Traumatic brain injury (TBI) has been under investigation for several decades. However, it was only recently that TBI research has claimed a prominent role in many neuroscience research programs. Unfortunately, despite this increased interest, improved clinical outcomes following TBI are due more to improved preventive measures, including helmets and airbags, than to clinical intervention. Indeed, most clinicians target the physical manifestations of injury, including increased intracranial pressure and bleeding, rather than underlying mechanisms of cognitive disruption. This is due to necessity, as over 200 clinical trials for TBI treatment have failed in producing an effective therapy.
Numerous physiological functions are disrupted following TBI, chief among them being energy metabolism. However, the underlying mechanism of this effect, as well as the potential impact of impaired energy generating capacity, has not been determined. Indeed, despite the efforts of numerous laboratories, even the extent and duration of post-traumatic energy changes are unclear. While a growing consensus appears to confirm a shift towards anaerobic metabolism after injury, a potential alteration in primary energy subtrates is currently not well understood. There appears to be a significant increase in the capacity of the brain to use “alternative” substrates for energy generation, including ketone bodies and long chain lipids. However, the full extent of these metabolic alterations, the underlying mechanisms driving these shifts, and the implications for both reduced aerobic metabolism and use of alternative substrates for energy generation has not been determined.
Numerous reports have speculated that energy disruptions may be caused by the potent inflammatory response after injury, calcium dystasis, or impaired amino acid metabolism, among many other candidates. In turn, disruptions in energy production may also be causing many of these secondary events that occur after an injury. Metabolic disturbance has also been attributed with disrupting neurotransmitter trafficking and release, inability to maintain ionic gradients, and numerous other cellular processes.
This significant and far reaching effect of post-traumatic changes in energy metabolism underscores the need to fully understand how these contribute to post-traumatic physiology. However, given the tremendous array of injury models, subspecialties, and technical advances, the literature in the field has become very diffuse and difficult to properly evaluate. The Research Topic, “Neuroenergetics of Traumatic Brain Injury”, will provide a definitive update by leading experts in the field of neuroenergetics. A single issue will allow the compilation and summary of progress achieved in hypotheses, interpretations, and techniques used to properly understand the state of the art in this field.
Traumatic brain injury (TBI) has been under investigation for several decades. However, it was only recently that TBI research has claimed a prominent role in many neuroscience research programs. Unfortunately, despite this increased interest, improved clinical outcomes following TBI are due more to improved preventive measures, including helmets and airbags, than to clinical intervention. Indeed, most clinicians target the physical manifestations of injury, including increased intracranial pressure and bleeding, rather than underlying mechanisms of cognitive disruption. This is due to necessity, as over 200 clinical trials for TBI treatment have failed in producing an effective therapy.
Numerous physiological functions are disrupted following TBI, chief among them being energy metabolism. However, the underlying mechanism of this effect, as well as the potential impact of impaired energy generating capacity, has not been determined. Indeed, despite the efforts of numerous laboratories, even the extent and duration of post-traumatic energy changes are unclear. While a growing consensus appears to confirm a shift towards anaerobic metabolism after injury, a potential alteration in primary energy subtrates is currently not well understood. There appears to be a significant increase in the capacity of the brain to use “alternative” substrates for energy generation, including ketone bodies and long chain lipids. However, the full extent of these metabolic alterations, the underlying mechanisms driving these shifts, and the implications for both reduced aerobic metabolism and use of alternative substrates for energy generation has not been determined.
Numerous reports have speculated that energy disruptions may be caused by the potent inflammatory response after injury, calcium dystasis, or impaired amino acid metabolism, among many other candidates. In turn, disruptions in energy production may also be causing many of these secondary events that occur after an injury. Metabolic disturbance has also been attributed with disrupting neurotransmitter trafficking and release, inability to maintain ionic gradients, and numerous other cellular processes.
This significant and far reaching effect of post-traumatic changes in energy metabolism underscores the need to fully understand how these contribute to post-traumatic physiology. However, given the tremendous array of injury models, subspecialties, and technical advances, the literature in the field has become very diffuse and difficult to properly evaluate. The Research Topic, “Neuroenergetics of Traumatic Brain Injury”, will provide a definitive update by leading experts in the field of neuroenergetics. A single issue will allow the compilation and summary of progress achieved in hypotheses, interpretations, and techniques used to properly understand the state of the art in this field.
