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”? A histologically low-grade meningioma can still threaten life through location and compression, while glioblastoma is biologically malignant yet extracranial metastasis is rare. “No lymphatics” is no longer a sufficient explanation because meningeal lymphatic vessels are recognised; multiple biological and anatomical barriers, treatment and limited survival contribute. Modern CNS diagnosis therefore integrates tumour type, molecular features and CNS WHO grade rather than relying on a simple benign/malignant binary or systemic TNM staging. ^[2][11]

Reading the pie chart: In the historical dataset reproduced on the slide, meningioma is the largest slice (23.2%), followed by glioblastoma (15.6%), nerve-sheath tumours (12.7%), oligodendroglial tumours (11.4%) and pituitary adenoma (9.8%). The slide itself warns that these proportions vary with study methods, country and age group; use the chart to appreciate diversity, not as a universal epidemiological distribution. ^[1]

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]

Why does this matter? Age and compartment narrow—but do not settle—the differential. The lecture's four unlabeled cases are an exercise in pattern recognition, not a histological answer key: the 5-year-old has a midline posterior-fossa mass (medulloblastoma is high on the list); the 65-year-old has a discrete posterior-fossa lesion (metastasis becomes more likely); the 35-year-old has a large central/skull-base mass; and the 30-year-old with HIV has an intracranial lesion requiring an opportunistic-infection/lymphoma differential. Imaging alone does not establish tissue type. ^[1]

Mechanisms of raised ICP from a brain tumour ^[1]:

1. Mass effect — the tumour itself occupies space
2. Peritumoural oedema — vasogenic oedema from disrupted BBB (tumour secretes VEGF)
3. CSF flow obstruction — e.g. posterior fossa tumour blocking the 4th ventricle → obstructive hydrocephalus
4. Venous congestion — e.g. midline meningioma compressing the superior sagittal sinus

What the four scans show: direct mass effect distorts adjacent brain/ventricles and shifts midline structures; vasogenic oedema is T2-bright white-matter swelling around the tumour; a posterior-fossa mass can obstruct the fourth ventricle and dilate the upstream ventricles; and a lesion abutting a major dural sinus can narrow venous outflow on venography. ^[1]

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 diagram shows subfalcine shift under the falx (possible ACA compression), uncal displacement through the tentorial notch (ipsilateral CN III compression), central downward transtentorial displacement, and tonsillar descent through the foramen magnum (brainstem/respiratory compromise). The arrows describe pressure-driven displacement, not four mutually exclusive syndromes; patterns can coexist. ^[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

Seizures arise most directly from irritated or infiltrated cerebral cortex, so a tumour-related first seizure strongly points to a supratentorial/cortical lesion. The slide's “supratentorial ✓ / infratentorial ✗” is a high-yield localisation rule, not a claim that a patient with a posterior-fossa tumour can never seize from another cause. ^[1][10]

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)

The lecture highlights specific tumour-location pairings:

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, usually vascular masses supplied substantially by dural branches outside the blood-brain barrier, so they often enhance avidly and uniformly. The “dural tail” is a helpful clue but is not specific to meningioma, and heterogeneous enhancement can occur with calcification, necrosis or higher-grade disease. ^[1][14]

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.

MR spectroscopy can support grading/differential diagnosis by measuring metabolites; it does not replace integrated imaging and tissue diagnosis. High choline suggests increased membrane turnover. ^[1][22]

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]

From radiology supporting material ^[5]:

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]

Antiseizure medication (e.g. levetiracetam): treat a verified tumour-related seizure. Do not routinely prescribe prophylaxis to a seizure-naive patient solely because a brain tumour is present. SNO/EANO also finds insufficient evidence to choose prophylaxis by tumour location or imaging features. When treatment is needed, avoid unnecessary enzyme-inducing drug interactions with systemic anticancer therapy. ^[1][10]

Steroids (e.g. dexamethasone): ^[1]

• Exclude infection first!
• ↓ cerebral oedema and relieve symptoms
• Peri-operative use or palliation
• S/E: DM, immunosuppression, peptic ulcer…

Steroid caveats: Dexamethasone is for symptomatic vasogenic oedema/mass effect, not the scan alone, and should be tapered as rapidly as clinically tolerated. If abscess is possible, urgent antimicrobial/source-control assessment is essential; steroid use is reserved for selected life-threatening oedema/mass effect. If primary CNS lymphoma is possible, avoid corticosteroids before tissue diagnosis whenever clinically safe because they can obscure pathology. ^[20][24]

Slide-era/local practice point: The deck lists perioperative tranexamic acid to reduce bleeding. It is not a universal medication for every brain-tumour operation; use depends on procedure-specific bleeding risk, contraindications and the local anaesthetic/neurosurgical protocol. ^[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:

The lecture describes several advanced techniques for brain tumour surgery:

The preceding historical images show trephined skulls and barber-surgeons. Their role is contextual: opening the skull long predates anaesthesia, antisepsis, microscopy and imaging; they are not a modern operative-technique sequence. ^[1]

1. Craniotomy — the visual sequence shows scalp reflection, a removable bone flap, tumour exposure and fixation plates when the flap is replaced. This distinguishes a craniotomy from a craniectomy, in which the bone is not replaced at the same operation. ^[1]

2. Neuronavigation (Frameless Stereotaxy) — the diagram shows the workflow: pre-operative scan → surgical planning → patient-to-image registration → tracked intraoperative navigation. It improves localisation, but accuracy can degrade after dural opening as tumour removal and CSF loss produce brain shift. ^[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

What the dose-distribution diagram shows: Whole-brain radiotherapy exposes the entire brain to a treatment dose, conventional focal radiotherapy narrows the field but still gives surrounding tissue a dose gradient, and stereotactic radiosurgery concentrates the highest dose tightly around a small target. The trade-off is intracranial coverage versus normal-brain exposure and neurocognitive toxicity. ^[1][12][13]

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]

The slide's ≈2.5–3 cm “limit” is a rule of thumb, not an absolute cut-off. Selection depends on tumour volume, location, oedema, prior therapy, number/total volume of metastases and normal-tissue constraints; larger lesions may be resected or treated with fractionated stereotactic radiotherapy. Current guidelines support SRS for selected patients with multiple lesions, not just a single small metastasis. ^[12][13]

Radiation necrosis can occur — this is a delayed complication where irradiated brain tissue becomes necrotic, mimicking tumour recurrence on imaging. ^[1]

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]

Management is risk-adapted: observation is first option for many incidental, asymptomatic suspected meningiomas; surgery is first option for symptomatic or growing accessible tumours, while radiosurgery/fractionated radiotherapy are options in selected settings. The slide's “recurrence ~15%” is not a universal rate—risk depends on WHO grade, molecular features, location, extent of resection and follow-up. ^[14]

Sex/hormone association: Meningiomas are more common in women and often express progesterone receptors; some change size during pregnancy, but receptor expression alone does not fully explain epidemiology or dictate treatment. ^[14]

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.

Classification update: The slide uses a histology-only WHO I–IV framework and the older name “glioblastoma multiforme.” WHO CNS5 integrates histology with molecular features. Adult-type diffuse gliomas are separated chiefly into astrocytoma, IDH-mutant; oligodendroglioma, IDH-mutant and 1p/19q-codeleted; and glioblastoma, IDH-wildtype, CNS WHO grade 4. An IDH-mutant grade 4 astrocytoma is no longer called glioblastoma. ^[11]

Glioblastoma, IDH-wildtype is a highly infiltrative adult diffuse glioma with high recurrence risk. The slide's “~14 months” is a historical cohort-level median, not an individual prognosis; outcome varies with age, performance, extent of safe resection, MGMT promoter methylation and therapy. ^[1][11]

The lecture shows classic GBM imaging:

• Heterogeneous enhancement — because of necrosis, haemorrhage, and variable vascularity
• Butterfly pattern — an infiltrative lesion crossing the corpus callosum. This is not pathognomonic for glioblastoma; primary CNS lymphoma and tumefactive demyelination are important mimics.

Treatment Principle for Glioblastoma

Maximal safe surgical removal where feasible. ^[1]

Chemoirradiation with temozolomide (TMZ) — standard therapy. An alkylating agent. Concomitant TMZ + ERT, then adjuvant TMZ. ^[1]

For an eligible newly diagnosed patient, the standard framework remains maximal safe resection (or biopsy when resection is unsafe), fractionated radiotherapy with concurrent temozolomide, then adjuvant temozolomide. The exact regimen is adapted for age, frailty and molecular markers—especially MGMT promoter methylation—rather than applied identically to everyone. ^[11]

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 Fields (TTFields) — the slide's device-and-mitosis diagram shows alternating electric fields disrupting dividing tumour cells. TTFields can be discussed as an adjunct during maintenance temozolomide for selected patients; adherence, scalp toxicity, access, burden and patient preference matter. ^[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

Actually 'vestibular schwannoma'. At cerebellopontine angle (CPA). Bilateral in NF2. Expands internal acoustic meatus. ^[1]

Clinical features: unilateral sensorineural hearing loss and tinnitus; larger lesions can cause cerebellar dysfunction, CN V symptoms, brainstem compression and hydrocephalus. Management options include observation, microsurgery, radiosurgery or fractionated radiotherapy, selected by symptoms, hearing, tumour size/growth, age, patient preference and centre expertise. ^[1][18]

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 intraoperative photograph labels the tumour between the retracted cerebellum and brainstem, with CN VII/VIII draped at its surface and the AICA and lower cranial nerves nearby. This visually explains the operative risks to hearing, facial function, swallowing/voice and brainstem vessels. ^[1]

Brain tumours are a major cause of raised ICP. Posterior-fossa tumours can obstruct the fourth ventricle and cause hydrocephalus. CSF diversion such as an EVD may be a temporising measure, but drainage strategy and timing relative to tumour surgery require neurosurgical control because abrupt pressure shifts can worsen herniation.

The endocrine perspective complements the neurosurgical view. Key additions:

• Order of hormone loss in hypopituitarism: GH → FSH/LH → ACTH → TSH ^[7]
• Prolactinoma: serum prolactin usually > 10× ULN (if only mildly elevated in a macroadenoma, think "stalk effect" — compression of the stalk interrupts dopamine delivery → mild hyperprolactinaemia, not a true prolactinoma) ^[7]

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.

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 — a seizure is unlikely to be caused directly by an infratentorial lesion
• 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 Caution: A dural-based avidly homogeneous frontal lesion in this demographic would suggest meningioma, but “dural-based” is absent and meningioma is not among the recorded choices. Of these options, adenocarcinoma metastasis is the least incompatible, yet enhancement alone is insufficient. Check the original paper/key rather than converting this incomplete stem into a false imaging rule.

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

For "describe the management of a patient with GBM":

1. Medical: dexamethasone for oedema, anticonvulsants if seizures (levetiracetam)
2. Surgical: maximal safe resection
3. Adjuvant: chemoirradiation with temozolomide (Stupp protocol: concurrent TMZ + RT, then adjuvant TMZ)
4. Adjuncts/recurrence: discuss TTFields during maintenance in selected patients; bevacizumab is mainly used for recurrent disease or oedema/symptom control rather than proven overall-survival benefit
5. Prognosis: explain that outcome is individual and depends on performance, age, molecular markers and treatment; the slide's ~14 months is historical