Epidemiology, Pathology, Clinical Features, and Diagnosis of Meningioma - UpToDate

5/25/2017 Epidemiology, pathology, clinical features, and diagnosis of meningioma UpToDate
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Epidemiology, pathology, clinical features, and diagnosis of meningioma
Author: John K Park, MD, PhD
Section Editors: Jay S Loeffler, MD, Patrick Y Wen, MD
Deputy Editor: April F Eichler, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2017. | This topic last updated: Dec 08, 2016.
INTRODUCTION — Meningiomas are the most frequent primary brain tumors (table 1 and figure 1). Although
most meningiomas are benign, their location in the central nervous system can cause serious morbidity or
mortality. (See "Incidence of primary brain tumors".)
The epidemiology, pathology, clinical presentation, and diagnosis of meningiomas will be reviewed here. Other
topics on meningioma include:
● Treatment of WHO grade I (benign) meningiomas (see "Management of known or presumed benign
(WHO grade I) meningioma")
● Treatment of WHO grade II and III meningiomas (see "Management of atypical and malignant (WHO
grade II and III) meningioma")
● Systemic therapy for recurrent meningioma (see "Systemic treatment of recurrent meningioma")
EPIDEMIOLOGY — Meningiomas are the most common primary central nervous system tumors and account
for about onethird of all primary brain and spinal tumors [1,2]. (See "Incidence of primary brain tumors".)
According to the Central Brain Tumor Registry in the United States (CBTRUS), there were 129,841 new
cases of meningioma diagnosed from 2008 to 2012 [3]. The estimated number of new cases per year in the
United States is nearly 26,000. The incidence rate varies by race, with blacks having a 1.2fold higher
incidence than whites [3].
The incidence of meningioma increases progressively with age, with a median age at diagnosis of 65 years
[3]. Meningiomas are rare in children [4], except in those with hereditary syndromes such as
neurofibromatosis type 2 (NF2) or antecedent therapeutic radiation therapy [5,6]. (See 'Risk factors' below.)
Meningiomas are more common in women, with a female to male ratio of about two or three to one [5,7,8].
For spinal meningiomas, which comprise about 10 percent of all meningiomas, the female to male ratio is
even higher, approximately nine to one. This female predominance is less pronounced or absent in those with
atypical or anaplastic meningiomas, children, and those with radiationinduced meningiomas.
Populationbased studies estimate that 80 to 90 percent of meningiomas are WHO grade I, approximately 10
to 15 percent are grade II, and 1 to 3 percent are grade III [3,7,9]. Hospitalbased studies, particularly from
tertiary care centers, have reported a higher proportion of grade II and III tumors [10,11].
RISK FACTORS — A number of factors have been studied for a possible relationship to the development of
meningiomas and other brain tumors. The factors most intensively investigated as having a potential etiologic
role in meningioma are discussed here. Factors associated with other types of brain tumors are reviewed
separately. (See "Risk factors for brain tumors".)
Ionizing radiation — Exposure to ionizing radiation is the most important acquired risk factor for meningioma
[8,12]. Radiationinduced meningiomas have a higher incidence of multiplicity and atypia compared with
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sporadic meningiomas. An increased risk of meningioma following a lengthy latency period has been
established in a variety of situations.
● Radiation therapy for malignancy – Therapeutic use of radiation can result in exposure of the central
nervous system either as a direct consequence of treatment or by incidental exposure. Clinical situations
in which this is particularly important include the following:
• Radiation therapy for primary malignancies of the central nervous system
• Radiation therapy for tumors in the head and neck region
• Prophylactic craniospinal irradiation to prevent central nervous system (CNS) relapse as a
component of treatment for acute leukemia or other malignancy
Although the absolute risk associated with radiation therapy is not known, the latency period is more than
20 years in many cases. Longterm followup of epidemiologic studies has observed that the incidence
continues to rise even after several decades, and that risk may be highest among patients treated at a
young age [6,13,14].
● Incidental radiation exposure – An association between radiation and the subsequent development of
meningioma has been observed in a number of other clinical settings:
• Tinea capitis – Until the 1950s, low doses of irradiation were used to treat tinea capitis. An analysis
of over 11,000 children treated for tinea capitis found a sevenfold increase in the incidence of
meningioma, with a mean latency of 36 years [8,15].
• Dental radiographs – Several studies have reported an increased risk of meningioma associated with
frequent dental radiographs [1621]. Across multiple studies, the reported risk has been highest for
multiple radiographs examinations and childhood exposure, primarily in an era when the dose of
dental radiographs was higher than with current technology [16,19,20,22]. Importantly, recall bias
can influence associations found in casecontrol studies such as these, and validation of dental
records was not performed in most of these studies [23].
• Diagnostic head computed tomography (CT) – Childhood exposure to diagnostic head CTs may also
be associated with an increased risk of brain tumors, including meningiomas [24,25]. (See
"Radiationrelated risks of imaging studies", section on 'Pediatrics'.)
• Atomic bomb exposure – An increased incidence of meningiomas has been observed in survivors of
the atomic explosions in Japan [26,27]. The increased incidence of meningioma was more
pronounced in those who received higher radiation doses and those who were younger at the time of
exposure [28].
Genetic predisposition — A genetic predisposition to meningioma is best characterized in patients with
neurofibromatosis type 2 (NF2) and schwannomatosis. Patients with multiple endocrine neoplasia type 1
(MEN1) also have an increased risk of meningioma, although at lower rates compared with neurofibromatosis
[29]. (See "Multiple endocrine neoplasia type 1: Clinical manifestations and diagnosis", section on 'Other
tumors'.)
Neurofibromatosis type 2 — NF2 is an autosomal dominant disorder predisposing to multiple tumors of
the nervous system. This disorder is caused by mutations in the NF2 gene, a tumor suppressor gene on
chromosome 22. (See "Neurofibromatosis type 2", section on 'Molecular pathogenesis'.)
Approximately onehalf of individuals with NF2 have meningiomas, and multiple meningiomas are often
present [30]. Most meningiomas are intracranial, although intradural, extramedullary spinal meningiomas are
also seen. (See "Neurofibromatosis type 2", section on 'Meningiomas'.)
The incidence increases with age, and lifetime risk of developing a meningioma may be as high as 75 percent
[31]. Patients with NF2 tend to develop meningiomas at an earlier age than those with sporadic meningiomas.
The meningiomas seen in patients with NF2 are more frequently atypical or anaplastic compared with
sporadic tumors [32,33].
Schwannomatosis — Meningiomas are recognized as part of the phenotype of schwannomatosis in
some patients. Patients with schwannomatosis have multiple schwannomas in the absence of bilateral
vestibular schwannomas; germline mutations in the tumor suppressor gene SMARCB1 are present in up to
50 percent of familial cases and a small proportion of sporadic cases. (See "Schwannomatosis", section on
'Other tumors'.)
Hormonal factors — Hormonal factors may have a role in the development of meningioma, as suggested by
several lines of evidence [1]:
● The incidence of meningioma is higher in postpubertal women compared with men
● The female:male ratio is highest during the peak reproductive years and decreases in older adults
● Progesterone and androgen receptors are present in approximately twothirds of patients, while estrogen
receptors have been identified in approximately 10 percent of cases [3436]
Multiple observational studies have explored a possible relationship between either hormone replacement
therapy or oral contraceptive use and the risk of meningioma, with mixed results [1,3743]. A metaanalysis of
six prospective casecontrol studies that included over 1600 meningioma cases found that everuse of
hormone therapy was associated with a small but significant increase in the risk of meningioma (relative risk
[RR] 1.35, 95% CI 1.21.5) [43]. In studies that distinguished between estrogenonly versus combined
estrogenprogestin hormone therapy, estrogen, but not combined therapy, was associated with increased risk
(RR 1.31). This is equivalent to an approximate absolute excess risk of 2 per 10,000 users over five years.
Some, but not all, studies have also suggested a protective effect of smoking and an increased risk with
higher body mass index (BMI), both of which could potentially be mediated through their effects on
endogenous estrogen levels [37,4042].
Inhibition of estrogen or progesterone receptors has not been shown to alter the natural history of recurrent
meningiomas. (See "Systemic treatment of recurrent meningioma", section on 'Hormonal therapy'.)
Breast cancer — A moderately increased risk of meningioma has been reported in women with breast
cancer, and a similar increase in the incidence of breast cancer has been observed in women with a history of
meningioma [1,44]. Whether this relationship is due to shared hormonal risk factors, other risk factors causing
both diseases, or an underlying genetic predisposition is unclear [1].
Obesity — A positive association between BMI and meningioma has been reported in several large
observational studies, with odds ratios ranging from 1.4 to 2.1 [37,40,4549]. This relationship might be
related to endogenous hormonal factors, since obesity is associated with higher levels of estrogens and other
growth factors.
High BMI is an established risk factor for a variety of other neoplasms, including esophageal adenocarcinoma,
endometrial cancer, colon cancer, and breast cancer [50]. (See "Epidemiology, pathobiology, and clinical
manifestations of esophageal cancer", section on 'Obesity and metabolic syndrome' and "Endometrial
carcinoma: Epidemiology and risk factors", section on 'Obesity' and "Factors that modify breast cancer risk in
women", section on 'Weight' and "Colorectal cancer: Epidemiology, risk factors, and protective factors",
section on 'Obesity'.)
Others — Several studies have analyzed the role of head trauma as an etiologic factor for brain tumors, with
conflicting results [22,5153]. Improved recall of a history of head trauma in patients with meningioma may
have contributed to bias in some of these studies.
Others have looked at a possible link between cell phone usage and the subsequent development of brain
tumors. At present, there is no conclusive evidence supporting a causal relationship. However, the prolonged
latency period seen with ionizing radiation suggests that longer followup is required [1]. (See "Risk factors for
brain tumors", section on 'Cellular telephones and radiofrequency radiation'.)
PATHOLOGY
WHO classification — Meningiomas are classified according to the World Health Organization (WHO)
schema, which is based upon morphologic criteria [54,55]. The WHO classification system divides
meningiomas into three groups (table 2):
● WHO grade I – Benign meningiomas (WHO grade I) (picture 1) are subdivided into a number of
subtypes (table 2). WHO grade I meningiomas do not meet any of the criteria for a higher grade lesion
based upon morphologic criteria. The treatment approach is the same for all of the subtypes of benign
meningiomas.
● WHO grade II – WHO grade II meningiomas include atypical, clear cell, and chordoid meningiomas.
Atypical meningiomas have increased mitotic activity (≥4 mitoses per 10 highpowered fields), brain
invasion, or three or more of the following features: increased cellularity, small cells with a high
nuclear:cytoplasmic ratio, prominent nucleoli, uninterrupted patternless or sheetlike growth, or foci of
spontaneous or geographic necrosis (picture 1).
● WHO grade III – WHO grade III (malignant) meningiomas include anaplastic, papillary, and rhabdoid
meningiomas. Anaplastic meningiomas have ≥20 mitoses per 10 highpowered fields and/or malignant
characteristics resembling carcinoma, sarcoma, or melanoma. Features that support the diagnosis of
malignant meningioma include the loss of usual meningioma growth patterns, infiltration of underlying
brain, abundant mitoses with atypical forms, and multifocal microscopic foci of necrosis (picture 1).
The WHO grading system correlates with outcome and thus has a major impact on treatment planning.
Patients with WHO grade II or grade III meningiomas are significantly more likely to have invasive disease, a
local recurrence following the initial treatment, and ultimately to have a shorter overall survival compared with
patients with a WHO grade I meningioma.
● Overall reported rates of recurrence for patients with grade I, II, and III meningiomas are 7 to 25, 30 to
50, and 50 to 94 percent, respectively, in various series [5660].
● Although WHO grade III meningiomas are considered malignant, distant metastasis is rare and the
primary issue is local recurrence, which necessitates additional treatment beyond surgery and ultimately
can cause death [61]. (See "Management of atypical and malignant (WHO grade II and III)
meningioma".)
Among grade I tumors, the presence atypical features may also have prognostic importance, although data
are more limited. In a study of 147 patients who underwent resection of a grade I meningioma, the fiveyear
recurrence rate was significantly higher for tumors with one or two atypical features compared with tumors
with no atypical features (31 versus 14 percent), independent of extent of resection [62].
Molecular pathogenesis — The bestcharacterized genetic alteration is loss of chromosome 22, which in
many cases is associated with mutations in the neurofibromatosis type 2 (NF2) gene located on the long arm
of chromosome 22. (See 'Neurofibromatosis type 2' above.)
NF2 mutations are also present in approximately onehalf of sporadic meningiomas, more commonly in those
with transitional or fibroblastic histologic subtypes and in higher grade tumors [63].
Genomic sequencing efforts have identified several oncogenic mutations in a small subset of nonNF2 mutant
meningiomas that have potential therapeutic implications. In two separate studies, mutations in Smoothened
(SMO), an activator of the Hedgehog pathway that is mutated in many basal cell carcinomas, were found in
approximately 5 percent of tumors, and mutations in vakt murine thymoma viral oncogene homolog 1
(AKT1), an activator of the phosphatidylinositol 3kinase (PI3K) pathway, were found in up to 13 percent of
tumors [64,65]. Mutations in TRAF7, a proapoptotic ubiquitin ligase, were identified in approximately one
quarter of tumors in one study [65]. The role of these mutations in the pathogenesis of meningioma, however,
is unclear. Another study found oncogenic mutations in PI3KA in approximately 7 percent of meningiomas,
mostly those located in the skull base [66].
Activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway also appears to be a
common alteration in meningioma that has potential therapeutic implications [67].
CLINICAL PRESENTATION — Meningiomas can arise anywhere from the dura, most commonly within the
skull and at sites of dural reflection (falx cerebri, tentorium cerebelli, venous sinuses) [68]. Other less common
sites include the optic nerve sheath and choroid plexus; approximately 10 percent arise in the spine. Very
rarely, meningiomas can arise at extradural sites [69].
Symptoms from a meningioma are determined by the location of the mass and by the time course over which
the tumor develops. Meningiomas are frequently extremely slow growing and often are asymptomatic. (See
"Clinical presentation and diagnosis of brain tumors", section on 'Clinical manifestations'.)
Asymptomatic tumors — Many meningiomas are asymptomatic or minimally symptomatic, and are
discovered incidentally on a neuroimaging study or at autopsy [7072]. Followup studies on patients with
asymptomatic meningiomas suggest that most such tumors either remain the same size or grow slowly over
prolonged periods [73,74].
In a systematic review and metaanalysis of incidental findings on brain MRI in nearly 20,000 children and
adults, meningioma was the most common incidental tumor, identified on 0.29 percent of MRIs [75]. The
prevalence of incidental findings, including meningioma, increased with age. A subsequent prospective,
populationbased study of brain MRI in 5000 healthy adults (mean age 65 years) identified meningioma in 2.5
percent of participants [76]. The most common locations were convexity (62 percent) and falx cerebri (15
percent).
Seizures — Seizures are present preoperatively in approximately 30 percent of patients who are diagnosed
with an intracranial meningioma [77]. The risk of seizure is higher in association with nonskull base location
(eg, convexity and parasagittal/falcine tumors) and tumors associated with peritumoral edema.
Focal findings — Characteristic focal deficits are caused by tumors in specific locations. Examples of such
lesions include:
● Visual changes – Visual changes, which are often unrecognized, are common in meningiomas involving
the optic pathways.
• Visual field defects may be caused by parasellar meningiomas
• Optic atrophy in one eye and papilledema in the other, the socalled FosterKennedy syndrome, can
be produced by parasellar or subfrontal meningiomas
• Progressive unilateral visual loss, which may be mistaken for optic neuritis, can be caused by optic
nerve sheath meningiomas
• Mild weakness of extraocular movements has been associated with cavernous sinus meningiomas
● Loss of hearing or smell – A cerebellopontine angle meningioma can produce sensorineural hearing loss.
Olfactory groove or sphenoid ridge meningiomas can cause anosmia due to compression of the olfactory
tract.
● Mental status changes – Mental status changes with apathy and inattention may result from surprisingly
large subfrontal or sphenoid ridge meningiomas. Similar or even larger sized tentorial notch and
intraventricular meningiomas are at times asymptomatic and diagnosed incidentally.
● Extremity weakness – Meningiomas at different sites can produce characteristic patterns of extremity
weakness.
• A parasagittal meningioma growing on the falx and compressing the motor strip can lead to bilateral
leg weakness in the absence of a spinal cord lesion
• Foramen magnum meningiomas may produce a subtly progressive sequence of ipsilateral arm, then
leg weakness, which is followed by contralateral leg and arm weakness that may be misdiagnosed as
multiple sclerosis
• Spinal meningiomas frequently present with progressive leg weakness and numbness
● Obstructive hydrocephalus – Large tumors in the posterior cranial fossa can cause obstructive
hydrocephalus, and present with papilledema and classic early morning headache.
NEUROIMAGING — Meningiomas have a very characteristic appearance on both magnetic resonance
imaging (MRI) and computed tomography (CT) (table 3).
On MRI, a typical meningioma is an extraaxial, duralbased mass that is isointense or hypointense to gray
matter on T1 and isointense or hyperintense on proton density and T2 weighted images. There is usually
strong, homogeneous contrast enhancement after gadolinium administration (image 1). Most meningiomas
show a characteristic marginal dural thickening that tapers peripherally (the "tail" sign) (image 2).
On CT, the typical meningioma is a welldefined extraaxial mass that displaces the normal brain. They are
smooth in contour, adjacent to dural structures, and sometimes calcified or multilobulated. Isointensity with
normal surrounding brain may make diagnosis difficult on a noncontrasted scan, but intravenous contrast
administration results in uniformly bright enhancement. Secondary involvement of adjacent bone (reactive
sclerosis, invasion, erosion) is uncommon with convexity meningiomas, but occurs in up to onehalf of skull
base tumors [78].
Differentiating an atypical or malignant meningioma from a benign meningioma purely on the basis of
neuroimaging is difficult. Features that may suggest the presence of a highgrade meningioma rather than a
benign meningioma include the following [61,7981]:
● Intratumoral cystic change
● Hyperostosis of the adjacent skull and/or bone destruction
● Extension of tumor through the skull base
● Peritumoral brain edema
● Low apparent diffusion coefficient (ADC) values
● Elevated cerebral blood volume
Positron emission tomography (PET) scanning has shown more intense uptake associated with higher grade
meningiomas in some, but not all, studies [82]. However, none of these neuroimaging findings is sufficiently
specific to be clinically useful. Furthermore, the initial therapeutic approach for most meningiomas is surgical
resection if feasible, depending upon the size and location of the lesion, as well as the patient’s overall
condition and symptoms. (See "Management of known or presumed benign (WHO grade I) meningioma".)
Prior to the development of MRI and CT, angiography was used to suggest the diagnosis of meningioma by
demonstrating arterial supply from meningeal vessels and the delayed vascular blush that is characteristic of
these lesions. The use of angiography now is limited to tumor embolization as a component of therapy. (See
"Management of known or presumed benign (WHO grade I) meningioma", section on 'Extent of resection'.)
DIFFERENTIAL DIAGNOSIS — While meningioma is by far the most common cause of a discrete, dural
based enhancing mass lesion, many other disease processes can involve the dura or subdural space,
resulting in an appearance on magnetic resonance imaging (MRI) or computed tomography (CT) that may
suggest meningioma. These include lymphoma, plasmacytoma, metastatic carcinoma, melanocytic
neoplasms, solitary fibrous tumor, gliosarcoma, inflammatory lesions such as sarcoidosis and granulomatosis
with polyangiitis, and infections such as tuberculosis [68,8385].
In general, MRI, CT, and positron emission tomography (PET) studies cannot reliably distinguish these
entities from meningioma. The presence of atypical imaging features, such as large or disproportionate
amount of associated edema, extensive bone involvement, or brain or leptomeningeal invasion, may be a clue
to an alternative etiology or to a higher grade meningioma, along with clinical features of systemic disease.
These and other clinical clues to rare alternative diagnoses are reviewed in the table (table 4).
DIAGNOSTIC EVALUATION — A definitive diagnosis of meningioma and classification as benign, atypical, or
malignant (World Health Organization [WHO] grades I, II, and III, respectively) requires histologic
confirmation. However, imaging studies often provide a tentative diagnosis and may be sufficient for empiric
treatment when obtaining tissue for pathologic confirmation entails too high a risk of causing further neurologic
deficits.
While the differential diagnosis of meningioma includes a wide range of neoplastic and nonneoplastic entities,
these are rare and almost always diagnosed after tissue is obtained, due to their clinical and radiographic
similarity to meningiomas. The utility of an extensive preoperative evaluation is uncertain.
History — The history in patients with a suspected meningioma should include an assessment of risk factors,
especially a history of prior therapeutic radiation. Radiationinduced meningiomas have a higher likelihood of
being high grade and of being multiple and recurrent. (See 'Ionizing radiation' above and "Management of
known or presumed benign (WHO grade I) meningioma", section on 'Radiationinduced meningiomas'.)
The history should also probe for conditions that may cause duralbased pathology mimicking meningioma,
including hematologic and nonhematologic malignancy, sarcoidosis, and tuberculosis (table 4). (See
'Differential diagnosis' above.)
Genetic syndromes predisposing to meningioma, such as neurofibromatosis type 2 (NF2) and
schwannomatosis, may be apparent by personal and family history by the time a meningioma is identified.
Lack of a family history does not rule these syndromes out, however, as de novo mutations frequently occur.
(See 'Genetic predisposition' above.)
Physical examination — Most patients with meningioma have a normal physical examination. Occasionally,
convexity tumors associated with prominent hyperostosis or direct bony extension may produce a palpable
bulge on the skull.
Physical stigmata of NF2 or schwannomatosis may include hearing loss (for NF2) and multiple palpable
schwannomas. (See "Neurofibromatosis type 2", section on 'Clinical features' and "Schwannomatosis",
section on 'Clinical features'.)
Laboratories — It seems reasonable to obtain a comprehensive metabolic panel and complete blood count,
as findings such as hypercalcemia or anemia might prompt additional testing for multiple myeloma or systemic
malignancy. We do not routinely obtain serum protein electrophoresis (SPEP), urinalysis, angiotensin
converting enzyme (ACE) level, or tuberculosis screening in otherwise healthy adults. More extensive
evaluation should be considered in immunocompromised hosts and in patients with atypical imaging features.
Cerebrospinal fluid analysis does not play a role in the diagnostic evaluation of meningioma but may be
indicated if there are atypical imaging features, such as leptomeningeal enhancement, suggesting
involvement of the subarachnoid space.
Imaging — Magnetic resonance imaging (MRI) provides the most complete assessment of suspected
meningiomas. Computed tomography (CT) may also be obtained to provide better definition of bony anatomy
and the degree of calcification associated with the lesion. (See 'Neuroimaging' above.)
We do not routinely obtain spinal imaging in patients with a suspected intracranial meningioma, but we do
advise obtaining a brain MRI in patients with a suspected spinal meningioma to look for intracranial masses
that may suggest either a tumor predisposition syndrome or an alternative diagnosis.
We obtain updated cancer staging (eg, chest, abdomen, and pelvis CT) in patients with known cancer but do
not routinely obtain these tests in otherwise healthy adults with history of cancer by history or ageappropriate
cancer screening. The presence of atypical neuroimaging findings, even in a patient without known cancer,
may also indicate the need for a more extensive cancer staging.
SUMMARY
● Meningiomas account for approximately onethird of primary central nervous system tumors, occurring
primarily in older individuals with a female predominance (table 1). (See 'Epidemiology' above.)
● The etiology of meningioma is not known in most cases. However, there is a clear association with
antecedent radiation exposure, which is associated with a latency period that may exceed 30 years.
Meningiomas are a frequent manifestation of neurofibromatosis type 2 (NF2), and somatic mutations in
the NF2 gene may also contribute to the development of sporadic meningiomas. (See 'Risk factors'
above and 'Molecular pathogenesis' above.)
● Meningiomas are classified according to the World Health Organization (WHO) grading system. WHO
grade I lesions are benign and generally have a favorable prognosis, while atypical (grade II) and
malignant (grade III) meningiomas are substantially more likely to recur. (See 'WHO classification'
above.)
● Meningiomas can arise anywhere from the dura, most commonly within the skull. Approximately 10
percent arise in the spinal cord. (See 'Clinical presentation' above.)
● Many meningiomas are slow growing and discovered incidentally on a neuroimaging study. These may
be asymptomatic or minimally symptomatic. (See 'Asymptomatic tumors' above.)
● Symptoms can vary widely, depending upon by the location of the mass. (See 'Focal findings' above.)
● On magnetic resonance imaging (MRI), a typical meningioma is an extraaxial, duralbased mass that is
isointense or hypointense to gray matter on T1, isointense or hyperintense on proton density and T2
weighted images, and associated with strong, homogeneous contrast enhancement after gadolinium
administration (table 3 and image 1). (See 'Neuroimaging' above.)
● The differential diagnosis of meningioma includes a wide range of neoplastic and nonneoplastic entities
(table 4). However, these are rare and almost always diagnosed after tissue is obtained, due to their
clinical and radiographic similarity to meningiomas. The utility of an extensive preoperative evaluation is
uncertain except in selected patients. (See 'Differential diagnosis' above and 'Diagnostic evaluation'
above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate, Inc. would like to acknowledge Dr. Peter Black, who
contributed to an earlier version of this topic review.
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Topic 5220 Version 15.0
GRAPHICS
Distribution of all primary brain and CNS tumors by site
Annual
Percent of
Histology incidence
total
rate*
Tumors of neuroepithelial tissue 29.9 6.62
Pilocytic astrocytoma 1.4 0.34
Diffuse astrocytoma 2.3 0.53
Anaplastic astrocytoma 1.7 0.38
Unique astrocytoma variants 0.3 0.07
Glioblastoma 15.1 3.20
Oligodendroglioma 1.1 0.25
Anaplastic oligodendroglioma 0.5 0.10
Oligoastrocytic tumors 0.9 0.20
Ependymal tumors 1.9 0.43
Glioma malignant, NOS 2.0 0.47
Choroid plexus 0.2 0.05
Other neuroepithelial tumors 0.03 0.01
Neuronal and mixed neuronalglial tumors 1.2 0.28
Tumors of the pineal region 0.2 0.04
Embryonal tumors 1.1 0.26

Tumors of cranial and spinal nerves 8.1 1.76
Nerve sheath tumors 8.1 1.76

Tumors of meninges 37.6 8.13
Meningioma 36.4 7.86
Mesenchymal tumors 0.4 0.08
Primary melanocytic lesions 0.04 0.01
Other neoplasms related to the meninges 0.8 0.18

Lymphomas and hematopoietic neoplasms 2.1 0.46
Lymphoma 2.0 0.44
Other hematopoietic neoplasms 0.07 0.01

Germ cell tumors and cysts 0.4 0.10
Germ cell tumors, cysts and heterotopias 0.4 0.10

Tumors of sellar region 16.3 3.68
Tumors of the pituitary 15.5 3.49
Craniopharyngioma 0.8 0.18
Chordoma/chondrosarcoma 156 0.1

Unclassified tumors 5.6 1.23
Hemangioma 1.5 0.34
Neoplasm, unspecified 4.0 0.88
All other 0.03 0.01
TOTAL 365,858 100.0
CBTRUS Statistical Report: NPCR and SEER Data from 2008 to 2012.
* Average annual ageadjusted incidence rate.
CBTRUS: Central Brain Tumor Registry of the United States; CNS: central nervous system; NOS: not otherwise specified;
NPCR: National Program of Cancer Registries; SEER: Surveillance, Epidemiology, and End Results Program.
Data from: Ostrom QT, Gittleman H, Fulop J, et al. CBTRUS Statistical Report: Primary Brain and Central Nervous System
Tumors Diagnosed in the United States in 20082012. Neuro Oncol 2015; 17 Suppl 4:iv1.
Graphic 81566 Version 8.0
Incidence rates of primary brain tumors by major
neuroepithelial tissue and meningeal histologic types and
age group
The category "All brain tumors" includes some specific types not individually shown
(tumors of cranial and spinal nerves, hemangioblastomas, primary lymphomas, germ
cell tumors, and tumors of the sellar region). The "Astrocytoma" category includes
diffuse astrocytomas, anaplastic astrocytomas, unique astrocytoma variants, and
astrocytomas not otherwise specified.
PNET: primitive neuroectodermal tumor.
Reproduced with permission from: Wrensch M, Minn Y, Chew T, et al. Epidemiology of
primary brain tumors: Current concepts and review of the literature. NeuroOncology
2002; 4:278. Copyright © 2002 Margaret Wrensch, MD.
Meningioma subtypes
WHO

grade
Meningiomas with low risk of recurrence or aggressive growth:
Meningothelial I
Fibrous (fibroblastic) I
Transitional (mixed) I
Psammomatous I
Angiomatous I
Microcystic I
Secretory I
Lymphoplasmacyterich I
Metaplastic I
Meningiomas with greater likelihood of recurrence and/or aggressive behavior:
Atypical * II
Clear cell (intracranial) II
Chordoid II
Rhabdoid III
Papillary III
Anaplastic (malignant) III
Meningiomas of any subtype with high proliferative index
* As of the 2016 edition of the WHO Classification of Tumours of the Central Nervous System [1], atypical
meningioma is defined as a tumor with increased mitotic activity (≥4 mitoses per ten high powered fields), brain
invasion, or three or more of the following features: increased cellularity, small cells with a high
nuclear:cytoplasmic ratio, prominent nucleoli, uninterrupted patternless or sheetlike growth, or foci of
spontaneous or geographic necrosis.
WHO: World Health Organization.
Reproduced with permission from: Perry A, Louis DN, Scheithauer BW, et al. Meningiomas. In: WHO Classification of
Tumours of the Central Nervous System, Louis DN, Ohgaki H, Wiestler OD, Cavenee WK (Eds), IARC Press, Lyon 2007.

[1] WHO Classification of Tumours of the Central Nervous System, Fourth Edition, Louis DN, Ohgaki H, Wiestler OD,
Cavenee WK (Eds), IARC, Lyon 2016.
Histologic appearance of meningioma, WHO grades IIII
Left panel: transitional meningioma (grade I) showing characteristic cellular whorls;
intranuclear pseudoinclusions are visible in some cells. Middle panel: Chordoid
meningioma (grade II) with cohesive epitheliallike cords of cells; small foci of more
typical arachnoidal differentiation are found in most of these tumors. Right panel:
anaplastic meningioma (grade III) consisting of pleiomorphic arachnoidal cells with
a high mitotic rate; foci of necrosis are widely distributed throughout most
anaplastic meningiomas.
Reproduced with permission from: Whittle IR, Smith C, Navoo P, Collie D.
Meningiomas. The Lancet 2004; 363:1536. Copyright ©2004 Elsevier.
Neuroimaging features of meningioma
Typical Atypical
Smooth contour Large or disproportionate amount of associated
Homogeneous enhancement edema
Dural tail Intratumoral cystic change
Calcification Extensive bone involvement
Brain or leptomeningeal invasion
Low apparent diffusion coefficient
Elevated cerebral blood volume
Intracranial meningioma
A 70yearold woman presented with a severalweek history of confusion. Panels
(A, B): Noncontrast and contrastenhanced head CT shows a large bifrontal
lesion with calcifications and surrounding edema. Panels (C, D): Noncontrast
and contrastenhanced T1weighted axial MR images of the head also
demonstrate large flow voids representing blood vessels in the center of the
tumor. Panel (E): Noncontrast T1weighted sagittal MR image. Panel (F):
Contrastenhanced T1weighted coronal MR image.
CT: computed tomography; MR: magnetic resonance.
Courtesy of John Park, MD, PhD.
Radiographic features of meningioma
A: Tail sign: tapering dural thickening (arrow) due to direct tumor involvement or
reactive change in the dura, is a highly characteristic sign of meningioma; note also
the small reactive arachnoid cyst, reflecting the extraaxial site of this lesion
(arrowhead). B: Reactive cerebral white matter changes. C: Bony reactive changes:
reactive bone sclerosis, reflected in the increased vault thickness (arrows) is seen
most commonly in patients with multiple meningiomas associated with
neurofibromatosis type 2; invasive tumors such as these can cause problematic
extracranial facial masses.
Reproduced with permission from: Whittle IR, Smith C, Navoo P, Collie D.
Meningiomas. The Lancet 2004; 363:1536. Copyright ©2004 Elsevier.
Differential diagnosis of meningioma
Neoplastic Clinical and imaging clues
Solitary fibrous tumor/hemangiopericytoma Heterogeneous enhancement; prominent bone
erosion
Lymphoma Lack of hyperostosis; low apparent diffusion
coefficient
Plasmacytoma Abnormal SPEP, UPEP; anemia; renal insufficiency
Metastatic carcinoma Edema; adjacent skull metastasis; known breast,
prostate, or lung cancer
Melanocytic neoplasms Posterior fossa or spinal cord location
Gliosarcoma Heterogenous enhancement, local invasion
Leiomyosarcoma Rare, primarily seen in HIVpositive patients
Nonneoplastic Clinical clues
Sarcoidosis Uncommon manifestation of neurosarcoidosis;
systemic disease may or may not be present
Granulomatosis with polyangiitis Constitutional symptoms, renal insufficiency
IgG4related disease Orbital location; multiple tumors; elevated serum
IgG4
RosaiDorfman disease Massive painless cervical lymphadenopathy and fever
Tuberculosis Endemic regions; immunocompromise; chronic
cough and constitutional symptoms
HIV: human immunodeficiency virus; IgG4: immunoglobulin G4; SPEP: serum protein electrophoresis; UPEP: urinary
protein electrophoresis.
Contributor Disclosures
John K Park, MD, PhD Nothing to disclose Jay S Loeffler, MD Nothing to disclose Patrick Y Wen,
MD Grant/Research/Clinical Trial Support: Acerta [Brain tumor (ACP196); Agios [Brain tumor (AG120,
AG881); Angiochem [Brain tumor (ANG1005); AstraZeneca [Brain tumor (Vandetanib)]; Kadmon [Brain
tumor 9tesevatinib); Karyopharm [Brain tumor (Selinexor)]; Merck [Brain tumor (Pembrolizumab)]; Novartis
[Brain tumor (Trametanib, dabrafenib, BGJ398, INC208)]; Oncoceutics [Brain tumor (ONC201)]; Vascular
Biogenics [Brain tumor (VB111)]; Roche [Brain tumor (Bevacizumab)]; SanofiAventis [Brain tumor
(Plerixafor)]. Speaker's Bureau: Merck [Brain tumor]. Consultant/Advisory Boards: Agios [Brain tumor
(AG120)]; Astra Zeneca [Brain tumor]; Cavion [Brain tumor (Mibefridil)]; Cortice Biosciences [Brain tumor
(TP12887)]; Foundation Medicine [Brain tumor (none)]; Genentech/Roche [Brain tumor (Bevacizumab)];
Monteris [Brain tumor (Neuroblate)]; Novartis [Brain tumor (LDK298)]; Novogen [Brain tumor (GDC0084);
Regeneron [Brain tumor (PD1 antibodies)]; Vascular Biogenics [Brain tumor (VB111)]; VBI Vaccines [Brain
tumors]. April F Eichler, MD, MPH Equity Ownership/Stock Options: Johnson & Johnson [Dementia
(galantamine), Epilepsy (topiramate)].
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multilevel review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
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5/25/2017 Epidemiology, pathology, clinical features, and diagnosis of meningioma ­ UpToDate

Tumors of neuroepithelial tissue 29.9 6.62

Pilocytic astrocytoma 1.4 0.34

Diffuse astrocytoma 2.3 0.53

Anaplastic astrocytoma 1.7 0.38

Unique astrocytoma variants 0.3 0.07

Glioblastoma 15.1 3.20

Oligodendroglioma 1.1 0.25

Anaplastic oligodendroglioma 0.5 0.10

Oligoastrocytic tumors 0.9 0.20

Ependymal tumors 1.9 0.43

Glioma malignant, NOS 2.0 0.47

Choroid plexus 0.2 0.05

Other neuroepithelial tumors 0.03 0.01

Neuronal and mixed neuronal­glial tumors 1.2 0.28

Tumors of the pineal region 0.2 0.04

Embryonal tumors 1.1 0.26

Nerve sheath tumors 8.1 1.76

Meningioma 36.4 7.86

Mesenchymal tumors 0.4 0.08

Primary melanocytic lesions 0.04 0.01

Other neoplasms related to the meninges 0.8 0.18

Lymphoma 2.0 0.44

Other hematopoietic neoplasms 0.07 0.01

Germ cell tumors, cysts and heterotopias 0.4 0.10

Tumors of the pituitary 15.5 3.49

Craniopharyngioma 0.8 0.18

Chordoma/chondrosarcoma 156 0.1

Hemangioma 1.5 0.34

Neoplasm, unspecified 4.0 0.88

All other 0.03 0.01

TOTAL 365,858 100.0

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5/25/2017 Epidemiology, pathology, clinical features, and diagnosis of meningioma UpToDate

Neuronal and mixed neuronalglial tumors 1.2 0.28