Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.
2 min synopsisUK scopeSources checked 27 Aug 2026Clinical review pending
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Escalate
Any sudden new cognitive, language, visual, gait or focal neurological deficit is an acute stroke until assessed through the hyperacute pathway. New confusion with physiological illness is delirium until proved otherwise. Do not attribute abrupt change to established vascular dementia or chronic white-matter disease without urgent glucose, observations, neurological assessment and imaging.
Synopsis
Recognise cognitive syndromes attributable to cerebrovascular injury, connect phenotype with strategic infarcts and small-vessel burden, identify mixed neurodegeneration, and prevent further brain injury without prescribing antithrombotic or cognitive medicine solely from an imaging label.
Vascular cognitive impairment spans objective cognitive decline without major dependency through to dementia caused wholly or partly by cerebrovascular disease.
Mechanisms include a strategic infarct, multiple cortical infarcts, subcortical small-vessel disease, cerebral haemorrhage, hypoperfusion and inherited arteriopathy; mixed Alzheimer and vascular pathology is common.
Executive dysfunction, slowed processing, impaired attention, apathy, gait change and urinary symptoms may be more prominent than early storage-memory loss in subcortical disease.
Key red flags
Strategic infarct
Abrupt new amnesia, language, executive or behavioural dysfunction after a small thalamic, hippocampal, caudate or dominant angular lesion may produce substantial cognitive disability.
Investigation priorities
01
Chronological patient and collateral historyFirst step
Link cognitive change to stroke events, stepwise deterioration or cumulative vascular disease and quantify functional loss.
Management branches
New deficitDo not miss acute stroke
Cognition or function changes suddenly, with or without an obvious focal sign.
1. Record last-known-well time, perform ABCDE, check glucose and activate the local stroke pathway for sudden language, neglect, visual, executive or memory change.
2. Obtain urgent brain and vascular imaging and assess reperfusion or haemorrhage management through the stroke team.
Key medicines
Clopidogrel after non-cardioembolic ischaemic strokeA common long-term secondary-prevention regimen is 75 mg orally once daily after the acute antiplatelet phase, selected according to current stroke guidance and individual tolerance.
High-intensity statin after ischaemic strokeCurrent secondary-prevention pathways commonly use atorvastatin 80 mg once daily unless interactions, adverse-effect risk or another clinical factor justifies a lower intensity.
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.