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.
- The course can be stepwise after recognised strokes, but small-vessel disease often produces a gradual trajectory; absence of obvious clinical stroke does not exclude vascular contribution.
- Imaging abnormalities must be anatomically and quantitatively sufficient to explain the syndrome. A few age-related white-matter hyperintensities do not establish vascular dementia.
- Use MRI where possible to characterise infarcts, white-matter disease, lacunes, microbleeds and haemorrhage, while integrating findings with functional and cognitive chronology.
- Prevent further stroke through mechanism-specific antithrombotic treatment when indicated, blood-pressure and lipid care, diabetes management, smoking cessation, activity and treatment of atrial fibrillation.
- Do not prescribe aspirin or anticoagulation solely to treat cognitive impairment or incidental white-matter change; each requires a recognised vascular indication and bleeding-risk review.
- NICE recommends cholinesterase inhibitors or memantine in vascular dementia only when comorbid Alzheimer disease, Parkinson disease dementia or dementia with Lewy bodies is suspected.
- Rehabilitation, gait and falls work, mood care, communication support and carer planning address disability even when cognitive drug options are limited.
Key red flags
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
Link cognitive change to stroke events, stepwise deterioration or cumulative vascular disease and quantify functional loss.
Management branches
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.
- 3. Treat delirium, seizure, infection and metabolic mimics in parallel, avoiding an assumption that previous dementia explains the event.
- 4. Defer stable cognitive classification until the acute syndrome and immediate post-stroke delirium have been reassessed.
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.It does not treat cognition directly and should not be started for white-matter change alone. Review bleeding, interactions, adherence and whether atrial fibrillation instead requires anticoagulation.
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.Check liver profile and interaction history and assess muscle symptoms. Statins are not prescribed specifically to slow Alzheimer disease or incidental cognitive impairment, and haemorrhage context may need specialist review.