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Diemen, Netherlands

Boelen P.A.,University Utrecht | Boelen P.A.,Arq Psychotrauma Expert Group
Journal of Trauma and Dissociation | Year: 2015

This study examined associations between the violence of a loss and the suddenness of a loss and symptom levels of prolonged grief disorder (PGD) and posttraumatic stress disorder (PTSD) after the death of a loved one. A further aim was to investigate whether peritraumatic distress (i.e., fear, helplessness, and horror) and peritraumatic dissociation mediate the emotional impact of violent losses and unexpected losses. We obtained self-reported data from 265 individuals bereaved in the previous 3 years by losses due to violent causes (17%) or illness (83%). Outcomes showed that participants who experienced violent losses (due to homicide, suicide, or accident) reported more PGD symptoms and PTSD symptoms compared to those confronted with illness loss. In this latter group, greater perceived unexpectedness was positively associated with PGD severity and PTSD severity. Multiple mediation analyses showed that the impact of violent loss and unexpectedness of the loss on PGD severity and PTSD severity was fully mediated by peritraumatic distress and dissociation; peritraumatic helplessness and peritraumatic dissociation (but not peritraumatic fear and horror) emerged as unique mediators. Findings suggest that both violent and unexpected losses exacerbate postloss psychopathology, which is at least partially because of such losses yielding more intense acute helplessness and dissociative responses. Copyright © Taylor & Francis Group, LLC. Source

Nawijn L.,University of Amsterdam | van Zuiden M.,University of Amsterdam | Frijling J.L.,University of Amsterdam | Koch S.B.J.,University of Amsterdam | And 3 more authors.
Neuroscience and Biobehavioral Reviews | Year: 2015

Post-traumatic stress disorder (PTSD) is a debilitating psychiatric disorder. An important diagnostic feature of PTSD is anhedonia, which may result from deficits in reward functioning. This has however never been studied systematically in PTSD. To determine if PTSD is associated with reward impairments, we conducted a systematic review of studies in which reward functioning was compared between PTSD patients and healthy control participants, or investigated in relation to PTSD symptom severity. A total of 29 studies were included, covering reward anticipation and approach ('wanting'), and hedonic responses to reward ('liking'). Overall, results were mixed, although decreased reward anticipation and approach and reduced hedonic responses were repeatedly observed in PTSD patients compared to healthy controls. Decreased reward functioning was seen more often in female than in male PTSD samples and most often in response to social positive stimuli. Though more research is needed, these findings are a first step in understanding the possible mechanisms underlying anhedonia in PTSD. © 2015 Elsevier Ltd. Source

Olff M.,University of Amsterdam | Olff M.,Arq Psychotrauma Expert Group | Polak A.R.,University of Amsterdam | Witteveen A.B.,University of Amsterdam | And 2 more authors.
Neurobiology of Learning and Memory | Year: 2014

Background: Posttraumatic stress disorder (PTSD) has been associated with neurocognitive deficits, such as impaired verbal memory and executive functioning. Less is known about executive function and the role of comorbid depression in PTSD. Recently, studies have shown that verbal memory impairments may be associated with comorbid depressive symptoms, but their role in executive function impairments is still unclear. Objective: To examine several domains of executive functioning in PTSD and the potentially mediating role of comorbid depressive symptoms in the relationship between executive function and PTSD. Method: Executive functioning was assessed in 28 PTSD patients and 28 matched trauma-exposed controls. The Cambridge Neuropsychological Test Automated Battery (CANTAB) with subtests measuring response inhibition (SST), flexibility/set shifting (IED), planning/working memory (OTS) and spatial working memory (SWM) was administered in PTSD patients and trauma-exposed controls. Regression analyses were used to assess the predictive factor of PTSD symptoms (CAPS) and depressive symptoms (HADS-D) in relation to executive function when taking into account the type of trauma. Pearson's correlations were used to examine the association between PTSD symptom clusters (CAPS) and executive function. The mediating effects of depression and PTSD were assessed using regression coefficients and the Sobel's test for mediation. Results: Our findings indicate that PTSD patients performed significantly worse on executive function than trauma-exposed controls in all domains assessed. PTSD symptoms contributed to executive functioning impairments (SST median correct, IED total errors, OTS latency to correct, SWM total errors and SWM strategy). Adding depressive symptoms to the model attenuated these effects. PTSD symptom clusters 'numbing' and to a lesser extent 'avoidance' were more frequently associated with worse executive function (i.e., IED total errors, OTS latency to correct and SWM total errors) than 'reexperiencing' and 'hyperarousal'. Depressive symptoms mediated the relation between PTSD and executive function on some executive function measures (IED total errors and OTS latency to correct), whereas PTSD did not mediate the relation between depression and executive function. Conclusions: PTSD patients perform worse on executive function. The impairments seem to be mostly associated with the less specific PTSD symptom cluster of 'numbing'. Depressive symptoms seem to mediate the relationship between PTSD and executive function. These findings may have clinical implications with regard to treatment indication and prognosis. © 2014 Elsevier Inc. Source

Christiansen D.M.,University of Aarhus | Christiansen D.M.,University of Southern Denmark | Elklit A.,University of Southern Denmark | Olff M.,University of Amsterdam | Olff M.,Arq Psychotrauma Expert Group
General Hospital Psychiatry | Year: 2013

Objective: Losing an infant or fetus late in pregnancy, during birth or in the first year of life is a potentially traumatic event for parents. However, little is known about the factors contributing to chronic posttraumatic stress reactions in this population. The present study examined chronic posttraumatic stress disorder (PTSD) symptoms and potential correlates in 634 mothers and fathers up to 18 years (M= 3.4 years) after the death of their infant. Methods: Members of a private national support organization for parents bereaved by infant death were contacted and asked to participate in the study. Participants filled out a questionnaire package including measures of PTSD (the Harvard Trauma Questionnaire), coping (the Coping Style Questionnaire), perceived social support (the Crisis Support Scale) and attachment (the Revised Adult Attachment Scale). Associations between variables were examined through the use of analyses of variance, correlation analyses and a regression analysis. Results: We found an estimated PTSD prevalence of 12.3%. Type of loss (pre-, peri- or postnatal) did not have any effect on PTSD severity, but lower gestational age was associated with more symptoms. Time since the loss, female sex, attachment avoidance, attachment anxiety, emotion-focused coping, rational coping, feeling let down and social support satisfaction accounted for 42% of the variance in PTSD severity. Conclusions: The study highlights the long-term impact of infant loss and points to attachment, coping and social support as important contributors to the development and maintenance of posttraumatic stress symptoms. © 2013 Elsevier Inc. Source

Mouthaan J.,Center for Anxiety Disorders | Sijbrandij M.,VU University Amsterdam | Sijbrandij M.,EMGO Institute for Health and Care Research | Luitse J.S.K.,Trauma Unit | And 5 more authors.
Psychoneuroendocrinology | Year: 2014

Background: Decreased activation of the hypothalamus-pituitary-adrenal (HPA) axis in response to stress is suspected to be a vulnerability factor for posttraumatic stress disorder (PTSD). Previous studies showed inconsistent findings regarding the role of cortisol in predicting PTSD. In addition, no prospective studies have examined the role of dehydroepiandrosterone (DHEA), or its sulfate form DHEAS, and the cortisol-to-DHEA(S) ratio in predicting PTSD. In this study, we tested whether acute plasma cortisol, DHEAS and the cortisol-to-DHEAS ratio predicted PTSD symptoms at 6 weeks and 6 months post-trauma. Methods: Blood samples of 397 adult level-1 trauma center patients, taken at the trauma resuscitation room within hours after the injury, were analyzed for cortisol and DHEAS levels. PTSD symptoms were assessed at 6 weeks and 6 months post-trauma with the Clinician Administered PTSD Scale. Results: Multivariate linear regression analyses showed that lower cortisol predicted PTSD symptoms at both 6 weeks and 6 months, controlling for age, gender, time of blood sampling, injury, trauma history, and admission to intensive care. Higher DHEAS and a smaller cortisol-to-DHEAS ratio predicted PTSD symptoms at 6 weeks, but not after controlling for the same variables, and not at 6 months. Conclusions: Our study provides important new evidence on the crucial role of the HPA-axis in response to trauma by showing that acute cortisol and DHEAS levels predict PTSD symptoms in survivors of recent trauma. © 2014 Elsevier Ltd. Source

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