gms | German Medical Science

59th Annual Meeting of the German Society of Neurosurgery (DGNC)
3rd Joint Meeting with the Italian Neurosurgical Society (SINch)

German Society of Neurosurgery (DGNC)

1 - 4 June 2008, Würzburg

The delayed passage of S100B from the cerebrospinal fluid to blood is associated with a better neurological function following acute brain injury

Die verzögerte Passage von S100B aus dem Liquor in das Blut ist nach akuten Hirnschädigungen mit einer verbesserten neurologischen Funktion verbunden

Meeting Abstract

  • corresponding author S. Meissner - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • A. Podlewski - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • R. Megele - Klinik für Neurochirurgie, Klinikum Amberg
  • M. Buchfelder - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
  • A. Kleindienst - Klinik für Neurochirurgie, Universität Erlangen-Nürnberg

Deutsche Gesellschaft für Neurochirurgie. Società Italiana di Neurochirurgia. 59. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3. Joint Meeting mit der Italienischen Gesellschaft für Neurochirurgie (SINch). Würzburg, 01.-04.06.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocDI.02.05

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2008/08dgnc155.shtml

Published: May 30, 2008

© 2008 Meissner et al.
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Outline

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Objective: S100B has been promoted as a clinical marker of brain damage for more than 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 (BBB) rather than to reflect cerebral S100B levels. Furthermore, the S100B release pattern following experimental injury suggests a participation of the neurotrophic protein in 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 28 patients with subarachnoid hemorrhage (SAH, H&H1 n=3, H&H2 n=5, H&H3 n=7, H&H4 n=4, H&H5 n=9) and in 15 patients with severe traumatic brain injury (TBI) treated with a ventricular drainage, 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). The percentage of S100B in serum of CSF was calculated. Neurological function was assessed daily by the Glasgow Coma Score (GCS). The Glasgow Outcome Score (GOS) at discharge determined recovery.

Results: Following SAH, the S100B serum concentration was highest on admission (0.20±0.27µg/l) and decreased thereafter steadily (0.09±0.04µg/l on day 10). Mean S100B CSF levels were continuously high for the first 5 days (54.13±9.27µg/l on admission), and decreased thereafter (7.80±7.78µg/l on day 10). Similarly, following TBI, the S100B serum concentration was highest on admission (0.47±0.39µg/l) and decreased thereafter steadily (0.12±0.12µg/l on day 10). Mean S100B CSF levels were continuously high for the first week (198.52±340.17µg/l on admission), and decreased thereafter (29.85±85.21µg/l on day 10). A high S100B serum concentration on day 1 predicted a worse neurological function on day 7 to 10 (p=0.045). However, calculating a ratio S100B serum/CSF, those patients with high ratios starting at day 4 had a significantly better neurological function (p=0.002).

Conclusions: Initially high S100B serum levels reflect the passive release from damaged cells and through a compromised BBB and predict a bad neurological function. Considering a half-life of S100B of few hours and a stimulated active S100B release serving repair mechanisms, a higher S100B serum/CSF ratio may be beneficial for neurological function.