Inflammation following stroke

Stroke is one of the leading causes of mortality and morbidity. The stroke process triggers an inflammatory reaction that may last up to several months. Suppression of inflammation using a variety of drugs reduces infarct volume and improves clinical outcomes in animal models of stroke. This benefit...

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Bibliographic Details
Published in:Journal of clinical neuroscience 2006, Vol.13 (1), p.1-8
Main Authors: Nilupul Perera, M., Ma, Henry K., Arakawa, Shuji, Howells, David W., Markus, Romesh, Rowe, Christopher C., Donnan, Geoffrey A.
Format: Article
Language:English
Subjects:
Animal stroke model
Animals
Disease Models, Animal
Fibrinolytic Agents - therapeutic use
Haemorrhagic stroke
Humans
Inflammation
Inflammation - etiology
Inflammation - prevention & control
Ischaemic stroke
Neuroprotection
Stroke - complications
Stroke - therapy
Time Factors
Tissue Plasminogen Activator - therapeutic use
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Summary:Stroke is one of the leading causes of mortality and morbidity. The stroke process triggers an inflammatory reaction that may last up to several months. Suppression of inflammation using a variety of drugs reduces infarct volume and improves clinical outcomes in animal models of stroke. This benefit occurs even with the initiation of therapy after 3 hours of onset of stroke, beyond the therapeutic window for thrombolysis with tPA. The use of neuroprotectants to suppress inflammation may widen the therapeutic time window for tPA while lessening its side-effects. Suppression of inflammation may also improve outcomes in animal models of haemorrhagic stroke. To date, clinical trials with anti-inflammatory agents in acute ischaemic stroke have failed to improve clinical outcomes. However, because of the potential for broader applicability across all aspects of stroke, a better understanding of anti-inflammatory mechanisms is important.
ISSN:0967-5868
1532-2653
DOI:10.1016/j.jocn.2005.07.005