The New Neurometabolic Cascade of Concussion

The New Neurometabolic Cascade of Concussion

2014 October ; 75(0 4): S24–S33 | Christopher C. Giza, M.D. and David A. Hovda, Ph.D.
The article by Giza and Hovda provides an updated overview of the biological underpinnings of concussion, highlighting the significant advancements in understanding the acute neurometabolic cascade following brain injury. The authors discuss how initial ionic flux and glutamate release lead to significant energy demands and metabolic crises in the injured brain, which can be linked to clinical symptoms such as migraines, cognitive impairment, and vulnerability to repeat injuries. Advanced neuroimaging techniques have enabled noninvasive monitoring of post-concussion pathophysiology, and there is growing concern about the risk of chronic or progressive neurobehavioral impairment. The paper also explores the connections between acute pathophysiology and long-term biological changes, including axonal dysfunction, altered neurotransmission, and protein degradation, which may underlie chronic sequelae. The authors emphasize the need for further research to better understand the timing of increased risk for repeated injuries and to develop interventions to prevent persistent deficits or neurodegeneration.The article by Giza and Hovda provides an updated overview of the biological underpinnings of concussion, highlighting the significant advancements in understanding the acute neurometabolic cascade following brain injury. The authors discuss how initial ionic flux and glutamate release lead to significant energy demands and metabolic crises in the injured brain, which can be linked to clinical symptoms such as migraines, cognitive impairment, and vulnerability to repeat injuries. Advanced neuroimaging techniques have enabled noninvasive monitoring of post-concussion pathophysiology, and there is growing concern about the risk of chronic or progressive neurobehavioral impairment. The paper also explores the connections between acute pathophysiology and long-term biological changes, including axonal dysfunction, altered neurotransmission, and protein degradation, which may underlie chronic sequelae. The authors emphasize the need for further research to better understand the timing of increased risk for repeated injuries and to develop interventions to prevent persistent deficits or neurodegeneration.
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