Stroke and TIA
Exam Tips
- In OSCEs, treat sudden focal neurology as stroke until proven otherwise: document exact onset/last-known-well, perform FAST and glucose immediately, and escalate urgently for brain imaging.
- Differentiate TIA from mimic by abrupt negative symptoms (loss of function) in a vascular territory; positive spreading symptoms suggest migraine/seizure.
- Know key UK prescribing sequences: aspirin 300 mg immediately for suspected TIA (if no bleed concern), clopidogrel 75 mg daily for long-term non-cardioembolic prevention, and anticoagulation for AF-related events when safe.
- In viva questions, justify why haemorrhage exclusion on CT precedes antithrombotics/thrombolysis, and state major bleeding contraindications clearly.
- Quote prognosis intelligently: highest recurrence risk is early after TIA/minor stroke, while long-term disability and recurrent vascular events remain common.
Definition
Stroke is an acute neurological syndrome caused by a cerebrovascular event, producing focal (or occasionally global) brain dysfunction that lasts more than 24 hours or causes death. In clinical practice it is classified as ischaemic infarction (most cases) or intracranial haemorrhage (intracerebral or subarachnoid), while transient ischaemic attack (TIA) causes similar sudden focal symptoms but resolves fully within 24 hours and has no acute infarction on imaging.
Pathophysiology
Most strokes are ischaemic, due to thrombotic or embolic arterial occlusion (large-artery atherosclerosis, cardioembolism such as atrial fibrillation, or small-vessel lipohyalinosis causing lacunar infarcts). Arterial blockage creates an infarct core with irreversible injury and a surrounding penumbra that is initially salvageable; energy failure causes glutamate-mediated excitotoxicity, calcium influx, oxidative stress, cytotoxic oedema, and then inflammatory injury. Haemorrhagic stroke results from vessel rupture (commonly hypertension-related small-vessel disease for intracerebral haemorrhage, or ruptured saccular aneurysm for subarachnoid haemorrhage), leading to mass effect, raised intracranial pressure, reduced perfusion, and blood-product neurotoxicity. TIAs reflect brief focal ischaemia without established infarction, but indicate unstable vascular disease and high early recurrent stroke risk. See Figure: cerebral arterial territories/Circle of Willis and ischaemic core-penumbra model in standard neurovascular textbooks.
Risk Factors
- Hypertension (most important modifiable risk factor for both ischaemic and haemorrhagic stroke)
- Atrial fibrillation (paroxysmal or persistent), valvular heart disease, recent myocardial infarction, heart failure
- Carotid atherosclerosis/stenosis and other atherothrombotic disease
- Diabetes mellitus
- Hyperlipidaemia
- Smoking
- Excess alcohol, cocaine or methamphetamine use
- Physical inactivity, obesity, poor diet
- Previous TIA or stroke
- Older age, male sex (earlier presentation), family history of stroke
- Hypercoagulable states (e. g, antiphospholipid syndrome, sickle cell disease)
- Migraine with aura (especially in younger women), and combined hormonal contraception in selected high-risk groups
- Chronic kidney disease and obstructive sleep apnoea
- Pregnancy/postpartum state and pre-eclampsia
- Arterial dissection, vasculitis, vascular malformations, and less commonly cerebral venous sinus thrombosis
Clinical Features
Symptoms
- Sudden unilateral face/arm/leg weakness or numbness
- Sudden speech disturbance (dysarthria, expressive/receptive dysphasia)
- Sudden monocular visual loss (amaurosis fugax), hemianopia, or diplopia
- Sudden vertigo, ataxia, imbalance, or dysphagia (posterior circulation features)
- Abrupt severe headache (especially thunderclap in subarachnoid haemorrhage)
- Transient episodes with complete recovery suggest TIA
Signs
- FAST-positive findings: facial asymmetry, arm drift/weakness, speech impairment
- Focal upper motor neuron signs (hyperreflexia, extensor plantar response) after hyperacute phase
- Visual field defects and gaze palsy
- Cerebellar signs (nystagmus, dysmetria, truncal ataxia)
- Reduced consciousness, meningism, or vomiting (more suggestive of haemorrhage/raised ICP)
- Irregularly irregular pulse indicating possible atrial fibrillation
Investigations
Management
Lifestyle Modifications
- Urgent emergency referral to hyperacute stroke unit; treat as time-critical
- Smoking cessation, alcohol reduction, Mediterranean-style diet, weight loss, regular aerobic activity
- Tight long-term control of blood pressure, diabetes, and lipids
- Driving/work counselling and structured stroke rehabilitation (physio, OT, speech and language therapy)
- Swallow screening before oral intake; aspiration prevention and nutrition/hydration planning
Pharmacological Treatment
Immediate antiplatelet (suspected TIA/minor ischaemic event once haemorrhage unlikely)
- Aspirin 300 mg stat, then 300 mg once daily until specialist review/imaging
Do not give aspirin if intracranial haemorrhage is known/suspected or active bleeding. Use caution with peptic ulcer disease and aspirin hypersensitivity.
Acute reperfusion for ischaemic stroke
- Alteplase 0.9 mg/kg IV (max 90 mg): 10% bolus over 1 minute, remainder over 60 minutes
Given in specialist stroke centres within thrombolysis window after imaging exclusion of haemorrhage. Contraindications include recent major bleeding/surgery, severe uncontrolled hypertension, and high bleeding risk.
Secondary antiplatelet prevention (non-cardioembolic ischaemic stroke/TIA)
- Clopidogrel 75 mg once daily long term
- If clopidogrel not tolerated: Aspirin 75 mg once daily plus modified-release dipyridamole 200 mg twice daily
After acute ischaemic stroke, aspirin 300 mg daily is commonly used initially (e. g, for 14 days) before long-term regimen. Check bleeding risk and drug interactions.
Anticoagulation for atrial fibrillation-related stroke prevention
- Apixaban 5 mg twice daily (reduce to 2.5 mg twice daily if dose-reduction criteria met)
- Rivaroxaban 20 mg once daily with food
- Dabigatran 150 mg twice daily
- Edoxaban 60 mg once daily
- Warfarin adjusted to INR 2.0-3.0 when DOAC unsuitable
Start timing after acute stroke depends on infarct size/haemorrhagic risk and specialist advice. Avoid anticoagulation in active major bleeding; review renal function and interacting drugs.
Lipid lowering
- Atorvastatin 80 mg at night (or maximally tolerated high-intensity statin)
Use unless contraindicated; monitor for myopathy/hepatotoxicity and interactions.
Blood pressure lowering for secondary prevention
- Ramipril 2.5 mg once daily, titrate up to 10 mg once daily
- Indapamide 2.5 mg once daily (or 1.5 mg modified-release once daily)
Individualise targets; avoid excessive acute BP lowering in hyperacute ischaemic stroke unless needed for thrombolysis eligibility or hypertensive emergency.
VTE prophylaxis in immobile stroke patients
- Intermittent pneumatic compression (first line mechanical prophylaxis)
- Low molecular weight heparin e. g, enoxaparin 40 mg subcutaneously once daily (selected patients)
Balance thrombosis prevention against intracranial/extracranial bleeding risk; avoid routine anticoagulant prophylaxis in high bleeding-risk patients.
Surgical / Interventional
- Mechanical thrombectomy for eligible anterior-circulation large-vessel occlusion (and selected posterior-circulation cases) within specialist time/imaging criteria
- Carotid endarterectomy for symptomatic carotid stenosis (typically 50-99% NASCET) as early as feasible after TIA/minor stroke
- Neurosurgical/endovascular aneurysm securing (coiling or clipping) for aneurysmal subarachnoid haemorrhage
- Selected decompressive hemicraniectomy for malignant middle cerebral artery infarction with life-threatening oedema
- Occasional haematoma evacuation/external ventricular drainage in selected intracerebral haemorrhage cases
Complications
- Early neurological deterioration, cerebral oedema, and haemorrhagic transformation
- Aspiration pneumonia, urinary infection, pressure sores, and sepsis
- Venous thromboembolism including pulmonary embolism
- Seizures and post-stroke epilepsy
- Cardiac complications (myocardial ischaemia, arrhythmias, heart failure)
- Persistent motor deficits, spasticity, contractures, falls, and fractures
- Dysphagia, dehydration, malnutrition, and poor oral health
- Cognitive impairment, vascular dementia, mood disorders, fatigue, and pain syndromes
- Urinary/faecal incontinence, sexual dysfunction, and reduced quality of life
- Recurrent stroke or recurrent TIA
Prognosis
Prognosis depends strongly on stroke subtype, age, premorbid status, and speed of reperfusion. UK outcomes have improved, but haemorrhagic stroke still carries substantially higher early mortality than ischaemic stroke, and subarachnoid haemorrhage has significant pre-hospital and 6-month mortality. TIA predicts high early recurrent stroke risk (greatest in the first days to weeks), so urgent assessment and secondary prevention are essential. Long-term disability is common, and recurrence risk remains clinically important over years, especially without aggressive vascular risk-factor control.
Sources & References
✅NICE Guidelines(1)
- Stroke and TIA[overview]
📖Textbook References(16)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1018)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1018)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1019)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1028, 1029)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1023, 1024)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1024)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 998)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 477, 478, 479)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 813)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 811)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 174)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 173, 174)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 146)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 128, 129)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 504)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 154, 155)[context]