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dc.contributor.authorBellander, Bo-Michael
dc.contributor.authorOlafsson, Ingvar Hakon
dc.contributor.authorGhatan, Per Hamid
dc.contributor.authorBro Skejo, Hanne Pernille
dc.contributor.authorHansson, Lars-Olof
dc.contributor.authorWanecek, Mikael
dc.contributor.authorSvensson, Mikael A
dc.date.accessioned2012-05-14T08:58:29Z
dc.date.available2012-05-14T08:58:29Z
dc.date.issued2011-01
dc.date.submitted2012-05-13
dc.identifier.citationActa Neurochir (Wien). 2011, 153(1):90-100en_GB
dc.identifier.issn0942-0940
dc.identifier.pmid20686797
dc.identifier.doi10.1007/s00701-010-0737-z
dc.identifier.urihttp://hdl.handle.net/2336/223474
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links field.en_GB
dc.description.abstractOBJECT: Complement 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. METHODS: Twenty 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)). RESULTS: Following 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. CONCLUSION: This 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.
dc.language.isoenen
dc.publisherSpringer Verlagen_GB
dc.relation.urlhttp://dx.doi.org/10.1007/s00701-010-0737-zen_GB
dc.rightsArchived with thanks to Acta neurochirurgicaen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAgeden_GB
dc.subject.meshBiological Markersen_GB
dc.subject.meshBrain Injuriesen_GB
dc.subject.meshComplement Activationen_GB
dc.subject.meshComplement Membrane Attack Complexen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshNerve Growth Factorsen_GB
dc.subject.meshPhosphopyruvate Hydrataseen_GB
dc.subject.meshS100 Proteinsen_GB
dc.subject.meshUp-Regulationen_GB
dc.subject.meshYoung Adulten_GB
dc.titleSecondary insults following traumatic brain injury enhance complement activation in the human brain and release of the tissue damage marker S100B.en
dc.typeArticleen
dc.contributor.departmentLandspitali The National University Hospital, Reykjavík, Iceland. Department of Clinical Neuroscience, Section for Neurosurgery, Karolinska University Hospital Solna, S-171 76 Stockholm, Sweden. bo-michael.bellander@karolinska.seen_GB
dc.identifier.journalActa neurochirurgicaen_GB
html.description.abstractOBJECT: Complement 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. METHODS: Twenty 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)). RESULTS: Following 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. CONCLUSION: This 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.


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