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Ice hockey, one of the most popular sports in the world, is a contact sport that is always associated with huge risks of traumatic brain injuries (TBIs) resulting from high-velocity impacts. Although technology in player protection equipment has advanced over the years, mild traumatic brain injuries (mTBIs) like concussion remain prevalent. Finite Element (FE) analysis presents a methodology to recreate accidents in an effort to study the effects of protective helmets and predict brain injuries. This study aimed at improving the response of an existing ice hockey helmet FE model during different impact conditions and reconstructing an ice hockey collision using FE simulations. First, the shear response of the Expanded Polypropylene (EPP) material for the helmet liner was improved by means of a single element simulation to replicate the experiments. Simulations of helmet drop tests were then performed to validate the helmet FE model. Two different designs of the helmet model were implemented, one with normal properties of the foam and the other with a softer foam. Actual cases of ice hockey accidents were then reconstructed using positioning and impact velocities as input from video analysis. As player to player collisions had not been reconstructed for ice hockey using two player models, it was decided to use two full body Human Body Models (HBMs) for the reconstruction. The biomechanical injury parameters for the accident reconstruction were plotted and compared with injury thresholds for concussion. The kinematic results achieved from the drop test simulations showed a considerable decrease in peak values for resultant accelerations, resultant rotational accelerations, and resultant rotational velocities. These results also exhibited better CORrelation and Analysis (CORA) scores than previously achieved. The biomechanical analysis of the accident reconstruction showed the strains in the brain for the concussed player to be more than the threshold for concussion, which confirms the validity of the reconstruction approach. The results of this study show an improved response of the helmet FE model under different impact conditions. They also present a methodology for ice hockey accident reconstruction using two full body HBMs.

There is an established bidirectional relation between substance use and traumatic brain injuries (TBIs). Despite the high rate of prescribing opioids for pain management following a TBI and the epidemic of opioid use disorder (OUD) in the United States, scarce research has specifically analyzed the association between TBI and OUD. In a series of three interrelated manuscripts, the present study will first examine the prevalence and features of TBIs among persons seeking treatment for OUD. Next, the present study will evaluate the association between TBI and indicators of risky health behaviors and OUD severity, including the risk of overdose and polysubstance use. The predictive ability of symptoms of posttraumatic stress disorder, anxiety, impulsivity, depression, and chronic pain on odds of having had a TBI will also be calculated. Last, a systematic review will be conducted to provide comprehensive guidelines for effective methods of tailoring OUD treatment to mitigate the effects of TBI on treatment outcomes. Altogether, the findings will aid in the understanding of the development of TBI for persons with OUD, provide insight into common clinical complexities for patients with OUD and TBI, and offer guidance on how best to tailor interventions to increase substance use treatment efficacy for persons with TBI.

Youth football players ages 8-12 may incur hundreds of repeated head impacts (RHI) each season. Evidence suggests concussive brain injury during childhood may disrupt normal developmental processes resulting in long-term impairments. However, little research has investigated the long-term effects of incurring RHI during critical periods of neurodevelopment. Rapid myelination and cerebral blood flow rates, peaks in regional cortical thickness and volumes of specific structures, refinement of regional connectivity, and other neurodevelopmental changes occurring in the brain from ages 10-12 could create a window of vulnerability to RHI. The objective of this research was to determine the relationship between exposure to RHI prior to age 12, during a critical period of neurodevelopment, and later-life brain structure and function. Former National Football League (NFL) players ages 40-65 were divided into two groups based on their age of first exposure (AFE) to RHI through tackle football: AFE <12 and AFE ≥12. In the first study, we observed significantly lower scores on objective tests of executive functioning, memory, and estimated verbal IQ in those who began playing football prior to age 12 compared to those who began playing at age 12 or older. Next, we used diffusion tensor imaging (DTI) to examine the structural integrity of the corpus callosum (CC) and observed that the AFE <12 group had significantly lower fractional anisotropy (FA) as well as a greater decline in FA with age in anterior CC regions than the AFE ≥12 group. Lastly, we used advanced DTI tractography techniques to examine seven CC regions. Significant differences between AFE groups in associations between CC diffusion measures and cognition, mood, and behavior were found. The results of this research suggest that incurring RHI through tackle football during a critical neurodevelopmental period prior to age 12 may result in later-life structural and functional consequences, including cognitive, mood, and behavioral impairments; alterations in white matter structure; and greater vulnerability of white matter to the normal aging process. If replicated with longitudinal designs, larger samples, and athletes whose highest level of play was youth, high school, or college, these findings may have implications for safety recommendations for youth sports.

Military-related blast-exposure and sports-related closed-head impact-injury are associated with traumatic brain injury (TBI) and chronic traumatic encephalopathy (CTE), a tau protein neurodegenerative disease. Despite growing awareness of links between TBI and CTE, the mechanisms underpinning this association, and relationship to concussive and subconcussive head injury, are poorly understood. This dissertation addresses the hypothesis that blast-exposure and impact-injury induce traumatic acceleration of the head and injurious forces in the brain that led to structural brain damage (TBI) and chronic sequelae, including CTE. This hypothesis was addressed in five specific aims: 1) develop a blast shock tube instrument and impact instrument to deliver relevant blast-exposure and impact-injury to mice, 2) validate a mouse model of single blast-exposure that recapitulates brain pathology in blast-exposed military veterans diagnosed with CTE, 3) validate a mouse model of single-repeat closed-head impact-injury that recapitulates brain pathology in contact sport athletes diagnosed with CTE, 4) match kinematics of blast and impact models using high-speed videography, 5) deploy kinematically-matched mouse models of single blast-exposure and single-repeat closed-head impact-injury to investigate mechanisms that trigger experimental concussion and post-traumatic sequelae. Blast and impact injuries were shown to cause similar CTE-linked brain pathologies, including microvasculopathy, neuroinflammation, astrogliosis, and phosphorylated tauopathy. Despite similarities in chronic consequences, blast-exposure and impact-injury produced different acute neurological responses. Surprisingly, impact-injured mice demonstrated signs of experimental concussion, whereas blast-exposed mice with comparable head kinematics did not. Computational modeling indicated that point loading of forces during impact, as opposed to distributed loading in blast, caused ipsilateral spikes in cortical shear stress which we conclude to be responsible for experimental concussion. The blast-exposure and impact-injury models have been and will continue to be invaluable tools for elucidating the mechanisms of and relationships between concussion, TBI, and CTE. / 2019-07-09T00:00:00Z

Children and adolescents with concussion display aberrant functional connectivity in some of the major neurocognitive networks. This includes the Default Mode Network, Central Executive Network and Salience Network. Using resting state fMRI, the purpose of this thesis was to explore the functional connectivity of cognition-related networks in youth experiencing concussion. With a prospective cohort study, the functional connectivity (defined as the temporal coherence between spatially separated brain regions) of children and adolescents ages 10-18 years old was evaluated in relation to a number of demographic and injury-specific factors including recovery length, age at the time of injury, symptom severity, and neurocognitive performance. The results showed two general trends: (1) a reduction in connectivity (i.e., hypoconnectivity) between the regions of the Default Mode Network, and (2) an increase in connectivity (i.e., hyperconnectivity) between additional sensory-related regions like the cerebellum and hippocampus. The Default Mode Network, which processes self-referential information, has a long-protracted development across childhood through adulthood. Given that the participants in this cohort exhibited reduced functional connectivity within the Default Mode Network and between the Default Mode Network and other neurocognitive networks suggests that this is an area of vulnerability in youth in the event of concussion. Increased connectivity between the Central Executive Network and Salience Network, and between cognitive- and sensory-related regions such as the hippocampus and cerebellum might be interpreted as a compensatory mechanism to supplement deficits of the Default Mode Network. This thesis sheds light on important concussion-related regions for future research to investigate further and delves into the possible neural mechanisms contributing to the cognitive, sensory, mood, and sleep disturbances in children and adolescents with concussion. / Dissertation / Doctor of Philosophy (PhD) / Your brain at rest is not resting. In fact, your many brain regions are continuously communicating even during rest to maintain important communication between them. This communication between brain regions is termed functional connectivity. When you receive a blow to the head, face, neck, or another part of your body that senses a biomechanical force to your brain, the functional connectivity (i.e., communication lines) between your brain regions may be altered. A blow of this nature is considered a concussion, also known as a mild traumatic brain injury. With disruptions to the typical functional connectivity between your brain regions following a concussion, you may experience difficulty in managing cognitive tasks, emotions, and body coordination. Among those most vulnerable to the effects of concussion are children and adolescents whose brains have yet to develop fully. The goal of this thesis was to evaluate the functional connectivity between brain regions of children and adolescents to determine how brain communication might be disrupted following concussion. These evaluations were done using functional magnetic resonance imaging (fMRI) of the brains of children and adolescents ages 10-18 years old. It was discovered that the functional connectivity of the frontal lobe is related severity of post-concussion symptoms such that individuals with worse symptoms had reduced functional connectivity in the frontal lobe compared to individuals who reported less severe symptoms. Further, children and adolescents with longer recovery periods have a different level of functional connectivity in the temporal lobe compared to youth with relatively shorter recovery periods. This might suggest that both of these regions could provide prognostic value in determining who might have worse symptoms or a longer recovery time following injury. In comparison to children and adolescents who have not had a concussion, children and adolescents experiencing a concussion are more likely to have abnormal functional connectivity between the hippocampus and cerebellum, which are particularly involved in processing sensory information and navigation. This was interpreted to mean that the brain responded to the concussion by increasing the communication between regions that might help a child with a concussion coordinate their bodies so that they can move from place to place. This was additionally supported by a further investigation which showed that children and adolescents have reduced communication between areas of the brain that might allow them to process information about the self (e.g., memories, sensations, relationships with others, etc.). Overall, the results demonstrated that following a concussion, children and adolescents may have a deficit in the functioning of the frontal lobe in a specific region that allows them to process cognitive and sensory information. This might explain why concussion leads to poor memory, body coordination, sensitivity to light and sounds, and even difficulty sleeping. Their brains might then compensate for the disruption by increasing alternate pathways of communication. Together these findings open gateways for future researchers to look more deeply at the specific regions affected by concussion in youth. It draws attention to the many neurocognitive, emotional, and somatic symptoms a child with a concussion exhibits and their symptoms’ underlying neurological processes.

High contact sports put athletes at a higher risk of sustaining a concussion. This work focused on assessing regional brain health in aging, retired Canadian Football League (rCFL) players years to decades after retirement. Advanced, quantitative magnetic resonance imaging (MRI) techniques were implemented to identify and quantify microstructural brain white matter damage, cognitive functional signal characteristics (fractal dimension (FD) and amplitude of low frequency fluctuations (ALFF) and fractional ALFF (fALFF)), and cerebral blood flow (CBF) dysregulation. Due to the high reproducibility of diffusion tensor imaging (DTI) and resting state functional MRI (rsfMRI), a Z-scoring approach exploring outliers relative to a large normative dataset was implemented to examine each rCFL subject individually. However, arterial spin labelling (ASL) data is more sensitive to scanner inconsistencies, therefore a group-wise analysis was performed with the CBF and ASL spatial coefficient of variance (ASL sCoV) data. Minimal microstructural damage was detected in the rCFL subjects, but a substantial amount of functional and CBF abnormalities were present. The FD was significantly reduced in 48 of 91 regions-of-interest (ROIs) examined, and the four rCFL subjects with the highest number of abnormal ROIs all exhibited worse motor speed, social functioning and general health scores than the other rCFL subjects. Furthermore, the ALFF analysis identified the cerebellum, parietal lobe ROIs, and central sub-cortical ROIs to be consistently abnormal. Finally, the temporal occipital fusiform cortex, superior parietal gyrus, caudate nucleus, and the cerebellum were significantly abnormal bilaterally based on CBF and ASL sCoV values, which also correlated with worse physical functioning and elevated daily chronic pain. This work adds to the growing literature that brain changes are present later in life that may be related to concussions and repetitive sub-concussive head impacts sustained years earlier. Several consistently damaged ROIs also correlated with adverse clinical presentations to indicate areas of future research. / Dissertation / Doctor of Philosophy (PhD) / Clinical concussion assessment has a limited ability to identify brain injury location and severity. Therefore, there is a need for more advanced diagnostic tools to provide meaningful, objective information to concussion patients and clinicians. The work presented in this thesis aimed to assess brain health using magnetic resonance imaging (MRI) techniques of retired professional football players with a complex history of concussions and repetitive sub-concussive impacts. Our research found concussion-related functional and cerebral blood flow brain abnormalities past that of normal aging, but minimal white matter damage, present in the retired athletes that also correlated with clinically testable health metrics such as motor speed, emotional well-being, and pain. Through personalized subject-specific analyses, this work provides further evidence of the effects of concussions later in life.

Subconcussive impacts have become a growing concern particularly with respect to contact sports. It is believed that minimal head impacts can cause cerebral perturbations that initiate an immune response creating a window of vulnerability. Evidence suggests that additional head insults sustained during this window of vulnerability elicit an exaggerated inflammatory response and exacerbate cognitive deficits. Therefore, determining the lower limits of systematic perturbation resulting from low-level impacts is of critical importance in expanding our understanding of cerebral vulnerability and recovery. However, the vast majority of experimental investigations of subconcussion fail to model single impact events and instead focus on cumulative insults. Additionally, these animal models employ impact magnitudes used to model mild Traumatic Brain Injury. The present investigation aimed to address this gap in knowledge through the utilization of a pneumatically controlled, closed-head, blunt impact device capable of producing repeatable, defined, subconcussive head impacts within a rat model. Thermography was used as a noninvasive measure of inflammation and system perturbations with respect to local (head) and global (thorax and abdomen) temperature changes. Cognitive function was assessed using an Open Field Test and Novel Object Recognition test. Neuroinflammation was measured by assessment of GFAP and iba-1 within the hippocampus and corpus callosum. To investigate the tolerance and the persistence of cerebral vulnerability, measurement outcomes were assessed at six timepoints of recovery, 0, 0.5, 1, 4, 7, and 14 days. Thermal disturbances were detected directly after impact, followed by an apparent recovery, 0.5- and 1-day post-impact. A latent temperature increase was observed after 4- and 7-days of recovery coinciding with decreased risk-avoidance behaviors, a modest upregulation of iba-1, and a marked downregulation of GFAP. Short-term memory deficits became apparent after 7-days of recovery. A decrease in locomotor activity and an upregulation of GFAP was observed concomitant to a persistent decrease in risk-avoidance despite thermal, short-term memory, and iba-1 measurements recovery 14-days post-impact. Overall, these results indicate that low magnitude subconcussive impacts can produce latent thermal, behavioral, and histological disturbances uncharacteristic for a head injury model suggestive of a biomechanical threshold of altered pathodynamics that fail to fully recover after 14 days.