7 Old age psychiatry7.5 Mental disorders in older people
7.5.2 Vascular dementia and vascular cognitive impairment
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Written by Resident Doctor Committee · Published
Definition and epidemiology
Vascular cognitive impairment ranges from mild cognitive decline caused by cerebrovascular disease to vascular dementia, which substantially disrupts everyday function.
Vascular dementia causes about one dementia in five, second only to Alzheimer's disease at about 60%.
It cannot be told from Alzheimer's disease with clinical certainty, and the two pathologies often coexist in older people.
Its risk factors are hypertension, diabetes, atrial fibrillation, smoking, dyslipidaemia and age, and a previous stroke roughly doubles dementia risk.
Cortical and subcortical dementia
Dementias are classed by where the pathology begins.
Class | Examples |
|---|---|
Cortical | Alzheimer's disease, frontotemporal dementia |
Subcortical | Small vessel vascular dementia, Huntington's disease, progressive supranuclear palsy |
Mixed | Dementia with Lewy bodies |
Subcortical dementias, such as subcortical ischaemic vascular dementia and Parkinson's and Huntington's disease, impair retrieval, so cues help recall.
Cortical dementias damage encoding, so cues help little.
Subtypes
Vascular cognitive impairment has three recognised syndromes: impairment after a single stroke, multi-infarct dementia, and progressive small vessel disease.
Subtype | Cause | Course | Features |
|---|---|---|---|
Post-stroke | A single stroke | Immediate decline, then variable recovery or progression | Depend on lesion site and reserve |
Multi-infarct dementia | Repeated embolic events, with cortical infarcts across several arterial territories | Abrupt onset, stepwise with plateaus | Accumulating focal deficits |
Binswanger's disease | Long-standing hypertension damaging small penetrating arteries | Slow, even subcortical decline | Psychomotor slowing, apathy, small-stepped gait, urinary symptoms |
Strategic infarct | One infarct at a site critical for memory and arousal | Sudden, with no further decline | Depend on site |
Each step in vascular decline reflects a new cerebrovascular event with incomplete recovery, whereas Alzheimer's disease begins insidiously and declines continuously.
Binswanger's disease (subcortical arteriosclerotic encephalopathy) shows diffuse deep white matter ischaemic change and lacunes on imaging.
Artery of Percheron occlusion causes bilateral paramedian thalamic infarction, with drowsiness at onset, apathy, amnesia and vertical gaze palsy.
CADASIL
CADASIL is an autosomal dominant small vessel disease caused by NOTCH3 mutations on chromosome 19, and a parent is often affected.
It begins in young or middle adulthood, around the forties, with migraine with aura, then transient ischaemic attacks, subcortical strokes and mood change, and it is progressive.
Imaging shows white matter change in the anterior temporal poles and external capsules.
Clinical features
Executive function and processing speed fail first, whereas Alzheimer's disease starts with episodic memory.
Gait and urinary symptoms come early, unlike typical Alzheimer's disease.
Upper motor neurone signs, such as clonus from corticospinal damage, are commoner than in degenerative dementia, and after a hemispheric stroke they are asymmetrical and lateralised.
Pseudobulbar affect (involuntary laughing or crying) and gait-predominant parkinsonism with a limited levodopa response can occur.
Depression is commonest in vascular dementia, affecting roughly a third to a half, and is linked to frontal-subcortical ischaemic damage and preserved insight.
Assessment
The Hachinski Ischaemic Score estimates the likelihood that vascular pathology underlies a dementia, weighting abrupt onset, stepwise course, stroke history, hypertension and focal neurology.
Because it rewards abrupt change, it can miss gradual subcortical disease.
Magnetic resonance imaging best shows infarcts, lacunes, white matter injury and microbleeds.
White matter lesions are common in older people without dementia, so imaging alone does not establish vascular dementia.
Management
Vascular dementia is managed by treating vascular risk factors such as blood pressure, lipids, diabetes, smoking and atrial fibrillation.
Statins and aspirin have no proven effect on the incidence or course of vascular cognitive impairment.
The National Institute for Health and Care Excellence advises against cholinesterase inhibitors or memantine for vascular dementia alone, but they can be considered when Alzheimer's disease or Lewy body disease coexists.
Prognosis
Survival averages about five years after diagnosis, often shorter than in Alzheimer's disease.