(Stroke. 2004;35:341.)
© 2004 American Heart Association, Inc.
Advances in Stroke 2003 |
From London Sciences Health Centre, University of Western Ontario, London, Ontario, Canada.
Correspondence to Dr Vladimir Hachinski, Department of Clinical Neurological Sciences, London Health Sciences Centre, 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. |
The generation of new information creates a parallel demand for its analysis, evaluation, and integration with current knowledge. When we introduced Advances in Stroke in the February 2003 issue of Stroke, 9 out of the top 10 accessed articles were from this series. This suggests that the succinct summaries of the most important developments in the previous year fulfilled a need. One remarkable aspect of the series was that it featured some articles co-authored by clinicians and basic scientists in clear language, bridging the common dichotomy between laboratory and clinical approaches.
The year 2003 witnessed the reporting of a strong association between the phosphodiesterase 4D gene and ischemic stroke in Iceland. This sets the stage for the study in other populations and for working out mechanisms. A disease mechanism that is becoming clearer is one explaining the association of hyperhomocysteinemia and stroke. At least part of the answer is that oxidative stress affects the structure and function of the cerebral blood vessels. It turns out that angiotensin II can also harm blood vessels, independently from its role in producing hypertension.
Imaging has unveiled the threat that white matter lesions and silent infarcts pose. Subjects with these changes are twice as likely to develop dementia and 3 times as prone to suffer a stroke than subjects of similar age who do not have them. When a stroke actually occurs, tPA remains the treatment of choice within the first 3 hours but always under the shadow of possible hemorrhage. Experimental data
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