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2014 ; 75 Suppl 4
(0 4
): S24-33
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The new neurometabolic cascade of concussion
#MMPMID25232881
Giza CC
; Hovda DA
Neurosurgery
2014[Oct]; 75 Suppl 4
(0 4
): S24-33
PMID25232881
show ga
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.
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