Acute effects of alcohol on trauma memories

Memory disturbances following a trauma are a characteristic feature of posttraumatic stress disorder. Despite alcohol’s frequent involvement in real-life traumatic events, our understanding of its contribution to trauma-related symptoms is unclear. The research in this thesis aimed to determine the way in which alcohol intoxication during a traumatic experience might influence memory for the event. Experiment 1 showed that alcohol impaired recognition associated with recollection with greater reductions as dose increased (0, 0.4, 0.6, 0.8g/kg); in contrast, recognition associated with familiarity was preserved. Experiments 2 and 3 utilised an analogue trauma film to examine how low (0.4g\kg) and high (0.8g/kg) doses of alcohol affected intrusive imagery and explicit memory for the footage. Alcohol during encoding resulted in a dose-dependent inverted U-shaped curve on intrusive imagery, with increased intrusions only following a low dose. Explicit memory for the footage was reduced in a dose-dependent linear manner. In addition, experiment 3 concurrently assessed same- and shifted-view object location recognition to determine the mechanisms that might underpin alcohol’s effects on trauma memory. Results showed that a low dose of alcohol selectively impaired shifted-view recognition, thought to rely on an allocentric representation. However, same-view recognition was preserved, suggesting a spared egocentric representational system. In contrast, the high dose disrupted both same- and shifted-view recognition, suggesting a global disruption in both memory systems. Experiment 4 examined the effects of alcohol (0.4/kg) on contextual fear acquisition and extinction and both same- and shifted-view recognition. Fear acquisition was unaffected by alcohol, whilst extinction learning was impaired with persistent conditioned responses throughout extinction. Alcohol-induced reductions in extinction learning were highly correlated with decreases in shifted-view recognition, supporting the role of contextual encoding in extinction. The findings of these studies suggest that alcohol dose-dependently influences trauma memories and this could result in a distinct set of trauma-related symptoms

The Influence of Neuroendocrine and Genetic Markers of Stress on Cognitive Processing and Intrusive Symptoms

This body of research investigated the influence of neuroendocrine and genetic elements of arousal on cognitive processes in the development of intrusive memories and flash-forward intrusions as related to Post-Traumatic Stress Disorder. Specifically, this thesis investigated various mechanisms that may underlie intrusive symptoms as postulated by prevalent theories of PTSD. Study 1 examined the distinctive relationship between peritraumatic dissociation and subsequent re-experiencing symptoms. Network analyses revealed strong positive edges between peritraumatic dissociation and subsequent amnesia, as well as the re-experiencing symptoms of physical reactivity to reminders, flashbacks, intrusions, and dreams, and to a lesser extent emotional numbness and hypervigilance. The finding that peritraumatic dissociation is related to subsequent re-experiencing symptoms is consistent with cognitive models that emphasize the role of dissociative experiences during a traumatic event in the etiology of PTSD re-experiencing symptoms. Study 2 aimed to determine whether peri-traumatic stress, as measured via salivary cortisol and salivary alpha-amylase, as well as pre-existing genetic polymorphisms on the FKBP5 gene increased dissociation and data-driven processing, and subsequently impacted intrusive memories related to a trauma film. The findings revealed that greater noradrenergic arousal predicted less intrusive memory distress in individuals who scored higher on data-driven processing and trait dissociation, and in FKBP5 low-risk carriers. For individuals who reported less data-driven processing and trait dissociation, and in FKBP5 high-risk carriers, as noradrenergic arousal increased, intrusive memory distress increased. This study also showed no association between data-driven processing with memory fragmentation, and fragmentation with intrusive memories. Whilst these findings support some aspect of cognitive models of PTSD as they indicate a role for data-driven processing and dissociation in intrusive symptoms, they highlight a threshold at which these variables stop moderating the relationship between arousal and intrusive memories and suggest that memory fragmentation is not related to intrusive memories. Study 3 examined the role of cognitive control in flash-forward intrusions in the context of an enduring stressor, the COVID-19 pandemic. In line with expectations, results showed that as cognitive control worsened, FKBP5 high-risk carriers reported more flash-forward distress, and low-risk carriers reported less distress. These findings are considered in the context of hippocampal changes and are consistent with emerging theories of PTSD. Lastly, study 4 sought to investigate the role of two neurological processes, pattern separation and pattern completion in intrusive memories in individuals with PTSD compared to trauma exposed controls. Consistent with existing literature, the data indicate that individuals with PTSD reported more data-driven processing, more intrusive symptoms, and demonstrated better behavioural pattern completion than trauma-exposed controls. These findings are in line with current cognitive models of PTSD, as they again indicate a role for data-driven processing in PTSD. However, study 4 found no support for the postulate that deficient pattern separation is a feature of PTSD and found an opposite effect for the role of pattern completion. Whilst these findings are inconsistent with theory, they are in line with existing experimental studies. Overall, the findings from this thesis provide insight into cognitive and biological models of PTSD and shed light on the mechanisms underlying the nature and development of intrusive symptoms

A Systematic Review and Meta-Analysis of the Incidence of Injury in Professional Female Soccer

The epidemiology of injury in male professional football is well documented and has been used as a basis to monitor injury trends and implement injury prevention strategies. There are no systematic reviews that have investigated injury incidence in women’s professional football. Therefore, the extent of injury burden in women’s professional football remains unknown. PURPOSE: The primary aim of this study was to calculate an overall incidence rate of injury in senior female professional soccer. The secondary aims were to provide an incidence rate for training and match play. METHODS: PubMed, Discover, EBSCO, Embase and ScienceDirect electronic databases were searched from inception to September 2018. Two reviewers independently assessed study quality using the Strengthening the Reporting of Observational Studies in Epidemiology statement using a 22-item STROBE checklist. Seven prospective studies (n=1137 professional players) were combined in a pooled analysis of injury incidence using a mixed effects model. Heterogeneity was evaluated using the Cochrane Q statistic and I2. RESULTS: The epidemiological incidence proportion over one season was 0.62 (95% CI 0.59 - 0.64). Mean total incidence of injury was 3.15 (95% CI 1.54 - 4.75) injuries per 1000 hours. The mean incidence of injury during match play was 10.72 (95% CI 9.11 - 12.33) and during training was 2.21 (95% CI 0.96 - 3.45). Data analysis found a significant level of heterogeneity (total Incidence, X2 = 16.57 P < 0.05; I2 = 63.8%) and during subsequent sub group analyses in those studies reviewed (match incidence, X2 = 76.4 (d.f. = 7), P <0.05; I2 = 90.8%, training incidence, X2 = 16.97 (d.f. = 7), P < 0.05; I2 = 58.8%). Appraisal of the study methodologies revealed inconsistency in the use of injury terminology, data collection procedures and calculation of exposure by researchers. Such inconsistencies likely contribute to the large variance in the incidence and prevalence of injury reported. CONCLUSIONS: The estimated risk of sustaining at least one injury over one football season is 62%. Continued reporting of heterogeneous results in population samples limits meaningful comparison of studies. Standardising the criteria used to attribute injury and activity coupled with more accurate methods of calculating exposure will overcome such limitations

11th International Coral Reef Symposium Abstracts

https://nsuworks.nova.edu/occ_icrs/1001/thumbnail.jp