Background

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

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: 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.

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. [2]

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.[3]
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

History
Meningiomas produce their symptoms by several mechanisms. They may cause symptoms by
irritating the underlying cortex, compressing the brain or the cranial nerves, producing
hyperostosis[4] and/or invading the overlying soft tissues, or inducing vascular injuries to the brain.
[5]
The signs and symptoms secondary to meningiomas may appear or become exacerbated during
pregnancy but usually abate or improve in the postpartum period.

Irritation: By irritating the underlying cortex, meningiomas can cause seizures. New-onset
seizures in adults justify neuroimaging (eg, MRI) to exclude the possibility of an intracranial
neoplasm.
Compression: Localized or nonspecific headaches are common. Compression of the
underlying brain can give rise to focal or more generalized cerebral dysfunction, as evinced by focal
weakness, dysphasia, apathy, and/or somnolence.
Stereotypic symptoms: Meningiomas in specific locations may give rise to the stereotyped
symptoms listed in the Table. These stereotypical symptoms are not pathognomonic of
meningiomas in these locations; they may occur with other conditions or lesions. Conversely,
meningiomas in these locations may remain asymptomatic or produce other unlisted symptoms.
Table. Symptoms and Signs Associated with Meningiomas in Specific Locations

(Open Table in a new window)

o
o
o
o

Location

Symptoms

Parasagittal

Monoparesis of the contralateral leg

Subfrontal

Change in mentation, apathy or disinhibited behavior, 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, III, IV, V, VI), 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, Brown-Sequard (hemispinal cord) syndrome

Optic nerve

Exophthalmos, 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 wing

Seizures; multiple cranial nerve palsies if the superior orbital fissure involved

Tentorial

May protrude within supratentorial and infratentorial compartments, producing

symptoms by compressing specific structures within these 2 compartments [6]

Foramen magnum

Paraparesis, sphincteric troubles, tongue atrophy associated with fasciculation

Vascular: This presentation, although rare, should be considered. Meningiomas of the skull
base may narrow and even occlude important cerebral arteries, possibly presenting either as
transient ischemic attack (TIA)like episodes or as stroke.
Miscellaneous
Intraventricular meningiomas may present with obstructive hydrocephalus.
Meningiomas in the vicinity of the sella turcica may produce panhypopituitarism.
Meningiomas that compress the visual pathways produce various visual field defects,
depending on their location.
Rarely, chordoid meningiomas can present with hematologic disturbances, namely
Castleman syndrome.[7]

Physical
The physical findings mirror the aforementioned symptoms and include signs due to raised
intracranial pressure, involvement of cranial nerves, compression of the underlying parenchyma, and
involvement of bone and subcutaneous tissues by the meningioma.

Raised intracranial pressure leads to papilledema, decreased mentation and, ultimately, to

brain herniation.

Involvement of the cranial nerves may lead to anosmia, visual field defects, optic atrophy,
diplopia, decreased facial sensation, facial paresis, decreased hearing, deviation of the uvula, and
hemiatrophy of the tongue.

Compression of the underlying parenchyma may give rise to pyramidal signs that are
exemplified by pronator drift, hyperreflexia, positive Hoffman sign, and presence of the Babinski
sign. Parietal-lobe syndrome may occur if the parietal lobes are compressed.
o
Compression of the dominant (usually left) parietal lobe may give rise to Gerstmann
syndrome: agraphia, acalculia, right-left disorientation, and finger agnosia.

Compression of the nondominant (usually right) parietal lobe leads to tactile and
visual extinction and neglect of the contralateral side.
o
Compression of the occipital lobes leads to a congruent homonymous hemianopsia.

Spinal meningiomas may give rise to a Brown-Sequard syndrome (ie, contralateral decreased
pain sensation, ipsilateral weakness, decrease in position sense), sphincteric weakness and,
ultimately, complete quadriparesis or paraparesis.
o

Causes

Trauma and viruses have been investigated as possible causative agents for development of
meningiomas. However, no definitive proof has yet been found.
The role of inflammation (eg, posttraumatic insult) resulting in the upregulation of COX-2 has
been investigated in the tumorogenesis of meningiomas. [8]
On the other hand, the role of radiation in the genesis of meningiomas has been shown.
Patients subjected to low-dose irradiation for tinea capitis may develop multiple
meningiomas decades later in the field of irradiation.
High-dose cranial irradiation may induce meningiomas after a short latency period.
Genetic causes have been implicated in the development of meningiomas.
The best-characterized and most common genetic alteration is the loss of the NF2
gene (NF2) on chromosome 22q[9] . NF2 encodes a tumor suppressor known as merlin (or
schwannomin).
Of interest, the meningioma locus is close to but probably different from the gene
responsible for NF2.
Up to 60% of sporadic meningiomas were found to harbor NF2 mutations.
Other cytogenetic alterations are chromosomal loss of 1p, 3p, 6q, and 14q.
Loss of chromosome 10 is associated with increased tumor grade, shortened time to
recurrence, and shortened survival.
Progression to anaplastic meningioma has been associated with involvement of
chromosomal site 17q.
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), loss of progesterone
receptors, increased expression of cyclooxygenase 2 and ornithine decarboxylase.
Monosomy of chromosome 7 is a rare cytogenetic change. However, it is frequently
reported in radiation-induced 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).
The most consistent chromosomal abnormality isolated in meningiomas is on the long
arm of chromosome 22.
Meningiomas can also be associated with different genetic syndromes, namely
Gorlin[10] and Rubinstein-Taybi syndromes[11] .
IMP3, an oncofetal RNA-binding protein, has been identified as a potential biomarker
in patients who have a high risk of recurrent meningioma. [12]
Several findings suggest an association between hormones and the risk for meningiomas,
including increased incidence in women versus men and the presence of estrogen, progesterone, and
androgen receptors on some of these tumors. However, the exact nature of this relationship and its
implication on the management of meningiomas remain under investigation.
Whether cell phone use increases the risk of meningiomas (and of brain tumors in general)
remains of great interest, especially with the recent tremendous increase in the use of these devices
worldwide. At present, the available data do not support such an association; however, all published
studies have relatively small sample sizes and a short period of follow-up. [13]

Differential Diagnoses

Brainstem Gliomas
Cavernous Sinus Syndromes
Complex Partial Seizures
Craniopharyngioma
Frontal Lobe Syndromes

Glioblastoma Multiforme
Low-Grade Astrocytoma
Neurofibromatosis, Type 1
Neurofibromatosis, Type 2
Oligodendroglioma
Persistent Idiopathic Facial Pain
Pituitary Tumors
Primary CNS Lymphoma

Laboratory Studies
No specific laboratory tests are used to screen for meningioma.

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.[14] See the images below.

Case 1: MRI of a meningioma on plaque.

Case 1: Bone-window CT reveals calcification of the meningioma.

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 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 T1weighted 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 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.

Procedures
Preoperative endovascular embolization of the vascular feeders from the external circulation may be
beneficial in extremely vascular meningiomas.[15] If this is the case, resection should be performed
shortly after embolization to decrease the likelihood of tumor revascularization.

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 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).

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,[16] clear
cell, choroid, lymphoplasmacyte-rich, papillary, and metaplastic variants.
Meningiomas may be associated with hyperostosis.[4] 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. [17]

Malignancy
The notion of malignancy in meningiomas is still vague.[18] Some histologic variants, such as papillary
meningioma, undoubtedly carry a less favorable prognosis than other histologic types. [19] 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

Meningothelial, fibroblastic, transitional, angiomatous,

microcystic, secretory, lymphoplasmacytic metaplastic,
psammomatous

Does not fulfill criteria for grade II or III

II (Atypical)

Chordoid, clear cell

4 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[20]

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. [21]
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. [22]

Medical Care

Medical care for meningiomas has been disappointing. It is restricted either to perioperative
drugs or to medications that are used after all other means of treatment have failed. [23]
The use of corticosteroids preoperatively and postoperatively has significantly decreased the
mortality and morbidity rates associated with surgical resection.
Antiepileptic drugs should be started preoperatively in supratentorial surgery and continued
postoperatively for no less than 3 months.
The current experience with chemotherapy is disappointing.
This modality of treatment is reserved for malignant cases after failure of surgery and
radiotherapy to control the disease.
The main drugs studied include temozolomide, which had no effect against recurrent
meningiomas in a phase 2 study[24] , and hydroxyurea (ribonucleotide reductase inhibitor); RU-486
(synthetic antiprogestin); and interferon-alpha. The last 3 drugs also showed disappointing results. A
recently published prospective phase 2 study of irinotecan (CPT-11) also failed to demonstrate any
efficacy.
The combination of interferon alpha and 5-fluorouracil synergistically reduces
meningioma cell proliferation in culture and warrants further investigation.
Some studies have shown a possible role of COX-2 inhibitors in the treatment of
recurrent meningiomas.[8]

The role of targeted chemotherapy to block the tumorogenic pathways of

meningiomas at specific sites is being extensively investigated. [25]
Molecules to block specific growth factors or enzymes are being developed. Atypical
meningioma (WHO grade II) and anaplastic meningioma (WHO grade III) showed increased fatty
acid synthase (FAS) expression. FAS inhibitor (cerulein) decreased meningioma cell survival in vitro.
Thus, increased FAS expression in human meningiomas represents a novel therapeutic target for
the treatment of unresectable or malignant meningiomas. [26]
Although most meningiomas grow slowly and have a low mitotic rate, clinical benefit has been
reported in many case series with either tumor regression or stasis after radiotherapy; however, these
results have not been confirmed in randomized trials. Oya et al reported on the natural history of
meningiomas.[27]The prospect of benign meningioma growth is an important factor to consider in their
proper management. Approximately 40% of 273 meningiomas (in 244 patients) grew within a 4-year
period. Lack of calcification, hyperintensity in T2 MRI, and peritumoral edema were predictors of
growth in follow up. In addition, age younger than 60 years and tumor size larger than 25 mm
(diameter) were also associated with a greater risk.
Radiotherapy is mainly used as adjuvant therapy for incompletely resected, high-grade and/or
recurrent tumors. It can also be used as primary treatment in some cases (optic nerve
meningiomas[28] and some unresectable tumors).[29, 30]
In general the ideal treatment of a benign meningioma is surgical resection if possible.
Hasegawa et al treated 46 patients with gamma knife radiation (GKR) as the initial treatment modality.
[31]
The lesions were falcine, convexity, or parasagittal. The study found GKR to be effective. The main
caveat was tumor size. Large tumors had the possibility of severe postirradiation edema. This was
actually more likely to occur with significant, baseline peritumoral edema. GKR may be selected over
surgery in patients with significant medical comorbidities.
Stereotactic radiosurgery has been shown to provide excellent local tumor control with
minimal toxicity.[32, 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.
It has been advocated as an effective management strategy for small meningiomas
and for meningiomas involving the skull base or the cavernous sinus.
It is used primarily to prevent tumor progression.
In a recently published series, the long-term follow up after radiosurgery was
reported; a tumor control rate of 94% was found after an average of 103 months.

Surgical Care
The constant principles in meningioma resection are the following: If possible, all involved or
hyperostotic bone should be removed. The dura involved by the tumor as well as a dural rim that is
free from tumor should be resected (duraplasty is performed). Dural tails that are apparent on MRI are
best removed, even though some may not be involved with the tumor. Make a provision for harvesting
a suitable dural substitute (pericranium or fascia lata). The surgeon also can use commercially
available dural substitutes. If feasible, always start by coagulating the arterial feeders to the
meningioma. See the images below.
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: 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.

Surgical strategies for managing meningiomas in specific locations are discussed in the sections that
follow.

Convexity meningioma

Opening the scalp and skull may be bloody because of the hypertrophy of blood vessels originating
from the external circulation.
The tumor may breach the sanctity of the dura and the bone, thus appearing subcutaneously.
The dural blood vessels should be coagulated before opening the dura to decrease tumor vascularity.
Usually the tumor is separated from underlying brain parenchyma by an arachnoid layer. This layer
may not be complete at the depth of the tumor. In this location, separating the tumor from the brain
may be difficult.
Unless the tumor is small and can be removed in 1 piece, the best strategy for excising convexity
meningiomas is to find the arachnoidal plane and dissect it gently.
Placing patties circumferentially around the tumor allows quick identification of this crucial plane at a
later time.
Coagulate the surface of the tumor, then core it and invaginate the outer layer to allow further
circumferential dissection.
Perform dural grafting.

Parasagittal meningiomas
These tumors may arise from the convexity and involve the superior sagittal sinus (SSS) by medial
extension, or they may arise from the falx and involve the SSS by upward extension. The former
subgroup is easier to treat surgically because of its superficial location.
The foremost consideration in surgically treating parasagittal meningiomas is to decide what to do
with the SSS. MRV is not yet sensitive enough to confirm unequivocally the complete occlusion of the
SSS.
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. If the SSS is completely obliterated by
tumor, it can be ligated safely and excised. The surgeon should be careful not to injure the veins that
run anteriorly and posteriorly to the tumor. These veins may provide crucial collateral circulation for
the venous drainage of the cerebrum and should be preserved at all costs.
If the SSS is only partially involved, the decision of whether to sacrifice it depends on the involved
segment.
The anterior third of the SSS can usually be sacrificed with impunity; the middle third, sacrificed at
times; and the posterior third, never ligated. In this author's experience, the SSS is never sacrificed
beyond the anterior third.
Some surgeons resect a partially involved sinus and reconstruct it later (either with a vein or
prosthetic graft).
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. If the sinus is occluded gradually by the tumor, the venous drainage will be diverted
over time through parasagittal veins.

Olfactory groove and tuberculum sellae meningiomas

To avoid undue retraction of the frontal lobes, these tumors are best approached through a low
craniotomy. This is achieved by removing the supraorbital rim.
A unilateral approach is usually sufficient. The midline burr hole should be placed just above the
frontonasal suture. By entering the frontal sinus and removing the orbital rim, a low approach is
provided.
To allow adequate visualization, the falx should be sectioned after ligating the most anterior aspect of
the SSS. Every attempt should be made to preserve at least one of the olfactory nerves.

These tumors receive their blood supply through various sources: the ethmoidal branches of the
ophthalmic arteries, branches from the middle meningeal artery, and the carotid arteries.
These tumors often invade the ethmoid sinuses and, at times, the sphenoid sinus.
Care should be taken to identify and preserve both optic nerves. 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.
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.
Removing the zygoma and the orbital rim allows wider exposure of the sphenoid wing, the middle
cranial fossa, the anterior cranial fossa, and the anterior clinoid.
Medial tumors may extend within the cavernous sinus.

Tentorial and torcular meningiomas

Tentorial meningiomas may be supplied by a multitude of vessels that arise from the tentorial leaf.
These should be coagulated thoroughly before one attempts to remove the tumor.
A major supply may be the Bernasconi-Cassinari artery, which arises from the cavernous portion of
the carotid artery and runs posteriorly to supply the tentorium.
This artery is usually not apparent on normal angiograms but may be conspicuous in angiograms of
tentorial meningiomas.
A definite attempt should be made at recognizing the Bernasconi-Cassinari artery during surgery and
coagulating it to decrease tumor vascularity.
Tentorial meningiomas often grow in both the infratentorial and supratentorial compartments and
should be approached accordingly.
Studying the preoperative angiogram is imperative in cases of torcular meningiomas to delineate the
patency of the different sinuses and the available collateral circulation. Removing these tumors
completely is often impossible because of partial involvement of the venous sinuses.

Cerebellopontine angle meningiomas

In acoustic neuromas, the facial nerve usually lies anterosuperiorly to the tumor and is encountered
late in surgery. This relationship is lost in cerebellopontine angle meningiomas, 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).
Before attempting to remove the tumor, the surgeon should first diminish its blood supply by
coagulating its supplying arteries from the dura. To do so, the interface of the tumor and the petrous
bone should be followed. A partial cerebellar resection may be necessary to avoid undue retraction of
the brain.

Meningiomas involving the cavernous sinus

The issue of meningiomas involving the cavernous sinus is currently an area of intense interest in
neurosurgery. No one doubts that, in experienced hands, such meningiomas can be treated
successfully.
The debate centers on 2 points: when to operate and how aggressive the resection should be. The
following opinion is a personal reflection on the matter, and diverging views may be found in the
literature.

Asymptomatic cavernous sinus meningiomas should not be operated but should be monitored
carefully by means of repeated physical examination and serial MRI.

Symptomatic meningiomas in otherwise healthy patients should be resected by

neurosurgeons who are trained for such procedures.
Avoid injuring the cranial nerves or the carotid artery. This author does not believe in the benefit of
bypassing and resecting the cavernous carotid artery in these cases.
The surgeon should remember that a multitude of processes may affect the cavernous sinus and
mimic a meningioma, including sarcoidosis and infection/inflammation that lead to the Tolosa-Hunt
syndrome.
Gamma knife may be a good treatment option in parasellar meningiomas. [34] Large tumors can be
partially resected and treated with gamma knife after resection. In a report by Jensen et al, a good
outcome was obtained, with an impressive 69% local tumor growth control.

Clival and petroclival meningiomas

These tumors represent some of the greatest challenges in neurosurgery; although partial resection is
relatively straightforward, complete resection remains a daunting task.
Partial resection usually does not translate into any benefit for the patient and only renders further
surgeries more difficult; therefore, every attempt should be made to complete the resection. If surgery
has to be interrupted for logistical reasons, the second operation should be scheduled the earliest
possible opportunity.
A multitude of approaches has been devised for these tumors. The traditional approaches such as the
suboccipital or the subtemporal are usually insufficient to allow complete removal. More extensive
approaches, such as the petrosal approach, are needed. This approach consists of combined
supratentorial and infratentorial craniotomies, associated with a simple mastoidectomy down to the
solid angle (ie, the bone encasing the inner ear). After the tentorium is split, the petroclival
meningioma can be visualized in its entirety.

Consultations
If the patient has neurofibromatosis, the neurosurgeon may want to refer the patient for genetic
counseling and for audiometric testing.
If the radiologic diagnosis is not clear cut, a detailed discussion with the radiologist should attempt to
rule out other pathologic entities, such as neurofibromas or sarcomas.
In specific cases, consulting a radiation oncologist may be appropriate.

Diet
No dietary restrictions are necessary in patients with meningiomas. If the patient is on perioperative
steroids, a low-salt diet is appropriate.

Activity
Patients with a meningioma who undergo surgery can resume their normal activities after an
adequate period of postoperative rest (1-3 mo).

Medication Summary
The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Corticosteroids
Class Summary
These agents reduce edema around tumor, frequently leading to symptomatic and objective
improvement in symptoms.
View full drug information

Dexamethasone (Decadron, Dexasone)

Postulated mechanisms of action of corticosteroids in brain tumors include reduction in vascular

permeability, cytotoxic effects on tumors, inhibition of tumor formation, and decreased CSF
production.

Further Inpatient Care

Before or after surgery, patients with skull-base meningiomas may have numerous disabilities, such
as diplopia, dysphasia, dysphagia, or motor weakness. These problems should be managed with a
multidisciplinary approach (eg, occupational therapy, physiotherapy, speech therapy).

Further Outpatient Care

Patients who undergo operation for meningiomas should receive regular follow-up with enhanced MRI
to check for possible recurrences.[35] Patients who are discharged home with antiepileptic agents
should be monitored by a neurologist.

Prognosis
Patients whose meningiomas are completely resected usually have an excellent prognosis.
Tumor size may play a role in determining outcome. In a study of 34 patients who underwent surgery
for CPA meningiomas, 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 (45.5% vs 5.9%, respectively). It was also found that deficits of the lower cranial nerves
occurred only in patients whose tumors extended into the jugular foramen. No association was found
between tumor extension into the internal acoustic canal and either postoperative complications or
cranial nerve deficits. Among all patients, 5.9% suffered postoperative facial nerve palsy.[36]
The following types of meningiomas are most likely to recur: incompletely excised, malignant, or
multiple tumors.