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Scholars Journal of Applied Medical Sciences | Volume-7 | Issue 07
Pathophysiology and Mechanism of Concussion
Anthony Muchiri Wangui, David Kaniaru, Mary Wambui
Published: July 30, 2019 | 53 71
DOI: 10.36347/sjams.2019.v07i07.033
Pages: 2441-2448
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Abstract
Concussion has been identified as a major concern and a risk to athletes and sportsmen especially those involved in contact sports. During concussion the brain is exposed to intense acceleration, deceleration and rotational forces, resulting in the stretching and distortion of the neural structures. A systematic review was performed to summarize and appraise the evidence of literature on pathophysiology of concussion. The review was guided and based on CCOHTA’S guidelines. Primary studies that were either describing pathophysiology, mechanism, occurrence, biomechanics of concussion were included. With the Population inclusive of all Patients of all ages with a clinical definition of concussion. Published literature was identified through a cross-database search of relevant DIALOG databases. parallel searches were performed on AgeLine, CINAHL, PubMed, The Cochrane Library, and the Health Economic Evaluations Database. Searches were limited to literature published from January 1995 (1990 for PubMed) onward, with results fused up to May 31, 2019. Published literature was identified through a cross-database search of relevant DIALOG databases. parallel searches were performed on AgeLine, CINAHL, PubMed, The Cochrane Library, and the Health Economic Evaluations Database. Searches were limited to literature published from January 1995 (1990 for PubMed) onward, with results fused up to May 31, 2019. The pathophysiology of concussion was discussed in three major sunheadings of Cerebral Blood Flow, Ionic Flux and Glutamate Release, The Diffuse Axonal Injury (DAI) and Second Impact Syndrome In concussion. In summary concussion leads to These changes are activated by the mechanical insult itself and lead to ionic disturbance, EAA “neurotoxicity,” initial mitochondrial dysfunction, ROS-mediated damage, energy metabolism depression, alteration of gene expression, and ultimately variation of NAA concentration, the “surrogate” marker of the dysfunctional neurons. Prospective longi