This Article Full Text Full Text (PDF) All Versions of this Article: 34/10/2331    most recent 01.STR.0000094580.14898.7Cv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bonelli, R. M. Search for Related Content PubMed PubMed Citation Articles by Bonelli, R. M.

(Stroke. 2003;34:2331.)
© 2003 American Heart Association, Inc.

Original Contributions

Editorial Comment—How to Treat Vascular Dementia?

University Clinic of Psychiatry, Karl-Franzens University Graz, Graz, Austria

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

In clinical practice, we deal with a great proportion of elderly people. Many times, we are able to identify cognitive deficits (although not too scarce, we overlook dementia in our patients). However, the further division into the several subtypes of dementing disorders may be complicated and laborious for patients, caregivers, and physicians due to noncompliance, incomplete clinical history, or missing medical equipment. Moreover, considerable clinical overlap makes treatment decisions difficult. So the good news, presented by Black et al in this issue,¹ is that the 3 most common forms of dementia—Alzheimer’s disease (AD), vascular dementia (VaD), and dementia with Lewy bodies—do have a common effective treatment schedule: acetylcholinesterase inhibitors (ACEI). Although their efficacy is, indeed, not overwhelming and a considerable proportion of patients will not profit by this medication, they still represent a ray of hope in the sad story of dementia treatment.

In the 1960s, it was widely recognized that AD was responsible for most cases of dementia in the elderly and that cerebral arteriosclerosis was a rare cause of dementia.² A decade later, research found out that some people develop dementia not due to arteriosclerosis of brain vasculature but rather as a consequence of a series of strokes, affecting different brain regions, and the term multi-infarct dementia was introduced.³ In the 1990s, it also became clear that several other mechanisms (ischemic white matter lesions, lacunes) may underlie vascular damage to the brain, which culminates in cognitive decline; therefore, the broader term vascular dementia was accepted⁴ and recognized as . . . [Full Text of this Article]

This article has been cited by other articles:

				J. P. Rowland, J. Rigby, A. C. Harper, and R. Rowland Cardiovascular monitoring with acetylcholinesterase inhibitors: a clinical protocol Adv. Psychiatr. Treat., May 1, 2007; 13(3): 178 - 184. [Abstract] [Full Text] [PDF]