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Mohammed T. Abou-Saleh

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Principles and Practice of Geriatric Psychiatry.Editors: Professor John R. M. Copeland, Dr <strong>Mohammed</strong> T. <strong>Abou</strong>-<strong>Saleh</strong> and Professor Dan G. BlazerCopyright & 2002 John Wiley & Sons LtdPrint ISBN 0-471-98197-4 Online ISBN 0-470-84641-048Vascular DementiaPeter HumphreyWalton Centre for Neurology and Neurosurgery, Liverpool UKEPIDEMIOLOGYFor many years, dementia was thought to be due to vasculardisease. This seemed logical, largely on the basis that atherosclerosisand dementia are common in the elderly. In the 1970sand 1980s, many papers appeared stressing that vascular dementiawas over-diagnosed 1 , and most came to the conclusion thatAlzheimer’s disease (AD) was the commonest cause of dementia,even in patients who had had a stroke. In recent years thependulum has swung a little back towards vascular disease being amore significant cause. Furthermore, the clear margins betweensome types of vascular dementia and AD have become blurred.Indeed, brain infarction may play an important part in determiningthe expression of the clinical symptoms of AD 2 .The epidemiology of vascular dementia is fraught withdifficulties because of the lack of a reliable definition to act as agold standard. Many groups have come to a different consensusabout the criteria for the diagnosis (e.g. DSM-IV, ADDTC,NINDS–AIREN, ICD-10 and Hachinski score) Not only is theclinical diagnosis ambiguous, partly because many patients havemixed dementia (i.e. both AD and vascular disease), but thepathological differentiation of the varying types of dementia isalso blurred. Does one then use clinical series, preferablycommunity-based, or autopsy series? Reliable data are verysparse. Referral bias remains a major problem in hospital basedseries. In a community-based study in those aged over 85 from theUSA, dementia was found in 30% 3 . In Europe and the USA,vascular disease accounts for 10–40% of all cases of dementia,whereas in Japan vascular disease is more common than AD; thelifetime risk of developing vascular dementia is approximately25% 4–6 . Pathological studies suggest that cases of mixed AD andvascular dementia may be as common as those with just vasculardementia.Equally good reasons can be made for thinking that vasculardementia remains both underdiagnosed and overdiagnosed 7,8 .Dementia is common following stroke occurring in approximately16% after the first stroke 9 .The risk factors for vascular dementia have rarely been studied inisolation to stroke. The major risk factors are age, race,hypertension, diabetes mellitus, hyperlipidaemia, smoking, transientischaemic attack and heart disease, especially ischaemic heartdisease and atrial fibrillation 10 . The level of education, volume ofcerebral loss, degree of cerebral atrophy and presence ofperiventricular white matter lesions are important in the developmentof dementia 11 . Other possible risk factors includepolycythaemia, homocysteinuria, hyperfibrinogenaemia, alcoholexcess and lack of physical exercise.Most of these risk factors predispose to the atheroscleroticprocess in all its many guises (e.g. large vessel atherosclerosis,small vessel lacunae and white matter leukoaraiosis). However,there are a number of other causes for vascular dementia whichare worthy of separate mention. In the last 10 years ourunderstanding that genetic factors can predispose to vasculardisease have gained increasing importance, with the detailedunderstanding of the families with cerebral autosomal dominantarteriopathy with subcortical infarcts and leukoencephalopathy(CADASIL), mitochondrial diseases and hereditary cerebralhaemorrhage with amyloid 12–14 . CADASIL has been shown tobe linked to chromosome 19: individuals are predisposed tomigraine, vascular events and dementia 12 . The genetics ofmitochondrial encephalomyopathy with lactic acid and strokelikeepisodes (MELAS) is of interest; only men are affected, withthe disease being transmitted only by the maternal line. Theclinical features include stroke-like episodes, lactic acidosis, shortstature and deafness 13 . The diagnosis is confirmed by DNAanalysis to look for point mutations in the RNA gene. Other rarecauses of multi-infarct dementia and stroke include the antiphospholipidsyndrome 15,16 , arteritis 17 and late effects of cranialradiotherapy, amongst others 18–20 .CLINICAL TYPESThe pathological findings in vascular dementia are diverse.Findings range from large cortical infarctions (Figure 48.1) tosmall discrete deep infarcts (Figure 48.2) and to diffuse areas ofwhite matter low-attenuation changes as seen on CT scan (Figure48.3). Several of these changes may co-exist in the same patient(Figure 48.4).Cortical InfarctsRISK FACTORSMultiple cortical thrombo-embolic infarcts are a common causeof multi-infarct dementia. This will follow embolic occlusionsfrom either the heart or the great vessels, primarily in the neck,e.g. carotid stenosis, or primary thrombosis in the major corticalarteries of the cerebral hemispheres, e.g. antiphospholipidsyndrome 15,16 and arteritis 17 . Dementia may rarely result frommultiple watershed infarcts in the territories between the middleand posterior cerebral arteries in the cortex: hypotension is theusual cause secondary to prolonged cardiac arrest.Principles and Practice of Geriatric Psychiatry, 2nd edn. Edited by J. R. M. Copeland, M. T. <strong>Abou</strong>-<strong>Saleh</strong> and D. G. Blazer&2002 John Wiley & Sons, Ltd

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