The clinical picture of vascular dementia has become more clear and more cloudy in recent years. As we described, while there is agreement that stroke often immediately precedes dementia, the criteria for a clinical diagnosis of VaD are widely variable. In addition, the relationship of stroke to Alzheimer's disease is also unclear. Thus, VaD is viewed today as being much less common than was originally thought. Instead, mixed dementia appears far more common than VaD.

Clinical awareness of MD lags far behind the fairly recent gains in our scientific knowledge of this common cause of dementia. Clearly, neu-ropathological studies identify a substantially higher rate of mixed dementia cases than clinical diagnoses suggest (Gold et al., 1997; Snowdon et al., 1997; Tomlinson et al., 1970). Collectively, studies suggest that one-third to one-half of dementia cases are not pure cases, but rather are caused by the presence of both Alzheimer and vascular pathologies. The low rate of accurate clinical diagnoses of MD appears to be largely a function of the absence of diagnostic markers, unclear diagnostic standards for VaD, and the inevitable complications of clinical diagnoses when more than one etiology is present. Although HIS scores and patterns of cognitive deficits do not reliably support clinical diagnosis of MD, accuracy does seem to improve with neuroimaging techniques.

The coexistence of AD and VaD is higher than chance, suggesting shared risk factors. Cerebrovascular disease increases the risk for not only VaD, but also AD. Furthermore, autopsy studies following ante-mortem data suggest that the interactive effects of these two disease processes are likely to result in the clinical expression of dementia. Debilitating cognitive impairment appears to result from the presence of multiple factors, for example, neurofibrillary tangles, as well as lacunar infarcts in subcortical regions (Snowdon et al., 1997). Further prospective studies that include both cognitive measures and neuropathological analyses at autopsy are necessary to understand this interactive process of AD and VaD.

The commonalities of these brain disorders are further evidenced by the overlapping symptomatology in MD, AD, and VaD. With both cortical and subcortical lesions, areas of impairment are widespread, including cognitive, affective, behavioral, and motor functioning. Some investigations have observed higher rates of depression, behavioral disturbance, and motor impairments in VaD and MD, which may reflect the additive component of subcortical damage. Nevertheless, distinctive symptom patterns are not obvious, and certainly there are no pathognomonic markers of MD. Rate of decline also appears more similar than distinct in these diseases, with the important caveat that mortality rates for VaD and MD are higher than for AD.

Greater recognition of MD will advance scientific knowledge of both AD and VaD. As we gain insight into the pathophysiology of these disease processes, this knowledge base will shed light on the expression and etiology of the diseases. Future research will address important unanswered questions such as identifying genetic and environmental risk factors, distinguishing the degree of incidental versus causal connections between AD and VaD, ascertaining the physiological threshold tolerance of MD that triggers the clinical expression of dementia, and identifying laboratory tests with satisfactory diagnostic accuracy.

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