Modelling Blast Brain Injury

Abstract

The consequences of blast traumatic brain injury (blast-TBI) in humans are largely determined by the characteristics of the trauma insult and, within certain limits, the individual responses to the lesions inflicted (Maas et al., Lancet Neurol. 2008;7:728–41). In blast-TBI, the mechanisms of brain vulnerability to the detonation of an explosive device are not completely understood. They most likely result from a combination of the different physical aspects of the blast phenomenon, specifically extreme pressure oscillations (blast overpressure wave), projectile penetrating fragments and acceleration–deceleration forces, creating a spectrum of brain injury that ranges from mild to severe blast-TBI (Hicks et al., J Trauma. 2010; 68:1257-63). The pathophysiology of penetrating and inertially driven blast-TBI has been extensively investigated for many years. However, the brain damage caused by blast overpressure is much less understood and is unique to this type of TBI (Chen et al., J Neurotrauma. 2009; 26:861–76). Indeed, there continues to be debate about how the pressure wave is transmitted and reflected through the brain and how it causes cellular damage (Nakagawa et al., J Neurotrauma. 2011; 28:1101–19). No single model can mimic the clinical and mechanical complexity resulting from a real-life blast-TBI (Chen et al., J Neurotrauma. 2009; 26:861–76). The different models, non-biological (in silico or surrogate physical) and biological (ex vivo, in vitro or in vivo), tend to complement each other.