Vascular dementia: past, present and future

Abstract

Summary Gold G, Fontana P, Zekry D. Vascular dementia:past, present and future. Schweiz Arch NeurolPsychiatr 2002;153:372–8. Knowledge and understanding of vascular demen-tia has greatly evolved since its first descriptions inthe 19th century. The term now refers to a broadconcept that encompasses many different patho-physiological mechanisms that include singlestrategic infarcts, multiple infarcts, small vessel disease, hypoperfusion and haemorrhage. Thisevolution has prompted the development of newclinical criteria. These include the ICD-10, DSM-IV and those developed by the State of CaliforniaAlzheimer’s Disease Diagnostic and TreatmentCenters (ADDTC) and by the National Institutefor Neurological Disorders and Stroke with sup-port from the Association Internationale pour laRecherche et l’Enseignement en Neurosciences(NINDS-AIREN).Most are relatively specific butsuffer from low sensitivity and, most importantly,they are not interchangeable. Clinicopathologicalcorrelation studies have shown that the ICD-10research criteria and the probable vascular de-mentia category of the ADDTC and NINDS-AIREN were unable to detect the vast majority ofvascular dementia cases. The best compromiseappears to be the possible vascular dementiacategory of the ADDTC that has a sensitivity of0.70 and a specificity of 0.78 for multi-infarctdementia. The important differences among thevarious diagnostic systems currently in use partlyexplain the marked variations in prevalence (5 to31 per 1000) among vascular dementia epidemio-logical studies. Specific epidemiological data forvascular dementia is not available in Switzerland,however, the prevalence of dementia in generalparallels that of other countries and increasessharply 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 whendementia occurs abruptly, is associated with focalneurological signs and symptoms and follows astepwise deteriorating course. However, over halfof the cases may present with a more variablecourse. The proposed neuropsychological patternfor vascular dementia includes marked deficits in attention, concentration and executive functionand less pronounced memory impairment com-pared to Alzheimer’s disease. Improved informa-tion retrieval with cueing is highly unusual inAlzheimer’s disease and common in vasculardementia. It is important to note that cognitive and behavioural consequences of vascular braindamage depend upon type, number, size andlocation of lesions.Mental slowing is suggestive ofsubcortical vascular dementia.Behavioural deficitsconsistent with a frontal lobe dysfunction have alsobeen described.Treatment options remain essentially preven-tive through interventions aimed at controllingvascular risk factors.Treatment of hypertension isparticularly important. It can reduce stroke risk by approximately 40% and cut dementia risk inhalf. Once dementia is present, the objective is to slow down its progress, prevent new cerebrallesions, maximise cognition and function andcontrol behaviour. In this situation, pharmacolog-ical options are limited. However, recent reports of acetylcholinesterase use in mixed and vasculardementia have shown encouraging results on cog-nition, function and behaviour and further studiesof these compounds are ongoing.Future prospectsinclude the development of diagnostic markersthat can help discriminate vascular dementia fromAlzheimer’s disease and the continued search forprognostic indicators that could help identifywhich individuals with mild cognitive changes willdevelop a true dementia. Further clinicopatho-logical correlation studies are also necessary tobetter identify the respective contributions of