Please use this identifier to cite or link to this item:
Title: Inflammation following stroke.
Austin 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
Issue Date: 1-Jan-2006
Publication information: 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.
Gov't Doc #: 16410192
DOI: 10.1016/j.jocn.2005.07.005
Journal: Journal of Clinical Neuroscience
Type: Journal Article
Subjects: Animals
Disease Models, Animal
Fibrinolytic Agents.therapeutic use
Inflammation.etiology.prevention & control
Time Factors
Tissue Plasminogen Activator.therapeutic use
Appears in Collections:Journal articles

Show full item record

Page view(s)

checked on Jul 19, 2024

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.