Key Facts

Vascular dementia is preventable and modifiable through cardiovascular risk factor management. Pure vascular dementia is less common than mixed AD/vascular pathology. No specific pharmacological treatment is available.

Epidemiology

~20% of all dementia. M > F. Prevalence increases with age and cardiovascular comorbidity. Post-stroke dementia: ~30% of stroke survivors develop dementia within 5 years. Mixed AD/vascular dementia likely accounts for a larger proportion than previously thought (~20-40%).

Aetiology

• Large vessel disease: multi-infarct dementia from recurrent cortical or subcortical infarcts
• Small vessel disease (most common subtype): hypertensive arteriopathy, cerebral amyloid angiopathy → lacunar infarcts, white matter disease (leukoaraiosis)
• Strategic infarct: single infarct in critical cognitive area (thalamus, angular gyrus, basal forebrain, hippocampus)
• Haemorrhagic: intracerebral haemorrhage, cerebral amyloid angiopathy
• Hypoperfusion: cardiac failure, post-cardiac arrest

Pathophysiology

Cerebrovascular disease causes neuronal death through ischaemia/infarction → cumulative cognitive impairment. Small vessel disease causes chronic hypoperfusion, disruption of subcortical white matter tracts, and disconnection of cortical-subcortical circuits → executive dysfunction, processing speed reduction. The relationship between vascular burden and dementia is not linear — location of lesions matters as much as volume.

Cognitive Profile

• Executive dysfunction: impaired planning, organising, multitasking, abstract thinking (prominent early)
• Processing speed: slowed thinking and responses
• Attention: poor sustained and divided attention
• Memory: relatively preserved initially (retrieval deficit rather than encoding — improves with cues); contrasts with AD where encoding is impaired

Other Features

• Stepwise decline (multi-infarct) or progressive (small vessel)
• Temporal relationship to stroke (may follow stroke by weeks-months)
• Gait disturbance: apraxic/small-stepped gait; falls
• Emotional lability: pseudobulbar affect (inappropriate laughing/crying)
• Focal neurological signs: pyramidal signs, visual field defects
• Urinary incontinence: early (subcortical pattern)
• Depression: common comorbidity

Red Flags

• Sudden cognitive decline after stroke → post-stroke dementia
• Young patient with vascular dementia → investigate for CADASIL (autosomal dominant; NOTCH3 gene), Fabry, vasculitis
• Lobar haemorrhages + dementia → cerebral amyloid angiopathy

Cognitive Assessment

• ACE-III, MoCA (better for executive/vascular pattern than MMSE)
• Executive function testing: trail-making test, verbal fluency, clock-drawing

Imaging

• MRI brain: gold standard; white matter hyperintensities (Fazekas scale), lacunar infarcts, cortical infarcts, cerebral atrophy, microbleeds (SWI/GRE)
  • Fazekas 0: no WMH; Fazekas 1: punctate; Fazekas 2: early confluent; Fazekas 3: confluent/extensive
• CT head: if MRI contraindicated; less sensitive for white matter disease

Bloods

• Vascular risk factor screen: HbA1c, fasting lipids, glucose, U&Es, TFTs, FBC
• Exclude reversible causes: B12, folate, TFTs, calcium
• If young: NOTCH3 (CADASIL), Fabry, vasculitis screen

Other

• ECG: AF screening
• Echocardiography: if embolic source suspected
• Carotid Doppler: significant carotid stenosis

Vascular Risk Factor Modification (Cornerstone)

• Hypertension: target BP <130/80 mmHg (NICE NG136); amlodipine, ramipril, indapamide
• Statins: atorvastatin 20-80mg OD for secondary prevention
• Diabetes: optimise HbA1c
• Anticoagulation: for AF (DOACs preferred — NICE NG196)
• Antiplatelet: clopidogrel 75mg OD for secondary prevention post-stroke/TIA
• Smoking cessation: NRT, varenicline, behavioural support
• Exercise: regular physical activity (30 min/day, 5 days/week)
• Diet: Mediterranean diet
• Weight management: target healthy BMI

Anti-Dementia Drugs

• ChEIs are NOT routinely recommended for pure vascular dementia (NICE TA217)
• May be considered for mixed AD/vascular dementia (treat the AD component)
• No specific drug treatment for vascular dementia

Non-Pharmacological

• Cognitive stimulation therapy
• Exercise programmes
• Rehabilitation (especially post-stroke cognitive rehabilitation)
• Social engagement, meaningful activities
• Carer support, Alzheimer's Society

Mood Management

• Depression: SSRIs (citalopram, sertraline)
• Pseudobulbar affect: SSRIs may help

Referral Criteria

• Memory assessment service: all suspected dementia
• Stroke services: if new vascular events
• Cardiology: AF management
• Genetics: if CADASIL or young-onset suspected

Highly variable. Stepwise decline with periods of stability or improvement. Mean survival from diagnosis ~5 years (shorter than AD in some studies). Prognosis depends on underlying vascular disease control. Post-stroke dementia: ~30% at 5 years. Mixed dementia: prognosis similar to AD. Vascular risk factor modification can slow progression but cannot reverse established damage. High risk of recurrent stroke and cardiovascular events.

Vascular Dementia Subtypes

Fazekas White Matter Hyperintensity Scale