Elucidating factors associated with adherence to treatment for physical and mental health conditions is important, given well-documented associations between non-adherence and poor treatment outcomes. Researchers have worked to identify such factors; however, most studies focus on adherence to medical, rather than, psychological treatments. Clarifying variables that predict adherence to psychotherapy is particularly important for individuals with post-traumatic stress disorder (PTSD), for whom treatment, which typically involves exposure to trauma-related stimuli and imagery, can be aversive. It may consequently be associated with high nonadherence rates, even though studies indicate that greater adherence to PTSD treatment relates to better treatment outcomes. Research needs to identify factors that increase or decrease the likelihood that affected individuals will enter and complete therapy. Although several studies to date have examined adherence to treatment for PTSD, this literature is limited on several fronts. First, studies on psychotherapy adherence have identified few consistent predictors of treatment adherence. Second, adherence to psychotherapy is rarely a central focus of treatment-related research; more typically, researchers treat adherence as secondary in importance to treatment outcomes. Third, little research on psychotherapy adherence has been theoretically driven. Fourth, little adherence research has focused on combat veterans with PTSD, who tend to have particularly poor treatment outcomes. Especially lacking is knowledge about predictors of adherence in veterans who have recently returned from combat; most research focuses on veterans of the Vietnam War, many of whom were initially traumatized decades earlier. The study tested the hypothesis that elevated reports of a specific type of PTSD symptom--avoidance/emotional numbing-- predicted poorer adherence to treatment in 160 veterans who received psychotherapy. No significant associations between avoidance and emotional numbing symptoms and adherence were found. However, emotional numbing was negatively related to psychotherapy adherence. Other variables typically related to PTSD and treatment outcomes were found to be important predictors of psychotherapy adherence and completion/noncompletion of therapy.

EMDR, eye movement desentization and reprocessing, är en evidensbaserad psykoterapeutisk metod för behandling av bl. a trauma. Syftet med undersökningen var att undersöka effekten av EMDR-behandling på patienter hos S:t Lukas. Frågeställningar: Hur skattar S:t Lukas patienter Posttraumatisk stress disorder (PTSD)-kriterierna återupplevande, undvikande och överspändhet, före och efter EMDR-behandling? Finns det utifrån bakgrundsvariablerna kön, ålder, typ av trauma, tidigare trauma samt antal behandlingstillfällen några skillnader i personernas skattningar före respektive efter behandlingen? Metod: I denna kvantitativa studie undersöktes 21 kvinnor och 9 män före och efter EMDR behandling. Självskattningsformuläret Impact of Event Scale-Revised, IES-R användes, vilket mäter PTSD-kriterierna återupplevande, undvikande och överspändhet. Resultat och diskussion: Resultaten från studien visar statistiskt signifikant symtomminskning i återupplevande, undvikande och överspändhet. Ingen av patienterna gav indikation på PTSD efter EMDR-behandlingen. Före behandlingen var genomsnittet för IES-värdet 2,8. Efter behandlingen hade genomsnittet för IES-värdet sjunkit till 0,7. Det finns statistiskt signifikanta skillnader mellan IES-värdet när olika bakgrundsvariabler särskiljs: yngre (personer under 40 år) har ett signifikant lägre IES-värde för återupplevande än äldre efter behandling, personer som utsatts för rån har ett signifikant högre IES-värde för överspändhet än personer som utsatts för andra trauma före behandling och personer som utsatts för rån har ett signifikant högre IES-värde för undvikande än personer som utsatts för andra trauma efter behandling. Det genomsnittliga IES-värdet minskade med 2,1 för kvinnor och 2,0 för män. Kvinnor och män svarar således på behandlingen på likartat sätt men de könsbundna variationerna i denna undersökning är inte signifikanta. Personer som utsatts för tidigare trauma har före behandling ett genomsnittligt högre IES-värde, 2,9, än personer som inte utsatts för tidigare trauma, 2,6. Skillnaden i IES-värde är emellertid inte statistiskt signifikant och efter behandling är IES-värdet i stort sett detsamma för de två grupperna.

Combat veterans often return from war with psychological as well as physical injuries. Armed service members who are bodily injured routinely go to hospitals for treatment, first at military hospitals and later in the U.S. Department of Veterans Affairs (VA) system. But those with psychological injuries like post-traumatic stress disorder (PTSD) often go years, if not a lifetime, without treatment, in large part because the VA denies their claims with dubious justification. Veterans’ service organizations like the Veterans of Foreign Wars (VFW), the American Legion, and others, as well as state and county governments, have knowledgeable service officers whose job is to help guide veterans through the VA system and through the many appeals that are often needed to get treatment and an adequate disability rating that could result in monetary payments. This report tells the story of one VFW post in Burnet, Texas, its veterans, their families, and how their success in getting treatment for PTSD has positively affected their lives. It has also enabled them, as they recover, to help other veterans seek treatment and win compensatory disability ratings too. The report focuses on one Vietnam veteran, who four decades after his discharge from the Army came to be treated for PTSD. / text

BACKGROUND: There have been prevailing gender differences in negative mental health outcomes for U.S. female service members (FSMs) returning from combat deployments with rates of depression and post-traumatic stress nearly twice that of their male peers. AIM: The aim of this research study was to examine the extent to which the absence or presence of social support, social conflict, and stressful life events either facilitated or hindered optimal mental health during the post-deployment period and shaped FSMs’ mental health in the context of the post-deployment experience. RESEARCH QUESTIONS: What was the nature of the relationship between social support, social conflict, and stressful life events and mental health symptoms (PTSD, depression, anxiety, and alcohol abuse) in FSMs after deployment to Iraq? And was the degree of social support or the degree of social conflict more highly associated with negative mental health symptoms (greater PTSD symptoms, greater depression symptoms, greater anxiety symptoms, and greater alcohol abuse symptoms) in FSMs after deployment to Iraq? THEORETICAL FRAMEWORK: The theoretical framework for this study was derived from Vaux’s theory of social support (Vaux, 1988) and from a model developed by Berkman and Glass (2000) that hypothesized how social support and social networks have direct effects on an individual’s physical, mental, and social health. These two frameworks were viewed from a feminist standpoint perspective. METHODS: This descriptive, correlational, cross-sectional design used a convenience sample of 150 active duty FSMs who were 6-12 months post-deployment from Iraq and stationed at Fort Campbell, Kentucky. FINDINGS: During preliminary exploratory data analyses and statistical assumption testing, significant between group differences were found between the officer and enlisted FSMs on four variables: annual household income, stressful life events, education, and prior exposure to violence (physical assault, sexual assault, or domestic violence). Additionally, significant differences emerged in bivariate correlations between the predictor and outcome variables when the 13 officer FSMs were separated out from the original sample during statistical analyses. These findings suggested these were two distinct populations; therefore, the sample was divided into two groups based on rank. For the officer FSMs, there were no significant bivariate correlations between social support, social conflict, or post-deployment stressful life events and any of the mental health outcomes although a one-tailed analysis was conducted due to low sample size (n = 13). In contrast, the two-tailed analysis of the enlisted FSMs (n = 137) showed significant positive bivariate correlations (p < .01) between social conflict and stressful life events and the outcome variables depression, PTSD, and anxiety symptom severity. Furthermore, the analysis demonstrated a significant inverse correlation between social support and the outcome variables depression, PTSD, and anxiety symptom severity. Hierarchical linear regression of the enlisted FSM group showed that depression symptom severity was best explained by the presence of comorbid PTSD symptoms and the absence of social support. The presence of social conflict was excluded in the final model, and stressful life events were not found to be significant in explaining depression symptom severity. Overall, comorbid PTSD symptom severity and the absence of social support accounted for 71% of the variance in depression symptom severity in this group of enlisted FSMs. In contrast, greater PTSD symptom severity in the post-deployment period was best explained by greater comorbid depression symptom severity, the presence of social conflict, and greater stressful life events. The absence of social support did not significantly contribute to the model for PTSD symptom severity. Comorbid depression symptom severity, stressful life events, and the presence of social conflict, which were entered in three steps, accounted for 74% of the variance in PTSD symptom severity reported by this group of enlisted FSMs. And finally, greater anxiety symptom severity was best explained by greater comorbid depression symptom severity, the presence of social conflict, and the absence of social support. The presence of social conflict had a stronger relationship with anxiety symptom severity than the absence of social support in the final model. In addition, the presence of more stressful life events did not significantly contribute to the overall variance in anxiety symptom severity. Comorbid depression symptom severity, the absence of social support, and the presence of social conflict accounted for 68% of the variance in anxiety symptoms reported by this group of enlisted FSMs. The implications and recommendations based on these findings span strategic planning for the military, nursing practice, and future research. / text

This research explores the relationship between social, cultural and politico-historical factors and the interpretation of events as causing disruption and significant distress in the lives of rural Zulu-speakers in KwaZulu Natal. Focus groups, each comprising a different category of first-language Zulu speakers were conducted, namely a youth group, a women's group, a group of traditional and faith healers and a group of community health workers, The groups were conducted in Zulu, recorded and then transcribed and translated into English. The translated transcripts were then analysed for common themes. It was found that explanatory systems of illnesses, based on the African worldview produce a tendency to cluster events into 'paths ofdistress' that are endowed with traumatic meaning. These paths are initiated by events that are significant in terms of people's history and culture. They are an attempt to describe how the connection and relationship between events, which are to a large extent outside ofone's control, contribute to aconcept of 'trauma' or'suffering' that implies disruption and distress on an ongoing and wider scale than is captured in the Western concept of PTSD. Aprofound sense offailure and a breakdown of community relationships and processes are some ofthe effects of such paths. / Thesis (M.A.)-University of Natal, Durban, 2003.

Post-traumatic stress disorder (PTSD), an anxiety disorder, may develop after experiencing or witnessing a severe traumatic event. Characteristic symptoms include hyper arousal and amnesic symptoms, while volume reductions in the hippocampus of these patients appear correlated with illness severity and the degree of cognitive deficit. Stress-induced increases in plasma cortisol have been implicated in this apparent atrophy of the hippocampus, although, clinical studies have described a marked suppression of plasma cortisol in PTSD. Given this hypocortisolemia, the basis for hippocampal neuro degeneration and cognitive decline remains unclear. While stress-related hippocampal structural changes have been linked to the neurotoxic effects of glucocorticoids and glutamate. NMDA-NO pathways have been found to play a causal role in anxiety-related behaviours. Prior exposure to trauma is an important risk factor for PTSD. In most instances the disorder becomes progressively worse over time, possibly with a delayed onset, suggesting a role for sensitization. In this study a time-dependent sensitization (TDS) model was used to induce PTSD-like sequelae in male Spraque-Dawley rats. The TDS-model is based on exposure to acute stressors, with a reminder of the trauma, in the form of re-exposure to one of the acute stressor, seven days later. NOS-activity, NMDA receptor parameters (Bmax and Kd) and GABA levels in the hippocampus of rats, as well as plasma corticosterone levels were determined 21 days after exposure to the TDS-model. Increased levels of corticosterone were measured after exposure to acute stress, but these levels were found to decrease below basal levels 21 days after the re-exposure, thus mimicking glucocorticoid levels in patients with PTSD. These findings may also imply that the increase in glucocorticoid levels after stress exposure is only the initial step in a cascade of events leading to neuronal damage in the hippocampus. This study also found that stress-restress evoked a long-lasting increase in hippocampal NOS activity that was accompanied by a reactive down-regulation of hippocampal NMDA receptors and dysregulation of inhibitory GABA pathways. Subsequently, animals were chronically treated with certain pharmacological agents prior to exposure to the TDS-model to determine possible approaches for inhibiting the induction of PTSD. Pre-treatment with fluoxetine, currently indicated in the treatment of PTSD. and the nNOS inhibitor, 7-nitroindazole, had no effect on the increased NOS activity measured 21 days afler exposure to the TDS-model. Pre-treatment with the iNOS inhibitor, aminoguanidine, however, resulted in inhibition of the observed increase in hippocampal NOS-activity, implicating a possible role for the iNOS isoform in the etiology of PTSD. Treatment with ketoconazole, an inhibitor of glucoccfticoid synthesis, resulted in inhibition of the increase in NOS-activity observed after exposure to TDS-stress, thus indicating a possible link between stress glucocorticoid-release and NO synthesis. These perturbations may have importance in explaining the increasing evidence for stress-related hippocampal degenerative pathology and cognitive deficits seen in patients with PTSD. Uncovering and understanding the role of NO in PTSD will hopefully lead to the development of selective therapeutic agents in disorders like PTSD. as well as providing a better understanding of basic processes underlying normal and pathological neuronal functions in PTSD. / Thesis (Ph.D. (Pharmacology))--North-West University, Potchefstroom Campus, 2004.

Introduction: This thesis evaluated the effectiveness of an educational intervention for Toronto Transit Commission (TTC) employees exposed to a traumatic event at work. Methods: This study used a sequential mixed methods design. The primary outcome was the proportion seeking mental health treatment after an educational intervention (BPI) compared to a group not receiving an educational intervention (TAU). Qualitative interviews aimed to understand what compelled participants to seek help and perceptions of the educational intervention. Results: 60 TAU and 50 BPI participants were recruited. A larger proportion of BPI participants sought specialty mental health treatment compared to the TAU (p=0.034). Reasons for seeking treatment were varied and we found overall positive responses to the educational intervention, particularly normalization of reactions. Conclusions: A greater proportion of those receiving the educational intervention sought help. However, the interviews showed that although the educational intervention was helpful, it was not central to this decision.

It is well documented that exposure to intimate partner violence (IPV) negatively affects children’s developmental outcomes (Chan & Yeung, 2009; Evans, Davies & DiLillo, 2008) and may lead to the expression of symptomatology consistent with post-traumatic stress disorder (PTSD) (Graham-Bermann, De Voe, Mattis, Lynch & Thomas, 2006; Kilpatrick & Williams,1998). Currently there is no consensus as to the nature of the influence of mother-child relationships on child outcomes such as post-traumatic stress symptoms in IPV-exposed families. The present study examined the role of maternal influences, such as the quality of mother-child interaction, maternal depression, and maternal violence history on sibling trauma outcomes. Results indicated that increased maternal depressive symptoms, maternal violence history, and negative mother-child interactions did not significantly predict post-traumatic stress symptoms in siblings exposed to IPV. Findings provided support for the notion of maternal compensatory strategies used to protect siblings from the detrimental consequences of IPV exposure.

Introduction: This thesis evaluated the effectiveness of an educational intervention for Toronto Transit Commission (TTC) employees exposed to a traumatic event at work. Methods: This study used a sequential mixed methods design. The primary outcome was the proportion seeking mental health treatment after an educational intervention (BPI) compared to a group not receiving an educational intervention (TAU). Qualitative interviews aimed to understand what compelled participants to seek help and perceptions of the educational intervention. Results: 60 TAU and 50 BPI participants were recruited. A larger proportion of BPI participants sought specialty mental health treatment compared to the TAU (p=0.034). Reasons for seeking treatment were varied and we found overall positive responses to the educational intervention, particularly normalization of reactions. Conclusions: A greater proportion of those receiving the educational intervention sought help. However, the interviews showed that although the educational intervention was helpful, it was not central to this decision.

Post-traumatic stress disorder (PTSD), an anxiety disorder, may develop after experiencing or witnessing a severe traumatic event. Characteristic symptoms include hyper arousal and amnesic symptoms, while volume reductions in the hippocampus of these patients appear correlated with illness severity and the degree of cognitive deficit. Stress-induced increases in plasma cortisol have been implicated in this apparent atrophy of the hippocampus, although, clinical studies have described a marked suppression of plasma cortisol in PTSD. Given this hypocortisolemia, the basis for hippocampal neuro degeneration and cognitive decline remains unclear. While stress-related hippocampal structural changes have been linked to the neurotoxic effects of glucocorticoids and glutamate. NMDA-NO pathways have been found to play a causal role in anxiety-related behaviours. Prior exposure to trauma is an important risk factor for PTSD. In most instances the disorder becomes progressively worse over time, possibly with a delayed onset, suggesting a role for sensitization. In this study a time-dependent sensitization (TDS) model was used to induce PTSD-like sequelae in male Spraque-Dawley rats. The TDS-model is based on exposure to acute stressors, with a reminder of the trauma, in the form of re-exposure to one of the acute stressor, seven days later. NOS-activity, NMDA receptor parameters (Bmax and Kd) and GABA levels in the hippocampus of rats, as well as plasma corticosterone levels were determined 21 days after exposure to the TDS-model. Increased levels of corticosterone were measured after exposure to acute stress, but these levels were found to decrease below basal levels 21 days after the re-exposure, thus mimicking glucocorticoid levels in patients with PTSD. These findings may also imply that the increase in glucocorticoid levels after stress exposure is only the initial step in a cascade of events leading to neuronal damage in the hippocampus. This study also found that stress-restress evoked a long-lasting increase in hippocampal NOS activity that was accompanied by a reactive down-regulation of hippocampal NMDA receptors and dysregulation of inhibitory GABA pathways. Subsequently, animals were chronically treated with certain pharmacological agents prior to exposure to the TDS-model to determine possible approaches for inhibiting the induction of PTSD. Pre-treatment with fluoxetine, currently indicated in the treatment of PTSD. and the nNOS inhibitor, 7-nitroindazole, had no effect on the increased NOS activity measured 21 days afler exposure to the TDS-model. Pre-treatment with the iNOS inhibitor, aminoguanidine, however, resulted in inhibition of the observed increase in hippocampal NOS-activity, implicating a possible role for the iNOS isoform in the etiology of PTSD. Treatment with ketoconazole, an inhibitor of glucoccfticoid synthesis, resulted in inhibition of the increase in NOS-activity observed after exposure to TDS-stress, thus indicating a possible link between stress glucocorticoid-release and NO synthesis. These perturbations may have importance in explaining the increasing evidence for stress-related hippocampal degenerative pathology and cognitive deficits seen in patients with PTSD. Uncovering and understanding the role of NO in PTSD will hopefully lead to the development of selective therapeutic agents in disorders like PTSD. as well as providing a better understanding of basic processes underlying normal and pathological neuronal functions in PTSD. / Thesis (Ph.D. (Pharmacology))--North-West University, Potchefstroom Campus, 2004.