Clinical Guides
Stroke and Transient Ischaemic Attack
An India-contextualised guide to urgent assessment of stroke and transient ischaemic attack, including reperfusion pathways, recurrence prevention, and coordinated post-stroke care. It is written for supervised learning, with attention to tissue-based definitions, swallowing safety, mechanism-led antithrombotics, referral capability, rehabilitation, caregiver communication, affordability and equitable follow-up in Indian services.
MedNext Academy | 12 min read
Stroke and Transient Ischaemic Attack
An India-contextualised guide to urgent assessment of stroke and transient ischaemic attack, including reperfusion pathways, recurrence prevention, and coordinated post-stroke care. It is written for supervised learning, with attention to tissue-based definitions, swallowing safety, mechanism-led antithrombotics, referral capability, rehabilitation, caregiver communication, affordability and equitable follow-up in Indian services.
Summary
Stroke is sudden neurological dysfunction caused by vascular injury; an ischaemic event reflects arterial occlusion and a haemorrhage reflects bleeding. A transient ischaemic attack (TIA) is a transient focal neurological syndrome without evidence of acute infarction on appropriate imaging. TIA is not a harmless mini-stroke and a resolving symptom is not automatically a TIA: persistent deficit or an acute infarct is stroke, while both require urgent assessment. Record the last-known-well time, glucose, airway and circulation, anticoagulant exposure and whether the deficit is disabling.
Immediate non-contrast CT excludes haemorrhage and important mimics; CT angiography can identify large-vessel occlusion, dissection and major stenosis. Selected ischaemic strokes may be eligible for intravenous thrombolysis within the licensed window, and selected proximal occlusions for thrombectomy, including some late or wake-up presentations after specialist imaging selection. A suspected TIA needs brain and vascular assessment, ECG and rapid specialist review rather than routine reassurance.
Across both presentations, screen swallowing before oral intake, prevent hypoxia, fever, hypoglycaemia and aspiration, and begin rehabilitation when safe. Secondary prevention is mechanism-led: antiplatelet treatment for most non-cardioembolic disease, anticoagulation for suitable cardioembolism, blood-pressure and lipid management, tobacco cessation and carotid or cardiac treatment when indicated. This reviewed draft remains reviewed and never replaces a local stroke protocol or specialist decision.
How Common Is It?
Stroke is a leading cause of acquired disability, but an imported incidence figure cannot describe an individual Indian patient's probability, mechanism or access to treatment. Case ascertainment varies with rural transport, death before hospital, CT availability, referral practices and whether recurrent events are counted. India has substantial hypertension, diabetes, tobacco exposure, dyslipidaemia, rheumatic heart disease and uneven access to stroke units, thrombolysis, thrombectomy and rehabilitation. Services should measure onset-to-door, door-to-imaging, swallowing screening, transfers and functional outcome rather than treatment counts alone.
TIA is a clinical emergency because the period after a transient episode can carry a substantial risk of completed stroke, especially when there is weakness or speech disturbance, atrial fibrillation, carotid disease, diabetes or recurrent symptoms. The risk is not safely estimated by an isolated score or by the patient's feeling that the symptoms have gone. MRI may show an infarct even when the examination is normal; a normal scan does not erase concerning chronology.
Trials often assume rapid ambulance transport and specialist follow-up. In India, a safe plan therefore includes a named service, affordable tests, clear return precautions, family education and a route for same-day or next-day review. Young age does not exclude dissection, cardioembolism, pregnancy-related disease or thrombophilia, while older age does not prove small-vessel disease. The burden includes cognitive, emotional, communication and caregiver effects, not only limb weakness.
Risk Factors
Hypertension is the most important modifiable risk factor for both infarction and intracranial haemorrhage. Diabetes, smoking and smokeless tobacco, dyslipidaemia, obesity, inactivity, chronic kidney disease, sleep apnoea and previous vascular disease add risk. Atrial fibrillation, rheumatic mitral stenosis, prosthetic valves, cardiomyopathy, recent infarction and ventricular thrombus can embolise. Carotid or intracranial atherosclerosis, small-vessel disease and arterial dissection require different prevention strategies; a risk-factor list cannot establish mechanism.
Ask about antiplatelets, anticoagulants and adherence; recent surgery, trauma, malignancy, infection, pregnancy or puerperium, migraine, seizure, stimulant exposure and family history. In a young person consider dissection after neck pain or trauma, cerebral venous thrombosis, antiphospholipid syndrome, sickle-cell disease, vasculitis and selected inherited disease when the phenotype supports them. In an older person, cerebral amyloid angiopathy or malignancy may be relevant to a haemorrhage pattern.
Social risk is clinical risk: distance from a stroke centre, ambulance access, medicine cost, literacy, language, caregiving, unsafe work and fragmented records alter outcomes. Risk reduction needs measured blood pressure, glucose and lipid review, smoking cessation, activity and diet counselling, sleep assessment, medication reconciliation and a plan the patient can obtain. Do not blame a patient for a system barrier. After TIA, recurrence prevention begins during the diagnostic encounter, not at an indefinite outpatient appointment.
Diagnosis
History
Establish exact onset, last-known-well, peak deficit, duration and recovery. Characterise weakness, numbness, aphasia, dysarthria, neglect, visual loss, diplopia, ataxia, facial asymmetry, seizure, headache, vomiting and collapse. Ask about baseline independence, previous events, atrial fibrillation, valve disease, vascular risks, pregnancy, anticoagulant name and last dose, antiplatelet use, recent procedures and bleeding. A witness, ambulance record or phone video may clarify a transient episode. Do not let symptom resolution delay assessment.
Examination
Stabilise airway, breathing and circulation; record temperature, oxygen saturation, blood pressure, glucose and rhythm. Perform a reproducible neurological examination including consciousness, language, neglect, visual fields, eye movements, pupils, facial movement, speech, power, sensation and coordination. Record an NIH Stroke Scale when trained, but remember that a low score can miss disabling aphasia, hemianopia or posterior-circulation disease. Look for meningism, trauma, arrhythmia, murmur, endocarditis, dissection and anticoagulant-related bleeding. Re-examine if symptoms fluctuate.
Investigations
Obtain urgent non-contrast CT. Add CT angiography from arch to vertex when large-vessel occlusion, dissection or significant carotid disease is possible; perfusion CT or diffusion MRI may support late-window selection in capable centres. MRI is useful for small infarcts, posterior fossa disease and TIA tissue definition but must not delay eligible reperfusion. Check glucose, blood count, electrolytes, renal and liver function, coagulation when relevant, ECG and pregnancy status when relevant. Arrange carotid imaging, echocardiography and prolonged rhythm monitoring according to mechanism. Document the imaging result, timing, severity and treatment question.
Differential Diagnosis
Hypoglycaemia can cause focal deficit and is immediately reversible; check it before attributing symptoms to stroke. Seizure may cause ictal signs or postictal weakness, but a first seizure with persistent focal findings still needs stroke imaging. Migraine aura often spreads gradually with positive visual or sensory symptoms, yet a first or atypical aura in an older person is a diagnosis of exclusion. Syncope is global loss of consciousness, although an arrhythmia can coexist.
Acute vestibular syndrome with inability to walk, direction-changing nystagmus, diplopia, limb ataxia or new hearing loss may be posterior circulation stroke rather than vestibular neuritis. Bell palsy, radiculopathy, peripheral neuropathy, functional neurological symptoms, tumour, subdural haematoma, cerebral venous thrombosis, encephalitis, meningitis and toxic-metabolic illness enter the differential according to context. Functional symptoms require positive inconsistency or incongruity, not a dismissive psychiatric label.
Thunderclap headache with neck stiffness raises subarachnoid haemorrhage; CT-negative cases may need specialist lumbar-puncture or vascular pathways. A CT that shows no bleed does not rule out early infarction. A transient deficit with diffusion-restricted infarction is ischaemic stroke rather than tissue-negative TIA, whereas haemorrhage excludes thrombolysis. Chronology, examination, imaging and recurrence pattern must be integrated before discharge or a prevention prescription.
Management
Activate a stroke team and transfer to a stroke-capable service. Correct hypoglycaemia, hypoxia, fever and seizures without delaying imaging. Eligible disabling ischaemic stroke may receive alteplase or tenecteplase within the licensed window after haemorrhage, blood pressure and contraindications are checked. Selected proximal large-vessel occlusion may benefit from thrombectomy as early as possible and, after advanced imaging selection, in a late window. These are specialist decisions; a low NIHSS does not make a disabling deficit benign.
For high-risk TIA or minor non-cardioembolic stroke, a short, protocol-defined course of dual antiplatelet therapy may be appropriate after haemorrhage is excluded; it is not routine for every TIA and is not a substitute for anticoagulation in atrial fibrillation. Most other non-cardioembolic events need antiplatelet therapy. Cardioembolic prevention requires rhythm assessment and appropriately timed anticoagulation, balancing infarct size and bleeding. Symptomatic carotid stenosis may need urgent vascular review.
For haemorrhage, stop and reverse relevant anticoagulants, manage blood pressure smoothly, treat raised intracranial pressure and involve neurocritical care or neurosurgery. Screen swallowing before food, drink or oral medicines. Prevent aspiration, pressure injury and venous thromboembolism; use intermittent pneumatic compression where appropriate. Begin coordinated physiotherapy, occupational, speech-language, cognitive and mood rehabilitation when medically stable. Give written safety-netting and a named follow-up owner.
Prescribing Information
No thrombolytic, reversal agent or antithrombotic dose should be copied from this guide. Verify the product label, weight, timing, imaging, blood pressure, anticoagulant exposure, platelet count, renal function, recent surgery, bleeding history and local protocol. Post-thrombolysis observation must include a plan for neurological deterioration and intracranial bleeding. Blood-pressure thresholds differ between reperfusion, uncomplicated infarction and intracerebral haemorrhage; indiscriminate rapid lowering can harm cerebral perfusion.
Aspirin is given only after haemorrhage is excluded. Dual antiplatelet therapy belongs to selected early minor stroke or high-risk TIA pathways and has a defined duration. Anticoagulation for atrial fibrillation is not started solely because a rhythm was seen: infarct burden, repeat imaging, haemorrhagic transformation, renal function, valve disease, pregnancy, interactions and adherence determine timing and choice. Mechanical valves and rheumatic mitral stenosis need specialist planning.
Start or intensify lipid-lowering and antihypertensive treatment according to the mechanism and clinical state. Review diabetes treatment, swallowing, renal and hepatic function, falls, constipation and medicine affordability. Explain generic names, purpose, duration, missed-dose instructions and bleeding warnings. Do not add an acid suppressant, supplement or traditional product automatically. Every discharge prescription should state who reviews it, when monitoring occurs and what symptoms require emergency help.
When to Refer
Every suspected stroke and every concerning TIA needs emergency or rapid specialist assessment, even when symptoms improve. Immediate transfer is required for persistent or recurrent face, arm, speech, visual, neglect, ataxic or consciousness deficit; severe headache; seizure with focal signs; anticoagulant exposure; suspected dissection; or posterior-circulation syndrome. Handover last-known-well, baseline function, glucose, blood pressure, examination or NIHSS, medicine and last-dose information, pregnancy, recent surgery and imaging.
Transfer to a thrombectomy-capable centre when CTA suggests proximal occlusion or local expertise cannot assess this promptly. Involve neurosurgery or neurocritical care for cerebellar or large haemorrhage, hydrocephalus, mass effect, vascular malformation, aneurysm concern, deteriorating consciousness or malignant infarction. Cardiology, vascular surgery, haematology, obstetric medicine, oncology or infectious-disease input should follow the suspected mechanism.
Before discharge, involve rehabilitation, speech and language, dietetics, psychology, social work and caregiver support according to need. Arrange rhythm monitoring, carotid review, echocardiography and risk-factor follow-up with named ownership. A referral in India must address transport, cost, records, language and appointment access. If advanced therapy is unavailable, document the limitation, use tele-stroke advice and transfer safely rather than offering false reassurance.
Red Flags
Worsening consciousness, anisocoria, repeated vomiting, severe headache, new pupillary abnormality, seizure, rapidly increasing weakness or respiratory compromise may indicate expanding haemorrhage, oedema, herniation or aspiration. New fever, hypoxia, chest pain, hypotension, arrhythmia or recurrent deficit requires immediate reassessment. A sudden headache or deterioration after thrombolysis is an emergency. Do not attribute decline to fatigue, sleep or rehabilitation without examining the patient.
High-risk patterns include malignant hemispheric infarction, basilar occlusion, cerebellar swelling, large-vessel occlusion, a disabling deficit with low NIHSS, anticoagulant-associated haemorrhage, intraventricular extension and uncontrolled blood pressure. A normal first CT does not exclude early infarction, posterior stroke or subarachnoid haemorrhage. Recurrent transient symptoms are not evidence of benign disease; they may signal an unstable source requiring admission or urgent intervention.
Complication warnings include coughing or wet voice with intake, reduced urine, a painful swollen calf, new breathlessness, delirium, depression, suicidal thinking, falls, shoulder injury and caregiver exhaustion. Families should call emergency services for new FAST symptoms rather than arrange unsafe private transport. Discharge with diagnostic uncertainty requires explicit return precautions, a 24-hour contact route and a plan for completing vascular, cardiac and brain assessment.
Indian Clinical Context
Indian stroke pathways range from district hospitals to comprehensive tertiary centres, with major differences in ambulance transport, CT and CTA, thrombolysis stock, thrombectomy, neurosurgery, reversal agents and rehabilitation. A hospital should map its actual 24-hour capability, referral phone numbers, transport time, tele-stroke support and receiving clinician. The Government of India national stroke guidance supports organised prevention, acute care, referral and rehabilitation, but it does not replace a locally tested protocol.
Cost and distance should trigger transparent escalation, not a false TIA label or an unchecked contraindication. Use generic names, public schemes and social-work support where available. Warfarin may be affordable but needs reliable INR monitoring; direct oral anticoagulants reduce monitoring burden but may be intermittently stocked or unaffordable. Explain the plan in the family's language and account for literacy, tobacco, traditional medicines, caregiving and fragmented records.
Rheumatic heart disease, intracranial atherosclerosis, hypertension, diabetes and tobacco exposure are important contexts, but ancestry is not a diagnostic shortcut. International reperfusion trials may not reflect local transfer delays, so services should audit time, equity and functional outcome. This guide makes no unsupported national burden estimate and does not override current Indian labels, state protocols, hospital formularies or bedside specialist judgement.
NMC Competency Mapping
This topic integrates NMC CBME competencies in neurological history and examination, emergency care, imaging and ECG interpretation, pharmacology, prevention, communication and rehabilitation. Learners should identify a disabling focal deficit, state last-known-well, check glucose and ABC stability, perform a structured examination and recognise that a low NIHSS can miss aphasia, hemianopia or posterior stroke. They should distinguish tissue-negative TIA from infarction-based stroke and explain why symptoms resolving does not end the emergency.
Diagnostic reasoning includes ischaemia, intracerebral and subarachnoid haemorrhage, seizure, migraine, hypoglycaemia, vestibular disease, venous thrombosis and functional symptoms. Learners should explain the roles and limits of CT, CTA, perfusion imaging, MRI, ECG, rhythm monitoring, echocardiography and carotid imaging. Pharmacology learning includes safe aspirin timing, selected dual antiplatelet pathways, anticoagulation timing, reversal, blood-pressure treatment, lipid lowering and swallow-safe administration. Independent prescribing, thrombolysis and reversal require supervised practice.
OSCEs can assess a transient aphasia case, wake-up large-vessel occlusion, apixaban-associated haemorrhage, dysphagia and family counselling. Community competencies include tobacco cessation, hypertension adherence, rehabilitation access and stroke warning education. Faculty should verify exact competency codes against the current NMC compendium and keep undergraduate outcomes separate from specialist procedural credentialing.
Key Exam Pearls for NEET PG
A TIA is transient focal neurological dysfunction without acute infarction; a transient deficit with diffusion-restricted infarction is ischaemic stroke. The first action in a suspected stroke is ABC assessment plus capillary glucose and urgent brain imaging, not an outpatient score. Non-contrast CT excludes haemorrhage; CTA detects large-vessel occlusion and dissection. A normal early CT does not exclude infarction or posterior stroke.
Thrombolysis is time-dependent and requires haemorrhage exclusion, blood-pressure and contraindication review. Mechanical thrombectomy is for selected large-vessel occlusion and can benefit selected late-window patients after advanced imaging. Aspirin follows exclusion of haemorrhage. Short dual antiplatelet therapy is restricted to selected minor non-cardioembolic stroke or high-risk TIA; atrial fibrillation generally requires anticoagulation rather than antiplatelet substitution. A symptomatic carotid lesion needs urgent vascular assessment.
Always screen swallowing before oral intake. In intracerebral haemorrhage, stop and reverse anticoagulation, control blood pressure smoothly and seek neurocritical or neurosurgical care. Secondary prevention is mechanism-led: pressure, lipids, diabetes, tobacco, rhythm, carotid disease and rehabilitation. Exam answers should include last-known-well, disabling deficit, glucose, CT, CTA when relevant, recurrence risk and explicit safety-netting. Patient-centred counselling, early mobilisation when safe, mood screening, communication access and caregiver teaching are part of recovery and should be documented alongside the neurological diagnosis.
Frequently Asked Questions
Is a completely resolved focal episode safe to manage as an outpatient without urgent imaging?
No. A resolved episode may be a TIA, a small infarct or a mimic, and early recurrence can be disabling. Arrange urgent specialist assessment with brain and vascular evaluation, ECG and mechanism-directed tests. Persistent, recurrent or disabling symptoms require emergency transfer. Do not let a reassuring examination after arrival erase the witness history or last-known-well time.
Should every patient with a suspected TIA receive aspirin before brain imaging?
The answer depends on the local emergency pathway and the possibility of haemorrhage or another dangerous diagnosis. Aspirin is appropriate after intracranial bleeding has been excluded and a clinician has considered allergy, active bleeding and the likely mechanism. Do not give antiplatelet treatment blindly to a patient with severe headache, anticoagulant exposure or symptoms that remain unresolved without urgent imaging and senior assessment.
Does a low NIH Stroke Scale score mean thrombolysis or thrombectomy is unnecessary?
No. A low score can conceal disabling aphasia, hemianopia, neglect, ataxia or posterior-circulation disease. Treatment eligibility depends on the deficit's functional impact, imaging, time, vessel status, contraindications and specialist assessment. Describe what the patient cannot do rather than relying on the number alone, and transfer promptly to a service that can evaluate reperfusion options.
What secondary prevention should begin after a confirmed non-cardioembolic TIA?
After haemorrhage and important mimics are excluded, a clinician should select antiplatelet treatment, assess for carotid disease and atrial fibrillation, manage blood pressure, diabetes and lipids, and address tobacco, activity, diet and medicine access. Selected high-risk cases may receive a short protocol-defined dual-antiplatelet course. The exact drugs and timing depend on bleeding risk, imaging, renal function and current Indian guidance; specialist follow-up must be rapid and named. The plan should also record adherence barriers, monitoring dates, rehabilitation needs, communication preferences, warning symptoms, and who is responsible for reviewing results and changing treatment.
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