Meningioma

What is a meningioma?

A meningioma is a tumor of the meninges that typically grows slowly and is benign in most cases.

A meningioma is a neoplasm arising from the arachnoid/meningothelial cell layer. It does not originate from brain tissue itself; however, as it enlarges, it can exert mass effect on the brain, cranial nerves, or vascular structures—leading to symptoms.

How common is it—and who is at higher risk?

Meningiomas account for approximately 34% of primary intracranial tumors and are the most common benign intracranial tumor.

The strongest factor associated with increased incidence is age. There is also a slightly higher prevalence in women. Many meningiomas are discovered incidentally on MRI/CT performed for an unrelated reason, particularly in older adults.

In population-based studies, incidental meningiomas are found in roughly 0.9% of individuals, and prevalence increases in adults older than 75 years.

Where do meningiomas arise, and where are they most often located?

They arise from meningothelial cells within arachnoid granulations and commonly develop adjacent to dural venous sinuses.

Most meningiomas are supratentorial and commonly occur:

• Along the convexity of the cranial vault.
• Parasagittal, near the superior sagittal sinus.
• At the skull base (e.g., sphenoid wing, olfactory groove, clival region), where they may involve cranial nerves.

Spinal meningiomas also occur (approximately 10% of cases) and may compress the spinal cord or nerve roots.

Which risk factors matter (age, radiation, NF2)?

Ionizing radiation is the clearest environmental risk factor. In a smaller subset of patients, inherited predisposition exists (e.g., NF2).

The best-established risk factors include:

• Age: incidence rises substantially with advancing age.
• Ionizing radiation: associated with a 6–10× higher incidence in specific exposed cohorts.
• NF2 (Neurofibromatosis type 2): inherited NF2 alterations can lead to multiple meningiomas.

Data on hormonal factors are more mixed. Topics such as head trauma or mobile phone use have been studied, but a consistent causal relationship has not been established.

In families with primary brain tumors, a higher risk has been observed among first-degree relatives—supporting a role for inherited susceptibility in some cases.

What symptoms can occur depending on location?

Symptoms depend not only on size, but—most importantly—on location and whether the tumor is associated with surrounding edema.

Common clinical presentations include:

• Headache or a pressure-like sensation.
• Seizures (especially with superficial convexity tumors in contact with the cerebral cortex).
• Focal neurologic deficits: weakness, sensory changes, speech/language difficulty, visual field loss.
• Cranial neuropathies at the skull base: double vision, facial numbness/tingling, hearing loss, balance disturbance.
• Behavior or personality changes with frontal lobe involvement.

How is it diagnosed (MRI/CT), and what do imaging features mean?

Contrast-enhanced brain MRI is the reference standard. CT is helpful for calcification/bony change and in urgent settings.

• Contrast-enhanced MRI: typically demonstrates an extra-axial mass with avid enhancement, often with adjacent dural enhancement (“dural tail”).
• CT: may reveal calcifications or hyperostosis of the adjacent bone.

Certain imaging features are associated with a higher likelihood of future growth and/or symptom development:

• Peritumoral edema.
• High T2 signal characteristics on MRI in specific patterns.
• Absence of calcification or irregular margins in selected cases.

Growth assessment is most accurately performed using volumetric analysis, rather than relying on a single linear diameter.

How are meningiomas graded (WHO I–III), and why does grading matter?

WHO grade helps predict recurrence risk and guides surveillance strategy and the need for adjuvant radiation therapy.

The WHO grading system broadly distinguishes:

• WHO I (benign): the majority of cases, with multiple subtypes (e.g., meningothelial, fibrous, transitional).
• WHO II (atypical): higher mitotic activity/cellularity and increased risk of recurrence.
• WHO III (anaplastic/malignant): more aggressive behavior, higher recurrence risk, and often the need for radiation therapy.

When is observation appropriate—and what do we monitor over time?

Small, asymptomatic meningiomas without significant compression of brain or critical neurovascular structures can often be monitored with periodic MRI.

Observation is a reasonable option when:

• The patient is asymptomatic or has mild, non-progressive symptoms.
• There is no meaningful compression of brain parenchyma or critical neurovascular structures.
• Growth is minimal or the tumor remains stable over time.

In epidemiologic series, a subset of incidental meningiomas enlarges over time (often in a roughly linear pattern), on the order of 2–3 mm/year, while volumetric studies suggest a higher proportion shows measurable growth by volume. Features such as edema, high T2 signal, irregular margins, or lack of calcification are associated with a higher likelihood of future growth.

In some clinical frameworks, a practical threshold prompting treatment consideration is volumetric growth > ~1 mL/year and/or the development or progression of edema.

When is surgery recommended—and what is the goal of the operation?

The goal is maximal safe resection—prioritizing neurological function while respecting critical nerves and vessels.

Surgery is typically considered when there is:

• Symptoms attributable to the tumor (seizures, progressive weakness, cranial neuropathy, etc.).
• Documented growth over time or new/worsening imaging-related impact (edema, mass effect).
• A location where safe gross-total resection is feasible with an acceptable neurologic risk profile.

Extent of resection has traditionally been described in grading systems (e.g., Simpson), where the ideal is complete tumor removal together with the dural attachment and any adjacent involved bone. In real-world practice, surgical strategy is individualized based on location (especially at the skull base) and the tumor’s relationship to cranial nerves and vascular structures.

When does radiation therapy / SRS play a role?

Radiation may serve as primary therapy for unresectable tumors, for residual/recurrent disease, and for higher WHO grade tumors.

Indications for radiation therapy include:

• Residual tumor after surgery (particularly when further resection would carry unacceptable risk).
• Recurrence after prior resection.
• WHO grade II–III or concern for aggressive biology, where adjuvant therapy is often discussed.
• Patients with significant comorbidities who are not surgical candidates, or locations where radical resection is not realistic.

Common approaches include:

• Fractionated external beam radiation (e.g., 50–54 Gy for benign tumors using appropriate fractionation schemes).
• SRS or stereotactic radiotherapy for selected smaller lesions/residual disease, depending on proximity to optic pathways/brainstem.
• Proton beam therapy in selected skull base tumors near the optic apparatus/pituitary region, where a sharper dose fall-off may reduce exposure to adjacent critical structures.

Technique selection depends on size, location, prior radiation exposure, and tolerance constraints of neighboring critical structures (optic nerves/chiasm, brainstem).

Recurrence and prognosis: what determines risk?

Recurrence risk is driven primarily by WHO grade and the extent of resection—making long-term MRI surveillance essential.

In general, higher WHO grade is associated with a greater likelihood of recurrence. Additionally, the more complete the resection, the better the likelihood of durable local control. Even after gross-total resection, long-term follow-up with MRI is recommended, as recurrence can occur years later.

For residual disease or WHO grade II/III tumors, durable control often requires a combined approach: surgery plus targeted radiation.