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.

Cavitation induced fracture of intact brain tissue

“…Both numerical simulations and experiments indicate that cavitation may be a damage mechanism contributing to TBI from blast [69]- [72]. The specific mechanism by which cavitation damages tissue is still unclear, be it bubble collapse, cell membrane interruption, blood-brain barrier disruption, or water jet formation [73]. Although cavitation-induced damage has been measured in brain slices and cell culture systems [74]- [76], there is still a missing link that connects cavitation to fracture.…”

Dependence on Anesthesiology Support in Victims With Combined Mine-Explosive Thoraco-Abdominal Injuries and Penetrating Head Injuries at the Stage of Preparation and Conducting of Aeromedical Evacuation

“…Explosive explosive injuries account for more than 50% of all injuries received in military battles, and the proportion of casualties among the civilian population is also increasing [1]. However, only limited research has been conducted on the pathophysiology of blast-induced brain injury, and the effect of changes in cerebral blood flow (CBF) or cerebral vascular reactivity on blast-induced brain injury has not been investigated [2]. Although secondary hypotension and hypoxemia are associated with increased mortality and morbidity after blunt head injury, the effect of secondary injury factors in blast injury is unknown [2].…”

“…However, only limited research has been conducted on the pathophysiology of blast-induced brain injury, and the effect of changes in cerebral blood flow (CBF) or cerebral vascular reactivity on blast-induced brain injury has not been investigated [2]. Although secondary hypotension and hypoxemia are associated with increased mortality and morbidity after blunt head injury, the effect of secondary injury factors in blast injury is unknown [2]. TBI itself causes cerebral hypoperfusion, reduced oxygen delivery to the brain, excitotoxicity, and disruption of cerebral blood flow autoregulation, which explains the vulnerability of the affected brain to hypoxia and hypotension caused by blood loss [2,3].…”

“…Although secondary hypotension and hypoxemia are associated with increased mortality and morbidity after blunt head injury, the effect of secondary injury factors in blast injury is unknown [2]. TBI itself causes cerebral hypoperfusion, reduced oxygen delivery to the brain, excitotoxicity, and disruption of cerebral blood flow autoregulation, which explains the vulnerability of the affected brain to hypoxia and hypotension caused by blood loss [2,3].…”

Activation of autophagy after blast-induced traumatic brain injury in mice

“…bTBI has a variety of injury mechanisms, resulting in its more complex clinical manifestations than general TBI [3]. Although there are many studies on various injury mechanism and treatment, no breakthrough has been made [4,5].…”