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Vascular cognitive impairment

Abstract

Cognitive impairment commonly accompanies clinical syndromes associated with vascular disease of the brain. Because of evolving definitional criteria, however, the frequency of cognitive impairment attributable to cerebrovascular disease is difficult to determine. Dementia occurs in up to one-third of elderly patients with stroke, a subset of whom have Alzheimer's disease (AD) rather than a pure vascular dementia syndrome. In fact, pure vascular dementia has been shown to be uncommon in most large autopsy series. A mixed etiology of AD and cerebrovascular disease is thought to become more common with increasing age, although no clinical criteria for the diagnosis of AD with cerebrovascular disease are currently available. Epidemiological studies have implicated subcortical small-vessel disease as a risk factor for cognitive impairment and dementia, but the cognitive expression and clinical significance of MRI white matter changes in individual patients is difficult to establish. The frequency of specific neuropathologic features of vascular cognitive impairment depends largely on study inclusion criteria. Cerebral meningocortical microangiopathies with distinctive clinicopathological profiles are associated with dementia in both sporadic cases and familial syndromes. In patients with AD, the contribution of amyloid-β protein to the degree of cognitive impairment has not been clearly defined.

Key Points

  • Several clinical subtypes of vascular cognitive impairment due to vascular disease are now recognized, ranging in severity from mild cognitive impairment to dementia

  • The risk of dementia after stroke is increased in older patients and in those with pre-existing cognitive impairment or cerebrovascular disease

  • The cognitive consequences of subcortical small-vessel disease is variable, suggesting that the subcortical white matter changes visualized on conventional MRI might be incomplete markers of the total burden of cerebrovascular disease

  • The cognitive profile of vascular cognitive impairment is predominantly subcortical, with prominent psychomotor slowing and executive deficits, but relatively preserved language and recognition memory

  • From a neuropathologic perspective, the morphologic substrates or correlates of vascular dementia are extremely heterogeneous

  • Cerebral microvascular diseases, both sporadic and genetically determined, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and cerebral amyloid angiopathy, are instructive in terms of providing pathologic models of age-related arteriopathies and their consequences for brain parenchyma

  • The brains of aged individuals are likely to show impaired function as a consequence of combined 'Alzheimerization' and cerebrovascular disease

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Figure 1: Conceptual framework for etiology and pathogenesis of ischemic vascular dementia, taking into account cerebrovascular disease, systemic factors and ischemic necrosis of the brain, as well as retrograde or downstream effects of focal ischemic lesions.
Figure 2: Microscopic appearance of brain lesions commonly encountered in the brains of individuals with cerebrovascular disease and dementia.
Figure 3: Lacunar infarcts.
Figure 4: Cerebral amyloid angiopathy, sporadic, with extensive old microinfarcts throughout the CNS.

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Acknowledgements

Work in H Vinters' laboratory is supported by PHS grants P50 AG 16570 and P01 AG 12435. The research of O Selnes is supported by PHS grant 35610 (NINCDS). Technical assistance provided by Justine Pomakian and Negar Khanlou. We thank Pamela Talalay for her editorial assistance.

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Correspondence to Ola A Selnes.

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Selnes, O., Vinters, H. Vascular cognitive impairment. Nat Rev Neurol 2, 538–547 (2006). https://doi.org/10.1038/ncpneuro0294

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