Vascular dementia

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

Reconstruct cognition around vascular events. Ask whether loss followed a stroke, appeared in steps or progressed steadily, and document focal deficits, gait, continence, mood and IADLs. Establish pre-stroke and post-stroke function through collateral. A dramatic ward decline can reflect delirium and deconditioning rather than a new stable dementia stage.

Examine pulse and rhythm, blood pressure including posture when safe, bruits only where clinically relevant, focal neurology, visual fields, speech, gait, parkinsonism and sensation. Cognitive testing should sample executive function and processing speed rather than relying on memory alone. Depression, apathy and aphasia can distort apparent performance.

MRI is preferred when feasible to show cortical and strategic infarcts, lacunes, white-matter hyperintensity, microbleeds and atrophy. CT identifies larger lesions and is often sufficient in acute stroke. Imaging must be proportional to the cognitive phenotype: common incidental small-vessel change does not establish causality.

Treat vascular risks according to primary or secondary prevention guidance and individual tolerance. Detect AF and use anticoagulation when indicated after stroke and bleeding assessment. Use antiplatelet therapy for non-cardioembolic vascular indications, not cognition. Control blood pressure and diabetes without provoking posture symptoms, renal injury or hypoglycaemia.

After ischaemic stroke, high-intensity statin treatment is usual unless contraindicated or a lower dose is required by interactions or adverse-effect risk. Smoking cessation, physical activity, diet and sleep-apnoea care support vascular health. Explain that prevention lowers future injury risk but does not reverse established infarcts.

Cognitive enhancers are not routine for pure vascular dementia. When collateral, phenotype or imaging suggests mixed Alzheimer or Lewy-body disease, a specialist may use an AChE inhibitor or memantine according to that comorbid indication. Review pulse, falls, weight and benefit as for the neurodegenerative subtype.

Rehabilitation addresses gait, weakness, communication, neglect, executive strategies and mood. OT adapts medicines, finances and home tasks; carers need strategies for apathy and initiation rather than assuming refusal. Review driving, swallowing, falls, continence, capacity and safeguarding and provide a named coordinator across stroke and memory services.

Key points

Vascular dementia requires cognitive decline interfering with function plus cerebrovascular disease judged sufficient to explain it; imaging lesions alone are not diagnosis.
The phenotype often emphasises slowed processing, attention, executive function, gait and focal findings more than isolated early amnesia.
Decline may be stepwise after strokes, but small-vessel disease can progress gradually; absence of obvious steps does not exclude it.
First investigate any sudden new deficit as acute stroke and any fluctuating inattention as delirium.
MRI better characterises infarcts, lacunes, white-matter disease and microbleeds; interpret burden, location and chronology together.
Assess AF, blood pressure, lipids, diabetes, smoking, activity and previous stroke while avoiding targets that cause falls or hypoglycaemia.
Secondary prevention follows the actual stroke or cardiovascular indication; do not give aspirin solely for a vascular-dementia label.
NICE advises AChE inhibitors or memantine in vascular dementia only when comorbid Alzheimer, Parkinson dementia or DLB is suspected.
Rehabilitation, cognitive support, hearing, vision, mood care, exercise and environmental adaptation remain central.
Use shared decisions to balance recurrent-stroke prevention against bleeding, posture, medicine burden, prognosis and goals.

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

Large-vessel infarction

Strategic or multiple cortical strokes disrupt memory, language, visuospatial and executive networks according to lesion location.

Cerebral small-vessel disease

Lacunes, white-matter injury and microbleeds damage frontal-subcortical connections, producing slowed processing, executive and gait dysfunction. This increases vulnerability across cognition, function and daily care.

Haemorrhagic and hypoperfusion injury

Intracerebral haemorrhage, cerebral amyloid angiopathy and severe hypoperfusion can leave persistent cognitive impairment. This increases vulnerability across cognition, function and daily care.

Mixed vascular-neurodegenerative disease

Vascular lesions commonly lower the threshold for symptoms from Alzheimer or Lewy-body pathology in later life.

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

1
Network disconnection
Infarcts and white-matter tract injury disconnect frontal, subcortical and cortical circuits needed for attention, planning and speed.
2
Cumulative lesion burden
Repeated overt or silent vascular injury reduces reserve, causing stepwise, fluctuating or gradually progressive decline. This influences cognition, mobility and everyday functional reserve.
3
Strategic-location effect
A small thalamic, hippocampal or angular-gyrus lesion can cause disproportionate cognitive change despite modest total volume.
4
Endothelial and perfusion dysfunction
Hypertension, diabetes and arteriopathy promote barrier damage, chronic ischaemia and impaired neurovascular coupling. This influences cognition, mobility and everyday functional reserve.
5
Interaction with neurodegeneration
Vascular injury and amyloid or tau pathology have additive effects, making clean clinical separation difficult. This influences cognition, mobility and everyday functional reserve.

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

Executive-speed phenotype

Slow processing, poor set shifting and reduced initiation dominate over isolated forgetting.

Focal cognitive pattern

Aphasia, neglect, visuospatial or memory syndrome maps to strategic or cortical vascular injury.

Gait and mood association

Short-stepped gait, falls, apathy, lability or depression accompanies frontal-subcortical disease.

Step after stroke

A dated cognitive and functional decrement follows a cerebrovascular event, with partial plateau or recovery.

New stroke syndromeRed flag

Sudden focal or cognitive deficit remains an emergency regardless of established dementia.

Mixed-disease phenotype

Progressive amnesia, hallucinations or parkinsonism exceeds what vascular location and burden explain.

Red flags requiring action

A new focal deficit or sudden step requires stroke or intracranial haemorrhage assessment rather than a routine memory appointment.
Acute inattention and fluctuation is delirium, which can be triggered by stroke, infection or medicines in vascular cognitive impairment.
Rapid progression without new vascular events, seizure or systemic features requires a non-vascular differential and specialist review.
Falls, early gait change, urinary symptoms and executive failure may indicate small-vessel disease but also hydrocephalus, Parkinsonism or drug harm.
Antiplatelet or anticoagulant treatment needs a separate vascular indication and bleeding assessment; dementia alone is not an indication.
A high vascular burden does not prove every cognitive symptom is vascular, because mixed Alzheimer pathology is common.

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
Collateral event-function timelineFirst step
Why
Connect vascular events to acquired decline.
Interpretation and limitations
Map strokes, steps, recovery, IADLs, gait and behaviour and separate acute delirium from stable loss.
02
Cognitive and neurological assessment
Why
Characterise executive and focal deficits.
Interpretation and limitations
Use accessible testing plus speech, fields, power, coordination, sensation, gait and parkinsonism examination.
03
MRI or CT brain
Why
Define cerebrovascular burden and alternatives.
Interpretation and limitations
Relate infarct location, lacunes, white-matter change, microbleeds and atrophy to phenotype rather than counting lesions.
04
Vascular risk assessment
Why
Find modifiable recurrent-injury drivers. within a safe older-adult assessment.
Interpretation and limitations
Assess ECG or rhythm for AF, pressure, lipids, diabetes, smoking, kidney function, weight and sleep-apnoea risk.
05
Delirium and contributor work-up
Why
Explain acute or disproportionate worsening.
Interpretation and limitations
Use 4AT, medicine review, mood, hearing, vision and targeted medical tests whenever trajectory changes.
06
Swallow and functional assessment
Why
Prevent secondary disability. within a safe older-adult assessment.
Interpretation and limitations
Assess aspiration, mobility, falls, continence, ADLs, IADLs, home and carer input through the stroke and CGA MDT.

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

Alzheimer disease

Prominent progressive episodic-memory encoding with medial temporal atrophy suggests Alzheimer dominance, though mixed disease is frequent.

Lewy-body dementia

Visual hallucinations, REM-sleep behaviour, parkinsonism and marked cognitive fluctuation point beyond ordinary vascular variability. Distinguish it through chronology, examination and targeted testing.

Delirium and depression

Acute inattention or mood-related slowing can mimic deterioration and require parallel assessment and treatment. Distinguish it through chronology, examination and targeted testing.

Normal-pressure hydrocephalus

Gait-predominant decline, urinary symptoms and ventriculomegaly may justify specialist CSF-dynamics assessment. Distinguish it through chronology, examination and targeted testing.

Medication and systemic disease

Sedatives, anticholinergics, hypotension, hypoglycaemia and organ failure can worsen executive performance and falls. Distinguish it through chronology, examination and targeted testing.

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

01Diagnostic sequenceLink phenotype, function and vascular injuryFirst stepPersistent cognitive decline occurs with stroke or vascular disease.

1Exclude acute stroke and delirium and obtain a dated collateral cognitive and functional trajectory.
2Complete executive, focal, mood and gait assessment with MRI or CT and vascular risk evaluation.
3Diagnose vascular or mixed dementia only when lesion burden and location plausibly fit the impairment.

02First-line preventionPrevent another vascular injury safelyFirst lineA cerebrovascular mechanism and modifiable risks are present.

1Determine cardioembolic, non-cardioembolic, haemorrhagic or primary-prevention context before prescribing antithrombotic therapy.
2Individualise pressure, lipid, diabetes, smoking, exercise and nutrition measures against posture, bleeding and treatment burden.
3Monitor adherence, organ function and functional adverse effects and coordinate stroke, primary and memory care.

03Mixed-disease routeTreat the supported comorbid subtypeSymptoms exceed a pure vascular explanation.

1Review amnestic, hallucination, fluctuation and parkinsonian clues with imaging and specialist assessment.
2Use AChE inhibitor or memantine only when comorbid Alzheimer, DLB or Parkinson dementia is suspected.
3Maintain vascular prevention, rehabilitation and carer support regardless of cognitive-drug response.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Prevent recurrent non-cardioembolic ischaemic events when a vascular indication is confirmed; it is not a treatment for dementia itself.

Antiplatelet therapy

Use the agent and dose specified by the person's TIA or non-cardioembolic stroke pathway, commonly clopidogrel 75 mg orally once daily for long-term secondary prevention.

Assess bleeding, haemoglobin, falls context, peptic history, interactions and adherence; do not combine antithrombotics without a defined indication.

Lipid-lowering secondary vascular prevention to reduce future events, not restoration of existing cognition.

Atorvastatin

After ischaemic stroke or TIA, NICE commonly recommends atorvastatin 80 mg orally once daily unless interactions, adverse-effect risk or preference require a lower dose.

Check liver profile and interactions, discuss muscle symptoms and goals, and individualise when frailty or treatment burden alters net benefit.

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

Recurrent stroke and disability

Further infarction or haemorrhage adds focal impairment, dysphagia, dependency and mortality. Anticipatory multidisciplinary prevention and review are therefore important.

Gait disorder and falls

Frontal-subcortical injury, weakness and impaired judgement combine with vascular medicines and postural hypotension. Anticipatory multidisciplinary prevention and review are therefore important.

Emotional and behavioural change

Apathy, depression, lability, disinhibition and slowed initiation affect rehabilitation and relationships. Anticipatory multidisciplinary prevention and review are therefore important.

Swallowing and continence difficulty

Stroke burden and executive impairment increase aspiration, malnutrition, urgency and care needs. Anticipatory multidisciplinary prevention and review are therefore important.

Polypharmacy and treatment harm

Aggressive pressure or glucose control, bleeding and interactions can undermine cognition, mobility and quality of life.

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

Review new focal or fluctuating change urgently rather than waiting for routine dementia follow-up.
Track blood pressure including posture, AF treatment, lipids, diabetes, renal function, bleeding and medicine adherence.
Follow gait, falls, swallowing, mood, IADLs and carer workload alongside cognition.
Reassess mixed pathology if amnesia, hallucinations, fluctuation or parkinsonism becomes prominent.
Align stroke, memory and primary-care plans so antithrombotic and monitoring ownership is explicit.

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

Stepwise is not mandatory

Small-vessel cognitive impairment can progress gradually without clinically recognisable strokes.

Location can outweigh volume

A strategic small infarct may be more cognitively important than extensive silent white-matter change.

Aspirin is not a dementia drug

Antithrombotic treatment requires its own vascular indication and benefit-harm assessment.

Mixed pathology is frequent

Alzheimer and vascular changes often contribute together rather than competing for a single label.

Apathy is not laziness

Frontal-subcortical injury impairs initiation and needs cueing and rehabilitation strategies.

Prevention cannot reverse infarction

The aim is avoiding further injury while adapting to established loss.

11Common pitfallsFrequent interpretation and management errors.

01
Calling incidental white-matter change the sole cause of cognitive symptoms.
02
Missing acute stroke because vascular dementia is already documented.
03
Giving antiplatelet treatment solely for a dementia label without a vascular indication.
04
Using donepezil routinely for pure vascular dementia contrary to NICE subtype guidance.
05
Pursuing aggressive pressure or glucose targets despite falls, posture symptoms or hypoglycaemia.
06
Neglecting depression, gait and carer support while focusing on brain imaging.