Stroke Medicine
Acute Ischaemic Stroke: Clinical Assessment, Reperfusion Eligibility, and Secondary Prevention — FCPS/MRCP Guide
- Definition & Core Concepts
- Vascular Territory Anatomy
- Classification by Territory and Mechanism
- Pathophysiology — Core and Penumbra
- Clinical Features and Localization
- Interpretation Framework: Ischaemic vs Mimic
- Differential Diagnosis
- Investigations
- Acute Management Pathway
- Complications
- Secondary Prevention
- Prognosis
- Red Flags and Must-Not-Miss Emergencies
- FCPS/MRCP Exam Pearls
- Common Viva Traps
- Practical Clinical Approach
- Frequently Asked Questions
- Medical Glossary
Acute ischaemic stroke is one of the most time-critical emergencies in clinical medicine. Every minute of delay in recognition and reperfusion results in the loss of approximately 1.9 million neurons. For FCPS and MRCP candidates, stroke is a core examination topic that tests your ability to combine rapid localization, imaging interpretation, reperfusion decision-making, physiological optimization, and long-term secondary prevention into a single coherent management plan. This article follows the FCPS/MRCP medicine-folder framework — giving you exam-ready structure alongside clear, reader-friendly clinical reasoning.
Definition and Core Concepts
Acute ischaemic stroke is defined as acute focal neurological dysfunction caused by cerebral, spinal, or retinal infarction due to arterial occlusion or critical hypoperfusion. It is distinct from TIA, in which no permanent infarction occurs, and from intracerebral haemorrhage, which requires urgent exclusion before any reperfusion is attempted.
The fundamental principle driving all hyperacute management is “time is brain” — the faster reperfusion is achieved, the more salvageable penumbra is preserved.
Vascular Territory Anatomy
Understanding which artery is affected guides both recognition and localization:
| Territory | Key Clinical Features |
|---|---|
| MCA — Middle Cerebral Artery | Face and arm > leg weakness; aphasia if dominant hemisphere; neglect if non-dominant |
| ACA — Anterior Cerebral Artery | Leg > arm weakness; abulia; frontal lobe signs |
| PCA — Posterior Cerebral Artery | Homonymous hemianopia; cortical blindness; thalamic sensory syndromes |
| Brainstem / Posterior Circulation | Diplopia, dysarthria, dysphagia, ataxia, crossed signs, reduced consciousness |
| Lacunar — Small Vessel | Pure motor hemiparesis; pure sensory stroke; sensorimotor stroke; ataxic hemiparesis |
Classification by Territory and Mechanism
By Vascular Territory
- Anterior circulation stroke (MCA, ACA, internal carotid)
- Posterior circulation stroke (PCA, basilar artery, cerebellar)
- Lacunar stroke (small-vessel penetrating arteries)
By Mechanism — TOAST Classification
- Large-artery atherosclerosis — carotid or intracranial large-vessel stenosis/occlusion
- Cardioembolism — atrial fibrillation, LV thrombus, valvular disease
- Small-vessel occlusion — lipohyalinosis of deep penetrating arteries
- Other determined cause — arterial dissection, vasculitis, paradoxical embolism via PFO, hypercoagulable states
- Undetermined / cryptogenic
Mechanism identification drives secondary prevention: antiplatelet vs anticoagulation, carotid intervention, PFO closure in selected young patients, or vasculitis treatment.
Pathophysiology — Core and Penumbra
Arterial occlusion causes an abrupt fall in cerebral blood flow (CBF). Two distinct zones result:
- Infarct core — CBF <10 mL/100g/min → irreversible neuronal death within minutes. Cannot be salvaged.
- Ischaemic penumbra — CBF ~10–20 mL/100g/min → functionally impaired but structurally viable. The target of reperfusion therapy.
Without timely reperfusion, the penumbra progressively converts into dead core. Every 15 minutes of delay to thrombolysis costs approximately one month of healthy life — the biological reality behind “time is brain.”
Clinical Features and Localization
Common Presentations
- Sudden hemiparesis or hemisensory loss
- Facial weakness (lower face in cortical; distinguish from peripheral VII palsy)
- Aphasia (expressive, receptive, or global) or dysarthria
- Homonymous visual field defect or diplopia
- Visuospatial neglect
- Ataxia with accompanying focal posterior signs
- Reduced consciousness in large hemispheric or brainstem strokes
Localization Pearls
- Aphasia → dominant hemisphere (usually left); MCA territory
- Neglect → non-dominant parietal/frontal (usually right); MCA territory
- Pure motor hemiparesis, no cortical signs → lacunar / internal capsule
- Leg predominant weakness → ACA territory
- Vertigo + diplopia + dysarthria + ataxia → posterior circulation until proven otherwise
- Crossed CN deficit + contralateral limb weakness → brainstem stroke
Interpretation Framework: Ischaemic Stroke vs Mimic
| Feature | Ischaemic Stroke | Common Mimic |
|---|---|---|
| Onset pattern | Sudden, maximal at onset; or stepwise in atherothrombotic | Gradual (tumour); follows seizure (Todd paresis) |
| Deficit character | Negative — loss of function: weakness, sensory loss, field defect | Positive features (jerking, spreading march) → seizure; bilateral → metabolic |
| Blood glucose | Usually normal | Hypoglycaemia (BG <3.0) mimics stroke — exclude first |
| Seizure clues | Not a primary feature of AIS | Todd paresis: witnessed convulsion, post-ictal confusion, clears over minutes–hours |
| Headache character | Usually absent; sudden severe headache → suspect SAH or ICH, not AIS | Migraine aura (positive spreading); SAH (thunderclap); subdural haematoma |
CT head first-pass checklist in hyperacute stroke:
- Priority 1 — exclude haemorrhage: any parenchymal hyperdensity = no thrombolysis
- Early ischaemic change: loss of insular ribbon, sulcal effacement, obscured lentiform nucleus
- Hyperdense vessel sign suggests thrombus — prompts urgent CTA
- Early ischaemic changes alone do not contraindicate thrombolysis; haemorrhage does
Differential Diagnosis
- Intracerebral haemorrhage — clinically indistinguishable; CT mandatory before reperfusion
- TIA — identical syndrome but fully resolved with no infarction on DWI
- Hypoglycaemia — commonest treatable mimic; check BG immediately
- Todd paresis (post-ictal) — witnessed seizure; clears within hours
- Migraine with aura — positive spreading aura, younger patient, prior history
- Functional neurological disorder — inconsistency, positive Hoover sign, psychiatric context
- Brain tumour / subdural haematoma — subacute onset; mass lesion on CT
- PRES / hypertensive encephalopathy — bilateral, posterior, severe hypertension
- Wernicke encephalopathy — malnourished / alcoholic; confusion + ataxia + ophthalmoplegia
Investigations
Hyperacute (Door to CT: target <25 minutes)
- Capillary blood glucose — mandatory, immediate
- Non-contrast CT head — exclude haemorrhage; early ischaemic change
- CT angiography (CTA) — when LVO suspected or thrombectomy pathway active
- ECG — detect AF, acute MI
- FBC, U&E, coagulation (INR, APTT), glucose
- SpO₂, temperature, bilateral BP
Early Inpatient / Aetiologic Workup
- MRI brain with DWI — confirms infarction; superior for lacunar and posterior fossa strokes
- Carotid duplex ultrasound or MRA / CTA of neck
- Echocardiography + prolonged cardiac monitoring / Holter for paroxysmal AF
- HbA1c, fasting lipid profile
- In young patients: thrombophilia screen, vasculitis panel, antiphospholipid antibodies
Acute Management Pathway
Step 1 — Immediate Stabilisation
- Airway: maintain patency; early anaesthetic input if GCS declining
- Breathing: oxygen only if SpO₂ <94% — routine O₂ in normoxic patients does not improve outcome
- Circulation: do not aggressively lower BP without specific indication
- Glucose: correct hypoglycaemia immediately before any other neurological decision
- NBM until swallow screen completed
- Onset time / last-known-well — document precisely; critical for reperfusion eligibility
Step 2 — Stroke Team Activation and Imaging
- Activate stroke pathway — parallel processing of all steps simultaneously
- Urgent non-contrast CT head ± CTA
- Assess NIHSS
Step 3 — Reperfusion Decision
IV Thrombolysis (alteplase or tenecteplase)
- Eligible ischaemic stroke within 4.5 hours of onset (or last-known-well)
- Requires: haemorrhage excluded on CT, known onset time, no major contraindications
- Contraindications: active bleeding, recent major surgery, prior ICH, therapeutic anticoagulation, BP >185/110 unresponsive to treatment, uncorrected BG
- Target BP ≤185/110 before; ≤180/105 during and after thrombolysis
Mechanical Thrombectomy
- Confirmed or suspected LVO — ICA, proximal MCA (M1/M2), basilar artery
- Extended window (up to 24 h) for selected patients with perfusion mismatch imaging
- Can be combined with IV thrombolysis (“bridging”) when both are indicated
- Transfer to thrombectomy-capable centre if required — time-critical
Step 4 — Antiplatelet Therapy
- Not thrombolysed + haemorrhage excluded → aspirin 300 mg promptly
- Post-thrombolysis → delay antiplatelets until 24-hour repeat CT excludes haemorrhagic transformation
- DAPT (aspirin + clopidogrel × 21 days) for minor stroke or high-risk TIA
Step 5 — Physiological Optimisation
- BP: permissive hypertension in hyperacute phase; lower only if >220/120 (non-reperfusion) or per post-thrombolysis protocol
- Glucose: target <10 mmol/L; correct hypoglycaemia immediately
- Temperature: paracetamol for fever; hyperthermia accelerates penumbral death
- Oxygenation: SpO₂ ≥94%
- Fluid: normal saline; avoid hypotonic fluids (worsen cerebral oedema)
Step 6 — Stroke Unit Care
- Early mobilisation when clinically safe
- DVT prophylaxis — compression stockings; LMWH when safe
- Formal swallow assessment by SLT
- Multidisciplinary rehab: physiotherapy, occupational therapy, speech therapy
- Neurological observation for deterioration (NIHSS, GCS, BP, glucose)
Complications
| Complication | Key Clinical Points |
|---|---|
| Haemorrhagic transformation | Especially post-thrombolysis; worsening deficit + headache + new CT hyperdensity; urgent repeat CT |
| Malignant MCA infarction | Cerebral oedema; declining GCS; herniation risk; consider decompressive craniectomy in eligible patients |
| Aspiration pneumonia | Commonest early infection; dysphagia-related; prevented by swallow screen + NBM protocol |
| DVT / PE | Immobility; compression stockings from admission; anticoagulation when haemorrhagically safe |
| Early neurological deterioration | Causes: haemorrhagic transformation, oedema, re-occlusion, metabolic disturbance, aspiration |
| Post-stroke depression | Up to 30% of survivors; impairs rehabilitation; screen proactively; treat with SSRI if confirmed |
| Pressure sores / contractures | Immobility-related; nursing repositioning + early physiotherapy are preventive essentials |
Secondary Prevention
The aetiology determines the prevention strategy — a high-yield examiner favourite:
| Mechanism | Prevention Strategy |
|---|---|
| All ischaemic strokes | High-intensity statin + BP control + lifestyle modification + diabetes optimisation + smoking cessation |
| Non-cardioembolic (atherosclerotic, lacunar) | Antiplatelet — aspirin alone, or DAPT for 21 days in minor stroke / high-risk TIA |
| AF-related (cardioembolic) | DOAC preferred in non-valvular AF; timing 2–14 days post-stroke based on infarct size and haemorrhagic risk |
| Symptomatic carotid stenosis ≥50% | CEA ideally within 2 weeks; statin + antiplatelet perioperatively |
| PFO in selected young patients (<60 y) | Percutaneous closure after MDT evaluation (CLOSE, RESPECT, REDUCE trial evidence) |
Prognosis
Outcome depends on stroke size, location, mechanism, age, comorbidities, collateral circulation, reperfusion speed, and complication prevention. The modified Rankin Scale (mRS) is the universal outcome measure.
- Large hemispheric infarcts → higher mortality from malignant oedema
- Posterior circulation strokes → can be devastating (basilar occlusion) or excellent recovery (PCA)
- Lacunar strokes → generally better functional recovery than cortical strokes at same NIHSS
- Organised stroke-unit care demonstrably improves survival and functional outcome
- Recurrence risk is highest in the first 48–72 hours — drives urgency of secondary prevention
- Posterior circulation stroke with declining consciousness — brainstem / large cerebellar infarct; rapidly fatal if labelled “labyrinthitis”
- Malignant MCA infarction — massive oedema with herniation; early neurosurgical referral for decompressive craniectomy
- Large cerebellar infarct with obstructive hydrocephalus — deterioration within hours; urgent CSF drainage or suboccipital decompression
- Worsening deficit after reperfusion — haemorrhagic transformation until proven otherwise; urgent repeat CT
- Thunderclap headache at onset — consider SAH or ICH before AIS; never thrombolyse without CT
- Stroke on therapeutic anticoagulation — specialist input needed before any reperfusion; reversal agent consideration
- The first imaging in hyperacute stroke = non-contrast CT — to exclude haemorrhage before any reperfusion
- Onset time / last-known-well is essential — document precisely; do not guess
- The ischaemic penumbra is salvageable — this is the biological basis for thrombolysis and thrombectomy
- MCA stroke is the classic exam territory — face/arm > leg weakness, aphasia (dominant), neglect (non-dominant)
- Hypoglycaemia must be excluded first — before imaging interpretation
- Oxygen is NOT given routinely — only if SpO₂ <94%
- BP is NOT aggressively lowered in hyperacute AIS without specific indication
- Swallow screen is mandatory BEFORE any oral intake
- Post-thrombolysis: delay antiplatelets until 24-hour repeat imaging
- AF-related stroke → eventual anticoagulation, not antiplatelet monotherapy
- Posterior circulation stroke is easily missed — any focal sign with dizziness = central until proven otherwise
- DAPT (aspirin + clopidogrel × 21 days) after minor stroke / high-risk TIA is evidence-based
- Labelling posterior stroke as benign vertigo — diplopia, dysarthria, dysphagia, facial numbness, or ataxia = central lesion
- Over-lowering BP in hyperacute AIS — penumbra depends on collateral perfusion; aggressive reduction worsens infarct unless specific indication
- Forgetting swallow screen — always mention this; it is a core stroke-unit safety standard
- Missing hypoglycaemia mimic — check glucose before any other neurological conclusion
- Delaying CTA in severe deficit — LVO must not be an afterthought; CTA and thrombectomy pathway run in parallel
- Antiplatelets immediately post-thrombolysis — delayed until 24-hour imaging; giving them immediately risks haemorrhagic conversion
- Antiplatelet monotherapy in AF-related stroke — AF = cardioembolic = anticoagulation needed
- Confusing core and penumbra — core is dead; penumbra is the entire justification for reperfusion therapy
- Recognise — FAST/BE-FAST; sudden focal deficit in any vascular territory
- Stabilise — ABC; glucose check and correction; SpO₂; document onset time
- Activate — stroke team / pathway; parallel processing of CT + clinical assessment
- Image — non-contrast CT head; add CTA if LVO suspected or thrombectomy pathway active
- Reperfusion decision — thrombolysis eligible? LVO confirmed → thrombectomy pathway?
- Optimise physiology — glucose, temperature, hydration, BP (context-dependent), oxygen only if needed
- Stroke unit — monitoring, swallow screen, DVT prophylaxis, NBM if dysphagia, early rehab referral
- Investigate aetiology — ECG/Holter, carotid imaging, echocardiography, bloods
- Secondary prevention — mechanism-driven: antiplatelet vs anticoagulation; statin; BP control; CEA if indicated
- Rehabilitation — MDT, early mobilisation, goal-setting, discharge planning, community follow-up
Frequently Asked Questions
What is the difference between TIA and acute ischaemic stroke?
TIA presents with identical focal neurological symptoms but resolves fully within 24 h (usually <60 min) and causes no permanent infarction on DWI-MRI. Acute ischaemic stroke causes a persistent deficit and demonstrates infarction on imaging. Both are emergencies with high early recurrence risk requiring urgent investigation and secondary prevention.
Why must CT head be done before thrombolysis?
Intracerebral haemorrhage is clinically indistinguishable from ischaemic stroke. CT reliably excludes haemorrhage within minutes. Giving thrombolysis to a patient with an unrecognised ICH is catastrophic — this step is non-negotiable.
When should antiplatelets be started after acute ischaemic stroke?
If not thrombolysed and haemorrhage excluded: aspirin 300 mg within 24 hours. Post-thrombolysis: delay for 24 hours until repeat CT excludes haemorrhagic transformation. DAPT (aspirin + clopidogrel × 21 days) applies to minor stroke or high-risk TIA.
What makes posterior circulation stroke easy to miss?
Isolated dizziness mimics peripheral vestibular disorders. The critical red flag is any accompanying focal sign — diplopia, dysarthria, dysphagia, facial numbness, limb ataxia, or altered consciousness. Never attribute dizziness to a peripheral cause if any of these are present.
When is anticoagulation started after cardioembolic stroke?
Timing follows infarct size and haemorrhagic risk. The “1-3-6-12” rule: TIA → day 1; minor stroke → day 3; moderate → day 6; large cortical infarct → day 12–14. Always confirm with the stroke team before initiating.
Medical Glossary — Key Stroke Terms
All underlined terms throughout this article have hover tooltips. The table below is a quick-reference summary:
| Term / Abbreviation | Meaning |
|---|---|
| AIS | Acute Ischaemic Stroke |
| TIA | Transient Ischaemic Attack — stroke symptoms that fully resolve with no infarction on imaging |
| LVO | Large Vessel Occlusion — proximal MCA, ICA, or basilar artery occlusion; target for mechanical thrombectomy |
| MCA / ACA / PCA | Middle / Anterior / Posterior Cerebral Artery — the three main cortical territories |
| Penumbra | Hypoperfused but viable brain tissue around the infarct core — rescued by reperfusion therapy |
| NIHSS | NIH Stroke Scale — 0–42 severity score used to guide management and track recovery |
| TOAST | Standard 5-category stroke aetiology classification |
| DWI-MRI | Diffusion-Weighted Imaging MRI — detects acute ischaemia within minutes of onset |
| CTA | CT Angiography — detects LVO and guides thrombectomy pathway |
| DOAC | Direct Oral Anticoagulant (e.g. apixaban, rivaroxaban, dabigatran) — preferred for AF-related stroke prevention |
| CEA | Carotid Endarterectomy — surgery for symptomatic carotid stenosis ≥50%; ideally within 2 weeks |
| mRS | Modified Rankin Scale — 0–6 functional outcome; 0–2 = independent |
| PFO | Patent Foramen Ovale — cardiac shunt enabling paradoxical embolism; cause of cryptogenic stroke in young patients |
| DAPT | Dual Antiplatelet Therapy — aspirin + clopidogrel for 21 days after minor stroke / high-risk TIA |
| ICH / SAH | Intracerebral Haemorrhage / Subarachnoid Haemorrhage — both are stroke mimics / differentials requiring CT exclusion |
| NBM | Nil By Mouth — no oral intake until swallow screen passed; prevents aspiration pneumonia |
| FAST / BE-FAST | Stroke recognition mnemonics: Face, Arm, Speech, Time / Balance, Eyes, Face, Arm, Speech, Time |
Medical Disclaimer: This article is written for educational purposes and FCPS/MRCP examination preparation. It does not constitute clinical advice. Clinical decisions must always be made by qualified healthcare professionals based on individual patient assessment, local guidelines, and current evidence. For emergency stroke management, always activate the local stroke protocol and involve the treating stroke team immediately.