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

Neuroprotective effect of hyperbaric oxygen therapy following experimental brain contusion

Neuroprotektiver Effekt der hyperbaren Sauerstofftherapie auf experimentelle Hirnkontusionen

Meeting Abstract

  • corresponding author C. Voigt - Klinik für Neurochirurgie, Universität Leipzig
  • A. Foerschler - Klinik für Radiologie, Universität Leipzig
  • M. Jaeger - Klinik für Neurochirurgie, Universität Leipzig
  • J. Meixensberger - Klinik für Neurochirurgie, Universität Leipzig
  • L. Küppers-Tiedt - Klinik für Neurologie, Universität Leipzig
  • M. U. Schuhmann - Klinik für Neurochirurgie, Universität Leipzig

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. DocFR.06.07

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2007/07dgnc102.shtml

Published: April 11, 2007

© 2007 Voigt et al.
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Outline

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Objective: Previous experimental research showed a positive effect of hyperbaric oxygen therapy (HBO) on infarct size in models of focal brain ischemia. In this pilot study we evaluated the effect of HBO on experimental brain contusions in rats using MR imaging. Clinical TBI studies from the last 15 years had repeatedly reported a possible clinical benefit from HBO therapy.

Methods: 10 SD rats were investigated 24h and 72h after Controlled Cortical Impact injury. 5 rats were treated with 100% oxygen at 2.5 atmospheres absolute, 5 were kept at normobaric room air for 60 min, beginning 1h after CCI. MRI scanning (Philips Intera, 1mm slice, T2, DWI) was performed 24h and 72h after injury in all animals. Lesion size was determined in T2 weighted MRI scans. The relative change of ADC values in the area of contusion was determined in comparison to the con-tralateral side.

Results: Lesion volume in T2 images decreased in the HBO animals within 24h (63.1±16.5 mm3 vs. 87.4±13.8 mm3, p<0.05). This decrease in contusion size continued in HBO animals till 72h, while there was a trend to even larger contusions in controls at this time (46.8±17.8 mm3 vs. 92.5±13.1 mm3, p<0.01). In addition, T2 hyperintensity within the contusion area was clearly milder in the treatment group. This was reflected in ADC mapping. The mean relative ADC increase at 24h of 26.8±2.3% in controls, was strongly attenuated after HBO therapy. 3 animals even showed a decrease in ADC values, resulting in a mean relative ADC change of 2.3±12.2% (p<0.01). 72h after the HBO, induced attenuation of relative ADC values was less compared to 24h, however still significantly lower than in controls 10.1±14.8% vs. 32.8±11.2%, p<0.02).

Conclusions: A 60-minute exposure to hyperbaric oxygen starting 1h after controlled cortical impact injury significantly attenuated the induced lesion size and the relative increase of ADC values in the contused area. Thus, HBO after trauma seems to have neuroprotective effects on contused brain and its penumbra as previously observed in models of focal brain ischemia. The effect of HBO in ischemia is thought to be mediated through improved oxygen supply to the tissue at risk, increased BBB integrity, attenuated vascular basal lamina degradation, down regulation of COX-2, reduced excitotoxicity, alterations in inflammation and apoptotic regulators affecting late neuronal damage. Further research has to clarify the role of HBO and the mechanisms of neuroprotection after traumatic brain injury.