Abstract
Blast-induced traumatic brain injury has been associated with neurodegenerative and neuropsychiatric disorders. To date, although damage due to oxidative stress appears to be important, the specific mechanistic causes of such disorders remain elusive. Here, to determine the mechanical variables governing the tissue damage eventually cascading into cognitive deficits, we performed a study on the mechanics of rat brain under blast conditions. To this end, experiments were carried out to analyse and correlate post-injury oxidative stress distribution with cognitive deficits on a live rat exposed to blast. A computational model of the rat head was developed from imaging data and validated against in vivo brain displacement measurements. The blast event was reconstructed in silico to provide mechanistic thresholds that best correlate with cognitive damage at the regional neuronal tissue level, irrespectively of the shape or size of the brain tissue types. This approach was leveraged on a human head model where the prediction of cognitive deficits was shown to correlate with literature findings. The mechanistic insights from this work were finally used to propose a novel protective device design roadmap and potential avenues for therapeutic innovations against blast traumatic brain injury.
Highlights
Blast-induced traumatic brain injury, arising in particular from the exposure to improvised explosive devices, has become a major problem for the armed forces[1] with mounting evidence pointing towards long-term neurodegenerative and neuropsychiatric disorders in veteran populations[2]
Post-Blast-induced traumatic brain injury (bTBI) pathologies are thought to be mechanically initiated by the early-time propagation of stress waves[3], cavitation effects[4], rapid acceleration of the head resulting from shock wave and blast wind interaction with the body[5], and secondary and tertiary injuries arising from subsequent impact, acceleration, and penetrating trauma[6,7]
We used a validated mild bTBI model in rats to expose individuals to blast conditions and, we performed a set of experimental techniques to characterise the distribution of oxidative stress reaction, a hallmark of secondary injury, across the brain and to relate these results to array of impairments in bTBI rats
Summary
Blast-induced traumatic brain injury (bTBI), arising in particular from the exposure to improvised explosive devices, has become a major problem for the armed forces[1] with mounting evidence pointing towards long-term neurodegenerative and neuropsychiatric disorders in veteran populations[2]. This work aims to provide new insights into the mechanical mechanisms of brain damage resulting from blast exposure by focussing on early-time events of primary blast loading and their correlation to post-injury biochemical and functional impairments. To this end, an in vivo/in silico methodology was developed to assess the consequences of blast on rats. We provide new, validated bTBI in silico models of rat and human subjects capable of testing future innovations in combat head protection from blast and further exploring links between physical injury phenomena and downstream biological processes
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