Quantification of Shockwave Transmission Through the Cranium Using an Experimental Model

Author(s):  
Alok S. Shah ◽  
Brian D. Stemper ◽  
Narayan Yoganandan ◽  
Barry S. Shender

Studies have hypothesized mechanisms for brain injury resulting from exposure to blast waves. Theories include shockwaves increasing fluid pressure within brain tissue by transmitting through bones and blood vessels 1, indirect brain tissue damage due to ischemia from pulmonary blast injury 2, and formation of mechanical stresses that can result in tissue distortion 3. Mechanical damage to brain tissue can occur due to skull flexure resulting in loads typically seen in impact-induced injury 4 or axonal shearing/stretching, due to linear or rotational accelerations resulting in Diffuse Axonal Injury (DAI) 5. Despite several investigations it remains unclear whether direct propagation of the shockwave through the cranium can deform brain tissue and result in mechanically-induced injury 6. Finite element 7, 8 and animal 9, 10 models provide information on mechanisms and outcomes of blast-induced mTBI (mild traumatic brain injury). However, validations of FEM studies were limited due to the paucity of high rate material properties. Animal tests were designed to understand mechanisms of shockwave transmission but most did not report intracranial pressures. Understanding blast injury mechanisms requires a better delineation of shockwave energy transfer through the head and the influence of factors including region-specific differences, and mechanical properties of brain simulant. A Post Mortem Human Subjects (PMHS) model was used in this study to examine these factors and provide an understanding of shockwave transmission through the tissues of the human head.

Author(s):  
Hesam Sarvghad-Moghaddam ◽  
Asghar Rezaei ◽  
Ashkan Eslaminejad ◽  
Mariusz Ziejewski ◽  
Ghodrat Karami

Blast-induced traumatic brain injury (bTBI), is defined as a type of acquired brain injury that occurs upon the interaction of the human head with blast-generated high-pressure shockwaves. Lack of experimental studies due to moral issues, have motivated the researchers to employ computational methods to study the bTBI mechanisms. Accordingly, a nonlinear finite element (FE) analysis was employed to study the interaction of both unprotected and protected head models with explosion pressure waves. The head was exposed to the incoming shockwaves from front, back, and side directions. The main goal was to examine the effects of head protection tools and the direction of blast waves on the tissue and kinematical responses of the brain. Generation, propagation, and interactions of blast waves with the head were modeled using an arbitrary Lagrangian-Eulerian (ALE) method and a fluid-structure interaction (FSI) coupling algorithm. The FE simulations were performed using Ls-Dyna, a transient, nonlinear FE code. Side blast predicted the highest mechanical responses for the brain. Moreover, the protection assemblies showed to significantly alter the blast flow mechanics. Use of faceshield was also observed to be highly effective in the front blast due to hindering of shockwaves.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Gozde Uzunalli ◽  
Seth Herr ◽  
Alexandra M. Dieterly ◽  
Riyi Shi ◽  
L. Tiffany Lyle

Abstract Background Blast-induced traumatic brain injury (bTBI) is a growing health concern due to the increased use of low-cost improvised explosive devices in modern warfare. Mild blast exposures are common amongst military personnel; however, these women and men typically do not have adequate recovery time from their injuries due to the transient nature of behavioral symptoms. bTBI has been linked to heterogeneous neuropathology, including brain edema, neuronal degeneration and cognitive abnormalities depending on the intensity of blast overpressure and frequency. Recent studies have reported heterogeneity in blood–brain barrier (BBB) permeability following blast injury. There still remains a limited understanding of the pathologic changes in the BBB following primary blast injuries. In this study, our goal was to elucidate the pathologic pattern of BBB damage through structural analysis following single and repetitive blast injury using a clinically relevant rat model of bTBI. Methods A validated, open-ended shock tube model was used to deliver single or repetitive primary blast waves. The pathology of the BBB was assessed using immunofluorescence and immunohistochemistry assays. All data were analyzed using the one-way ANOVA test. Results We have demonstrated that exposure to repetitive blast injury affects the desmin-positive and CD13-positive subpopulations of pericytes in the BBB. Changes in astrocytes and microglia were also detected. Conclusion This study provides analysis of the BBB components after repetitive blast injury. These results will be critical as preventative and therapeutic strategies are established for veterans recovering from blast-induced traumatic brain injury.


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