Methodology to Study Attenuation of a Blast Wave Through the Cranium

Abstract

The purpose of the study was to quantify attenuation of open field shockwaves passing through the PMHS (Post Mortem Human Subject) cranium. A better understanding of the relationship between shockwave characteristics external to the cranium and insults experienced by the brain is essential for understanding injury mechanisms, validation of finite element models, and development of military safety devices for soldiers in the field. These relationships are being developed using experimental PMHS techniques. Our existing shock tube produced open field shockwaves by increasing input pressure behind a Mylar membrane using compressed nitrogen until the membrane burst. Increasing membrane thickness resulted in greater bursting pressure and peak shockwave pressure. Peak pressure decreased predictably with greater distance from the shock tube outlet. Input pressures between 1.6 and 3.2 MPa resulted in peak shockwave pressures between 45 kPa and 90 kPa measured between 40 and 60 cm from the shock tube exit. The experimental protocol consisted of obtaining a PMHS head, filling the voided cranium with Sylgard gel, and securing the head in front of the shock tube using a Hybrid III dummy neck. Pressure transducers were mounted on the external cranium surface on the ipsilateral side and on the internal cranium surface on the ipsilateral and contralateral sides. Because the specimen was tested in multiple orientations, the ipsilateral side referred to the frontal or temporal sides. Transducers were mounted prior to adding the Sylgard gel. Data from all tests indicated shockwave rise times less than 10 μs external to the skull and internal to the skull on the ipsilateral side. Therefore, the sampling rate was 10 MHz using a digital oscilloscope. Shockwave characteristics were quantified including peak overpressure, peak underpressure, and duration of positive phase. The results show peak overpressure attenuations between 14 and 26% from the external ipsilateral transducer to the contralateral transducers in frontal and lateral orientation. In addition, there was a 93–96% reduction in the rate of onset between those transducers. Each characteristic may affect injury type/severity. This setup can be used to understand injury mechanisms for blast-induced mTBI, to quantify effects of interventions (e.g., helmets) on attenuation of open field blast waves, and for validation of finite element models.

Behavioral Outcomes Differ between Rotational Acceleration and Blast Mechanisms of Mild Traumatic Brain Injury

“…Although not thoroughly investigated here, differences are likely attributable to pathologies affecting different brain regions, as evident in our prior MRI studies, or differing mechanisms of tissue damage based on injury model. Rotational acceleration produces inertially modulated strain-based injuries ( 57 ) whereas shock wave exposure mechanisms are less clear and have been hypothesized to create tissue damage through blast wave propagation via thoracic mechanisms, ischemic brain damage, head acceleration, direct skull deformation resulting in neuronal damage, or strain-induced tissue damage due to shock wave interaction with brain tissues ( 7 , 12 , 15 , 33 , 35 , 53 , 58 – 62 ). Nonetheless, these findings suggest that mTBI outcomes are dependent upon the mechanism of injury that has both clinical and experimental implications.…”

“…Other studies have focused on the interaction of the shock wave with brain tissues, resulting in brain tissue shear stresses ( 11 ). This mechanism is particularly relevant, given that our group has shown in a post-mortem human subject model that shock wave overpressure enters the cranium and interacts with the intracranial contents with the Friedlander waveform essentially intact, although the magnitude is somewhat attenuated ( 12 ). Once inside the cranium, the shock wave can interact with brain tissues on a local level to produce extensive neuronal death or altered neuronal function, loss of glial cells, and astrocytosis ( 13 , 14 ).…”

Effects of Blast Overpressure on Neurons and Glial Cells in Rat Organotypic Hippocampal Slice Cultures

“…Therefore, injuries and associated behavioral deficits were directly attributable to shockwave overpressure and not head rotational acceleration, skull flexure, thoracic mechanisms, or pulmonary ischemia. The concept of direct propagation of the shockwave through the cranium was proven in theory by our group using a post-mortem human subject model ( 24 ). That study determined that shockwave overpressures propagate intact through the skull and maintain the characteristic Friedlander waveform inside the cranium without significant loss of peak overpressure magnitude for blast exposures from the frontal and lateral directions.…”

Acute death of astrocytes in blast-exposed rat organotypic hippocampal slice cultures

“…It has been proposed that blast overpressure indirectly causes brain injury either via skull deformation, head acceleration, ischemia, or thoracic mechanisms [ 17 – 23 ]. However, research from our group, in addition to the results of other experts in the field, suggests that a blast shock wave can transverse the cranium intact and generate tissue stress and strain leading to neuronal damage [ 24 – 29 ]. Correspondingly, data from in vitro bTBI models [ 30 – 33 ], including our recent findings [ 34 ], imply that blast overpressure can directly damage neurons and glial cells.…”