Vascular dementia: Past, present and future

Abstract

Knowledge and understanding of vascular dementia has greatly evolved since its first descriptions in the 19th century. The term now refers to a broad concept that encompasses many different pathophysiological mechanisms that include single strategic infarcts, multiple infarcts, small vessel disease, hypoperfusion and haemorrhage. This evolution has prompted the development of new clinical criteria. These include the ICD-10, DSM-IV and those developed by the State of California Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC) and by the National Institute for Neurological Disorders and Stroke with support from the Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN). Most are relatively specific but suffer from low sensitivity and, most importantly, they are not interchangeable. Clinicopathological correlation studies have shown that the ICD-10 research criteria and the probable vascular dementia category of the ADDTC and NINDS-AIREN were unable to detect the vast majority of vascular dementia cases. The best compromise appears to be the possible vascular dementia category of the ADDTC that has a sensitivity of 0.70 and a specificity of 0.78 for multi-infarct dementia. The important differences among the various diagnostic systems currently in use partly explain the marked variations in prevalence (5 to 31 per 1000) among vascular dementia epidemiological studies. Specific epidemiological data for vascular dementia is not available in Switzerland, however, the prevalence of dementia in general parallels that of other countries and increases sharply with age from 2.7% in individuals aged 65 to 69 to 24.8% in people who are 90 years old or older. Vascular dementia should be suspected when dementia occurs abruptly, is associated with focal neurological signs and symptoms and follows a stepwise deteriorating course. However, over half of the cases may present with a more variable course. The proposed neuropsychological pattern for vascular dementia includes marked deficits in attention, concentration and executive function and less pronounced memory impairment compared to Alzheimer's disease. Improved information retrieval with cueing is highly unusual in Alzheimer's disease and common in vascular dementia. It is important to note that cognitive and behavioural consequences of vascular brain damage depend upon type, number, size and location of lesions. Mental slowing is suggestive of subcortical vascular dementia. Behavioural deficits consistent with a frontal lobe dysfunction have also been described. Treatment options remain essentially preventive through interventions aimed at controlling vascular risk factors. Treatment of hypertension is particularly important. It can reduce stroke risk by approximately 40% and cut dementia risk in half. Once dementia is present, the objective is to slow down its progress, prevent new cerebral lesions, maximise cognition and function and control behaviour. In this situation, pharmacological options are limited. However, recent reports of acetylcholinesterase use in mixed and vascular dementia have shown encouraging results on cognition, function and behaviour and further studies of these compounds are ongoing. Future prospects include the development of diagnostic markers that can help discriminate vascular dementia from Alzheimer's disease and the continued search for prognostic indicators that could help identify which individuals with mild cognitive changes will develop a true dementia. Further clinicopathological correlation studies are also necessary to better identify the respective contributions of vascular and degenerative lesions in mixed dementia cases.