PATHOGENESIS OF LEUKOARAIOSIS - A REVIEW

Citation
L. Pantoni et Jh. Garcia, PATHOGENESIS OF LEUKOARAIOSIS - A REVIEW, Stroke, 28(3), 1997, pp. 652-659
Citations number
114
Categorie Soggetti
Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
28
Issue
3
Year of publication
1997
Pages
652 - 659
Database
ISI
SICI code
0039-2499(1997)28:3<652:POL-AR>2.0.ZU;2-I
Abstract
Background Changes in the cerebral hemispheric white matter, detectabl e with increasing frequency by modern neuroimaging methods, are associ ated with aging and conceivably may contribute to the development of s pecific cognitive deficits. The pathogenesis of these cerebral white m atter abnormalities (sometimes described as leukoaraiosis) is unknown. This review evaluates the available evidence in support of the hypoth esis that the etiology of leukoaraiosis is related to a specific type of cerebral ischemia and highlights mechanisms by which ischemic injur y to the brain may induce selected structural alterations limited to t he cerebral white matter. Summary of Review The review is based on the critical analysis of over 100 publications (most appearing in the las t decade) dealing with the anatomy and physiology of the arterial circ ulation to the cerebral white matter and with the pathogenesis of leuk oaraiosis. Conclusions A significant number of clues support the hypot hesis that some types of leukoaraiosis may be the result of ischemic i njury to the brain. Structural changes affecting the small intraparenc hymal cerebral arteries and arterioles that are associated with aging and with stroke risk factors, altered cerebral blood flow autoregulati on, and the conditions created by the unique arterial blood supply of the hemispheric white matter each seem to contribute to the developmen t of leukoaraiosis. To the best of our ability to interpret current in formation, the type of ischemic injury that is most likely responsible for these while matter changes involves transient repeated events cha racterized by moderate drops in regional cerebral blood flow that indu ce an incomplete form of infarction. This hypothesis could be tested i n appropriate experimental models.