Post-stroke inflammatory response: effects of stroke evolution and outcome.
Recovery after stroke is often hindered by further neurologic deterioration, which can affect up to 45% of patients. It has been suggested that one of the major causes of this neurologic deterioration may be post-ischemic cerebral inflammation. This review presents the basis of pathophysiologic mechanisms of post-stroke inflammation and discusses possible targets and routes for therapeutic intervention.
Tan
Kiat T
KT
Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Dudley Road, Birmingham B18 7QH, UK.
Lip
Gregory Y H
GY
Blann
Andrew D
AD
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000032:analysis; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects; D015850:Interleukin-6 / Q000097:blood; D020521:Stroke / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein