• Gunes A Aygok, Anthony Marmarou, Panos Fatouros, Birgit Kettenmann, and Ross M Bullock.
• Department of Neurosurgery, Virginia Commonwealth University Medical Center, 1001 East Broad Street, Suite 235, P.O. Box 980508, Richmond, VA 23298-0508, USA. gaaygok@vcu.edu
• Acta Neurochir. Suppl. 2008 Jan 1; 102: 57-61.

BackgroundWe believe that in traumatic brain injury (TBI), the reduction of N-acetyl aspartate (NAA) occurs in the presence of adequate cerebral blood flow (CBF) which would lend support to the concept of mitochondrial impairment. The objective of this study was to test this hypothesis in severely injured patients (GCS 8 or less) by obtaining simultaneous measures of CBF and NAA.MethodsFourteen patients were studied of which six patients presented as diffuse injury at admission CT, while focal lesions were present in eight patients. CBF using stable xenon method was measured at the same time that NAA was measured by magnetic resonance proton spectroscopy (1HMRS) in the MR suite. Additionally, diffusion weighted imaging (DWI) and maps of the apparent diffusion coefficient (ADC) were assessed.FindingsIn diffuse injury, NAA/Cr reduction occurred uniformly throughout the brain where the values of CBF in all patients were well above ischemic threshold. In focal injury, we observed ischemic CBF values in the core of the lesions. However, in areas other than the core, CBF was above ischemic levels and NAA/Cr levels were decreased.ConclusionsConsidering the direct link between energy metabolism and NAA synthesis in the mitochondria, this study showed that in the absence of an ischemic insult, reductions in NAA concentration reflects mitochondrial dysfunction.

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