Cerebrospinal Fluid Cavitation as a Mechanism of Blast-Induced Traumatic Brain Injury: A Review of Current Debates, Methods, and Findings

Abstract

Cavitation has gained popularity in recent years as a potential mechanism of blast-induced traumatic brain injury (bTBI). This review presents the most prominent debates on cavitation; how bubbles can form or exist within the cerebrospinal fluid (CSF) and brain vasculature, potential mechanisms of cellular, and tissue level damage following the collapse of bubbles in response to local pressure fluctuations, and a survey of experimental and computational models used to address cavitation research questions. Due to the broad and varied nature of cavitation research, this review attempts to provide a necessary synthesis of cavitation findings relevant to bTBI, and identifies key areas where additional work is required. Fundamental questions about the viability and likelihood of CSF cavitation during blast remain, despite a variety of research regarding potential injury pathways. Much of the existing literature on bTBI evaluates cavitation based off its prima facie plausibility, while more rigorous evaluation of its likelihood becomes increasingly necessary. This review assesses the validity of some of the common assumptions in cavitation research, as well as highlighting outstanding questions that are essential in future work.

Keywords: BTBI; blastinjury; cavitation; cerebrospinal fluid; injury-head trauma.

Figure 1

Outstanding questions and debates in cavitation research described in this review. The largest bubble represents the central question of cavitation in bTBI research. Underlying questions and their theoretical solutions are labeled in the second largest bubble clusters, with logistical questions and possible approaches shown in the smallest clusters.

Figure 2

Planar Friedlander waveform adapted from Chandra et al. (37). In the figure, the instantaneous overpressure p⁺ at time t is defined using the peak overpressure p^*, positive phase duration t_d, and decay constant b.