gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

Correlation of cerebral monitoring and histopathological results in a standardized trauma model in sheep

Zerebrales Monitoring und histopathologischer Befund - Untersuchung zur Korrelation am standardisierten Trauma Modell des Schafs

Meeting Abstract

  • corresponding author C. Greiner - Department of Neurosurgery, Universität Münster
  • M. Hasselblatt - Insitute of Neuropathology, Universität Münster
  • H. D. Stubbe - Department of Anesthesiology and Intensive Care, Universität Münster
  • C. Rickert - Gerhard-Domack-Institute of Pathology, University of Münster
  • H. Wassmann - Department of Neurosurgery, Universität Münster

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. DocP056

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

Published: May 4, 2005

© 2005 Greiner 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.




The underlying mechanisms of severe traumatic brain injuries (TBI) are complex. Multiple factors are responsible for the patient’s outcome. Various experimental models imitate only single mechanisms of the TBI. We present our first results of a modified standardized head impact model in sheep, which will make a validation of different therapeutic regimes possible.


Fifteen sheep (3 SHAM) were instrumented with monitoring probes (arterial and sinus sagital catheters, intracranial pressure monitoring (ICP), internal carotid flow- and polarographic tissue O2 probes (ptiO2). During anaesthesia and mechanical ventilation, standardized TBI was induced by temporo-parietal head impact triggered by a non-penetrating stunner with adjustable forces. Time of investigation was 14h following TBI. Histopathology of the brain was investigated with different staining-methods and immunohistochemistry.


Head impact increased ICP from 9.5±1.2 to 22.5±7 mmHg and decreased internal carotid blood flow (ICBF) from 170±15 to 115±10 ml/min. Initial ptiO2 was 23.6±2.6 mmHg before and 9.7±2.2 mmHg 1h after TBI, respectively. Cerebral metabolic rate of oxygen (CMRO2) dropped from 9.8±1.4 to 6.8±2.0 1h after TBI. All brains (n=12) showed a generalized edema, eleven demonstrated a traumatic subarachnoid haemorrhage, in nine combined with intracranial contusions (contre-coup). In eleven brains, diffuse axonal injury could be demonstrated. All data are mean±SD. Immunohistochemistry (TUNEL, Caspase 3) for evaluation of apoptosis is still in progress.


This modified experimental head impact model demonstrates comparable monitoring data and similar patterns of neuropathological damage in all investigated animals. It is now applied for standardized investigation of therapeutic regimes (e.g. hyperbaric oxygenation) to prevent secondary brain damage.