• Nikolaus Plesnila.
• Laboratory of Experimental Neurosurgery, Department of Neurosurgery and Institute for Surgical Research, University of Munich Medical Center, Grosshadern, Marchioninistr 15, 81377 Munich, Germany. plesnila@med.uni-muenchen.de
• Prog. Brain Res. 2007 Jan 1;161:393-400.

AbstractAmong the secondary events occurring after traumatic brain injury (TBI) pathologically increased intracranial pressure (ICP) correlates most closely with poor outcome. In addition to infusion of hypertonic solutions, e.g. mannitol, and other medical measures, decompression of the brain by surgical removal of a portion of the cranium (craniectomy) has been used for many decades as an intuitive strategy for the treatment of post-traumatic ICP increase. The lack of evidence-based clinical and controversial experimental data, however, resulted in decompressive craniectomy to be recommended by most national and international guidelines only as a third tier therapy for the treatment of pathologically elevated ICP. Ongoing clinical trials on the use of decompressive craniectomy after TBI may clarify many aspects of the clinical application of this technique, however, some important pathophysiological issues, e.g. the timing of decompression craniectomy, its effect on brain edema formation, and its role for secondary brain damage, are still widely discussed and can only be addressed in experimental settings. The aim of the current review was therefore to summarize and discuss recent experimental data dealing with the use of decompression craniectomy following TBI. The present results suggest that surgical decompression effectively prevents secondary brain damage when performed early enough. Although caution should be taken when transferring conclusions drawn from experimental settings to the clinical situation, the current literature suggests that the timing of decompression may be of utmost importance in order to exploit the full neuroprotective potential of craniectomy following TBI.

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