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|Title:||Inflammation following stroke.|
|Authors:||Nilupul Perera, M;Ma, Henry K;Arakawa, Shuji;Howells, David William;Markus, Romesh;Rowe, Christopher C;Donnan, Geoffrey A|
|Affiliation:||National Stroke Research Institute, Austin Health, University of Melbourne, Level 1, Neurosciences Building, 300 Waterdale Road, Heidelberg Heights, Victoria 3081, Australia. email@example.com|
|Citation:||Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia; 13(1): 1-8|
|Abstract:||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.|
|Internal ID Number:||16410192|
Disease Models, Animal
Fibrinolytic Agents.therapeutic use
Inflammation.etiology.prevention & control
Tissue Plasminogen Activator.therapeutic use
|Appears in Collections:||Journal articles|
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