Thesis (Ph.D.)--Baylor University, 2006. / Includes bibliographical references (p. 123-135).

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Traumatic brain injury (TBI) remains an important cause of morbidity and mortality within society. TBI may result in both focal and diffuse brain injury. Diffuse traumatic axonal injury (TAI) is an important pathological substrate of TBI, and can be associated with a range of clinical states, ranging from concussion through to death, the clinical severity being associated with a number of factors related to the injury. A retrospective study was conducted using 406 cases with TBI, from the archive of the Academic Department of Pathology (Neuropathology) University of Edinburgh, during the period from1982 and 2005. This cohort was sequential and provided a unique description of the range of pathologies associated with fatal TBI within the Edinburgh catchment area. All the data was collected on a proforma and analysed to provide a description of the incidence in the injury patterns among the Edinburgh cohort. This cohort was then used to provide cases to try and critically assess the mechanisms of axonal injury in TBI. A study was undertaken to investigate TAI in an experimental model of non-impact head injury in a gyrencephalic mammalian model (piglet model) and in human autopsy materials using immunohistochemical analysis of a range of antibodies, and to define the distribution of axonal injury with flow and neurofilament markers in TAI. A further objective was to examine the expression of β-APP as an indicator of impaired axonal transport, three neurofilament markers targeting NF-160, NF-200, and the phosphorylated form of the neurofilament heavy chain (NFH), in different anatomical regions of piglet and human brains. The double immunofluorescence labelling method was then employed to investigate the hypothesis of co-localisation between β-APP and each one of the previous neurofilament markers. The animal studies showed significant differences in NF-160 between sham and injured 3-5 days old piglet cases (6 hour survival) and between 3-5 days sham and injured, when stained with SMI-34 antibody. In 4 weeks old piglet cases (6 hour survival), immunoreactivity of β-APP was significantly higher in injured than control. No other significant differences for any of the antibodies were noted, based on age, velocity, and survival time. Human results suggested that the brainstem had a higher level of β-APP and NF-160 than the corpus callosum and internal capsule. Co-localisation of β-APP with NFs was not a consistent feature of TAI in piglet and human brains, suggesting that markers of impaired axonal transport and neurofilament accumulation are sensitive to TAI, but may highlight different populations involved in the evolution of TAI.

In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. At post-injury days (PIDs) 1, 7, and 28, brain tissue from sham and brain-injured adult, male rats was processed for Golgi, glial fibrillary acidic protein (GFAP), or silver stain and analyzed to quantify BLA dendritic branch intersections, activated astrocytes, and regional neuropathology, respectively. Compared to sham, brain-injured rats at all PIDs showed enhanced dendritic branch intersections in both pyramidal and stellate BLA neuronal types, as evidenced by Sholl analysis. GFAP staining in the BLA was significantly increased at PID1 and 7 in comparison to sham. However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.

A dissertation submitted to the Faculty of Arts. University of the Witwatersrand, Johannesburg, in partial fulfilment of the requirements for the Degree of Master of Arts (Clinical Psycholoqy). Johannesburg, August 1996 / This study aims to explore the relationship between intrusion and avoidance symptoms as described in the diagnostic category in the DSM-IV (American Psychiatric Association, 1994) and frequency and level of exposure to traumatogenic events. The effects of lay counselling after the event were taken into account in the analysis, and the sample consisted of voluntary First National Bank employees, who were exposed to more than one bank robbery between December 1989 and 1992. The hypotheses of the study were that an increasing number of exposures to potentially traumatogenic events, and increasing levels of exposure to potentially traurnatoqenic events would be related to the development of avoidant and intrusion symptoms. Further, it was hypothesised that the interaction of these two variables would also be significantly related to the development of avoidant and intrusive symptoms and the nature of this interaction was explored. The scale used to measure the symptoms was the impact of Events Scale (Horowitz, 1979). Level of exposure was measured on a four point scale, which included extreme exposure with physical injury; direct threat and coafrontatlon: indirect contact with the perpetrators, and the fourth category was indirect exposure, or secondary victimisation. The results indicated that level of exposure had a significant relationship with the development of both intrusion and avoidance symptoms. Contrary to expectations, frequency of exposure was not found to be related to symptomology and it was speculated that this might have been because of the crudeness of the measure. In this regard it is of note that level of exposure as measured in this study included frequency of exposure. The results indicated further that post trauma counselling was not significantly related to symptomology. The implications of these findings were discussed in the light of the general literature in PTSD.

Every year an estimated 42 million people worldwide suffer a mild traumatic brain injury (MTBI) or concussion, with approximately 3.6 million sports related concussions occurring yearly in the United States alone (Bailes, 2015, Azad et al., 2015). An MTBI is an acute brain injury resulting from mechanical energy to the head from external forces (Bailes 2015). Symptoms of an MTBI include visual disturbances, dizziness, nausea and vomiting, light sensitivity, loss of balance, and a general feeling of fatigue (Bailes 2015). MTBI’s are first diagnosed through changes in ImPACT baseline scores as well as Vestibular Ocular Motor Screening (Mucha et al., 2014). Repetitive MTBI and/or repetitive sub-concussive head trauma have been tentatively linked to increased risk for a variety of neurodegenerative diseases including chronic traumatic encephalopathy (CTE) (Gardner et al., 2015). The major limitation of the link between MTBI and CTE is that CTE can only be diagnosed post-mortem (Azad et al., 2015). Due to that limitation, the prevalence of CTE is unknown and the amount of MTBI or sub-concussive trauma exposure necessary to produce CTE is unclear (Gardner et al., 2015). Newer methods of research including SNTF immunostaining and L-COSY are being further developed and studied to better diagnose MTBI and its link to CTE by exploring changes in brain protein formation and brain neurochemistry (Johnson et al., 2015, Lin et al., 2015). Through research development and case studies on professional American football players and boxers, a link between MTBI, particularly repetitive MTBI and CTE has been formed (Maroon et al., 2014).

Postmortem brains from young athletes with a history of repetitive concussive head injury and military service personnel with history of blast neurotrauma revealed evidence of parenchymal contusion, myelinated axonopathy, microvasculopathy, neuroinflammation, neurodegeneration, and phosphorylated tauopathy consistent with chronic traumatic encephalopathy (CTE) (L. E. Goldstein et al., 2012). The mechanisms by which head trauma induces acute concussion and chronic sequelae are unknown. To elucidate the mechanistic connection between traumatic brain injury (TBI), acute concussion and chronic sequelae, including CTE, require the use of animal models. This doctoral dissertation investigated the hypothesis that closed-head impact injury in mice triggers acute neurological signs associated with sport-related concussion as well as brain pathologies and functional sequelae associated with CTE. To test this hypothesis, we developed a mouse model of impact neurotrauma that utilizes a momentum transfer device to induce non-skull deforming head acceleration, triggering transient neurological signs consistent with acute concussion and traumatic brain injury (TBI) in unanesthetized C57BL/6 mice. The Boston University Concussion Scale (BUCS) was developed to assess neurological signs that are consistent with acute concussion in humans. Mice exhibited contralateral circling and limb weakness, locomotor abnormalities, and impaired gait and balance that recapitulate acute concussion in humans. Concussed mice recovered neurological function within three hours, but demonstrated persistent myelinated axonopathy, microvasculopathy, neuroinflammation, and phosphorylated tauopathy consistent with early CTE. Concussive impact injury also induced blood-brain barrier disruption, neuroinflammation (including infiltration peripheral monocytes and activation microglia), impaired hippocampal axonal conduction, and defective long-term potentiation (LTP) of synaptic transmission in medial prefrontal cortex. Kinematic analysis during impact injury revealed head acceleration of sufficient intensity to induce acute concussion, traumatic brain injury (TBI), early CTE-linked pathology, and related chronic sequelae. Surprisingly, the presence or degree of concussion measured by BUCS did not correlate with brain injury. Moreover, concussion was observed following impact injury but not blast exposure under conditions that induce comparable head kinematics. Empirical pressure measurements and dynamic modeling revealed greater pressure on the head and compression wave loading in the brain during impact compared to blast neurotrauma. These findings suggest acute concussion is triggered by focal loading of energy that transit the brain before onset of macroscopic head motion. By contrast, the forces associated with rapid head motion is sufficient to induce CTE-linked pathology. Our results indicate that while acute concussion and chronic sequelae may be triggered by the same insult, the pathophysiological responses underpinning these effects are engaged through distinct mechanisms and time domains. Our results indicate that concussion is neither necessary nor sufficient to induce acute brain injury or chronic sequelae, including CTE. / 2018-02-17T00:00:00Z

Thesis (M MSc (Clinical Psychology))--University of Limpopo,2010. / The phenomenon of trauma from violent crime is deeply rooted within the South African community (Human Rights Watch, 2008). Various studies has researched the resulting post-traumatic stress reaction (PTSR) of the trauma victim, with far-reaching implications for an understanding of the emotional, cognitive, physiological, and social level of functioning of the victim (Edwards, 2005). Punctuating from the general systems theory, however, it is clear that the trauma victim does not function in isolation, but forms part of certain circular patterns of interaction within a family system. Change in one part of this system will induce change in the system as a whole (Becvar & Becvar, 2006). The aim of this research project was to move away from exclusively focusing on the trauma victim and to investigate the effects, if any, on the whole family system if one of its members experienced a PTSR. Data was collected from qualitative interviews with a family member of each trauma victim, someone who had not directly experienced the traumatic incident. The data was transcribed verbatim and analysed, in accordance with qualitative methodology by three independent, systemically trained clinicians. The findings indicate that there is a significant effect on the whole family system, and that all the members of this system experience some form of PTSR as a secondary traumatic experience. The ability of the system to cope effectively with this environmental demand is based largely on the effectiveness of its patterns of communication. These findings have important implications for our understanding of the phenomenon of trauma, trauma prevention and intervention strategies.

Thesis (Ph. D.)--Auburn University, 2008. / Abstract. Vita. Includes bibliographical references (p. 49-57).