Citation

Chen Y, Huang W, Constantini S. Front. Neurol. 2013; 4: 119.

Affiliation

BrightstarTech, Inc. Clarksburg, MD, USA.

Copyright

(Copyright © 2013, Frontiers Research Foundation)

DOI

10.3389/fneur.2013.00119

PMID

23966976

PMCID

PMC3743039

Abstract

The initial mechanism of blast-induced TBI is different from that of sports-related concussion. However, both the two conditions can trigger a comparable pathophysiological cascade (i.e., secondary neuronal damage), thus leading to progressive neuronal cell death, neural loss, and axonal degeneration in the brain. Secondary neuronal damage should be the major contributor to ultimate neurologic and psychological impairments following various brain insults including blast-induced TBI and sports-related concussion. CTE is a result of secondary neuronal damage triggered by sports-related concussion. It is similar to long-term neuropsychiatric and neurological consequences of blast-induced TBI. This may be the reason why blast-induced TBI and sports-related concussion are considered to have the same injury mechanisms. Abnormal tau protein deposition in some specific regions of the brain is only a marker of the presence of neuronal cell death, loss or degeneration, and cannot be used to specifically diagnose blast-induced TBI and sports-related head trauma.

Language: en