Authored & revised by Pulathi Senaratna(Founder & Senior Editor) · Updated 7 Nov 2026
✓ Clinically reviewed by Medipaedia Editorial Board on 7 Nov 2026mID 10061
⚡ At-a-Glance Clinical Summary Card
ICD-10: I63.9ICD-11: 8B11
⚡ High-Yield Clinical Summary
Acute ischaemic stroke is a sudden neurological deficit resulting from focal cerebral hypoperfusion, diagnosed via non-contrast computed tomography and multimodal neuroimaging (ASPECTS quantification and NIHSS scoring), and managed urgently through intravenous thrombolysis and mechanical endovascular thrombectomy.
🩺 Specialty:
Radiology & Medical Imaging
🎯 Classic Triad / Hallmark Presentation:
Sudden-onset focal neurological deficit conforming to a vascular territory (FAST: Contralateral hemiparesis, facial droop, aphasia/dysarthria, gaze deviation, or homonymous hemianopia) + NIHSS quantification + Hyperdense MCA sign / loss of insular ribbon on non-contrast CT
🔬 Gold-Standard Diagnostic Test:
Immediate Non-Contrast CT Head (to exclude haemorrhage and calculate ASPECTS score) + CT Angiography (arch-to-vertex for Large Vessel Occlusion in ICA/M1/M2/Basilar) + CT Perfusion (core-to-penumbra mismatch in 6–24h window)
💊 First-Line Treatment Protocol:
IV Thrombolysis within 4.5 hours of onset (Alteplase 0.9 mg/kg or Tenecteplase 0.25 mg/kg after excluding haemorrhage; keep BP <185/110 mmHg) + Mechanical Endovascular Thrombectomy within 6–24 hours for anterior/posterior Large Vessel Occlusion + Aspirin 300 mg started 24h post-thrombolysis after repeat CT
Acute ischaemic stroke (ASPECTS and NIHSS) is a critical medical emergency defined by the sudden cessation of cerebral blood flow within a specific vascular territory, resulting in rapid neurological dysfunction and potential permanent brain infarction if reperfusion is not achieved promptly1, 2. The syndrome is evaluated clinically via the National Institutes of Health Stroke Scale (NIHSS) to quantify severity and anatomically via the Alberta Stroke Program Early CT Score (ASPECTS) on non-contrast computed tomography to evaluate structural integrity and exclude intracranial haemorrhage1, 6. Immediate diagnostic triage combines non-contrast computed tomography, computed tomography angiography to identify large vessel occlusions, and computed tomography perfusion to quantify the salvageable ischaemic penumbra, guiding hyperacute interventions including intravenous thrombolysis and mechanical endovascular thrombectomy2, 3, 5.
1. Etiology & Risk Factors
Cardioembolic Infarction (~20–30%): Most frequently caused by non-valvular or valvular atrial fibrillation, left ventricular thrombus following acute myocardial infarction, rheumatic heart disease, infective or non-bacterial thrombotic endocarditis, and prosthetic heart valves, leading to large-vessel embolisation.
Large Artery Atherosclerosis (~20–25%): Atheromatous plaque disruption, ulceration, or in-situ thrombosis within the extracranial or intracranial internal carotid artery, middle cerebral artery, or vertebrobasilar system, causing artery-to-artery embolism or local branch occlusion.
Small Vessel Occlusion / Lacunar Infarction (~20–25%): Lipohyalinosis and microatheroma affecting small penetrating perforating arteries (lenticulostriate, thalamogeniculate, paramedian branches), commonly associated with chronic uncontrolled hypertension and diabetes mellitus.
Cryptogenic Stroke / Embolic Stroke of Undetermined Source (ESUS) (~25%): Infarctions without an identifiable cardiac or large-artery source despite comprehensive diagnostic workup, frequently linked to occult paroxysmal atrial fibrillation, patent foramen ovale, or aortic arch atheroma.
Other Determined Etiologies (<5%): Cervicocephalic arterial dissections (internal carotid or vertebral arteries), hypercoagulable states (antiphospholipid syndrome, malignancy, factor V Leiden), vasculitis (primary CNS vasculitis, giant cell arteritis), cerebral venous sinus thrombosis, and genetic arteriopathies (CADASIL)1, 2.
Modifiable Vascular Risk Factors: Systemic arterial hypertension (the single most potent modifiable risk factor), cigarette smoking, dyslipidaemia, type 2 diabetes mellitus, heavy alcohol consumption, obstructive sleep apnoea, obesity, and physical inactivity.
Non-Modifiable Risk Factors: Advancing age, male sex, genetic predisposition, and positive family history of cerebrovascular disease3, 6.
2. Pathophysiology
The interruption of cerebral blood flow below the critical threshold of approximately 10 to 18 mL/100g/min triggers an immediate bioenergetic failure within brain tissue1, 2. Deprivation of oxygen and glucose halts oxidative phosphorylation, causing rapid adenosine triphosphate (ATP) depletion, failure of ATP-dependent Na+/K+-ATPase membrane pumps, and massive intracellular accumulation of sodium and water, resulting in cytotoxic oedema1, 4. Concurrently, depolarisation of neuronal membranes opens voltage-gated calcium channels, prompting excessive extracellular release of the excitatory neurotransmitter glutamate, which binds to NMDA and AMPA receptors and floods intracellular spaces with neurotoxic calcium ions2, 3. This calcium surge activates destructive intracellular enzymes, including phospholipases, endonucleases, and proteases, which dismantle cell membranes and cytoskeletal proteins, culminating in necrotic cell death within the ischaemic core1, 5. Surrounding the irreversibly damaged core lies the ischaemic penumbra—a zone of marginally perfused tissue where collateral blood flow sustains cellular viability without supporting normal electrical activity2, 3. Within the penumbra, persistent moderate hypoperfusion, peri-infarct depolarisations, and delayed apoptotic signalling drive progressive tissue injury over hours, establishing the central pathophysiological target for hyperacute reperfusion therapies (intravenous thrombolysis and mechanical thrombectomy) designed to salvage salvageable brain tissue before the penumbra undergoes irreversible infarction3, 5, 6.
3. Clinical Presentation & Classic Clinical Signs
History & Cardinal Symptoms: Patients present with abrupt, focal neurological deficits that evolve over minutes to hours, typically without pain. Hallmark manifestations follow specific vascular distributions, summarised by the FAST mnemonic (Face drooping, Arm weakness, Speech difficulty, Time to call emergency services). Additional symptoms include sudden monocular or binocular visual loss (amaurosis fugax or homonymous hemianopia), ataxia, vertigo, sudden severe headache (often preceding haemorrhagic transformation or posterior circulation dissection), and acute confusional state or altered mental status1, 2.
Physical Examination & Named Clinical Signs:
Contralateral Hemiparesis & Facial Droop: Upper motor neurone facial weakness sparing the forehead and contralateral arm/leg weakness, characteristic of middle cerebral artery trunk or superior division occlusion1, 6.
Aphasia & Neglect Syndromes: Expressive (Broca) or receptive (Wernicke) aphasia resulting from dominant hemisphere involvement; contralateral hemispatial neglect, anosognosia, and constructional apraxia resulting from non-dominant hemisphere lesions2, 4.
Gaze Deviation: Forced conjugate deviation of the eyes toward the side of the cerebral lesion ("looking at the lesion") due to disruption of frontal eye fields, or away from the hemiparetic side in pontine lesions3, 5.
Homonymous Hemianopia: Loss of vision in the temporal half of one visual field and the nasal half of the other, pointing to optic tract or optic radiation involvement1, 2.
Horner Syndrome: Ptosis, miosis, and anhidrosis caused by disruption of oculosympathetic pathways, frequently associated with internal carotid artery dissection6.
Immediate Non-Contrast Computed Tomography (NCCT) Head combined with computed tomography angiography (CTA) and computed tomography perfusion (CTP). NCCT rapidly excludes intracranial haemorrhage and quantifies early ischaemic changes via ASPECTS; CTA identifies large vessel occlusion (ICA, M1/M2 segments, basilar artery); CTP delineates core infarct from salvageable penumbra1, 2, 5.
Laboratory Panel
Urgent point-of-care blood glucose (to exclude hypoglycaemia mimicking stroke), complete blood count with platelet count (threshold <50,000/µL contraindicates thrombolysis), coagulation profile (PT/INR, aPTT; INR >1.7 contraindicates thrombolysis), serum electrolytes, renal function panel (creatinine for contrast administration), and cardiac biomarkers (troponin to evaluate cardiogenic origin or myocardial infarction)2, 3, 6.
Imaging / Radiology (X-ray, US, CT, MRI)
NCCT reveals early signs of acute ischaemia: loss of the grey-white matter differentiation in the basal ganglia or insular ribbon, sulcal effacement, and the hyperdense middle cerebral artery (MCA) sign (thrombus within the vessel lumen). Brain MRI with diffusion-weighted imaging (DWI) demonstrates restricted diffusion within minutes of symptom onset, while fluid-attenuated inversion recovery (FLAIR) helps date the age of the infarct1, 4, 5.
ECG / Histopathology / Procedural
12-lead ECG and continuous telemetry identify new-onset or paroxysmal atrial fibrillation, acute ST-segment elevation myocardial infarction, or left ventricular hypertrophy. Transthoracic and transoesophageal echocardiography evaluate cardioembolic sources (patent foramen ovale, vegetation, mural thrombus). Carotid duplex ultrasound assesses degrees of internal carotid artery stenosis2, 3, 6.
5. Staging, Classification & Clinical Scoring Systems
NIHSS (National Institutes of Health Stroke Scale)
Quantifies stroke severity across 11 neurological domains (level of consciousness, extraocular movements, visual fields, facial palsy, motor function, ataxia, sensory, language, dysarthria, extinction/inattention). Scores range from 0 to 42: 0 (no stroke), 1–4 (minor stroke), 5–15 (moderate stroke), 16–20 (moderate-severe stroke), 21–42 (severe stroke). Scores >6 strongly predict large vessel occlusion and benefit from endovascular therapy1, 2, 6.
ASPECTS (Alberta Stroke Program Early CT Score)
Topographic semi-quantitative scoring system dividing the middle cerebral artery (MCA) territory into 10 regions on axial non-contrast CT (caudate, lentiform nucleus, internal capsule, insular cortex, and M1 through M6 cortical regions). Each involved region subtracts 1 point from 10. A score of 10 represents a normal CT, while a score <6 indicates extensive ischaemic injury (>1/3 of MCA territory), predicting poor functional recovery and increased risk of haemorrhagic transformation following reperfusion therapy1, 5, 6.
Modified Rankin Scale (mRS)
Assesses global functional disability post-stroke at 90 days. Scores range from 0 (no symptoms) to 6 (death). Scores of 0–2 represent functional independence and are the primary clinical trial efficacy endpoint for stroke reperfusion therapies3, 4, 6.
TOAST Classification
Categorises ischaemic stroke etiology into five subtypes to guide secondary prevention: (1) Large-artery atherosclerosis, (2) Cardioembolism, (3) Small-vessel occlusion (lacunar), (4) Stroke of other determined etiology, and (5) Stroke of undetermined etiology (cryptogenic)2, 3.
6. Differential Diagnosis
Differential Condition
Distinguishing Clinical, Biochemical & Imaging Features
Hypoglycaemia
Presents with acute focal neurological deficits, altered mental status, diaphoresis, and tremors; distinguished instantly by point-of-care capillary blood glucose measurement (<3.9 mmol/L or <70 mg/dL) and rapid reversal of symptoms following intravenous dextrose administration1, 2.
Todd Paralysis
Transient focal neurological deficit (typically motor weakness or aphasia) following a focal or generalised epileptic seizure. Neuroimaging reveals no acute ischaemia; symptoms resolve completely within 24 to 48 hours, often accompanied by epileptiform discharges on electroencephalography3, 6.
Hemiplegic Migraine / Migraine Aura
Characterised by fully reversible visual, sensory, or motor aura symptoms preceding or accompanying a headache. Onset is usually gradual with marching symptoms (spreading depression), contrasting with the abrupt, maximal-at-onset deficit of an ischaemic stroke2, 4.
Intracranial Mass / Brain Tumour / Abscess
Can present with subacute focal neurological deficits or precipitate acute stroke-like symptoms due to local oedema, haemorrhage, or seizure. Non-contrast CT and MRI reveal a mass lesion with surrounding vasogenic oedema and mass effect rather than a vascular-territory hypodensity1, 5.
7. Management & Treatment Protocol
Initial Stabilization & Resuscitation: Secure airway, breathing, and circulation (ABCs). Administer supplemental oxygen only if oxygen saturation drops below 94%. Correct hypovolaemia with isotonic crystalloids (normal saline). Manage hyperglycaemia aggressively with sliding-scale regular insulin to maintain blood glucose between 7.8 and 10.0 mmol/L (140–180 mg/dL). Avoid aggressive blood pressure lowering in the hyperacute phase unless blood pressure exceeds 220/120 mmHg or thrombolysis is planned1, 2, 5.
First-Line Medical / Pharmacological Therapy:
Intravenous Thrombolysis (IVT): Indicated within 4.5 hours of symptom onset for eligible patients. Lower blood pressure strictly below 185/110 mmHg prior to initiation.
Alteplase: Administer at 0.9 mg/kg total dose (maximum 90 mg); give 10% of the calculated dose as an initial intravenous bolus over 1 minute, followed by the remaining 90% infused continuously over 60 minutes2, 3, 4.
Tenecteplase: Emerging alternative administered as a single weight-based bolus of 0.25 mg/kg (maximum 25 mg), offering greater ease of administration and superior recanalisation rates in large vessel occlusions3, 6.
Antiplatelet Therapy: Administer oral Aspirin 300 mg loading dose within 24 to 48 hours of stroke onset, delayed until 24 hours post-thrombolysis following a repeat neuroimaging scan that excludes intracranial haemorrhage1, 2.
Secondary Prevention: Long-term antiplatelet therapy (Clopidogrel 75 mg once daily or Aspirin plus Dipyridamole) for non-cardioembolic strokes; therapeutic anticoagulation (Direct Oral Anticoagulants such as Apixaban 5 mg twice daily, Rivaroxaban 20 mg once daily, or Warfarin adjusted to target INR 2.0–3.0) for cardioembolic strokes resulting from atrial fibrillation, initiated 4 to 14 days post-stroke depending on infarct size. High-intensity statin therapy (Atorvastatin 80 mg once daily) for all patients with atherosclerotic aetiology2, 3, 5.
Surgical / Interventional Indications:
Mechanical Endovascular Thrombectomy (EVT): Indicated within 6 hours of symptom onset (and up to 24 hours in selected patients with salvageable tissue demonstrated on CTP or MR perfusion) for anterior circulation large vessel occlusions (internal carotid artery or M1/M2 segments of the middle cerebral artery) and basilar artery occlusions, using stent retrievers and/or aspiration catheters2, 3, 5, 6.
Decompressive Hemicraniectomy: Urgent neurosurgical intervention for patients under 60 years old with malignant middle cerebral artery infarctions (massive space-occupying oedema leading to midline shift and herniation) performed within 48 hours of symptom onset to reduce mortality1, 6.
8. Complications & Prognosis
Acute Complications: Haemorrhagic transformation of the infarct (ranging from asymptomatic petechial haemorrhages to fatal parenchymal haematomas, significantly heightened by thrombolytic therapy), malignant cerebral oedema and elevated intracranial pressure, acute symptomatic seizures, aspiration pneumonia, deep vein thrombosis, pulmonary embolism, and pressure ulceration1, 2, 4.
Chronic Complications: Post-stroke spasticity, chronic neuropathic pain, central post-stroke pain syndrome, major depressive disorder ("post-stroke depression"), cognitive impairment and vascular dementia, and permanent physical disability2, 3.
Prognosis: Acute ischaemic stroke remains a leading cause of long-term adult disability and mortality worldwide. Prognosis is heavily dictated by patient age, baseline stroke severity (NIHSS score), initial neuroimaging extent (ASPECTS score), timely achievement of arterial recanalisation, and prompt admission to a specialized acute stroke unit1, 2, 5, 6.
🎓 Board Exam Pearls & Clinical Pitfalls
Exam Pearl 1: The Alberta Stroke Program Early CT Score (ASPECTS) grades the 10-point non-contrast CT regions of the middle cerebral artery territory; a score under 6 signifies extensive established ischaemia and predicts poor functional outcomes after reperfusion.
Clinical Pitfall 2: Failing to maintain blood pressure strictly below 185/110 mmHg prior to and during the first 24 hours following intravenous thrombolysis dramatically increases the risk of fatal symptomatic intracranial haemorrhage.
Board Pearl 3: The National Institutes of Health Stroke Scale (NIHSS) quantifies stroke severity on a 0 to 42 point scale, where scores above 25 indicate severe neurological impairment and strongly correlate with proximal large vessel occlusion.
📚 Verified PubMed & Guideline References (7) — click any reference to open the source
