Meningioma is the most common extra-axial intracranial tumor, originating from arachnoid cap cells. It constitutes approximately 37% of all primary intracranial tumors. The vast majority are WHO grade 1 (benign), with a 2-3 times higher incidence in women compared to men. Typical locations include the parasagittal region, convexity, sphenoid wing, olfactory groove, tuberculum sellae, and cerebellopontine angle. They are generally slow-growing, well-circumscribed tumors, and many are discovered incidentally.
Age Range
40-70
Peak Age
55
Gender
Female predominant
Prevalence
Very Common
Meningioma is a generally slow-growing extra-axial tumor arising from cap cells of arachnoid villi. The tumor is supplied by dural blood vessels and develops a broad-based dural attachment as it grows; this manifests on MRI as the characteristic 'dural tail sign' — representing reactive dural thickening and/or tumoral infiltration. The CSF cleft between tumor and brain is the most reliable indicator of extra-axial location, demonstrating intact pia mater. Meningiomas are fibrovascular in nature, and the dense vascular network leads to homogeneous contrast enhancement. Calcification in the form of psammoma bodies is common. Pressure effect on bone may cause hyperostosis (reactive bone thickening) or bone invasion. Progesterone receptor positivity explains the female predominance and accelerated growth during pregnancy.
Linear dural contrast enhancement that tapers conically in both directions from the tumor's dural attachment margin on T1 post-contrast sequences. Enhancement decreases and disappears with increasing distance from the tumor base. While highly characteristic of meningioma, it is not pathognomonic — it can also be seen in dural metastasis, lymphoma, and granulomatous diseases. Histopathologically, the dural tail represents reactive fibrovascular dural thickening and/or neoplastic infiltration. The possibility of neoplastic infiltration along the dural tail should be considered in surgical planning.
On non-contrast CT, an isodense to slightly hyperdense extra-axial mass is observed relative to brain parenchyma. The hyperdense appearance is due to high cellularity and calcification. Psammomatous calcification is detected in 20-25% of cases, showing scattered, punctate, or coarse calcification patterns. Hyperostosis (reactive bone thickening) of adjacent bone is common, especially in convexity and sphenoid wing meningiomas. Bone destruction suggests atypical/malignant meningioma. Peritumoral edema is variable, depending on size and location.
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An isodense to slightly hyperdense extra-axial mass measuring approximately _x_x_ cm is identified in the right/left ___ region with broad-based dural attachment, containing foci of calcification.
Contrast-enhanced CT demonstrates intense, homogeneous enhancement. Homogeneous enhancement is the most typical contrast pattern of meningioma. Heterogeneous enhancement suggests cystic degeneration, necrosis, or suspicion of higher grade. The dural tail sign may be visible on contrast-enhanced CT but is more conspicuous on MRI. The intensity of enhancement reflects the tumor's rich vascular structure.
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On contrast-enhanced series, the mass demonstrates intense, homogeneous enhancement. Tapering dural enhancement (dural tail sign) is present at the lesion margins.
On T1-weighted sequences, an isointense extra-axial mass relative to gray matter is observed. The T1 hypointense CSF cleft between tumor and brain parenchyma is the most reliable indicator of extra-axial location. The mass has broad-based dural attachment and displaces adjacent cortical gray matter inward (buckling sign). On T1 post-contrast sequences, intense homogeneous enhancement with prominent dural tail sign is observed.
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On T1-weighted sequences, an isointense extra-axial mass is observed relative to gray matter with CSF cleft between tumor and brain parenchyma. Post-contrast T1 sequences demonstrate intense homogeneous enhancement and dural tail sign.
On T2-weighted sequences, meningioma generally appears iso-to-hyperintense relative to gray matter. T2 signal intensity correlates with histological subtype: meningothelial type is generally hyperintense, fibroblastic and transitional types are isointense, and calcified psammomatous type appears hypointense. The CSF cleft is prominently visible as hyperintense on T2, confirming extra-axial location. Peritumoral vasogenic edema is variable; it may be more prominent in parasagittal and convexity meningiomas. Secretory meningiomas are characterized by marked peritumoral edema.
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On T2-weighted sequences, the mass demonstrates iso/hyperintense signal relative to gray matter with hyperintense CSF cleft between tumor and brain parenchyma.
On FLAIR sequences, meningioma generally appears mildly hyperintense relative to gray matter. The CSF cleft is suppressed on FLAIR (CSF signal eliminated) but the tumor-brain interface is clearly evaluated. Peritumoral vasogenic edema is detected more conspicuously on FLAIR than T2 — especially cortical surface edema may be masked on T2 due to adjacency to CSF. FLAIR is also useful for evaluating the dural tail sign. Intratumoral cystic components may not be suppressed on FLAIR (due to proteinaceous content), allowing differentiation from simple CSF.
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On FLAIR sequences, the mass demonstrates mildly hyperintense signal with vasogenic edema in the surrounding parenchyma.
Diffusion restriction in meningiomas is variable and correlates with histological subtype. Typical WHO grade 1 meningiomas generally do not show restricted diffusion (ADC normal or slightly elevated). Atypical (grade 2) and anaplastic (grade 3) meningiomas may show restricted diffusion due to increased cellularity (low ADC). ADC values are inversely proportional to tumor grade — low ADC indicates higher grade risk. Mean ADC values: grade 1 ≈ 0.9-1.1, grade 2 ≈ 0.7-0.9, grade 3 ≈ 0.6-0.8 x10⁻³ mm²/s. DWI also aids in meningioma-schwannoma differential diagnosis.
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On DWI, the mass shows no significant/significant diffusion restriction with ADC values of ___ x10⁻³ mm²/s.
On perfusion MRI, meningiomas generally show elevated rCBV, but values vary over a wide range. Richly vascular angiomatous meningiomas show very high rCBV, while fibroblastic type may show low rCBV. Meningioma perfusion curve characteristically shows a 'non-return' pattern — lacking blood-brain barrier as a dural tumor, contrast continuously leaks into tumor interstitium. This pattern is valuable for differentiation from intra-axial tumors. Normal peritumoral rCBV (non-infiltrative tumor) is critical for differentiation from GBM.
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Perfusion MRI demonstrates elevated rCBV in the mass with a non-return perfusion curve pattern consistent with extra-axial tumor.
The most characteristic finding on MR spectroscopy for meningioma is the alanine (Ala) peak — a doublet peak at 1.47 ppm that inverts on PRESS sequence. Alanine is a highly specific metabolite for meningioma, rarely detected in other brain tumors. Additionally, elevated choline (cell membrane turnover) and absent NAA (non-neuronal tumor) are observed. Glutamate/glutamine complex may also be elevated. Creatine is generally low. Lipid-lactate peak may be seen in some meningiomas and can suggest higher grade.
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MR spectroscopy demonstrates alanine peak at 1.47 ppm, elevated choline, and absent NAA in the mass, consistent with meningioma.
On SWI sequences, susceptibility foci related to calcification may be observed within the meningioma — as punctate or coarse hypointense areas. Dilated tumor vascular structures (flow voids) appear as prominent hypointense linear structures on SWI. Diffuse calcification in psammomatous type meningioma creates marked susceptibility artifact on SWI. SWI also demonstrates displacement of perilesional cortical veins, supporting extra-axial location. Phase information aids in differentiating calcification from hemosiderin.
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On SWI sequences, susceptibility foci related to calcification and dilated vascular structures are observed within the mass.
Criteria
Most common subtype. Lobular architecture, indistinct intercellular borders, whorl formation, psammoma bodies. Characterized by cellular uniformity.
Distinct Features
Generally T2 hyperintense on MRI (high cellular water content), intense homogeneous enhancement, minimal peritumoral edema. Elevated rCBV on perfusion MRI.
Criteria
Characterized by fibroblast-like cell structure with dense collagen and reticulin fibers. Whorl formation shows fibroblastic variations.
Distinct Features
On MRI, T2 isointense-to-hypointense (dense collagen content shortens T2 time), homogeneous enhancement, ADC values may be lower compared to meningothelial type. Calcification more common on CT.
Criteria
Increased mitotic activity (≥4 mitoses/10 HPF) and/or at least 3 atypical features: increased cellularity, small cells, prominent nucleoli, sheeting growth, areas of necrosis. Brain invasion alone qualifies for grade 2.
Distinct Features
On MRI, irregular margins, heterogeneous enhancement, areas of necrosis, restricted diffusion (low ADC), marked peritumoral edema, mushroom-shaped growth pattern. High recurrence risk (30-40%).
Criteria
Markedly increased mitotic activity (≥20 mitoses/10 HPF) and/or carcinoma, sarcoma, or melanoma-like histology. Characterized by aggressive biological behavior.
Distinct Features
On MRI, marked heterogeneous enhancement, extensive necrosis, irregular margins, brain parenchyma invasion, marked restricted diffusion (lowest ADC values), mushroom-shaped aggressive growth. Median recurrence time <2 years.
Distinguishing Feature
Schwannoma: 'ice cream cone' mass widening internal auditory canal at CPA, heterogeneous enhancement, T2 hyperintense. Meningioma: broad-based dural attachment, dural tail sign, homogeneous enhancement, no IAC widening.
Distinguishing Feature
Dural metastasis: known primary malignancy history, multiple dural lesions, bone destruction (hyperostosis in meningioma), irregular enhancement, rapid growth. Meningioma: slow growth, homogeneous enhancement, hyperostosis, dural tail.
Distinguishing Feature
Primary CNS lymphoma (dural form): markedly restricted diffusion (very low ADC), low rCBV, shrinkage with steroids, homogeneous enhancement. Meningioma: variable diffusion, alanine peak on MRS, hyperostosis, no steroid response.
Distinguishing Feature
GBM (gliosarcoma with dural extension): intra-axial origin, ring-shaped heterogeneous enhancement, central necrosis, elevated rCBV, lipid-lactate peak on MRS. Meningioma: extra-axial, CSF cleft, homogeneous enhancement, alanine peak on MRS, dural tail sign.
Urgency
routineManagement
WHO derece 1 meningiomlarda Simpson derece I-III cerrahi rezeksiyon altın standarttır. Asemptomatik küçük meningiomlar izlenebilir (seri MRG). Cerrahi uygun değilse stereotaktik radyocerrahi (SRS) alternatiftir. Derece 2-3 meningiomlarda adjuvan radyoterapi.Biopsy
Not NeededFollow-up
Asemptomatik insidental meningiom: 3-6 ay sonra ilk kontrol MRG, ardından büyüme yoksa yıllık takip. Cerrahi sonrası: 3 ay ve 1 yılda kontrastlı MRG. Subtotal rezeksiyon veya yüksek derece: 3-6 ayda bir kontrastlı MRG.The vast majority of meningiomas are benign (WHO grade 1) and grow slowly. Asymptomatic incidental meningiomas can be monitored with serial MRI. Surgical resection is preferred for symptomatic lesions (neurological deficit, seizure, headache). The Simpson grading system evaluates extent of resection and recurrence risk. For locations near critical structures (cavernous sinus, brainstem), stereotactic radiosurgery is considered due to high surgical risk. Adjuvant radiotherapy is recommended for atypical and malignant meningiomas.
Most meningiomas are WHO Grade 1 with favorable prognosis. Small asymptomatic meningiomas can be followed with serial MRI. Surgical resection is the primary treatment for symptomatic or growing lesions. Atypical (Grade 2) and anaplastic (Grade 3) meningiomas have a more aggressive course and may require adjuvant radiotherapy.