Vascular dementia

Impairment of blood supply to the brain used to be considered to be the main cause of dementia in the elderly, until it was recognized that such a mechanism is rarely, if ever, implicated. Multiple small strokes, referred to as multi-infarct dementia, were subsequently identified as the principal mechanism, both clinically and at autopsy (Hachinski et al. 1974).

In most neuropathological and clinical series, vascular dementia is the most common cause after Alzheimer's disease, accounting for some 10–20% of dementia cases alone, and an important concomitant of Alzheimer's disease or other degenerative dementias. The incidence of vascular dementia may be falling with better management of vascular risk factors. It is also believed that many cases of dementia with Lewy bodies were previously diagnosed clinically as vascular dementia. If cases of dementia where there is a vascular component are considered, then there is no doubt that vascular disease is a major cause or contributor to cognitive impairment (Hachinski and Bowler 1993).

The term "vascular dementia" is preferable to ‘multi-infarct dementia’ as it reflects the considerable heterogeneity of the condition and includes cases due to haemorrhage, small lacunar infarcts, large cortical infarcts, and vasculitides. In comparison to Alzheimer's disease, there is a paucity of epidemiological data on vascular dementia. In part, this is due to the fact that patients with major strokes are often excluded, and yet, in one study, up to 25% of patients 3 months after a stroke were considered to have dementia using DSM-IV criteria, and up to 60% had cognitive impairment (Pohjasvaara et al. 1997).

More recently, the NINCDS-AIREN criteria (Roman 1998) have been developed, which require the appearance of cognitive impairment within 3 months of a stroke, or sudden onset and fluctuation of cognitive impairment. In view of the potential contribution of focal neuropsychological deficits from a discrete stroke, the cognitive criteria for dementia are that there should be memory impairment plus at least two other domains. There should also be relevant vascular changes on imaging which are thought to be directly related. However, very different proportions of cases are diagnosed as vascular dementia, depending upon the use of NINCDS-AIREN, DSM-IV, or ICD-10 criteria. (Wetterling et al. 1996).

Three main vascular pathologies are believed to be associated with vascular dementia; namely, single discrete cortical infarcts, multiple infarcts (multi-infarct dementia), and subcortical arteriosclerotic encephalopathy (Binswanger's disease). In reality, these may overlap.

Single discrete infarcts, for example, in right middle cerebral and posterior cerebral artery territories and thalamic infarcts, can present with a picture suggestive of dementia. Much more common, however, is the accumulation of deficits from multiple single cortical and/or subcortical infarcts.

Men are more commonly affected than women, and there is usually a vascular history, particularly of hypertension. There is a gradual accumulation of cognitive deficits with episodes of confusion or focal neurology. If there are mainly subcortical infarcts, patients tend to have a subcortical pattern of cognitive deficit with cognitive slowing and additional motor features. Some may develop an extrapyramidal syndrome, and in others a pseudobulbar palsy can be prominent with pathological laughing and crying. Neuropathologically, multiple small subcortical infarcts appear to be more important in vascular dementia than single large infarcts (Esiri et al. 1997).

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