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Acute stress reactivity and intrusive memory development: a randomized trial using an adjusted trauma film paradigm

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Abstract

Understanding the neurobiological and cognitive processes underlying the development of posttraumatic stress disorder (PTSD) and its specific symptoms may facilitate preventive intervention development. Severe traumatic stress and resulting biological stress system activations can alter contextual memory processes. This may provide a neurobiological explanation for the occurrence of intrusive memories following trauma. Investigating the associations between temporal aspects and individual variation in peri- and post-traumatic hypothalamic pituitary adrenal (HPA) axis and sympathetic nervous system (SNS) stress reactivity and memory processing may increase our understanding of intrusive symptom development. The experimental trauma film paradigm is commonly used for this purpose but lacks robust SNS and HPA axis activation. Here, we performed an RCT to investigate the effect of an adjusted trauma film paradigm containing an added brief psychosocial stressor on HPA and SNS stress reactivity throughout the experiment and intrusive memory frequency in the following week in healthy males (N=63, mean age=22.3). Secondary, we investigated effects on film-related declarative memory accuracy and intrusion-related characteristics, and associations between acute HPA and SNS stress reactivity, film-related memory, glucocorticoid receptor functioning and intrusion frequency and characteristics. Participants were randomized to the socially-evaluated cold pressor test (seCPT n=29) or control condition (warm water n=34) immediately prior to a trauma film. Linear Mixed Models revealed increased acute SNS and cortisol reactivity, lower recognition memory accuracy and more intrusions that were more vivid and distressing during the following week in the seCPT compared to control condition. Linear regression models revealed initial associations between cortisol and alpha amylase reactivity during the experimental assessment and subsequent intrusions, but these effects did not survive multiple comparison corrections. Thus, with this adjustment, we increased the translational value of the trauma film paradigm as it appears to elicit a stronger stress response that is likely more comparable to real-life trauma. The adapted paradigm may be useful to investigate individual variation in biological and cognitive processes underlying early post-trauma PTSD symptoms and could advance potential preventive interventions.

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... Simulating the biological conditions that lead to PTSD in an experimental setting will allow better quality diagnostic and treatment tools to be developed. Recent research has suggested that increased frequency of intrusive memories of the film content are reported by participants who undergo a stress task prior to trauma film viewing (Hilberdink et al., 2022), although one study recently suggested that this only occurs if there is a corresponding increase in cortisol following stress (Schultebraucks et al., 2019). This finding aligns with our understanding that negative and intrusive memories are consolidated as a result of cortisol reactivity following stress (Roozendaal & McGaugh, 2011) -if participants do not have a cortisol response after film viewing, they will not necessarily report intrusive memories (Chou et al., 2014). ...
... At the beginning of the experiment, the first salivary sample and the first SUDS rating were collected. Then, the cold pressor test and trauma film paradigm commenced (for a similar method, see Hilberdink et al, 2022). This manipulation was intended to increase participant stress levels in the stress group via integration of the cold-pressor test into the trauma film viewing. ...
... While previous studies have shown that stress reactivity and related biological responses are positively associated with intrusive memory frequency (Cheung et al., 2015;Hilberdink et al., 2022;Nicholson et al., 2014), viewing traumatic imagery or film does not necessarily invoke a biological stress response (Otte et al., 2016). Recently, Hilberdink et al. (2022) showed that inclusion of a socially evaluated cold-pressor task prior to trauma film viewing significantly increased the number of reported intrusive memories relative to control, and that this was positively associated with the biological stress responses measured in saliva. ...
... A potential mechanism by which the COVID-19 outbreak may have affected mental health is the modulation of memory processes. Stress has been shown to promote associative learning (Merz et al., 2016;Peyrot et al., 2020) and analogue intrusions (Hilberdink et al., 2022;Schultebraucks et al., 2019) by altering neurochemical processes during memory formation. To our knowledge, no study to date has investigated whether the stress brought about by the COVID-19 outbreak might have affected analogue PTSD symptoms and associative learning. ...
... Our first finding was that COVID-19-related distress was associated with increased intrusion load, which is in line with previous studies showing that a psychosocial stressor before analogue trauma exposure results in higher intrusion load (Hilberdink et al., 2022) and supports the idea that biological stress responses predict subsequent intrusions (Schultebraucks et al., 2019). Moreover, our findings align with the assumption that the COVID-19 outbreak had the potential to increase allostatic load (Fofana et al., 2020). ...
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Background: The COVID-19 outbreak in early 2020 was associated with an immediate increase in mental health problems in a significant percentage of the general population. Therefore, it is crucial to investigate how the COVID-19 pandemic – as a psychosocial stressor – affected the aetiological processes of mental disorders. Previous research has shown that stress potentiates associative (fear) learning and analogue symptoms of posttraumatic stress disorder (PTSD) and that analogue PTSD symptoms can emerge in response to associative learning. Objective: We investigated whether distress in response to the COVID-19 outbreak support the development of intrusions and rumination after exposure to a non-COVID-19-related analogue trauma. Moreover, we examined if these effects are mediated by the strength of associative learning during analogue trauma. Method: 122 undergraduate university students participated in an online experiment between March and July 2020. They completed questionnaires measuring distress and rumination related to the COVID-19 outbreak. On a subsequent day, they went through an associative learning task, in which neutral stimuli were paired with the appearance of a highly aversive film clip. Subjective ratings were assessed as indicators of associative learning. On the next day, participants documented film-related intrusions and rumination. Results: COVID-19-related distress but not rumination was associated with post-film intrusion and rumination load. These effects were mediated by associative learning. Conclusions: The current findings are in line with the assumptions that stress enhanced both associative learning and PTSD symptoms. Specifically, they indicate that prolonged psychosocial stress – like during the COVID-19 outbreak – is linked to individual differences in memory processing of aversive events. Further confirmatory research is needed to replicate these results.
... The persistent reexperiencing of the traumatic experience characterizing chronic PTSD is accompanied by elevated systemic levels of oxidative stress and inflammation, due to sustained activation of the hypothalamic-pituitary-adrenal axis (77,78). This maladaptive stress response can provoke a constant state of alert, hyperarousal, and altered fear response (79), further exacerbating intrusive memories in a maladaptive loop (80,81). By limiting the access of the consciousness and attention to intrusive memories (55), the memory control system may break this negative cycle, reducing hippocampal damage caused by intrusion-related stress and their associated negative emotions. ...
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The hippocampus’s vulnerability to trauma-induced stress can lead to pathophysiological disturbances that precipitate the development of posttraumatic stress disorder (PTSD). The mechanisms of resilience that foster remission and mitigate the adverse effects of stress remain unknown. We analyzed the evolution of hippocampal morphology between 2016/2017 and 2018/2019, as well as the memory control mechanisms crucial for trauma resilience. Participants were individuals exposed to the 2015 Paris terrorist attacks ( N = 100), including chronic ( N = 34) and remitted ( N = 19) PTSD, and nonexposed ( N = 72). We found that normalization of inhibitory control processes, which regulate the resurgence of intrusive memories in the hippocampus, not only predicted PTSD remission but also preceded a reduction in traumatic memories. Improvement in control mechanisms was associated with the interruption of stress-induced atrophy in a hippocampal region that includes the dentate gyrus. Human resilience to trauma is characterized by the plasticity of memory control circuits, which interacts with hippocampal neuroplasticity.
... Some relevant functional domains are difficult to monitor in laboratory settings, such as sleep for example. For other relevant functional domains detailed experimental tasks have been formulated, such as for example for intrusions (Asselbergs et al., 2023;Hilberdink et al., 2022;James et al., 2016), avoidance (Sheynin et al., 2017) and fear learning and extinction (Milad et al., 2008;Wen et al., 2022). These tasks are often long and involve an emotional component. ...
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Background: Individuals greatly differ in their responses to acute stress, ranging from resilience to vulnerability that may yield stress-related psychopathology. Stress-related psychopathologies involve, by definition, substantial modifications across multiple behavioural domains, including impaired cognitive, affective and social functioning. Nevertheless, and despite extensive investigation of individual variability in stress responsivity, no study to date simultaneously assessed the impact of acute stress across multiple behavioural domains within a given individual. Objective: To address this critical gap, 84 healthy female participants (mean age 24.45 ± 3.02, range 19-35) underwent an established acute stress induction procedure and completed three behavioural tasks, probing the functional domains of positive, cognitive and social processing, both before and after the acute stress procedure. Method: A novel behavioural profiling algorithm was implemented to identify individuals whose performance was substantially impacted by stress across all three functional domains. Results: Approximately 30% of participants exhibited substantial deviation in their performance from before to after stress in all three tasks, hereon defined as stress-affected. Stress-affected participants did not differ in their psychological and physiological responses to the acute stress procedure from the other stress-unaffected 70% of the sample. However, follow-up assessments in 66 of these participants revealed higher levels of stress six months following the procedure among the stress-affected compared to the stress-unaffected group. Stress-affected individuals also reported more aversive childhood experiences, such that the odds of participants who were sexually abused at an early age to be affected behaviourally by acute stress later in life increased by more than five-fold. Conclusions: Taken together, these findings suggest that being affected by acute stress across multiple functional domains is associated with future stress sensitivity and past childhood sexual abuse. Probing individual differences in the impact of acute stress across domains of functionality may better align with the multi-dimensional nature of stress responsivity, uncovering latent vulnerability.
... Nevertheless, the actual research shows a contrary situation. The film paradigm seems to trigger a more robust stress response, which may be more similar to reallife trauma (Hilberdink et al., 2022). Moreover, the types of trauma (body, sex, traffic, disgust) caused by the themes of different films have different direct subjective and physiological responses (Arnaudova and Hagenaars, 2017). ...
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Some people develop symptoms of posttraumatic stress disorder (PTSD) after having experienced a traumatic event, whereas others do not. Intrusive memories are a cardinal symptom of PTSD and a better understanding of encoding and consolidation of intrusive memory may yield important insights on differences in the response to trauma. The primary aim of this study is to investigate whether psychosocial stress induction (Trier Social Stress Test) versus active control (placebo version) leading to respective biological stress responses during the encoding and consolidation of a film-elicited analogue trauma influences the development of intrusive memories over the course of 7 consecutive days. We hypothesized that the activation of the biological stress system increases the number of intrusive memories over the course of 7 days. This single-blind randomized placebo-controlled study examined 122 young healthy women. Biological stress response was measured by salivary cortisol, salivary α-amylase activity, and heart rate variability. Generalized linear mixed models were used to analyze longitudinal effects of activation of biological stress response on self-reported number of intrusive memories. Cross-validated regularized regression (least absolute shrinkage and selection operator) was applied for data-driven feature selection including known biological and psychological predictors. Corroborating our hypothesis, biological stress-responders to the Trier Social Stress Test reported significantly more intrusive memories after trauma film. A priori designed post hoc tests point at significantly more intrusions on Day 1 and 2 in biological stress responders. Least absolute shrinkage and selection operator regression revealed salivary cortisol, salivary α-amylase activity, heart rate variability, subjectively rated distress, fear, and (on trend level) dissociation during the trauma film as relevant predictors of intrusive memories. A heightened biological stress response in young women is associated with more intrusive memories the first days after experiencing a trauma analogue. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
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Intrusive memories of a traumatic event can be distressing and disruptive, and comprise a core clinical feature of post-traumatic stress disorder (PTSD). Intrusive memories involve mental imagery-based impressions that intrude into mind involuntarily, and are emotional. Here we consider how recent advances in cognitive science have fueled our understanding of the development and possible treatment of intrusive memories of trauma. We conducted a systematic literature search in PubMed, selecting articles published from 2008 to 2018 that used the terms “trauma” AND (“intrusive memories” OR “involuntary memories”) in their abstract or title. First, we discuss studies that investigated internal (neural, hormonal, psychophysiological, and cognitive) processes that contribute to intrusive memory development. Second, we discuss studies that targeted these processes using behavioural/pharmacological interventions to reduce intrusive memories. Third, we consider possible clinical implications of this work and highlight some emerging research avenues for treatment and prevention, supplemented by new data to examine some unanswered questions. In conclusion, we raise the possibility that intrusive memories comprise an alternative, possibly more focused, target in translational research endeavours, rather than only targeting overall symptoms of disorders such as PTSD. If so, relatively simple approaches could help to address the need for easy-to-deliver, widely-scalable trauma interventions.
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Background: Women have a two to three times higher risk of developing post-traumatic stress disorder (PTSD) compared to men. Several factors are involved explaining this difference (Christiansen & Hansen, 2015 Christiansen, D. M., & Hansen, M. (2015). Accounting for sex differences in PTSD: A multi-variable mediation model. European Journal of Psychotraumatology, 6, 26068. doi:10.3402/ejpt.v6.26068[Taylor & Francis Online] [Google Scholar]). Both psychosocial and biological explanations (e.g. oxytocin related) have been suggested and will be reviewed in this paper. To date, we are still behind in gender- and sex-sensitive research and reporting. Prevalence and type of trauma: The lifetime prevalence of PTSD is about 10–12% in women and 5–6% in men. There are similar differences between the sexes for (comorbid) disorders such as major depression and anxiety disorders. PTSD subcluster scores have been found to be increased in women, e.g. for re-experiencing and anxious arousal (Charak et al., 2014 Charak, R., Armour, C., Elklit, A., Angmo, D., Elhai, J. D., & Koot, H. M. (2014). Factor structure of PTSD, and relation with gender in trauma survivors from India. European Journal of Psychotraumatology, 5, 1. doi:10.3402/ejpt.v5.25547[Taylor & Francis Online] [Google Scholar]). Men and women experience different types of trauma, both in private life and at work (e.g. police officers, Van der Meer et al., 2017 van der Meer, C. A. I., Bakker, A., Smit, A. S., van Buschbach, S., den Dekker, M., Westerveld, G. J., … Olff, M. (2017). Gender and age differences in trauma and PTSD among Dutch treatment-seeking police officers. Journal of Nervous & Mental Disease, 205(2), 87–2. doi:10.1097/NMD.0000000000000562 [Google Scholar]), with women being exposed to more high-impact trauma (e.g. sexual trauma) than men, and at a younger age. Trauma early in life has more impact, especially when it involves type II trauma interfering with neurobiological development and personality. Traumatic stress affects different areas of the brains of boys and girls at different ages. Acute phase, stress-coping and psychotherapy: In the acute phase, women generally score higher than men on acute subjective responses, e.g. threat perception, peritraumatic dissociation and known predictors of PTSD. Women handle stressful situations differently and have evolved differentially to support these different behaviours. For instance, women in stressful situations may use a tend-and-befriend response rather than the fight-or-flight response that is often assumed. Emotion-focused, defensive and palliative coping are more prevalent in women, while problem-focused coping is higher in men. Women seek more social support, the lack of it being the most consistent predictor of negative outcome of trauma. Women have been shown to benefit more from psychotherapy then men in the reduction of PTSD symptoms. Psychobiological reactions and effects of oxytocin: Although only 2% of psychobiological research has been conducted in females (mainly rats), sex differences have been shown. Women appear to have a more sensitized hypothalamus–pituitary–axis than men, while men appear to have a sensitized physiological hyperarousal system. PTSD has consistently been associated with amygdala hyperactivity, ventromedial prefrontal cortex (vmPFC) hypoactivity and reduced communication (functional connectivity) between the vmPFC and amygdala, with the lower PFC control over the amygdala providing an explanation for the excessive fear response in PTSD. We hypothesized that the oxytocin system, which is associated with social support, fear and stress responses, was likely to play a sex-specific role in the stress response. In recently traumatized patients, we found that the effects of administration of oxytocin on amygdala reactivity to emotional stimuli depend on stimulus valence and sex (Frijling, 2017 Frijling, J. L. (2017). Preventing PTSD with oxytocin: Effects of oxytocin administration on fear neurocircuitry and PTSD symptom development in recently trauma-exposed individuals. European Journal of Psychotraumatology, 8(1), 1302652. doi:10.1080/20008198.2017.1302652[Taylor & Francis Online] [Google Scholar]). In PTSD patients, we showed sex-specific routes for the effects of single oxytocin administration on the potential to diminish anxiety (fear learning) and fear expression by the amygdala: increased inhibitory control of the vmPFC over the centromedial nucleus in men and fewer excitatory dorsal anterior cingulate cortex projections to the basolateral nucleus in women. So, while our findings add to accumulating evidence that oxytocin administration could potentially enhance treatment response in PTSD, the routes in men and women differ (Frijling, 2017 Frijling, J. L. (2017). Preventing PTSD with oxytocin: Effects of oxytocin administration on fear neurocircuitry and PTSD symptom development in recently trauma-exposed individuals. European Journal of Psychotraumatology, 8(1), 1302652. doi:10.1080/20008198.2017.1302652[Taylor & Francis Online] [Google Scholar]). Gender policy: In summary, all of these sex and gender differences in brain and behaviour together may explain why PTSD is more prevalent in women than in men. Clearly, we should not simplify. There are no male or female stereotypes, but some features are more common in women and others in men. To fully understand the differences, we need more gender- and sex-sensitive research as well as reporting (e.g. see the gender policy of the European Association of Science Editors). In 2016, the European Journal of Psychotraumatology was the first to implement a gender policy (Olff, 2016 Olff, M. (2016). Five years of European Journal of Psychotraumatology. European Journal of Psychotraumatology, 7, 31350. doi:10.3402/ejpt.v7.31350[Taylor & Francis Online] [Google Scholar]), i.e. authors are asked to: report the sex of research subjects, justify single-sex studies, discriminate between sex and gender (mostly for human research), analyse how sex or gender impact the results, and discuss sex and gender issues when relevant. This should not only apply to the field of psychotrauma, but deserves a much broader implementation. In doing so, we hope to obtain information that will improve sex- and gender-specific approaches to helping those affected by psychotrauma.
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A better understanding of psychological trauma is fundamental to clinical psychology. Following traumatic event(s), a clinically significant number of people develop symptoms, including those of Acute Stress Disorder and/or Post Traumatic Stress Disorder. The trauma film paradigm offers an experimental psychopathology model to study both exposure and reactions to psychological trauma, including the hallmark symptom of intrusive memories. We reviewed 74 articles that have used this paradigm since the earliest review (Holmes & Bourne, 2008) until July 2014. Highlighting the different stages of trauma processing, i.e. pre, peri and post trauma, the studies are divided according to manipulations before, during and after film viewing, for experimental as well as correlational designs. While the majority of studies focussed on the frequency of intrusive memories, other reactions to trauma were also modelled. We discuss the strengths and weaknesses of the trauma film paradigm as an experimental psychopathology model of trauma, consider ethical issues, and suggest future directions. By understanding the basic mechanisms underlying trauma symptom development, we can begin to translate findings from the laboratory to the clinic, test innovative science-driven interventions, and in the future reduce the debilitating effects of psychopathology following stressful and/or traumatic events.
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Evidence suggests that previous trauma reduces the cortisol response to subsequent stressors. We examined the relation of this response to intrusive memory, and the potential moderating roles of sympathetic reactions. Pre-existing trauma-related factors and the cardiac defense response were assessed before 58 healthy participants viewed a trauma film. Salivary cortisol and alpha-amylase (sAA) were collected pre-, peri- and post-film. Intrusive memories about the film were recorded for a week. Cortisol increased whereas sAA decreased after the film. Those with more recent traumatic experiences and greater subclinical PTSD symptoms had lower cortisol concentration post-film. Lower cortisol levels predicted greater vividness of intrusions. Positive correlations between cortisol and the frequency of intrusion were only present among individuals with more sympathetic activations. These findings suggest the contribution of insufficient cortisol secretion to over-consolidation of traumatic memory, and highlight the variation attributable to individual differences and different memory characteristics.
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Most people will experience or witness a traumatic event. A common occurrence after trauma is the experience of involuntary emotional memories of the traumatic event, herewith "flashbacks". Some individuals, however, report no flashbacks. Prospective work investigating psychological factors associated with an absence of flashbacks is lacking. We performed an individual participant data meta-analysis on 16 experiments (n = 458) using the trauma film paradigm to investigate the association of emotional response to traumatic film footage and commonly collected baseline characteristics (trait anxiety, current depression, trauma history) with an absence of analogue flashbacks. An absence of analogue flashbacks was associated with low emotional response to the traumatic film footage and, to a lesser extent, low trait anxiety and low current depression levels. Trauma history and recognition memory for the film were not significantly associated with an absence of analogue flashbacks. Understanding why some individuals report an absence of flashbacks may aid preventative treatments against flashback development.
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Intrusive memories are a common feature of many psychological disorders. Recent evidence has potentially extended cognitive models of intrusions by identifying the role of biological markers of arousal at the time of consolidation in subsequent memory for emotional events. This study investigated the role of arousal during consolidation in the development of intrusive memories. Seventy-eight university students (37 men and 41 women) viewed 20 negative and 20 neutral images. Half the participants then underwent a cold pressor test (High Stress), immersing their hand in ice water, while the remaining participants immersed their hand in warm water (Low Stress). Samples of salivary alpha-amylase (sAA) and cortisol were collected from participants at baseline and following the stressor challenge. Participants completed a delayed free recall test and intrusion questionnaires two days later. Participants in the High Stress condition reported more intrusions of negative images than participants in the Low Stress condition. An interaction variable in a linear regression of increased noradrenergic and cortisol values predicted intrusive memories of emotional stimuli for men but not women. These findings are consistent with recent evidence of the combined effects of noradrenaline and corticoid responses to stress on emotional memories, and also with increasing evidence of gender differences in how stress hormones influence formation of emotional memories. These findings point to possible mechanisms by which development of intrusions may be prevented after consolidation of traumatic experiences.
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This brief report presents an experiment testing the effect of immersion on emotional responses and cognitive genre categorisation of film viewers. Immersion of a film presentation was varied by presenting an animated movie either in a 3D-viewing condition (low immersive condition) or in a CAVE condition (high immersive condition, comparable to virtual reality experience). Viewers rated their emotions and categorised the movies into four basic film genres (action, drama, comedy, and non-fiction). Two distinct types of emotion were measured: Fictional World emotions (e.g., sadness) in response to the presented fictional events and Artefact emotions in response to the film as an artefact (e.g., fascination). Results showed that stronger immersion led to more intense emotions but did not influence genre categorisation. In line with expectations, both types of emotional response were intensified by high immersion. The results are explained by suggesting that highly immersive cinema has its impact on a basic dimension of emotion, namely arousal that underlies both types of emotions.
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The common approach to the multiplicity problem calls for controlling the familywise error rate (FWER). This approach, though, has faults, and we point out a few. A different approach to problems of multiple significance testing is presented. It calls for controlling the expected proportion of falsely rejected hypotheses – the false discovery rate. This error rate is equivalent to the FWER when all hypotheses are true but is smaller otherwise. Therefore, in problems where the control of the false discovery rate rather than that of the FWER is desired, there is potential for a gain in power. A simple sequential Bonferroni-type procedure is proved to control the false discovery rate for independent test statistics, and a simulation study shows that the gain in power is substantial. The use of the new procedure and the appropriateness of the criterion are illustrated with examples.
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Background: Flashbacks (intrusive memories of a traumatic event) are the hallmark feature of Post Traumatic Stress Disorder, however preventative interventions are lacking. Tetris may offer a 'cognitive vaccine' [1] against flashback development after trauma exposure. We previously reported that playing the computer game Tetris soon after viewing traumatic material reduced flashbacks compared to no-task [1]. However, two criticisms need to be addressed for clinical translation: (1) Would all games have this effect via distraction/enjoyment, or might some games even be harmful? (2) Would effects be found if administered several hours post-trauma? Accordingly, we tested Tetris versus an alternative computer game--Pub Quiz--which we hypothesized not to be helpful (Experiments 1 and 2), and extended the intervention interval to 4 hours (Experiment 2). Methodology/principal findings: The trauma film paradigm was used as an experimental analog for flashback development in healthy volunteers. In both experiments, participants viewed traumatic film footage of death and injury before completing one of the following: (1) no-task control condition (2) Tetris or (3) Pub Quiz. Flashbacks were monitored for 1 week. Experiment 1: 30 min after the traumatic film, playing Tetris led to a significant reduction in flashbacks compared to no-task control, whereas Pub Quiz led to a significant increase in flashbacks. Experiment 2: 4 hours post-film, playing Tetris led to a significant reduction in flashbacks compared to no-task control, whereas Pub Quiz did not. Conclusions/significance: First, computer games can have differential effects post-trauma, as predicted by a cognitive science formulation of trauma memory. In both Experiments, playing Tetris post-trauma film reduced flashbacks. Pub Quiz did not have this effect, even increasing flashbacks in Experiment 1. Thus not all computer games are beneficial or merely distracting post-trauma - some may be harmful. Second, the beneficial effects of Tetris are retained at 4 hours post-trauma. Clinically, this delivers a feasible time-window to administer a post-trauma "cognitive vaccine".
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Little information exists on the lifetime prevalence of traumatic events and posttraumatic stress disorder (PTSD) in the general population of the Netherlands. A national representative sample of 1087 adults aged 18 to 80 years was selected using random digit dialing and then surveyed by telephone using the Composite International Diagnostic Interview (CIDI) to determine the prevalence of trauma and DSM-IV PTSD. The lifetime prevalence of any potential trauma was 80.7%, and the lifetime prevalence of PTSD was 7.4%. Women and younger persons showed higher risk of PTSD. It was concluded that PTSD is a fairly common disorder and exposure to trauma is high throughout the population. Unexpectedly, prevalence rates resemble those found in the United States and are higher than in several other European countries.
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Background: Flashbacks are the hallmark symptom of Posttraumatic Stress Disorder (PTSD). Although we have successful treatments for full-blown PTSD, early interventions are lacking. We propose the utility of developing a 'cognitive vaccine' to prevent PTSD flashback development following exposure to trauma. Our theory is based on two key findings: 1) Cognitive science suggests that the brain has selective resources with limited capacity; 2) The neurobiology of memory suggests a 6-hr window to disrupt memory consolidation. The rationale for a 'cognitive vaccine' approach is as follows: Trauma flashbacks are sensory-perceptual, visuospatial mental images. Visuospatial cognitive tasks selectively compete for resources required to generate mental images. Thus, a visuospatial computer game (e.g. "Tetris") will interfere with flashbacks. Visuospatial tasks post-trauma, performed within the time window for memory consolidation, will reduce subsequent flashbacks. We predicted that playing "Tetris" half an hour after viewing trauma would reduce flashback frequency over 1-week. Methodology/principal findings: The Trauma Film paradigm was used as a well-established experimental analog for Post-traumatic Stress. All participants viewed a traumatic film consisting of scenes of real injury and death followed by a 30-min structured break. Participants were then randomly allocated to either a no-task or visuospatial ("Tetris") condition which they undertook for 10-min. Flashbacks were monitored for 1-week. Results indicated that compared to the no-task condition, the "Tetris" condition produced a significant reduction in flashback frequency over 1-week. Convergent results were found on a clinical measure of PTSD symptomatology at 1-week. Recognition memory between groups did not differ significantly. Conclusions/significance: Playing "Tetris" after viewing traumatic material reduces unwanted, involuntary memory flashbacks to that traumatic film, leaving deliberate memory recall of the event intact. Pathological aspects of human memory in the aftermath of trauma may be malleable using non-invasive, cognitive interventions. This has implications for a novel avenue of preventative treatment development, much-needed as a crisis intervention for the aftermath of traumatic events.
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Participants in 2 experiments watched a filmed story and then left the lab--with instructions not to think about the film, with instructions to think about the film, or with no instructions. Memories of the film, assessed on participants' return to the lab some 5 hr later, showed reliable effects of thought suppression on memory for the sequence of events in the film. Participants who suppressed thoughts of the film were less able to retrieve the order of events by several measures than were those in the other groups, even thought their retrieval of the events themselves as assessed by recognition, free recall, and cued recall was not generally impaired.
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Meta-analyses were conducted on 14 separate risk factors for posttraumatic stress disorder (PTSD), and the moderating effects of various sample and study characteristics, including civilian/military status, were examined. Three categories of risk factor emerged: Factors such as gender, age at trauma, and race that predicted PTSD in some populations but not in others; factors such as education, previous trauma, and general childhood adversity that predicted PTSD more consistently but to a varying extent according to the populations studied and the methods used; and factors such as psychiatric history, reported childhood abuse, and family psychiatric history that had more uniform predictive effects. Individually, the effect size of all the risk factors was modest, but factors operating during or after the trauma, such as trauma severity, lack of social support, and additional life stress, had somewhat stronger effects than pretrauma factors.
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The article describes features of trauma memories in post-traumatic stress disorder (PTSD), including characteristics of unintentional re-experiencing symptoms and intentional recall of trauma narratives. Reexperiencing symptoms are usually sensory impressions and emotional responses from the trauma that appear to lack a time perspective and a context. The vast majority of intrusive memories can be interpreted as re-experiencing of warning signals, i.e., stimuli that signalled the onset of the trauma or of moments when the meaning of the event changed for the worse. Triggers of re-experiencing symptoms include stimuli that have perceptual similarity to cues accompanying the traumatic event. Intentional recall of the trauma in PTSD may be characterised by confusion about temporal order, and difficulty in accessing important details, both of which contribute to problematic appraisals. Recall tends to be disjointed. When patients with PTSD deliberately recall the worst moments of the trauma, they often do not access other relevant (usually subsequent) information that would correct impressions/predictions made at the time. A theoretical analysis of re-experiencing symptoms and their triggers is offered, and implications for treatment are discussed. These include the need to actively incorporate updating information ("I know now ...") into the worst moments of the trauma memory, and to train patients to discriminate between the stimuli that were present during the trauma ("then") and the innocuous triggers of re-experiencing symptoms ("now").
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Background Impaired contextual fear inhibition is often associated with posttraumatic stress disorder (PTSD). Our previous work has demonstrated that more hippocampal activation during a response inhibition task after trauma exposure was related to greater resilience and fewer future PTSD symptoms. In the current study, we sought to extend our previous findings by employing a contextual fear conditioning and extinction paradigm to further determine the role of the hippocampus in resilience and PTSD in the early aftermath of trauma. Methods Participants (N = 28) were recruited in the Emergency Department shortly after experiencing a traumatic event. A contextual fear inhibition task was conducted in a 3 T MRI scanner approximately two months post-trauma. Measures of resilience (CD-RISC) at time of scan and PTSD symptoms three months post-trauma were collected. The associations between hippocampal activation during fear conditioning and during the effect of context during extinction, and post-trauma resilience and PTSD symptoms at three-months were assessed. Results During fear conditioning, activation of the bilateral hippocampal region of interest (ROI) correlated positively with resilience (r = 0.48, p = 0.01). During the effect of context during extinction, greater bilateral hippocampal activation correlated with lower PTSD symptoms three months post-trauma after controlling for baseline PTSD symptoms, age and gender (r=-0.59, p=0.009). Conclusions Greater hippocampal activation was related to post-trauma resilience and lower PTSD symptoms three months post-trauma. The current study supports and strengthens prior findings suggesting the importance of hippocampus-dependent context processing as a mechanism for resilience versus PTSD risk, which could be a potential mechanistic target for novel early interventions.
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The common approach to the multiplicity problem calls for controlling the familywise error rate (FWER). This approach, though, has faults, and we point out a few. A different approach to problems of multiple significance testing is presented. It calls for controlling the expected proportion of falsely rejected hypotheses — the false discovery rate. This error rate is equivalent to the FWER when all hypotheses are true but is smaller otherwise. Therefore, in problems where the control of the false discovery rate rather than that of the FWER is desired, there is potential for a gain in power. A simple sequential Bonferronitype procedure is proved to control the false discovery rate for independent test statistics, and a simulation study shows that the gain in power is substantial. The use of the new procedure and the appropriateness of the criterion are illustrated with examples.
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Progress in clinical and affective neuroscience is redefining psychiatric illness as symptomatic expression of cellular/molecular dysfunctions in specific brain circuits. Post-traumatic stress disorder (PTSD) has been an exemplar of this progress, with improved understanding of neurobiological systems subserving fear learning, salience detection, and emotion regulation explaining much of its phenomenology and neurobiology. However, many features remain unexplained and a parsimonious model that more fully accounts for symptoms and the core neurobiology remains elusive. Contextual processing is a key modulatory function of hippocampal-prefrontal-thalamic circuitry, allowing organisms to disambiguate cues and derive situation-specific meaning from the world. We propose that dysregulation within this context-processing circuit is at the core of PTSD pathophysiology, accounting for much of its phenomenology and most of its biological findings. Understanding core mechanisms like this, and their underlying neural circuits, will sharpen diagnostic precision and understanding of risk factors, enhancing our ability to develop preventive and “personalized” interventions.
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Introduction: Stress hormones such as cortisol are involved in modulating emotional memory. However, little is known about the influence of cortisol on the formation of intrusive memories after a traumatic event. The aim of this study was to examine whether cortisol levels during encoding and consolidation of an intrusion-inducing trauma film paradigm would influence subsequent intrusion formation. Material and methods: In an experimental, double-blind, placebo-controlled study a trauma film paradigm was used to induce intrusions in 60 healthy women. Participants received a single dose of either 20 mg hydrocortisone or placebo before watching a trauma film. Salivary cortisol and alpha-amylase as well as blood pressure were measured during the experiment. The consecutive number of intrusions, the vividness of intrusions, and the degree of distress evoked by the intrusions resulting from the trauma film were assessed throughout the following seven days. Results: Hydrocortisone administration before the trauma film resulted in increased salivary cortisol levels but did not affect the consecutive number of intrusions, the vividness of intrusions, and the degree of distress evoked by the intrusions throughout the following week. Conclusions: These results indicate that pharmacologically increased cortisol levels during an experimental trauma film paradigm do not influence consecutive intrusive memories. Current data do not support a prominent role of exogenous cortisol on intrusive memories, at least in healthy young women after a relatively mild trauma equivalent.
Article
Background and objectives: Cognitive and information processing theories of Post-Traumatic Stress Disorder (PTSD) assert that trauma intrusions are characterized by poor contextual embedding of visuospatial memories. Therefore, efficient encoding of visuospatial contextual information might protect against intrusions. We tested this idea using indices of visuospatial memory embedding along with the trauma film paradigm. Methods: Individual differences in spatial configuration learning, as well as the degree to which visual recognition memory depends on its visual encoding context (i.e., memory contextualization), were assessed in 81 healthy participants. Next, participants viewed a distressing film. Intrusions and other PTSD analogue symptoms were assessed subsequently. Results: Participants displaying stronger memory contextualization developed fewer intrusions and PTSD analogue symptoms. Spatial configuration learning was unrelated to memory contextualization and, contrary to prior findings, predicted higher levels of intrusions. Limitations: Due to the analogue design, our findings may not translate directly to clinical populations. Furthermore, due to the correlational design of the study, causal relations remain to be tested. Conclusions: Our results suggest a protective role for the ability to integrate memories in their original visual learning context against the development of PTSD symptoms.
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Neuroendocrine studies examining the hypothalamic-pituitar3'-adrenal (HPA) axis under baseline conditions and in response to neuroendocrine challenges have supported the hypothesis of altered HPA functioning in posttraumatic stress disorder (PTSD). However, to date, there is much debate concerning the nature of HPA changes in PTSD. Furthermore , in studies showing parallel findings in PTSD and major depressive disorder there is controversy regarding whether the HPA alterations suggest a specific pathophysiolog'y of PTSD, or, rather, reflect comorbid major depressive disorder. This review summarizes findings of HPA axis dysfunction in both PTSD and major depressive disorder, and shows distinct patterns of HPA changes, which are probably due to db~'erent mechanisms of action for cortisol and its regulatory factors.
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Background: Intrusive memories of traumatic events are a core feature of post-traumatic stress disorder but little is known about the neurobiological formation of intrusions. The aim of this study was to determine whether the activity of the noradrenergic system during an intrusion-inducing stressor would influence subsequent intrusive memories. Method: We conducted an experimental, double-blind, placebo-controlled study in 118 healthy women. Participants received a single dose of either 10 mg yohimbine, stimulating noradrenergic activity, or 0.15 mg clonidine, inhibiting noradrenergic activity, or placebo. Subsequently, they watched an established trauma film which induced intrusions. The number of consecutive intrusions resulting from the trauma film, the vividness of the intrusions, and the degree of distress evoked by the intrusions were assessed during the following 4 days. Salivary cortisol and α-amylase were collected before and after the trauma film. Results: A significant time × treatment interaction for the number of intrusions and the vividness of intrusions indicated a different time course of intrusions depending on treatment. Post-hoc tests revealed a delayed decrease of intrusions and a delayed decrease of intrusion vividness after the trauma film in the yohimbine group compared with the clonidine and placebo groups. Furthermore, after yohimbine administration, a significant increase in salivary cortisol levels was observed during the trauma film. Conclusions: Our findings indicate that pharmacological activation of the noradrenergic system during an emotionally negative event makes an impact on consecutive intrusive memories and their vividness in healthy women. The noradrenergic system seems to be involved in the formation of intrusive memories.
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Objective: Intraclass correlation coefficient (ICC) is a widely used reliability index in test-retest, intrarater, and interrater reliability analyses. This article introduces the basic concept of ICC in the content of reliability analysis. Discussion for researchers: There are 10 forms of ICCs. Because each form involves distinct assumptions in their calculation and will lead to different interpretations, researchers should explicitly specify the ICC form they used in their calculation. A thorough review of the research design is needed in selecting the appropriate form of ICC to evaluate reliability. The best practice of reporting ICC should include software information, "model," "type," and "definition" selections. Discussion for readers: When coming across an article that includes ICC, readers should first check whether information about the ICC form has been reported and if an appropriate ICC form was used. Based on the 95% confident interval of the ICC estimate, values less than 0.5, between 0.5 and 0.75, between 0.75 and 0.9, and greater than 0.90 are indicative of poor, moderate, good, and excellent reliability, respectively. Conclusion: This article provides a practical guideline for clinical researchers to choose the correct form of ICC and suggests the best practice of reporting ICC parameters in scientific publications. This article also gives readers an appreciation for what to look for when coming across ICC while reading an article.
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Traumatic experiences can lead to a range of mental health problems with posttraumatic stress disorder (PTSD) leading as the most documented disorder following trauma. Epidemiological research has found the rate of exposure to trauma to far outweigh the prevalence of PTSD. Indicating that most people do not develop PTSD following a traumatic event, this phenomenon has led to an interest in evaluating risk factors to determine who develops PTSD. Risk factors for the development of psychopathology following trauma exposure fall into three categories: pre-trauma, peri-trauma and post-trauma factors. Pre-trauma factors can include age, gender, race/ethnicity, education, prior psychopathology, and neurobiological factors. Peri-trauma factors can include the duration/severity of trauma experience and the perception that the trauma has ended. Post-trauma factors can include access to needed resources, social support, specific cognitive patterns, and physical activity. To date, several important risk factors have been found to impact the risk of developing PTSD including gender, age, education, IQ, race and ethnicity, sexual orientation, pre-trauma psychopathology, prior trauma exposure, familial psychiatric history, and neurobiological factors. This article outlines the state of research findings on pretraumatic, peritraumatic, and posttraumatic risk factors for the development of PTSD and associated psychopathology following trauma.
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Previous evidence on endocrine risk markers for posttraumatic stress disorder (PTSD) has been inconclusive. Here, we report results of the first prospective study to investigate whether long-term hair cortisol levels and experimentally-induced cortisol stress reactivity are predictive of the development of PTSD symptomatology in response to trauma during military deployment. Male soldiers were examined before deployment to Afghanistan and at a 12-month post-deployment follow-up using dimensional measures for psychopathological symptoms. The predictive value of baseline (i) hair cortisol concentrations (HCC, N=90) and (ii) salivary cortisol stress reactivity (measured by the Trier Social Stress Test, N=80) for the development of PTSD symptomatology after being exposed to new-onset traumatic events was analyzed. Baseline cortisol activity significantly predicted PTSD symptom change from baseline to follow-up upon trauma exposure. Specifically, our results consistently revealed that lower HCC and lower cortisol stress reactivity were predictive of a greater increase in PTSD symptomatology in soldiers who had experienced new-onset traumatic events (explaining 5% and 10.3% of variance, respectively). Longitudinal analyses revealed an increase in HCC from baseline to follow-up and a trend for a negative relationship between HCC changes and the number of new-onset traumatic events. Additional pre-deployment analyses revealed that trauma history was reflected in lower HCC (at trend level) and that HCC were negatively related to stressful load. Our data indicate that attenuated cortisol secretion is a risk marker for subsequent development of PTSD symptomatology upon trauma exposure. Future studies are needed to confirm our findings in other samples. Copyright © 2015 Elsevier Ltd. All rights reserved.
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We show that a Poisson structure can be induced on the affine moduli space of (semisimple) representations of an associative algebra from a suitable Lie algebra structure on the zeroth Hochschild homology of the algebra. In particular this applies to necklace Lie algebra for path algebras of doubled quivers and preprojective algebras. We call such structures H0-Poisson structures, and show that they are well behaved for Azumaya algebras and under Morita equivalence.
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Posttraumatic stress disorder (PTSD) is an anxiety disorder that may develop in response to a traumatic event. Approximately 10% of trauma-exposed individuals subsequently develop PTSD. It is hypothesized that the development of PTSD is associated with biological vulnerability factors, which are already present prior to the onset of symptoms. In this review we present an overview of currently identified vulnerability factors in the glucocorticoid (GC) signaling pathway for the development of PTSD. In addition, the implications of the identified vulnerability factors for potential preventive intervention strategies, including glucocorticoid receptor (GR) agonists and oxytocin, are discussed. Summarized, the findings of these studies indicate that individuals vulnerable for development of PTSD have dysregulations on various levels of the GC-signaling cascade: i.e. low levels of circulating levels of cortisol shortly after trauma, high GR number in peripheral blood mononuclear cells (PBMCs), high GILZ mRNA expression and low FKBP5 expression in PBMCs prior to trauma, and high sensitivity of T-cells for regulation by GCs prior to trauma. Furthermore, single nucleotide polymorphisms in the GR and FKBP5 genes have been found to be associated with increased risk for PTSD. Collectively, the identified vulnerability factors tentatively suggest that the development of PTSD may be preceded by a high sensitivity of various cells for regulation by GCs. The identification of these vulnerability factors may ultimately aid selective targeting of preventive interventions towards individuals at risk for PTSD. In addition, the identification of these vulnerability factors may eventually result in new preventive pharmacological strategies for PTSD.
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Neuroendocrine studies examining the hypothalamic-pituitary-adrenal (HPA) axis under baseline conditions and in response to neuroendocrine challenges have supported the hypothesis of altered HPA functioning in posttraumatic stress disorder (PTSD). However, to date, there is much debate concerning the nature of HPA changes in PTSD. Furthermore, in studies showing parallel findings in PTSD and major depressive disorder there is controversy regarding whether the HPA alterations suggest a specific pathophysiology of PTSD, or, rather, reflect comorbid major depressive disorder. This review summarizes findings of HPA axis dysfunction in both PTSD and major depressive disorder, and shows distinct patterns of HPA changes, which are probably due to different mechanisms of action for cortisol and its regulatory factors.
Article
Stressful events activate the amygdala and a network of associated brain regions. Studies in both humans and rodents indicate that noradrenaline has a prominent role in this activation. Noradrenaline induces a hypervigilant state that helps to remember the event. This mnemonic effect is enhanced when the situation is so stressful that substantial amounts of corticosteroids are released and reach the amygdala. The combination of the two hormones leads to optimal strengthening of contacts and thus memory. Yet, rises in corticosteroid levels that are not precisely synchronized with noradrenaline release do not act synergistically but rather prevent or suppress the effect of noradrenaline. This dynamic interaction illustrates the adaptive and potentially protective capacity of corticosteroids regarding traumatic memories.
Article
Recent years have seen a growing interest in salivary α-amylase (sAA) as a non-invasive marker for sympathetic nervous system (SNS) activity. Saliva offers many advantages as a biomarker fluid and sAA is one of its most plentiful components. sAA is a digestive enzyme that breaks down starch, which provides a simple means of quantification by measuring its enzymatic activity. This commentary will address a number of common misconceptions and methodological issues that surround the use of sAA as a marker of SNS activity and limit its utility in biobehavioral research. The usefulness of sAA as an SNS marker is undermined by the fact that the parasympathetic nerves also play a significant role in sAA release. Local parasympathetic nerves regulate sAA activity via: (1) α-amylase release from glands that are solely or mainly parasympathetically innervated; (2) via synergistic sympathetic-parasympathetic effects on protein secretion (known as 'augmented secretion'); and (3) via effects on salivary flow rate. Regarding methodology, we discuss why it is problematic: (1) to ignore the contribution of salivary flow rate; (2) to use absorbent materials for saliva collection, and; (3) to stimulate saliva secretion by chewing. While these methodological problems can be addressed by using standardized and timed collection of unstimulated saliva, the physiological regulation of sAA secretion presents less resolvable issues. We conclude that at present there is insufficient support for the use and interpretation of sAA activity as a valid and reliable measure of SNS activity.
Article
This study sought to characterize the variability of the acute cortisol response following trauma and its relationship to posttraumatic stress disorder (PTSD). Forty eight participants were recruited within 24h of a traumatic accident requiring hospital admission. A saliva sample was collected at 08.00 h and 16.00 h 2 days, 1 month and 6 months after hospital admission, together with 24-h urine collection. Participants completed a dexamethasone suppression test (0.5mg DEX at 21.00 h) at each follow up, together with self-report questionnaires. The Clinician Administered PTSD Scale (CAPS) was administered at 1 and 6 months to identify PTSD. Prevalence of PTSD was 27% at 1 month and 21% at 6 months. PTSD symptoms at 6 months were negatively correlated with salivary cortisol at 08.00 h on day 2 (r=-0.36, p=0.04), but positively correlated with 16.00 h cortisols (r=0.41, p=0.03). A lower rise in cortisol at 08.00 h on day 2 was associated with an increase in risk of PTSD at both 1 month (OR=1.411 (1.017, 1.957)) and 6 months (OR=1.411 (1.066, 1.866)). At 1 month, 70% of participants with PTSD suppressed cortisol to more than 90% of pre-dex levels compared with 25% without PTSD (χ(2)=6.77, p=0.034). Urinary cortisol excretion was not different between groups at any time point. The findings support a hypothesis that sensitization of the HPA axis and enhanced suppression of cortisol following the dexamethasone suppression test are established early in the disease process.
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To understand mental disorders, analogue paradigms provide an indispensable contribution. In posttraumatic stress disorder (PTSD), the stressful film paradigm is a frequently used analogue approach: Films depicting traumatic events are shown to non-clinical participants in order to elicit stress responses analogue to responses to traumatic events in real life. Previous studies used a large variety of films, which is problematic with regard to the comparability of results. The main goal of this study was to identify a film clip that (a) consistently provokes stress reactions and (b) provokes reactions that are as similar as possible to traumatic stress. We randomly exposed 105 male and female participants to one of four stressful films, differing, e.g., in content and origin. Intrusive memories of the film, reported immediately after the film and during a diary phase of three days, as well as distress, heart rate, and several mood states were measured. A film clip depicting rape elicited the most consistent reactions that were characterized by a higher heart rate, more distress and more intrusive memories, compared to the other three clips. Intrusive memories across all films were especially related to an increase in heart rate and disgust in response to the film.
Article
Attempts to suppress traumatic material may be involved in the development and maintenance of post-traumatic stress disorder (PTSD). In order to investigate this possibility, analogue post-traumatic intrusions were induced in normal participants by means of a distressing film. For comparison, a second film was used to induce intrusions about polar bears. It was hypothesized that the suppression of these intrusions would produce an immediate decrease but a delayed increase ("rebound effect") in their frequency. It was also predicted that the rebound effect would be larger for the analogue traumatic intrusions. Each film was followed by two consecutive time periods during which participants' thoughts were recorded. During the first period, the suppression group was instructed to suppress thoughts about the film whilst the control group merely recorded their thoughts. During the second period, both groups merely recorded their thoughts. The results supported the immediate decrease hypothesis for both types of intrusion. As predicted, there was a rebound effect for analogue traumatic intrusions although not for polar bear thoughts. Several methodological issues relating to the findings are highlighted. The possible implications of a rebound effect with trauma-relevant intrusions are discussed with reference to PTSD.
Article
Study protocols in endocrinological research and the neurosciences often employ repeated measurements over time to record changes in physiological or endocrinological variables. While it is desirable to acquire repeated measurements for finding individual and group differences with regard to response time and duration, the amount of data gathered often represents a problem for the statistical analysis. When trying to detect possible associations between repeated measures and other variables, the area under the curve (AUC) is routinely used to incorporate multiple time points. However, formulas for computation of the AUC are not standardized across laboratories, and existing differences are usually not presented when discussing results, thus causing possible variability, or incompatibility of findings between research groups. In this paper, two formulas for calculation of the area under the curve are presented, which are derived from the trapezoid formula. These formulas are termed 'Area under the curve with respect to increase' (AUCI) and 'Area under the curve with respect to ground' (AUCG). The different information that can be derived from repeated measurements with these two formulas is exemplified using artificial and real data from recent studies of the authors. It is shown that depending on which formula is used, different associations with other variables may emerge. Consequently, it is recommended to employ both formulas when analyzing data sets with repeated measures.