Dementia, Vascular

BASICS

Vascular dementia (also known as vascular cognitive impairment) is a heterogeneous disorder caused by the sequelae of cerebrovascular disease that manifests in cognitive impairment affecting memory, thinking, learning, language, behavior, judgment, and executive dysfunction.

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, obstructive sleep apnea) (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
  • Smoking
  • Diabetes (especially with frequent hypoglycemia)
  • Atherosclerotic heart disease; HTN; atrial fibrillation; PVD
  • Hyperlipidemia
  • Obstructive sleep apnea
  • 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.
  • Sleep apnea should be treated.
  • 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.

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