• Bo-Michael Bellander, Ingvar Hakon Olafsson, Per Hamid Ghatan, Hanne Pernille Bro Skejo, Lars-Olof Hansson, Mikael Wanecek, and Mikael A Svensson.
• Department of Clinical Neuroscience, Section for Neurosurgery, Karolinska University Hospital Solna, S-171 76 Stockholm, Sweden. bo-michael.bellander@karolinska.se
• Acta Neurochir (Wien). 2011 Jan 1;153(1):90-100.

ObjectComplement activation has been suggested to play a role in the development of secondary injuries following traumatic brain injury (TBI). The present study was initiated in order to analyze complement activation in relation to the primary brain injury and to secondary insults, frequently occurring following TBI.MethodsTwenty patients suffering from severe TBI (Glasgow coma score ≤ 8) were included in the study. The "membrane attack complex," C5b9, which is the cytolytic end product of the complement system was analyzed in cerebrospinal fluid (CSF). The degree of brain tissue damage was assessed using the release of S100B and neuron-specific enolase (NSE) to the CSF and blood. The blood-brain barrier was assessed using the CSF/serum quotient of albumin (Q (A)).ResultsFollowing impact, initial peaks (0-48 h) of C5b9, S100B, and NSE with a concomitant loss of integrity of the blood-brain barrier were observed. Secondary insults at the intensive care unit were monitored. Severe secondary insults were paralleled by a more pronounced complement activation (C5b9 in CSF) as well as increased levels of S100B (measured in CSF), but not with NSE.ConclusionThis human study indicates that complement activation in the brain is triggered not only by the impact of trauma per se but also by the amount of secondary insults that frequently occur at the scene of accident as well as during treatment in the neurointensive care unit. Complement activation and in particular the end product C5b9 may in turn contribute to additional secondary brain injuries by its membrane destructive properties.

32 keywords...

hide…