Research on cavitation as a bTBI mechanism has been conducted in a variety of fields, using multiple approaches and outcome measures. These computational models and experimental outcomes are explored in later sections of this review, but range from finite element (FE) models to shock tube experiments. Computational approaches and a range of experimental techniques are being applied to cavitation problems. Further, the specific manner through which cavitation may lead to cellular and tissue damage is similarly unclear.Ĭavitation research has greatly expanded in the last 5 years, in terms of number of publications, as well as variety in study designs ( 10– 13). However, there is currently no conclusive evidence that realistic blast scenarios lead to CSF cavitation. Cavitation refers to the formation and subsequent collapse of bubbles formed in response to local pressure fluctuations within a fluid. One of the most commonly theorized bTBI mechanisms involves the formation and bursting of cavitation bubbles within the cerebrospinal fluid (CSF), appearing in literature as early as the 1950's ( 9). Thus, hindering the critical design of optimal protective gear to mitigate bTBI and improve treatment plans for persons exposed to blast waves.
A single blast exposure, without secondary injury (e.g., blunt and penetrating injury, for example, due to shrapnel), can lead to pathological symptoms, cognitive deficits, behavioral changes, and mood disorders ( 6).ĭespite an array of research on likely TBI mechanisms, there is not a clear and unified injury pathway in the case of blast injury ( 7, 8). In the first three quarters of 2019 alone, 15,262 cases of bTBI were diagnosed, and these numbers only represent the first blast exposure reported by a given service member, meaning the number of injuries is even larger when repeated blast exposures to the same individual are taken into account ( 5). 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).
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