Alcohol use disorder (AUD) and post-traumatic stress disorder (PTSD) are debilitating conditions that often co-occur, with an estimated 41-79% comorbidity rate. A major concern with the co-occurrence of these disorders is the tendency for one to exacerbate the other. Specifically, symptoms related to PTSD are a significant risk factor for the development of AUD, and alcohol abuse worsens PTSD symptoms. This cycle, along with a lack of effective pharmacological treatment options, leads to significant behavioral and physiological deficits. Additionally, remission for comorbid AUD and PTSD is much more difficult to attain due to exacerbated symptomology and a lack of FDA-approved medications. In recent years, cannabidiol (CBD), a non-psychoactive compound found in cannabis, has been a focus of study due to its therapeutic potential. Researchers have demonstrated the anxiolytic and anti-inflammatory effects of CBD in both humans and animals, showing its promise as a novel therapeutic agent in the treatment of psychiatric disorders. The purpose of this study is to investigate the hypothesis that CBD will reduce fear-related behaviors and neuroinflammation in a rat model of comorbid AUD and PTSD. Our AUD/PTSD model utilized restraint stress and chronic intermittent ethanol exposure procedures. To investigate changes in future stress sensitivity all animals were exposed to a contextual fear conditioning paradigm, which was used to train the animals to associate environmental and auditory cues (environment appearance and tone) with an aversive stimulus (mild foot-shock). 30 minutes prior to each conditioning session, rats received an intraperitoneal injection of CBD (20mg/kg) or 0.9% Saline. Once the animals learned to associate the cues with a shock, they were exposed to an extinction learning procedure that involved presentation of the cue alone (no shock). This procedure parallels exposure therapy in humans, allowing for the assessment adaptations to fear learning. The amount of time the rats remain still (freezing) during the tone represents fear-related behavior. Our current results indicate rats with a history of stress and alcohol exposure displayed significantly higher freezing behaviors and this effect was significantly decreased with CBD treatment. This suggests that when CBD is administered during fear learning, it is able to attenuate heightened stress sensitivity associated with AUD/PTSD. To evaluate how CBD mediates the neuroinflammatory response associated with AUD and PTSD, brains from the rats were extracted and analyzed for the inflammatory cytokine tumor necrosis factor a (TNF-a). Specific regions of interest included the medial prefrontal cortex and hippocampus, areas associated with anxiety, memory, and addiction. Neuroinflammation analyses are still ongoing, however it is predicted that rats who received CBD will show a reduction in inflammation in the medial prefrontal cortex and hippocampus. Taken together, the current results show promise for CBD to reduce enhanced fear-related behavior associated with comorbid AUD and PTSD.

The development of posttraumatic stress disorder (PTSD) and severe weather phobia (SWP) symptoms in relation to weather-related trauma was examined. Participants were college students (N = 815) enrolled at Mississippi State University. Findings suggest that distinct factors (specifically, disorder-specific cognitions and anxiety sensitivity) contribute to the development of PTSD and in the onset of SWP symptoms following exposure to weather-related trauma. A weather trauma model taking into account disorder-specific cognitive vulnerabilities, previous exposure to weather-related trauma, and levels of anxiety sensitivity is suggested to provide an explanation for these differences. The results suggest that prevention and treatment efforts should address learned fear response, aim at reducing anxiety sensitivity, and target disorder-specific cognitions.

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African Americans have reported higher levels of Posttraumatic Stress Disorder (PTSD) symptoms than their Caucasian counterparts in some studies. Variables hypothesized to contribute to differential levels of PTSD symptoms between African Americans and Caucasians that have not been adequately explored in these studies include ethnicity, resource loss, religious coping, and social support. The purpose of this study was to test portions of a model that characterizes the relationship between traumatic events and PTSD symptoms in African Americans and Caucasians. It was hypothesized that ethnicity, perceived ethnic identity, socioeconomic status (SES), resource loss, religious coping, family support, and professional support would be significant predictors of PTSD symptoms. Data from 59 African American children and adolescents, aged 4 to 20, and 54 of their Caucasian counterparts from the Residential Fire Project were used to examine the role of ethnicity, SES, resource loss, religious coping, family support, and professional support in the development of PTSD symptoms. Data from 86 African Americans and 417 Caucasians, aged 15 to 21 from the National Comorbidity Survey (NCS), were used to examine the role of ethnicity, perceived ethnic identity, SES, religious coping, family support, mental healthcare, and non-mental healthcare in the development of PTSD symptoms. Participants in the Fire Project were interviewed individually, and completed self-report questionnaires. Results indicated that only resource loss factors contributed significantly to the prediction of variance in PTSD symptoms. Participants in the NCS were also interviewed individually. Results indicated that mental healthcare, family support, SES, ethnicity, and religious coping contributed significantly to the prediction of variance in PTSD symptoms in this sample. Findings are discussed within a psychosocial model. / Master of Science

Every day people are exposed to crimes in Sweden, which can lead to both emotional and practical difficulties. Having the opportunity to get support and help after a traumatic incident can reduce the negative consequences of a crime, such as posttraumatic stress disorder and secondary victimization. In many communities in Sweden there are local support services for the crime victims, but in the district of Östra Norrbotten there are no support activities that specifically address this issue. The purpose of this thesis is to investigate if the police in Östra Norrbotten feel that they can offer the crime victim sufficient support or refer to such support. Eight police officers in the district were interviewed to learn about their experiences. The results show that the majority of respondents felt that there are gaps in the field they can´t provide the crime victims to a support that they deem as sufficient or refer to such support. The fact that crime victims do not receive support can lead to negative impact on the recovery from all events. / <p>Validerat; 20130317 (global_studentproject_submitter)</p>

Re-experiencing trauma in the form of intrusive, image-based memories (here referred to as flashbacks) is a hallmark symptom of Post-Traumatic Stress Disorder (PTSD). There are successful treatments available for full-blown PTSD; however, these can only be administered one month post trauma. There are limited interventions that can be administered to reduce flashbacks in the early aftermath of trauma. The overarching aim of this thesis was to use an experimental psychopathology approach, the trauma film paradigm, to investigate the reduction of flashbacks post-trauma using the cognitive task, Tetris. Chapter 1 provides a literature review of experimental research that has used the trauma film paradigm. Chapter 2 reviews experimental work on disrupting memory reconsolidation in humans. Chapter 3 details pilot work on the development of an experimental protocol based upon these literature reviews. Experiment 1 (Chapter 4) investigated disrupting reconsolidation for a 24 hour old analogue trauma (aversive film material) using the cognitive task, Tetris. A procedure designed to disrupt flashback reconsolidation (a memory reactivation task for the film followed by playing the computer game Tetris) was compared with a no-task Control. Compared to Control, those in the Tetris condition reported fewer flashbacks to the film in an intrusion diary across the subsequent week and on convergent measures of flashback frequency. Experiment 2 (Chapter 5) provided a test of replication for findings from Experiment 1, in addition to extending findings by dismantling the procedure’s component parts. Participants who underwent Tetris only (without memory reactivation) or memory reactivation (without Tetris) did not demonstrate a reduction in flashbacks and were comparable to the no-task control condition. Both a memory reactivation task plus Tetris in combination were critical for reducing subsequent flashbacks for a consolidated memory for a trauma film. Experiment 3 (Chapter 6) tested whether playing Tetris could help disrupt flashback memories for an analogue trauma (film) if administered prior to film viewing, relative to a no-task control condition. Results showed that playing Tetris before a trauma film did not reduce flashbacks, as demonstrated via an intrusion diary and convergent flashback measures. Chapters 7 reviews email feedback relating to playing Tetris after experiencing real-life adversity from members of the public. Chapter 8 explores a form of treatment for trauma in a NHS, complex patient setting. Chapter 9 discusses the findings from all chapters with reference to their implications and limitations, and new directions for future research. Overall, findings using analogue trauma suggest that memory reactivation followed by playing Tetris may be promising for development as a post-trauma ‘cognitive vaccine’ to disrupt the both the consolidation and potential reconsolidation of flashback memories.