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 0-470-84641-0VASCULAR DEMENTIA 25534. Scheinberg P. Dementia due to vascular disease—a multifactorialdisorder. Stroke 1988; 19: 1291–9.35. Meyer JS, Judd BW, Tawakina T et al. Improved cognition aftercontrol of risk factors for multi-infarct dementia. J Am Med Assoc1986; 256: 2203–9.36. Caselli RJ. Giant cell (temporal) arteritis: a treatable cause for multiinfarctdementia. Neurology 1990; 40: 753–5.37. Tatemichi TK, Desmond DW, Prohovnik I et al. Dementia associatedwith bilateral carotid occlusions: neuropsychological and haemodynamiccourse after extracanial to intracranial bypass surgery.J Neurol Neurosurg Psychiat 1995; 58: 633–6.38. Frackowiak RSJ, Pozzilli C, Legg NJ et al. Regional cerebral oxygensupply and utilization in dementia. Brain 1981; 104: 753–78.39. Fazekas F. Neuroimaging of dementia. Curr Opin Neurol Neurosurg1990; 3: 103–7.40. Forette F, Seux M-L, Staessen JA et al. Prevention of dementia inrandomised double-blind placebo-controlled systolic hypertension inEurope (Syst-Eur) trial. Lancet 1998; 352: 1347–51.41. Antiplatelet Trialists’ Collaboration. Collaborative overview ofrandomised trials of antiplatelet therapy. Br Med J 1994; 308:81–106.42. Davis SM, Donnan GA. Secondary prevention for stroke afterCAPRIE and ESPS-2. Cerebrovasc Dis 1998; 8: 73–7.43. Diener H, Cunha L, Forbes C et al. European Stroke PreventionStudy (ESPS)2. Dipyridamole and acetylsalicylic acid in secondaryprevention of stroke. J Neurol Sci 1996; 143: 1–13.44. Caprie Steering Committee. A randomised blinded trial of clopidogrelversus aspirin in patients at risk of ischaemic events (CAPRIE).Lancet 1996; 348: 1329–39.45. European Atrial Fibrillation Study Group. Secondary prevention ofnon-rheumatic atrial fibrillation after transient ischaemic attack orminor stroke. Lancet 1993; 342: 1255–62.46. Gorter, J.W., Algra, A., Van Gijn et al. SPIRIT: predictors ofanticoagulant-related bleeding complications in patients after cerebralischaemia. Cerebrovasc Dis 1997; 7(suppl. 4): 3.Vascular Dementia Subgroups:Multi-infarct Dementia and Subcortical White Matter DementiaIngmar SkoogSahlgrenska University Hospital, Go¨teborg, SwedenUntil the 1960s, almost all dementias of old age were consideredsecondary to ‘‘hardening of the arteries’’ and chronic ischaemia.In the next decades, vascular causes of dementia came to beconsidered rare, and multi-infarct dementia (MID) almost its onlycause. The term ‘‘vascular dementia’’ (VaD) was introduced in the1990s to emphasize that several cerebrovascular disorders mightcause dementia.An ischaemic stroke increases the risk for dementia severalfold1 . The dementias related to stroke are MID and strategicinfarct dementia. MID is related to multiple small or large braininfarcts, often too small individually to produce a major clinicalincident. The typical patient has a history of stroke or transitoryischaemic attacks with acute focal neurological symptoms andsigns. The clinical picture includes sudden onset, stepwisedeterioration and a fluctuating course of the dementia. In theearly stages, the cognitive impairment may have a largevariability, depending on the site of the lesions. However, in alarge minority of cases the dementia may have a gradual onset,with a slowly progressive course 2 and without focal signs orinfarcts on brain imaging (especially when computed tomographyhas been used), which makes it difficult to differentiate from AD.It has been suggested that the dementia may be related to thelocation or the volume of the infarcts. The risk factors suggestedfor MID are similar to those in stroke, including advanced age,male sex, hypertension, diabetes mellitus, smoking and cardiacdiseases 3 .Ischaemic white matter lesions (WMLs) were first described incases of dementia by Durand-Fardel in 1854, followed byBinswanger in 1894, and by Alzheimer in 1898. Fewer than 50autopsied cases were described up to 1980 4 . In the 1980s, whenWMLs became possible to discern on brain imaging, they weresuddenly reported in thousands of patients. Before the advent ofbrain imaging, the level of interest in white matter disordersamong pathologists was low and the white matter was notroutinely evaluated in most patients. The pathologic descriptionincludes marked or diffuse demyelination and moderate loss ofaxons, with astrogliosis and incomplete infarction in subcorticalstructures of both hemispheres, and arteriosclerotic changes, withhyalinization or fibrosis and thickening of the vessel walls andnarrowing of the lumen of the small penetrating arteries andarterioles in the white matter. The main hypothesis regarding thecause of WMLs is that long-standing hypertension causeslipohyalinosis and thickening of the vessel walls, with narrowing ofthe lumen of the small perforating arteries and arterioles whichnourish the deep white matter 4 . The dementia is probably causedby subcortical–cortical or cortico–cortical disconnection, and isgenerally of a subcortical type with extrapyramidal signs,especially psychomotor retardation. A frontal lobe syndromewith apathy, loss of drive and emotional blunting is common.Regarding the subtypes of VaD, there is a discussion betweenlumpers and splitters. In the NINDS–AIREN criteria 6 , MID andWMLs are lumped together and it has been questioned whetherpresent scientific knowledge permits anything more than a broaddefinition of VaD. Focal neurological deficits and brain infarctsare common in subjects with WMLs, and the presence of WMLsare reported to increase the risk for dementia in subjects withstroke. The reason for the common co-occurrence of stroke andWMLs may be that they share similar risk factors, mainlyhypertension. However, not all demented subjects with WMLshave cortical infarcts in their brains, and not all individuals withMID have WMLs. Therefore, it may be better to adopt thesplitting view to better categorize these entities, with the understandingthat there is a large overlap.There is also an overlap between VaD and AD. WMLs havebeen described in a high proportion of cases with AD on bothbrain imaging and at autopsy, and they seem to be more commonin late-onset than in early-onset AD 4 . It has even been suggestedthat white matter degeneration precedes and causes the corticalatrophy in AD 5 . A considerable proportion of subjects from thegeneral population fulfilling the research criteria for AD or VaD