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

Relevance of spontaneous perifocal depolarizations for secondary contusion expansion after CCI in mice

Die Rolle von perifokalen Depolarisationen für den sekundären Hirnschaden nach experimentellem Schädel-Hirn-Trauma bei der Maus

Meeting Abstract

  • corresponding author R. Trabold - Neurochirurgische Universitätsklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • L. von Baumgarten - Institut für Chirurgische Forschung, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • T. Back - Neurologische Klinik Mannheim, Ruprecht-Karls-Universität Heidelberg
  • N. Plesnila - Neurochirurgische Universitätsklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München

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 008

The electronic version of this article is the complete one and can be found online at:

Published: April 11, 2007

© 2007 Trabold et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Spontaneous perifocal depolarizations (SD) are responsible for lesion progression following cerebral ischemia. Since SDs were also observed in TBI patients, but their role for secondary brain damage is unclear yet, we aimed to address this question in an experimental study.

Methods: C57/Bl6 mice were subjected to controlled cortical impact (CCI; 6 m/s, 0.5mm). DC-potential, EEG and laser-Doppler flow (LDF) were continuously measured in peri-contusional tissue for 3 h. In a second line of experiments additional SDs were induced by cortical application of KCl (2µl 1 M solution every 10 min for 100 min). 24 h after trauma brains were removed for the quantification of contusion volume.

Results: Trauma induced one negative DC shift within the first 10 min in all animals. In 5/7 animals 1-3 SDs were observed within the next 3 h. In the second series of experiments cortical KCl application induced 10-11 DC-shifts within 2 h in all animals while control animals showed the same pattern as observed in the first line of experiments. 24 h after CCI contusion volume was not different between groups (20.8±2.6 mm3 vs. 21.1±3.71 mm3 in controls).

Conclusions: Our data show that SDs are infrequently observed after CCI and that the additional induction of SDs does not aggravate post-traumatic brain damage. We conclude from these findings that SDs are most likely not involved in mechanisms leading to secondary brain damage after experimental TBI.