Stroke — Symptoms, Causes & Treatment | MyMedicPlus

Stroke is a sudden disruption of blood supply to part of the brain, causing focal neurological deficits that persist for more than 24 hours (distinguishing it from a transient ischaemic attack, which resolves completely within 24 hours). It is the third leading cause of death globally and the leading cause of adult disability, affecting approximately 15 million people per year worldwide — of whom 5.5 million die and another 5 million are left with permanent disability. Stroke is classified into ischaemic stroke (87% of cases) — caused by thrombotic or embolic occlusion of a cerebral artery leading to brain infarction — and haemorrhagic stroke (13%) — which includes intracerebral haemorrhage (ICH, from rupture of a blood vessel into brain tissue) and subarachnoid haemorrhage (SAH, from rupture of a cerebral aneurysm into the subarachnoid space). The UK stroke FAST acronym (Face, Arms, Speech, Time) prompts public recognition and emergency response. Stroke is a time-critical medical emergency — 'time is brain' — every minute of ischaemic stroke without reperfusion treatment causes the death of approximately 1.9 million neurons. Mechanical thrombectomy for large vessel occlusion (LVO) is one of the most effective acute treatments in medicine.

Hypertension is the single most important modifiable risk factor for both ischaemic and haemorrhagic stroke — controlling blood pressure to below 130/80 mmHg reduces stroke risk by 40%. Atrial fibrillation (AF) increases ischaemic stroke risk 5-fold through cardioembolism — coagulation of blood in the fibrillating left atrial appendage, releasing clots to the cerebral circulation; anticoagulation with DOACs reduces this risk by 64%. Diabetes mellitus: independent risk factor for ischaemic stroke (RR 2-6, increasing with poor glycaemic control). Smoking: doubles ischaemic stroke risk through endothelial damage, platelet aggregation, and carotid atherosclerosis; risk reverts to non-smoker levels within 5 years of cessation. Hypercholesterolaemia: elevated LDL promotes carotid and intracranial atherosclerosis; high-intensity statin therapy reduces stroke risk by 25-30%. Carotid artery stenosis: symptomatic internal carotid artery (ICA) stenosis above 70% carries 15-20% 2-year stroke risk — carotid endarterectomy (CEA) reduces this risk. Patent foramen ovale (PFO): present in 25-30% of adults; may facilitate paradoxical embolism from deep venous thrombosis in young cryptogenic stroke patients — PFO closure reduces recurrent stroke. Obesity, physical inactivity, excessive alcohol (above 14 units/week), and sleep apnoea are additional modifiable risk factors. Prior TIA (transient ischaemic attack): 10-15% stroke risk within 3 months, highest in the first 48 hours.

All stroke symptoms are sudden in onset — this is the defining characteristic distinguishing stroke from other neurological conditions. FAST acronym: Face drooping (sudden unilateral facial weakness or droop — ask patient to smile); Arm weakness (unilateral arm weakness — patient cannot raise both arms and keep them elevated, with one arm drifting down — pronator drift); Speech difficulty (sudden dysarthria — slurred speech, or aphasia — inability to speak or understand language); Time — call 999/911 immediately. Additional neurological symptoms: sudden visual loss in one eye (amaurosis fugax — transient monocular blindness from retinal artery occlusion); sudden diplopia (double vision); sudden hemianopia (loss of half the visual field — typically contralateral to the lesion); hemispatial neglect (unawareness of one side of the body or visual space — right hemisphere strokes); vertigo, ataxia, and incoordination (posterior circulation stroke affecting the brainstem or cerebellum); sudden severe headache ('thunderclap headache — worst headache of my life') suggesting subarachnoid haemorrhage; sudden dysphagia; and hemiplegia or hemiparesis. The NIHSS (National Institutes of Health Stroke Scale — 0-42) quantifies neurological deficit severity and guides treatment decisions. Posterior circulation strokes (vertebrobasilar territory) cause the 'four D's' — diplopia, dysarthria, dysphagia, and dizziness.

Non-contrast CT head: available 24/7, performed immediately on arrival to exclude haemorrhage before thrombolysis — identifies ICH as hyperdense (bright white) area; also detects early ischaemic changes (ASPECTS scoring). CT angiography (CTA) of the intracranial and extracranial vasculature: essential for detecting large vessel occlusion (LVO) — identifies occlusion location and guides thrombectomy eligibility; performed immediately alongside non-contrast CT in all stroke patients. CT perfusion (CTP): identifies the ischaemic penumbra (salvageable tissue) vs irreversible infarct core — guides thrombectomy in late-presenting patients (4.5-24 hours from onset, DEFUSE-3 and DAWN trial criteria). MRI brain with diffusion-weighted imaging (DWI): most sensitive for acute ischaemia — positive within minutes of onset; shows ischaemic changes as bright on DWI with corresponding dark area on apparent diffusion coefficient (ADC) map. Blood tests: urgent blood glucose (hypoglycaemia is the most important stroke mimic), full blood count, INR/APTT (before thrombolysis), renal function, troponin. ECG: identifies AF (the most important cardioembolic source) — prolonged cardiac monitoring (7-30 days Holter) detects paroxysmal AF missed on standard ECG. Echocardiography (TTE/TOE): identifies cardioembolic sources (left atrial thrombus, valvular disease, patent foramen ovale, intracardiac tumour). Carotid Duplex ultrasound: quantifies ICA stenosis — guides endarterectomy decision.

Ischaemic stroke — acute reperfusion therapy: IV alteplase (recombinant tPA — 0.9 mg/kg, maximum 90 mg, with 10% as IV bolus and remainder over 60 minutes) within 4.5 hours of confirmed symptom onset — reduces death and disability by 30% (NNT 9 for favourable outcome); contraindicated in haemorrhage, recent surgery, anticoagulation. Tenecteplase (0.25 mg/kg IV) is an alternative being adopted in many centres. Mechanical thrombectomy (endovascular clot retrieval using stent retrievers or aspiration catheters) for confirmed LVO (internal carotid, middle cerebral artery M1/M2, basilar artery) — up to 24 hours in selected patients with salvageable penumbra; highly effective (NNT 2.6 for functional independence vs standard care in HERMES meta-analysis); significantly improves functional outcomes. Aspirin 300 mg after haemorrhage excluded; statin therapy (atorvastatin 80 mg); early blood pressure management (permissive hypertension in first 24 hours — avoid aggressive BP lowering that reduces cerebral perfusion); dedicated stroke unit care — reduces 30-day mortality and disability by 20% compared to general wards. Haemorrhagic stroke (ICH): blood pressure lowering to systolic below 140 mmHg within 1 hour reduces haematoma expansion; reverse anticoagulation (prothrombin complex concentrate for warfarin, idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors); neurosurgery for selected cases (cerebellar haemorrhage above 3 cm — immediate surgery; accessible supratentorial haematoma with neurological deterioration). SAH: CT head then lumbar puncture (xanthochromia) to confirm; nimodipine 60 mg every 4 hours for 21 days to prevent vasospasm; cerebral angiography and endovascular coiling (preferred) or surgical clipping of the aneurysm.

Acute complications: cerebral oedema with malignant middle cerebral artery (MCA) infarction — occurs in 10-15% of MCA territory strokes; causes fatal brain herniation without intervention; decompressive hemicraniectomy (surgical removal of bone flap — DESTINY-II trial) reduces mortality from 78% to 29% in patients aged 60 and above. Haemorrhagic transformation: ischaemic infarction may haemorrhage, particularly after thrombolysis or in cardioembolic strokes. Aspiration pneumonia: dysphagia affects 40-70% of acute stroke patients — aspiration from impaired swallow reflex is the most common cause of pneumonia and death in the first week; mandatory dysphagia screening (water swallow test by trained nursing staff) before oral intake. Deep venous thrombosis (DVT) and pulmonary embolism (PE): from immobility — prophylactic LMWH, compression stockings, and early mobilisation are essential. Chronic disability: hemiplegia, aphasia (affecting language production and/or comprehension), vascular dementia, post-stroke depression (40% — underrecognised and undertreated; SSRIs modestly improve functional recovery), central post-stroke pain (burning dysaesthetic pain in the hemiplegic limbs), epilepsy (5-10% develop post-stroke seizures — delayed seizures indicate established epilepsy requiring anticonvulsants), and spasticity. Recurrent stroke risk: 10% in the first year after ischaemic stroke without secondary prevention.

Primary prevention: control blood pressure to below 130/80 mmHg (the most important intervention — each 10 mmHg reduction in systolic BP reduces stroke risk by 22%); anticoagulation with DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) for AF patients with CHA2DS2-VASc score above 1 in men or above 2 in women; high-intensity statin therapy (atorvastatin 40-80 mg — reduces LDL to below 1.8 mmol/L); smoking cessation; regular aerobic exercise (150 minutes weekly); Mediterranean diet; glycaemic control in diabetes; alcohol moderation (below 14 units weekly). Secondary prevention after ischaemic stroke or TIA: dual antiplatelet therapy (aspirin 75 mg plus clopidogrel 75 mg for 21 days for minor ischaemic stroke or high-risk TIA — CHANCE trial), then clopidogrel 75 mg alone long-term (preferred over aspirin alone); ACE inhibitor plus indapamide (perindopril/indapamide — PROGRESS trial — reduces recurrence regardless of baseline blood pressure); high-intensity statin; anticoagulation for cardioembolic stroke from AF (start within 2-14 days depending on infarct size and haemorrhagic risk); carotid endarterectomy within 48 hours for symptomatic ICA stenosis above 70% (CEA reduces 5-year absolute stroke risk by 16%); PFO closure in selected young cryptogenic stroke patients.

Call emergency services immediately if you or anyone nearby shows any FAST symptoms: Face drooping on one side, Arm weakness (cannot raise both arms equally), Speech difficulty (slurred, strange, or absent) — and Time means call now. Note the exact time symptoms began. Do not drive yourself — call an ambulance. TIA (mini-stroke — symptoms fully resolved) is also a medical emergency requiring same-day emergency department assessment — the 48-hour stroke risk after TIA is 10%. Sudden severe 'thunderclap' headache (worst headache ever, instantaneous onset) requires emergency assessment for subarachnoid haemorrhage. Early treatment with thrombolysis (within 4.5 hours) or thrombectomy (within 24 hours) dramatically reduces death and disability. Time lost is brain lost — do not delay.