Vascular Dementia

Vascular dementia is a major neurocognitive disorder resulting from cerebrovascular disease. It is the second commonest cause of dementia overall after Alzheimer disease. It frequently coexists with Alzheimer pathology in the same individual (mixed dementia), a common and clinically important scenario given the shared risk factors and association with advancing age.

Vascular dementia has several clinical and pathological subtypes:

• Post-stroke dementia, developing after one or more clinically apparent, discrete stroke events.
• Subcortical ischaemic vascular dementia, reflecting the cumulative effect of chronic small vessel disease, frequently without any single, clearly identifiable clinical stroke.
• Less commonly, dementia related to strategic infarct location or to significant intracerebral haemorrhage.

Presentation and course vary with the subtype and the pattern of cerebrovascular pathology.

Pathophysiology and classification

• Post-stroke dementia reflects the cumulative cognitive impact of one or more clinically apparent strokes. The pattern and severity of impairment reflect the location, size, and number of infarcts or haemorrhages.
• The decline is characteristically, though not invariably, stepwise: discrete episodes of worsening follow each new vascular event, with periods of relative stability between. This is a useful distinguishing feature from the smooth, gradually progressive decline typical of Alzheimer disease. It is not universal, and its absence does not exclude a vascular contribution.
• Subcortical ischaemic vascular dementia reflects chronic cerebral small vessel disease, producing diffuse white matter ischaemic change and multiple small, often clinically silent lacunar infarcts.
• This subtype frequently presents with a gradual, insidious decline that can closely resemble a primary neurodegenerative dementia. The stepwise pattern is often absent, so careful clinical and radiological assessment is needed to identify the vascular contribution.
• Shared vascular risk factors (hypertension, diabetes, hyperlipidaemia, smoking, and atrial fibrillation) are important, modifiable contributors to the development and progression of vascular dementia across all subtypes. Aggressive vascular risk factor management has direct treatment implications.

• Presentation varies with the subtype and the location and pattern of cerebrovascular pathology. Post-stroke dementia often shows a more classical stepwise decline.
• Subcortical ischaemic vascular dementia more typically presents with gradual decline and prominent early executive dysfunction and psychomotor slowing. This contrasts with the early, prominent episodic memory impairment typical of Alzheimer disease.
• Gait disturbance is often an early and relatively prominent feature. It reflects involvement of the frontal-subcortical white matter pathways for gait and postural control in the small vessel disease subtype.
• Urinary symptoms and mood disturbance are commonly associated. Depression and apathy are frequently prominent and sometimes precede overt cognitive decline.
• The picture overlaps with normal pressure hydrocephalus (see hydrocephalus), which can complicate diagnosis.
• Focal neurological signs reflecting prior clinically apparent strokes may be present, providing supportive evidence of a vascular contribution.
• Vascular and Alzheimer pathology frequently coexist (mixed dementia), so the presentation often shows features of both rather than a "pure" vascular dementia syndrome. Careful, full clinical and radiological assessment, not clinical presentation alone, is frequently needed to characterise the contribution of each process.

• Full clinical assessment is the foundation of diagnosis, following the general principles for major neurocognitive disorder. It includes a detailed history, with specific enquiry about prior clinically apparent stroke or transient ischaemic attack and a full assessment of vascular risk factors. Formal cognitive assessment characterises the pattern of domain involvement.
• Structural neuroimaging is essential. Magnetic resonance imaging is generally preferred over computed tomography because it is more sensitive for small vessel disease changes.
• Imaging should show significant cerebrovascular disease: territorial infarcts (post-stroke dementia), extensive white matter hyperintensity, and multiple lacunar infarcts (subcortical ischaemic vascular dementia).
• The pattern, location, and extent of vascular pathology support the diagnosis, together with careful clinical correlation of the timing of any vascular events against the onset or progression of cognitive symptoms.
• Established diagnostic criteria generally require objective evidence of significant cerebrovascular disease on neuroimaging and a plausible temporal or clinical relationship between this pathology and the cognitive decline. The pattern of cognitive impairment should also be consistent with a vascular rather than purely degenerative aetiology.
• In practice, vascular and Alzheimer pathology frequently coexist, so some diagnostic overlap and uncertainty about the relative contribution of each is common. Acknowledge this rather than forcing an artificially precise, single diagnostic label.
• Identify the underlying vascular risk factors as an integral part of evaluation: blood pressure, glucose and lipid profile, and screening for atrial fibrillation and other cardiac sources of embolism where clinically indicated. This confirms the vascular contribution and guides risk factor management to prevent further vascular events and cognitive decline.

• Aggressive, full vascular risk factor management is the primary, essential strategy. It means optimal control of hypertension, diabetes, and hyperlipidaemia, and smoking cessation. Add antiplatelet or anticoagulant therapy where indicated by the vascular pathology and risk profile.
• This prevents further vascular events and may slow further cognitive decline. It is a more directly modifiable approach than the limited options for the primary neurodegenerative dementias.
• Cholinesterase inhibitors and memantine, the mainstay of symptomatic Alzheimer disease treatment, have shown limited, generally modest evidence of benefit in pure vascular dementia, though they may give some symptomatic benefit.
• A treatment trial may reasonably be considered in mixed dementia with a significant coexisting Alzheimer pathology component.
• Manage behavioural and psychological symptoms, including the frequently prominent depression and apathy, and the broader psychosocial and functional support needs, following the general principles for major neurocognitive disorder.
• Multidisciplinary supportive care is essential. It includes physiotherapy for the frequently prominent gait disturbance and falls risk, occupational therapy, and psychosocial support for the affected individual and their family.
• Vascular and primary neurodegenerative pathology frequently coexist, and vascular risk factor management helps prevent further vascular contribution to decline whether or not a degenerative process is present. An integrated approach addresses both the vascular risk factors and the general principles of major neurocognitive disorder management.
• Regular, structured multidisciplinary follow up supports longitudinal management throughout the progressive course.