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(Stroke. 2004;35:386.)
© 2004 American Heart Association, Inc.

Advances in Stroke 2003

Vascular Cognitive Impairment

J. V. Bowler, MD, FRCP

From the Department of Neurology, Royal Free Hospital, London, UK.

Correspondence to Dr. John V. Bowler, Royal Free Hospital, Dept of Neurology, London NW3 2QG, UK. E-mail j.bowler@rfc.ucl.ac.uk

Key Words: Advances in Stroke • cognitive disorders

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Developments in the field of vascular cognitive impairment over the past year have been evolutionary rather than revolutionary and spread across many aspects. However, even evolutionary changes may be radical, and it is in 3 particular aspects—those of treatment, prevention, and the evaluation of white matter disease—that evolution has been at its most rapid.

Treatment

Since 2002, 5 large, randomized studies of the symptomatic treatment of probable and possible vascular dementia have been published. This is a radical development, and these few studies exceed everything that has been published before. These comprise 2 studies of the anticholinesterase donepezil in vascular dementia,^1,2 2 studies of the NMDA receptor antagonist memantine in mild to moderate vascular dementia,^3,4 and a study of the anticholinesterase galantamine in "probable vascular dementia and Alzheimer’s disease combined with cerebrovascular disease."⁵

While these findings are exciting and represent new developments, there are a number of cautions. The first is the relatively modest benefits seen in all these trials. For the anticholinesterases, the benefit on the ADAS-Cog⁶ amounts to about 3 points and to <1 point on the Mini-Mental State Examination (MMSE).⁷ While statistically significant, these effects are so slight that they may not be useful routine treatments but perhaps treatments that should be tried in all but maintained only in individual responders.

These drugs were originally developed for Alzheimer’s disease on the basis of the cholinergic hypothesis; much is made of the presence of a cholinergic deficit in vascular dementia, which probably occurs because of ischemic damage to the . . . [Full Text of this Article]

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