Acute ischaemic stroke recognition and imaging

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Acute ischaemic stroke results from arterial occlusion with threatened but potentially salvageable brain around an irreversibly injured core. Time matters, but modern selection combines time, clinical disability, premorbid status, vessel anatomy and tissue imaging. The first clinician should identify a stroke syndrome, establish last-known-well, assess immediate physiology and supply the stroke team with anticoagulants, recent surgery or bleeding, baseline function and contact details for witnesses or family.

Recognition extends beyond facial droop, arm weakness and speech disturbance. Homonymous visual loss, neglect, gaze deviation, isolated aphasia, abrupt limb ataxia, dysarthria with diplopia and crossed brainstem findings can be vascular. Common mimics include hypoglycaemia, seizure with Todd paresis, migraine, intoxication, infection-related recrudescence of an old deficit and functional neurological disorder. Thrombolysis safety requires urgent expert discrimination, yet seeking perfect diagnostic certainty must not create avoidable delay.

Imaging has distinct questions. Non-contrast CT asks whether there is blood, a large established infarct or another lesion. CTA asks where the artery is blocked and whether carotid or vertebral pathology is present. CT perfusion or MRI mismatch can estimate viable tissue in selected extended or unknown-onset cases. Imaging interpretation belongs within a reperfusion-capable stroke network: a subtle early ischaemic sign should inform risk without delaying transfer or treatment while awaiting a non-essential report.

Key points

Stroke should be suspected when a focal neurological deficit begins suddenly, even when FAST is negative, symptoms are mild, the patient is young or posterior circulation features dominate.
Record the exact last-known-well time, not merely the discovery time; wake-up and unknown-onset strokes may still be eligible for advanced-imaging-selected reperfusion.
Stabilise airway, breathing and circulation, check capillary glucose, temperature, oxygen saturation and seizure activity, but run these actions in parallel with emergency stroke-team activation.
Urgent non-contrast CT excludes haemorrhage and major structural mimics but can look normal in early ischaemia; a normal scan never rules out acute ischaemic stroke.
Add CT angiography promptly when thrombectomy could be relevant, and use perfusion CT or MRI-based selection according to the treatment window and the local comprehensive stroke pathway.
Assess a structured deficit score such as NIHSS while remembering that it can underweight disabling aphasia, hand weakness, gait ataxia and posterior circulation signs.
Do not routinely lower moderately raised blood pressure before reperfusion assessment; extreme pressure, thrombolysis thresholds and other hypertensive emergencies require protocol-led treatment.
Keep the patient nil by mouth until a trained swallow screen, avoid unnecessary transfer delay, and repeat examination and imaging if neurological deterioration occurs.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Large-artery thromboembolism

Atherosclerotic plaque, cervical arterial disease or an embolus can occlude a major intracranial vessel, causing cortical, brainstem or cerebellar deficits and creating potential thrombectomy anatomy.

Cardioembolism

Atrial fibrillation, recent myocardial injury, intracardiac thrombus or valve disease can generate emboli that lodge abruptly in cerebral arteries, often producing cortical or multi-territory infarction.

Small-vessel occlusion

Disease of penetrating arterioles, associated particularly with hypertension, diabetes and ageing, causes compact deep infarcts with pure motor, sensory or other lacunar syndromes.

Less common arterial mechanisms

Dissection, vasculitis, hypercoagulability and selected haematological or genetic arteriopathies are especially relevant in younger people, recurrent events or unusual vascular distributions.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Arterial occlusion
Thrombus or embolus abruptly reduces blood flow to a cerebral territory, depriving neurons and glia of oxygen and glucose while collateral vessels variably sustain surrounding tissue.
2
Core and penumbra formation
Severely hypoperfused tissue develops irreversible energy failure, while less compromised penumbral tissue remains electrically silent but potentially recoverable if reperfusion occurs before secondary injury.
3
Infarction and swelling
Persistent ischaemia triggers excitotoxicity, ionic failure, cytotoxic oedema and inflammation. Tissue injury expands with time and can produce mass effect or haemorrhagic transformation.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Middle cerebral artery syndrome

Contralateral face and arm-predominant weakness or sensory loss, gaze preference, aphasia or neglect suggests an MCA event; a proximal occlusion may produce a dense combination.

Anterior cerebral artery syndrome

Contralateral leg-predominant weakness, abulia, impaired initiation and urinary incontinence can arise from medial frontal or callosal ischaemia.

Posterior cerebral artery syndrome

A homonymous visual field defect, visual agnosia, memory disturbance or thalamic sensory syndrome may occur without the classic FAST features.

Lacunar phenotype

Pure motor, pure sensory, ataxic hemiparesis or dysarthria–clumsy hand syndromes suggest small-vessel disease, but clinical phenotype alone cannot exclude a treatable large-vessel occlusion.

Posterior circulation warning

Sudden severe imbalance, diplopia, dysarthria, dysphagia, nystagmus or crossed sensory and motor findings should prompt vertebrobasilar assessment even if limb power is preserved.

Cortical signs

Aphasia, neglect, gaze deviation, visual field loss, apraxia and extinction support cortical involvement and help localise the likely occluded arterial territory.

Red flags requiring action

Falling consciousness, vomiting, new pupillary asymmetry or progressive hemiplegia may indicate large infarction, haemorrhagic transformation, seizure or raised intracranial pressure and needs immediate reassessment.
Sudden headache with meningism, anticoagulant use or marked hypertension requires urgent exclusion of intracranial haemorrhage even when focal deficit suggests ischaemia.
Fluctuating brainstem signs, quadriparesis or reduced consciousness can reflect basilar occlusion and should trigger immediate comprehensive-stroke-centre discussion.
Hypoxia, hypotension, severe hypoglycaemia or hyperglycaemic crisis threatens brain and systemic survival and must be corrected alongside imaging, not before calling the stroke team.
A seizure at onset does not exclude stroke; persistent focal deficit or an occlusion on angiography still requires specialist reperfusion consideration.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Capillary glucose and physiological screenFirst step
Why
Find immediate mimics and correct physiological variables that worsen cerebral injury.
Interpretation and limitations
Hypoglycaemia can produce focal signs; reassess after correction while persisting deficits remain on the acute-stroke pathway.
02
Non-contrast CT brain
Why
Exclude haemorrhage, identify a large established infarct and detect important structural mimics before reperfusion or antiplatelet treatment.
Interpretation and limitations
Early ischaemia may be invisible; loss of grey–white differentiation, sulcal effacement or a hyperdense artery supports infarction but treatment decisions require expert context.
03
CT angiography of head and neck
Why
Identify intracranial large-vessel occlusion, arterial stenosis or dissection and enable thrombectomy triage.
Interpretation and limitations
Interpret occlusion site, collateral circulation and access anatomy; do not withhold time-critical CTA solely for a modest creatinine abnormality without balancing neurological benefit.
04
CT perfusion or MRI mismatch imaging
Why
Estimate infarct core and salvageable tissue in selected late-window, wake-up or diagnostically difficult presentations.
Interpretation and limitations
Automated maps can be artefact-prone and thresholds vary; selection must follow the local stroke network and current national guidance rather than a standalone colour map.
05
NIH Stroke Scale
Why
Quantify neurological deficit, communicate severity and follow early change using a reproducible examination.
Interpretation and limitations
A low score can still represent disabling aphasia, visual loss or hand dysfunction and may miss posterior circulation severity; treatment is not decided by the score alone.
06
ECG and baseline blood tests
Why
Detect atrial fibrillation and establish glucose, count, renal function and coagulation information relevant to treatment safety.
Interpretation and limitations
Do not wait for tests that are not clinically required before reperfusion; targeted coagulation information matters when anticoagulant exposure or coagulopathy is possible.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Hypoglycaemia or metabolic disturbance

Low glucose, electrolyte change and intoxication can cause focal or global deficits; bedside physiology may reveal a reversible mimic but does not preclude simultaneous stroke.

Seizure with postictal deficit

Witnessed convulsion, gaze deviation or a deficit that improves steadily supports Todd paresis, although acute stroke can itself trigger seizures and may still require vascular imaging.

Migraine aura

Gradually spreading positive visual or sensory symptoms followed by headache favour aura, whereas abrupt maximal negative loss and persistent disability are more typical of ischaemia.

Functional neurological disorder

Positive inconsistency, preserved automatic movement or a recognised functional pattern supports FND, but assessment should not delay reperfusion decisions when a disabling vascular syndrome remains plausible.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01CODEFirst minutes of suspected strokeFirst stepA new sudden focal neurological deficit is present or has only partly improved.

1Activate the acute stroke team, record last-known-well and discovery time, establish premorbid function and obtain a concise witness history.
2Assess airway, breathing, circulation, capillary glucose, oxygen saturation, temperature and seizure activity while securing intravenous access without delaying transfer.
3Document the focal examination and NIHSS, anticoagulant name and last dose, recent procedures, bleeding history and current blood pressure.
4Transfer directly to emergency brain and arterial imaging through the fastest local pathway and keep the patient nil by mouth pending swallow screening.

02IMAGEImaging sequenceThe patient reaches a centre able to perform urgent stroke imaging.

1Obtain non-contrast CT immediately to distinguish haemorrhage from ischaemia and assess early established injury or another structural diagnosis.
2Perform CTA without avoidable delay when large-vessel occlusion is plausible or thrombectomy eligibility is being assessed.
3Add perfusion CT or MRI according to onset window, wake-up status and network protocol when tissue-based selection may extend treatment opportunity.
4Transmit images and clinical details rapidly to the thrombectomy centre; do not allow transfer arrangements to wait for non-essential local investigations.

03MIMICStroke mimic remains possibleThe history, examination or imaging suggests seizure, migraine, metabolic disease or functional symptoms.

1Correct hypoglycaemia, hypoxia or other immediate disturbance and repeat the focused neurological assessment promptly.
2Seek positive mimic evidence such as witnessed ictal activity, a spreading aura pattern or internal inconsistency while still excluding vascular occlusion.
3Discuss treatment risk and diagnostic probability with the stroke specialist, because seizure or migraine can accompany true cerebral ischaemia.
4AlternativeIf reperfusion is not given, document the reasoning and arrange the appropriate alternative investigation and safety-net rather than using a vague mimic label.

04WORSENEarly neurological deteriorationConsciousness, NIHSS, headache, vomiting or vital signs worsen after initial imaging or treatment.

1Repeat ABC assessment and glucose, check for seizure, aspiration, hypotension, fever and treatment-related angioedema or bleeding.
2Obtain urgent repeat brain imaging and vascular review to identify haemorrhagic transformation, re-occlusion, oedema or a missed posterior lesion.
3EscalationEscalate immediately to stroke, critical care and neurosurgical teams when decompression, airway protection or another intervention may be needed.
4Communicate change and ceiling-of-care decisions clearly while maintaining oxygenation, normoglycaemia and appropriate blood-pressure targets.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Provides early antiplatelet therapy for acute ischaemic stroke when reperfusion-related timing and swallowing safety permit.

Aspirin

Give 300 mg orally, rectally or by enteral tube once daily after intracranial haemorrhage has been excluded, generally within 24 hours; wait 24 hours after thrombolysis and re-image first.

Do not give before haemorrhage is excluded, during the first 24 hours after thrombolysis, or when bleeding or a specialist anticoagulation plan changes the balance.

Controls markedly elevated pressure safely enough to permit thrombolysis or treats a concurrent hypertensive emergency.

Intravenous labetalol

Use protocol-led intravenous boluses or infusion only when blood pressure exceeds a reperfusion threshold or another emergency indication exists; exact dosing follows local stroke policy.

Rapid excessive reduction can impair penumbral perfusion; avoid or modify in bradycardia, heart block, decompensated heart failure and significant bronchospasm.

Corrects hypoxaemia that could worsen cerebral and systemic injury during acute stroke assessment.

Oxygen

Titrate supplemental oxygen to the locally specified target when saturation is below the recommended range; do not administer routinely to a non-hypoxic patient.

Use controlled targets in people at risk of hypercapnic respiratory failure and investigate the reason for hypoxia, including aspiration or pulmonary oedema.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cerebral oedema and herniation

Large hemispheric or cerebellar infarcts can swell, compress ventricles or brainstem and reduce consciousness, requiring repeat imaging and early neurocritical or neurosurgical assessment.

Haemorrhagic transformation

Damaged vessels may leak into infarcted tissue spontaneously or after reperfusion, ranging from minor petechiae to symptomatic haematoma with acute neurological deterioration.

Aspiration and immobility harm

Dysphagia, weakness and reduced alertness increase pneumonia, venous thrombosis, pressure injury and deconditioning unless stroke-unit swallowing and mobility care begin promptly.

Persistent disability and recurrence

Loss of motor, language, visual, cognitive or balance function can restrict independence, while an untreated embolic or vascular mechanism leaves continuing risk of another stroke.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat neurological observations and NIHSS at protocol-defined intervals, with immediate escalation for any new deficit, headache, vomiting or reduced consciousness.
Track blood pressure closely around reperfusion decisions and avoid unplanned lowering outside the thresholds agreed by the stroke team.
Monitor oxygen saturation, temperature, capillary glucose and cardiac rhythm, correcting clinically important abnormalities without causing hypoglycaemia or hypotension.
Perform and document a trained swallow screen before any oral food, fluid or medication, then refer promptly for specialist swallowing assessment if failed.
After thrombolysis or thrombectomy, follow access-site, bleeding, angioedema and post-procedure imaging protocols in the specialist unit.
Review venous thromboembolism risk, hydration, continence, skin pressure, positioning and early mobilisation once reperfusion and neurological stability permit.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Last well is decisive

A patient found aphasic at 08:00 after going to bed well at 22:00 has a last-known-well time of 22:00, although advanced imaging may still identify treatment eligibility.

Normal CT is expected

Non-contrast CT is excellent for blood but insensitive to early small infarction, so normal appearances must not be used to dismiss a convincing stroke syndrome.

Disability beats score alone

Isolated aphasia, hemianopia or dominant-hand weakness can be life-changing despite a low NIHSS and deserves explicit specialist treatment consideration.

CTA changes destination

Demonstrating a proximal occlusion can trigger direct transfer to a thrombectomy centre and is not merely an aetiological test for later review.

Posterior signs are undercounted

Gait, eye movements, bulbar function and severe truncal ataxia need direct examination because common scales emphasise anterior circulation deficits.

Recrudescence has a trigger

Old deficits may recur during infection or metabolic stress, but a new stroke must still be excluded before attributing symptoms to recrudescence.

11Common pitfallsFrequent interpretation and management errors.

01
Do not wait for spontaneous improvement before activating the stroke team; rapidly improving symptoms can recur and may remain disabling.
02
Do not interpret a normal early CT as evidence against ischaemic stroke or postpone angiography when thrombectomy is plausible.
03
Do not equate FAST negativity or a low NIHSS with absence of posterior circulation or otherwise disabling stroke.
04
Do not lower blood pressure reflexively to normal values before the reperfusion team defines the appropriate target.
05
Do not give aspirin before haemorrhage is excluded or within 24 hours after thrombolysis without the required follow-up imaging.
06
Do not let renal blood tests, routine chest radiography or non-essential cannulation create a preventable reperfusion delay.