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Vascular dementia is a heterogeneous disorder caused by the sequel of cerebrovascular disease that manifests in cognitive impairment affecting memory, thinking, language, behavior, and judgment.
- 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); arteriosclerotic dementia; poststroke dementia; senile dementia due to hardening of the arteries; Binswanger disease. Diagnostic and Statistical Manual of Mental Disorders (DSM-5) categorizes vascular dementia as mild or major VCD.
Second most common cause of dementia after Alzheimer dementia in the elderly
About 6 to 12 cases/1,000/person age >70 years
- Incidence of vascular dementia is declining in high-income countries in the past several decades likely due to better management of vascular risks.
- ~1.2–4.2% in those age >65 years
- 14–32% prevalence of dementia after a stroke
Etiology and Pathophysiology
On autopsy of those with dementia, many have significant vascular pathology that is present, but this is not necessarily correlated clinically with vascular dementia. 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: 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.
- Noninfarct ischemic changes and atrophy
- Transient ischemic attack (TIA)/stroke
- Vascular, demographic, genetic factors
- Vascular disease (i.e., hypertension [HTN], peripheral vascular disease [PVD], atrial fibrillation, hyperlipidemia, diabetes)
- Cerebral autosomal dominant arteriopathy with subcortical infarcts (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 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
- Previous stroke
- Diabetes (especially with frequent hypoglycemia)
- Atrial fibrillation
- Metabolic syndrome
- Coronary atherosclerotic heart disease (1)
- Optimization and aggressive treatment of vascular risk factors, such as HTN, diabetes, and hyperlipidemia (2)[C]
- HTN is the single most modifiable risk factor and 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 (3)[B].
- Lifestyle modification: weight loss, physical activity, smoking cessation
- Medication management for vascular risk reduction: aspirin usage, statin therapy for hyperlipidemia, antihypertensive therapy (4)[B]
Commonly Associated Conditions
- Cerebral amyloid angiopathy (CAA) causes ischemic white matter damage due to amyloid deposition in penetrating cortical vessels.