Incidence: most common extraaxial tumor: 15–18% of intracranial tumors in adults; 1–2% of primary brain tumors in children; 33% of all incidental intracranial neoplasms

Origin: derived from meningothelial cells concentrated in arachnoid villi (= “arachnoid cap cells”), which penetrate the dura (villi are numerous in large dural sinuses, in smaller veins, along root sleeves of exiting cranial + spinal nerves, choroid plexus)

Histologic classification:

• benign behavior pattern
  1. fibroblastic (fibrous) type = interwoven bands of spindle cells + collagen + reticulin fibers
  2. transitional (mixed) type
     = features of meningothelial + fibroblastic forms
     • aggressive imaging appearance
  3. meningothelial (syncytial) type = forming a syncytium of closely packed cells with indistinct borders
  4. angioblastic (malignant) type
     = probably hemangiopericytoma / hemangioblastoma arising from vascular pericytes

Peak age: 45 (range, 35–70) years; rare <20 years (in children >50% malignant); M÷F = 1÷2 to 1÷4

In pediatric age group:

• NO gender predilection
• Higher risk of sarcomatous change
• Consider association with neurofibromatosis type 2

Associated with: NF2 (multiple meningiomas, occurrence in childhood), basal cell nevus syndrome

• 10% of patients with multiple meningiomas have type 2 neurofibromatosis!
• Most common radiation-induced CNS tumor with latency period of 19–35 years varying with dosage!

Types:

1. Globular meningioma (most common):
   compact rounded mass with invagination of brain; flat at base; contact to falx / tentorium / basal dura / convexity dura
2. Meningioma en plaque:
   pronounced hyperostosis of adjacent bone, particularly along base of skull; difficult to distinguish hyperostosis from tumor cloaking the inner table (DDx: Paget disease, chronic osteomyelitis, fibrous dysplasia, metastasis)
3. Multicentric meningioma (2–9%):
   16% in autopsy series; tendency to localize to a single hemicranium; present clinically at earlier age; global / mixed; CSF seeding is exceptional; in 50% associated with neurofibromatosis type 2

Location:

1. Supratentorial (90%)
   1. convexity = lateral hemisphere (20–34%)
   2. parasagittal = medial hemisphere (18–22%):
      falcine meningioma (5%) below superior sagittal sinus, usually extending to both hemispheres
   3. sphenoid ridge + middle cranial fossa (17–25%)
   4. frontobasal at olfactory groove (10%)
2. Infratentorial (9–15%)
   1. cerebellar convexity (5%)
   2. tentorium cerebelli (2–4%)
   3. cerebellopontine angle (2–4%)
   4. clivus (<1%)
3. Spine (12%)

Atypical location:

1. cerebellopontine angle (<5%)
2. optic nerve sheath (<2%)
3. intraventricular (0.5–3.7%): 80% in atrium (L >R), 15% in 3^rd, 5% in 4^th ventricle ← infolding of meningeal tissue during formation of choroid plexus
   • Most common trigonal intraventricular mass in adulthood!
4. ectopic = extradural (<1%): intradiploic space, outer table of skull, scalp, paranasal sinus, parotid gland, parapharyngeal space, mediastinum, lung, adrenal gland

Plain film:

• hyperostosis at site close to / within bone (exostosis, enostosis, sclerosis):
  • Hyperostosis does NOT indicate tumor infiltration!
• blistering at paranasal sinuses (ethmoid, sphenoid) ± sclerosis (= pneumosinus dilatans)
• enlarged meningeal grooves (if location in vault)
• enlarged foramen spinosum
• calcification (= psammoma bodies)

CT:

• sharply demarcated well-circumscribed slowly growing mass
• hyperdense (70–75% ← highly cellular nature or psammomatous calcifications) / isodense lesion on NECT
• calcifications (15–20–25%) in circular / radial pattern (DDx: osteoma)
• “cortical buckling” of underlying brain
• “intraosseous meningioma” = permeation of bone with intra- and extracerebral soft-tissue component (DDx: fibrous dysplasia)
• hyperostosis of adjacent bone (18%)
• intense uniform enhancement on CECT ← absence of blood-brain barrier:
  • “dural tail” = wide attachment to adjacent dura mater
• minimal peritumoral edema (in up to 75%):
  • NO correlation between tumor size + amount of edema (DDx: intraaxial lesion)
• cystic component: major in 2%, minor in 15%

MR (100% detection rate with gadolinium DTPA):

• hypo- to isointense on T1WI + iso- to hyperintense on T2WI (intensity depends on amount of cellularity versus collagen elements):
  • tends to follow cortical signal intensity
  • homogeneous / heterogeneous texture (← tumor vascularity, cystic changes, calcifications)
• arcuate bowing of white matter + cortical effacement
• tumor-brain interface ← low-intensity vessels + high-intensity cerebrospinal cleft on T2WI
• contrast enhancement for 3–60 min on T1WI as high as 148% above enhancement of brain parenchyma
• “dural tail” sign (in 60–72%)
• encasement + narrowing of vessels
• elevated alanine peak (1.5 ppm) + glutamate–glutamic acid peak (2.1–2.5 ppm)

Angio:

• “mother-in-law” phenomenon (contrast material shows up early and stays late into venous phase)
• “sunburst” / “spoke-wheel” pattern of tumor vascularity with hypervascular cloudlike stain
• early draining vein (rare: perhaps in angioblastic meningioma)
• en plaque meningioma is poorly vascularized

Vascular supply:

1. External carotid artery (almost always):
   1. vault: middle meningeal artery
   2. sphenoid plane + tuberculum: recurrent meningeal branch of ophthalmic a.
   3. tentorium: meningeal branch of meningohypophyseal trunk of ICA
   4. clivus + posterior fossa: vertebral artery / ascending pharyngeal artery
   5. falx: partly middle meningeal artery + others
2. Internal carotid artery (rare):
   1. intraventricular: choroidal vessels

Cx: local invasion of venous sinuses