Current Pathogenetic Concepts of Vascular Cognitive Impairment

Abstract

The term vascular cognitive impairment designates a heterogenous group of disorders ranging from mild cognitive impairment to full-blown dementia -vascular dementia -resulting from cerebrovascular lesions involving various brain areas. Current clinical criteria show moderate sensitivity (50-56%) and variable specifi city (range 64-98%). The prevalence in autopsy series ranges from 0.03 to 58% (mean 8-15% in Western series, 22-35% in Japan). Major morphological types -multi-infarct and subcortical vascular encephalopathy, strategic infarct dementia, lacunar state, cortical granular atrophy (rare), and ischemic encephalopathy -are caused by atherosclerosis of major cerebral arteries and small vessel disease, resulting from systemic, cardiac and local vascular disease or cerebral amyloid angiopathy. Pathogenesis of vascular dementia is multifactorial, and pathophysiology affects brain areas and neurological networks involved in cognition, memory, behavior, and executive functions. Vascular brain injury in elderly persons often coexists with Alzheimer-type lesions and other pathologies resulting in mixed dementia. However, these lesions are also present in many non-demented elderly subjects. The heterogeneity of clinical manifestations, cerebrovascular pathology and their pathogenic factors result in limitations of the accuracy of diagnostic criteria for vascular dementia. Therefore, standardized and reproducible neuropathological criteria for the assessment of cerebrovascular lesions associated with cognitive impairment in order to elucidate contribution of cerebrovascular disease to cognitive impairment are urgently needed.

Diagnóstico do comprometimento cognitivo vascular: recomendações do Departamento Científico de Neurologia Cognitiva e do Envelhecimento da Academia Brasileira de Neurologia

“…As lesões cerebrais vasculares compreendem as modalidades isquêmicas (infartos, microinfartos, lacunas, hiperintensidades da substância branca, espaços perivasculares alargados) e hemorrágicas (infartos hemorrágicos, hemorragias cerebrais e microhemorragias), que se apresentam de modo variável, não havendo uma lesão neuropatológica única para a caracterização do CCV, assim como não há critérios amplamente aceitos em relação à localização e quantidade necessária de lesões para o diagnóstico neuropatológico de CCV [34][35][36][37] . Diversos eventos neuropatológicos parecem contribuir para a ocorrência de DCV, entre eles, perda da integridade da substância branca com consequente desconexão entre áreas estratégicas para as redes cognitivas 16 , alterações da cascata de coagulação 38 , dos oligodendrócitos 39 , modificações das células endoteliais 40 , com alterações na perfusão sanguínea cerebral.…”

Vascular Brain Disease in Geriatric Neuropsychiatry

“…In addition, the variation in the prevalence of VaD between the eighth and tenth decades of life was not significant in one study (from 10.2 to 9.9%) [16,17]. Mixed dementia, on the other hand, showed that prevalence between these age groups increased, advancing from 4.7 to 7.1% of subjects [16,17]. Another study conducted in the USA showed that VaD was responsible for 21% of dementia cases among those 80 years of age, but this rate corresponded to only 16% of cases older than 80.…”

“…A European study, for example, showed that the prevalence of VaD reduced when populations aged 60 and 90 were compared-15 and 8.7%, respectively [16]. In addition, the variation in the prevalence of VaD between the eighth and tenth decades of life was not significant in one study (from 10.2 to 9.9%) [16,17]. Mixed dementia, on the other hand, showed that prevalence between these age groups increased, advancing from 4.7 to 7.1% of subjects [16,17].…”

Diagnosis of vascular cognitive impairment: recommendations of the scientific department of cognitive neurology and aging of the Brazilian Academy of Neurology

“…Cerebral vascular injuries comprise the ischemic (infarcts, microinfarcts, lacunae, white matter hyperintensities, enlarged perivascular spaces) and hemorrhagic lesions (hemorrhagic infarcts, cerebral hemorrhages, and microhemorrhages), which present in a variable way, with no single neuropathological lesion characterizing VCI. In addition, there are no widely accepted criteria in relation to the location and number of lesions necessary for the neuropathological diagnosis of VCI [34][35][36][37] . Several neuropathologic events seem to contribute to the occurrence of VCI, including loss of white matter integrity with consequent disconnection between strategic areas for cognitive networks 16 , changes in the coagulation cascade 38 and oligodendrocytes 39 , and changes in endothelial cells with alterations in cerebral blood perfusion 40 .…”