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Vascular dementia

Last updated: January 4, 2021

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Vascular dementia (VD) describes gradual cognitive decline caused by small or large vessel disease. Important risk factors include hypertension, diabetes mellitus, hyperlipidemia, and advanced age. Large vessel changes primarily lead to thrombotic and/or embolic vascular occlusion, resulting in localized infarctions. In contrast, small vessel changes generally lead to more diffuse lesions. Common symptoms are cognitive impairment, motor disorders, and changes in behavior. The severity of symptoms and the mode of onset (insidious or sudden) depend on the number of vascular events and the extent of cerebral damage. Vascular dementia is primarily a clinical diagnosis that is supported by evidence of cerebrovascular lesions on imaging. Management consists of treating underlying conditions (e.g., hypertension) and, in some cases, antiplatelet drugs.

  • Second most common type of dementia (15–20% of cases) [1]
  • Prevalence increases with age (∼ 1–4% in patients ≥ 65 years).

Epidemiological data refers to the US, unless otherwise specified.

Lesions of the smaller (microangiopathy) and larger (macroangiopathy) cerebral arteries share common risk factors and pathological features but produce distinct clinical entities. [3]

Small vessel disease [3][4]

Large vessel disease

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. [5]

Dementia due to small vessel disease [6]

  • Symptoms tend to progress gradually or stepwise and comparatively slower than in multi-infarct dementia.
  • Generally associated with signs of subcortical pathology:

Dementia due to large vessel disease [6]

  • 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” in “Stroke”.

VD is a clinical diagnosis (as with all dementias; see “Mini-Mental State Examination”) based on medical history and clinical features, which is supported by imaging findings.

  • Brain MRI: : multiple cortical infarcts, subcortical infarcts (lacunes), and white matter lesions (periventricular and in the semioval center) [8]
  • Brain CT scan: microangiopathic lesions located in white matter, multiple lacunar lesions in the subcortical brain regions
  • Functional imaging (PET-CT): may be helpful in distinguishing between VD and Alzheimer disease (AD)
    • VD: hypoperfusion and hypometabolism more pronounced in the frontal lobe
    • AD: hypoperfusion and hypometabolism more pronounced in the parietal and temporal lobes
  • 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
  • Laboratory tests: (e.g., glucose levels, TSH): to rule out other potential causes or comorbidities

The differential diagnoses listed here are not exhaustive.

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.

  1. Wolters FJ, Ikram MA. Epidemiology of Vascular Dementia. Arterioscler Thromb Vasc Biol. 2019; 39 (8): p.1542-1549. doi: 10.1161/atvbaha.119.311908 . | Open in Read by QxMD
  2. CADASIL. https://rarediseases.org/rare-diseases/cadasil/. . Accessed: January 4, 2021.
  3. Iemolo F, Duro G, Rizzo C, Castiglia L, Hachinski V, Caruso C. Pathophysiology of vascular dementia.. Immun Ageing. 2009; 6 : p.13. doi: 10.1186/1742-4933-6-13 . | Open in Read by QxMD
  4. Caplan LR, Siesjo BK, Weir B et al.. Primer on Cerebrovascular Diseases. ACADEMIC PRESS ; 1997
  5. Jellinger KA. Pathology and pathogenesis of vascular cognitive impairment-a critical update. Frontiers in Aging Neuroscience. 2013; 5 . doi: 10.3389/fnagi.2013.00017 . | Open in Read by QxMD
  6. 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): p.2672-713. doi: 10.1161/STR.0b013e3182299496 . | Open in Read by QxMD
  7. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  8. Heiss WD, Rosenberg GA, Thiel A, Berlot R, de Reuck J. Neuroimaging in vascular cognitive impairment: a state-of-the-art review.. BMC Med. 2016; 14 (1): p.174. doi: 10.1186/s12916-016-0725-0 . | Open in Read by QxMD