Ricardo J. Komotar, Robert M. Starke, Eric J. Arias, Matthew C. Garrett, Marc L. Otten, Maxwell B. Merkow, Benjamin Hassid, J. Mocco, Michael E. Sughrue, Grace H. Kim, William J. Mack, Andrew F. Ducruet and E. Sander Connolly Pages 287 - 292 ( 6 )
Recent evidence has shown that after the initial occlusion, a large portion of stroke patients achieve some degree of reperfusion either through collateral circulation or clot dissolution. However, it appears that this reperfusion may lead to increased inflammation-induced damage. Even though the exact mechanism of this secondary injury is unclear, several experimental studies have indicated an intimate connection between complement and this secondary form of damage. We review the available literature and attempt to identify promising clinical therapeutic targets.
Complement, stroke, reperfusion, ischemia
Department of Neurosurgery, Columbia University, 710 West 168th Street, Room 431, New York, NY 10032, USA.