ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Epidemiology, pathology, clinical features, and diagnosis of meningioma

Epidemiology, pathology, clinical features, and diagnosis of meningioma
Literature review current through: May 2024.
This topic last updated: Apr 23, 2024.

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 (CNS) can cause serious morbidity or mortality.

The epidemiology, pathology, clinical presentation, and diagnosis of meningiomas will be reviewed here. Other topics on meningioma include:

Treatment of World Health Organization (WHO) grade 1 (benign) meningiomas (see "Management of known or presumed benign (WHO grade 1) meningioma")

Treatment of WHO grade 2 and 3 meningiomas (see "Management of atypical and malignant (WHO grade 2 and 3) meningioma")

Systemic therapy for recurrent meningioma (see "Systemic treatment of recurrent meningioma")

EPIDEMIOLOGY — Meningiomas are the most common primary central nervous system (CNS) tumors and account for approximately one-third of all primary brain and spinal tumors [1,2].

According to the Central Brain Tumor Registry in the United States (CBTRUS), there are approximately 37,000 new cases of meningioma diagnosed yearly in the US [2]. The estimated annual incidence rate in the US is 9.7 per 100,000 population. The incidence rate varies by race, with Black Americans having a 1.2-fold higher incidence than White Americans [2].

The incidence of meningioma increases progressively with age, with a median age at diagnosis of 65 years. Meningiomas are rare in children [3], except in those with hereditary syndromes such as NF2-related schwannomatosis or antecedent therapeutic radiation therapy [4,5]. (See 'Risk factors' below.)

Meningiomas are more common in females, with a female-to-male ratio of approximately two or three to one [6,7]. For spinal meningiomas, which comprise approximately 10 percent of all meningiomas, the female-to-male ratio is even higher, approximately nine to one. This female predominance is highest in middle-aged adults (35 to 54 years) and less pronounced or absent in those with atypical or anaplastic meningiomas, children, and those with radiation-induced meningiomas.

Population-based studies estimate that 80 to 85 percent of meningiomas are World Health Organization (WHO) grade 1, approximately 15 to 18 percent are grade 2, and 1 to 3 percent are grade 3 [8]. Hospital-based studies, particularly from tertiary care centers, have reported a higher proportion of grade 2 and 3 tumors [9,10].

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 [11,12]. Radiation-induced meningiomas have a higher incidence of multiplicity and atypia compared with sporadic meningiomas (image 1). 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 (CNS) 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 CNS

Radiation therapy for tumors in the head and neck region

Prophylactic craniospinal irradiation to prevent 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. Long-term follow-up 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 [5,13-17]. In a cohort of over 4000 childhood cancer survivors exposed to cranial radiation, the cumulative risk of meningioma was 5.6 percent by age 40 years [15]. Cumulative incidence was highest among patients younger than five years at initial cancer diagnosis (10 percent); additional risk factors included female sex and increasing dose of radiation. A smaller study found a 12 percent cumulative incidence of meningioma by 40 years after exposure to cranial radiation in childhood [16].

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 [11,18].

Dental radiographs – Several studies have reported an increased risk of meningioma associated with frequent dental radiographs [19-24]. Across multiple studies, the reported risk has been highest for multiple radiograph examinations and childhood exposure, primarily in an era when the dose of dental radiographs was higher than with current technology [19,22,23,25]. Importantly, recall bias can influence associations found in case-control studies such as these, and validation of dental records was not performed in most of these studies [26].

Diagnostic head computed tomography (CT) – Childhood exposure to diagnostic head CTs may also be associated with an increased risk of brain tumors, including meningiomas [27,28]. (See "Radiation-related risks of imaging", section on 'Children and adolescents'.)

Atomic bomb exposure – An increased incidence of meningiomas has been observed in survivors of the atomic explosions in Japan [29,30]. 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 [31].

Genetic predisposition — A genetic predisposition to meningioma is best characterized in patients with NF2-related schwannomatosis (NF2) and other forms of schwannomatosis. Patients with multiple endocrine neoplasia type 1 (MEN1) also have an increased risk of meningioma, although at lower rates compared with neurofibromatosis [32]. (See "Multiple endocrine neoplasia type 1: Clinical manifestations and diagnosis", section on 'Other tumors'.)

NF2-related schwannomatosis — NF2-related schwannomatosis (NF2) is an autosomal dominant disorder predisposing to multiple tumors of the nervous system. This disorder is caused by mutations in the NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor (NF2) gene, a tumor suppressor gene on chromosome 22. (See "NF2-related schwannomatosis (formerly neurofibromatosis type 2)", section on 'Molecular pathogenesis'.)

Approximately one-half of individuals with NF2 have meningiomas, and multiple meningiomas are often present [33]. Most meningiomas are intracranial, although intradural, extramedullary spinal meningiomas are also seen. (See "NF2-related schwannomatosis (formerly 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 [34]. 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 [35,36].

Other schwannomatoses — Meningiomas are recognized as part of the phenotype of other forms of schwannomatosis in some patients. Patients with non-NF2-related 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 "Schwannomatoses related to genetic variants other than NF2", 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 females compared with males.

The female-to-male ratio is highest during the peak reproductive years and decreases in older adults.

Progesterone and androgen receptors are present in approximately two-thirds of meningiomas, while estrogen receptors have been identified in approximately 10 percent of cases [37-39].

Some, but not all, studies have 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 [40-44].

Exogenous estrogens and progestins — Multiple observational studies have explored a possible relationship between exogenous estrogen and progestin exposure (eg, menopausal hormone therapy or oral contraceptive use) and the risk of meningioma, with mixed results [1,40-47].

Menopausal hormone therapy – A meta-analysis of six prospective case-control studies that included over 1600 meningioma cases found that ever-use of hormone therapy was associated with a small but statistically significant increase in the risk of meningioma (relative risk [RR] 1.35, 95% CI 1.2-1.5) [47]. In studies that distinguished between estrogen-only versus combined estrogen-progestin 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.

Hormonal contraception – Combined estrogen-progestin oral contraceptives (COCs) have not been associated with excess risk. Prolonged use (≥1 year) of high-dose medroxyprogesterone acetate (depo medroxyprogesterone acetate [DMPA], also known as DepoProvera) may be associated with a small increase in risk compared with nonuse, although absolute event rates are very low (0.05 versus 0.01 percent) [48].

High-dose cyproterone — Cyproterone has both anti-androgenic and progestogenic properties. When used in high doses as an anti-androgen, it is associated with a 5- to 20-fold increase in the risk of meningioma with increasing cumulative doses (eg, ≥25 mg per day over several years) [48,49]. It is contraindicated in people with a history of meningioma and should be discontinued if meningioma is diagnosed [50]. (See "Management of known or presumed benign (WHO grade 1) meningioma", section on 'Patients with hormone exposure'.)

Cyproterone is not available in the United States but is used in Europe and elsewhere at high doses (eg, ≥25 mg per day) for conditions that include advanced prostate cancer, severe hypersexuality in males, hirsutism, and androgen suppression in transgender females. Based on a European Medicines Agency (EMA) safety committee review, the occurrence of both single and multiple meningiomas has been reported in association with cyproterone, primarily at doses of 25 mg/day and above [48,51]. The estimated incidence of meningioma with cumulative exposure to ≥3 g of cyproterone acetate is 24 per 100,000 person-years [49].

In a case-control study of >1000 resected cyproterone-associated meningiomas in France, the median age at presentation was lower compared with nonexposed resected meningioma cases (47 versus 61 years), and there was a predilection for middle skull base location (39 versus 23 percent) [52]. In a separate French study that included 210 patients exposed to cyproterone or one of two other progestins who underwent MRI screening, the rate of meningioma detection was 7 percent; seven of these patients (47 percent) had multiple meningiomas [53]. The most common tumor locations were convexity (62 percent), middle skull base (21 percent), and anterior skull base (16 percent).

Available data have not shown a risk of meningioma with the lower doses of cyproterone (1 to 2 mg in combination with ethinylestradiol or estradiol valerate) used for contraception, acne, and hirsutism. As a precaution, the EMA recommends avoiding cyproterone in people with a meningioma, even at these low doses [50].

Others

Breast cancer – A moderately increased risk of meningioma has been reported in females with breast cancer, and, conversely, an increase in the incidence of breast cancer has been observed in females with a history of meningioma [1,54,55]. The magnitude of risk is not well established. A meta-analysis of 13 observational studies estimated a nearly 10-fold increase in the prevalence of breast cancer in females with meningioma compared with prevalence in the general population (odds ratio 9.87, 95% CI 7.31-13.32), although heterogeneity among studies was high and possible publication bias was identified [55].

Whether the association is due to shared hormonal risk factors, other risk factors causing both diseases, or an underlying genetic predisposition is unclear [1]. Given shared risks, clinicians should emphasize the importance of breast cancer screening in females with meningioma. (See "Screening for breast cancer: Strategies and recommendations".)

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 [40,41,44,56-60]. 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 [61]. (See "Epidemiology and risk factors for esophageal cancer", section on 'Obesity and metabolic syndrome' and "Endometrial carcinoma: Epidemiology, risk factors, and prevention", section on 'Obesity' and "Factors that modify breast cancer risk in women", section on 'Weight and body fat in postmenopausal women' and "Epidemiology and risk factors for colorectal cancer", section on 'Obesity'.)

Head trauma – Several studies have analyzed the role of head trauma as an etiologic factor for brain tumors, with conflicting results [25,62-64]. Improved recall of a history of head trauma in patients with meningioma may have contributed to bias in some of these studies.

Cell phones – 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 follow-up is required [1]. (See "Risk factors for brain tumors", section on 'Cellular phones and radiofrequency fields'.)

PATHOLOGY

WHO classification — Meningiomas are classified according to the 2021 World Health Organization (WHO) Classification of Tumors of the Central Nervous System, which is based upon morphologic and molecular criteria [65-68]. The WHO classification recognizes three grades of meningioma, which can be assigned to 15 morphologic subtypes:

WHO grade 1 – Benign meningiomas (WHO grade 1) (picture 1 and image 2) span 13 subtypes. WHO grade 1 meningiomas do not meet any of the criteria for a higher-grade lesion based upon morphologic and molecular criteria. The treatment approach is the same for all of the subtypes of benign meningiomas.

WHO grade 2 – WHO grade 2 meningiomas include specific morphologic subtypes (clear cell and chordoid meningiomas), tumors with increased mitotic activity (4 to 19 mitoses per 10 high-powered fields) or brain invasion, and tumors with three or more of the following features: increased cellularity, small cells with a high nuclear-to-cytoplasmic ratio, prominent nucleoli, uninterrupted patternless or sheet-like growth, and foci of spontaneous or geographic necrosis (picture 1 and image 3).

WHO grade 3 – WHO grade 3 (malignant) meningiomas have ≥20 mitoses per 10 high-powered fields; malignant characteristics resembling carcinoma, sarcoma, or melanoma; or a high-risk molecular feature (telomerase reverse transcriptase [TERT] promoter mutation or homozygous cyclin-dependent kinase inhibitor 2A/B [CDKN2A/B] deletion) (picture 1 and image 4). (See 'Molecular risk stratification' below.)

The WHO classification system correlates with outcome and thus has a major impact on treatment planning. Patients with WHO grade 2 or grade 3 meningiomas are significantly more likely to have invasive disease, a local recurrence following the initial treatment, and, ultimately, a shorter overall survival compared with patients with a WHO grade 1 meningioma.

Overall reported rates of recurrence for patients with grade 1, 2, and 3 meningiomas are 7 to 25, 30 to 50, and 50 to 94 percent, respectively, in various series [69-73].

Although WHO grade 3 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 [74]. (See "Management of atypical and malignant (WHO grade 2 and 3) meningioma".)

Among grade 1 tumors, the presence of atypical features may also have prognostic importance, although data are more limited. In a study of 147 patients who underwent resection of a grade 1 meningioma, the five-year 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 [75].

Molecular risk stratification — A growing number of individual molecular genetic alterations have been identified that are associated with more aggressive biology and worse outcomes, including mutations in the TERT promoter region, CDKN2A/B deletion, and loss of trimethylation of lysine 27 of histone 3 (H3K27me3) [76-79].

TERT alterationsTERT gene alterations in particular have been associated with an aggressive clinical course. In a multicenter retrospective study of 677 patients with meningioma, the prevalence of TERT gene alterations was 5, 8, and 15 percent for WHO grade 1, 2, and 3 tumors, respectively [80]. Median recurrence-free and overall survival were 14 months and 4.8 years for TERT-mutated tumors, compared with 8.4 and 13.3 years for TERT-wildtype tumors. While this may be partially explained by the higher relative incidence of WHO grade 3 tumors in the TERT-mutated group, the adverse effect on survival appeared to be independent of WHO grade in a multivariable analysis.

CDKN2A/B deletion – In a study of 528 meningiomas, homozygous deletion of CDKN2A/B was identified exclusively in grade 2 (27 percent) and grade 3 tumors (73 percent) [81]. The median time to progression after surgery was substantially shorter in tumors carrying CDKN2A/B deletion (8 versus 101 months). Co-occurring TERT promoter mutations were present in three of six CDKN2A/B-deleted tumors that were tested for both alterations.

H3K27me3 loss – Loss of immunohistochemical staining for H3K27me3 is associated with increased risk for recurrence, especially in WHO grade 2 tumors [82-84]. In a large retrospective cohort of over 1100 meningiomas, H3K27me3 loss was observed in 3.1 percent of grade 1 tumors, 10.4 percent of grade 2 tumors, and 17.7 percent of grade 3 tumors [82]. On multivariate analysis, H3K27me3 loss was predictive of decreased recurrence-free survival (risk ratio [RR] 1.80), independent of sex, extent of resection, tumor grade, and proliferation index.

Classification of meningiomas into molecular groups by DNA and RNA profiling as well as the integration of molecular and morphologic features may also improve upon the prediction of biologic behavior and prognosis [85-88]. A three-tiered integrated grading scheme (Integrated Grades 1, 2, and 3) based on mitotic count, chromosomal copy-number data, and CDKN2A deletion status has been proposed, which more accurately predicts risk of recurrence than the WHO grading system [89]. Further validation is necessary, however, before this scheme can be used to guide treatment decisions.

Molecular pathogenesis — The best-characterized genetic alteration is loss of chromosome 22, which in many cases is associated with mutations in the NF2 gene located on the long arm of chromosome 22. (See 'NF2-related schwannomatosis' above.)

NF2 mutations are also present in approximately one-half of sporadic meningiomas, more commonly in those with transitional or fibroblastic histologic subtypes and in higher-grade tumors [90].

Genomic sequencing efforts have identified several oncogenic mutations in a small subset of non-NF2 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 v-akt murine thymoma viral oncogene homolog 1 (AKT1), an activator of the phosphatidylinositol 3-kinase (PI3K) pathway, were found in up to 13 percent of tumors [91,92]. Mutations in TRAF7, a proapoptotic ubiquitin ligase, were identified in approximately one-quarter of tumors in one study [92]. 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 [93].

Many of these mutations appear to be most prevalent in anterior skull base tumors. In a series of 62 anterior skull base meningiomas, SMO mutations were present in 7 tumors (11 percent), all but one of which were in the olfactory groove, and AKT1 mutations were present in 12 tumors (19 percent) [94]. Other studies suggest that PI3KA mutations also occur primarily in skull base tumors and might be overrepresented in progestin-exposed tumors [93,95].

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 [96].

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) [97]. 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 [98].

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 "Overview of the clinical features and diagnosis of brain tumors in adults", section on 'Clinical manifestations'.)

Asymptomatic tumors — Many meningiomas are asymptomatic or minimally symptomatic, and are discovered incidentally on a neuroimaging study or at autopsy [99-103]. Follow-up studies on patients with asymptomatic meningiomas suggest that most such tumors either remain the same size or grow slowly over prolonged periods [104,105].

In a systematic review and meta-analysis of incidental findings on brain magnetic resonance imaging (MRI) in nearly 20,000 children and adults, meningioma was the most common incidental tumor, identified on 0.29 percent of MRIs [106]. The prevalence of incidental findings, including meningioma, increases with age. In population-based studies of brain MRI in older adult volunteers (mean age 65 to 70 years), meningiomas are identified in approximately 2.5 percent of participants [107,108]. The most common locations are convexity (62 percent) and falx cerebri (15 percent) [107].

Seizures — Seizures are present preoperatively in approximately 30 percent of patients who are diagnosed with an intracranial meningioma [109]. The risk of seizure is higher in association with non-skull 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 so-called Foster-Kennedy 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 MRI and CT (table 2 and image 2).

On MRI, a typical meningioma is an extra-axial, dural-based mass that is isointense or hypointense to gray matter on T1-weighted images and isointense or hyperintense on proton density and T2-weighted images. A thin cerebrospinal fluid (CSF)-isointense rim ("CSF cleft") indicates the absence of tumor extension into the brain, and there is usually intense, homogeneous contrast enhancement after gadolinium administration (image 2). Many meningiomas show marginal dural thickening that tapers peripherally (the "dural tail" sign).

On noncontrast CT, the typical meningioma is a well-defined extra-axial mass that displaces normal brain. They are smooth in contour, adjacent to dural structures, and sometimes calcified or multilobulated (image 2 and image 3). Due to hypercellularity, psammomatous calcification, or both, meningiomas may be hyperdense compared with cortex. Involvement of adjacent bone (reactive hyperostosis, invasion, erosion) may occur in up to one-half of skull base meningiomas (image 2) [110].

Differentiating an atypical or malignant meningioma from a benign meningioma purely on the basis of neuroimaging is difficult. Features on MRI that may suggest the presence of a high-grade meningioma rather than a benign meningioma include the following [74,111-114]:

Absence of CSF-isointense cleft around tumor margin or frank invasion of brain parenchyma

Intratumoral cystic or necrotic change (image 4)

Extension of tumor through the skull base

Low apparent diffusion coefficient (ADC) values

Elevated relative cerebral blood volume on perfusion-weighted MRI

However, none of these neuroimaging findings are sufficiently sensitive or specific. 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 1) meningioma".)

18-F Fluorodeoxyglucose (FDG) positron emission tomography (PET) scanning has shown more intense uptake associated with higher-grade meningiomas in some, but not all, studies and is of limited diagnostic value [115]. Novel PET tracers, including specific somatostatin receptor ligands (eg, gallium Ga-68 DOTATATE), hold more promise for both diagnosis and treatment planning but are not yet widely available for clinical use [116-118].

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 1) 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 MRI or CT that may suggest meningioma (table 3). These include solitary fibrous tumor (image 5), dural metastasis (image 6) or lymphoma, gliosarcoma, plasmacytoma, and some inflammatory lesions such as sarcoidosis and granulomatosis with polyangiitis [97,116,119-121].

In general, MRI, CT, and 18-F fluorodeoxyglucose (FDG) 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, marked hypo- or hyperintensity on T2-weighted images, absence of a dural tail, destruction of adjacent bone, or brain or leptomeningeal invasion, may be a clue to an alternative etiology or to a higher-grade meningioma [122]. These and other clinical clues to rare alternative diagnoses are reviewed in the table (table 3).

DIAGNOSTIC EVALUATION — A definitive diagnosis of meningioma and classification as benign, atypical, or malignant (World Health Organization [WHO] grades 1, 2, and 3, 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 non-neoplastic 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. Radiation-induced 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 1) meningioma", section on 'Radiation-induced meningiomas'.)

The history should also probe for conditions that may cause dural-based pathology mimicking meningioma, including hematologic and nonhematologic malignancy and sarcoidosis (table 3). (See 'Differential diagnosis' above.)

Genetic syndromes predisposing to meningioma, such as NF2-related schwannomatosis (NF2) and other forms of 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 spontaneous mutations can 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 "NF2-related schwannomatosis (formerly neurofibromatosis type 2)", section on 'Clinical features' and "Schwannomatoses related to genetic variants other than NF2", 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 — MRI with contrast provides the most complete assessment of suspected meningiomas. Imaging protocols that focus on a specific region (eg, orbits, sella/pituitary, cerebellopontine angle) may help to adequately image small meningiomas [123]. CT may also be of value to define adjacent hyperostosis or tumoral calcification. (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 (image 7) to look for intracranial masses that may suggest either a tumor predisposition syndrome or an alternative diagnosis.

We obtain cancer staging (eg, chest, abdomen, and pelvis CT) in patients with known cancer but do not routinely obtain these tests in otherwise healthy adults who have undergone age-appropriate 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 AND RECOMMENDATIONS

Epidemiology – Meningiomas account for approximately one-third of primary central nervous system (CNS) tumors, occurring primarily in older individuals with a female predominance (table 1). (See 'Epidemiology' above.)

Etiology – 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 NF2-related schwannomatosis, and somatic mutations in the NF2 gene may also contribute to the development of sporadic meningiomas. (See 'Risk factors' above and 'Molecular pathogenesis' above.)

Pathology – Meningiomas are classified according to the World Health Organization (WHO) grading system. WHO grade 1 lesions are benign and generally have a favorable prognosis, while atypical (grade 2) and malignant (grade 3) meningiomas are substantially more likely to recur. (See 'WHO classification' above.)

Location – Meningiomas can arise anywhere from the dura, most commonly within the skull (image 2). Approximately 10 percent arise in the spinal cord (image 7). (See 'Clinical presentation' above.)

Clinical presentation – Many meningiomas are slow growing and discovered incidentally on a neuroimaging study. These may be asymptomatic or minimally symptomatic. Symptoms of large tumors can vary widely, depending upon by the location of the mass. (See 'Clinical presentation' above.)

Imaging – On MRI, a typical meningioma is an extra-axial, dural-based 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 (image 2). (See 'Neuroimaging' above.)

Differential diagnosis – The differential diagnosis of meningioma includes a wide range of neoplastic and non-neoplastic entities (table 3). However, these are rare and almost always diagnosed after tissue is obtained, due to their clinical and radiographic similarity to meningiomas (image 5). (See 'Differential diagnosis' above.)

Diagnosis – A definitive diagnosis of meningioma and classification as benign, atypical, or malignant requires histologic confirmation at the time of biopsy or surgery. For small and minimally symptomatic tumors, the diagnosis is based on characteristic imaging findings. (See 'Diagnostic evaluation' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Peter Black, MD, PhD, who contributed to an earlier version of this topic review.

  1. Wiemels J, Wrensch M, Claus EB. Epidemiology and etiology of meningioma. J Neurooncol 2010; 99:307.
  2. Ostrom QT, Price M, Neff C, et al. CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2016-2020. Neuro Oncol 2023; 25:iv1.
  3. Liu Y, Li F, Zhu S, et al. Clinical features and treatment of meningiomas in children: report of 12 cases and literature review. Pediatr Neurosurg 2008; 44:112.
  4. Marosi C, Hassler M, Roessler K, et al. Meningioma. Crit Rev Oncol Hematol 2008; 67:153.
  5. Banerjee J, Pääkkö E, Harila M, et al. Radiation-induced meningiomas: a shadow in the success story of childhood leukemia. Neuro Oncol 2009; 11:543.
  6. Claus EB, Bondy ML, Schildkraut JM, et al. Epidemiology of intracranial meningioma. Neurosurgery 2005; 57:1088.
  7. Cao J, Yan W, Li G, et al. Incidence and survival of benign, borderline, and malignant meningioma patients in the United States from 2004 to 2018. Int J Cancer 2022; 151:1874.
  8. Ostrom QT, Gittleman H, Truitt G, et al. CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2011-2015. Neuro Oncol 2018; 20 Suppl 4:iv1.
  9. Willis J, Smith C, Ironside JW, et al. The accuracy of meningioma grading: a 10-year retrospective audit. Neuropathol Appl Neurobiol 2005; 31:141.
  10. Pearson BE, Markert JM, Fisher WS, et al. Hitting a moving target: evolution of a treatment paradigm for atypical meningiomas amid changing diagnostic criteria. Neurosurg Focus 2008; 24:E3.
  11. Umansky F, Shoshan Y, Rosenthal G, et al. Radiation-induced meningioma. Neurosurg Focus 2008; 24:E7.
  12. Braganza MZ, Kitahara CM, Berrington de González A, et al. Ionizing radiation and the risk of brain and central nervous system tumors: A systematic review. Neuro Oncol 2012; 14:1316.
  13. Friedman DL, Whitton J, Leisenring W, et al. Subsequent neoplasms in 5-year survivors of childhood cancer: the Childhood Cancer Survivor Study. J Natl Cancer Inst 2010; 102:1083.
  14. Taylor AJ, Little MP, Winter DL, et al. Population-based risks of CNS tumors in survivors of childhood cancer: the British Childhood Cancer Survivor Study. J Clin Oncol 2010; 28:5287.
  15. Bowers DC, Moskowitz CS, Chou JF, et al. Morbidity and Mortality Associated With Meningioma After Cranial Radiotherapy: A Report From the Childhood Cancer Survivor Study. J Clin Oncol 2017; 35:1570.
  16. Kok JL, Teepen JC, van Leeuwen FE, et al. Risk of benign meningioma after childhood cancer in the DCOG-LATER cohort: contributions of radiation dose, exposed cranial volume, and age. Neuro Oncol 2019; 21:392.
  17. Withrow DR, Anderson H, Armstrong GT, et al. Pooled Analysis of Meningioma Risk Following Treatment for Childhood Cancer. JAMA Oncol 2022; 8:1756.
  18. Ron E, Modan B, Boice JD Jr, et al. Tumors of the brain and nervous system after radiotherapy in childhood. N Engl J Med 1988; 319:1033.
  19. Preston-Martin S, Yu MC, Henderson BE, Roberts C. Risk factors for meningiomas in men in Los Angeles County. J Natl Cancer Inst 1983; 70:863.
  20. Preston-Martin S, Mack W, Henderson BE. Risk factors for gliomas and meningiomas in males in Los Angeles County. Cancer Res 1989; 49:6137.
  21. Ryan P, Lee MW, North B, McMichael AJ. Amalgam fillings, diagnostic dental x-rays and tumours of the brain and meninges. Eur J Cancer B Oral Oncol 1992; 28B:91.
  22. Longstreth WT Jr, Phillips LE, Drangsholt M, et al. Dental X-rays and the risk of intracranial meningioma: a population-based case-control study. Cancer 2004; 100:1026.
  23. Claus EB, Calvocoressi L, Bondy ML, et al. Dental x-rays and risk of meningioma. Cancer 2012; 118:4530.
  24. Lin MC, Lee CF, Lin CL, et al. Dental diagnostic X-ray exposure and risk of benign and malignant brain tumors. Ann Oncol 2013; 24:1675.
  25. Preston-Martin S, Paganini-Hill A, Henderson BE, et al. Case-control study of intracranial meningiomas in women in Los Angeles County, California. J Natl Cancer Inst 1980; 65:67.
  26. Calnon WR. Shortcomings of study on dental x-rays and risk of meningioma. Cancer 2013; 119:464.
  27. Pearce MS, Salotti JA, Little MP, et al. Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study. Lancet 2012; 380:499.
  28. Davis F, Il'yasova D, Rankin K, et al. Medical diagnostic radiation exposures and risk of gliomas. Radiat Res 2011; 175:790.
  29. Grant IS. Necrotising fasciitis. Lancet 1994; 344:1770.
  30. Plyusnin A, Vapalahti O, Vasilenko V, et al. Dobrava hantavirus in Estonia: does the virus exist throughout Europe? Lancet 1997; 349:1369.
  31. Preston DL, Ron E, Yonehara S, et al. Tumors of the nervous system and pituitary gland associated with atomic bomb radiation exposure. J Natl Cancer Inst 2002; 94:1555.
  32. Asgharian B, Chen YJ, Patronas NJ, et al. Meningiomas may be a component tumor of multiple endocrine neoplasia type 1. Clin Cancer Res 2004; 10:869.
  33. Goutagny S, Kalamarides M. Meningiomas and neurofibromatosis. J Neurooncol 2010; 99:341.
  34. Evans DG, Huson SM, Donnai D, et al. A clinical study of type 2 neurofibromatosis. Q J Med 1992; 84:603.
  35. Perry A, Giannini C, Raghavan R, et al. Aggressive phenotypic and genotypic features in pediatric and NF2-associated meningiomas: a clinicopathologic study of 53 cases. J Neuropathol Exp Neurol 2001; 60:994.
  36. Larson JJ, van Loveren HR, Balko MG, Tew JM Jr. Evidence of meningioma infiltration into cranial nerves: clinical implications for cavernous sinus meningiomas. J Neurosurg 1995; 83:596.
  37. Carroll RS, Zhang J, Dashner K, et al. Androgen receptor expression in meningiomas. J Neurosurg 1995; 82:453.
  38. Blankenstein MA, Verheijen FM, Jacobs JM, et al. Occurrence, regulation, and significance of progesterone receptors in human meningioma. Steroids 2000; 65:795.
  39. Carroll RS, Zhang J, Black PM. Expression of estrogen receptors alpha and beta in human meningiomas. J Neurooncol 1999; 42:109.
  40. Jhawar BS, Fuchs CS, Colditz GA, Stampfer MJ. Sex steroid hormone exposures and risk for meningioma. J Neurosurg 2003; 99:848.
  41. Benson VS, Pirie K, Green J, et al. Lifestyle factors and primary glioma and meningioma tumours in the Million Women Study cohort. Br J Cancer 2008; 99:185.
  42. Lee E, Grutsch J, Persky V, et al. Association of meningioma with reproductive factors. Int J Cancer 2006; 119:1152.
  43. Claus EB, Calvocoressi L, Bondy ML, et al. Exogenous hormone use, reproductive factors, and risk of intracranial meningioma in females. J Neurosurg 2013; 118:649.
  44. Muskens IS, Wu AH, Porcel J, et al. Body mass index, comorbidities, and hormonal factors in relation to meningioma in an ethnically diverse population: the Multiethnic Cohort. Neuro Oncol 2019; 21:498.
  45. Wigertz A, Lönn S, Mathiesen T, et al. Risk of brain tumors associated with exposure to exogenous female sex hormones. Am J Epidemiol 2006; 164:629.
  46. Blitshteyn S, Crook JE, Jaeckle KA. Is there an association between meningioma and hormone replacement therapy? J Clin Oncol 2008; 26:279.
  47. Benson VS, Kirichek O, Beral V, Green J. Menopausal hormone therapy and central nervous system tumor risk: large UK prospective study and meta-analysis. Int J Cancer 2015; 136:2369.
  48. Roland N, Neumann A, Hoisnard L, et al. Use of progestogens and the risk of intracranial meningioma: national case-control study. BMJ 2024; 384:e078078.
  49. Weill A, Nguyen P, Labidi M, et al. Use of high dose cyproterone acetate and risk of intracranial meningioma in women: cohort study. BMJ 2021; 372:n37.
  50. Cyproterone-containing medicinal products: Restrictions in use of cyproterone due to meningioma risk. European Medicines Agency. Available at: https://www.ema.europa.eu/en/medicines/human/referrals/cyproterone-containing-medicinal-products (Accessed on March 30, 2021).
  51. Restrictions in use of cyproterone due to meningioma risk. EMA/14775/2020. European Medicines Agency. Available at: https://www.ema.europa.eu/en/documents/referral/cyproterone-article-31-referral-restrictions-use-cyproterone-due-meningioma-risk_en-0.pdf (Accessed on March 30, 2021).
  52. Champeaux-Depond C, Weller J, Froelich S, Sartor A. Cyproterone acetate and meningioma: a nationwide-wide population based study. J Neurooncol 2021; 151:331.
  53. Samoyeau T, Provost C, Roux A, et al. Meningioma in patients exposed to progestin drugs: results from a real-life screening program. J Neurooncol 2022; 160:127.
  54. Custer BS, Koepsell TD, Mueller BA. The association between breast carcinoma and meningioma in women. Cancer 2002; 94:1626.
  55. Degeneffe A, De Maertelaer V, De Witte O, Lefranc F. The Association Between Meningioma and Breast Cancer: A Systematic Review and Meta-analysis. JAMA Netw Open 2023; 6:e2318620.
  56. Johnson DR, Olson JE, Vierkant RA, et al. Risk factors for meningioma in postmenopausal women: results from the Iowa Women's Health Study. Neuro Oncol 2011; 13:1011.
  57. Michaud DS, Bové G, Gallo V, et al. Anthropometric measures, physical activity, and risk of glioma and meningioma in a large prospective cohort study. Cancer Prev Res (Phila) 2011; 4:1385.
  58. Wiedmann M, Brunborg C, Lindemann K, et al. Body mass index and the risk of meningioma, glioma and schwannoma in a large prospective cohort study (The HUNT Study). Br J Cancer 2013; 109:289.
  59. Schildkraut JM, Calvocoressi L, Wang F, et al. Endogenous and exogenous hormone exposure and the risk of meningioma in men. J Neurosurg 2014; 120:820.
  60. Niedermaier T, Behrens G, Schmid D, et al. Body mass index, physical activity, and risk of adult meningioma and glioma: A meta-analysis. Neurology 2015; 85:1342.
  61. Lauby-Secretan B, Scoccianti C, Loomis D, et al. Body Fatness and Cancer--Viewpoint of the IARC Working Group. N Engl J Med 2016; 375:794.
  62. Preston-Martin S, Pogoda JM, Schlehofer B, et al. An international case-control study of adult glioma and meningioma: the role of head trauma. Int J Epidemiol 1998; 27:579.
  63. Inskip PD, Mellemkjaer L, Gridley G, Olsen JH. Incidence of intracranial tumors following hospitalization for head injuries (Denmark). Cancer Causes Control 1998; 9:109.
  64. Preston-Martin S, Henderson BE, Yu MC. Epidemiology of intracranial meningiomas: Los Angeles Country, California. Neuroepidemiology 1983; 2:164.
  65. Louis DN, Perry A, Reifenberger G, et al. The 2016 World Health Organization Classification of Tumors of the Central Nervous System: A summary. Acta Neuropathol 2016; 131:803.
  66. WHO Classification of Tumours of the Central Nervous System, 4th ed, Louis DN, Ohgaki H, Wiestler OD, Cavenee WK (Eds), International Agency for Research on Cancer, 2016.
  67. Louis DN, Perry A, Wesseling P, et al. The 2021 WHO Classification of Tumors of the Central Nervous System: a summary. Neuro Oncol 2021; 23:1231.
  68. Central Nervous System Tumours, 5th ed, WHO Classification of Tumours Editorial Board (Ed), International Agency for Research on Cancer, 2021.
  69. 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. p.164.
  70. Yang SY, Park CK, Park SH, et al. Atypical and anaplastic meningiomas: prognostic implications of clinicopathological features. J Neurol Neurosurg Psychiatry 2008; 79:574.
  71. Pasquier D, Bijmolt S, Veninga T, et al. Atypical and malignant meningioma: outcome and prognostic factors in 119 irradiated patients. A multicenter, retrospective study of the Rare Cancer Network. Int J Radiat Oncol Biol Phys 2008; 71:1388.
  72. Palma L, Celli P, Franco C, et al. Long-term prognosis for atypical and malignant meningiomas: a study of 71 surgical cases. J Neurosurg 1997; 86:793.
  73. Perry A, Scheithauer BW, Stafford SL, et al. "Malignancy" in meningiomas: a clinicopathologic study of 116 patients, with grading implications. Cancer 1999; 85:2046.
  74. Hanft S, Canoll P, Bruce JN. A review of malignant meningiomas: diagnosis, characteristics, and treatment. J Neurooncol 2010; 99:433.
  75. Marciscano AE, Stemmer-Rachamimov AO, Niemierko A, et al. Benign meningiomas (WHO Grade I) with atypical histological features: correlation of histopathological features with clinical outcomes. J Neurosurg 2016; 124:106.
  76. Juratli TA, McCabe D, Nayyar N, et al. DMD genomic deletions characterize a subset of progressive/higher-grade meningiomas with poor outcome. Acta Neuropathol 2018; 136:779.
  77. Sahm F, Schrimpf D, Olar A, et al. TERT Promoter Mutations and Risk of Recurrence in Meningioma. J Natl Cancer Inst 2016; 108.
  78. Goutagny S, Nault JC, Mallet M, et al. High incidence of activating TERT promoter mutations in meningiomas undergoing malignant progression. Brain Pathol 2014; 24:184.
  79. Juratli TA, Thiede C, Koerner MVA, et al. Intratumoral heterogeneity and TERT promoter mutations in progressive/higher-grade meningiomas. Oncotarget 2017; 8:109228.
  80. Mirian C, Duun-Henriksen AK, Juratli T, et al. Poor prognosis associated with TERT gene alterations in meningioma is independent of the WHO classification: an individual patient data meta-analysis. J Neurol Neurosurg Psychiatry 2020; 91:378.
  81. Sievers P, Hielscher T, Schrimpf D, et al. CDKN2A/B homozygous deletion is associated with early recurrence in meningiomas. Acta Neuropathol 2020; 140:409.
  82. Behling F, Fodi C, Gepfner-Tuma I, et al. H3K27me3 loss indicates an increased risk of recurrence in the Tübingen meningioma cohort. Neuro Oncol 2021; 23:1273.
  83. Nassiri F, Wang JZ, Singh O, et al. Loss of H3K27me3 in meningiomas. Neuro Oncol 2021; 23:1282.
  84. Katz LM, Hielscher T, Liechty B, et al. Loss of histone H3K27me3 identifies a subset of meningiomas with increased risk of recurrence. Acta Neuropathol 2018; 135:955.
  85. Sahm F, Schrimpf D, Stichel D, et al. DNA methylation-based classification and grading system for meningioma: a multicentre, retrospective analysis. Lancet Oncol 2017; 18:682.
  86. Nassiri F, Mamatjan Y, Suppiah S, et al. DNA methylation profiling to predict recurrence risk in meningioma: development and validation of a nomogram to optimize clinical management. Neuro Oncol 2019; 21:901.
  87. Nassiri F, Liu J, Patil V, et al. A clinically applicable integrative molecular classification of meningiomas. Nature 2021; 597:119.
  88. Maas SLN, Stichel D, Hielscher T, et al. Integrated Molecular-Morphologic Meningioma Classification: A Multicenter Retrospective Analysis, Retrospectively and Prospectively Validated. J Clin Oncol 2021; 39:3839.
  89. Driver J, Hoffman SE, Tavakol S, et al. A molecularly integrated grade for meningioma. Neuro Oncol 2022; 24:796.
  90. Choy W, Kim W, Nagasawa D, et al. The molecular genetics and tumor pathogenesis of meningiomas and the future directions of meningioma treatments. Neurosurg Focus 2011; 30:E6.
  91. Brastianos PK, Horowitz PM, Santagata S, et al. Genomic sequencing of meningiomas identifies oncogenic SMO and AKT1 mutations. Nat Genet 2013; 45:285.
  92. Clark VE, Erson-Omay EZ, Serin A, et al. Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO. Science 2013; 339:1077.
  93. Abedalthagafi M, Bi WL, Aizer AA, et al. Oncogenic PI3K mutations are as common as AKT1 and SMO mutations in meningioma. Neuro Oncol 2016; 18:649.
  94. Strickland MR, Gill CM, Nayyar N, et al. Targeted sequencing of SMO and AKT1 in anterior skull base meningiomas. J Neurosurg 2017; 127:438.
  95. Peyre M, Gaillard S, de Marcellus C, et al. Progestin-associated shift of meningioma mutational landscape. Ann Oncol 2018; 29:681.
  96. Pachow D, Andrae N, Kliese N, et al. mTORC1 inhibitors suppress meningioma growth in mouse models. Clin Cancer Res 2013; 19:1180.
  97. Whittle IR, Smith C, Navoo P, Collie D. Meningiomas. Lancet 2004; 363:1535.
  98. Mattox A, Hughes B, Oleson J, et al. Treatment recommendations for primary extradural meningiomas. Cancer 2011; 117:24.
  99. Vernooij MW, Ikram MA, Tanghe HL, et al. Incidental findings on brain MRI in the general population. N Engl J Med 2007; 357:1821.
  100. Annegers JF, Schoenberg BS, Okazaki H, Kurland LT. Epidemiologic study of primary intracranial neoplasms. Arch Neurol 1981; 38:217.
  101. Nakasu S, Hirano A, Shimura T, Llena JF. Incidental meningiomas in autopsy study. Surg Neurol 1987; 27:319.
  102. Islim AI, Mohan M, Moon RDC, et al. Incidental intracranial meningiomas: a systematic review and meta-analysis of prognostic factors and outcomes. J Neurooncol 2019; 142:211.
  103. Cleary JO, Yeung J, McMeekin H, et al. The significance of incidental brain uptake on 68Ga-DOTATATE PET-CT in neuroendocrine tumour patients. Nucl Med Commun 2016; 37:1197.
  104. Niiro M, Yatsushiro K, Nakamura K, et al. Natural history of elderly patients with asymptomatic meningiomas. J Neurol Neurosurg Psychiatry 2000; 68:25.
  105. Go RS, Taylor BV, Kimmel DW. The natural history of asymptomatic meningiomas in Olmsted County, Minnesota. Neurology 1998; 51:1718.
  106. Morris Z, Whiteley WN, Longstreth WT Jr, et al. Incidental findings on brain magnetic resonance imaging: systematic review and meta-analysis. BMJ 2009; 339:b3016.
  107. Bos D, Poels MM, Adams HH, et al. Prevalence, Clinical Management, and Natural Course of Incidental Findings on Brain MR Images: The Population-based Rotterdam Scan Study. Radiology 2016; 281:507.
  108. Cerhan JH, Butts AM, Syrjanen JA, et al. Factors Associated With Meningioma Detected in a Population-Based Sample. Mayo Clin Proc 2019; 94:254.
  109. Englot DJ, Magill ST, Han SJ, et al. Seizures in supratentorial meningioma: a systematic review and meta-analysis. J Neurosurg 2016; 124:1552.
  110. Pieper DR, Al-Mefty O, Hanada Y, Buechner D. Hyperostosis associated with meningioma of the cranial base: secondary changes or tumor invasion. Neurosurgery 1999; 44:742.
  111. Hsu CC, Pai CY, Kao HW, et al. Do aggressive imaging features correlate with advanced histopathological grade in meningiomas? J Clin Neurosci 2010; 17:584.
  112. Zhang H, Rödiger LA, Shen T, et al. Perfusion MR imaging for differentiation of benign and malignant meningiomas. Neuroradiology 2008; 50:525.
  113. Nagar VA, Ye JR, Ng WH, et al. Diffusion-weighted MR imaging: diagnosing atypical or malignant meningiomas and detecting tumor dedifferentiation. AJNR Am J Neuroradiol 2008; 29:1147.
  114. Hwang WL, Marciscano AE, Niemierko A, et al. Imaging and extent of surgical resection predict risk of meningioma recurrence better than WHO histopathological grade. Neuro Oncol 2016; 18:863.
  115. Rogers L, Gilbert M, Vogelbaum MA. Intracranial meningiomas of atypical (WHO grade II) histology. J Neurooncol 2010; 99:393.
  116. Nowosielski M, Galldiks N, Iglseder S, et al. Diagnostic challenges in meningioma. Neuro Oncol 2017; 19:1588.
  117. Galldiks N, Albert NL, Sommerauer M, et al. PET imaging in patients with meningioma-report of the RANO/PET Group. Neuro Oncol 2017; 19:1576.
  118. Perlow HK, Nalin AP, Handley D, et al. A Prospective Registry Study of 68Ga-DOTATATE PET/CT Incorporation Into Treatment Planning of Intracranial Meningiomas. Int J Radiat Oncol Biol Phys 2024; 118:979.
  119. Johnson MD, Powell SZ, Boyer PJ, et al. Dural lesions mimicking meningiomas. Hum Pathol 2002; 33:1211.
  120. Tu PH, Giannini C, Judkins AR, et al. Clinicopathologic and genetic profile of intracranial marginal zone lymphoma: A primary low-grade CNS lymphoma that mimics meningioma. J Clin Oncol 2005; 23:5718.
  121. Tan LA, Kasliwal MK, Wewel J, et al. Neurosarcoidosis mimicking bilateral posterior fossa tentorial meningiomas. J Neurooncol 2015; 125:435.
  122. Starr CJ, Cha S. Meningioma mimics: five key imaging features to differentiate them from meningiomas. Clin Radiol 2017; 72:722.
  123. Kahraman-Koytak P, Bruce BB, Peragallo JH, et al. Diagnostic Errors in Initial Misdiagnosis of Optic Nerve Sheath Meningiomas. JAMA Neurol 2019; 76:326.
Topic 5220 Version 48.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟