Since the original descriptions of postconcussive pathophysiology, there has been a significant increase in interest and ongoing research to study the biological underpinnings of concussion. The initial ionic flux and glutamate release result in significant energy demands and a period of metabolic crisis for the injured brain. These physiological perturbations can now be linked to clinical characteristics of concussion, including migrainous symptoms, vulnerability to repeat injury, and cognitive impairment. Furthermore, advanced neuroimaging now allows a research window to monitor postconcussion pathophysiology in humans noninvasively. There is also increasing concern about the risk for chronic or even progressive neurobehavioral impairment after concussion/mild traumatic brain injury. Critical studies are underway to better link the acute pathobiology of concussion with potential mechanisms of chronic cell death, dysfunction, and neurodegeneration. This “new and improved” article summarizes in a translational fashion and updates what is known about the acute neurometabolic changes after concussive brain injury. Furthermore, new connections are proposed between this neurobiology and early clinical symptoms as well as to cellular processes that may underlie long-term impairment.
ABBREVIATIONS:
APP, amyloid precursor protein
BOLD, blood oxygen level-dependent
DTI, diffusion tensor imaging
FA, fractional anisotropy
fMRI, functional magnetic resonance imaging
FPI, fluid percussion injury
GABA, γ-aminobutyric acid
mTBI, mild traumatic brain injury
NAA,N-acetylaspartate
NMDAR,N-methyl-D-aspartate receptor
TBI, traumatic brain injury
