A meningioma is a dural-based, extra-axial tumour of arachnoid cap cells and the commonest primary intracranial tumour, 41.7 percent of all primary brain and CNS tumours [1]. On MRI it is a broad-based mass, isointense to grey matter, that enhances avidly, displaces the brain across a CSF cleft and often has a dural tail; on CT it is iso- to hyperdense with calcification or hyperostosis. Imaging does not grade it: grade is histological and, since 2021, partly molecular [2][3].
This page is a working reference for reporting: the features and named signs with the numbers behind them, the atypical appearances that trip people up, what imaging can and cannot say about grade and brain invasion, the mimics, SSTR PET, how to handle an incidental meningioma, and progestogen-associated meningioma, which radiologists are now expected to recognise.
- Key facts for practice and radiology board exams
- What is a meningioma?
- Where do meningiomas occur?
- MRI and CT features of meningioma
- Named signs of meningioma
- Atypical appearances of meningioma
- Can imaging predict meningioma grade or brain invasion?
- WHO 2021 grading and cIMPACT-NOW update 8
- SSTR PET in meningioma
- Differential diagnosis of a dural-based mass
- Incidental meningioma: what to recommend
- Progestogen-associated meningioma
- Treatment and post-treatment imaging
- How to report a meningioma
- Quiz
- Frequently asked questions
- References
Key facts for practice and radiology board exams
- Commonest primary intracranial tumour: 41.7 percent of all primary brain and CNS tumours and 56.8 percent of non-malignant ones, commoner in women [1]. About 20 percent are found incidentally [4].
- Extra-axial signs: broad dural base, CSF cleft with trapped vessels, grey-white junction buckling. Dural tail in up to 72 percent, but not specific [5][6].
- Signal: T1 iso to hypo, T2 iso to hyper relative to grey matter, avid homogeneous enhancement [5]. MRS: raised choline, low creatine, alanine doublet at 1.47 ppm (overlaps lactate at 1.33 ppm) [5][7].
- Angiography: dural (external carotid) supply in a sunburst pattern; mother-in-law sign, the blush comes early and stays late [8].
- WHO CNS5 (2021): one tumour type, 15 subtypes. Grade 2 by mitoses 4 to 19 per 10 high-power fields, brain invasion, chordoid or clear cell subtype, or 3 of 5 atypical features. Grade 3 by 20 or more mitoses, frank anaplasia, TERT promoter mutation or CDKN2A/B homozygous deletion [2][4].
- cIMPACT-NOW update 8 (2025): grade 1 morphology with 1p deletion plus 22q deletion or NF2 variant becomes grade 2 [3].
- Higher grade on imaging: cystic change is the most specific feature (93.4 percent), irregular tumour-brain interface the most accurate (79.7 percent) [9]; lower ADC (0.79 versus 0.92 x 10-3 mm2/s) [10].
- SSTR PET (68Ga-DOTATATE or DOTATOC) detects meningioma with high sensitivity and specificity; best for extent, bone involvement, and recurrence versus scar [11].
- Incidental meningioma: IMPACT progression risk 3.9, 24.2 and 51.6 percent for low, medium and high risk [12]. Calcification is reassuring; T2 hyperintensity, oedema and volume over 10 cm3 are not [4].
- Progestogens: cyproterone acetate (odds ratio 19.2), nomegestrol and chlormadinone acetate, and injectable medroxyprogesterone raise meningioma risk, typically at the anterior and middle skull base; many shrink after the drug stops [13][14][15].
What is a meningioma?
Meningiomas arise from arachnoid cap (meningothelial) cells, which are most numerous at the arachnoid granulations and along the dural venous sinuses. That explains the distribution: parasagittal, convexity and skull base locations dominate, and a meningioma can occur anywhere arachnoid cells are found, including the ventricles (choroid plexus stroma), the optic nerve sheath and the spinal canal.
CBTRUS 2017 to 2021 data place meningioma at 41.7 percent of all primary brain and CNS tumours [1], with incidence rising after 65 and again after 85 years [4]. The best-validated risk factor is cranial irradiation, with a linear dose-response relation and the highest risk after treatment under the age of 10 [4][16]. Genetic syndromes are the other main group: NF2-related schwannomatosis (multiple meningiomas, often with vestibular schwannomas; see the neurofibromatosis and NF2 articles and Radiology OSCE Case 271) and familial multiple spinal clear cell meningiomas from SMARCE1 variants [17]. Exogenous progestogens are now a recognised, reversible cause (see below).
Where do meningiomas occur?
Supratentorial convexity, parasagittal and falcine meningiomas are the commonest, followed by the skull base. Location matters for the report because it sets the surgical risk and the structures to comment on.
| Location | What to look for and report |
|---|---|
| Convexity | Easiest to resect. Comment on hyperostosis, transosseous extension and the CSF cleft. See Radiology OSCE Case 261. |
| Parasagittal and falcine | Superior sagittal sinus invasion with partial or complete occlusion, which is much commoner than arterial compromise [5]; bilateral growth across the falx. See Radiology OSCE Case 232. |
| Sphenoid wing and spheno-orbital | Hyperostosis, proptosis, optic canal and superior orbital fissure involvement; the typical site of en plaque and progestogen-associated meningiomas [14]. |
| Olfactory groove, planum sphenoidale, tuberculum sellae | Anosmia and visual loss; relation to the anterior cerebral arteries, optic chiasm and cribriform plate. |
| Parasellar and cavernous sinus | Encasement of the cavernous internal carotid artery, which can narrow its lumen [5]; extension through foramina and along the trigeminal nerve. |
| Cerebellopontine angle | Second commonest CPA mass after vestibular schwannoma; a dural tail favours meningioma because a schwannoma is not typically associated with one [5]. |
| Tentorium, petroclival, foramen magnum | Brainstem compression, basilar and vertebral artery encasement, venous sinus relations. |
| Intraventricular | 0.5 to 3 percent, usually the trigone of the lateral ventricle in adults [5]. |
| Optic nerve sheath | 0.4 to 1.3 percent [5]; tubular enhancement around a spared nerve (tram-track sign). |
| Intraosseous | About two-thirds of extradural meningiomas and under 2 percent of all meningiomas; expansile hyperostotic or lytic calvarial lesion [18]. |
| Spinal | Mostly women, thoracic predilection, intradural extramedullary with a broad dural base; en plaque and foraminal tumours recur more [19]. |
MRI and CT features of meningioma
| Sequence or modality | Typical finding | Pearls |
|---|---|---|
| T1 | Isointense to slightly hypointense to grey matter [5] | Fat in lipomatous or metaplastic subtypes; blood products if haemorrhagic |
| T2 and FLAIR | Isointense to slightly hyperintense to grey matter [5] | Signal predicts consistency: T2 hyperintense tumours tend to be softer [20]. Very high T2 signal suggests the microcystic subtype (1.6 percent) [5] |
| Peritumoral oedema | Variable vasogenic oedema in the adjacent brain | Some subtypes, such as lymphoplasmacyte-rich, cause oedema out of proportion to size [4]; marked oedema with an irregular interface suggests brain invasion [21] |
| Post-contrast T1 | Avid, homogeneous enhancement; dural tail in up to 72 percent [4] | Non-enhancing areas are calcification, cyst or necrosis |
| DWI and ADC | Most are not markedly restricted | Low ADC favours higher grade [10]; very low ADC with a dural mass also raises lymphoma |
| SWI or T2* | Susceptibility from calcification [5] | Flow voids at the vascular pedicle |
| MR spectroscopy | Raised choline, low creatine, alanine doublet at 1.47 ppm [5] | Alanine overlaps lactate (1.33 ppm) and is not always present; raised glutamine and glutamate help when alanine is absent [7][22]. Lactate suggests a more aggressive tumour [7] |
| Perfusion (DSC, ASL) | Hypervascular tumour | Estimates vascularity before embolisation and, with MRS, helps separate meningioma from malignant mimics [20] |
| Unenhanced CT | Iso- to hyperdense extra-axial mass; calcification in a proportion | One of the classic hyperdense lesions on unenhanced CT; best for calcification and bone |
| Bone on CT | Hyperostosis (commonest), osteolysis, enlarged skull base foramina, pneumosinus dilatans | Hyperostosis in 20 percent of a review series [5] but 75 percent of a surgical series, where 7 of 30 hyperostotic bones contained tumour [23] |
| Angiography (DSA, CTA, MRA) | Dural supply in a sunburst pattern, pial supply at the periphery; persistent blush | Assess sinus patency and embolisation candidacy [20] |
Named signs of meningioma
| Sign | Modality | What it is | How much weight to give it |
|---|---|---|---|
| CSF cleft sign | T2 MRI | Rim of CSF, often with flow voids, between tumour and cortex | Strong sign of an extra-axial location [5]; loss with an irregular interface suggests brain invasion [21] |
| Grey-white matter buckling | MRI, CT | Cortex and white matter displaced inward, not expanded | Supports extra-axial location |
| Dural tail sign | Post-contrast T1 | Enhancing dura tapering away from the mass | Up to 72 percent of meningiomas [4], but also metastasis, lymphoma, schwannoma, granulomatous disease [6] |
| Sunburst or spoke-wheel pattern | DSA, MRI | Dural feeders radiating from a central pedicle | Characteristic of a dural blood supply; can be shown noninvasively [8] |
| Mother-in-law sign | DSA, dynamic MRA or perfusion | Tumour blush arrives early and persists into the late venous phase | Classic angiographic sign of a hypervascular meningioma [8] |
| Hyperostosis | CT, radiograph | Thickened, sclerotic bone next to the dural base | Reactive or invaded; do not assume it is only reactive [23] |
| Pneumosinus dilatans | CT | Expanded paranasal sinus next to a planum or anterior skull base meningioma | Location clue |
Atypical appearances of meningioma
Most diagnostic errors come from the minority that do not look like the textbook case.
| Appearance | Imaging | Main pitfall |
|---|---|---|
| En plaque | Flat sheet of thickened enhancing dura, marked hyperostosis; sphenoid ridge and convexity [5] | Bone mimics fibrous dysplasia, Paget disease or sclerotic metastasis; the dural component is easy to miss without contrast |
| Calcified or burnt-out | Densely calcified, very hyperdense on CT, low T2 and SWI signal, little enhancement; usually psammomatous | Calcification is associated with slower growth [24][4]; mistaken for an osteoma or calcified granuloma |
| Cystic or microcystic | Intratumoral or peritumoral cysts; microcystic subtype very bright on T2 [5] | Mimics glioma or haemangioblastoma; cystic change is the most specific imaging feature of higher grade [9] |
| Intraventricular | Well-defined, enhancing trigonal mass, calcified in a proportion [5] | Choroid plexus papilloma, ependymoma, metastasis |
| Intraosseous | Expansile hyperostotic or lytic calvarial or orbital lesion [18] | Fibrous dysplasia, metastasis, myeloma |
| Haemorrhagic | Acute blood within or around the tumour; commoner under 30 and over 70 years, convexity and intraventricular locations [5] | Presents as a haematoma that hides the tumour |
| Intra-axial-appearing | Deep cortical invasion, oedema, heterogeneous enhancement | Mimics high-grade glioma; look for a dural attachment |
| Multiple (meningiomatosis) | Two or more separate meningiomas | Consider NF2-related schwannomatosis, prior radiation, progestogen exposure and SMARCE1 in spinal clear cell tumours [17] |
Can imaging predict meningioma grade or brain invasion?
Partly. Imaging raises or lowers the probability of a higher-grade tumour, but grade remains a tissue diagnosis. The numbers are useful for how strongly to word a report.
| Feature | Performance for high grade or invasion | Source |
|---|---|---|
| Cystic change | Specificity 93.4 percent for high grade | Meta-analysis of 24 studies [9] |
| Irregular tumour-brain interface | Accuracy 79.7 percent, PPV 65.0 percent, AUC 0.788 for high grade | [9] |
| Mass effect | Sensitivity 81.0 percent, NPV 90.7 percent for high grade | [9] |
| Heterogeneous enhancement | AUC 0.703 for high grade | [9] |
| Mean ADC | 0.92 (low grade) versus 0.79 (high grade) x 10-3 mm2/s; sensitivity 69, specificity 82 percent | Meta-analysis of 25 studies, 1,552 tumours [10] |
| Tumour-brain interface for brain invasion | AUC 0.860 alone; 0.935 combined with lobulation, finger-like protrusion, mushroom sign, bone invasion, size and ADC | 675 patients, 108 with invasion [21] |
Radiomics models now predict integrated molecular risk and 1p loss from preoperative MRI in research cohorts, but they are not ready for clinical use [25]. The practical message is to report the features, not a grade: describe the interface, the CSF cleft, oedema, cysts, ADC and bone destruction, and flag a suspected higher-grade or invasive tumour because it changes the extent of resection and the case for radiotherapy.
WHO 2021 grading and cIMPACT-NOW update 8
The fifth edition WHO classification (CNS5) treats meningioma as one type with 15 subtypes, grades it with Arabic numerals as CNS WHO grade 1 to 3 within the tumour type, and introduced the first molecular grading criteria [2]. Brain invasion alone remains sufficient for grade 2 [4]; papillary or rhabdoid morphology alone is no longer enough for grade 3 [2].
| CNS WHO grade | Criteria (any one) | Subtypes |
|---|---|---|
| Grade 1 | Fewer than 4 mitoses per 10 high-power fields and no grade 2 or 3 criteria | Meningothelial, fibrous, transitional, psammomatous, angiomatous, microcystic, secretory, lymphoplasmacyte-rich, metaplastic |
| Grade 2 | 4 to 19 mitoses per 10 high-power fields; brain invasion; chordoid or clear cell subtype; 3 of 5 of sheeting, hypercellularity, small cell change, macronucleoli, spontaneous necrosis [4]. cIMPACT-NOW 8: grade 1 morphology with 1p deletion plus 22q deletion or an NF2 variant [3] | Chordoid, clear cell (almost all SMARCE1-deficient) [4], atypical |
| Grade 3 | 20 or more mitoses per 10 high-power fields; frank anaplasia (sarcoma-, carcinoma- or melanoma-like); TERT promoter mutation; CDKN2A/B homozygous deletion [2][3] | Anaplastic; papillary and rhabdoid by criteria rather than morphology alone |
Beyond the WHO criteria, DNA methylation profiling separates meningiomas into biologically distinct classes that predict recurrence better than histology [26], and an integrated molecular-morphologic score outperformed WHO grading (c-index 0.744 versus 0.699) [27]. For the radiologist this explains two things: why an apparently benign-looking grade 1 tumour can recur early, and why post-operative imaging intervals are increasingly set by molecular risk rather than by grade alone [4].
SSTR PET in meningioma
Almost all meningiomas express somatostatin receptor 2, so 68Ga-DOTATATE or DOTATOC PET shows them with high contrast [4]. The joint EANM, EANO, RANO and SNMMI 2024 guideline sets procedure standards and lists the indications [11], building on the 2017 RANO/PET recommendations [28]:
- Uncertain diagnosis of a dural lesion, for example meningioma versus metastasis or lymphoma.
- Tumour extent, including bone, skull base, cavernous sinus and falx involvement that MRI underestimates, and radiotherapy target delineation [11][4].
- Recurrence versus post-treatment scar after surgery or radiotherapy [11].
- Selection for radioligand therapy (177Lu-DOTATATE), which remains investigational [29][11].
Pitfalls: the pituitary gland shows high physiological uptake, with slight uptake in vessels, choroid plexus and salivary glands; active inflammatory lesions such as granulomatous disease and neurosarcoidosis take up tracer; and brain metastases and gliomas can show slightly increased uptake [11].
Differential diagnosis of a dural-based mass
| Diagnosis | Features that favour it over meningioma |
|---|---|
| Solitary fibrous tumour (formerly haemangiopericytoma) [2] | No calcification or hyperostosis, may erode the skull, heterogeneous enhancement with prominent internal flow voids, narrow stalk-like or broad dural attachment [5]; higher ADC values than atypical meningioma on histogram analysis [30] |
| Dural metastasis | Known primary (breast, lung, prostate, renal), multiplicity, adjacent calvarial destruction, typically T2 hyperintense [5]; can have a dural tail [6] |
| Lymphoma | Marked diffusion restriction (low ADC), T2 iso to hypointense, may extend across the calvarium without destroying it; dural tail possible [6] |
| IgG4-related and granulomatous pachymeningitis, sarcoid, tuberculosis | Diffuse or multifocal smooth dural thickening, T2 hypointensity, other organ involvement; see the pachymeningeal thickening mnemonic [31][5] |
| Vestibular schwannoma (CPA) | Centred on and expanding the internal auditory canal, acute angle with the petrous bone, cystic change; not typically associated with a dural tail [5] |
| Peripheral glioma or other intra-axial tumour | No CSF cleft, expands rather than displaces cortex; a dural tail does not exclude it [6] |
| Hyperostosis mimics | Fibrous dysplasia (ground-glass, no dural component), Paget disease, sclerotic metastasis; look for enhancing dura |
Incidental meningioma: what to recommend
An incidental meningioma is a common report. About 20 percent of meningiomas are found incidentally, most grow slowly (on average under 5 percent volume per year), and 5 to 8 percent of patients develop symptoms over about 4 years [4]. The 2021 EANO guideline supports a watch-and-scan strategy for many asymptomatic, often elderly, patients [29]. There is no guideline-fixed interval; an MRI at 6 to 12 months to exclude rapid growth and an alternative diagnosis is a reasonable first step [32].
| Feature | Direction of risk |
|---|---|
| Calcification | Lower risk of progression [4] |
| T2 hyperintensity | Higher risk [4] |
| Peritumoral oedema | Higher risk [4]; also associated with symptom development [33] |
| Volume over 10 cm3 (or diameter 3 cm or more) | Higher risk [4][33] |
| Non-skull base location, close to a dural venous sinus | Higher risk [4] |
| Comorbidity and poor performance status | Death from other causes more likely than intervention [12] |
The IMPACT tool combines these clinical and MRI factors. In its 2026 external validation in 1,248 patients from 33 centres in 15 countries, 10-year progression-free survival was 85.7 percent; progression occurred in 3.9 percent of low-risk, 24.2 percent of medium-risk and 51.6 percent of high-risk meningiomas (C-statistic 0.80), and 40.5 percent of patients died of unrelated causes without progression or intervention [12]. An age-adjusted Charlson comorbidity index of 6 or more with a performance status of 2 to 4 predicted death from other causes over intervention [12]. Growth is not inevitable but is not rare either: 35.4 percent grew in a cohort followed for at least 10 years [24]. Treatment has real morbidity, and 94 percent of operated incidental meningiomas are grade 1 [33], so the report should describe risk features rather than imply urgency.
Progestogen-associated meningioma
French national data changed practice. With high-dose cyproterone acetate, meningioma incidence was 23.8 versus 4.5 per 100,000 person-years (adjusted hazard ratio 6.6), rising to 21.7 above a cumulative 60 g, and the tumours clustered at the anterior and middle skull base, particularly spheno-orbital [14]. Patients were operated on at a median of 47 rather than 61 years [34]. A case-control study of 18,061 operated women then extended the signal to other progestogens [13], and a cohort study of 1.06 million women quantified it for nomegestrol acetate [35].
| Progestogen | Risk of operated meningioma | Source |
|---|---|---|
| Cyproterone acetate | Odds ratio 19.21 | [13] |
| Nomegestrol acetate | Odds ratio 4.93; relative risk 12.0 above 6 g cumulative; back to baseline 1 year after stopping | [13][35] |
| Chlormadinone acetate | Odds ratio 3.87 | [13] |
| Medroxyprogesterone acetate (injectable) | Odds ratio 5.55 | [13] |
| Medrogestone | Odds ratio 3.49 | [13] |
| Promegestone | Odds ratio 2.39 | [13] |
| Progesterone, dydrogesterone, levonorgestrel intrauterine systems | No excess risk | [13] |
Reporting point: multiple or skull base meningiomas in a younger woman or a transgender woman should prompt the question of progestogen exposure. Stopping the drug is often the first treatment: in a 2026 series of 137 meningiomas, 88 percent showed a volumetric response after cyproterone acetate was withdrawn, and the volume change at 3 months predicted the final response [15]. A baseline and a 3 to 6 month MRI after withdrawal is therefore a useful recommendation.
Treatment and post-treatment imaging
- Observation for many asymptomatic tumours [29].
- Surgery is the standard for symptomatic or growing tumours; gross total resection including the involved dura is often curative [29]. The 1957 Simpson grade of resection still has prognostic value, but chasing a lower Simpson grade at the cost of morbidity, for example at the skull base or a patent sinus, gives little benefit [36][4].
- Radiosurgery or fractionated radiotherapy for residual, recurrent or inoperable tumours and after resection of higher-grade tumours; the benefit after gross total resection of grade 2 tumours is being tested in ROAM/EORTC-1308 and NRG BN-003 [29][4].
- Systemic therapy has no standard of care; bevacizumab and multikinase inhibitors have shown modest activity, and SSTR radioligand therapy is investigational [29][4].
- Post-treatment imaging: contrast MRI documents residual tumour and growth, and SSTR PET helps when recurrence and post-therapeutic scar cannot be separated on MRI [11].
How to report a meningioma
- Location, size in three dimensions (volume if under surveillance) and comparison with prior imaging.
- Extra-axial evidence: CSF cleft, dural base, dural tail; state if the cleft is lost or the interface is irregular.
- Features that raise concern for higher grade: cysts, heterogeneous enhancement, low ADC, marked oedema, bone destruction [9][10].
- Bone: hyperostosis, lysis, transosseous or extracranial extension, skull base foramina, orbit.
- Vessels and sinuses: sinus invasion or occlusion, arterial encasement and narrowing, candidate feeders for embolisation.
- Mass effect: midline shift, herniation, hydrocephalus, optic apparatus or brainstem compression.
- For incidental tumours: calcification, T2 signal, oedema and proximity to a venous sinus, which drive the follow-up plan [4][12].
- Context: multiplicity, prior cranial radiation, NF2 features, and progestogen exposure in the appropriate patient.
Quiz
Multiple meningiomas can be associated with which of the following genetic mutations?
- Mutation in the NF1 gene on the long arm of chromosome 21
- Mutation in the NF2 gene on the long arm of chromosome 22
- Mutation in the NF1 gene on the short arm of chromosome 21
- Mutation in the NF2 gene on the short arm of chromosome 22
More meningioma cases: left frontal meningioma with dural tail and CSF cleft, falcine meningioma, frontoparietal meningioma with MR spectroscopy and multiple meningiomas in NF2.
Frequently asked questions
References
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- Champeaux-Depond C, Weller J, Froelich S, Sartor A. Cyproterone acetate and meningioma: a nationwide-wide population based study. J Neurooncol. 2021;151(2):331-338.
- Nguyen P, Roland N, Neumann A, Hoisnard L, Passeri T, Duranteau L, et al. Prolonged use of nomegestrol acetate and risk of intracranial meningioma: a population-based cohort study. Lancet Reg Health Eur. 2024;42:100928.
- Dadario NB, Sughrue ME. Simpson’s Grading Scale for WHO Grade I Meningioma Resection in the Modern Neurosurgical Era: Are We Really Asking the Right Question? J Neurol Surg B Skull Base. 2024;85(2):145-155.
Further reading: Osborn’s Brain, the standard neuroradiology text for extra-axial tumours.
Case co-authored by TeamGyan members Dr Mansi Sarmalkar and Dr Bhargavi Sovani. Updated September 2026.
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