Vascular cognitive impairment

Abstract

For the greater part of the 20th century dementia was routinely attributed to arteriosclerosis and consequent chronic cerebral ischaemia. This view changed with the increasing recognition of Alzheimer’s disease (AD) and the demonstration that infarcts and not chronic ischaemia were the basis of what came to be termed multi-infarct dementia (MID). The term “vascular dementia” subsequently replaced MID as it was recognised that there were many different aetiologies apart from multiple infarcts. However, by the end of the 20th century, the increasingly recognised AD overshadowed VaD to the extent that some authors reported that MID was rare. Because AD was thought to be the major cause of dementia, its criteria became those applied to all dementia. AD was separated from VaD using clinical features thought to reflect vascular risk factors, vascular events, and the manifestations of systemic and cerebral vascular disease, typically codified using the ischaemic score (table 1). The basis of the definition has resulted in the criteria for VaD emphasising memory loss and usually the progression and irreversibility of cognitive decline, none of which are necessarily the case. In addition, they also define dementia as the level of cognitive impairment at which normal daily functions are impaired and therefore will identify only late cases, so underestimating the prevalence of cognitive impairment caused by vascular disease and denying patients the benefit of early preventative treatment. Regulatory bodies, which increasingly determine what may be done and to whom, have a tendency to adhere rigidly to published data. If data exist only for advanced disease, then expensive drugs may only be available for advanced disease, at least within guidelines. This important early stage is termed vascular cognitive impairment (VCI). The importance of VCI lies in the fact that vascular disease is the largest single identifiable risk factor for dementia apart from age and the only one currently treatable. Indeed, the concept can be taken further; while the prevention of progression of VCI is analogous to secondary prevention, primary prevention requires the recognition of the presence of risk factors in a susceptible host, termed “brain-at-risk” (fig 1).