The vascular dementias are a heterogeneous group of disorders in terms of aetiology, histopathology, pathogenetic mechanisms, and clinical appearance. In the majority of cases cognitive impairment is not caused by large cortical and subcortical territorial and watershed infarcts (multi-infarct dementia), but are due to a combination of subcortical microinfarcts (lacunes) and severe ischemic white matter changes, both indicating cerebral small-vessel disease. The subcortical variants of vascular dementia are clinically characterised by impairment of executive function and by changes in personality. Hence they are dissimilar to the clinical picture of Alzheimer's disease. On the other hand they often lack the abrupt onset and stepwise deterioration seen in multi-infarct dementia. Functional brain imaging has significantly contributed to unveiling the causal relationships between vascular lesions and cognitive deficits. It has been demonstrated that disruption of subcortico-cortical connections and of intercortical association pathways play a major pathogenetic role. The repertoire of symptomatic treatments for vascular dementias is extremely limited to date but may improve in the near future. Positive results are available from clinical trials with galantamine, donepezil, and memantine.     «

The vascular dementias are a heterogeneous group of disorders in terms of aetiology, histopathology, pathogenetic mechanisms, and clinical appearance. In the majority of cases cognitive impairment is not caused by large cortical and subcortical territorial and watershed infarcts (multi-infarct dementia), but are due to a combination of subcortical microinfarcts (lacunes) and severe ischemic white matter changes, both indicating cerebral small-vessel disease. The subcortical variants of vascular...     »