Stroke Emergency — Symptoms, Causes & Treatment | MyMedicPlus

Stroke is a medical emergency caused by sudden disruption of cerebral blood supply, resulting in focal neurological deficits. Every minute without reperfusion treatment, approximately 1.9 million neurons and 14 billion synapses are irreversibly lost — hence the phrase 'time is brain.' Ischemic stroke (87%) results from arterial occlusion: thrombotic (in situ clot from atherosclerosis or small vessel disease) or embolic (clot from a distant source such as the heart in atrial fibrillation, carotid plaque, or paradoxical embolism through a patent foramen ovale). Hemorrhagic stroke (13%) results from intracerebral hemorrhage (ICH — most commonly from hypertension or cerebral amyloid angiopathy) or subarachnoid hemorrhage (SAH — most commonly from rupture of an intracranial aneurysm, presenting with thunderclap headache). Together, stroke and transient ischemic attack (TIA) affect approximately 15 million people annually worldwide, causing 5.5 million deaths and leaving a further 5 million permanently disabled. Stroke is the 3rd leading cause of death and the leading cause of acquired adult disability globally. Immediate recognition using FAST (Face drooping, Arm weakness, Speech difficulty, Time to call) and emergency treatment are the cornerstones of stroke management.

Ischemic stroke causes: atrial fibrillation accounts for 20-30% of ischemic strokes via a cardioembolic mechanism — AF causes a 5-fold increase in stroke risk, effectively prevented by anticoagulation with DOACs (apixaban, rivaroxaban, edoxaban, dabigatran); large vessel atherosclerosis of the carotid or intracranial arteries causes thrombotic or artery-to-artery embolic stroke; small vessel disease (lipohyalinosis from chronic hypertension) causes lacunar infarctions in the deep perforating arteries; and paradoxical embolism through a patent foramen ovale (PFO). Hemorrhagic stroke causes: hypertension is the most common cause of spontaneous intracerebral hemorrhage (ICH — typically affecting the basal ganglia, thalamus, cerebellum, or pons); cerebral amyloid angiopathy (CAA) causes lobar hemorrhage in elderly patients; anticoagulant use (warfarin, DOACs) significantly increases ICH risk; arteriovenous malformations (AVMs) cause hemorrhage in younger patients; cocaine use causes vasospasm and ICH; and ruptured intracranial aneurysm causes subarachnoid hemorrhage (SAH) presenting with sudden severe 'thunderclap' headache. Hypertension is the single most important modifiable risk factor for both ischemic and hemorrhagic stroke, present in up to 80% of stroke patients. Other modifiable risk factors: diabetes mellitus, smoking (2x stroke risk), hypercholesterolaemia, obesity, and physical inactivity.

Use the FAST acronym to recognise stroke: Face drooping on one side (ask the person to smile — does one side droop?); Arm weakness (ask the person to raise both arms — does one arm drift downward?); Speech difficulty (slurred speech, strange or garbled speech, inability to speak, or inability to understand speech — aphasia or dysarthria); Time — call emergency services (999/911) immediately at the first sign. Do not wait for all four symptoms to be present — any single FAST symptom requires an emergency call. Additional symptoms: sudden loss of vision in one or both eyes (amaurosis fugax — transient monocular blindness suggests carotid artery disease); diplopia (double vision) or blurred vision; sudden severe 'thunderclap' headache reaching maximum intensity within seconds — the worst headache of the patient's life — is highly specific for subarachnoid hemorrhage; sudden loss of balance or coordination, dizziness, or difficulty walking (cerebellar or posterior circulation stroke); sudden confusion or disorientation; and hemineglect (ignoring one side of the body, more common in right hemisphere strokes). All stroke symptoms are sudden in onset — gradual-onset symptoms rarely indicate stroke. A transient ischemic attack (TIA or 'mini-stroke') presents identically but all symptoms resolve completely within 24 hours (usually within minutes); it is equally a medical emergency.

Immediate non-contrast CT head: the first investigation performed 24/7 in all stroke centres — excludes hemorrhagic stroke (acute blood appears hyperdense on CT) before thrombolysis is given, and detects early ischemic changes (subtle cortical swelling, loss of grey-white differentiation, hyperdense MCA sign). CT angiography (CTA) of the head and neck: performed simultaneously — identifies large vessel occlusion (LVO of the M1/M2 MCA, basilar artery) mandating mechanical thrombectomy decision; detects intracranial aneurysm in SAH. MRI diffusion-weighted imaging (DWI): the most sensitive test for acute ischemia — positive within minutes of infarction; MRI FLAIR sequences help estimate infarct age in wake-up stroke or unknown onset (DWI-FLAIR mismatch identifies potentially treatable patients). Point-of-care blood glucose: hypoglycaemia below 3.5 mmol/L mimics stroke and must be excluded immediately before treatment is given. ECG: detects atrial fibrillation as a cardioembolic aetiology requiring anticoagulation rather than antiplatelet therapy. Coagulation screen (INR, APTT): determines thrombolysis eligibility. Blood tests: CBC, renal function, troponin (to detect cardiac embolism), lipid profile. National Institutes of Health Stroke Scale (NIHSS): standardised neurological assessment scoring 0-42 — quantifies stroke severity, guides treatment decisions, and predicts prognosis. Target door-to-needle time: under 60 minutes (ideally under 45 minutes).

Ischemic stroke — acute reperfusion: IV alteplase (tPA) 0.9 mg/kg (maximum 90 mg) administered within 4.5 hours of symptom onset — reduces death or severe disability by 30%; tenecteplase 0.25 mg/kg (single IV bolus) is an emerging equally effective alternative with simpler administration. Target door-to-needle time is under 60 minutes (ideally under 45 minutes). Mechanical thrombectomy (MT): stent retriever or aspiration catheter technique for confirmed large vessel occlusion (M1/M2 MCA, basilar artery) — can be performed up to 24 hours in patients with salvageable brain tissue on CT perfusion or DWI-FLAIR mismatch; NNT of 2.6 for independent functional recovery (mRS 0-2); the most effective acute intervention in stroke medicine. Hemorrhagic stroke: systolic BP target below 140 mmHg within 1 hour of symptom onset (INTERACT2 trial); reverse anticoagulation with 4-factor prothrombin complex concentrate (PCC — Beriplex or Octaplex) for warfarin-related ICH; idarucizumab (Praxbind) for dabigatran reversal; andexanet alfa for factor Xa inhibitor reversal; neurosurgical evacuation for cerebellar hemorrhage above 3 cm or accessible ICH with progressive neurological deterioration. SAH: nimodipine 60 mg orally every 4 hours to reduce cerebral vasospasm; neurosurgical clipping or endovascular coiling of ruptured aneurysm. All stroke patients: admission to a dedicated stroke unit — Cochrane meta-analysis of 31 trials demonstrates 18-22% reduction in mortality and 20% reduction in disability regardless of stroke type; aspirin 300 mg (ischemic stroke only, after hemorrhage excluded by CT head); statin therapy; dysphagia screen before any oral intake; DVT prophylaxis with LMWH and graduated compression stockings.

Acute: cerebral oedema (malignant middle cerebral artery infarction affects 10-15% of large MCA strokes — hemicraniectomy within 48 hours reduces mortality from 78% to 29% per the DESTINY II trial), symptomatic hemorrhagic transformation of ischemic infarction (occurs in 6% of thrombolysed patients and independently in 10-40% of large infarcts), and transtentorial herniation causing brain death. Subacute: aspiration pneumonia (occurs in approximately 30% of stroke patients from dysphagia — the most common early medical complication and leading cause of early death after stroke), urinary tract infection, deep vein thrombosis and pulmonary embolism (prophylactic LMWH and graduated compression stockings are standard of care), and pressure ulcers from immobility. Chronic: hemiplegia or hemiparesis (50% of survivors), aphasia (35%), persistent dysphagia (10-15%), vascular dementia, post-stroke depression (30-40% — requires active screening and treatment), post-stroke epilepsy (5-10% within first year), central post-stroke pain syndrome, and shoulder subluxation with spasticity. Recurrent stroke risk is approximately 15% at 5 years; highest risk is in the first 48 hours after TIA or minor stroke.

Call emergency services (999/911) immediately if any FAST symptoms develop — do not drive to hospital, do not wait to see if symptoms improve. Every minute of delay increases neuronal loss and worsens long-term outcome. For TIA (transient ischemic attack — symptoms fully resolved): same-day emergency assessment and urgent brain imaging are mandatory as the 48-hour stroke risk after TIA is 10-20%; do not drive, and attend A&E immediately. Secondary prevention after ischemic stroke or TIA: dual antiplatelet therapy (aspirin 300 mg then clopidogrel — dual therapy for 21 days for minor stroke or TIA, then clopidogrel 75 mg monotherapy); anticoagulation for atrial fibrillation (DOACs preferred over warfarin for non-valvular AF — 64% reduction in cardioembolic stroke); high-intensity statin (atorvastatin 40-80 mg daily, target LDL below 1.8 mmol/L); antihypertensive therapy (ACE inhibitor plus thiazide diuretic, target BP below 130/80 mmHg); and carotid endarterectomy within 2 weeks for symptomatic ICA stenosis above 50-70%.

Stroke is an absolute medical emergency — call 999/112 immediately at the first sign of stroke. Use the FAST test: Face drooping (unilateral), Arm weakness (one arm drifts down), Speech difficulty (slurred, confused, or unable to speak), Time to call 999. Do not wait to see if symptoms improve — even transient symptoms (TIA) require emergency assessment as TIA carries a 10-20% risk of stroke within 48 hours (highest in the first 24 hours). For suspected TIA, do not drive — call 999 or attend A&E immediately. Time is critical: thrombolysis (alteplase or tenecteplase) must be given within 4.5 hours of stroke onset; mechanical thrombectomy (endovascular clot retrieval) is effective up to 24 hours in selected patients. While waiting for the ambulance: do not give the person food, drink, or medication (aspirin is contraindicated until brain haemorrhage is excluded by CT); keep the person calm and lying on their side if unconscious; record the time symptoms first appeared (essential for thrombolysis decision). Post-TIA prevention starts immediately: antiplatelet therapy (aspirin 300 mg then clopidogrel), statin, antihypertensive, and carotid imaging — every hour of delay in post-TIA management increases the risk of early stroke.