gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

The delayed release of S100B following acute brain damage may reflect an endogenous neuroprotective or neurotrophic response

Die verzögerte Freisetzung von S100B nach akuter Hirnschädigung mag Ausdruck einer endogenen neuroprotektiven oder neurotrophen Reaktion sein

Meeting Abstract

  • corresponding author B. Leiner - Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
  • I. Y. Eyüpoglu - Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
  • D. Grass - Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
  • M. Buchfelder - Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
  • A. Kleindienst - Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocP 049

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2007/07dgnc304.shtml

Veröffentlicht: 11. April 2007

© 2007 Leiner et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: S100B has been promoted as a clinical marker of brain damage for a decade, and high serum S100B levels are considered to correlate with the severity of injury and a poor prognosis. However, experimental research demonstrated S100B serum levels to be altered by the blood-brain-barrier rather than to reflect cerebral S100B levels measured by MR proton spectroscopy. Furthermore, the S100B release pattern following experimental injury suggests a participation of the neurotrophic protein in delayed repair mechanisms. The present study was designed to elucidate the relevance of increased S100B serum levels in patients following acute brain damage and to compare them with cerebral S100B levels.

Methods: In 12 consecutive patients with traumatic brain injury or subarachnoid hemorrhage treated with a ventricular drainage (6 male, 6 female, mean age 45 years), we measured S100B in serum and in the cerebrospinal fluid (CSF) for 10 days (Elecsys® S100 Immunoassay, Roche Diagnostics, measuring range 0.005-39µg/l). Neurological deterioration was assessed daily by the Glasgow Coma Score (GCS). The Glasgow Outcome Score (GOS) at discharge determined recovery.

Results: The mean S100B concentration in serum was highest on admission (0.18±0.05µg/l) and decreased thereafter steadily (0.10±0.02µg/l on day 10). Mean S100B CSF levels were continuously high for the first week following injury (26.11±3.73µg/l on admission, 21.16±9.59µg/l on day 7), and decreased thereafter (4.88±1.81µg/l on day 10). For the individual patient, S100B levels in serum and in CSF did not correlate (r=0.108). The S100B concentration in CSF was closer related to the GCS (r=-0.336) and the GOS (r=-0.339) than in serum (r=-0.228 respectively r=-0.259).

Conclusions: The time course of cerebral S100B levels in patients with acute brain injury suggests a stimulated and delayed release initiated by the insult that may reflect an endogenous neuroprotective or neurotrophic response. Whenever available, S100B measurements in CSF should be preferred over serum measurements. The predictive value of S100B for the prognosis following brain injury remains questionable.