Brain Tumour — Types, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Brain tumours are abnormal growths of cells within or adjacent to the brain. Primary brain tumours arise from brain tissue itself — most commonly gliomas (astrocytoma, glioblastoma, oligodendroglioma), meningiomas (from the meninges — most common benign brain tumour), and pituitary adenomas. Secondary (metastatic) brain tumours arise from cancer that has spread from elsewhere — more common than primary tumours, originating typically from lung, breast, colorectal, renal, and melanoma primaries. Approximately 308,000 primary brain tumour cases occur globally each year. The 2021 WHO CNS tumour classification integrates molecular markers — IDH mutation, MGMT methylation, 1p/19q codeletion, TERT promoter mutation — into tumour grading, replacing purely histological classification. IDH-mutant gliomas have significantly better prognosis than IDH-wildtype tumours of the same histological grade. Glioblastoma (IDH-wildtype grade 4 astrocytoma) is the most aggressive primary brain tumour, with a median overall survival of 14-16 months with optimal Stupp protocol treatment. Secondary (metastatic) brain tumours outnumber primary tumours — occurring in 20-30% of all cancer patients during the disease course.

The cause of most primary brain tumours is unknown. Confirmed risk factors include ionising radiation exposure (e.g., previous cranial radiation for childhood leukaemia), rare hereditary syndromes (neurofibromatosis 1 and 2, Li-Fraumeni syndrome, tuberous sclerosis, Von Hippel-Lindau disease, Gorlin syndrome), and age (risk increases with age for most types). Despite public concern, current evidence does NOT confirm that mobile phone use, electromagnetic fields, or power lines cause brain tumours. Glioblastoma (GBM) is the most common and aggressive primary brain tumour — median survival 15 months with optimal treatment. Immunosuppression (HIV/AIDS, post-transplant) increases the risk of primary CNS lymphoma. Epstein-Barr virus (EBV) is strongly implicated in primary CNS lymphoma in immunocompromised patients. Previous therapeutic cranial irradiation increases secondary brain tumour risk by 2-10-fold within 10-15 years of treatment.

Symptoms depend on tumour location, size, and growth rate. Common presentations include: new-onset headaches (often worse in the morning, associated with nausea/vomiting from raised intracranial pressure); focal neurological deficits (weakness, numbness, aphasia, visual field defects depending on tumour location); seizures (new-onset in an adult always requires brain imaging); cognitive changes (memory problems, personality changes, concentration difficulties); and papilloedema (optic disc swelling) from raised ICP. Pituitary tumours cause hormonal disturbances, visual field defects, and headaches. Metastatic tumours may present with multiple focal deficits. Cerebellar tumours present with ataxia (unsteady gait), nystagmus, and intention tremor rather than focal limb weakness. Brain stem tumours cause cranial nerve palsies, long tract signs, and dysphagia. Lhermitte's sign (electric shock sensation on neck flexion) suggests cervical spinal or posterior fossa pathology.

MRI with gadolinium contrast is the gold standard imaging modality — it provides superior soft tissue detail and characterises tumour type, grade, and location better than CT. CT with contrast is used acutely (bleeding, urgent assessment) and in patients with MRI contraindications. MRI spectroscopy, perfusion MRI, and functional MRI map tumour biology and eloquent brain areas to guide surgery. Stereotactic biopsy or surgical resection provides definitive histological diagnosis and molecular characterisation (IDH1/2 mutation, MGMT methylation, 1p/19q codeletion) — essential for grading and treatment planning per the 2021 WHO CNS tumour classification. Liquid biopsy (circulating tumour DNA from blood) is an emerging tool for monitoring glioblastoma response and detecting recurrence without repeat surgical biopsy. PET-CT with amino acid tracers (FET, DOPA) improves delineation of tumour extent and differentiates recurrence from treatment effect.

Surgical resection is the cornerstone of treatment — maximising safe tumour removal (extent of resection correlates with improved survival) while preserving neurological function using intraoperative MRI, awake craniotomy, and fluorescence-guided surgery (5-ALA). Radiotherapy: stereotactic radiosurgery (Gamma Knife, CyberKnife) for small lesions; fractionated external beam radiotherapy for larger tumours. Glioblastoma standard of care: surgery + concurrent temozolomide chemotherapy + radiotherapy (Stupp protocol) then adjuvant temozolomide for 6 months. Bevacizumab (VEGF inhibitor) for recurrent GBM. TTFields (Tumour Treating Fields — electrical fields via scalp electrodes) improve GBM survival. Immunotherapy trials ongoing. Dexamethasone reduces peritumoral oedema. For primary CNS lymphoma: high-dose methotrexate-based chemotherapy achieves complete remission in 40-60% of patients; whole-brain radiotherapy is used for refractory disease but carries significant neurocognitive toxicity. Electric field therapy (TTFields — alternating electrical fields via scalp transducers) combined with temozolomide improves glioblastoma 5-year survival from 5% to 13% in the phase III EF-14 trial. Steroid-sparing agents (bevacizumab) reduce corticosteroid requirements and associated toxicity.

Untreated brain tumours cause progressive neurological deterioration from direct tissue invasion, oedema, and raised intracranial pressure. Herniation (downward displacement of brain tissue through the tentorium cerebelli from mass effect) is life-threatening, causing coma and death without emergency neurosurgical intervention. Uncontrolled seizures impair quality of life and carry risk of status epilepticus. Rapidly growing tumours like glioblastoma have a median survival of only 3 months without treatment. Even benign tumours cause significant morbidity from compression of critical brain structures if untreated.

Currently there are no proven dietary or lifestyle measures to prevent primary brain tumours. Minimise unnecessary radiation exposure (medical imaging should only be ordered when clinically indicated). Patients with hereditary brain tumour syndromes benefit from genetic counselling and regular surveillance MRI. For patients undergoing treatment: corticosteroids reduce tumour-related oedema; anti-epileptic drugs prevent seizures; physiotherapy and occupational therapy maintain function; cognitive rehabilitation addresses treatment-related cognitive changes. Rehabilitation and palliative care teams provide essential support for patients and families, particularly in high-grade glioma.

Call emergency services immediately for: sudden onset of the 'worst headache of my life' (possible subarachnoid haemorrhage from ruptured aneurysm); new focal weakness, speech difficulty, or vision loss of sudden onset (possible stroke or acute haemorrhage into a tumour); first-ever seizure in an adult (any new seizure in an adult requires urgent brain imaging within 24 hours); or sudden confusion, drowsiness, or loss of consciousness. See your GP urgently (within 2 weeks) for: new persistent headaches that are progressive, worse in the morning, or wake you from sleep; any new neurological symptom (persistent weakness, clumsiness, numbness, visual change, speech difficulty, or balance problems); personality or cognitive change noticed by family members; or new onset headache in a patient over 50. Do not dismiss progressive headaches as 'just stress' — the combination of morning headache with nausea and projectile vomiting is a classic raised intracranial pressure presentation requiring emergency assessment.