Description

• Vascular dementia (previously known as multi-infarct dementia) was first mentioned by Thomas Willis in 1672. It was later further described in the late 19th century by Binswanger and Alzheimer as a separate entity from dementia paralytica caused by neurosyphillis. This concept has evolved tremendously since the advent of neuroimaging modalities.
• Synonym(s): Vascular cognitive impairment (VCI); Vascular cognitive disorder (VCD); Arteriosclerotic dementia; Post-stroke dementia; Senile dementia due to hardening of the arteries; Binswanger disease

Epidemiology

Second most common cause of dementia after Alzheimer dementia in the elderly.

Incidence
About 6–12 cases/1,000/person age >70 years

• ~1.2–4.2% in those age >65 years
• 14–32% prevalence of dementia after a stroke

Risk Factors

• Age
• Previous stroke
• Smoking
• Diabetes
• Hypertension (HTN)
• Atrial fibrillation
• Peripheral vascular disease (PVD)
• Hyperlipidemia
• Metabolic syndrome
• Coronary atherosclerotic heart disease

• Cerebral autosomal dominant arteriopathy (CADASIL) is caused by a mutation in the NOTCH3 gene on chromosome 19 that results in leukoencephalopathy and subcortical infarcts. This is clinically manifested in recurrent strokes and associated cognitive decline.
• Apolipoprotein E gene type: Those with ApoE4 subtypes are at higher risk of developing both vascular and Alzheimer dementia.
• Amyloid precursor protein (APP) gene: Leads to a form of vascular dementia called heritable cerebral hemorrhage with amyloidosis (1).

General Prevention

• Optimization and aggressive treatment of vascular risk factors, such as HTN, diabetes, and hyperlipidemia
• HTN is the single most modifiable risk factor and treatment for it must be optimized.
• Lifestyle modification: Weight loss, physical activity, smoking cessation
• Medication management for vascular risk reduction: Aspirin usage, statin therapy for hyperlipidemia, antihypertensive therapy

Pathophysiology

Upon autopsy of those with dementia, ⅓ have significant vascular pathology present, but this is not necessarily correlated clinically with vascular dementia (2). No set pathologic criteria exist for the diagnosis of vascular dementia such as those that exist for Alzheimer dementia:

• Large vessel disease: Cognitive impairment that follows a stroke
• Small vessel disease: Includes white matter changes (leukoaraiosis), subcortical infarcts, and incomplete infarction. This is usually the most common cause of multi-infarct dementia.
• Subcortical ischemic vascular disease: Due to small vessel involvement within cerebral white matter, brain stem, and basal ganglia. Lacunar infarcts and deep white matter changes are typically included in this category (3).
• Noninfarct ischemic changes and atrophy (4)

Etiology

• Transient ischemic attack (TIA)/stroke
• Vascular, demographic, genetic factors
• Vascular disease (i.e., hypertension, PVD, atrial fibrillation, hyperlipidemia, diabetes)

Commonly Associated Conditions

• CADASIL
• Cerebral amyloid angiopathy (CAA): Accumulation of amyloid in cerebral vasculature resulting in infarctions and hemorrhages