Alterations in cerebral energy metabolism induced by traumatic brain injury

Energy metabolism of the brain is unique, possessing high aerobic metabolism with no significant capacity for anaerobic glycolysis and limited tissue stores of glucose. A steady supply of oxygen and glucose is essential in order to maintain cerebral function and integrity. Extensive research in experimental and human head injury has been conducted regarding the delivery of oxygen and outcome. This research has provided evidence which indicates that in addition to the availability of oxygen and glucose, other factors, such as perturbation of mitochondrial energy transducing processes which also follow head trauma, play significant roles. In this paper, the salient findings from biochemical studies of experimental and clinical brain injury are summarized and indicate that the mitochondrial respiratory chain-linked oxidative phosphorylation and calcium transport are compromised by trauma-induced brain injury and support the idea that oxidative stress and perturbation of cellular calcium homeostasis play significant roles in traumatic brain injury.