vascular dementia

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Vascular dementia, also known as vascular cognitive impairment, is the second most common cause of dementia after the far more common Alzheimer disease. It is primarily seen in patients with atherosclerosis and chronic hypertension and results from the accumulation of multiple white matter lesions or cortical infarcts, although cerebral hemorrhages can be variably included .

Terminology

It is also possible to divide vascular dementia into subtypes, although no general agreement has been reached, and there is some overlap between them .

  • small vessel dementia (Binswanger disease)
  • cortical vascular dementia roughly equivalent to multi-infarct dementia
  • strategic infarct dementia
  • thalamic dementia

    • Epidemiology

    Incidence has been variably reported but is strongly correlated with age, seen in only 1% of patients over the age of 55 years of age, but in over 4% of patients over 71 years of age . To add to the confusion, given the prevalence of Alzheimer disease, the two are commonly seen together . Additionally, some patients develop accelerated vascular changes due to specific underlying disease (e.g. CADASIL and Fabry disease), and thus their demographics will be quite separate from the general population.

    Clinical presentation

    The presenting signs and symptoms are dependent on the areas affected and thus this is highly variable. Additionally, as these infarcts are accumulated in a stepwise fashion, deterioration is similarly stepwise rather than smoothly gradual.

    Generally, cortical dementia and strategic infarct dementia, usually due to large vessel occlusion, have a definable time of onset and specific deficits related to the region affected .

    Subcortical or small vessel dementia, in contrast, has a more insidious onset and vaguer 'executive function' deficits . The later is therefore understandably more frequently in the differential list of other dementias.

    Radiographic features

    Some authors have suggested that leukoaraiosis should involve at least 25% of the white matter in order to qualify for vascular dementia on imaging . Moreover, increasing white matter lesions on imaging correlating with increasing cognitive decline is thought to be another feature in favor of vascular dementia .

    CT/MRI

    Both CT and MRI are able to provide evidence of ischemic damage, however, MRI is more sensitive, especially to white matter small vessel ischemic change as well as to microhemorrhages seen in cerebral amyloid angiopathy and chronic hypertensive encephalopathy.

    It is beyond the scope of this article to describe all patterns of vascular damage, and the reader is referred to:

    Treatment and prognosis

    As befits a heterogeneous group of conditions, no single treatment exists, with the majority of effort going into treating individual risk factors for ongoing vascular damage (e.g. hypertension, smoking, hypercoagulation, atherosclerosis).

    Similarly, no single prognosis can be given, being largely dependent on the underlying cause and the degree to which successful treatment can be initiated.

    Siehe auch:
    und weiter:
    Assoziationen und Differentialdiagnosen zu multi-infarct dementia: