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.

This content is only available via PDF.
You do not currently have access to this content.