From neuronal and vascular impairment to dementia

Citation
Pp. De Deyn et al., From neuronal and vascular impairment to dementia, PHARMACOPS, 32, 1999, pp. 17-24
Citations number
79
Categorie Soggetti
Neurosciences & Behavoir
Journal title
PHARMACOPSYCHIATRY
ISSN journal
01763679 → ACNP
Volume
32
Year of publication
1999
Supplement
1
Pages
17 - 24
Database
ISI
SICI code
0176-3679(199903)32:<17:FNAVIT>2.0.ZU;2-B
Abstract
This paper reviews aspects of existing knowledge and recent concepts relate d to the development of vascular dementia which, after Alzheimer's disease, is the most frequent type of dementia. The disorder may result from cerebr ovascular disorders, including multi-infarct dementia due to thromboembolic disease, other less common vasculopathies and ischemic brain damage second ary to systemic hypotension. Characteristic clinical features are stepwise cognitive deterioration resulting from repeated strokes and the presence of focal signs and symptoms. The clinical distinction between Alzheimer's dis ease and vascular dementia may be difficult and strict criteria (NINDS/ AIR EN) have recently been adopted as standard guidelines for research studies. Vascular dementia and Alzheimer's disease can co-exist, so-called "mixed d ementia", and the presence of cerebrovascular disease may worsen Alzheimer dementia. Indeed, there is often a vascular component in the pathogenesis o f dementia. The pathogenesis of vascular dementia is complex. Post-stroke p atients are at increased risk; some predisposing or risk factors are the vo lume, number and site (whether strategic or not) of cerebral injuries, dist al field vascular injury with reduced cerebral blood flow, white matter isc hemia due to small vessel disease, the co-existence of vascular disease and Alzheimer's dementia, and the presence of cognitive decline prior to strok e. There is increasing evidence of a complex relationship between vascular dementia and Alzheimer's disease. When post-stroke dementia is progressive this may reflect associated Alzheimer's disease either unrecognized or asym ptomatic prior to the stroke. The apolipoprotein E4 genotype is a risk fact or for ischemic stroke, vascular dementia and Alzheimer dementia. Although dementia is usually irreversible, it is now accepted that cognitive impairm ent may be delayed, stabilized or sometimes reversed. The treatment of vasc ular dementia consists of two approaches: preventive measures, including at tempts to control risk factors for stroke and the use of antiplatelet agent s and/or surgery, and the treatment of cognitive symptoms. Nootropic and va sodilator agents have been reported to improve cognitive impairment from va rious causes. Ongoing research is attempting to show their specific benefit in vascular dementia.