Rate- and Region-Dependent Mechanical Properties of Göttingen Minipig Brain Tissue in Simple Shear and Unconfined Compression.

Traumatic brain injury (TBI), particularly from explosive blasts, is a major cause of casualties in modern military conflicts. Computational models are an important tool in understanding the underlying biomechanics of TBI but are highly dependent on the mechanical properties of soft tissue to produce accurate results. Reported material properties of brain tissue can vary by several orders of magnitude between studies, and no published set of material parameters exists for porcine brain tissue at strain rates relevant to blast. In this work, brain tissue from the brainstem, cerebellum, and cerebrum of freshly euthanized adolescent male Göttingen minipigs was tested in simple shear and unconfined compression at strain rates ranging from quasi-static (QS) to 300 s-1. Brain tissue showed significant strain rate stiffening in both shear and compression. Minimal differences were seen between different regions of the brain. Both hyperelastic and hyper-viscoelastic constitutive models were fit to experimental stress, considering data from either a single loading mode (unidirectional) or two loading modes together (bidirectional). The unidirectional hyper-viscoelastic models with an Ogden hyperelastic representation and a one-term Prony series best captured the response of brain tissue in all regions and rates. The bidirectional models were generally able to capture the response of the tissue in high-rate shear and all compression modes, but not the QS shear. Our constitutive models describe the first set of material parameters for porcine brain tissue relevant to loading modes and rates seen in blast injury.

Effect of stride length on the running biomechanics of healthy women of different statures.

BACKGROUND: Tibial stress fracture is a debilitating musculoskeletal injury that diminishes the physical performance of individuals who engage in high-volume running, including Service members during basic combat training (BCT) and recreational athletes. While several studies have shown that reducing stride length decreases musculoskeletal loads and the potential risk of tibial injury, we do not know whether stride-length reduction affects individuals of varying stature differently. METHODS: We investigated the effects of reducing the running stride length on the biomechanics of the lower extremity of young, healthy women of different statures. Using individualized musculoskeletal and finite-element models of women of short (N = 6), medium (N = 7), and tall (N = 7) statures, we computed the joint kinematics and kinetics at the lower extremity and tibial strain for each participant as they ran on a treadmill at 3.0 m/s with their preferred stride length and with a stride length reduced by 10%. Using a probabilistic model, we estimated the stress-fracture risk for running regimens representative of U.S. Army Soldiers during BCT and recreational athletes training for a marathon. RESULTS: When study participants reduced their stride length by 10%, the joint kinetics, kinematics, tibial strain, and stress-fracture risk were not significantly different among the three stature groups. Compared to the preferred stride length, a 10% reduction in stride length significantly decreased peak hip (p = 0.002) and knee (p < 0.001) flexion angles during the stance phase. In addition, it significantly decreased the peak hip adduction (p = 0.013), hip internal rotation (p = 0.004), knee extension (p = 0.012), and ankle plantar flexion (p = 0.026) moments, as well as the hip, knee, and ankle joint reaction forces (p < 0.001) and tibial strain (p < 0.001). Finally, for the simulated regimens, reducing the stride length decreased the relative risk of stress fracture by as much as 96%. CONCLUSIONS: Our results show that reducing stride length by 10% decreases musculoskeletal loads, tibial strain, and stress-fracture risk, regardless of stature. We also observed large between-subject variability, which supports the development of individualized training strategies to decrease the incidence of stress fracture.

A Strain Rate-Dependent Constitutive Model for Göttingen Minipig Cerebral Arteries.

Computational simulations of traumatic brain injury (TBI) are commonly used to advance understanding of the injury-pathology relationship, tissue damage thresholds, and design of protective equipment such as helmets. Both human and animal TBI models have developed substantially over recent decades, partially due to the inclusion of more detailed brain geometry and representation of tissues like cerebral blood vessels. Explicit incorporation of vessels dramatically affects local strain and enables researchers to investigate TBI-induced damage to the vasculature. While some studies have indicated that cerebral arteries are rate-dependent, no published experimentally based, rate-sensitive constitutive models of cerebral arteries exist. In this work, we characterize the mechanical properties of axially failed porcine arteries, both quasi-statically (0.01 s-1) and at high rate (>100 s-1), and propose a rate-sensitive model to fit the data. We find that the quasi-static and high-rate stress-stretch curves become significantly different (p < 0.05) above a stretch of 1.23. We additionally find a significant change in both failure stretch and stress as a result of strain rate. The stress-stretch curve is then modeled as a Holzapfel-Gasser-Ogden material, with a Prony series added to capture the effects of viscoelasticity. Ultimately, this paper demonstrates that rate dependence should be considered in the material properties of cerebral arteries undergoing high strain-rate deformations and provides a ready-to-use model for finite element implementation.

The importance of modeling the human cerebral vasculature in blunt trauma.

BACKGROUND: Multiple studies describing human head finite element (FE) models have established the importance of including the major cerebral vasculature to improve the accuracy of the model predictions. However, a more detailed network of cerebral vasculature, including the major veins and arteries as well as their branch vessels, can further enhance the model-predicted biomechanical responses and help identify correlates to observed blunt-induced brain injury. METHODS: We used an anatomically accurate three-dimensional geometry of a 50th percentile U.S. male head that included the skin, eyes, sinuses, spine, skull, brain, meninges, and a detailed network of cerebral vasculature to develop a high-fidelity model. We performed blunt trauma simulations and determined the intracranial pressure (ICP), the relative displacement (RD), the von Mises stress, and the maximum principal strain. We validated our detailed-vasculature model by comparing the model-predicted ICP and RD values with experimental measurements. To quantify the influence of including a more comprehensive network of brain vessels, we compared the biomechanical responses of our detailed-vasculature model with those of a reduced-vasculature model and a no-vasculature model. RESULTS: For an inclined frontal impact, the predicted ICP matched well with the experimental results in the fossa, frontal, parietal, and occipital lobes, with peak-pressure differences ranging from 2.4% to 9.4%. For a normal frontal impact, the predicted ICP matched the experimental results in the frontal lobe and lateral ventricle, with peak-pressure discrepancies equivalent to 1.9% and 22.3%, respectively. For an offset parietal impact, the model-predicted RD matched well with the experimental measurements, with peak RD differences of 27% and 24% in the right and left cerebral hemispheres, respectively. Incorporating the detailed cerebral vasculature did not influence the ICP but redistributed the brain-tissue stresses and strains by as much as 30%. In addition, our detailed-vasculature model predicted strain reductions by as much as 28% when compared to current reduced-vasculature FE models that only include the major cerebral vessels. CONCLUSIONS: Our study highlights the importance of including a detailed representation of the cerebral vasculature in FE models to more accurately estimate the biomechanical responses of the human brain to blunt impact.

Animal Orientation Affects Brain Biomechanical Responses to Blast-Wave Exposure.

In this study, we investigated how animal orientation within a shock tube influences the biomechanical responses of the brain and cerebral vasculature of a rat when exposed to a blast wave. Using three-dimensional finite element (FE) models, we computed the biomechanical responses when the rat was exposed to the same blast-wave overpressure (100 kPa) in a prone (P), vertical (V), or head-only (HO) orientation. We validated our model by comparing the model-predicted and the experimentally measured brain pressures at the lateral ventricle. For all three orientations, the maximum difference between the predicted and measured pressures was 11%. Animal orientation markedly influenced the predicted peak pressure at the anterior position along the midsagittal plane of the brain (P = 187 kPa; V = 119 kPa; and HO = 142 kPa). However, the relative differences in the predicted peak pressure between the orientations decreased at the medial (21%) and posterior (7%) positions. In contrast to the pressure, the peak strain in the prone orientation relative to the other orientations at the anterior, medial, and posterior positions was 40-88% lower. Similarly, at these positions, the cerebral vasculature strain in the prone orientation was lower than the strain in the other orientations. These results show that animal orientation in a shock tube influences the biomechanical responses of the brain and the cerebral vasculature of the rat, strongly suggesting that a direct comparison of changes in brain tissue observed from animals exposed at different orientations can lead to incorrect conclusions.

Regional Changes in Density and Microarchitecture in the Ultradistal Tibia of Female Recruits After U.S. Army Basic Combat Training.

Musculoskeletal injuries, such as stress fracture, are responsible for over 10-million lost-duty days among U.S. Army Soldiers. During Basic Combat Training (BCT), an 8- to 10-week program that transforms civilians into Soldiers, women are four times more likely than men to sustain a stress fracture. In this work, we performed high-resolution peripheral quantitative computed tomography scans on the ultradistal tibia of 90 female recruits [age = 21.5 ± 3.3 (mean ± standard deviation) years] before the start of BCT and after 8 weeks into BCT. Then, we divided the scanned bone volume into four sectors-lateral, posterior, medial, and anterior-and computed the bone density and microarchitectural parameters in each of the four sectors pre- and post-BCT. We used linear mixed models to estimate the mean difference for bone density and microarchitectural parameters, while controlling for age, race, and pre-BCT body mass index. Our results revealed that the total volumetric bone mineral density, trabecular volumetric bone mineral density, and trabecular thickness increased (p < 0.05) in each of the four sectors. In addition, cortical thickness and trabecular bone volume/total volume increased in both medial and posterior sectors (p < 0.05). Overall, six and five out of nine parameters improved in the medial and posterior sectors, respectively, after BCT. In conclusion, the heightened physical activity during BCT led to the most beneficial bone adaptation in the medial and posterior sectors of the ultradistal tibia, which is indicative of higher loading in these sectors during activities performed in the course of BCT.

Region specific anisotropy and rate dependence of Göttingen minipig brain tissue.

Traumatic brain injury is a major cause of morbidity in civilian as well as military populations. Computational simulations of injurious events are an important tool to understanding the biomechanics of brain injury and evaluating injury criteria and safety measures. However, these computational models are highly dependent on the material parameters used to represent the brain tissue. Reported material properties of tissue from the cerebrum and cerebellum remain poorly defined at high rates and with respect to anisotropy. In this work, brain tissue from the cerebrum and cerebellum of male Göttingen minipigs was tested in one of three directions relative to axon fibers in oscillatory simple shear over a large range of strain rates from 0.025 to 250 s-1. Brain tissue showed significant direction dependence in both regions, each with a single preferred loading direction. The tissue also showed strong rate dependence over the full range of rates considered. Transversely isotropic hyper-viscoelastic constitutive models were fit to experimental data using dynamic inverse finite element models to account for wave propagation observed at high strain rates. The fit constitutive models predicted the response in all directions well at rates below 100 s-1, after which they adequately predicted the initial two loading cycles, with the exception of the 250 s-1 rate, where models performed poorly. These constitutive models can be readily implemented in finite element packages and are suitable for simulation of both conventional and blast injury in porcine, especially Göttingen minipig, models.

Differences in running biomechanics between young, healthy men and women carrying external loads.

During U.S. Army basic combat training (BCT), women are more prone to lower-extremity musculoskeletal injuries, including stress fracture (SF) of the tibia, with injury rates two to four times higher than those in men. There is evidence to suggest that the different injury rates are, in part, due to sex-specific differences in running biomechanics, including lower-extremity joint kinematics and kinetics, which are not fully understood, particularly when running with external load. To address this knowledge gap, we collected computed tomography images and motion-capture data from 41 young, healthy adults (20 women and 21 men) running on an instrumented treadmill at 3.0 m/s with loads of 0.0 kg, 11.3 kg, or 22.7 kg. Using individualized computational models, we quantified the running biomechanics and estimated tibial SF risk over 10 weeks of BCT, for each load condition. Across all load conditions, compared to men, women had a significantly smaller flexion angle at the trunk (16.9%-24.6%) but larger flexion angles at the ankle (14.0%-14.7%). Under load-carriage conditions, women had a larger flexion angle at the hip (17.7%-23.5%). In addition, women had a significantly smaller hip extension moment (11.8%-20.0%) and ankle plantarflexion moment (10.2%-14.3%), but larger joint reaction forces (JRFs) at the hip (16.1%-22.0%), knee (9.1%-14.2%), and ankle (8.2%-12.9%). Consequently, we found that women had a greater increase in tibial strain and SF risk than men as load increases, indicating higher susceptibility to injuries. When load carriage increased from 0.0 kg to 22.7 kg, SF risk increased by about 250% in women but only 133% in men. These results provide quantitative evidence to support the Army's new training and testing doctrine, as it shifts to a more personalized approach that shall account for sex and individual differences.

A biomechanical-based approach to scale blast-induced molecular changes in the brain.

Animal studies provide valuable insights on how the interaction of blast waves with the head may injure the brain. However, there is no acceptable methodology to scale the findings from animals to humans. Here, we propose an experimental/computational approach to project observed blast-induced molecular changes in the rat brain to the human brain. Using a shock tube, we exposed rats to a range of blast overpressures (BOPs) and used a high-fidelity computational model of a rat head to correlate predicted biomechanical responses with measured changes in glial fibrillary acidic protein (GFAP) in rat brain tissues. Our analyses revealed correlates between model-predicted strain rate and measured GFAP changes in three brain regions. Using these correlates and a high-fidelity computational model of a human head, we determined the equivalent BOPs in rats and in humans that induced similar strain rates across the two species. We used the equivalent BOPs to project the measured GFAP changes in the rat brain to the human. Our results suggest that, relative to the rat, the human requires an exposure to a blast wave of a higher magnitude to elicit similar brain-tissue responses. Our proposed methodology could assist in the development of safety guidelines for blast exposure.

Cerebral Vasculature Influences Blast-Induced Biomechanical Responses of Human Brain Tissue.

Multiple finite-element (FE) models to predict the biomechanical responses in the human brain resulting from the interaction with blast waves have established the importance of including the brain-surface convolutions, the major cerebral veins, and using non-linear brain-tissue properties to improve model accuracy. We hypothesize that inclusion of a more detailed network of cerebral veins and arteries can further enhance the model-predicted biomechanical responses and help identify correlates of blast-induced brain injury. To more comprehensively capture the biomechanical responses of human brain tissues to blast-wave exposure, we coupled a three-dimensional (3-D) detailed-vasculature human-head FE model, previously validated for blunt impact, with a 3-D shock-tube FE model. Using the coupled model, we computed the biomechanical responses of a human head facing an incoming blast wave for blast overpressures (BOPs) equivalent to 68, 83, and 104 kPa. We validated our FE model, which includes the detailed network of cerebral veins and arteries, the gyri and the sulci, and hyper-viscoelastic brain-tissue properties, by comparing the model-predicted intracranial pressure (ICP) values with previously collected data from shock-tube experiments performed on cadaver heads. In addition, to quantify the influence of including a more comprehensive network of brain vessels, we compared the biomechanical responses of our detailed-vasculature model with those of a reduced-vasculature model and a no-vasculature model for the same blast-loading conditions. For the three BOPs, the predicted ICP values matched well with the experimental results in the frontal lobe, with peak-pressure differences of 4-11% and phase-shift differences of 9-13%. As expected, incorporating the detailed cerebral vasculature did not influence the ICP, however, it redistributed the peak brain-tissue strains by as much as 30% and yielded peak strain differences of up to 7%. When compared to existing reduced-vasculature FE models that only include the major cerebral veins, our high-fidelity model redistributed the brain-tissue strains in most of the brain, highlighting the importance of including a detailed cerebral vessel network in human-head FE models to more comprehensively account for the biomechanical responses induced by blast exposure.

Investigation of the direct and indirect mechanisms of primary blast insult to the brain.

The interaction of explosion-induced blast waves with the head (i.e., a direct mechanism) or with the torso (i.e., an indirect mechanism) presumably causes traumatic brain injury. However, the understanding of the potential role of each mechanism in causing this injury is still limited. To address this knowledge gap, we characterized the changes in the brain tissue of rats resulting from the direct and indirect mechanisms at 24 h following blast exposure. To this end, we conducted separate blast-wave exposures on rats in a shock tube at an incident overpressure of 130 kPa, while using whole-body, head-only, and torso-only configurations to delineate each mechanism. Then, we performed histopathological (silver staining) and immunohistochemical (GFAP, Iba-1, and NeuN staining) analyses to evaluate brain-tissue changes resulting from each mechanism. Compared to controls, our results showed no significant changes in torso-only-exposed rats. In contrast, we observed significant changes in whole-body-exposed (GFAP and silver staining) and head-only-exposed rats (silver staining). In addition, our analyses showed that a head-only exposure causes changes similar to those observed for a whole-body exposure, provided the exposure conditions are similar. In conclusion, our results suggest that the direct mechanism is the major contributor to blast-induced changes in brain tissues.

A 3-D Finite-Element Minipig Model to Assess Brain Biomechanical Responses to Blast Exposure.

Despite years of research, it is still unknown whether the interaction of explosion-induced blast waves with the head causes injury to the human brain. One way to fill this gap is to use animal models to establish "scaling laws" that project observed brain injuries in animals to humans. This requires laboratory experiments and high-fidelity mathematical models of the animal head to establish correlates between experimentally observed blast-induced brain injuries and model-predicted biomechanical responses. To this end, we performed laboratory experiments on Göttingen minipigs to develop and validate a three-dimensional (3-D) high-fidelity finite-element (FE) model of the minipig head. First, we performed laboratory experiments on Göttingen minipigs to obtain the geometry of the cerebral vasculature network and to characterize brain-tissue and vasculature material properties in response to high strain rates typical of blast exposures. Next, we used the detailed cerebral vasculature information and species-specific brain tissue and vasculature material properties to develop the 3-D high-fidelity FE model of the minipig head. Then, to validate the model predictions, we performed laboratory shock-tube experiments, where we exposed Göttingen minipigs to a blast overpressure of 210 kPa in a laboratory shock tube and compared brain pressures at two locations. We observed a good agreement between the model-predicted pressures and the experimental measurements, with differences in maximum pressure of less than 6%. Finally, to evaluate the influence of the cerebral vascular network on the biomechanical predictions, we performed simulations where we compared results of FE models with and without the vasculature. As expected, incorporation of the vasculature decreased brain strain but did not affect the predictions of brain pressure. However, we observed that inclusion of the cerebral vasculature in the model changed the strain distribution by as much as 100% in regions near the interface between the vasculature and the brain tissue, suggesting that the vasculature does not merely decrease the strain but causes drastic redistributions. This work will help establish correlates between observed brain injuries and predicted biomechanical responses in minipigs and facilitate the creation of scaling laws to infer potential injuries in the human brain due to exposure to blast waves.

Does Blast Exposure to the Torso Cause a Blood Surge to the Brain?

The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (<1%). In summary, our analyses show that the indirect mechanism causes a sudden and abundant stream of blood to rapidly propagate from the torso through the neck to the cerebral vasculature. This blood surge causes a considerable increase in the wall shear stresses in the brain vasculature network, which may lead to functional and structural effects on the cerebral veins and arteries, ultimately leading to vascular pathology. In contrast, our findings do not support the notion of strain-induced brain-tissue damage due to the indirect mechanism.

A 3-D Rat Brain Model for Blast-Wave Exposure: Effects of Brain Vasculature and Material Properties.

Exposure to blast waves is suspected to cause primary traumatic brain injury. However, existing finite-element (FE) models of the rat head lack the necessary fidelity to characterize the biomechanical responses in the brain due to blast exposure. They neglect to represent the cerebral vasculature, which increases brain stiffness, and lack the appropriate brain material properties characteristic of high strain rates observed in blast exposures. To address these limitations, we developed a high-fidelity three-dimensional FE model of a rat head. We explicitly represented the rat's cerebral vasculature and used high-strain-rate material properties of the rat brain. For a range of blast overpressures (100 to 230 kPa) the brain-pressure predictions matched experimental results and largely overlapped with and tracked the incident pressure-time profile. Incorporating the vasculature decreased the average peak strain in the cerebrum, cerebellum, and brainstem by 17, 33, and 18%, respectively. When compared with our model based on rat-brain properties, the use of human-brain properties in the FE model led to a three-fold reduction in the strain predictions. For simulations of blast exposure in rats, our findings suggest that representing cerebral vasculature and species-specific brain properties has a considerable influence in the resulting brain strain but not the pressure predictions.

Validation of Laboratory Animal and Surrogate Human Models in Primary Blast Injury Studies.

Blast-induced neurotrauma has affected more than 300,000 service members. It is important to understand the effect of single and repeated shock-blast wave exposures on the neuropsychological behavior of soldiers, to offer them better protection, diagnostics, and treatment. Preclinical animal models and helmet design studies on human surrogate models have relied on the use of compression gas-driven shock tubes. Traditional shock tubes are so simple that if not carefully designed and operated, the test results can easily introduce detrimental artifacts clouding the conclusions. In this work, we present live-fire test results of an instrumented human surrogate head-neck model and compare with the data obtained in a carefully designed shock tube. We present various features incorporated in the shock tube design that led to better fidelity between live-fire and laboratory shock-blast conditions. The effect of specimen placement, choice of driver gas, pressure and volume of driver, end-plate conditions, and measurement techniques all determine the successful replication of live-fire loading conditions. These parameters become more important when conducting animal testing as the totality of loading will dictate the injury severity and type which ultimately will determine the mechanisms of blast-induced neurotrauma and hence their prevention and treatment strategies.

Use of hydrogel spacer for improved rectal dose-sparing in patients undergoing radical radiotherapy for localized prostate cancer: First Canadian experience.

We describe the initial experience using a hydrogel spacer (SpaceOAR) to separate the prostate-rectum interspace in patients planned to undergo radical hypofractionated, image-guided, intensity-modulated radiotherapy (IG-IMRT). We depict and discuss the impact of SpaceOAR in the context of hypofractionated IG-IMRT, and the particular considerations for its applications in the Canadian setting.

Tailoring the Blast Exposure Conditions in the Shock Tube for Generating Pure, Primary Shock Waves: The End Plate Facilitates Elimination of Secondary Loading of the Specimen.

The end plate mounted at the mouth of the shock tube is a versatile and effective implement to control and mitigate the end effects. We have performed a series of measurements of incident shock wave velocities and overpressures followed by quantification of impulse values (integral of pressure in time domain) for four different end plate configurations (0.625, 2, 4 inches, and an open end). Shock wave characteristics were monitored by high response rate pressure sensors allocated in six positions along the length of 6 meters long 229 mm square cross section shock tube. Tests were performed at three shock wave intensities, which was controlled by varying the Mylar membrane thickness (0.02, 0.04 and 0.06 inch). The end reflector plate installed at the exit of the shock tube allows precise control over the intensity of reflected waves penetrating into the shock tube. At the optimized distance of the tube to end plate gap the secondary waves were entirely eliminated from the test section, which was confirmed by pressure sensor at T4 location. This is pronounced finding for implementation of pure primary blast wave animal model. These data also suggest only deep in the shock tube experimental conditions allow exposure to a single shock wave free of artifacts. Our results provide detailed insight into spatiotemporal dynamics of shock waves with Friedlander waveform generated using helium as a driver gas and propagating in the air inside medium sized tube. Diffusion of driver gas (helium) inside the shock tube was responsible for velocity increase of reflected shock waves. Numerical simulations combined with experimental data suggest the shock wave attenuation mechanism is simply the expansion of the internal pressure. In the absence of any other postulated shock wave decay mechanisms, which were not implemented in the model the agreement between theory and experimental data is excellent.

A parametric approach to shape field-relevant blast wave profiles in compressed-gas-driven shock tube.

Detonation of a high-explosive produces shock-blast wave, shrapnel, and gaseous products. While direct exposure to blast is a concern near the epicenter, shock-blast can affect subjects, even at farther distances. When a pure shock-blast wave encounters the subject, in the absence of shrapnels, fall, or gaseous products the loading is termed as primary blast loading and is the subject of this paper. The wave profile is characterized by blast overpressure, positive time duration, and impulse and called herein as shock-blast wave parameters (SWPs). These parameters in turn are uniquely determined by the strength of high explosive and the distance of the human subjects from the epicenter. The shape and magnitude of the profile determine the severity of injury to the subjects. As shown in some of our recent works (1-3), the profile not only determines the survival of the subjects (e.g., animals) but also the acute and chronic biomechanical injuries along with the following bio-chemical sequelae. It is extremely important to carefully design and operate the shock tube to produce field-relevant SWPs. Furthermore, it is vital to identify and eliminate the artifacts that are inadvertently introduced in the shock-blast profile that may affect the results. In this work, we examine the relationship between shock tube adjustable parameters (SAPs) and SWPs that can be used to control the blast profile; the results can be easily applied to many of the laboratory shock tubes. Further, replication of shock profile (magnitude and shape) can be related to field explosions and can be a standard in comparing results across different laboratories. Forty experiments are carried out by judiciously varying SAPs such as membrane thickness, breech length (66.68-1209.68 mm), measurement location, and type of driver gas (nitrogen, helium). The effects SAPs have on the resulting shock-blast profiles are shown. Also, the shock-blast profiles of a TNT explosion from ConWep software is compared with the profiles obtained from the shock tube. To conclude, our experimental results demonstrate that a compressed-gas shock tube when designed and operated carefully can replicate the blast time profiles of field explosions accurately. Such a faithful replication is an essential first step when studying the effects of blast induced neurotrauma using animal models.

Blast-induced biomechanical loading of the rat: an experimental and anatomically accurate computational blast injury model.

Blast waves generated by improvised explosive devices (IEDs) cause traumatic brain injury (TBI) in soldiers and civilians. In vivo animal models that use shock tubes are extensively used in laboratories to simulate field conditions, to identify mechanisms of injury, and to develop injury thresholds. In this article, we place rats in different locations along the length of the shock tube (i.e., inside, outside, and near the exit), to examine the role of animal placement location (APL) in the biomechanical load experienced by the animal. We found that the biomechanical load on the brain and internal organs in the thoracic cavity (lungs and heart) varied significantly depending on the APL. When the specimen is positioned outside, organs in the thoracic cavity experience a higher pressure for a longer duration, in contrast to APL inside the shock tube. This in turn will possibly alter the injury type, severity, and lethality. We found that the optimal APL is where the Friedlander waveform is first formed inside the shock tube. Once the optimal APL was determined, the effect of the incident blast intensity on the surface and intracranial pressure was measured and analyzed. Noticeably, surface and intracranial pressure increases linearly with the incident peak overpressures, though surface pressures are significantly higher than the other two. Further, we developed and validated an anatomically accurate finite element model of the rat head. With this model, we determined that the main pathway of pressure transmission to the brain was through the skull and not through the snout; however, the snout plays a secondary role in diffracting the incoming blast wave towards the skull.