This Article Full Text Full Text (PDF) All Versions of this Article: 36/2/177    most recent 01.STR.0000154894.22403.3av1 Alert me when this article is cited Alert me if a correction is posted 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 Google Scholar Google Scholar Articles by Hachinski, V. Search for Related Content PubMed PubMed Citation Articles by Hachinski, V. Pubmed/NCBI databases Medline Plus Health Information Stroke

(Stroke. 2005;36:177.)
© 2005 American Heart Association, Inc.

Advances in Stroke 2004

Introduction

From London Health Sciences Center, University of Western Ontario, London, Ontario, Canada.

Correspondence to Dr Vladimir Hachinski, University of Western Ontario, London Health Sciences Center, 339 Windermere Rd, London, Ontario N6A 5A5 Canada.

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

Advances in stroke in 2004 have been varied and many, from unraveling the genetics of intracerebral aneurysms to showing the high cost-effectiveness of even short-term care in stroke units.

After a slow beginning and a few false starts, the study of the genetics of stroke is picking up pace. Familial intracerebral aneurysms (IA) tend to be larger and more often multiple compared with sporadic ones. Familial IAs can show anticipation in certain kindred, manifesting in children some 20 years earlier than the mean age of subarachnoid hemorrhage in the parents. A locus near the elastin gene has been identified in one family, suggesting elastin abnormalities as a potential cause of strategically weakened vessels.

Polymorphism of the COX-2 gene has shown an association with ischemic events, a highly relevant finding in view of the recent reports regarding increased rates of stroke and myocardial infarction among consumers of two widely sold COX-2 inhibitors. COX-2 is expressed preferentially in some organs, such as the brain. It can be upregulated dramatically by inflammatory mediators and by cerebral ischemia in neurons, vascular cells, and inflammatory cells invading the brain. Contrariwise, inhibition of COX-2 in ischemic models of stroke attenuates the damage, even if given as late as 24 hours after injury, suggesting a new therapeutic target in the management of acute ischemic stroke.

Nitric oxide (NO) is a potent and major mediator of endothelium-dependent relaxation and thus a regulator of tone in large arteries and brain microvessels. It reacts extremely well with superoxide, resulting in . . . [Full Text of this Article]