Experimental induction of peritraumatic dissociation: The role of negative affect and pain and their psychophysiological and neural correlates

While research has elucidated processes underlying dissociative symptoms in patients with posttraumatic stress disorder, little is known about the circumstances under which trauma-related dissociation initially arises. To experimentally investigate causes and concomitants of peritraumatic dissociation, we subjected sixty-nine healthy women to aversive-audiovisual and painful-electrical stimulation in a 2(aversive/neutral film) x 2(pain/no pain) within-subject design while recording psychophysiological and fMRI-BOLD responses. Afterwards, participants rated negative-affect, pain, and dissociation for each condition. Using Bayesian multilevel regression models, we examined (1) whether aversive-audiovisual and painful-electrical stimulation elicit higher dissociation-levels than control conditions and (2) whether stronger negative-affect and pain responses (operationalized via self-report, psychophysiological, and neural markers) correlate with higher dissociation-levels. Several key findings emerged: Both aversive-audiovisual and painful-electrical stimulation elicited dissociation. Dissociation was linked to higher self-reported negative-affect, but we did not find enough evidence linking it to psychophysiological and neural negative-affect markers. However, dissociation was associated with higher levels of self-reported pain, a skin-conductance-response-based pain marker, and the fMRI-BOLD-based Neurologic-Pain-Signature. Results indicate that both aversive-audiovisual and painful stimuli can independently cause dissociation. Critically, pain responses captured via self-report, psychophysiological, and neural markers were consistently linked to higher dissociation-levels suggesting a specific, evolutionary meaningful, contribution of pain to the rise of dissociation

Estradiol during (analogue-)trauma: Risk- or protective factor for intrusive re-experiencing?

Intrusions, a key symptom of posttraumatic stress disorder (PTSD), can occur in the form of images but also as pain sensations. Similar to audiovisual intrusions, the frequency and persistence of pain intrusions varies greatly between individuals. In the current study, we examined whether peritraumatic circulating 17β-estradiol (E2) levels are a biologic factor associated with subsequent audiovisual (i.e., film) and pain intrusion development, and whether peritraumatic stress levels modulate this relationship. Forty-one free-cycling women participated in an ecologically informed trauma-pain-conditioning (TPC) paradigm, using trauma-films and pain as unconditioned stimuli. Independent variables were salivary peritraumatic E2 levels and stress indexed by salivary cortisol and self-reported state-anxiety during TPC. Outcomes were film- and pain-intrusions occurring during daily-life in the week following TPC and a Memory-Triggering-Task in response to conditioned stimuli 24 h after TPC. In the week after analogue-trauma, higher peritraumatic E2 levels were associated with a greater probability of experiencing film-intrusions in the beginning of the week, which switched to a lower probability toward the end of the week. This time-dependent relationship between E2 and film-intrusions only held for higher state-anxious women. In contrast, results indicated a consistent inverse relationship between peritraumatic E2 levels and pain-intrusions during daily-life and Memory-Triggering-Task. Together, these data suggest that higher peritraumatic E2 levels could be associated with lower long-term visual trauma intrusions, as well as lower pain-intrusions, and thereby possibly constitute a protective biologic factor for PTSD and potentially also for chronic pain

Development and Validation of the German Version of the Dissociative Subtype of PTSD Scale (DSPS)

The present study will develop and evaluate a German Version of the Dissociative Subtype of PTSD Scale (DSPS; Wolf et al., 2017)

Experimental Induction of Peritraumatic Dissociation: The Role of Negative Affect and Pain and Their Psychophysiological and Neural Correlates

While research has elucidated processes underlying dissociative symptoms in patients with posttraumatic stress disorder, little is known about the circumstances under which trauma-related dissociation initially arises. To experimentally investigate causes and concomitants of peritraumatic dissociation, we subjected sixty-nine healthy women to aversive-audiovisual and painful-electrical stimulation in a 2(aversive/neutral film) x 2(pain/no pain) within-subject design while recording psychophysiological and fMRI-BOLD responses. Afterwards, participants rated negative-affect, pain, and dissociation for each condition. Using Bayesian multilevel regression models, we examined (1) whether aversive-audiovisual and painful-electrical stimulation elicit higher dissociation-levels than control conditions and (2) whether stronger negative-affect and pain responses (operationalized via self-report, psychophysiological, and neural markers) correlate with higher dissociation-levels. Several key findings emerged: Both aversive-audiovisual and painful-electrical stimulation elicited dissociation. Dissociation was linked to higher self-reported negative-affect, but we did not find enough evidence linking it to psychophysiological and neural negative-affect markers. However, dissociation was associated with higher levels of self-reported pain, a skin-conductance-response-based pain marker, and the fMRI-BOLD-based Neurologic-Pain-Signature. Results indicate that both aversive-audiovisual and painful stimuli can independently cause dissociation. Critically, pain responses captured via self-report, psychophysiological, and neural markers were consistently linked to higher dissociation-levels suggesting a specific, evolutionary meaningful, contribution of pain to the rise of dissociation

Intrusive memories as conditioned responses to trauma cues: an empirically supported concept?

Intrusions in posttraumatic stress disorder (PTSD) are clinically understood as conditioned responses (CRs) to trauma-cues; however, experimental evidence for this is limited. We subjected 84 healthy participants to a differential conditioned-intrusion paradigm, where neutral faces served as conditioned stimuli (CS) and aversive film clips as unconditioned stimuli (US). While one group only completed acquisition, another group additionally received extinction. Subsequently, participants provided detailed e-diary intrusion reports. Several key findings emerged: First, participants in both groups re-experienced not only US but also CS as content of their intrusions. Second, intrusions were triggered by stimuli resembling CS, US, and experimental context. Third, extinction reduced probability and severity of US intrusions, and accelerated their decay, and this was particularly the case in participants showing greater cognitive (US-expectancy) and physiological (SCR) differential responding to CS+ vs. CS- at end of acquisition (i.e., conditionability). Similarly, CS-intrusion probability and severity was reduced by extinction in participants with greater cognitive conditionability. These results support conditioning’s role in re-experiencing in two critical ways: (1) Conditioning during trauma provides cues that not only function as triggers, but also as content of intrusions; (2) After strong conditioning, weakening the original CS-US relationship via extinction prevents intrusion formation after analogue-trauma