Meningioma

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Meningiomas are typically dural-based tumours derived from meningothelial cells. Their extra-axial position may displace rather than invade brain, yet location can make even a small lesion consequential. Convexity tumours may cause seizure or contralateral weakness; parasagittal tumours can affect leg function or venous sinuses; sphenoid-wing, planum and tuberculum lesions may threaten vision; posterior-fossa and foramen-magnum lesions can affect cranial nerves, long tracts or CSF flow.

A radiological appearance can be strongly suggestive but is not identical to histological diagnosis. Dural metastasis, solitary fibrous tumour and inflammatory lesions can mimic meningioma. MRI characterises the mass, oedema and soft-tissue relationships; CT is useful for bone change and calcification. Tissue permits subtype and CNS WHO grading when surgery is performed. Most are grade 1, but higher grade or recurrent tumours behave more aggressively and need different postoperative decisions.

Management is individual rather than size-only. Incidental asymptomatic lesions can often be observed, especially when intervention risk exceeds likely benefit. Growth, symptoms, threatened vision, mass effect and uncertainty favour treatment. Surgery can relieve pressure and provide tissue but risks neurological deficit, venous injury, cranial-nerve injury and CSF leak. Radiosurgery or fractionated radiotherapy can control selected lesions, residual disease or recurrence. NICE NG99 bases postoperative choices on grade and completeness of excision, and EANO emphasises observation for incidental asymptomatic disease and surgery for growing or symptomatic tumours.

Key points

Meningiomas arise from meningothelial cells and are usually extra-axial; many are incidental, but symptoms depend on location, size, oedema, venous involvement and pressure effects.
Standard contrast-enhanced structural MRI is the initial diagnostic test under NICE NG99; add CT when bone involvement or hyperostosis needs assessment.
Observation is appropriate for many incidental asymptomatic suspected meningiomas, while growing or symptomatic lesions prompt specialist discussion of surgery or radiotherapy.
Grade cannot be confirmed from imaging alone. Histology assigns CNS WHO grade, and grade together with extent of resection strongly shapes recurrence risk and follow-up.
Surgical ambition is balanced against neurological, vascular and cranial-nerve risk; deliberate subtotal resection followed by monitoring or radiotherapy can be safer than injurious total removal.
New symptoms during surveillance require clinical review and appropriate imaging rather than waiting automatically for the next routine scan.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Meningothelial origin

Tumour develops from arachnoid cap or related meningothelial cells and commonly attaches to dura. Location reflects meningeal anatomy rather than brain parenchymal lineage.

Predisposition and exposure

NF2-related schwannomatosis and prior cranial irradiation increase risk. Hormonal associations exist, but routine endocrine manipulation is not an established universal treatment.

Mostly sporadic disease

Most meningiomas arise without an identifiable inherited syndrome. Multiple tumours, young age or associated schwannomas may justify genetics assessment.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Extra-axial compression
Growth displaces brain and can impair local cortical networks. Slow expansion permits adaptation, so a large lesion may precede recognition until compensation fails.
2
Peritumoural oedema
Vascular and tumour-brain interactions can produce oedema disproportionate to size, increasing seizure risk, focal deficit and intracranial pressure.
3
Bone and sinus involvement
Tumour may induce hyperostosis, invade skull or encase venous sinuses and arteries. These relationships strongly influence resectability and operative morbidity.
4
Grade-related recurrence
Higher CNS WHO grade and residual viable tumour increase recurrence probability. Biology and extent therefore jointly determine adjuvant and surveillance decisions.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Convexity and cortical effects

Focal seizure, progressive unilateral weakness, sensory loss or language disturbance may result from cortical compression and oedema. Establish laterality and recovery after seizure rather than attributing all deficits to a postictal state.

Skull-base cranial nerves

Ask about visual acuity, field loss, diplopia, facial numbness, hearing change, dysphagia and voice change. Slow progression can be subtle, and formal testing often detects more than bedside complaint.

Frontal and parasagittal change

Collateral history may reveal apathy, disinhibition, executive failure, gait change or leg-predominant weakness. Venous sinus involvement influences both symptoms and surgical risk.

Pressure and hydrocephalusRed flag

Headache, vomiting, papilloedema and drowsiness can occur with large tumours, extensive oedema or obstruction of CSF pathways. Acute change requires emergency imaging despite an earlier slow-growth pattern.

Incidental lesion context

Clarify why imaging was obtained, whether symptoms localise to the lesion, prior scans, cancer history and comorbidity. Coexistence does not prove that the meningioma explains every headache or cognitive complaint.

Growth and atypical behaviour

Compare identical planes and sequences across scans. Rapid volumetric growth, irregular invasion or disproportionate oedema increases concern but still does not establish grade without tissue.

Red flags requiring action

New seizure, persistent postictal deficit or failure to recover usual consciousness.
Rapidly worsening focal weakness, speech or visual change, gait impairment, pupil abnormality or declining alertness.
Papilloedema, repeated vomiting or progressive headache with drowsiness suggesting significant oedema, hydrocephalus or mass effect.
Progressive visual loss, optic atrophy or field defect with a skull-base, planum, sphenoid-wing or parasellar lesion.
Documented growth, new neurological symptoms or radiological features atypical for a routine grade 1 tumour.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Standard structural MRI brainFirst step
Why
Define the suspected extra-axial lesion, enhancement, dural attachment, oedema, venous-sinus relationship and proximity to eloquent structures.
Interpretation and limitations
NICE specifies T2, FLAIR, DWI and T1 pre- and post-contrast volume sequences as the initial test. A typical appearance supports a radiological diagnosis but cannot confirm WHO grade.
02
CT head with bone windows
Why
Assess hyperostosis, calcification, bone erosion and skull-base anatomy when bone involvement is suspected.
Interpretation and limitations
Hyperostosis can support meningioma and alter operative planning, whereas destructive change may broaden the differential. CT complements rather than replaces soft-tissue MRI.
03
Formal visual and cranial-nerve assessment
Why
Quantify function threatened by skull-base and parasellar tumours before deciding whether observation remains safe.
Interpretation and limitations
Document acuity, colour vision, pupils, fields, ocular movements and other relevant cranial nerves. Progressive field loss can justify treatment even when overall tumour dimensions change little.
04
Histopathology and CNS WHO grade
Why
Confirm diagnosis and grade after resection or biopsy and identify features that change recurrence risk.
Interpretation and limitations
Imaging cannot supply grade. Interpret pathology alongside resection extent and current WHO criteria; sampling, prior radiation and recurrent disease may complicate assessment.
05
Serial MRI comparison
Why
Measure growth and new oedema in an observed or treated tumour using a consistent protocol.
Interpretation and limitations
Small linear differences may reflect technique. Sustained volumetric growth and new clinical deficit are more meaningful than one borderline measurement, and imaging anxiety should be acknowledged.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Dural metastasis

Cancer history, multiple lesions, destructive bone change or rapid evolution may suggest metastasis. Tissue may be needed when systemic treatment would differ.

Solitary fibrous tumour

This distinct mesenchymal tumour can mimic a vascular dural mass. Pathology and molecular classification separate it from meningothelial meningioma.

Schwannoma

Cranial-nerve-centred lesions, especially vestibular masses, follow nerve anatomy and produce characteristic deficits; imaging origin helps distinguish them.

Inflammatory dural disease

IgG4-related disease, granulomatous inflammation and infection can thicken dura. Systemic clues and tissue become important when imaging is atypical.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Incidental pathwayAsymptomatic radiological meningiomaFirst stepImaging for another reason shows a small typical meningioma without neurological deficit or threatened function.

1Confirm that symptoms do not localise to the lesion, review prior imaging and assess age, comorbidity, tumour site, oedema and intervention risk.
2Discuss at the appropriate specialist service and agree active monitoring when expected benefit of immediate treatment is low.
3Use an individual MRI and clinical-review schedule, explain uncertainty and anxiety, and bring review forward for any new neurological symptom or convincing growth.

02Treatment pathwayGrowing or symptomatic meningiomaSerial growth, seizure, focal deficit, threatened vision, mass effect or diagnostic uncertainty makes continued observation unsafe or unacceptable.

1Define treatment goals with the patient: tissue diagnosis, decompression, preservation of vision or neurological function and durable control.
2Balance resection extent against venous sinus, cranial nerve, vascular and eloquent-brain risk; maximal safe removal may intentionally leave adherent tumour.
3Choose surgery, radiosurgery or fractionated radiotherapy through MDT review, considering size, site, grade information, prior treatment and the person’s preferences.
4After tissue diagnosis, combine CNS WHO grade and Simpson resection extent to select active monitoring, further surgery or radiotherapy under NICE NG99.
5Verify the plan with postoperative imaging, neurological assessment, pathology review and an explicit recurrence-surveillance schedule.

03Recurrence pathwayResidual or recurrent diseaseFollow-up shows convincing growth after subtotal resection, radiotherapy or previous apparently complete excision.

1Confirm true progression on comparable imaging and reassess symptoms, performance, grade and previous radiation field.
2Review reoperation and radiation options in a specialist MDT because feasibility and toxicity differ from first treatment.
3When local options are exhausted, prioritise symptom control, rehabilitation and clinical-trial discussion; routine systemic therapy has no established broad role.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Seizure and deficit

Cortical compression and oedema can cause focal seizure, weakness, language disturbance or cognitive change, with functional consequences beyond tumour size.

Visual or cranial neuropathy

Skull-base tumours can progressively injure optic and other cranial nerves; delayed treatment may leave irreversible loss despite later control.

Hydrocephalus and herniation

Posterior-fossa obstruction, large tumour or severe oedema can impair CSF flow and create life-threatening pressure gradients requiring urgent intervention.

Treatment morbidity

Surgery and radiation can cause neurological deficit, vascular injury, CSF leak, radionecrosis or hypopituitarism depending on site and technique.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During active monitoring, combine neurological review with standard structural MRI at an interval based on grade certainty, tumour site, size, growth and patient factors.
After surgery, document new deficits and obtain postoperative imaging to establish residual tumour before applying grade- and extent-specific follow-up.
Measure visual fields and acuity serially for lesions near optic pathways because functional decline may precede a dramatic size change.
Review seizure control, cognition, gait, cranial-nerve function and rehabilitation needs rather than treating scan stability as complete clinical stability.
Arrange earlier clinical review and imaging for new or changing neurological symptoms at any time, including between planned surveillance visits.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Simpson grade has context

Resection extent describes operative completeness but does not stand alone. Modern decisions also incorporate WHO grade, imaging residual, anatomical risk and whether radiotherapy is available.

Safe subtotal surgery

Leaving tumour attached to a critical artery, venous sinus or cranial nerve can preserve function. Planned monitoring or radiotherapy may yield a better outcome than injurious anatomical completeness.

Symptoms need localisation

An incidental meningioma and headache commonly coexist. Causation is stronger when the neurological deficit, oedema or pressure effect matches tumour location and changes with treatment.

Radiology cannot grade

Diffusion, oedema and growth can raise suspicion, but WHO grade is pathological. Avoid promising benign behaviour solely from a typical dural tail.

Vision changes urgency

Slow field loss may be under-recognised by the patient. Formal visual testing can convert an apparently asymptomatic skull-base lesion into a function-threatening tumour needing treatment discussion.

11Common pitfallsFrequent interpretation and management errors.

01
Treating every incidental suspected meningioma immediately without weighing natural history, operative harm and patient preference.
02
Calling a lesion grade 1 from imaging alone or assuming a dural tail is pathognomonic.
03
Pursuing complete excision when adherence to a venous sinus, artery or cranial nerve makes neurological injury likely.
04
Using one fixed surveillance interval for all radiological, postoperative and higher-grade meningiomas.
05
Waiting for the next routine scan when seizure, visual decline, new deficit or drowsiness develops.

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