Mechanisms of blast-induced Traumatic Brain Injury (BTBI), particularly those linked to the primary pressure wave, are still not fully understood. One possible BTBI mechanism is cavitation in the cerebrospinal fluid (CSF) caused by CSF tensile failure, which is likely to increase strain and strain rate in the brain tissue near the CSF. Blast loading of the head can generate rarefaction (expansion) waves and rapid head motion, which both can produce tensile forces in the CSF. However, it is not clear which of these mechanisms is more likely to cause CSF tensile failure. In this study, we used a high-fidelity 3-dimensional computational model of the human head to test whether the CSF tensile failure increases brain deformation near the brain/CSF boundary and to determine the key failure mechanisms. We exposed the head model to a frontal blast wave and predicted strain and strain rate distribution in the cortex. We found that CSF tensile failure significantly increased strain and strain rate in the cortex. We then studied whether the rapid head motion or the rarefaction wave causes strain and strain rate concentration in cortex. We isolated these two effects by conducting simulations with pure head motion loading (i.e. prescribing the skull velocity but eliminating the pressure wave) and pure blast wave loading (i.e. eliminating head motion by fixing the skull base). Our results showed that the strain increase in the cortex was mainly caused by head motion. In contrast, strain rate increase was caused by both rapid head motion and rarefaction waves, but head motion had a stronger effect on elevating strain rate. Our results show that rapid motion of the head produced by blast wave is the key mechanism for CSF tensile failure and subsequent concentration of strain and strain rate in cortex. This finding suggests that mitigation of rapid head motion caused by blast loading needs to be addressed in the design of protective equipment in order to prevent the tensile failure of CSF.

爆炸引起的颅脑外伤（BTBI）的机制，特别是与原发性压力波有关的机制，仍未被完全了解。一种可能的BTBI机制是由CSF拉伸衰竭引起的脑脊液（CSF）的空化，这很可能会增加CSF附近脑组织的应变和应变率。头部的爆炸载荷会产生稀疏（膨胀）波和快速的头部运动，这两者都会在CSF中产生拉力。但是，尚不清楚这些机制中的哪一个更可能导致CSF拉伸破坏。在这项研究中，我们使用了人类头部的高保真3D计算模型来测试CSF拉伸衰竭是否会增加大脑/ CSF边界附近的大脑变形，并确定关键的失效机制。我们将头部模型暴露于额叶冲击波，并预测皮层中的应变和应变率分布。我们发现脑脊液拉伸失败显着增加了皮质中的应变和应变率。然后，我们研究了头部的快速运动或稀疏波是否会引起皮质中的应变和应变率集中。我们通过进行纯头部运动载荷（即规定颅骨速度但消除压力波）和纯爆炸波载荷（即通过固定颅骨基座消除头部运动）的模拟来隔离这两种效果。我们的结果表明，皮质中的应变增加主要是由于头部运动引起的。相反，应变率的增加是由头部的快速运动和稀疏波引起的，但是头部运动对提高应变率的影响更大。我们的研究结果表明，爆炸产生的头部快速运动是导致CSF拉伸破坏以及随后的皮质集中应变和应变率的关键机制。这一发现表明，在保护设备的设计中需要解决由爆炸载荷引起的快速头部运动的减轻，以防止CSF的拉伸破坏。