GC108 A Mass In The Brain Brain Tumours
Brain tumours are abnormal growths of cells within the brain or central spinal canal, classified as primary or metastatic, and benign or malignant, that can cause neurological dysfunction through mass effect, infiltration, or raised intracranial pressure.
A Mass in the Brain: Brain Tumours
This lecture by Prof. Gilberto Leung (GC 108) is the definitive neurosurgical brain tumour session for the HKUMed summative exams. It covers three pillars:
- Pathology & Clinical Presentation — classification of brain tumours, the age-location-histology triad, and the four cardinal presentations (raised ICP, focal deficits, seizures, other location-specific symptoms).
- Principles of Management & Brain Tumour Surgery — medical therapy, surgical principles/techniques, radiation therapy, and radiosurgery.
- Specific Tumour Types — cerebral metastasis, meningioma, glioma (GBM), pituitary adenoma, and acoustic neuroma.
How this fits into clinical practice and exams: Brain tumours are a favourite topic because they cross neurosurgery, neurology, radiology, endocrinology, and oncology. Exam questions test your ability to (a) guess the tumour type from age + location + imaging, (b) understand the logic of management, and (c) know complications of treatment, especially transsphenoidal surgery.
Learning Objectives from the Slide Deck [1]:
- Presentation: raised ICP, seizure, focal deficit — correlate with anatomy
- Pathology: age, location, systemic disease (cancer, NF2)
- Imaging: location, enhancement pattern, common DDx
- Medical therapy: anticonvulsants (supratentorial) and steroids
- Surgery: indications for resecting metastasis
- Use of radiosurgery
- Chemoirradiation for GBM
- Treatment principles for pituitary adenoma & complications of transsphenoidal surgery
1. Pathology — Overview & Classification
Primary brain tumours can be benign (e.g. meningioma, pituitary adenoma), "intermediate" (histologically benign but tendency to recur or dedifferentiate, e.g. some low-grade gliomas, craniopharyngioma), or malignant (e.g. glioblastoma). [1]
Secondary (Metastasis) are the commonest intracranial lesions in adults. Their incidence is increasing due to effective systemic therapy making cancer a "chronic disease." Common origins: lung, breast, colon… melanoma has the highest propensity to metastasise to the brain. [1]
Why "not always clear-cut"? The lecture emphasises this explicitly. A meningioma is "benign" histologically but can compress vital structures and kill. A glioblastoma is malignant but virtually never metastasises outside the CNS (no lymphatic drainage from the brain). So the traditional benign/malignant binary from systemic oncology does not map neatly onto intracranial tumours. TNM staging is not useful for primary brain tumours [2].
| Cellular Origin | Tumour Examples |
|---|---|
| Meninges | Meningioma |
| Neuroepithelial tissue | Astrocytoma, GBM |
| Sellar | Pituitary adenoma |
| Nerve sheath | Schwannoma, neurofibroma |
| Neuronal | Gangliocytoma |
| Embryonal | Medulloblastoma |
| Lymphoid cells | Lymphoma |
| Germ cell | Germinoma, teratoma |
| Malformative | Craniopharyngioma |
High Yield — Classify by Origin
The lecture lists this table explicitly. In MCQs, you may be given a pathology description and asked to identify the cellular origin. Know each pairing cold.
This is one of the most exam-tested concepts in the lecture.
In adults: the three commonest intracranial tumours are metastases, glioma, and meningioma, and they are predominantly supratentorial. [1]
Commonest solid tumour in children: medulloblastoma, cerebellar astrocytoma, ependymoma, germ cell tumour — predominantly infratentorial (posterior fossa). [1]
| Feature | Adults | Children |
|---|---|---|
| Common location | ~70-85% supratentorial | ~70% infratentorial (age 2-12) |
| Common tumours | Metastasis, glioma, meningioma | Medulloblastoma, cerebellar astrocytoma, ependymoma, germ cell |
| Overall commonest | Metastasis (secondary) | Pilocytic astrocytoma (Grade I) |
Why does this matter? Because when you see a brain mass on imaging, the patient's age and the tumour location immediately narrow your differential. The lecture's "What is it likely to be?" slide shows four cases:
- F/5 → posterior fossa → think medulloblastoma or cerebellar astrocytoma
- F/65 → supratentorial dura-based → think meningioma or metastasis
- M/35 → intra-axial supratentorial → think glioma
- M/30 HIV+ve → multiple ring-enhancing lesions → think CNS lymphoma or toxoplasmosis [1]
Exam Trap — HIV + Brain Mass
In an immunosuppressed patient, always consider CNS lymphoma AND toxoplasmosis. Both can present with multiple ring-enhancing lesions. Toxoplasmosis is treated empirically first; if no response, biopsy for lymphoma.
2. Clinical Presentation
The lecture organises presentation into four categories:
Mechanisms of raised ICP from a brain tumour [1]:
- Mass effect — the tumour itself occupies space
- Peritumoural oedema — vasogenic oedema from disrupted BBB (tumour secretes VEGF)
- CSF flow obstruction — e.g. posterior fossa tumour blocking the 4th ventricle → obstructive hydrocephalus
- Venous congestion — e.g. midline meningioma compressing the superior sagittal sinus
Clinical features of raised ICP (from supporting material [3][4]):
- Headache: generalised, dull, worse in the morning (nocturnal hypoventilation → ↑PaCO₂ → cerebral vasodilation → ↑ICP), relieved by vomiting, worsened by bending/coughing/straining
- Nausea and vomiting (area postrema stimulation; posterior fossa lesions especially)
- Papilloedema on fundoscopy
- ↓ Consciousness
- Cushing's triad (hypertension, bradycardia, irregular respiration) — a late sign of impending herniation
- CN VI palsy (false localising sign — the long course makes it vulnerable)
Brain herniation due to tumour — the lecture includes a slide showing herniation patterns. These include subfalcine (under the falx → ACA compression), transtentorial (uncal → CN III palsy + contralateral hemiplegia), and tonsillar (cerebellar tonsils through foramen magnum → respiratory arrest). [1]
Loss of function due to: neuronal destruction, pressure effect, or oedema (reversible with steroids). This enables clinical localisation. [1]
The lecture gives specific examples:
- Aphasia — dominant hemisphere (usually left) frontal (Broca's) or temporal (Wernicke's)
- Right lower limb weakness — left parasagittal/medial motor cortex (leg area is medial on the homunculus)
- Truncal ataxia — cerebellar vermis (midline cerebellar lesion)
- Cognitive/personality change — frontal lobe
| Lobe | Deficits |
|---|---|
| Frontal | Motor deficits, personality change (apathy or disinhibition), expressive aphasia, urinary incontinence, anosmia (olfactory groove meningioma) |
| Temporal | Receptive aphasia, contralateral superior quadrantanopia, complex partial seizures, memory impairment |
| Parietal | Sensory deficits, contralateral inferior quadrantanopia, Gerstmann syndrome (dominant), hemispatial neglect (non-dominant) |
| Occipital | Contralateral homonymous hemianopia (macular sparing), visual hallucinations |
| Cerebellum | Ataxia, nystagmus, projectile vomiting, obstructive hydrocephalus → raised ICP |
Seizures result from neuronal hyperactivity. The mechanism is unclear. Seizures occur with supratentorial lesions ✓ but NOT infratentorial lesions ✗. [1]
Why? Seizures originate from cortical grey matter. The cerebellum and brainstem (infratentorial structures) do not generate typical seizure activity; their circuits are different. Slow-growing tumours (meningioma, low-grade glioma) are more often associated with seizures than rapidly growing ones because slow growth allows peri-tumoral cortical irritation without outright destruction [2].
Seizure types mentioned:
- Partial (focal) / grand mal (generalised tonic-clonic)
- Complex partial seizure — temporal lobe epilepsy with mesial temporal sclerosis
- Gelastic seizure — from hypothalamic hamartoma (laughing seizures — a classic exam factoid)
High Yield — Seizures: Supratentorial Only
If asked "which brain tumour presentation is unlikely with a posterior fossa tumour?" → Seizure. This is directly from the lecture slide. Infratentorial tumours present with raised ICP, cerebellar signs, and cranial nerve palsies — NOT seizures.
The lecture highlights specific tumour-location pairings:
| Tumour | Presentation |
|---|---|
| Acoustic neuroma | Deafness, tinnitus, (rarely) hemifacial spasm |
| Trigeminal schwannoma | CN V neuralgia |
| Pituitary adenoma | Bitemporal hemianopia, hormonal hyper/hyposecretion |
| Craniopharyngioma | Failure to thrive (in children) |
3. Neuroimaging for Brain Tumours
This is heavily tested. The lecture explains the physics from first principles:
Meningioma typically shows intense dura-based homogenous enhancement (no BBB as ECA supply ++). [1]
Why? Meningiomas are extra-axial tumours supplied by external carotid artery (ECA) dural branches. These vessels lack a blood-brain barrier, so iodinated or gadolinium contrast leaks freely into the tumour → intense, uniform enhancement. The "dural tail" sign (thickening of adjacent dura that enhances) is characteristic.
Low-grade glioma shows heterogeneous weaker enhancement (BBB relatively intact). [1]
Why? Low-grade gliomas are intra-axial and grow slowly. The BBB is relatively preserved, so less contrast leaks through → minimal or patchy enhancement.
Malignant glioma (GBM) — vascular + leaky BBB → strong heterogeneous enhancement, often ring-enhancing with central necrosis. [1]
Why? GBM induces massive neoangiogenesis (VEGF-driven) with abnormal, leaky vessels. The contrast extravasates through these vessels → bright enhancement. The centre is necrotic (no vessels) → doesn't enhance → creates the classic "ring-enhancing" pattern.
| Tumour | Enhancement Pattern | Why? |
|---|---|---|
| Meningioma | Intense, homogeneous, dural tail | ECA supply, no BBB |
| Low-grade glioma | Minimal/weak, heterogeneous | BBB relatively intact |
| High-grade glioma (GBM) | Strong, heterogeneous, ring-enhancing | Leaky BBB, neoangiogenesis, central necrosis |
| Metastasis | Ring-enhancing or homogeneous | Variable BBB disruption |
| CNS lymphoma | Homogeneous (immunocompetent), ring-enhancing (HIV) | Diffuse infiltration |
MR Spectroscopy can differentiate high-grade from low-grade lesions by measuring chemical compositions. High choline indicates high cellular turnover. [1]
Why choline? Choline is a marker of membrane turnover. Rapidly dividing cells (high-grade tumours) need to make more cell membranes → ↑choline peak. N-acetylaspartate (NAA) is a neuronal marker that decreases when neurons are destroyed. So the classic high-grade glioma MRS pattern is: ↑Cho, ↓NAA, ↑Cho/NAA ratio. A lactate peak may also appear (anaerobic metabolism in hypoxic tumour core).
PET for brain tumour — malignant lesion tends to be hypermetabolic. [1]
Uses FDG (fluorodeoxyglucose). Limitation: normal brain is very metabolically active, so background uptake is high, making small tumours harder to detect. Amino acid PET (e.g. C-11 methionine) is superior in brain tumour imaging.
Functional MRI (fMRI) & DTI Tractography — aids surgical planning by locating functionally important structures (e.g. motor cortex, Broca's and Wernicke's areas). [1]
Why? Before surgery, the neurosurgeon needs to know where eloquent cortex is relative to the tumour. fMRI detects BOLD signal changes during tasks (e.g. tapping fingers → motor cortex lights up). DTI (Diffusion Tensor Imaging) maps white matter tracts (e.g. corticospinal tract, arcuate fasciculus) by following the direction of water diffusion along axons. Together, they guide "maximal safe resection."
A bleeding glioblastoma can mimic haemorrhagic stroke. Pituitary apoplexy causes acute visual loss, hormonal crisis, and SAH. A cerebral aneurysm can mimic a sellar tumour! [1]
Exam Trap — Tumour Mimics
A rapidly expanding sellar mass on imaging is not always a pituitary tumour. It could be a cerebral aneurysm (especially an internal carotid artery aneurysm in the cavernous sinus). Always consider vascular pathology before biopsy/surgery in the sellar region. The lecture explicitly shows this as a mimic.
From radiology supporting material [5]:
| Feature | Intra-axial | Extra-axial |
|---|---|---|
| Definition | Within brain parenchyma | Outside brain parenchyma (dural, meningeal, etc.) |
| Claw sign | Present (parenchyma wraps around mass) | Absent |
| CSF cleft | Absent | Present (rim of CSF between lesion and brain) |
| Dural tail | Absent | Often present (meningioma) |
| Perilesional oedema | Common | Less common |
| Examples | Glioma, metastasis, abscess, lymphoma | Meningioma, schwannoma, epidermoid |
4. Principles of Management
Treatment options: General medication therapy, surgical biopsy & resection, radiation therapy, chemotherapy, target therapy, immunotherapy. [1]
Principles: Aim at cure if feasible. Preserve life. Preserve function. Preserve personhood. Maximise quality of life. Do not treat scan. [1]
'Do Not Treat Scan'
This principle means: don't reflexively operate on every radiological abnormality. A non-functioning incidental tumour in a frail elderly patient may be best observed. Treatment decisions must consider the whole patient — their age, fitness, neurological status, quality of life, and prognosis.
Anticonvulsant (e.g. phenytoin, levetiracetam): [1]
- Prophylaxis or treatment (if already seizure)
- Not for infratentorial lesion
Why not for infratentorial? As discussed above, infratentorial lesions don't cause cortical seizures.
Steroids (e.g. dexamethasone): [1]
- Exclude infection first!
- ↓ cerebral oedema and relieve symptoms
- Peri-operative use or palliation
- S/E: DM, immunosuppression, peptic ulcer…
Why exclude infection first? If the "tumour" is actually an abscess, giving steroids (immunosuppression) without antibiotics would be catastrophic. Also, if it's CNS lymphoma, steroids cause acute lymphocyte lysis → tumour shrinks temporarily, reducing diagnostic yield on subsequent biopsy [3].
Tranexamic acid — perioperatively to reduce bleeding. [1]
Principles: Obtain histological diagnosis. Maximal safe removal. Preserve life. Preserve function. "Resection margin" is difficult (concept doesn't apply like in systemic oncology). [1]
Key surgical decisions:
- Whether/When to resect?
- How to resect?
- How much to resect?
The lecture gives four exemplar scenarios:
| Scenario | Approach |
|---|---|
| CNS Lymphoma | Biopsy only (treated with chemo ± RT, not surgery) |
| Meningioma | Total resection (curative intent) |
| Glioma in eloquent area | Subtotal removal (preserve function) |
| Non-functioning incidentaloma | Observe (do not treat scan) |
High Yield — CNS Lymphoma = Biopsy ONLY
CNS lymphoma is treated with high-dose methotrexate-based chemotherapy ± whole-brain radiotherapy. Surgical resection is NOT indicated because lymphoma is diffusely infiltrative and chemosensitive. Furthermore, steroids must be withheld (if possible) before biopsy because they lyse lymphoma cells and reduce diagnostic yield.
The lecture describes several advanced techniques for brain tumour surgery:
1. Craniotomy — a bone flap is cut and reflected to access the tumour, then replaced [1].
2. Neuronavigation (Frameless Stereotaxy) — uses pre-operative MRI/CT co-registered with intraoperative markers to guide the surgeon in real-time to the tumour's location [1][3].
3. Microsurgery — operating under microscope magnification for precision [1].
4. Electrophysiological Monitoring — SSEP (somatosensory evoked potentials), MEP (motor evoked potentials), BAEP (brainstem auditory evoked potentials), motor mapping — alert surgeons of iatrogenic injury. [1] Example: BAEP during acoustic neuroma surgery to preserve hearing.
5. Awake Craniotomy & Speech Cortex Mapping — Electrical stimulation over speech cortex induces speech arrest → speech cortex mapped out & preserved. [1] Used when tumour is near Broca's or Wernicke's area. Patient is awake and speaking during surgery; if stimulation at a point causes speech arrest, that cortex is eloquent and must not be resected.
6. Intraoperative MRI — Identify residual tumour, confirm total removal. [1] The surgeon can scan mid-operation to see if tumour remains.
Aim: deliver high treatment dose to tumour bed, minimise radiation to normal tissue. Balance between treatment efficacy and side-effects. [1]
Types:
- Conventional external beam radiotherapy (ERT/EBRT) — fractionated doses over weeks
- Radiosurgery — focused radiation beams converge onto the tumour in a single or few sessions
Radiosurgery: Focused radiation beams converge onto tumour. X-knife uses x-ray; Gamma knife uses gamma ray. Cyberknife uses real-time imaging & moves to adjust to movement. [1]
Size limit for radiosurgery ≈ 2.5-3 cm, but can treat multiple lesions. [1]
Radiation necrosis can occur — this is a delayed complication where irradiated brain tissue becomes necrotic, mimicking tumour recurrence on imaging. [1]
Radiation Necrosis vs Tumour Recurrence
Both show ring-enhancing lesions on MRI. Differentiation requires MR perfusion (recurrence = hyperperfused; necrosis = hypoperfused), MR spectroscopy (recurrence = ↑Cho; necrosis = ↑lipid/lactate), or PET (recurrence = hypermetabolic; necrosis = hypometabolic). This is a common exam pitfall.
5. Specific Tumour Types
5A. Cerebral Metastasis
Commonest intracranial tumour overall. Rising incidence as cancer survival improves. Spread via haematogenous route or direct invasion. [1]
Common origins: lung, breast, colon, kidney, melanoma… [1]
May present BEFORE the primary disease is discovered. May develop when the primary disease is long in remission and without extraneural metastasis. [1]
Multiple lesions in a cancer patient can be something else — the lecture shows four differential diagnoses for multiple brain lesions: cysticercosis, CNS lymphoma, toxoplasmosis, metastases. [1]
A cancer patient with a solitary brain mass:
Cannot presume to be metastasis. DDx: primary brain tumour, abscess… History & examination crucial. Look for primary & screen for other foci. SPECT. Serum tumour markers (!). Surgery + histology if in doubt. [1]
High Yield — Solitary Brain Mass in Cancer Patient ≠ Automatic Metastasis
The lecture explicitly warns you not to assume a solitary brain mass in a cancer patient is metastatic. It could be a primary brain tumour or even an abscess (immunosuppressed patients on chemotherapy). You MUST work it up properly.
Tend to resect if: single lesion, something to palliate (e.g. raised ICP, focal deficit), low risk of causing deficit, young & fit, systemic disease under control, reasonable life expectancy. [1]
Aim: symptomatic palliation, maintain/improve quality of life, prolong life expectancy. Cure is uncommon but not impossible. [1]
"Do No Harm!" — If the patient is too frail or has widespread systemic disease, management is dexamethasone, and at most WBRT. [1]
| Treatment | Median Survival |
|---|---|
| Untreated | ~1 month |
| WBRT alone | ~3-6 months |
| Surgery + WBRT | ~12 months or more |
Rarely surgery alone. WBRT has significant S/E and radiosurgery is now preferred. Drugs that cross BBB may improve outcome further. [1]
High Yield — Survival Numbers for Metastasis
These survival figures are commonly tested as a general framework. Remember the order: untreated (1 month) < WBRT (3-6 months) < Surgery + WBRT (≥12 months). Modern practice increasingly uses stereotactic radiosurgery instead of WBRT to avoid neurocognitive side effects.
From arachnoid cap cells. Risk factors: female sex, radiation-induced, NF2. [1]
Dura-based lesion with dural tail and strong homogenous contrast enhancement. [1]
Mostly benign. Can be atypical or malignant. [1]
First choice: Surgery (can be easy or very difficult depending on location). Radiosurgery is effective. Generally good outcome. Recurrence ~15%. [1]
Why female predominance? Meningiomas express progesterone receptors. They may enlarge during pregnancy and are more common in women.
Why NF2? Neurofibromatosis type 2 involves mutations in the merlin/schwannomin gene on chromosome 22. This predisposes to bilateral vestibular schwannomas AND multiple meningiomas. The lecture shows a slide of NF2 with meningioma. [1]
Why "easy or very difficult"? A convexity meningioma (on the brain surface) can be resected completely and safely. A skull base meningioma encasing the internal carotid artery (the lecture shows "Encasing ICA") is extremely challenging because you cannot sacrifice the ICA without causing a massive stroke.
From astrocytes, oligodendrocytes, ependymal cells… Commonly astrocytoma (WHO Grade I-IV). [1]
GBM (Grade IV): Middle-aged or above. Infiltrative, rapid growth, invasive. Almost always recurs. Life expectancy ~14 months. [1]
The lecture shows classic GBM imaging:
- Heterogeneous enhancement — because of necrosis, haemorrhage, and variable vascularity
- Butterfly lesion — GBM crossing the corpus callosum to involve both hemispheres (pathognomonic)
Treatment for Malignant Glioma (WHO III or IV)
Maximal safe surgical removal where feasible. [1]
Chemoirradiation with temozolomide (TMZ) — standard therapy. An alkylating agent. Concomitant TMZ + ERT, then adjuvant TMZ. [1]
This is the Stupp protocol: 6 weeks of concurrent radiotherapy + daily TMZ, followed by 6 cycles of adjuvant TMZ (5 days every 28-day cycle). It improved median survival from ~12 months to ~14.6 months.
Anti-angiogenesis agents — e.g. bevacizumab. [1]
Bevacizumab is a monoclonal antibody against VEGF. It reduces tumour oedema and improves symptoms (↓steroid requirement) but has not conclusively improved overall survival.
Tumour Treating Field (TTF) — a wearable device that delivers alternating electric fields to the scalp, disrupting tumour cell mitosis. Added to standard TMZ in the landmark EF-14 trial, it improved median survival to ~20.9 months. [1]
Prognostic molecular markers (from supporting material [4]):
- MGMT promoter methylation — methylated MGMT silences the DNA repair enzyme → TMZ is more effective → better prognosis
- IDH mutation — IDH1/2 mutant gliomas have better prognosis than IDH-wildtype
5D. Pituitary Adenoma
20-25% prevalence at autopsy. Micro ( < 1 cm) or Macro ( > 1 cm). [1]
'Functioning' or 'Non-functioning'. [1]
Common presentations: Visual (bitemporal hemianopia), Hormonal (hyper/hyposecretion), Cranial nerve palsy, Bleeding (apoplexy), Hydrocephalus (at III ventricle). [1]
Why bitemporal hemianopia? The optic chiasm sits directly above the pituitary gland. A pituitary macroadenoma growing superiorly compresses the chiasm from below. The crossing fibres (nasal retina fibres from each eye, which carry temporal visual field information) are most vulnerable → loss of both temporal visual fields.
The lecture provides a decision algorithm:
| Tumour Type | First-Line Treatment |
|---|---|
| Prolactinoma | Medical: bromocriptine or cabergoline (dopamine agonists) |
| GH-secreting, ACTH-secreting, TSH-secreting | Surgery first |
| Non-functioning macroadenoma | Surgery (or radiosurgery) |
For prolactinoma: bromocriptine / cabergoline. For GH, ACTH, TSH-secreting: surgery first (or radiosurgery). [1]
High Yield — Prolactinoma = Medical Treatment First
Prolactinoma is the ONE functional pituitary adenoma treated primarily with medication. Dopamine agonists (cabergoline is preferred due to fewer side effects and better efficacy) suppress prolactin secretion AND shrink the tumour. Surgery is reserved for drug-resistant cases or intolerance. This was tested in the 2022 Fourth Summative MCQ Q69. [6]
Why medical treatment works for prolactinoma but not other adenomas? Prolactin-secreting cells (lactotrophs) are uniquely under tonic dopaminergic inhibition from the hypothalamus. Dopamine agonists mimic this physiological suppression, causing both antisecretory effects and tumour shrinkage. Other pituitary adenoma types (GH, ACTH, TSH) don't have this degree of pharmacological responsiveness (somatostatin analogues for GH-omas are a second-line option, not as effective as dopamine agonists for prolactinomas).
This is directly listed as "Essential Knowledge" on the summary slide. [1]
| Complication | Explanation |
|---|---|
| Mortality | Very rare |
| Hypopituitarism | Can cause shock (cortisol insufficiency) |
| Diabetes insipidus (DI) | Polyuria, haemoconcentration — damage to posterior pituitary/stalk |
| CSF leakage & meningitis | Breach of dural/arachnoid barrier → ascending infection. Diagnosed by beta-2-transferrin positivity in nasal fluid |
| Visual loss | Close monitoring post-op — may indicate haematoma or oedema at chiasm |
| ENT symptoms | Epistaxis, anosmia, sinusitis |
| Vascular injury | Internal carotid artery injury — catastrophic |
| Intracranial haemorrhage | Rare but serious |
| Pneumocephalus | Air in cranial cavity — seen on post-op CT |
CSF leakage is detected by beta-2-transferrin positivity in nasal fluid. [1]
High Yield — Beta-2-Transferrin
Beta-2-transferrin is a protein found ONLY in CSF (and perilymph/vitreous humour). If a patient post-transsphenoidal surgery develops clear nasal discharge, testing it for beta-2-transferrin confirms CSF rhinorrhoea. This requires antibiotics to prevent meningitis and may require surgical repair.
An emergency!! Acute haemorrhagic infarction +/- SAH. Headache, visual loss, coma… Acute cortisol insufficiency requiring replacement (which can predispose DI). Give cortisol before T4. Urgent surgery for decompression. [1]
Why give cortisol before T4? In hypopituitarism, if you give thyroid hormone (T4) before replacing cortisol, you accelerate metabolism without adequate cortisol to support the stress response → adrenal crisis (potentially fatal). This is a classic endocrine teaching point. Cortisol replacement must always precede thyroid replacement in panhypopituitarism.
Why can cortisol replacement predispose to DI? Cortisol normally helps suppress ADH secretion to some degree, but more importantly, in the context of pituitary apoplexy with partial posterior pituitary damage, the cortisol deficiency itself may be masking DI (cortisol is needed for free water excretion). When you replace cortisol, the masking effect is removed → DI becomes apparent → polyuria.
Actually 'vestibular schwannoma'. At cerebellopontine angle (CPA). Bilateral in NF2. Expands internal acoustic meatus. [1]
Clinical features: Sensorineural hearing loss, tinnitus. Cerebellar dysfunction. Brainstem compression & hydrocephalus. Occasionally CN V or VII symptoms. Treatment: Surgery or radiosurgery. [1]
Why sensorineural hearing loss (SNHL)? The tumour arises from the Schwann cells of the vestibular branch of CN VIII, but it is intimately related to the cochlear branch in the tight internal acoustic meatus. As it grows, it compresses the cochlear nerve → unilateral SNHL. This is gradual, which is why severe spinning vertigo is uncommon (the vestibular system compensates gradually).
Why CN V and VII? As the tumour grows into the CPA, it can compress adjacent cranial nerves. The facial nerve (CN VII) runs very close to CN VIII and is usually stretched over the tumour but remains functional (it's thick and resilient). Trigeminal nerve (CN V) involvement causes facial numbness or neuralgia. [3]
Why NF2? NF2 is characterised by bilateral vestibular schwannomas. Bilateral acoustic neuromas in a young patient = NF2 until proven otherwise.
The lecture shows the intraoperative view: Tumour & CN VII & VIII, lower cranial nerves, brainstem, AICA (anterior inferior cerebellar artery), cerebellum retracted. [1]
This concept appears in the lecture (context of why steroids work for tumour oedema) and is important for exam discrimination:
| Feature | Vasogenic Oedema | Cytotoxic Oedema |
|---|---|---|
| Aetiology | Tumours, abscess | Ischaemia |
| Pathophysiology | Extracellular fluid leakage from capillaries → white matter; disrupted BBB | Intracellular swelling due to defective Na/K ATPase; intact BBB |
| CT appearance | Pronounced grey-white matter differentiation | Loss of grey-white matter differentiation |
| Response to steroids | YES — steroids reduce vascular permeability | NO — the BBB is intact; the problem is intracellular |
Why this matters clinically: Steroids (dexamethasone) dramatically reduce vasogenic oedema around tumours, leading to rapid clinical improvement. They do NOT help in acute ischaemic stroke (cytotoxic oedema). This is a fundamental distinction.
7. Integration with Related Material
Brain tumours are one of the main causes of raised ICP. Posterior fossa tumours can obstruct CSF flow through the 4th ventricle → obstructive hydrocephalus. Treatment may include EVD (external ventricular drain) as a temporising measure before definitive tumour surgery.
The endocrine perspective complements the neurosurgical view. Key additions:
Bitemporal hemianopia from pituitary tumour, visual field defects from various tumour locations.
Tumour haemorrhage can mimic traumatic haemorrhage or haemorrhagic stroke. Always consider underlying tumour in spontaneous "stroke" in unusual locations or young patients.
8. Exam Intelligence
2020 Fourth Summative MCQ Q59 [8]:
"A 30-year-old woman was found to have a tumour in the left side of the posterior cranial fossa. Which is the MOST LIKELY clinical presentation?"
- A. Grand mal seizure ← WRONG — infratentorial lesions don't cause seizures
- B. Headache worse on erect than supine ← WRONG — ICP headache is worse supine/morning
- C. Left homonymous hemianopia ← WRONG — this localises to right optic radiation/tract
- D. Trigeminal neuralgia ← CORRECT — posterior fossa tumour (e.g. CPA tumour) can compress CN V
2020 Fourth Summative MCQ Q60 [8]:
"A 45-year-old woman with a frontal lobe tumour showing homogenous contrast enhancement on MRI. Most likely diagnosis?"
- A. Adenocarcinoma ← consider if metastatic, but not the best answer for homogeneous enhancement
- B. Brain abscess ← ring-enhancing, not homogeneous
- C. Low-grade astrocytoma ← minimal enhancement
- D. Medulloblastoma ← posterior fossa in children The answer is most likely meningioma (not listed as this is from a separate version) — but among the options, the best fit for homogeneous enhancement of a frontal lobe tumour in a middle-aged woman would be adenocarcinoma (metastasis) since gliomas and abscess don't show homogeneous enhancement.
2022 Fourth Summative MCQ Q69 [6]:
"A 30-year-old woman with amenorrhoea and galactorrhoea, sellar tumour, prolactin 10x ULN. Most appropriate management?"
- A. Bromocriptine ← CORRECT — prolactinoma treated medically first
- B. OCP ← treats symptoms, not the tumour
- C. Temozolomide ← for glioma
- D. Transsphenoidal resection ← not first-line for prolactinoma
| Trap | Correct Answer |
|---|---|
| Assuming all brain masses in cancer patients are metastases | Must exclude primary brain tumour, abscess; biopsy if doubt |
| Seizures from infratentorial tumours | Seizures = supratentorial ONLY |
| Giving steroids to suspected CNS lymphoma before biopsy | Steroids lyse lymphoma cells → ↓diagnostic yield |
| Giving T4 before cortisol in pituitary apoplexy | Always replace cortisol FIRST |
| Ring-enhancement after radiation = tumour recurrence | May be radiation necrosis — needs MRS/PET/perfusion to differentiate |
| Mild hyperprolactinaemia with macroadenoma = prolactinoma | May be "stalk effect" (not a functioning prolactinoma) |
| Meningioma = always benign | Can be atypical or malignant; recurrence ~15% |
For "describe the management of a patient with GBM":
- Medical: dexamethasone for oedema, anticonvulsants if seizures (levetiracetam)
- Surgical: maximal safe resection
- Adjuvant: chemoirradiation with temozolomide (Stupp protocol: concurrent TMZ + RT, then adjuvant TMZ)
- Supportive: consider bevacizumab, TTF
- Prognosis: median survival ~14 months
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MCQ: A 5-year-old child presents with morning headaches, vomiting, and truncal ataxia. CT shows a posterior fossa mass. What is the most likely diagnosis? → Medulloblastoma (or cerebellar pilocytic astrocytoma)
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SAQ: List four mechanisms by which a brain tumour causes raised ICP. → Mass effect, peritumoural oedema, CSF flow obstruction, venous congestion
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MCQ: Which brain tumour is NOT treated by surgical resection? → CNS lymphoma (biopsy only)
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SAQ: A 60-year-old man with known lung cancer presents with seizures and a single ring-enhancing brain lesion. Outline your management. → Steroids (dexamethasone) → exclude abscess/primary brain tumour → staging (look for other metastases) → if solitary + fit + systemic disease controlled → resection + post-op radiosurgery/WBRT. If unfit → WBRT or radiosurgery ± palliative care.
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MCQ: What imaging feature is characteristic of meningioma? → Dura-based, homogeneous enhancement, dural tail sign
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SAQ: List five complications of transsphenoidal pituitary surgery. → Hypopituitarism (adrenal crisis), DI, CSF leak/meningitis, visual loss, vascular injury, epistaxis, pneumocephalus
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Viva: Why is bromocriptine/cabergoline the first-line treatment for prolactinoma? → Prolactin secretion is under tonic dopaminergic inhibition. Dopamine agonists mimic physiological suppression → reduce prolactin + shrink tumour. Surgery reserved for resistant cases.
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MCQ: A patient with pituitary apoplexy requires hormone replacement. Which hormone must be replaced first? → Cortisol (before T4)
High Yield Summary
Brain tumours — the essentials you cannot walk into the exam without knowing:
- Classification: Primary (benign/intermediate/malignant) vs Secondary (metastasis = commonest in adults). Classify primary tumours by cellular origin.
- Age-Location-Histology: Adults = supratentorial (metastasis, glioma, meningioma). Children = infratentorial (medulloblastoma, cerebellar astrocytoma, ependymoma).
- Four presentations: Raised ICP (mass, oedema, CSF obstruction, venous congestion), focal deficits, seizures (supratentorial ONLY), location-specific symptoms.
- Imaging: Meningioma = homogeneous enhancement + dural tail (no BBB). Low-grade glioma = weak enhancement. GBM = ring-enhancing + necrosis. MRS: ↑Cho = high-grade. fMRI/DTI for surgical planning.
- Management principles: Cure if feasible, preserve function, do not treat scan. Steroids for oedema (exclude infection/lymphoma first). Anticonvulsants for supratentorial tumours only.
- Metastasis surgery: Resect if single, something to palliate, low deficit risk, fit patient, systemic disease controlled. Median survival: untreated 1 month → WBRT 3-6 months → Surgery + WBRT ≥12 months.
- Meningioma: Arachnoid cap cells, female > male, NF2, surgery first, recurrence ~15%.
- GBM: Grade IV, infiltrative, ~14 months survival. Maximal safe resection + chemoirradiation (TMZ).
- Pituitary adenoma: Prolactinoma = medical (cabergoline/bromocriptine). All others = surgery first. Transsphenoidal approach. Complications: hypopituitarism, DI, CSF leak, visual loss.
- Pituitary apoplexy: Emergency. Replace cortisol BEFORE T4. Urgent decompression.
- Acoustic neuroma: Vestibular schwannoma at CPA, SNHL, bilateral = NF2.
- CNS lymphoma = biopsy only, no steroids before biopsy.
Active Recall - Brain Tumours
[1] Lecture slides: GC 108. A mass in the brain brain tumours.pdf (all pages/slides) [2] Senior notes: Maksim Surgery Notes.pdf (p. 361-362, Brain tumours section) [3] Senior notes: Ryan Ho Neurology.pdf (p. 161-167, Intracranial Tumours section) [4] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p. 521-534, Brain tumours section) [5] Senior notes: Ryan Ho Radiology.pdf (p. 23, Intracranial Tumours — intra vs extra-axial) [6] Past papers: 2022 Fourth Summative MCQ.pdf (Q69) [7] Senior notes: Ryan Ho Endocrine.pdf (p. 106-107, Pituitary Tumours section) [8] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q59, Q60)
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