• Clinical science

Vascular dementia (Vascular cognitive impairment)

Epidemiology

  • Second most common type of dementia (10–20% of cases).
  • Prevalence increases with age (∼ 1–4% in patients ≥ 65 years)

References:[1]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

References:[1]

Pathophysiology

Lesions of the smaller (microangiopathy) and larger (macroangiopathy) cerebral arteries share common risk factors and pathological features but produce distinct clinical entities.

Small vessel disease

  • Predominantly caused by lipohyalinosis, microatheroma and/or amyloid beta deposition ) of cerebral vessels → thickening of the intima and/or the vessel wall, inflammation, thromboembolisms → vessel stenosis, occlusion or rupture → cerebral ischemia → VD
  • Mainly causes infarcts or chronic ischemia in subcortical white matter; (e.g., internal capsule) and/or in small penetrating arteries (lacunes) → diffuse white matter disease (infarctions or chronic ischemia), subcortical lacunar infarct, or the combination of both (known as Binswanger's disease, which has multiple synonyms)

Large vessel disease

References:[1][2][3][4]

Clinical features

Symptoms depend on the location of ischemic events and therefore vary widely between individuals, but a progressive impairment of daily life is common. Because of the diverse clinical picture, the term “vascular cognitive impairment” is gaining popularity over VD .

Dementia due to small vessel disease

  • Symptoms tend to progress gradually or stepwise and comparatively slower than in multi-infarct dementia
  • Generally associated with signs of subcortical pathology
    • Early symptoms
      • Impaired memory
      • Reduced executive functioning
      • Loss of visuospatial abilities
      • Confusion
      • Apathy
      • Motor disorders (e.g., gait disturbance; , urinary incontinence)
    • Later symptoms:
      • Further cognitive decline: loss of judgement, disorientation
      • Mood disorders (e.g., euphoria, depression)
      • Behavioral changes (e.g., aggressiveness)
    • Advanced stages:
      • Further motor deterioration: dysphagia, dysarthria

Dementia due to large vessel disease

  • Usually sudden onset
  • Multi-infarct dementia: typically, stepwise deterioration
  • Generally associated with signs of cortical pathology
    • Cognitive impairment in combination with asymmetric or focal deficits (e.g., unilateral visual field defects, hemiparesis, Babinski reflex present)
    • Symptoms depend on the affected cerebral region(s): see “Clinical features” of stroke

References:[1][4][5][6]

Subtypes and variants

Diagnostics

VD is a clinical diagnosis (as with all dementias; see the Mini-mental state examination) based on medical history and clinical features, which is supported by imaging findings.

  • Ultrasound
    • Doppler examination of critical vessels (particularly the carotid arteries) for signs of cerebrovascular risk (e.g., atherosclerosis)
    • Echocardiography to evaluate the risk of cardioembolic events
  • Cranial CT
    • Microangiopathic lesions located in white matter, multiple lacunar lesions
    • Functional imaging via PET-CT may be helpful in distinguishing between VD and Alzheimer's disease (AD).
      • VD: hypoperfusion and hypometabolism more pronounced in the frontal lobe
      • AD: hypoperfusion and hypometabolism more pronounced in the parietal and temporal lobes
  • Cranial MRI: : multiple lacunar and white matter lesions (periventricular and in the semioval center)
  • Conduct laboratory tests to rule out other potential causes or comorbidities (e.g., glucose levels, TSH)

References:[1][5]

Differential diagnoses

The differential diagnoses listed here are not exhaustive.

Treatment

VD results in an irreversible loss of cognitive skills; management is therefore aimed at symptomatic treatment of dementia (e.g., memory therapy) and prevention of additional ischemic events.

References:[5]

  • 1. Wright CB. Etiology, clinical manifestations, and diagnosis of vascular dementia. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/etiology-clinical-manifestations-and-diagnosis-of-vascular-dementia. Last updated July 11, 2016. Accessed December 29, 2016.
  • 2. Caplan LR, Siesjo BK, Weir B et al. Primer on Cerebrovascular Diseases. ACADEMIC PRESS; 1997.
  • 3. Jellinger KA. Pathology and pathogenesis of vascular cognitive impairment-a critical update. Frontiers in Aging Neuroscience. 2013; 5. doi: 10.3389/fnagi.2013.00017.
  • 4. Gorelick PB, Scuteri A, Black SE, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the american heart association/american stroke association. Stroke. 2011; 42(9): pp. 2672–713. doi: 10.1161/STR.0b013e3182299496.
  • 5. Alagiakrishnan K. Vascular Dementia. In: Welton RS. Vascular Dementia. New York, NY: WebMD. http://emedicine.medscape.com/article/292105. Updated November 1, 2016. Accessed December 29, 2016.
  • 6. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. New York, NY: McGraw-Hill Education; 2015.
last updated 09/03/2018
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