Blast Response of Protective Armor Concepts Using an Arm Surrogate

Simmonds, K. E.; Bagchi, Amit; Matic, Peter; Leung, Alan C.; Pogue, W. M.; Thompson, A.; Strain, John; Gauvin, J. E.

doi:10.1115/imece2010-39025

Cited by 1 publication

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“…Reconstructions of actual human blast exposures can also be used to greater benefit in validating models and elucidating mechanisms. Helmet mounted sensor systems have been fielded since at least 2009 ( 59 ), so there should be some body of data available to compare exposures with resulting injuries. There is also the potential to utilize bodies of data related to human exposure to muzzle blasts of cannon ( 84 ), exposure of entry teams to breaching blasts ( 10 , 85 ), and exposure of room occupants near flash grenades.…”

Section: Discussionmentioning

confidence: 99%

The Complexity of Biomechanics Causing Primary Blast-Induced Traumatic Brain Injury: A Review of Potential Mechanisms

Courtney

Courtney²

2015

Front. Neurol.

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Primary blast-induced traumatic brain injury (bTBI) is a prevalent battlefield injury in recent conflicts, yet biomechanical mechanisms of bTBI remain unclear. Elucidating specific biomechanical mechanisms is essential to developing animal models for testing candidate therapies and for improving protective equipment. Three hypothetical mechanisms of primary bTBI have received the most attention. Because translational and rotational head accelerations are primary contributors to TBI from non-penetrating blunt force head trauma, the acceleration hypothesis suggests that blast-induced head accelerations may cause bTBI. The hypothesis of direct cranial transmission suggests that a pressure transient traverses the skull into the brain and directly injures brain tissue. The thoracic hypothesis of bTBI suggests that some combination of a pressure transient reaching the brain via the thorax and a vagally mediated reflex result in bTBI. These three mechanisms may not be mutually exclusive, and quantifying exposure thresholds (for blasts of a given duration) is essential for determining which mechanisms may be contributing for a level of blast exposure. Progress has been hindered by experimental designs, which do not effectively expose animal models to a single mechanism and by over-reliance on poorly validated computational models. The path forward should be predictive validation of computational models by quantitative confirmation with blast experiments in animal models, human cadavers, and biofidelic human surrogates over a range of relevant blast magnitudes and durations coupled with experimental designs, which isolate a single injury mechanism.

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