Brain Tumour
Summary
Brain tumours are abnormal growths arising from intracranial structures, classified as primary (originating within the CNS) or secondary (metastatic). Primary brain tumours include gliomas, meningiomas, pituitary adenomas, and schwannomas, while metastases from systemic cancers are the most common intracranial malignancies in adults. Presentation depends on tumour location and includes headache, seizures, focal neurological deficits, and personality changes. Diagnosis requires neuroimaging (MRI) and often histopathological confirmation. Management is multimodal, involving surgery, radiotherapy, and chemotherapy depending on tumour type. Prognosis varies dramatically from excellent (benign meningioma) to very poor (glioblastoma, median survival 15 months).
Key Facts
- Epidemiology: Primary brain tumours: 7-8 per 100,000/year; metastases 10x more common
- Most common primary tumour: Meningioma (benign); Glioblastoma (malignant)
- Most common sources of metastases: Lung (50%), Breast (15%), Melanoma (10%), Renal, Colorectal
- Peak age: Glioblastoma: 55-65 years; Medulloblastoma: Childhood
- Classic presentation triad: Headache + Nausea/vomiting + Papilloedema (raised ICP)
- Imaging gold standard: MRI with gadolinium contrast
- Glioblastoma survival: Median 15 months with optimal treatment
- Important classification: WHO Grade I-IV for gliomas
- Treatment cornerstone: Maximal safe surgical resection
- Stupp protocol: Surgery + RT + Temozolomide for glioblastoma
Clinical Pearls
"Worst Headache Pattern": Brain tumour headaches are classically worse on waking (raised ICP during recumbent sleep), worse with Valsalva (coughing, straining), and progressive over weeks.
"New Seizures in Adults": Any new-onset seizure in an adult over 25 requires brain imaging. Seizures are the presenting feature in 20-40% of brain tumours.
"Metastases > Primary": In adults, brain metastases outnumber primary brain tumours 10:1. Always consider a primary cancer workup.
"The Eloquent Cortex": Surgery near motor, sensory, language, or visual cortex requires awake craniotomy with cortical mapping to preserve function.
"Steroid Response": Dexamethasone dramatically reduces peritumoural oedema within hours. If a patient with suspected brain tumour improves on steroids, it supports (but doesn't confirm) the diagnosis.
Why This Matters Clinically
Brain tumours cause significant morbidity including cognitive impairment, seizures, and functional disability. Early recognition and referral to specialist neuro-oncology services improves outcomes. Even for aggressive tumours, treatment can provide meaningful survival extension and symptom palliation. Understanding the diverse presentations and appropriate referral pathways is essential for all clinicians.[1,2]
Incidence & Prevalence
| Tumour Type | Incidence (per 100,000/year) | Notes |
|---|---|---|
| All primary brain tumours | 7-8 | Including benign |
| Malignant primary brain tumours | 3-4 | Gliomas predominate |
| Metastatic brain tumours | 70-80 | 10x more common than primary |
| Glioblastoma | 3.2 | Most common malignant primary |
| Meningioma | 2.3 | Most common benign |
| Pituitary adenoma | 0.8 | Often incidental |
Demographics
| Factor | Details |
|---|---|
| Age | Bimodal: paediatric peak (medulloblastoma, ependymoma) and adult peak (glioma, metastases) |
| Sex | Gliomas: M > F (1.4:1); Meningiomas: F > M (2:1) |
| Trend | Incidence increasing, partly due to improved imaging detection |
| Survival | Highly variable by tumour type |
Risk Factors
| Factor | Relative Risk | Notes |
|---|---|---|
| Ionising radiation | 3-10x | Therapeutic RT, atomic bomb survivors |
| Genetic syndromes | High | NF1/NF2 (schwannomas, meningiomas), Li-Fraumeni, Turcot, VHL |
| Family history | 2x | First-degree relative with brain tumour |
| Age | Variable | Increases with age for glioma |
| Immunosuppression | 3-5x | CNS lymphoma (HIV, transplant) |
| Mobile phone use | No proven link | Extensively studied; no causal relationship established |
Mechanism
Step 1: Cellular Origin
- Brain tumours arise from various cell types: astrocytes (astrocytoma), oligodendrocytes, ependymal cells, meningeal cells, or Schwann cells
- Genetic mutations accumulate (TP53, PTEN, EGFR, IDH1/2, 1p/19q co-deletion)
- Transformation from low-grade to high-grade (secondary glioblastoma) can occur
Step 2: Tumour Growth
- Uncontrolled proliferation within fixed intracranial space
- Neovascularisation (VEGF-driven) provides blood supply
- Tumour cells infiltrate along white matter tracts (gliomas)
- Meningiomas compress but rarely invade brain parenchyma
Step 3: Mass Effect
- Growing tumour displaces normal brain tissue
- Compression of adjacent structures causes focal deficits
- Obstruction of CSF pathways → hydrocephalus
- Herniation syndromes if space-occupying effect severe
Step 4: Peritumoural Oedema
- Vasogenic oedema due to leaky tumour blood vessels (disrupted BBB)
- Oedema often exceeds tumour volume
- Contributes significantly to symptoms and mass effect
- Responsive to corticosteroids (dexamethasone)
Step 5: Secondary Effects
- Increased intracranial pressure → headache, vomiting, papilloedema
- Neuronal irritation → seizures
- Invasion of functional cortex → focal neurological deficits
- Hormone disruption (pituitary tumours) → endocrinopathy
WHO Classification of CNS Tumours (2021)
| Grade | Tumour Types | Behaviour |
|---|---|---|
| Grade 1 | Pilocytic astrocytoma, Meningioma (most), Schwannoma | Benign, potentially curable with surgery |
| Grade 2 | Diffuse astrocytoma (IDH-mutant), Oligodendroglioma | Low-grade, infiltrative but slow-growing |
| Grade 3 | Anaplastic astrocytoma, Anaplastic oligodendroglioma | Malignant, tendency to progress |
| Grade 4 | Glioblastoma (IDH-wildtype), Diffuse midline glioma | Highly malignant, poor prognosis |
Molecular Markers
| Marker | Significance |
|---|---|
| IDH1/2 mutation | Better prognosis in gliomas; distinguishes secondary from primary GBM |
| 1p/19q co-deletion | Oligodendroglioma marker; better prognosis, chemosensitive |
| MGMT methylation | Predicts response to temozolomide in glioblastoma |
| EGFR amplification | Common in primary glioblastoma; therapeutic target |
| H3K27M mutation | Diffuse midline glioma; very poor prognosis |
Symptoms by Category
| Category | Symptoms |
|---|---|
| Raised ICP | Headache (classically worse on waking, progressive), nausea/vomiting, visual obscurations, cognitive slowing |
| Seizures | Focal or generalised; presenting feature in 20-40% |
| Focal deficits | Hemiparesis, hemisensory loss, visual field defect, dysphasia, ataxia |
| Cognitive/Behavioural | Memory impairment, personality change, disinhibition (frontal), apathy |
| Endocrine (pituitary) | Amenorrhoea, galactorrhoea, acromegaly, Cushing's, hypopituitarism |
| Visual (pituitary) | Bitemporal hemianopia from chiasmal compression |
Symptoms by Location
| Location | Typical Symptoms |
|---|---|
| Frontal lobe | Personality change, disinhibition, expressive dysphasia (dominant), contralateral weakness, seizures |
| Temporal lobe | Memory disturbance, receptive dysphasia (dominant), complex partial seizures, upper quadrantanopia |
| Parietal lobe | Sensory loss, spatial neglect (non-dominant), apraxia, lower quadrantanopia |
| Occipital lobe | Homonymous hemianopia, visual hallucinations |
| Posterior fossa | Ataxia, nystagmus, cranial nerve palsies, hydrocephalus |
| Brainstem | Cranial nerve deficits, long tract signs, ataxia, locked-in syndrome |
| Sellar/suprasellar | Bitemporal hemianopia, pituitary dysfunction |
Signs
| Finding | Significance |
|---|---|
| Papilloedema | Raised intracranial pressure |
| Focal weakness | Motor cortex or internal capsule involvement |
| Visual field defect | Location-specific (hemianopia, quadrantanopia) |
| Dysphasia | Dominant hemisphere lesion |
| Cerebellar signs | Posterior fossa tumour |
| Cranial nerve palsy | Base of skull, brainstem, or meningeal involvement |
| False localising signs | VI nerve palsy with raised ICP |
Red Flags
[!CAUTION] Red Flags — Urgent Imaging Required:
- New-onset seizures in adults (especially >25 years)
- Progressive headache with morning vomiting
- Papilloedema on fundoscopy
- Rapid neurological deterioration
- Cushing's triad (hypertension, bradycardia, irregular respirations) — impending herniation
- New focal neurological deficit without clear alternative cause
- Personality or cognitive change with no psychiatric history
Structured Neurological Examination
General Inspection:
- Consciousness level (GCS)
- Cognitive state (orientation, attention, memory)
- Speech and language assessment
- Signs of raised ICP (altered alertness, posturing)
Cranial Nerves:
- Fundoscopy (papilloedema essential)
- Visual fields to confrontation
- Pupil responses (III nerve, herniation)
- Eye movements (brainstem lesions)
- Facial power and sensation
- Hearing assessment
Motor System:
- Tone (increased with upper motor neurone lesions)
- Power (pyramidal pattern weakness)
- Reflexes (hyperreflexia, clonus)
- Plantar response (Babinski sign)
- Pronator drift (subtle weakness)
Sensory System:
- Light touch, pinprick, temperature
- Proprioception, vibration
- Cortical sensory function (graphaesthesia, stereognosis)
- Neglect testing (parietal lesions)
Cerebellar Examination:
- Coordination (finger-nose, heel-shin)
- Dysdiadochokinesis
- Gait assessment
- Romberg's test
- Nystagmus
Key Signs to Detect
| Sign | Technique | Significance |
|---|---|---|
| Papilloedema | Fundoscopy | Raised ICP |
| Visual field defect | Confrontation | Localising value |
| Pronator drift | Arm extension with eyes closed | Subtle pyramidal weakness |
| Homonymous hemianopia | Visual field testing | Posterior lesion (optic tract to occipital cortex) |
| Bitemporal hemianopia | Visual field testing | Chiasmal compression (pituitary) |
| Cerebellar signs | Coordination testing | Posterior fossa lesion |
First-Line Imaging
| Investigation | Indication | Key Findings |
|---|---|---|
| CT Head (non-contrast) | Emergency assessment, screening | Mass effect, hydrocephalus, haemorrhage, calcification |
| CT Head (contrast) | If MRI not immediately available | Enhancing masses |
| MRI Brain (with gadolinium) | Gold standard for all suspected brain tumours | Tumour extent, oedema, enhancement pattern, relationship to eloquent areas |
MRI Features by Tumour Type
| Tumour | T1 (Pre-contrast) | T1 (Post-gadolinium) | T2/FLAIR |
|---|---|---|---|
| Glioblastoma | Hypointense centre, isointense rim | Ring enhancement with necrosis | High signal with extensive oedema |
| Meningioma | Isointense | Homogeneous intense enhancement, dural tail | Isointense, minimal oedema |
| Metastasis | Hypointense | Ring or nodular enhancement | Disproportionate oedema |
| Low-grade glioma | Hypointense | Minimal/no enhancement | High signal, diffuse |
Laboratory Investigations
| Investigation | Rationale |
|---|---|
| FBC, U&E, LFTs, coagulation | Pre-surgical baseline |
| Tumour markers (AFP, βHCG) | Suspected germ cell tumour (young patients) |
| Pituitary hormone panel | Sellar/suprasellar lesions |
| CSF cytology | Leptomeningeal disease (if safe to LP) |
Staging/Further Investigations
| Investigation | Indication |
|---|---|
| CT Chest/Abdomen/Pelvis | Metastatic tumour — identify primary |
| PET scan | Primary cancer search, recurrence vs radiation necrosis |
| MR Spectroscopy | Differentiating tumour from other pathology |
| Perfusion MRI | Assessing tumour grade, treatment response |
| Stereotactic biopsy | Histological diagnosis if resection not feasible |
Management Algorithm
SUSPECTED BRAIN TUMOUR
↓
┌────────────────────────────────────────────────────────┐
│ INITIAL ASSESSMENT │
│ - Urgent CT Head if emergency (seizure, acute focal │
│ deficit, reduced consciousness) │
│ - MRI Brain with gadolinium (gold standard) │
│ - Assess for raised ICP and herniation risk │
└────────────────────────────────────────────────────────┘
↓
┌────────────────────────────────────────────────────────┐
│ SUPPORTIVE CARE │
├────────────────────────────────────────────────────────┤
│ ➤ Dexamethasone 8-16 mg/day (reduces oedema) │
│ ➤ PPI cover (omeprazole) │
│ ➤ Anticonvulsants if seizures (levetiracetam) │
│ ➤ VTE prophylaxis │
│ ➤ Urgent neurosurgical referral │
└────────────────────────────────────────────────────────┘
↓
┌────────────────────────────────────────────────────────┐
│ TUMOUR-SPECIFIC MANAGEMENT │
├────────────────────────────────────────────────────────┤
│ GLIOBLASTOMA (Grade 4): │
│ ➤ Maximal safe resection │
│ ➤ Stupp protocol: RT 60 Gy + Temozolomide │
│ ➤ Adjuvant Temozolomide x6 cycles │
│ ➤ Consider tumour treating fields (Optune) │
│ ➤ Median survival: 15 months │
├────────────────────────────────────────────────────────┤
│ LOW-GRADE GLIOMA (Grade 2): │
│ ➤ Resection if feasible │
│ ➤ Post-op RT ± chemotherapy (high-risk features) │
│ ➤ Surveillance for low-risk │
├────────────────────────────────────────────────────────┤
│ MENINGIOMA: │
│ ➤ Observation if small and asymptomatic │
│ ➤ Surgery for symptomatic/growing lesions │
│ ➤ Radiotherapy for unresectable/recurrent │
├────────────────────────────────────────────────────────┤
│ BRAIN METASTASES: │
│ ➤ Treat underlying malignancy │
│ ➤ Limited (1-3): Stereotactic radiosurgery or surgery│
│ ➤ Multiple: Whole brain radiotherapy (WBRT) │
│ ➤ Targeted therapy (if molecular targets present) │
├────────────────────────────────────────────────────────┤
│ PITUITARY ADENOMA: │
│ ➤ Prolactinoma: Dopamine agonist (cabergoline) │
│ ➤ Other functioning: Trans-sphenoidal surgery │
│ ➤ Non-functioning: Surgery if compressive │
└────────────────────────────────────────────────────────┘
Surgical Principles
| Principle | Details |
|---|---|
| Maximal safe resection | Remove as much tumour as safely possible while preserving function |
| Awake craniotomy | For tumours near eloquent cortex; allows intraoperative mapping |
| Stereotactic biopsy | When resection not feasible; confirms histology |
| Debulking | Palliative reduction of mass effect |
| CSF diversion | VP shunt or ETV for obstructive hydrocephalus |
Adjuvant Therapy
| Treatment | Indication | Notes |
|---|---|---|
| Radiotherapy | Post-operative glioblastoma, anaplastic gliomas, unresectable tumours | 60 Gy in 30 fractions (standard glioblastoma) |
| Temozolomide | Glioblastoma (Stupp protocol), anaplastic gliomas | Oral alkylating agent; MGMT methylation predicts response |
| Stereotactic radiosurgery | Small tumours, metastases, recurrence | Gamma Knife, CyberKnife |
| Bevacizumab | Recurrent glioblastoma | Anti-VEGF; reduces oedema; no survival benefit |
| Immunotherapy | Limited indications; clinical trials | Checkpoint inhibitors under investigation |
Symptom Management
| Symptom | Treatment |
|---|---|
| Peritumoural oedema | Dexamethasone 8-16 mg/day; taper when possible |
| Seizures | Levetiracetam (preferred; fewer interactions), Sodium valproate, Lacosamide |
| Headache | Steroids, paracetamol, weak opioids; avoid NSAIDs pre-surgery |
| Venous thromboembolism | LMWH; IVC filter if anticoagulation contraindicated |
| Nausea | Antiemetics (ondansetron, cyclizine) |
| Depression/Anxiety | SSRIs, psychological support |
Early (Days-Weeks)
| Complication | Incidence | Management |
|---|---|---|
| Cerebral oedema | Common | Dexamethasone, osmotherapy |
| Raised ICP / Herniation | Variable | Emergency: Mannitol, hyperventilation, decompressive surgery |
| Seizures | 20-40% | Antiepileptic drugs |
| Haemorrhage into tumour | 2-5% | May require emergency surgery |
| Post-operative infection | 2-4% | Antibiotics, wound care |
| CSF leak | 2-5% | Surgical repair |
| Neurological deficit | Variable | Depends on surgery site; rehabilitation |
Late (Months-Years)
| Complication | Notes |
|---|---|
| Tumour recurrence | Almost universal for malignant gliomas |
| Radiation necrosis | Mimics recurrence; can occur months to years after RT |
| Cognitive decline | Due to tumour, treatment, or radiation |
| Endocrine dysfunction | Post-RT or from tumour location |
| Secondary malignancy | Rare late effect of radiation |
| Psychosocial impact | Depression, loss of independence |
Survival by Tumour Type
| Tumour Type | Median Survival | 5-Year Survival |
|---|---|---|
| Glioblastoma | 15 months (with treatment) | <% |
| Anaplastic astrocytoma | 2-3 years | 20-30% |
| Low-grade glioma (IDH-mutant) | 10-15 years | 70-80% |
| Oligodendroglioma (1p/19q codeleted) | 15-20 years | >0% |
| Meningioma (Grade I) | Near-normal | >0% |
| Brain metastases | 6-12 months | <% |
Prognostic Factors
| Good Prognosis | Poor Prognosis |
|---|---|
| Younger age | Older age (>5 for glioblastoma) |
| Good performance status (KPS ≥70) | Poor performance status |
| IDH1/2 mutation | IDH wildtype |
| 1p/19q co-deletion | No co-deletion |
| MGMT promoter methylation | MGMT unmethylated |
| Complete resection | Subtotal resection/biopsy only |
| Low tumour grade | High grade (Grade 4) |
Key Guidelines
| Guideline | Organisation | Year | Key Points |
|---|---|---|---|
| Brain tumours (primary) and brain metastases in adults (NG99) | NICE | 2018/2021 | Imaging pathways, referral, supportive care |
| CNS Tumour Management | EANO | 2021 | Molecular classification, treatment algorithms |
| Glioblastoma Clinical Practice Guidelines | ASCO-SNO | 2022 | Stupp protocol, recurrence management |
Landmark Trials
Stupp Trial (2005)
- n=573 patients with glioblastoma
- Compared RT alone vs RT + concurrent/adjuvant Temozolomide
- Result: Median survival 14.6 vs 12.1 months (HR 0.63)
- Clinical impact: Established standard of care for glioblastoma
- PMID: 15758009
EF-14 Trial (2017) — Tumour Treating Fields
- Added TTFields to standard therapy in newly diagnosed glioblastoma
- Improved median survival from 16 to 20.9 months
- PMID: 29260225
RTOG 0525 (2013)
- Dose-dense temozolomide in glioblastoma
- No survival benefit over standard dosing
- PMID: 23940225
EORTC 22033-26033 (2016)
- RT vs Temozolomide in low-grade glioma
- Similar efficacy; IDH status predictive
- PMID: 27686946
Evidence Strength
| Intervention | Level | Source |
|---|---|---|
| Surgery + RT + Temozolomide for glioblastoma | 1a | Stupp trial, meta-analyses |
| SRS for limited brain metastases | 1b | RCTs |
| Dexamethasone for oedema | 2a | Observational, clinical practice |
| Levetiracetam for seizures | 2b | Comparative studies |
What is a Brain Tumour?
A brain tumour is an abnormal growth of cells inside the brain or surrounding structures. Tumours can be "primary" (starting in the brain) or "secondary" (spreading from cancer elsewhere in the body, called metastases).
Why does it happen?
In most cases, we don't know exactly why brain tumours develop. They occur when brain cells start to grow abnormally. Some risk factors include previous radiation treatment and certain genetic conditions. Mobile phones have been extensively studied and are not proven to cause brain tumours.
What are the symptoms?
Symptoms depend on where the tumour is and how fast it's growing:
- Headaches: Often worse in the morning, made worse by coughing or straining
- Seizures (fits): May be the first sign
- Weakness or numbness: Usually affecting one side of the body
- Vision problems: Blurred vision or loss of part of vision
- Speech difficulty: Trouble finding words or understanding
- Personality changes: Mood swings, confusion, or unusual behaviour
How is it treated?
Treatment depends on the type of tumour:
- Surgery: To remove as much tumour as safely possible
- Radiotherapy: High-energy beams to kill tumour cells
- Chemotherapy: Tablets or injections to slow tumour growth
- Steroids: To reduce swelling around the tumour
What to expect?
This depends on the type of tumour. Some brain tumours are completely curable with surgery. Others require ongoing treatment. Your medical team will explain your individual situation and support you through treatment.
When to seek help urgently
Seek immediate medical attention if you experience:
- Sudden severe headache
- New seizure (fit) or worsening seizures
- Sudden weakness, numbness, or vision loss
- Severe drowsiness or confusion
- Difficulty breathing or very slow heart rate
Guidelines
-
National Institute for Health and Care Excellence (NICE). Brain tumours (primary) and brain metastases in adults (NG99). 2018, updated 2021. nice.org.uk/guidance/ng99
-
Weller M, van den Bent M, Preusser M, et al. EANO guidelines on the diagnosis and treatment of diffuse gliomas of adulthood. Nat Rev Clin Oncol. 2021;18(3):170-186. PMID: 33293629
Key Trials
-
Stupp R, Mason WP, van den Bent MJ, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med. 2005;352(10):987-996. PMID: 15758009
-
Stupp R, Taillibert S, Kanner A, et al. Effect of Tumor-Treating Fields Plus Maintenance Temozolomide vs Maintenance Temozolomide Alone on Survival in Patients With Glioblastoma: A Randomized Clinical Trial. JAMA. 2017;318(23):2306-2316. PMID: 29260225
-
Gilbert MR, Wang M, Aldape KD, et al. Dose-dense temozolomide for newly diagnosed glioblastoma: a randomized phase III clinical trial. J Clin Oncol. 2013;31(32):4085-4091. PMID: 24101040
Reviews
-
Louis DN, Perry A, Wesseling P, et al. The 2021 WHO Classification of Tumors of the Central Nervous System: a summary. Neuro Oncol. 2021;23(8):1231-1251. PMID: 34185076
-
Ostrom QT, Cioffi G, Waite K, et al. CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2014-2018. Neuro Oncol. 2021;23(12 Suppl 2):iii1-iii105. PMID: 34608945
-
The Brain Tumour Charity. Patient resources. thebraintumourcharity.org
High-Yield Exam Topics
| Topic | Key Points |
|---|---|
| Classification | Primary vs metastatic; WHO grading 1-4; IDH status |
| Glioblastoma | Ring enhancement, necrosis, 15-month survival, Stupp protocol |
| Metastases | More common than primary; lung, breast, melanoma sources |
| Raised ICP | Headache worse on waking, papilloedema, Cushing's triad |
| Herniation syndromes | Uncal (III nerve palsy → fixed dilated pupil), tonsillar |
| Steroid use | Dexamethasone reduces oedema; always cover with PPI |
Sample Viva Questions
Q1: A 60-year-old presents with progressive headache, worse in the mornings, and a new-onset seizure. MRI shows a ring-enhancing mass with central necrosis. What is the likely diagnosis and management?
Model Answer: The presentation and imaging are highly suggestive of glioblastoma (WHO Grade 4). Immediate management includes dexamethasone (8-16 mg/day) to reduce oedema, PPI cover, and levetiracetam for seizures. Urgent neurosurgical referral for maximal safe resection. Post-operative management follows the Stupp protocol: concurrent chemoradiotherapy (60 Gy with temozolomide) followed by adjuvant temozolomide. Molecular testing for IDH status and MGMT methylation guides prognosis and may influence treatment intensity.
Q2: What are the differences between primary and secondary brain tumours?
Model Answer: Primary brain tumours arise from CNS tissue (gliomas, meningiomas, schwannomas). They are less common than secondary tumours but include the most common adult malignancy (glioblastoma). Secondary (metastatic) tumours spread from cancers elsewhere — most commonly lung, breast, melanoma, renal cell carcinoma. Metastases are typically located at the grey-white junction, may be multiple, and have disproportionate surrounding oedema. Management differs: primary tumours require CNS-specific treatment, while metastases require treatment of the underlying malignancy alongside CNS intervention.
Q3: Why is dexamethasone used in brain tumour management?
Model Answer: Dexamethasone is a potent glucocorticoid that reduces vasogenic peritumoural oedema by stabilising the blood-brain barrier and reducing capillary permeability. Tumour vessels are leaky, causing significant oedema that contributes to mass effect and symptoms. Dexamethasone provides rapid symptom relief within hours to days. However, it has significant side effects (hyperglycaemia, immunosuppression, myopathy, psychiatric effects) and should be tapered as soon as feasible, particularly after definitive treatment.
Common Exam Errors
| Error | Correct Approach |
|---|---|
| Forgetting to check for papilloedema | Always include fundoscopy in neurological examination |
| Not considering metastases in adults | Metastases are 10x more common than primary tumours |
| Ordering LP in raised ICP | Contraindicated — risk of herniation |
| Forgetting PPI with steroids | Always prescribe PPI with dexamethasone |
| Missing molecular testing | IDH, 1p/19q, MGMT guide prognosis and treatment |
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.