Vascular Dementia

Introduction

Vascular dementia is cognitive decline caused by cerebrovascular disease - the cumulative effect of large vessel infarcts, small vessel disease, or both, on brain structure and function. It is the second commonest cause of dementia after Alzheimer's disease, accounting for a substantial minority of cases in pure form, with a further significant proportion of patients having mixed dementia, combining vascular and Alzheimer pathology.¹

For general dementia assessment and screening, see ²; this article covers the features, subtypes and management specific to a vascular aetiology, which differs meaningfully from Alzheimer's in both presentation and treatment.

Subtypes

Risk factors

The risk factors mirror those for stroke and atherosclerotic vascular disease generally, since the underlying process is the same.

• Hypertension - the single most important modifiable risk factor, particularly for small vessel disease
• Diabetes mellitus
• Atrial fibrillation and other cardioembolic sources
• Smoking
• Dyslipidaemia
• Prior stroke or transient ischaemic attack
• Obesity and physical inactivity

Pathophysiology

Vascular cognitive impairment results from the cumulative effect of ischaemic injury on the brain networks that support cognition, rather than from a single degenerative protein deposition process as in Alzheimer's disease.

• Large vessel disease: atherothrombotic or cardioembolic occlusion producing discrete cortical or subcortical infarcts. Cognitive consequences depend on the volume of tissue lost and, critically, on its location
• Small vessel disease: arteriolosclerosis and lipohyalinosis of the deep penetrating arterioles supplying the white matter and basal ganglia, producing lacunar infarcts and diffuse white matter ischaemia. Hypertension is the dominant driver
• Disconnection: damage to subcortical white matter tracts interrupts the frontal-subcortical circuits linking prefrontal cortex to basal ganglia and thalamus, which is why executive function, processing speed and gait are affected disproportionately early - the cortex itself may be relatively intact
• Hypoperfusion: chronic reduction in cerebral blood flow, and watershed infarction following episodes of profound hypotension, contribute in some patients
• Mixed pathology: vascular injury lowers the threshold at which coexisting Alzheimer pathology becomes clinically apparent, so the two processes are additive rather than merely coincidental

Clinical features

A key distinguishing feature from typical Alzheimer's disease is the early pattern of cognitive deficit: vascular dementia more often impairs executive function, processing speed and attention early, with episodic memory relatively better preserved until later in the disease, the reverse of the typical Alzheimer's pattern.

• Executive dysfunction: difficulty planning, organising, and shifting between tasks
• Slowed processing speed: taking noticeably longer to complete familiar tasks or respond in conversation
• Gait and mobility problems: particularly in subcortical small vessel disease - a shuffling, broad-based, or 'marche à petits pas' gait, sometimes with early falls
• Mood change: depression and emotional lability are common, sometimes preceding overt cognitive decline
• Focal neurological signs: may be present, reflecting the underlying vascular lesions - pyramidal signs, pseudobulbar palsy
• Urinary symptoms: urgency and incontinence occur relatively early compared with Alzheimer's disease
• A history of stroke, TIA, or known cerebrovascular risk factors is common, though not universal, particularly in subcortical small vessel disease which can be clinically silent until dementia manifests

Investigations

As for dementia generally, first-line assessment excludes reversible causes with the standard blood panel (see ²), followed by imaging that is particularly important in suspected vascular dementia to demonstrate the vascular burden.

• MRI brain (preferred over CT) - shows infarcts (cortical or subcortical), white matter hyperintensities (leukoaraiosis) reflecting chronic small vessel ischaemia, and cerebral microbleeds (best seen on susceptibility-weighted/gradient-echo sequences)
• CT head - a reasonable alternative where MRI is unavailable or contraindicated, though less sensitive for small vessel disease and microbleeds
• Cardiovascular risk assessment: blood pressure, lipid profile, HbA1c, and screening for atrial fibrillation (ECG, and further rhythm monitoring if indicated)
• Carotid imaging where there is a history suggesting large artery disease as a contributing source

Diagnosis requires both a clinically consistent pattern of cognitive decline and imaging evidence of cerebrovascular disease sufficient to plausibly account for it - imaging findings alone, in the absence of a matching clinical picture, are common incidental findings in older people (see ³) and do not by themselves establish the diagnosis.

Distinguishing vascular from Alzheimer dementia

Management

Cardiovascular risk reduction is the core treatment

Unlike Alzheimer's disease, there is no specific cognitive-enhancing drug licensed for pure vascular dementia. Management centres on secondary prevention of further cerebrovascular injury, which is what actually slows progression, alongside symptomatic and supportive care.

• Antiplatelet therapy (e.g. aspirin or clopidogrel) following ischaemic stroke/TIA, per standard secondary stroke prevention guidance
• Anticoagulation where atrial fibrillation or another cardioembolic source is identified
• Blood pressure control - a particularly important target given hypertension's central role in small vessel disease, though targets should be individualised in frail older patients to avoid symptomatic hypotension and falls
• Statin therapy for secondary prevention where appropriate
• Diabetes control
• Smoking cessation - see ⁴
• Physical activity and cardiovascular risk factor optimisation generally

Cognitive drugs in mixed dementia

Where there is a significant coexisting Alzheimer's component (mixed dementia), a trial of a cholinesterase inhibitor or memantine may be considered by a specialist, targeting the Alzheimer's element specifically, but this is not standard treatment for pure vascular dementia.

Symptomatic and supportive management

• Falls and gait assessment, given the prominence of mobility impairment - see ⁵
• Mood assessment and treatment, since depression is common and treatable
• Continence assessment, given the relatively early urinary involvement
• Cognitive stimulation and structured activity, as for dementia generally
• Carer support and post-diagnostic planning, as described in ²

Prevention

Vascular dementia is, in principle, the most preventable of the common dementias, because its risk factors are the modifiable risk factors for stroke and atherosclerosis - and because population-level improvements in blood pressure control and smoking rates have been accompanied by falling age-specific dementia incidence in several high-income countries.

• Midlife hypertension control carries the strongest evidence of any single modifiable factor - treating hypertension in midlife reduces later dementia risk, and blood pressure lowering trials have shown reductions in incident cognitive impairment
• Smoking cessation, which reduces both stroke risk and the direct vascular endothelial damage that drives small vessel disease
• Diabetes control, since diabetes accelerates both large and small vessel disease
• Detecting and anticoagulating atrial fibrillation, preventing the cardioembolic strokes that cause multi-infarct disease - opportunistic pulse checks in older patients are a cheap, high-yield intervention
• Physical activity, dietary pattern and weight management, acting through the shared cardiometabolic pathway
• Addressing hearing loss and social isolation, which are independently associated with dementia risk across subtypes

The practical implication is that cardiovascular risk management in midlife is also dementia prevention, and framing it that way in a consultation is often more motivating to a patient than an abstract discussion of stroke or myocardial infarction risk alone.

Specific vascular dementia syndromes

A few named entities are worth recognising, both because they appear in exam questions and because they change management or counselling.

Suspect CADASIL in a patient presenting with early-onset stroke or vascular cognitive impairment, a history of migraine with aura, a strong family history of early stroke or dementia, and an unexpectedly heavy white matter disease burden for their age - particularly involving the anterior temporal poles, which is relatively characteristic. Recognition matters because it changes family counselling entirely, even though management remains largely supportive and focused on conventional risk factor control.

Red flags

Prognosis

The course is variable: multi-infarct disease can show a stepwise pattern with periods of relative stability punctuated by acute declines, while subcortical small vessel disease tends towards a more gradually progressive course. Overall prognosis is influenced heavily by ongoing vascular risk - patients with well-controlled risk factors and no further vascular events have a better trajectory than those with recurrent cerebrovascular events, which is the central rationale for aggressive secondary prevention as the mainstay of management.

Median survival after diagnosis is generally shorter than in Alzheimer's disease, reflecting both the cognitive illness itself and the competing cardiovascular mortality that comes with the same underlying vascular burden - patients frequently die of myocardial infarction or stroke rather than of the dementia. This dual risk is worth bearing in mind when discussing prognosis and planning care, since it means cardiovascular events, not only cognitive decline, should feature in anticipatory care planning conversations.