• Most common primary intracranial tumour: ~37-38% of all primary CNS tumours (CBTRUS 2023 data)
• Annual incidence: approximately 8-9 per 100,000 population (age-adjusted)
• Prevalence increases with age — peak incidence in the 6th-7th decades of life
• Secondary (metastatic) brain tumours are 6-10× more common than primary brain tumours overall ^[2], but among primary tumours, meningioma is the most frequent

• Female predominance: F:M ratio approximately 2-3:1 for intracranial meningiomas
  • Why? Meningiomas frequently express progesterone receptors (found in ~70% of meningiomas) and sometimes oestrogen receptors (~30%). Hormonal stimulation is believed to promote growth. This explains:
    • Increased incidence in women of reproductive age
    • Tumour growth acceleration during pregnancy (increased progesterone)
    • Association with exogenous hormone use (HRT, OCP)
  • For spinal meningiomas, the female predominance is even more pronounced (up to 4:1)
• Exception: Atypical and anaplastic (WHO Grade 2-3) meningiomas show a less pronounced or even reversed sex ratio (M ≈ F or slight male predominance), suggesting different biology

• Rare in children (< 2% of all meningiomas) — when they occur in children, think of NF2
• Incidence rises steeply after age 40

• Meningiomas are the most common primary brain tumour in Hong Kong, consistent with global data
• Hong Kong Cancer Registry data shows a steady incidence, with the ageing population contributing to rising absolute numbers
• Relatively high prevalence of incidental meningiomas detected on MRI performed for other indications (e.g., headache workup, stroke screening)

The brain and spinal cord are enveloped by three meningeal layers (outer to inner):

1. Dura mater ("tough mother") — thick, fibrous, outermost layer; fused to periosteum of skull. Contains dural venous sinuses (superior sagittal sinus, transverse sinus, etc.)
2. Arachnoid mater ("spider-like mother") — thin, avascular, web-like membrane. Contains arachnoid cap cells (also called meningothelial cells) — the cells of origin for meningiomas
3. Pia mater ("tender mother") — delicate, highly vascular, adheres directly to brain surface

Arachnoid cap cells cluster at:

• Arachnoid granulations (Pacchionian granulations) — projections of arachnoid into dural venous sinuses, responsible for CSF resorption back into venous blood
• Along the dura wherever the arachnoid contacts it

This is why meningiomas characteristically arise at the dural surface and are found in predictable locations corresponding to where arachnoid granulations are concentrated.

Understanding WHERE meningiomas grow is critical because the tumour's location determines the clinical presentation (focal neurological deficits) and surgical accessibility.

In adults, 70% of brain tumours are supratentorial — the common types are metastatic brain tumours, meningioma, and gliomas (e.g. GBM) ^[2].

Meningiomas derive their blood supply primarily from dural (meningeal) arteries, most commonly:

• Middle meningeal artery (branch of maxillary artery from external carotid) — supplies convexity and sphenoid wing meningiomas
• Meningohypophyseal trunk (from intracavernous ICA) — cavernous sinus meningiomas
• Tentorial branches of ICA and posterior meningeal arteries

This rich dural blood supply explains:

• The intense, homogeneous enhancement on contrast imaging
• The characteristic "dural tail" sign on MRI (enhancing thickened dura extending from the tumour)
• The tendency for significant intraoperative bleeding — preoperative embolisation is sometimes performed to reduce vascularity

Meningiomas arise from arachnoid cap cells (meningothelial cells). These are specialised cells at the tips of arachnoid granulations. They are of mesenchymal origin (not neural), which is why meningiomas are classified separately from neuroepithelial tumours (gliomas).

The molecular landscape of meningiomas has been increasingly elucidated and is relevant both for understanding pathophysiology and for emerging targeted therapies:

Meningiomas produce symptoms through several mechanisms:

1. Direct compression of adjacent brain parenchyma → focal neurological deficits (the specific deficit depends on the eloquent cortex or white matter tracts compressed)

2. Vasogenic oedema (most apparent on FLAIR MRI) ^[2]: Disruption of the blood-brain barrier by tumour-secreted factors (especially VEGF) → protein-rich fluid leaks into the extracellular space of surrounding brain → oedema → additional mass effect. This oedema is the component most responsive to corticosteroids (dexamethasone reduces VEGF expression and restores BBB integrity)

3. Venous sinus compression/obstruction: Particularly parasagittal meningiomas that invade or compress the superior sagittal sinus → impaired venous drainage → ↑blood volume → raised ICP ^[4]. This mechanism is distinct from mass effect alone.

4. Cranial nerve compression: Extra-axial location means meningiomas often compress cranial nerves as they grow (e.g., olfactory groove meningioma → CN I compression → anosmia; CPA meningioma → CN VII/VIII compression)

5. Hyperostosis: Meningiomas can stimulate reactive bone thickening (hyperostosis) of the overlying skull — this is relatively specific to meningiomas and can cause a palpable bony swelling or proptosis (sphenoid wing meningioma with hyperostosis → lateral orbital wall thickening → proptosis)

6. CSF obstruction → Hydrocephalus (e.g., intraventricular meningioma blocking the foramen of Monro; posterior fossa meningioma compressing the 4th ventricle)

7. Seizures: Cortical irritation by the tumour. Usually associated with slow-growing tumours that involve cortex, e.g. meningioma, low-grade glioma ^[2]. Seizures affect 50-80% of primary tumours and 10-20% of secondary tumours ^[4]. Convexity and parasagittal meningiomas are most epileptogenic because they directly abut the cortex.

The WHO classifies meningiomas into 3 grades based on histological features, mitotic index, and molecular markers. This grading is the single most important prognostic factor.

Important update (WHO CNS5, 2021): Brain invasion alone is now sufficient to upgrade a meningioma to Grade 2, even if it otherwise looks histologically benign. Additionally, TERT promoter mutations or homozygous CDKN2A/B deletion in an otherwise low-grade meningioma upgrades it to Grade 3. This reflects the integration of molecular markers into grading — a paradigm shift.

As discussed in the anatomy section, meningiomas are also classified by their anatomical site (convexity, parasagittal, skull base, spinal, etc.). This is clinically more immediately useful because it determines symptoms and surgical approach.

Cardinal presentation of brain tumours ^[4]:

• High-grade diseases tend to present with subacute onset of S/S of ↑ICP
• Low-grade diseases tend to present with slowly progressive focal neurological S/S
  • Focal neurological deficits, i.e. negative symptoms
  • Epilepsy, i.e. positive symptom

Since meningiomas are predominantly slow-growing (WHO Grade 1), they most commonly present with:

1. Slowly progressive focal neurological deficits (most common presentation)
2. Seizures (particularly convexity and parasagittal locations)
3. Incidental finding on neuroimaging (increasingly common in the MRI era — up to 2% of brain MRIs in older adults incidentally detect a meningioma)
4. Headache ± features of raised ICP (when tumour is large enough)

A meningioma can grow surprisingly large before becoming symptomatic because:

• It is extra-axial (compresses rather than destroys brain)
• The brain has remarkable plasticity and can accommodate slow compression
• Patients may unconsciously compensate for gradual neurological decline

The CPA is a common exam scenario. The two most common CPA tumours are vestibular schwannoma (acoustic neuroma) and meningioma.

NF2 is associated with meningioma, ependymoma, acoustic (vestibular) schwannoma ^[10]. In an exam scenario, if you see bilateral CPA masses → think NF2 with bilateral vestibular schwannomas ± meningiomas.

Other CPA differentials (less common): epidermoid cyst (non-enhancing, restricts diffusion like "cauliflower"), arachnoid cyst, glomus jugulare tumour, metastasis.

Differential diagnosis of sellar mass ^[12][13][14]:

How to distinguish parasellar meningioma from pituitary macroadenoma on imaging:

Spinal meningiomas are the second most common intradural extramedullary tumour (after schwannoma).

Aetiology of raised ICP ^[5]:

• SOL: tumour, abscess, haematoma
• Cerebral oedema: trauma, infection, post-stroke
• Hydrocephalus: obstructive (IVH, tumour), communicating (post-meningitis, post-SAH)
• Idiopathic intracranial hypertension (IIH)

The key differentiating factor for meningioma: neuroimaging reveals an extra-axial, dural-based, enhancing mass. In contrast, IIH shows normal brain parenchyma (± empty sella, flattened posterior globes, tortuous optic nerves).

Seizures from brain tumours always supratentorial ^[17]. The DDx of new-onset seizure in adults includes:

• Most commonly a meningioma (found incidentally in ~2% of brain MRIs in older adults)
• Must exclude: dural metastasis (especially in patients with a history of malignancy), SFT, inflammatory dural disease
• If imaging is classic for meningioma (broad base, homogeneous enhancement, dural tail, ± calcification, no bone destruction) and the patient is asymptomatic → serial MRI follow-up is appropriate without biopsy

• Think NF2 first ^[10][11]: bilateral vestibular schwannomas, ependymomas, café-au-lait spots (fewer than NF1)
• Also consider: radiation-induced (history of prior cranial/head & neck radiotherapy, especially for NPC in Hong Kong context)
• Rarely: meningiomatosis (diffuse meningeal involvement) — must exclude leptomeningeal carcinomatosis or meningeal sarcoidosis

• A flat, carpet-like meningioma that spreads along the dural surface rather than forming a discrete mass
• Most common along the sphenoid wing → causes hyperostosis → proptosis
• DDx: fibrous dysplasia (ground-glass bone on CT), Paget's disease of skull, intraosseous metastasis

These are used for pre-operative planning, diagnostic uncertainty, or grading assessment:

Specifically requested when meningioma is suspected, to assess:

• Hyperostosis: Reactive bone thickening — helps confirm the diagnosis
• Bone invasion/erosion: Suggests higher-grade behaviour
• Skull base anatomy: Pre-surgical planning for skull base meningiomas
• Calcification: CT better for calcified tumour ^[14] — calcification within the mass is common and supports the diagnosis

• Role: Pre-operative assessment of vascular supply and venous sinus involvement
• Allows pre-operative embolisation of feeding vessels (usually middle meningeal artery branches) to reduce intraoperative bleeding
• Shows classic "sunburst" or "mother-in-law blush" pattern: prolonged tumour stain from the dural arterial supply
• Increasingly being replaced by MR angiography (MRA) and CT angiography (CTA) for non-invasive vascular assessment, but DSA remains the gold standard for embolisation

Essential when meningioma is near the visual pathway (tuberculum sellae, olfactory groove, sphenoid wing, suprasellar):

Only relevant for parasellar/suprasellar meningiomas that may compress the pituitary gland or stalk:

• Pituitary hormone profile: GH, IGF-1, prolactin, ACTH, cortisol, TSH, fT4, FSH, LH, oestradiol/testosterone
• Serum prolactin: Important to distinguish from prolactinoma. In meningioma, prolactin may be mildly elevated (typically < 3-5× ULN) due to stalk effect (compression of the pituitary stalk interrupts dopamine delivery from the hypothalamus → release of prolactin inhibition → modest hyperprolactinaemia). This is fundamentally different from a prolactinoma where prolactin is typically > 10× ULN ^[22].

• Indicated when the patient presents with seizures
• Shows focal slowing or epileptiform discharges overlying the meningioma
• Not diagnostic for meningioma specifically but helps characterise seizure semiology and guide anticonvulsant management
• Less useful diagnostically than imaging, but important for seizure management and pre-surgical epilepsy evaluation

• Rarely needed for typical meningiomas (imaging is usually sufficient for presumptive diagnosis, and tissue is obtained at definitive surgery)
• Stereotactic biopsy ^[2] is indicated when:
  • Imaging is atypical and the diagnosis is uncertain (e.g., could be lymphoma, metastasis, or inflammatory disease)
  • The lesion is in an inoperable location and tissue diagnosis is needed to guide non-surgical therapy (e.g., radiation planning)
  • The patient is not a surgical candidate but tissue diagnosis would change management

While there are no blood tests specific for meningioma, standard pre-operative and baseline investigations include:

Not every meningioma requires treatment. Since meningiomas are predominantly slow-growing benign tumours (WHO Grade 1 in ~80%), many — particularly small, incidental ones — will remain stable for years or even decades. Intervening on every meningioma would expose patients to unnecessary surgical risks.

• Incidental, asymptomatic meningioma (no mass effect, no oedema, no neurological deficit)
• Small size (typically < 2-3 cm)
• Elderly patients or those with significant comorbidities making surgery high-risk
• Location that would make surgery risky (e.g., small cavernous sinus meningioma)
• No documented growth on initial interval imaging

• Baseline MRI with gadolinium
• First follow-up MRI at 6 months (to establish early growth trajectory)
• If stable: subsequent MRI at 12-monthly intervals for 3-5 years, then can lengthen to every 1-2 years
• If growth documented (typically > 2-3 mm/year linear growth or volumetric increase) or new symptoms → reassess and proceed to treatment

• Approximately 60-70% of incidental meningiomas show no significant growth over 5 years
• Growth is more likely in: younger patients, calcification-absent tumours, T2-hyperintense tumours, and tumours with peritumoral oedema on initial imaging

High-dose glucocorticoids: reduction of cerebral oedema ^[4]:

• Use: PO (or IV if severe) dexamethasone 10 mg then 4 mg Q4H or 8 mg BD ^[4]

Why dexamethasone specifically?

• Dexamethasone is the steroid of choice for cerebral oedema because:
  • It has minimal mineralocorticoid activity → less sodium/water retention (important in a patient with raised ICP where fluid overload would be detrimental)
  • Long half-life (~36 hours) → convenient dosing
  • Potent anti-inflammatory and anti-oedema effect: reduces VEGF expression and restores BBB integrity → ↓vasogenic oedema → ↓mass effect → clinical improvement (often within hours)

Mechanism in detail: Meningiomas (and surrounding compressed brain) secrete VEGF → disrupted BBB in perilesional brain → vasogenic oedema. Dexamethasone suppresses VEGF transcription and stabilises endothelial tight junctions → oedema resolves.

Side effects of prolonged steroid use (important in the peri-operative period):

• Peptic ulcer (need prophylaxis) — prescribe a PPI (e.g., omeprazole) concurrently
• Immunosuppression — increased infection risk peri-operatively
• Diabetes mellitus — check blood glucose regularly; may need insulin sliding scale ^[4]
• Steroid myopathy, osteoporosis, adrenal suppression (if prolonged)

Anticonvulsants: treatment or secondary prophylaxis of seizures, usually levetiracetam (Keppra) ^[4]:

• NOT for infratentorial lesions (cerebellar cortex is inhibitory → infratentorial tumours don't cause seizures) ^[4]
• Usually not for primary prophylaxis ^[4] — routine prophylactic anticonvulsants are NOT recommended for brain tumour patients who have not had a seizure (AAN guidelines). There is no evidence that prophylactic AEDs reduce first seizure risk, and they add side effects.
• Treatment of seizures: Levetiracetam is preferred because:
  • Minimal hepatic enzyme induction (unlike carbamazepine, phenytoin) → fewer drug interactions with chemotherapy agents and dexamethasone
  • Good tolerability profile
  • IV formulation available for acute use
• Secondary prophylaxis: Continue AEDs after a first tumour-related seizure; duration depends on post-surgical seizure control and tumour grade

If a meningioma presents with signs of impending herniation (↓consciousness, "blown pupil," Cushing's triad):

• Provides tissue diagnosis and WHO grading (the only way to definitively grade)
• Achieves cytoreduction → ↓mass effect, ↓oedema, ↓seizure risk
• Curative in many Grade 1 meningiomas with complete resection
• Provides immediate symptom relief (especially raised ICP, compression symptoms)

The Simpson Grade (1957, still widely used) classifies the completeness of meningioma resection and directly correlates with recurrence risk:

Prognosis: recurrence affected by extent of resection and histology ^[4]. Simpson Grade I/II resection is the goal whenever safely achievable. However, pursuing Simpson I at the cost of major neurological deficit (e.g., sacrificing the motor cortex or a cranial nerve) is NOT justified — the principle is maximal removal within the safety limit ^[4].

Surgical approach ^[4]:

• Craniotomy: flap of bone cut and reflected — Standard for most meningiomas; the bone flap is replaced at the end of surgery
• Burr hole: often for biopsy — Rarely used alone for meningioma; occasionally for stereotactic biopsy when diagnosis is uncertain ^[4]
• Craniectomy: burr hole + removal of surrounding bone — Used when the bone is invaded by tumour (hyperostosis, bone invasion) and cannot be replaced; cranioplasty later
• Transphenoidal: for pituitary / parasellar lesions ^[4] — Can be used for selected tuberculum sellae/planum sphenoidale meningiomas (endoscopic endonasal approach)

Image-guided surgery ^[4]:

• Frameless stereotaxy: Pre-operative MRI is co-registered with the patient's anatomy via skull fiducial markers → allows real-time intraoperative navigation of instruments relative to the tumour and critical structures (motor cortex, language areas identified on fMRI, white matter tracts identified on DTI tractography ^[9])

Functional monitoring ^[4]:

• Evoked potentials: Somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) → detect inadvertent injury to sensory/motor pathways during resection
• Awake craniotomy: For meningiomas near language cortex (dominant hemisphere) → patient is awake during the critical resection phase; intraoperative electrical stimulation of cortex → observe speech response to map speech cortex → guide resection to avoid affecting speech ^[4]

Pre-operative embolisation:

• For large, highly vascular meningiomas (especially convexity, parasagittal)
• Performed 24-48 hours before surgery via DSA
• Embolic agents (PVA particles, Gelfoam) injected into feeding dural arteries (usually middle meningeal artery)
• Purpose: reduce intraoperative blood loss and improve surgical field visibility
• Not always necessary; decision made by neurosurgeon and neuroradiologist

Why SRS works for meningioma: Meningiomas are well-circumscribed, sharply demarcated from brain, and have predictable geometry — ideal for focused high-dose radiation. The radiation damages tumour cell DNA, particularly the slow-dividing meningothelial cells, leading to growth arrest or slow regression. SRS achieves tumour control rates of 90-95% at 10 years for Grade 1 meningiomas.

• Surgical approach: Transphenoidal ^[4] (endoscopic endonasal) for tuberculum sellae/planum sphenoidale meningiomas; or pterional/subfrontal craniotomy
• Pre-operative: Pituitary hormone profile mandatory; distinguish from pituitary adenoma
• Post-operative: Monitor for diabetes insipidus, CSF rhinorrhoea, and hypopituitarism
• Visual monitoring: Pre- and post-operative formal visual field testing; visual improvement is expected in ~60-80% of patients with pre-operative visual loss

• If the SSS is patent or only partially invaded: Attempt complete resection including sinus wall repair or reconstruction
• If the SSS is completely occluded: Can safely resect the involved sinus segment (venous collaterals have already formed)
• If the SSS is partially patent and collaterals have NOT formed: Resecting the sinus risks massive venous infarction → leave the sinus-involved portion → treat residual with SRS/FSRT
• MR venography pre-operatively is essential to plan this decision

• Complete surgical resection is virtually impossible without causing permanent cranial nerve palsy (CN III, IV, V1, V2, VI all traverse the cavernous sinus)
• Primary SRS or FSRT is the preferred approach for most cavernous sinus meningiomas
• Surgery is reserved for: debulking if tumour extends outside the cavernous sinus causing significant mass effect, or if tissue diagnosis is needed

• Very rare; presents with progressive monocular visual loss
• FSRT is first-line (surgery would sacrifice the optic nerve)
• Observation if vision is still good and tumour is small
• Surgery only if blind in that eye (orbital exenteration) or for cosmetic/compressive indications

• Most are intradural, extramedullary, thoracic, WHO Grade 1
• Surgery is curative in the vast majority — en bloc resection with dural margin
• Approach: posterior laminectomy or laminoplasty
• Excellent prognosis: recurrence rate < 5% after complete resection

Increased ICP due to: ^[2]

• Tumour mass effect
• Vasogenic oedema (most apparent on FLAIR MRI): disrupted BBB, tumour-secreting VEGF
• Hydrocephalus: obstructive / communicating (leptomeningeal carcinomatosis)
• Obstruction of cerebral venous drainage (e.g. superior sagittal sinus thrombosis) ^[2]

If ICP rises sufficiently and cannot be compensated, brain herniation occurs — this is the most immediately life-threatening complication of meningioma:

Why does hypertension + bradycardia occur in Cushing's triad?

• Rising ICP compresses the brainstem → ischaemia of medullary vasomotor centre → massive sympathetic discharge → systemic hypertension
• The baroreceptors in the carotid sinus/aortic arch detect this hypertension → reflex vagal (parasympathetic) activation → bradycardia
• Respiratory depression: direct compression of the medullary respiratory centre
• This is a last-ditch compensatory response — Cushing's triad means brainstem compression is imminent and intervention is urgent

The slowly growing meningioma progressively compresses adjacent brain, leading to irreversible neurological damage if left untreated:

Key teaching point: This is why neurosurgeons advocate timely intervention for meningiomas near eloquent structures — the goal is to operate before irreversible damage occurs. "Watch and wait" is appropriate for small, asymptomatic tumours away from critical structures, but becomes increasingly risky when the tumour approaches the optic apparatus, motor cortex, or brainstem.

• Seizures affect 50-80% of primary brain tumours ^[17]
• Usually associated with slow-growing tumours that involve cortex, e.g. meningioma, low-grade glioma ^[2]
• Chronic seizures can lead to:
  • Status epilepticus: Prolonged seizure activity → neuronal excitotoxicity → permanent brain damage
  • Todd's paralysis: Temporary post-ictal focal weakness (minutes to hours); important not to confuse with stroke
  • Psychosocial impact: Driving restrictions, employment difficulties, social stigma, depression
  • Anti-epileptic drug side effects: Cognitive dulling, hepatotoxicity, teratogenicity (if reproductive age)
  • SUDEP (Sudden Unexpected Death in Epilepsy): Rare but a recognised risk of ongoing seizures

Meningiomas in certain locations can obstruct CSF pathways:

If untreated, hydrocephalus → raised ICP → all the consequences listed above ^[5].

Complications of CSF shunts (if required for hydrocephalus) ^[23]:

• Mechanical failure: shunt blockage (most common), migration, fracture
• Shunt infection (most serious): S. epidermidis, S. aureus
• Overshunting: postural headache, can lead to subdural haematoma (stretching of bridging veins)

• Parasagittal and falcine meningiomas can compress or invade the superior sagittal sinus or its tributary cortical veins
• If a draining vein is occluded acutely (by tumour growth or peri-operatively), venous back-pressure in the upstream cortex rises dramatically → venous infarction → often haemorrhagic (because the infarcted venous territory becomes congested with blood that cannot drain)
• This is a catastrophic complication that can cause sudden neurological deterioration, massive cerebral oedema, and death

• Although the majority of meningiomas are Grade 1, a subset will undergo malignant transformation over time:
  • Grade 1 → Grade 2 (atypical) → Grade 3 (anaplastic)
• This is relatively rare but well-documented, particularly in:
  • Recurrent meningiomas (each recurrence has a higher chance of grade progression)
  • Meningiomas with certain molecular features (e.g., TERT promoter mutation, CDKN2A/B deletion)
  • Radiation-induced meningiomas (from prior cranial RT)
• Grade progression means: faster growth, increased recurrence risk, more aggressive local invasion, and rarely, extracranial metastasis

• Extracranial metastasis is rare in brain tumours (∵ no lymphatic drainage) ^[4]
• However, anaplastic (Grade 3) meningiomas can very rarely metastasise to lungs, liver, bone, or lymph nodes
• This is extremely uncommon and almost exclusively seen in Grade 3 disease
• The SFT/haemangiopericytoma (formerly "meningeal haemangiopericytoma"), which is often confused with meningioma, has a much higher propensity for extracranial metastasis — important to distinguish histologically

• Brain tumour patients (including meningiomas) have an increased risk of venous thromboembolism (VTE) — DVT and PE
• Mechanism: tumour cells release tissue factor and other procoagulant substances; immobility from neurological deficits; perioperative state
• Incidence: up to 20-30% of brain tumour patients develop VTE during their disease course
• This is an important consideration in both the pre-operative and post-operative periods

• Intraoperative bleeding: Meningiomas are highly vascular (dural arterial supply) → significant blood loss during surgery, especially for large convexity or parasagittal tumours
• Post-operative haematoma: Extradural, subdural, or intraparenchymal haematoma in the surgical cavity → may require urgent re-operation
• Risk reduction: Pre-operative embolisation of feeding arteries (usually middle meningeal artery); meticulous haemostasis at surgery

• Surgical manipulation of brain → reactive oedema in the surrounding parenchyma
• May cause transient worsening of neurological deficits in the first few post-operative days
• Managed with continued dexamethasone; usually resolves within days to weeks
• If draining veins are sacrificed during surgery → venous congestion → more severe oedema

• CSF rhinorrhoea ^[22]: CSF leaks through the nose, most commonly after skull base surgery (transphenoidal or anterior cranial fossa approach)
• Will require antibiotics to prevent ascending meningitis, as well as decision to go back to OT for repair ^[22]
• Mechanism: Defect in the dural closure or skull base reconstruction → CSF drains through pneumatised sinuses (sphenoid, ethmoid, frontal) into the nasal cavity
• Risk: Ascending bacterial meningitis — bacteria travel retrograde from the nasal cavity through the CSF defect into the subarachnoid space
• Management: Lumbar drain to reduce CSF pressure (allows dural defect to heal); if persistent → surgical repair of defect (fat/fascia graft + fibrin sealant)

• Post-operative cortical irritation (blood products, surgical manipulation, oedema) → seizures
• Usually occur within the first 72 hours post-operatively
• Managed with anticonvulsants (levetiracetam); some neurosurgical centres use a short 7-day prophylactic peri-operative AED course

• Brain tumour patients are at particularly high risk of VTE peri-operatively (tumour-associated hypercoagulability + immobilisation + surgery)
• Prophylaxis: Sequential compression devices intra-operatively; LMWH started 24-48 hours post-operatively (after confirmed haemostasis on post-op CT)

• Altered CSF dynamics after surgery; blood products in CSF can block arachnoid granulations → communicating hydrocephalus
• Intraventricular blood (if enters ventricles) can cause obstructive hydrocephalus
• May require EVD temporarily or VP shunt if persistent

Prognosis: recurrence affected by extent of resection and histology ^[4]:

Recurrence can occur years to decades after apparently complete resection — this is why lifelong MRI surveillance is recommended.