Indiana University-Purdue University Indianapolis (IUPUI) / Traumatic brain injury (TBI) is a critical public health issue in the United States, affecting about 2.8 million people annually. Extensive cell death and neural degeneration directly and diffusively caused by the initial mechanical insult results in a wide range of neurological complications post-trauma. Learning and memory dysfunction is one of the most common complains. Hippocampal neuronal loss, together with other mechanisms, largely contributes to learning and memory impairment as well as other cognitive dysfunctions post-trauma. To date, no FDA-approved drug is available to target cell death or improve learning and memory following TBI. It is of great interest to develop alternative approaches targeting neural repair instead. Neural stem/progenitor cells (NSCs) in the adult hippocampus undergo life-long neurogenesis supporting learning and memory functions, thus hold great promise for post-traumatic neuronal replacement. The previous studies demonstrated that TBI transiently increase NSC proliferation. However, it is debated on whether TBI affects neurogenesis. The mechanism of TBI-enhanced NSC proliferation remains elusive. In the current studies, I have investigated post-traumatic neurogenesis after different injury severities, evaluated integration of post-injury born neurons, illustrated a molecular mechanism mediating TBI-enhanced NSC proliferation, proposed a de novo state of NSCs, and tested effects of a pharmacological approach on spatial learning and memory function recovery. My results demonstrated that post-traumatic neurogenesis is affected by injury severities, partially explained the pre-existing inconsistency among works from different groups. Post-injury born neurons integrate in neural network and receive local and distal inputs. TBI promotes functional recruitment of post-injury born neurons into neural circuits. Mechanistically, mechanistic target of rapamycin (mTOR) pathway is required primarily for TBI-enhanced NSC proliferation; NSCs feature a de novo alert state, in which NSCs are reversibly released from quiescence and primed for proliferation. Furthermore, my data demonstrated a beneficial role of ketamine in improving post-traumatic spatial learning possibly by activating mTOR signal in NSCs and/or promoting neuronal activity of post-injury born neurons. Together, my data support the feasibility of neurogenesis mediated neuronal replacement, provide a target for enhancing post-traumatic NSC proliferation and subsequent neurogenesis, and prove a potential pharmacological approach benefiting post-traumatic functional recovery in learning and memory. / 2021-11-04

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Student Number : 0102295F - MA research dissertation - School of Psychology - Faculty of Arts / A review of trauma literature indicated that in comparison to PTSD there is very little research into the effects of secondary trauma, especially with regards to trauma workers. The present study explored the psychological impact of trauma workers who work with victims of violent crimes. Both Figley’s (1995) trauma transmission model and Dutton and Rubenstein (1995) ecological model were used to develop a refined trauma model for trauma workers in South Africa, which formed the theoretical basis for the current research. This model looked at the relationships between specific key variables (level of exposure to traumatic material, empathy, and level of perceived social support) and secondary traumatic stress, and their interrelationship. In the present study relevant information was gathered from volunteer trauma workers (N=64) using self-report measures. Data was analysed using the following statistical techniques: Descriptive statistics, Pearson’s Correlation Coefficients, Two Independent Sample T-Test, and a Moderated Multiple Regression. Results indicated that the trauma workers, to some extent, experienced symptoms of secondary traumatic stress. In addition, it was found that previous exposure to traumatic material, level of empathy, and level of perceived social support have a significant relationship with secondary traumatic stress. Social support was not found to have a moderating effect, but empathy emerged as a consistent moderator between the trauma workers previous exposure to traumatic material and secondary traumatic stress. Results also revealed that ones qualification made no difference in the development of secondary traumatic stress. In summary, this study expanded on knowledge into the effects of criminal violence in South Africa, particularly with concern to trauma workers, a population often ignored. This study was considered to be a contribution to trauma literature as it provides much needed empirical evidence.

Thesis is submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Faculty of Humanities, University of the Witwatersrand, Johannesburg, 1998 / The study was directed at exploring the social and personal construction of meaning of male victims of violent crime. Three inter-related goals were identified: the extension of the nascent narrative/thematic tradition of analysis in the traumatic stress field; the deepening of appreciation of the experience of criminal victimization; and the exploration o f the role of social construction in the cognitive schematic adjustment of victims. In this instance the examination of the role of social construction was focussed centrally on the juxtaposition of the subject roles associated with masculinity and victimization. On the basis of both clinical observation and theory, it was postulated that aspects of masculine identification would create difficulties for men attempting to adjust to involuntary exposure to a context in which they were clearly victimized. The thesis provides comprehensive coverage of theory straddling cognitive adjustment to psychological trauma, mainstream and critical social psychological theory on victimization, developmental and descriptive dimensions of theory on masculinity and a range of literature on criminal victimization. The theoretical conceptualization underpinning the study offers a unique integration of this body of knowledge. In order to investigate the research question, ten adult, white, English speaking,South African men who had experienced a life-threatening, criminally motivated attack were interviewed about the event and their subsequent responses. The study was located within the qualitative research tradition allowing for the development of theory, and fox depth of description and interpretation. Semi-structured interviews were recorded and tnmscribdl w batim . Interview transcripts were subjected to a thematic content analysis by means of a computer-aided text interpretation. Frequency figures were calculated, but the emphasis of the analysis was in the area of descriptive and interpretive dimensions. Three central themes emerged as signi fi cant; those of Control, Disillusionment and Anger. Multiple facets of each theme are addressed, including centrally the interface between thematic dimensions and the social construction of masculinity. A meta-theoretical discourse analytic commentary is provided, addressing for example, the rob of the “hero” discourse in interviewee’s reports. In addition, the clinical implications of the data are explored. The study provides evidence of the inter-relationship between social and personal construction o f meaning in the aftermath of tramatization. It is suggested that in the context of victimization the social construction of masculinity is both more intractable and more permeable than might be supposed.

This thesis presents research aimed at elucidating neurophysiological and neuropsychological correlates of two psychiatric disorders, schizophrenia and PTSD. Although psychiatric disorders are not traditionally known for featuring cognitive deficits, research over the past three decades has revealed that deficits in many aspects of cognitive functioning are present across a wide range of disorders. Here, we aim to further our understanding of these deficits and provide evidence of the clinical utility of neurophysiological correlates of cognitive dysfunction. The cause and course of cognitive deficits in PTSD is poorly understood, and an investigation of one potential explanatory mechanism, dissociative symptomatology, is presented in the first part of this thesis. Our results suggest that dissociative symptomatology plays a role in cognitive dysfunction in PTSD, as among the clinical variables tested (including PTSD symptomatology, dissociative symptoms, depressive symptoms, and anxiety symptoms) dissociative symptoms were the only significantly correlated variables to cognitive dysfunction in a sample of combat-trauma exposed veterans with and without PTSD. In the second part of this thesis, we investigate the potential clinical utility of a neurophysiological biomarker for semantic processing deficits, the N400, in schizophrenia. Our results indicate that N400 measures are stable over a one week period and therefore may be clinically useful as a neurophysiological biomarker for semantic processing abnormalities in schizophrenia. Overall, these two studies contribute to our knowledge of cognitive deficits in psychiatric disorders and demonstrate their complexity as well as their potential to provide clinically useful tools to aid in the identification of novel treatments targeted at ameliorating cognitive deficits in schizophrenia and PTSD. / Thesis / Master of Science (MSc)

The current study aimed to focus on Post-Traumatic Stress Disorder (PTSD) symptoms in parents who have a child diagnosed with a rare genetic syndrome called CHARGE Syndrome. While previous studies have investigated related factors to parental PTSD (Reda & Hartshorne, 2008; Wulffaert et al., 2009), this study was one of the first to focus on parental PTSD symptomology and possible traumatic experiences related to CHARGE (e.g., medical complications). Specific concerns related to PTSD addressed in the current study included trauma histories, the number of surgeries a child underwent, and parent stress levels. One hundred and ninety-seven parents completed surveys that met inclusion criteria for the study. Findings indicated that 48% of parents showed signs of PTSD based on reported symptomology. Additionally, higher parent stress levels were found to be contributed to greater symptomology presentation. Overall outcomes of the study demonstrate that PTSD and parent stress levels may affect parents' abilities to adequately provide the needed emotional support and care for their children with CHARGE Syndrome without support. This study paves the way for additional research in this area to focus on the screening and development of treatment resources for parents of children with CHARGE Syndrome. Future directions and limitations were discussed in detail.

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