Exposure to the blast wave can cause life-threatening injuries and fatalities, with the outcome depending on factors such as how close the individual is to the source and the overpressure (i.e., shock wave) amplitude created ( 3). The bTBI occurs when a blast wave, created by detonating improvised explosive devices (IEDs), propagates through the head of an individual ( 2– 4). There have been over 383,000 traumatic brain injuries (TBIs) reported by military service members since 2000, with blast-induced traumatic brain injury (bTBI) being the most common injury ( 1). 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. 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. Fundamental questions about the viability and likelihood of CSF cavitation during blast remain, despite a variety of research regarding potential injury pathways. 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. 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.
The Bentil Group, Department of Mechanical Engineering, Iowa State University, Ames, IA, United StatesĬavitation has gained popularity in recent years as a potential mechanism of blast-induced traumatic brain injury (bTBI).
0 kommentar(er)
