Cardiac vagal control, regulatory processes and depressive symptoms: Re-investigating the moderating role of sleep quality

Lower cardiac vagal control (CVC), which is often understood as an indicator for impaired regulatory processes, is assumed to predict the development of depressive symptoms. As this link has not been consistently demonstrated, sleep quality has been proposed as a moderating factor. However, previous studies were limited by non-representative samples, cross-sectional data, and focused on CVC as a physiological indicator for impaired regulatory processes, but neglected corresponding subjective measures. Therefore, we investigated whether sleep quality moderates the effects of CVC (quantified by high-frequency heart rate variability) and self-reported regulatory processes (self- and emotion-regulation) on concurrent depressive symptoms and on depressive symptoms after three months in a representative sample (N = 125). Significant interactions between CVC and sleep quality (in women only), as well as self-/emotion-regulation and sleep quality emerged, whereby higher sleep quality attenuated the relation between all risk factors and current depressive symptoms (cross-sectional data). However, there were no significant interactions between those variables in predicting depressive symptoms three months later (longitudinal data). Our cross-sectional findings extend previous findings on sleep quality as a protective factor against depressive symptoms in the presence of lower CVC and subjective indices of impaired regulatory processes. In contrast, our conflicting longitudinal results stress the need for further investigations

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

Structural neuroimaging of hippocampus and amygdala subregions in posttraumatic stress disorder: A scoping review

Numerous studies have explored the relationship between posttraumatic stress disorder (PTSD) and the hippo-campus and the amygdala because both regions are implicated in the disorder’s pathogenesis and pathophysiology. Nevertheless, those key limbic regions consist of functionally and cytoarchitecturally distinct substructures that may play different roles in the etiology of PTSD. Spurred by the availability of automatic segmentation software, structural neuroimaging studies of human hippocampal and amygdala subregions have proliferated in recent years. Here, we present a preregistered scoping review of the existing structural neuroimaging studies of the hippocampus and amygdala subregions in adults diagnosed with PTSD. A total of 3513 studies assessing subregion volumes were identified, 1689 of which were screened, and 21 studies were eligible for this review (total N = 2876 individuals). Most studies examined hippocampal subregions and reported decreased CA1, CA3, dentate gyrus, and subiculum volumes in PTSD. Fewer studies investigated amygdala subregions and reported altered lateral, basal, and central nuclei volumes in PTSD. This review further highlights the conceptual and methodological limitations of the current literature and identifies future directions to increase understanding of the distinct roles of hippocampal and amygdalar subregions in posttraumatic psychopathology

Cardiac Vagal Control, Regulatory Processes and Depressive Symptoms: Re-Investigating the Moderating Role of Sleep Quality

Lower cardiac vagal control (CVC), which is often understood as an indicator for impaired regulatory processes, is assumed to predict the development of depressive symptoms. As this link has not been consistently demonstrated, sleep quality has been proposed as a moderating factor. However, previous studies were limited by non-representative samples, cross-sectional data, and focused on CVC as a physiological indicator for impaired regulatory processes, but neglected corresponding subjective measures. Therefore, we investigated whether sleep quality moderates the effects of CVC (quantified by high-frequency heart rate variability) and self-reported regulatory processes (self- and emotion-regulation) on concurrent depressive symptoms and on depressive symptoms after three months in a representative sample (N = 125). Significant interactions between CVC and sleep quality (in women only), as well as self-/emotion-regulation and sleep quality emerged, whereby higher sleep quality attenuated the relation between all risk factors and current depressive symptoms (cross-sectional data). However, there were no significant interactions between those variables in predicting depressive symptoms three months later (longitudinal data). Our cross-sectional findings extend previous findings on sleep quality as a protective factor against depressive symptoms in the presence of lower CVC and subjective indices of impaired regulatory processes. In contrast, our conflicting longitudinal results stress the need for further investigations