What is vascular dementia?

Cerebrovascular disease (CVD) and dementia frequently coexist in elderly pa tients. The question of whether the CVD causes the dementia depends on how 'dementia' is defined. Traditional definitions specified that dementia invo lved a decline in intellectual ability as a core feature. However, revised definitions have since stipulated two key elements. 1) a global rather than focal neurobehavioural deficit and 2) impairment in activities of daily li ving (ADL). When applied to CVD, these latter concepts of dementia raise di fficulty. Focal cerebrovascular lesions in the cortex generate location-specific neur obehavioural deficits that are part of the dementia syndrome, but, even in combination, do not represent a global intellectual decline. Most cerebrovascular lesions are associated with physical symptoms that mak e if difficult to evaluate whether cognitive impairments have an independen t impact on ADL. The majority of neurobehavioural symptoms in CVD are caused by small-vessel -type subcortical lesions and are dissimilar to those seen in Alzheimer's d isease. There are several pathogenetic mechanisms, however, by which large-vessel o r small-vessel CVD can cause global cognitive and intellectual impairments, allowing a diagnosis of vascular dementia (VaD). An accumulation of ischaemic lesions in the cortex may produce global intel lectual impairment particularly if they affect important areas of the brain . Single small infarcts, or haemorrhages in strategic subcortical locations, may interfere with specific circuits connecting the prefrontal cortex to th e basal ganglia, or with nonspecific thalamocortical projections. This may generate combinations of executive dysfunction, personality change or apath y which are associated with hypoperfusion and hypometabolism predominantly in frontal cortical areas. Extensive white matter lesions probably affect cognitive function through a loss of axons, producing a functional disconnection of the cortex. This ca n manifest as significant reductions in blood flow and metabolism in fronta l, temporal and parietal cortical areas, which do not show any structural d amage. Given the diversify of aetiological factors, pathological changes and patho genetic mechanisms associated with VaD, several distinct syndromes must be distinguished Further study is needed to demonstrate that this emerging con cept can improve diagnosis, guide treatment and stimulate research.