Dementia, Vascular

Description

• Vascular dementia (previously known as multi-infarct dementia) was first mentioned by Thomas Willis in 1672. Later, it was further described in the late 19th century by Binswanger and Alzheimer as a separate entity from dementia paralytica caused by neurosyphilis. This concept has evolved tremendously since the advent of neuroimaging modalities.
• Synonym(s): vascular cognitive impairment (VCI); vascular cognitive disorder (VCD); Binswanger disease; Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) categorizes vascular dementia as mild or major VCD.

Epidemiology

Common cause of dementia in the elderly, and it frequently overlaps with Alzheimer dementia

Incidence
About 6 to 12 cases per 1,000/person aged >70 years

Prevalence

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

Etiology and Pathophysiology

No set pathologic criteria exist for the diagnosis of vascular dementia such as those that exist for Alzheimer dementia. Pathology includes the following:

• Large vessel disease: cognitive impairment that follows a stroke
• Small vessel disease (subcortical) includes white matter changes, subcortical infarcts, and incomplete infarction. This is usually the most common cause of multi-infarct dementia. Lacunar infarcts and deep white matter changes are typically included in this category.
• Transient ischemic attack (TIA)/stroke
• Vascular, demographic, genetic factors
  • Vascular disease (i.e., hypertension [HTN], peripheral vascular disease [PVD], atrial fibrillation, hyperlipidemia, diabetes) (1)[B],(2)[C]

Genetics

• Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (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, migraine with aura, and vascular dementia.
• Apolipoprotein E (ApoE) 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

Risk Factors

• Age (risk doubles every 5 years)
• Previous stroke
• Tobacco use
• Diabetes (especially with frequent hypoglycemia)
• Atherosclerotic heart disease; HTN; atrial fibrillation; PVD
• Hyperlipidemia
• Metabolic syndrome
• Low socioeconomic status (3)[C]

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 the treatment for it must be optimized.
• Smoking is associated with white matter changes on imaging, which may be associated with small vessel disease and vascular dementia progression.
• Lifestyle modification: weight loss, physical activity, smoking cessation
• Hearing loss should be corrected.
• Depression and social isolation should be evaluated.
• Cognitively stimulating activity can be beneficial.
• Medication management for vascular risk reduction: aspirin usage, statin therapy for hyperlipidemia, antihypertensive therapy (4)[B]

Commonly Associated Conditions

• CADASIL
• Cerebral amyloid angiopathy (CAA) causes ischemic white matter damage due to amyloid deposition in penetrating cortical vessels.