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A significant advance in the clinical characterization of vascular dementia (VaD) occurred in the 1970s when V. Hachinski described the term multi-infarct dementia (MID). A number of factors have contributed to difficulty in the development and implementation of diagnostic criteria for VaD. All diagnostic criteria have focused on the two most important issues in VaD: the presence of dementia, and the presence of vascular disease of sufficient severity to cause cognitive deficits. However, there is a great variability in their approach to these two core issues. The most difficult aspect in the diagnosis of VaD is to separate the presence of an ongoing neurodegenerative disease from true VaD. Constitutional and cerebrovascular risk factors and previous strokes have been associated with the presence of VaD. Therefore, detailed clinical, laboratory, neuroimaging, and neuropsychological assessments are necessary for the accurate diagnosis of VaD.
Gordon T. Plant, Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK,
Jorge Ghiso, Departments of Pathology and Psychiatry, New York University School of Medicine, New York, New York, USA,
Janice L. Holton, Queen Square Brain Bank, Department of Molecular Pathogenesis and Division of Neuropathology, Institute of Neurology, London WC1N 3BG, UK,
Blas Frangione, Departments of Pathology and Psychiatry, New York University School of Medicine, New York, New York, USA,
Tamas Revesz, Queen Square Brain Bank, Department of Molecular Pathogenesis and Division of Neuropathology, Institute of Neurology, London WC1N 3BG, UK
In this chapter we review a number of conditions which have in common cerebral amyloid angiopathy (CAA) (Table 14.1). However, and particularly in the context of dementia, it is now possible to make a clear distinction in this group of diseases. The distinction relates to the pathological processes which primarily lead to dementia.
Both sporadic and familial CAA from any cause can lead to dementia as a consequence of the angiopathy itself. The discussion regarding the causes of dementia in such instances may be closely related to the discussion in arteriosclerotic vascular dementia (Chapter 13). CAA occurring in Alzheimer's disease (AD) may contribute to the dementia by similar mechanisms. The clinico-pathological consequences of the CAA may be in some cases insignificant; in others there may be diffuse white matter rarefaction very similar to hypertensive Binswanger's encephalopathy (Chapter 13); or there may be recurrent haemorrhage. The haemorrhages themselves are usually large and lobar – with characteristic distribution – but occasionally smaller, deep haemorrhages of the type associated with hypertensive lacunar disease may occur. Finally areas of infarction may be seen but this rarely dominates the clinical picture. Lobar cerebral haemorrhage seems to occur particularly in those cases in which fibrinoid necrosis and microaneurysm formation occur – these are the hallmarks of severe amyloid angiopathy (Vonsattel et al., 1991). Ischaemic white matter changes (leukoencephalopathy or leukoariosis) can occur even when the vessels in the affected white matter do not show evidence of angiopathy, the ischaemia presumably being secondary to involvement of the penetrating cortical vessels (Dubas et al., 1985; Vonsattel et al., 1991). Yoshimura et al.
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