<p>Explosions are associated with more than 80% of the casualties in the Iraq and Afghanistan wars. Given the widespread use of thoracic protective armor, the most prevalent injury for combat personnel is blast-related traumatic brain injury (TBI). Almost 20% of veterans returning from duty had one or more clinically confirmed cases of TBI. In the decades of research prior to 2000, neurotrauma was under-recognized as a blast injury and the etiology and pathology of these injuries remains unclear.</p><p>This dissertation used the finite element (FE) method to address many of the biomechanics-based questions related to blast brain injuries. FE modeling is a powerful tool for studying the biomechanical response of a human or animal body to blast loading, particularly because of the many challenges related to experimental work in this field. In this dissertation, novel FE models of the human and ferret head were developed for blast and blunt impact simulation, and the ensuing response of the brain was investigated. The blast conditions simulated in this research were representative of peak overpressures and durations of real-world explosives. In general, intracranial pressures were dependent on the peak pressure of the impinging blast wave, but deviatoric responses in the brain were dependent on both peak pressure and duration. The biomechanical response of the ferret brain model was correlated with in vivo injury data from shock tube experiments. This accomplishment was the first of its kind in the blast neurotrauma field.</p><p>This dissertation made major contributions to the field of blast brain injury and to the understanding of blast neurotrauma. This research determined that blast brain injuries were brain size-dependent. For example, mouse-sized brains were predicted to have approximately 7 times larger brain tissue strains than the human-sized brains for the same blast exposure. This finding has important implications for in vivo injury model design, and a scaling model was developed to relate animal experimental models to humans via scaling blast duration by the fourth-root of the ratio of brain masses. </p><p>This research also determined that blast neurotrauma is correlated to deviatoric metrics of the brain tissue rather than dilatational metrics. In addition, strains in the blasted brain were an order-of-magnitude lower than expected to produce injury with traditional closed-head TBI, but an order-of-magnitude higher in strain rate. The 50th percentile peak principle strain metric of values of 0.6%, 1.8%, and 1.6% corresponded to the 50% risk of mild brain bleeding, moderate brain bleeding, and apnea respectively. These findings imply that the mechanical thresholds for brain tissue are strain-based for primary blast injury, and different from the thresholds associated with blunt impact or concussive brain injury because of strain rate effects.</p><p>The conclusions in this dissertation provide an important guide to the biomechanics community for studying neurotrauma using in vivo, in vitro, and in silico models. Additionally, the injury risk curves developed in this dissertation provide an injury risk metric for improving the effectiveness of personal protective equipment or evaluating neurotrauma from blast.</p> / Dissertation

Mild traumatic brain injury (mTBI) accounts for approximately 73-83% of all traumatic brain injuries (TBI) and continues to be a serious clinical challenge [1]. The role of injury mechanism in TBI has been widely debated, and it is believed that although there are differences between diffuse and focal TBI, the resulting injury is not influenced by the way in which it was acquired [1], [2]. It is known that TBIs can cause cognitive impairments that are often due to injury experienced in the hippocampus [2]. In response to insult, quiescent neural stem cell (NSC) populations within the dentate gyrus region of the hippocampus become activated. Stem cell differentiation following injury is hypothesized to be unique for diffuse and impact TBIs, primarily due to the differences in mechanotransduction pathways triggered by each respective injury. By quantifying the lineage of stem cells through immunohistochemistry, this study examined the dentate gyrus following mTBI in a rodent model, and the contribution that injury mechanism plays in mTBI outcomes. Additionally, the behavioral effects of mTBI were assessed through open field testing at 72 hours and four weeks following injury. Overall, these findings indicated that after four weeks following mTBI, there are not significant differences between impact and blast both from an immunohistochemical and behavioral standpoint. Despite there being few differences between injury groups, these findings help clarify the role of injury mechanism not only in the context of neurogenesis, but they also inform future studies addressing preventative and treatment strategies for mTBI. / Master of Science / Mild traumatic brain injury (mTBI) accounts for approximately 73-83% of all traumatic brain injuries (TBI) [1]. There are two main ways in which a mTBI can occur: through diffuse or focal injury. A diffuse injury is due to the brain experiencing a force that does not physically come into contact with the head, such as a shockwave from an explosion. These types of injuries typically affect the entire head. Impact injuries on the other hand, are caused by the head encountering an object at a force that causes injury to the brain. These injuries tend to be focal, as the entire head rarely comes into contact with an object. Both diffuse and focal injuries can cause mTBI, and there is a current debate questioning if the mode of injury has an impact on the damage experienced by the brain [1], [2]. However, it is also known that mTBI can cause cognitive impairments such as changes in behavior, memory, and even mental health, which can occur in the hippocampus of the brain [2]. Within the hippocampus, there is a small subset of cells referred to as neural stem cells (NSC) that become active following injury. The activation of these cells is believed to be in response to injury in the brain. Furthermore, NSCs have the ability to differentiate into various cell types within the brain, including astrocytes, oligodendrocytes, and neurons. Each of these cell types perform an integral role in the function of the brain. It is hypothesized that the response of NSCs in the hippocampus is unique depending on if an injury was acquired through diffuse or impact mechanisms. To investigate this, the lineage of NSCs was quantified within the hippocampus following blast and impact mTBI in a rodent model. Additionally, the behavioral effects of diffuse and impact injury were investigated at 72 hours and four weeks following injury. Despite there being no significant differences in outcomes between injury groups, these findings help clarify the role of injury mechanism not only in the context of NSC response, but they also inform future studies addressing preventative and treatment strategies for mTBI.

Introduction. Road traffic injuries are the eighth leading cause of death globally and the leading cause of death among young people aged 15-29. Of individuals killed or injured in road traffic injuries, a large group comprises occupants sustaining a thorax injury in frontal crashes. The elderly are particularly at risk, as they are more fragile. The evaluation of the frontal crash performance of new vehicles is normally based on barrier crash tests. Such tests are only representative of a small portion of real-life crashes, but it is not feasible to test vehicles in all real-life conditions. However, the rapid development of computers opens up possibilities for simulating whole populations of real-life crashes using so-called stochastic simulations. This opportunity leads to the aim of this thesis, which is to develop and validate a simplified, parameterized, stochastic vehicle simulation model for the evaluation of passive restraint systems in real-life frontal crashes with regard to rib fracture injuries. Methods. The work was divided into five phases. In phase one, the geometry and properties of a finite element (FE) generic vehicle buck model were developed based on data from 14 vehicles. In the second phase, a human FE model was validated for oblique frontal crashes. This human FE model was then used to represent the vehicle occupant. In the third phase, vehicle buck boundary conditions were derived based on real-life crash data from the National Automotive Sampling System (NASS) and crash test data from the Insurance Institute for Highway Safety. In phase four, a validation reference was developed by creating risk curves for rib fracture in NASS real-life crashes. Next, these risk curves were compared to the risk of rib fractures computed using the generic vehicle buck model. In the final phase, injury mechanisms in nearside oblique frontal crashes were evaluated. Results. In addition to an averaged geometry, parametric distributions for 27 vehicle and boundary condition parameters were developed as guiding properties for the stochastic model. Particular aspects of the boundary conditions such as pulse shape, pulse angle and pulse severity were analyzed in detail. The human FE model validation showed that the kinematics and rib fracture pattern in frontal oblique crashes were acceptable for this study. The validation of the complete FE generic vehicle buck model showed that the model overestimates the risk of rib fractures. However, if the reported under-prediction of rib fractures (50-70%) in the NASS data is accounted for using statistical simulations, the generic vehicle buck model accurately predicts injury risk for senior (70-year-old) occupants. The chest injury mechanisms in nearside oblique frontal crashes were found to be a combination of (I) belt and airbag loading and (II) the chest impacting the side structure. The debut of the second mechanism was found for pulse angles of about 30 degrees. Conclusion. A parameterized FE generic passenger vehicle buck model has been created and validated on a population of real life crashes in terms of rib fracture risk. With the current validation status, this model provides the possibility of developing and evaluating new passive safety systems for fragile senior occupants. Further, an injury mechanism responsible for the increased number of outboard rib fractures seen in small overlap and near-side oblique frontal impacts has been proposed and analyzed. / Vinnova Project: Real Life Safety Innovations