gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

Quantification of secondary brain damage after controlled cortical impact in mice

Quantifizierung des sekundären Hirnschadens nach Kontusionstrauma (Controlled Cortical Impact) bei der Maus

Meeting Abstract

  • corresponding author Christian A. Erös - Institute for Surgical Research, University of Munich, Munich
  • S. W. Kim - Institute for Surgical Research, University of Munich, Munich
  • K. Zweckberger - Institute for Surgical Research, University of Munich, Munich
  • R. Zimmermann - Institute for Surgical Research, University of Munich, Munich
  • A. Baethmann - Institute for Surgical Research, University of Munich, Munich
  • N. Plesnila - Institute for Surgical Research, University of Munich, Munich

Deutsche Gesellschaft für Neurochirurgie. Ungarische Gesellschaft für Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie. Köln, 25.-28.04.2004. Düsseldorf, Köln: German Medical Science; 2004. DocDI.04.06

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2004/04dgnc0184.shtml

Published: April 23, 2004

© 2004 Erös et al.
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Outline

Text

Objective

The most important constituents of secondary brain damage from traumatic brain injury (TBI) with contusions, are brain edema formation and delayed contusion expansion. In order to quantify secondary brain damage after the controlled cortical impact (CCI) model we investigated contusion volume and brain edema formation during the first 24 hourd after trauma.

Methods

Male C57/Bl6 mice (n=48) were craniotomized and subjected to CCI (8 m/s, 1 mm). The craniotomy was closed thereafter. Brain water content and contusion volume were assessed 6, 12, 24, and 48h and 15 min, 6, 12, and 24h after trauma, respectively.

Results

Brain water content increased continuously from 78.1±0.4 % in sham operated animals to a maximum of 81.1±0.7 % (p<0.05) in the ipsilateral hemisphere 24 h after CCI. No significant increase was detected on the contralateral side. The contusion was clearly demarcated already 15 min after trauma (19.4±4.0 mm3). 6 and 24 h later the contusion increased to 131% (25.4±3.1 mm3; p<0.05 vs. 15 min) and 171% (33.2±3.0 mm3; p<0.05 vs. 15 min and 6h) of its initial volume 15 min after CCI (100%), respectively.

Conclusions

The size of a cortical contusion is expanding significantly after closed head CCI. This secondary contusion expansion is paralleled by brain edema formation. These data demonstrate on a quantitative basis that parenchymal loss in the vicinity of a cortical contusion is an ongoing process and amendable to therapy due to its delayed character.