Brain metastases

Key points

• Brain metastases are more common than malignant primary brain tumours and most often arise from lung, breast, melanoma, renal and colorectal cancers.
• Presentation includes headache, focal deficit, seizure, cognitive or personality change, ataxia and occasionally haemorrhage or an incidental staging-scan finding.
• Emergency non-contrast CT is first line for acute deterioration because it rapidly identifies haemorrhage, hydrocephalus and dangerous mass effect.
• Contrast-enhanced MRI is the preferred definitive intracranial staging test; it detects small posterior-fossa, cortical and leptomeningeal lesions better and guides surgery or stereotactic radiotherapy.
• Restage extracranial disease and review the primary histology and molecular profile because systemic options and expected survival shape intracranial treatment.
• A solitary or atypical lesion, unknown primary, long cancer-free interval or discordant systemic picture often needs surgical or stereotactic biopsy before irreversible treatment.
• First-line symptomatic treatment for clinically important vasogenic oedema is dexamethasone at the lowest effective dose, with a planned taper after surgery, radiation or systemic response.
• Do not give routine corticosteroid to every asymptomatic small metastasis, because hyperglycaemia, infection, myopathy, delirium and reduced immunotherapy efficacy can outweigh benefit.
• Treat a tumour-related seizure with a low-interaction antiseizure medicine; do not prescribe prophylactic antiseizure medication indefinitely to a patient who has never seized.
• Surgical resection is preferred for selected large, accessible, symptomatic solitary or dominant lesions, particularly when tissue, decompression and rapid neurological improvement are needed.
• Stereotactic radiosurgery or fractionated stereotactic radiotherapy provides high local control for limited lesions or selected total intracranial volume and for many postoperative cavities.
• Whole-brain radiotherapy is reserved for selected extensive disease or situations unsuitable for focal treatment; discuss expected intracranial benefit against fatigue, alopecia and cognitive harm.
• CNS-active systemic treatment may be central in targetable lung cancer, HER2-positive breast cancer and melanoma, but symptomatic local mass effect usually needs prompt local therapy rather than waiting for systemic response.
• Management is based on performance, neurological function, lesion number and volume, extracranial control, molecular options, prognosis and patient goals—not lesion count alone.

1. 1
   Blood-borne seeding

   Circulating tumour cells lodge in small vessels, often at the grey–white junction or watershed regions, cross the neurovascular unit and establish one or multiple deposits.

2. 2
   Vasogenic oedema amplifies symptoms

   Tumour-disrupted capillaries leak fluid into white matter, creating deficits and pressure far beyond the enhancing deposit; corticosteroids reduce this oedema rather than killing tumour.

3. 3
   Location outweighs diameter

   A small motor-cortex, brainstem or posterior-fossa lesion can cause major disability, while a larger frontal deposit may initially produce only subtle cognitive change.

4. 4
   Haemorrhage and seizure complicate deposits

   Fragile tumour vessels can bleed and cortical irritation can generate focal or bilateral tonic–clonic seizures, sometimes revealing a previously occult metastasis.

5. 5
   Leptomeningeal spread follows CSF

   Tumour coating meninges and nerve roots produces multifocal cranial, spinal and radicular symptoms and requires a different whole-neuraxis and systemic management strategy.

• Review neurological examination, cognition, headache, vomiting, gait, swallowing and seizure frequency at each contact and give a direct route for same-day deterioration.
• Reconcile dexamethasone dose at every visit and record a taper, monitoring glucose, infection, sleep, mood, proximal strength and adrenal-risk education.
• Use MRI after local or systemic treatment at an interval matched to biology and symptoms, then regularly enough to detect treatable recurrence without replacing clinical assessment.
• After stereotactic radiation, review radiation dose maps and serial imaging before labelling enlarging enhancement recurrence; seek advanced imaging or tissue for meaningful uncertainty.
• Monitor extracranial disease and systemic drug toxicity in parallel because intracranial control alone may not improve function or survival when systemic cancer progresses.
• Track antiseizure adherence, adverse effects, rescue plan, legal driving restrictions, falls and caregiver understanding after any seizure.
• Assess rehabilitation, communication aids, work, capacity, advance-care preferences and family burden early, with specialist palliative care available during active oncology treatment.

1. 01

   Calling new confusion medication related without examining for focal signs or imaging the brain.

2. 02

   Using a normal acute CT to exclude small, posterior-fossa or leptomeningeal metastases.

3. 03

   Assuming a solitary lesion is metastatic solely because the patient previously had cancer.

4. 04

   Giving high-dose dexamethasone indefinitely without a definitive treatment and taper plan.

5. 05

   Starting prophylactic antiseizure medication in every seizure-naive patient.

6. 06

   Choosing treatment by lesion count while ignoring volume, location, systemic control and function.

7. 07

   Waiting for systemic therapy to shrink a large lesion causing dangerous mass effect.

8. 08

   Giving whole-brain radiotherapy automatically when focused treatment or supportive care is more appropriate.

9. 09

   Calling all post-stereotactic enhancement progression without considering radionecrosis.

10. 10

    Separating intracranial decisions from primary-cancer biology, rehabilitation and palliative priorities.