Mohammed T. Abou-Saleh

Principles and Practice of Geriatric Psychiatry.Editors: Professor John R. M. Copeland, Dr Mohammed T. Abou-Saleh and Professor Dan G. BlazerCopyright & 2002 John Wiley & Sons LtdPrint ISBN 0-471-98197-4 Online ISBN 0-470-84641-047Pathology of Vascular DementiaJ. M. MacKenzieGrampian University Hospitals NHS Trust, Aberdeen, UKCerebrovascular disease is usually considered to be the secondcommonest cause of dementia, although the precise prevalenceand the frequency of combination with Alzheimer’s disease (AD)is very variable. In the West, approximately 15% of autopsystudiedcases of dementia have been attributed to vascular diseasealone and 8–18% to a combination of vascular disease and AD 1,2 .However, this has been challenged in a recent autopsy study ofpatients in a dementia clinic, where dementia could not beattributed in any case to vascular disease alone 3 . Vasculardementia is commoner in the Far East than in the West andstill remains the commonest form of dementia in Japan 4 . In theWest, it may also be commoner than AD in the very elderly 5 .Estimates based on death certification and clinical diagnosiswithout pathological confirmation are liable to be significantlyinaccurate 6,7 .If it is difficult to determine how frequent vascular dementia is,it is also difficult to define what it is. For example, the terms‘‘arteriosclerotic’’ and ‘‘multi-infarct’’ dementia are often usedsynonymously and these, together with a lacunar state andBinswanger’s disease, have been grouped together 8 . In practice,three separate forms of vascular dementia can be identified,although there is often overlap between these: multi-infarctdementia; dementia due to single strategically-placed infarcts;and dementia due to diffuse white matter damage 9 .MULTI-INFARCT DEMENTIAMultiple areas of infarction involving both cortical and subcorticallocations, separated in both time and space, may beassociated with dementia, although in its pure form this isprobably uncommon 10 . The location of the infarcts is probablymore important than the volume of tissue lost (100 ml is the oftquotedfigure) 1,11 . Dementia may occur with relatively little tissueloss, particularly if infarcts are strategically located (see below)and the effect of subsequent infarcts may be synergistic ratherthan additive 12 .Multiple small infarcts of deep white matter or grey structures(‘‘lacunar state’’) may also be associated with dementia, althoughthis often overlaps with dementia due to diffuse white matterdamage 13 . Patients with a pure lacunar syndrome show features ofa subcortical dementia—psychomotor slowing, poor concentration,indecision and apathy—without features of corticaldysfunction 9 . Hypertension is the most important risk factor fordementia of this kind and that is particularly true for dementiadue to multiple lacunar infarcts 13,14 .DEMENTIA DUE TO SINGLE STRATEGICALLYPLACED INFARCTSDementia may result from single infarcts involving certain areasof the brain, such as the angular gyrus of the dominant parietallobe, the medial thalamic nuclei and head of the caudate nucleus,especially if bilateral, the globus pallidus, basal forebrain andhippocampus 9,15 . The cognitive effects of infarction of the angulargyrus may closely resemble AD, although the sudden onset of thecognitive deficit may point to the correct diagnosis 16 .DEMENTIA DUE TO DIFFUSE WHITE MATTERDAMAGEWhilst white matter damage due to multiple infarcts may be thesubstrate of dementia, there are also forms of more diffuse whitematter damage due to small-vessel disease which result indementia, and these are probably commoner than dementia dueto single or multiple infarcts 17 .Binswanger’s disease is considered to be a well-establishedclinicopathological entity: ischaemic periventricular leukoencephalopathymanifested clinically by subcortical frontalexecutive dysfunction, parkinsonism, urinary incontinence,mood changes and pseudobulbar palsy 18 . However, it is still thesubject of considerable controversy regarding both its frequency 19and its relationship with the radiological entity of ‘‘leukoaraiosis’’—theappearance of low attenuation areas in the whitematter on CT scanning 20 . CT abnormalities are common in theelderly and may not be associated with dementia 21,22 and theclinical significance of leukoaraiosis remains incompletelydefined 23 . It certainly does not equate to Binswanger’s disease,despite suggestions to the contrary 24 .A review of the pathological features of all the reported cases ofBinswanger’s disease in the world literature, 1912–1986, togetherwith Fisher’s review, reveals that the vast majority of casesdesignated as Binswanger’s disease show consistent pathologicalchanges 25,26 . The general autopsy shows evidence of prolongedsystemic hypertension. The brain is of average weight but there isdiffuse dilatation of the lateral and third ventricles, withrarefaction, discoloration and a rubbery texture of the periventricularwhite matter, particularly in the occipital regions. Thearteries of the Circle of Willis are affected by atheroma, which in60% of cases is severe. Lacunar infarcts are usually present butone-third of brains also contain large infarcts. Microscopically,there is incomplete diffuse demyelination, with gliosis andmicroinfarcts affecting the periventricular white matter butsparing the subcortical fibres, corpus callosum, anteriorPrinciples and Practice of Geriatric Psychiatry, 2nd edn. Edited by J. R. M. Copeland, M. T. Abou-Saleh and D. G. Blazer&2002 John Wiley & Sons, Ltd