Cerebrovascular Disease and Dementia (PDF)

the aging process, which can be described as a combination of milder degenerative and cerebrovascular changes among which the latter may be difficult to single out from a superimposed vascular dementing disease. In the literature, VaD is usually described as VaD or VaD plus other disorders, but VaD plus aging is rarely considered. The importance of aging in this context is emphasized by the finding that VaD is the most common form of organic dementia after the age of 85 (Amar and Wilcock, 1996). Normal aging with its gray and especially white matter loss, degenerative changes and small, silent vascular lesions can be viewed as predisposing to dementia due to a reduction of brain reserve capacity.

This brings an aged individual closer to the level of insufficiency where only minor additional lesions may be required to precipitate dementia. The degenerative aging changes, though milder, repeat much of the pathology of Alzheimer’s disease (AD). Senile plaques and neurofibrillary tangles are the most obvious of these. The latter are particularly pronounced in the entorhinal area of the hippocampus, an area vital to memory processing. There is also an amyloid angiopathy, sometimes as severe as that seen in AD, in which it can vary considerably in severity. More important, however, there is as in AD, a progressive loss of synapses in the cortex often amounting to as much as 40–50% in the oldest cases (Liu et al, 1996). The vascular lesions, accepted as an inevitable consequence of aging, are mainly expressed as a varying number of complete small infarcts in the gray and white matter and incomplete white matter infarcts, shown as white matter lucencies on imaging.

When sufficiently pronounced, the various lesions co-operate with the aging process to produce a dementia which may be named ‘summational dementia’ (Brun et al, 1992), since many of the changes are not demonstrable clinically, no single lesion can be held responsible and thus no conventional label can be applied. Before this stage is reached, however, the reduced reserve capacity may co-operate with any disease to produce dementia, which then appears to progress more quickly in the aged than in the younger patient with greater reserve capacity. Thus the more advanced the age, the less severe the lesion required to cause dementia. This then also means that even a minor stroke may seem to cause dementia, resulting in a clinical mislabeling of the condition, since the stroke is just the final straw and would not have resulted in dementia in a younger patient with greater reserve capacity.