Microcavitation: the key to modeling blast traumatic brain injury?

Abstract

Traumatic brain injuries (TBIs) are a significant source of deaths and disabilities worldwide with an associated healthcare burden in the billions of dollars [1]. Brain injuries generally result from either direct impact, blast or rapid acceleration and deceleration of the brain, and their severity is graded neurosymptomatically from mild to severe using the Glasgow Coma Scale. While these injuries, which in their mild form include concussions, are generally initiated by mechanical stress waves traveling through the brain resulting in exceeding tissue damage quantified as either compressive, tensile or shearing strains [2–4], blast TBIs have a slightly different origin, and as thus their injury mechanism and pathology remain an active topic of research [5,6]. In blast waves generated from explosions, including improvised explosive devices (IEDs) [6,7], the initial blast-generated shock wave profile features a sudden increase in pressure, often referred to as overpressure, followed by a low magnitude long-range negative pressure tail [5,7]. This profile is significantly different from most civilian blunt head impact scenarios, which, at least initially, are almost entirely composed of fast traveling pressure waves [5]. These shock-like pressure profiles introduce significant pressure changes across the brain on the order of a microto submilliseconds, whereas typical blunt trauma stresses change over the course of milliseconds and above. The classification of blast TBI has its own categorization from primary to quaternary blast injury [6]. Secondary to quaternary blast injuries have correlates in the civilian world whereas primary blast injuries that are classified by the interaction of the blast wave itself with the brain are unique to military and law enforcement personnel. Details of the origin of the injury and its pathology have remained elusive. Part of the challenge in dissecting the details of blast injury lies in the complex physical interaction between the fast moving pressure wave and the compliant brain. Furthermore, our understanding of the deformation behavior of soft brain tissue and its relationship to specific neuropathologies is still in its infancy. Although the initial blast wave is generally a pure pressure wave, it can turn into part pressure and part shear wave upon encountering the complex geometry of the human head and brain. While the traversing pressure wave will cause the tissue to undergo changes in volume, the shear wave can generate significant changes in shape, or shearing strains. In addition, part of the original pressure wave can reflect off a boundary of lower impedance, which is marked by either changes in tissue density or compliance, resulting in a negative, tensile, pressure reflection wave [8]. While a significant body of work has begun to detail the interaction of the compressive part of the wave with brain tissue and its cells [9–12], we will focus our attention here on the negative, or tensile character of the pressure wave. Recent experimental and finite element investigations simulating blasts to the head and brain have shown that these negative, tensile region of pressure can give rise to the phenomenon known as cavitation, which generally denotes the formation of vapor bubbles from a liquid [13,14]. Cavitation Microcavitation: the key to modeling blast traumatic brain injury?