Modelling the impact of emotion dysregulation and event centrality on posttraumatic distress

Abstract

Posttraumatic stress disorder (PTSD) is the most frequent of the common psychopathological responses to trauma and is known to increase risk of comorbid mental health difficulties, physical health issues, and impaired psychosocial functioning. An increasing body of research has directed efforts to understand PTSD within the context of emotion regulation, a multidimensional construct that encapsulates one’s ability to identify, monitor, and evaluate emotional experiences, as well as to regulate these in a manner that enables the individual to reach and maintain goals against contextual demands.

Cognitive models of PTSD provide a complementary framework to understand the mechanisms through which emotion regulation influences the development of PTSD. According to these models, there is a cognitive pathway to posttraumatic distress, via generation of new (or strengthening of previous) appraisals of the world as predominantly dangerous, and the self as predominantly incompetent. Emotional distress emerges when these appraisals are incongruent to valued individual goals. Alongside these processes, core PTSD symptoms, such as intrusions, reflect underlying cognitive processes aimed at integrating incongruent trauma-related appraisals with prior appraisals regarding the world and the self. Within such models information processing acts to down-regulate posttraumatic distress and symptomatology by resolving discrepancies between pre-trauma and post-trauma beliefs, and by restoring a sense of the world as relatively safe, and of the self as relatively competent.

Empirical evidence has demonstrated the association of both emotion regulation and trauma-related beliefs with PTSD and highlighted the presence of pronounced emotion dysregulation and negative appraisals among individuals exposed to interpersonal trauma during early stages of life, emphasizing the influence of developmental factors (e.g. attachment) upon these processes. This is consistent with propositions from contemporary developmental theories of emotion regulation and their impact in terms of self-related and interpersonal responses to trauma.

The main aim of this thesis was to model the differential impact of different types of stressors on PTSD, as mediated by emotion dysregulation and appraisal processes. This was conducted in both online community (Study I) and clinical (Study II) samples. In doing so, the thesis sought to expand the application of mediation modelling of posttraumatic distress, to concurrently investigate in a single path analysis model the unique contribution of different types of stressors to mechanisms involved in posttraumatic response.

The first chapter of the thesis presents an overview of contemporary issues in the presentation and aetiology of PTSD, and the debate surrounding the merit of using narrowly defined criteria to differentiate between traumatic and non-traumatic stressors when considering a diagnosis for PTSD. Thereafter, Chapter 2 presents an overview of the main cognitive and emotion-focussed models of PTSD presentation and maintenance, leading into the justification for the empirical studies. Three different types of stressors were examined; interpersonal adversity (experiences of abuse and neglect), non-interpersonal trauma, and non-traumatic stressors that did not involve abuse or neglect. This distinction enabled empirical investigation of the impact of non-traumatic stressors (which do not meet diagnostic criteria for trauma) as potential predictors of posttraumatic distress. Drawing from the aforementioned theoretical and empirical contributions, a path model for the association of trauma exposure to posttraumatic distress was constructed, with emotion dysregulation and event centrality (the latter indicating dominance of stressor-related appraisals) as mediators.

Chapter 3 presents the underlying methodology for the empirical studies, procedures used, the measurement battery, and planned analyses. In line with cognitive models of PTSD, the modelling assumed a serial mediation form, with emotion dysregulation specified to impact on event centrality.

Chapters 4 and 5 presents the results of the modelling. Hypotheses were investigated in two cross-sectional studies, applied to an online community sample (N = 375; Chapter 4); and a clinical sample of individuals receiving treatment for PTSD and other trauma related presentations (N = 106; Chapter 5) sample respectively. Both studies indicated the significance of the serial mediation process through emotion dysregulation and event centrality. However, there was contrasting evidence relevant to the contribution of each type of stressor to the mediation model. The online community study indicated significant mediation pathways for both interpersonal adversity and non-traumatic stressors, and significant direct effects from traumatic stressors and non-traumatic stressors on posttraumatic distress. In contrast, results from the clinical sample indicated that interpersonal adversity was the only stressor with direct effects on emotion dysregulation, event centrality, and posttraumatic distress, and the only one to initiate indirect pathways to posttraumatic distress through both mediators.

Finally, in Chapter 6 (Discussion) these results are contextualised with reference to the presentation of PTSD and the core psychological mechanisms introduced in Chapters 1 and 2. In particular, the findings illustrate the need to be more critical of strictly defined criteria for trauma to inform healthcare provision, and the potential merit of intensifying efforts to prevent interpersonal adversity during early years of life, given it was the only predictor in both studies shown to predict risk for posttraumatic distress through emotion dysregulation.