Avances en la fisiopatología de la demencia vascular

Abstract

AbstractThe prevalence, morphology, and pathogenesis of vascular dementia (VaD), recently termed vascular cognitive impairment (VCI), and of mixed dementia (Alzheimer disease + vascular encephalopathy) are a matter of dicussion and no validated neuropathologic criteria for these disorders are currently available. In Western memory clinic-based series, VaD/CVI is suggested in 8-10% of cognitively impaired elderly subjects; its prevalence in autopsy series ranges from 0.03 to 58% with reasonable values of 5-15%. Fairly unusual as an isolated nosological entity, VaD appears to correlate with focal, multifocal or diffuse cortical and/or subcortical microinfarcts and lacunes often affecting strategically important brain areas (thalamus, frontobasal and/or limbic systems), hemispheric white matter and, less often, large brain areas. They result from systemic, cardiac or local large or small vessel disease. The lesion pattern in «pure» VaD with predominant multiple small (subcortical) lesions related to microangiopathies differs from that in mixed dementia (AD + VaD), more often associated with large infarcts, suggesting different pathogenesis of both types. In very old subjects selective hippocampal sclerosis may be associated with multiple other vascular pathologies. Minor cerebrovascular lesions, except for severe amyloid angiopathy, appear not essential for cognitive decline in full-blown AD, while both mild AD-type pathology and small vessel disease may interact synergistically in “unmasking” or promoting dementia. AD pathology is significantly less severe in the presence of cerebrovascular lesions. Further studies are neededed to validate diagnostic criteria for VaD/VCI and to clarify the impact of vascular lesions on cognitive impairment.