Arq Psychotrauma Expert Group

Diemen, Netherlands

Arq Psychotrauma Expert Group

Diemen, Netherlands
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Frijling J.L.,Brain Imaging Center | Koch S.B.J.,Brain Imaging Center | Nawijn L.,Brain Imaging Center | Veltman D.J.,VU University Amsterdam | Olff M.,Arq Psychotrauma Expert Group
Social Cognitive and Affective Neuroscience | Year: 2015

There is a need for effective, early post-trauma preventive interventions for post-traumatic stress disorder (PTSD). Attenuating amygdala hyperreactivity early post-trauma, a likely PTSD vulnerability factor, may decrease PTSD risk. Since oxytocin modulates amygdala reactivity to emotional stimuli, oxytocin administration early post-trauma may be a promising candidate for PTSD prevention. In a randomized double-blind placebo-controlled fMRI study, we investigated effects of a single intranasal oxytocin administration (40 IU) on amygdala reactivity to happy, neutral and fearful faces in 41 recently trauma-exposed men and women showing moderate to high distress after initial post-trauma screening. We explored treatment interactions with sex. Participants were scanned within 11 days post-trauma. Compared with placebo, oxytocin significantly increased right amygdala reactivity to fearful faces. There was a significant treatment by sex interaction on amygdala reactivity to neutral faces, with women showing increased left amygdala reactivity after oxytocin. These findings indicate that a single oxytocin administration may enhance fearful faces processing in recently trauma-exposed individuals and neutral faces processing in recently trauma-exposed women. These observations may be explained by oxytocin-induced increased salience processing. Clinical implications of these findings for PTSD prevention should be further investigated. Trial register: Netherlands Trial Registry; Boosting Oxytocin after trauma: Neurobiology and the Development of Stress-related psychopathology (BONDS); NTR3190;;. © The Author (2015). Published by Oxford University Press.

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.

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.

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.

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.

Boelen P.A.,University Utrecht | Boelen P.A.,Arq Psychotrauma Expert Group | Reijntjes A.,University Utrecht | Smid G.E.,Foundation Centrum 45
Journal of Anxiety Disorders | Year: 2015

This study examined associations of Prospective IU and Inhibitory IU with symptom-levels of Prolonged Grief Disorder (PGD), Posttraumatic Stress-Disorder (PTSD), and depression in a sample of bereaved individuals. Specifically, 265 bereaved individuals completed measures of IU, PGD, PTSD, and depression in the first year after the death of a loved one; 134 participants again completed symptom-measures six months later. Cross-sectional analyses showed that Inhibitory IU (but not Prospective IU) was positively associated with symptom-levels of PTSD and depression (but not PGD), even when controlling for neuroticism, worry, and rumination. Prospective analyses showed that Prospective IU (but not Inhibitory IU) at baseline, predicted PGD severity six months later (but not PTSD or depression at follow-up) while controlling for baseline symptom-levels. The findings support the notion that IU is a vulnerability factor for different emotional problems, including those developing after the death of a loved one. Clinical implications of these findings are discussed. © 2016 Elsevier Ltd

Vermetten E.,Leiden University | Vermetten E.,Arq Psychotrauma Expert Group | Spiegel D.,Stanford University
Current Psychiatry Reports | Year: 2014

Psychological trauma can have devastating consequences on emotion regulatory capacities and lead to dissociative processes that provide subjective detachment from overwhelming emotional experience during and in the aftermath of trauma. Dissociation is a complex phenomenon that comprises a host of symptoms and factors, including depersonalization, derealization, time distortion, dissociative flashbacks, and alterations in the perception of the self. Dissociation occurs in up to two thirds of patients with borderline personality disorder (BPD). The neurobiology of traumatic dissociation has demonstrated a heterogeneity in posttraumatic stress symptoms that, over time, can result in different types of dysregulated emotional states. This review links the concepts of trauma and dissociation to BPD by illustrating different forms of emotional dysregulation and their clinical relevance to patients with BPD. © Springer Science+Business Media New York 2014.

Frijling J.L.,University of Amsterdam | Van Zuiden M.,University of Amsterdam | Koch S.B.J.,University of Amsterdam | Nawijn L.,University of Amsterdam | And 3 more authors.
Neuropsychopharmacology | Year: 2016

Approximately 10% of trauma-exposed individuals go on to develop post-traumatic stress disorder (PTSD). Neural emotion regulation may be etiologically involved in PTSD development. Oxytocin administration early post-trauma may be a promising avenue for PTSD prevention, as intranasal oxytocin has previously been found to affect emotion regulation networks in healthy individuals and psychiatric patients. In a randomized double-blind placebo-controlled between-subjects functional magnetic resonance (fMRI) study, we assessed the effects of a single intranasal oxytocin administration (40 IU) on seed-based amygdala resting-state FC with emotion regulation areas (ventromedial prefrontal cortex (vmPFC), ventrolateral prefrontal cortex (vlPFC)), and salience processing areas (insula, dorsal anterior cingulate cortex (dACC)) in 37 individuals within 11 days post trauma. Two resting-state scans were acquired; one after neutral- and one after trauma-script-driven imagery. We found that oxytocin administration reduced amygdala-left vlPFC FC after trauma script-driven imagery, compared with neutral script-driven imagery, whereas in PL-treated participants enhanced amygdala-left vlPFC FC was observed following trauma script-driven imagery. Irrespective of script condition, oxytocin increased amygdala-insula FC and decreased amygdala-vmPFC FC. These neural effects were accompanied by lower levels of sleepiness and higher flashback intensity in the oxytocin group after the trauma script. Together, our findings show that oxytocin administration may impede emotion regulation network functioning in response to trauma reminders in recently trauma-exposed individuals. Therefore, caution may be warranted in administering oxytocin to prevent PTSD in distressed, recently trauma-exposed individuals. © 2016 American College of Neuropsychopharmacology. All rights reserved.

Nijdam M.J.,University of Amsterdam | De Vries G.-J.,University of Amsterdam | Gersons B.P.R.,University of Amsterdam | Gersons B.P.R.,Arq Psychotrauma Expert Group | And 2 more authors.
Journal of Clinical Psychiatry | Year: 2015

Objective: Neuropsychological studies have consistently demonstrated impaired verbal memory in posttraumatic stress disorder (PTSD). Trauma-focused treatment for PTSD is thought to rely on memory, but it is largely unknown whether treatment outcome is influenced by memory performance. The aim of the study, therefore, was to examine the relationship between verbal memory performance and treatment response to trauma-focused psychotherapy. Method: Participants were referred to our outpatient clinic and recruited between December 2003 and January 2009 upon diagnosis of PTSD according to DSM-IV. Secondary analyses of a randomized controlled trial comparing eye movement desensitization and reprocessing therapy (n = 70) and brief eclectic psychotherapy (n = 70), a cognitive-behavioral intervention, are reported. Response to treatment was measured by self-reported PTSD symptom severity (Impact of Event Scale - Revised) over 17 weeks. Pretreatment verbal memory measures (California Verbal Learning Test, Rivermead Behavioral Memory Test) were included in the mixed linear model analyses in order to investigate the influence of memory on treatment outcome. Results: Pretreatment encoding, short-term retrieval, long-term retrieval, and recognition performance were significantly associated with treatment response in terms of self-reported PTSD symptom severity for both treatments (P = .013). Receiver operating characteristic curves predicting treatment response with pretreatment memory indices showed that 75.6% of the patients could be correctly classified as responder. Conclusions: Poor verbal memory performance represents a risk factor for worse treatment response to trauma-focused psychotherapy. Memory measures can be helpful in determining which patients are unable to benefit from trauma-focused psychotherapy. Future research should explore how treatment perspectives of patients with poor verbal memory can be improved. © Copyright 2015 Physicians Postgraduate Press, Inc.

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.

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