Metabolic Dysfunction Following Traumatic Brain Injury

  • Hovda D
  • Giza C
  • Bergsneider M
  • et al.
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Abstract

The major objective of this chapter is to provide insight on neurometabolic/ neurochemical cascade and pathophysiological processes underlying the brain responses to biomechanical concussive forces. Specifi cally, I will provide you with a brief, yet simple and straightforward notion of mild traumatic brain injury, also known as concussion. I would like to stress that concussion: (a) is an injury to the brain caused by biomechanical forces; it is not ischemia or stroke; (b) results in regional and temporal cellular alteration and may produce cell death; (c) produces a state of energy crisis and subsequent metabolic diaschisis ; (d) changes the priorities for fuel; and (e) can contribute to the acquisition of posttraumatic stress and more chronic neurological degeneration related to disease. Both animal models and human studies strongly suggest that there is nothing " mild " about mild TBI at the cellular level .

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Hovda, D. A., Giza, C. C., Bergsneider, M., & Vespa, P. M. (2014). Metabolic Dysfunction Following Traumatic Brain Injury. In Concussions in Athletics (pp. 205–215). Springer New York. https://doi.org/10.1007/978-1-4939-0295-8_11

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