Modelling Blast Brain Injury

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 [1]. In blast-TBI the mechanisms of brain vulnerability to the detonation of an explosive device are not entirely understood. They most likely result from a combination of the different physical aspects of the blast phenomenon, specifically extreme pressure oscillations (blast-overpressure wave – primary blast), projectile penetrating fragments (secondary blast) and acceleration-deceleration forces (tertiary blast), creating a spectrum of brain injury that ranges from mild to severe blast-TBI [2]. The pathophysiology of penetrating and inertially-driven blast-TBI has been extensively investigated for many years. However, the brain damage caused by blast-overpressure (primary blast) is much less understood and is unique to this type of TBI [3]. Indeed, there continues to be debate about how the pressure wave is transmitted and reflected through the brain and how it causes cellular damage [4]. No single model can mimic the clinical and mechanical complexity resulting from a real life blast-TBI [3]. The different models, non-biological (in silico or surrogate physical) and biological (ex vivo, in vitro or in vivo), tend to complement each other.