Cavitation in blast induced traumatic brain injury: the occurrence, mechanism, threshold and implication

Abstract

Blast induced traumatic brain injury (BTBI) has been a prevalent injury in recent conflicts, due to the vast use of improvised explosive devices. However, the mechanisms for BTBI remain unclear, particularly those linked to the primary blast waves. Recent neuropathological analysis have shown damage in the brain tissue close to the cerebrospinal fluid (CSF) in blast compared with non-blast TBI cases. CSF cavitation is a potential mechanism for this interface injury. This project aims to deepen the current understanding of CSF cavitation in the human head under blast exposures. Both computational and experimental studies have been carried out to investigate the occurrence, mechanism, threshold and implication of blast induced CSF cavitation. Firstly, several commonly used methods for simulating blast wave propagation in air and its interaction with the human head were critically assessed. Together with a new meshing topology, a finite element method was proposed, which was used as a guideline for blast simulation in this project. Next, using a high-fidelity human head FE model, the CSF cavitation effect on brain response under blast exposure was investigated. It was found that CSF cavitation significantly increased strain and strain rate in the cortex. To experimentally investigate CSF cavitation, a novel human head physical surrogate was developed and exposed to both blast and impact loadings. Particularly, the dissolved air in the CSF surrogate was kept at a similar level with in-vivo human CSF. It was shown that blast, and not impact, can produce CSF cavitation. A novel mechanism for the formation and collapse of cavitation in the CSF was proposed, which is based on the transmission and interaction of pressure waves in the skull and intracranial soft tissues. The blast induced pressure waves in the skull and intracranial soft tissues are respectively responsible for cavitation formation and collapse. Next, more blast tests were conducted with the physical surrogate to determine the pressure threshold for CSF cavitation. Finally, using the human head FE model, it was found that the incident overpressure, not the positive phase duration, determines the cavitation severity in CSF. It was also found that blasts characterized as non-lethal can already produce severe CSF cavitation. This project provides new understandings to CSF cavitation in BTBI. The findings about cavitation onset and collapse in the CSF may explain the concentration of pathology at the CSF/brain tissue interface in BTBI cases. The new experimental and computational methods and findings can guide the diagnosis of BTBI by focusing on interfaces and the evaluation and improvement of protective equipment.