• Ribal S Darwish and Nana S Amiridze.
• Department of Anesthesiology, Critical Care Medicine Division, University of Maryland Medical Center, 22 S. Greene Street, Baltimore, MD 21201-1595, USA. Rdarwish@anes.umm.edu
• Neurocrit Care. 2010 Jun 1;12(3):337-41.

BackgroundThe intrinsic pathway of apoptosis has been proposed as one mechanism of cell death after traumatic brain injury (TBI). This study tested the hypothesis that cytochrome c and activated caspase-9 are released into the cerebrospinal fluid (CSF) after severe TBI and that their presence correlates with mitochondrial injury and severity of neurologic outcome.MethodsNine adult patients with severe TBI (GCS < or = 8) underwent placement of intraventricular catheters for monitoring and management of intracranial pressure. CSF was sampled at catheter insertion (2-26 h after injury) and at intervals of 24, 48, and 72 h thereafter. Control samples were obtained from patients undergoing spinal anesthesia (ASA1). CSF levels of cytochrome c and activated caspase-9 were measured using ELISA.ResultsCytochrome c was detected in 18 (51.4%) samples, in the range of 0.08-5 ng/ml; mean value for cytochrome c was 0.44 ng/ml (SD +/- 0.632). Activated caspase-9 was detected in 10 samples (28.6%); mean value was 0.28 ng/ml (SD +/- 0.39). R (s) between cytochrome c and Glasgow outcome score (GOS) was -0.25 (P = 0.14), and between GOS and activated caspase-9 was -0.35 (P = 0.04). R calculated based on linear regression of activated caspase-9 and cytochrome c concentrations was 0.18. Control CSF samples had no detectable levels of either marker (detection level for cytochrome c was 0.08 ng/ml and 0.20 for activated caspase-9).ConclusionsWe concluded that activated caspase-9 and cytochrome c are present in the CSF of patients with severe TBI. Activated caspase-9 shows weak correlation with poor neurologic outcome.

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