Abstract
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.
Highlights
AND BACKGROUNDBlast-induced traumatic brain injury is not a new battlefield injury1
Physiological responses are mediated by the vagus nerve [13, 38]; shows that pressure waves initiated in the thorax can cause cerebral effects [17, 37] EEG signals were immediately suppressed even in vagotomized animals [39]
In animals with torso protection only, acute and chronic responses in the brain were significantly less than in animals with head protection only or that experienced whole body exposure. These results suggest that, for this level of exposure, thoracic, and other mechanisms contributed to the BACKGROUNDBlast-induced traumatic brain injury (bTBI); the thoracic mechanism was a significant contributor to the overall injury, which was dramatically reduced by thoracic protection
Summary
Blast-induced traumatic brain injury (bTBI) is not a new battlefield injury. Beginning in the late 1990s and increasingly since, bTBI has gained military. Mechanisms of primary bTBI and public prominence in the U.S as an injury that needs to be prevented as well as treated. Between 2000 and 2014, more than 300,000 American soldiers were diagnosed with traumatic brain injury of any type [2]2. The sharp increase in mild TBI beginning in 2006, as well as field data indicating that 50–80% of battlefield injuries have been due to blast exposure, are consistent with the increase in mild TBI cases resulting from blast exposure [3, 4]. Effective solutions are needed for military, humanitarian, and economic reasons
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