Interface-driven human brain injury mechanisms in blast exposure: A fluid–structure interaction model

Q3 Medicine
Joseph Amponsah , Archibong Archibong-Eso , Y.A.K. Fiagbe , Richard Bruce , Tabbi Wilberforce Awotwe , Samuel Adjei
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引用次数: 0

Abstract

Blast-induced traumatic brain injury (bTBI) presents a significant challenge for military personnel and civilians exposed to explosions. Beyond combat, bTBI can arise from civilian incidents like industrial accidents (chemical-plant or mining blasts), accidental demolition blasts, fireworks factory explosions, and residential gas-leak detonations. The precise mechanisms by which blast waves damage the brain are still developing. Studies suggest that bTBI is primarily an interface-driven injury, where mechanical forces concentrate at anatomical boundaries including gray–white matter junctions, cortical sulci, cerebrospinal fluid (CSF) spaces, and perivascular structures. Recent research has shown that fluid structure interaction (FSI) simulations are instrumental in capturing shock wave transmission through the skull, CSF, and brain tissue, directly informing the design of protective gear. Here, we developed a high-resolution FSI model of the human head with approximately five million elements and detailed anatomical features (sulci, gyri, CSF compartments, vascular structures) to examine these biomechanical interactions. We employed Friedlander waveform to simulate the blast wave, with adjustments for attenuation through the skull and pressure transmission into the CSF and brain, with peak overpressures ranging from 100 to 1000 kPa and durations up to 6 ms. Our findings indicate that local CSF pressures dropping below its vapor pressure (around –90 kPa) can initiate cavitation, particularly within sulcal and ventricular spaces. This cavitation is accompanied by elevated shear stresses at adjacent gray–white matter interfaces, with strain rates exceeding 250 s−1, co-localizing with diffuse axonal injury (DAI) thresholds. Higher overpressures (500 kPa) also induced intraventricular cavitation and elevated periventricular strain rates. Blast orientation significantly influenced injury distribution, lateral blasts resulted in more diffuse stress fields, while frontal blasts localized damage to anterior cortical regions.
爆炸暴露中界面驱动的人脑损伤机制:一个流固耦合模型
爆炸引起的创伤性脑损伤(bTBI)对暴露在爆炸中的军事人员和平民来说是一个重大挑战。除战斗外,创伤性脑损伤还可能由民用事故引起,如工业事故(化工厂或矿山爆炸)、意外爆破、烟花工厂爆炸和住宅瓦斯泄漏爆炸。爆炸冲击波损伤大脑的确切机制仍在研究中。研究表明,脑损伤主要是一种界面驱动型损伤,机械力集中在解剖边界,包括灰质交界处、皮质沟、脑脊液间隙和血管周围结构。最近的研究表明,流体结构相互作用(FSI)模拟有助于捕捉冲击波通过颅骨、脑脊液和脑组织的传输,直接为防护装置的设计提供信息。在这里,我们开发了一个高分辨率的人类头部FSI模型,其中包含大约500万个元素和详细的解剖特征(脑沟、脑回、脑脊液室、血管结构),以检查这些生物力学相互作用。我们采用Friedlander波形来模拟爆炸冲击波,并对冲击波通过颅骨的衰减和压力传递到脑脊液和大脑进行了调整,峰值超压范围为100至1000kpa,持续时间长达6ms。我们的研究结果表明,局部脑脊液压力低于其蒸汽压(约- 90kpa)可引发空化,特别是在脑沟和脑室间隙。这种空化伴随着邻近灰质界面剪切应力的升高,应变速率超过250 s−1,与弥漫性轴索损伤(DAI)阈值共定位。较高的超压(500kpa)也会引起室内空化和室周应变率升高。爆炸方向对损伤分布有显著影响,侧面爆炸使应力场更分散,而正面爆炸使损伤局限于前皮质区。
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来源期刊
Medicine in Novel Technology and Devices
Medicine in Novel Technology and Devices Medicine-Medicine (miscellaneous)
CiteScore
3.00
自引率
0.00%
发文量
74
审稿时长
64 days
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