attempt should be made at recognizing the Bernasconi-Cassinari artery during surgery and coagulating it to decrease tumor vascularity. the facial nerve usually lies anterosuperiorly to the tumor and is encountered late in surgery. Before attempting to remove the tumor. and the carotid arteries. in experienced hands. Removing the zygoma and the orbital rim allows wider exposure of the sphenoid wing. Tumor arterial supply and perforator arteries to the hypothalamus must be differentiated because both arise from the anterior circulation. Sphenoid-wing meningiomas Sphenoid-wing meningiomas present either as en plaque meningiomas or as globular masses. such meningiomas can be treated successfully. This artery is usually not apparent on normal angiograms but may be conspicuous in angiograms of tentorial meningiomas. at times. because the facial nerve may lie along the posterior tumor edge and can be injured early in surgery (unless care is taken to identify it).

More extensive approaches. Dexasone) . associated with a simple mastoidectomy down to the solid angle (ie. [34] Large tumors can be partially resected and treated with gamma knife after resection. Consultations If the patient has neurofibromatosis. the petroclival meningioma can be visualized in its entirety. After the tentorium is split. Corticosteroids Class Summary These agents reduce edema around tumor. View full drug information Dexamethasone (Decadron. the second operation should be scheduled the earliest possible opportunity. consulting a radiation oncologist may be appropriate. with an impressive 69% local tumor growth control. If the radiologic diagnosis is not clear cut.  Symptomatic meningiomas in otherwise healthy patients should be resected by neurosurgeons who are trained for such procedures. the bone encasing the inner ear). a good outcome was obtained. If the patient is on perioperative steroids. Medication Summary The goals of pharmacotherapy are to reduce morbidity and prevent complications. Clival and petroclival meningiomas These tumors represent some of the greatest challenges in neurosurgery. although partial resection is relatively straightforward. Diet No dietary restrictions are necessary in patients with meningiomas. If surgery has to be interrupted for logistical reasons. therefore. This author does not believe in the benefit of bypassing and resecting the cavernous carotid artery in these cases. the neurosurgeon may want to refer the patient for genetic counseling and for audiometric testing. Activity Patients with a meningioma who undergo surgery can resume their normal activities after an adequate period of postoperative rest (1-3 mo). A multitude of approaches has been devised for these tumors. are needed. Partial resection usually does not translate into any benefit for the patient and only renders further surgeries more difficult. In a report by Jensen et al. including sarcoidosis and infection/inflammation that lead to the Tolosa-Hunt syndrome. Gamma knife may be a good treatment option in parasellar meningiomas. such as neurofibromas or sarcomas. The traditional approaches such as the suboccipital or the subtemporal are usually insufficient to allow complete removal. This approach consists of combined supratentorial and infratentorial craniotomies. such as the petrosal approach. In specific cases. Avoid injuring the cranial nerves or the carotid artery. a low-salt diet is appropriate. complete resection remains a daunting task. frequently leading to symptomatic and objective improvement in symptoms. Asymptomatic cavernous sinus meningiomas should not be operated but should be monitored carefully by means of repeated physical examination and serial MRI. The surgeon should remember that a multitude of processes may affect the cavernous sinus and mimic a meningioma. every attempt should be made to complete the resection. a detailed discussion with the radiologist should attempt to rule out other pathologic entities.

cytotoxic effects on tumors. In a study of 34 patients who underwent surgery for CPA meningiomas.[36] The following types of meningiomas are most likely to recur: incompletely excised. occupational therapy. inhibition of tumor formation. dysphagia. and decreased CSF production. It was also found that deficits of the lower cranial nerves occurred only in patients whose tumors extended into the jugular foramen. . speech therapy). Tumor size may play a role in determining outcome. such as diplopia. Further Inpatient Care Before or after surgery. or motor weakness.[35] Patients who are discharged home with antiepileptic agents should be monitored by a neurologist. physiotherapy. Further Outpatient Care Patients who undergo operation for meningiomas should receive regular follow-up with enhanced MRI to check for possible recurrences. dysphasia. malignant.9% suffered postoperative facial nerve palsy.9%. 5. Prognosis Patients whose meningiomas are completely resected usually have an excellent prognosis. Among all patients. Agarwal et al found that the rate of permanent cranial nerve deficits was significantly greater in patients with tumors of more than 3 cm in size than in those with smaller meningiomas (45. patients with skull-base meningiomas may have numerous disabilities.Postulated mechanisms of action of corticosteroids in brain tumors include reduction in vascular permeability. These problems should be managed with a multidisciplinary approach (eg. respectively). No association was found between tumor extension into the internal acoustic canal and either postoperative complications or cranial nerve deficits.5% vs 5. or multiple tumors.