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Background: Intrusive memories of psychologically traumatic events bring distress both sub-clinically and clinically. This parallel-group, two-arm randomised controlled trial evaluated the effect of a brief behavioural intervention on reducing intrusive memories in frontline healthcare workers exposed to traumatic events during the COVID-19 pandemic. Methods: Participants with at least two intrusive memories of work-related trauma in the week before recruitment were randomised 1:1 to an imagery-competing task intervention (n = 73) or attention-based control task (n = 71). The number of intrusive memories was assessed at baseline and 5 weeks after the guided session (primary endpoint). Results: The intervention significantly reduced intrusive memory frequency compared with control [intervention Mdn = 1.0 (IQR = 0–3), control Mdn = 5.0 (IQR = 1–17); p < 0.0001, IRR = 0.30; 95% CI = 0.17–0.53] and led to fewer post-traumatic stress-related symptoms at 1, 3 and 6 month follow-ups (secondary endpoints). Participants and statisticians were blinded to allocation. Adverse events data were acquired throughout the trial, demonstrating safety. There was high adherence and low attrition. Conclusions: This brief, single-symptom, repeatable digital intervention for subclinical-to-clinical samples after trauma allows scalability, taking a preventing-to-treating approach after trauma. Trial registration: 2020–07-06, ClinicalTrials.gov identifier: NCT04460014. [ABSTRACT FROM AUTHOR]

Objectives: Embedded in the Collaborative Research Center "Fear, Anxiety, Anxiety Disorders" (CRC‐TRR58), this bicentric clinical study aims at identifying biobehavioral markers of treatment (non‐)response by applying machine learning methodology with an external cross‐validation protocol. We hypothesize that a priori prediction of treatment (non‐)response is possible in a second, independent sample based on multimodal markers. Methods: One‐session virtual reality exposure treatment (VRET) with patients with spider phobia was conducted on two sites. Clinical, neuroimaging, and genetic data were assessed at baseline, post‐treatment and after 6 months. The primary and secondary outcomes defining treatment response are as follows: 30% reduction regarding the individual score in the Spider Phobia Questionnaire and 50% reduction regarding the individual distance in the behavioral avoidance test. Results: N = 204 patients have been included (n = 100 in Würzburg, n = 104 in Münster). Sample characteristics for both sites are comparable. Discussion This study will offer cross‐validated theranostic markers for predicting the individual success of exposure‐based therapy. Findings will support clinical decision‐making on personalized therapy, bridge the gap between basic and clinical research, and bring stratified therapy into reach. The study is registered at ClinicalTrials.gov (ID: NCT03208400). [ABSTRACT FROM AUTHOR]

Objectives: Inhibitory control deficits are considered a key pathogenic factor in anxiety disorders. To assess inhibitory control, the antisaccade task is a well-established measure that assesses antisaccade performance via latencies and error rates. The present study follows three aims: (1) to investigate inhibitory control via antisaccade latencies and errors in an antisaccade task, and their associations with multiple measures of fear in patients with spider phobia (SP) versus healthy controls (HC), (2) to investigate the modifiability of antisaccade performance via a fear-specific antisaccade training in patients with SP and HC, and (3) to explore associations between putative training-induced changes in antisaccade performance in SPs and changes in diverse measures of fear. Methods: Towards aim 1, we assess antisaccade latencies (primary outcome) and error rates (secondary outcome) in an emotional antisaccade task. Further, the baseline assessment includes assessments of psychophysiological, behavioral, and psychometric indices of fear in patients with SP and HCs. To address aim 2, we compare effects of a fear-specific antisaccade training with effects of a prosaccade training as a control condition. The primary and secondary outcomes are reassessed at a post-1-assessment in both SPs and HCs. Aim 3 employs a cross-over design and is piloted in patients with SP, only. Towards this aim, primary and secondary outcomes, as well as psychophysiological, behavioral, and psychometric measures of fear are reassessed at a post-2-assessment after the second training block. Conclusion: This study aims to better understand inhibitory control processes and their modifiability in spider phobia. If successful, antisaccade training may assist in the treatment of specific phobia by directly targeting the putative underlying inhibitory control deficits. This study has been preregistered with ISRCTN (ID: ISRCTN12918583) on 28th February 2022. [ABSTRACT FROM AUTHOR]

Background: The neuropeptide oxytocin (OXT) plays a role in the regulation of eating behavior and metabolism. OXT functioning is altered in patients with eating and weight disorders, and a variant of the oxytocin receptor gene (OXTR) has been associated with impulsive eating behavior as it is seen in patients with binge eating disorder (BED). Gene × environment interactions could play a role in BED. One mechanism mediating this interaction is the epigenetic alteration of gene expression. We therefore investigated if DNA methylation of the OXTR differs between individuals with obesity depending on a comorbid BED. We analyzed DNA methylation of the OXTR in peripheral blood of 227 individuals on the obesity spectrum (mean age: 40.3 ± 13.1 yrs; mean BMI: 38.6 ± 7.3 kg/m2), 130 of which were diagnosed with BED. Results: There were no overall differences in OXTR methylation between participants with and those without BED (p > 0.05), while both subgroups were comparable regarding age and body mass index (BMI), but significantly differed in sex distribution (p = 0.035). We found no relationship between mean DNA methylation and BMI or self-reported eating disorder (ED) pathology. Analyzing potential sex differences revealed a significantly lower OXTR DNA methylation in male participants with BED as compared to those without BED (p = 0.017). No such difference was found in the female subsample (p > 0.05). Conclusions: Clinically significant binge eating pathology might be associated with lower OXTR DNA methylation exclusively in males. The differential DNA methylation of OXTR in males with BED supports the view that BED represents a phenotype within the obesity spectrum that is characterized by specific vulnerability factors. A better understanding of the epigenetic underpinnings of the OXT system might contribute to the refinement of OXT administration approaches as potential interventions in eating and weight disorders. [ABSTRACT FROM AUTHOR]

Background: The neuropeptide oxytocin (OXT) plays a role in the regulation of eating behavior and metabolism. OXT functioning is altered in patients with eating and weight disorders, and a variant of the oxytocin receptor gene (OXTR) has been associated with impulsive eating behavior as it is seen in patients with binge eating disorder (BED). Gene × environment interactions could play a role in BED. One mechanism mediating this interaction is the epigenetic alteration of gene expression. We therefore investigated if DNA methylation of the OXTR differs between individuals with obesity depending on a comorbid BED. We analyzed DNA methylation of the OXTR in peripheral blood of 227 individuals on the obesity spectrum (mean age: 40.3 ± 13.1 yrs; mean BMI: 38.6 ± 7.3 kg/m2), 130 of which were diagnosed with BED. Results: There were no overall differences in OXTR methylation between participants with and those without BED (p > 0.05), while both subgroups were comparable regarding age and body mass index (BMI), but significantly differed in sex distribution (p = 0.035). We found no relationship between mean DNA methylation and BMI or self-reported eating disorder (ED) pathology. Analyzing potential sex differences revealed a significantly lower OXTR DNA methylation in male participants with BED as compared to those without BED (p = 0.017). No such difference was found in the female subsample (p > 0.05). Conclusions: Clinically significant binge eating pathology might be associated with lower OXTR DNA methylation exclusively in males. The differential DNA methylation of OXTR in males with BED supports the view that BED represents a phenotype within the obesity spectrum that is characterized by specific vulnerability factors. A better understanding of the epigenetic underpinnings of the OXT system might contribute to the refinement of OXT administration approaches as potential interventions in eating and weight disorders. [ABSTRACT FROM AUTHOR]

This meta-analysis examined inhibitory control performance in the antisaccade task across mental disorders. Following PRISMA guidelines, we analyzed data from k = 146 studies (n = 13,807 participants) on antisaccade performance. Effect sizes were estimated using random-effects models and restricted maximum-likelihood estimation, with robustness tests for study heterogeneity and publication bias. Most disorders displayed elevated error rates, with schizophrenia showing the greatest impairments, followed by autism spectrum disorder, bipolar disorder and attention deficit hyperactivity disorder. Small to medium impairments were also found in eating disorders, major depressive disorder, obsessive-compulsive disorder and substance use disorder. Results were robust against corrections for publication bias and largely unaffected by confounding variables. Prolonged latencies were observed in schizophrenia, attention deficit hyperactivity disorder, bipolar disorder and obsessive compulsive disorder, with smaller and less robust effect sizes. Results indicate inhibitory control deficits in the antisaccade task across mental disorders, especially evident for error rates. While present in most disorders, results imply varying degrees of impairments, ranging from small to large in effect sizes, with largest impairments in schizophrenia. • We conducted the first comprehensive transdiagnostic meta-analysis of the antisaccade task in mental disorders. • Most of the investigated disorders showed impaired antisaccade performance, with largest effects in schizophrenia. • Impairments were generally larger and more robust for antisaccade error rates compared to antisaccade latencies. • Results imply aberrant inhibitory control as a possible transdiagnostic correlate of psychopathology. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) and anxiety disorders (ANX) share core symptoms such as negative affect and often co-exist. Magnetic-resonance imaging (MRI) research suggests shared neuroanatomical/neurofunctional underpinnings. So far, studies considering transdiagnostic and disorder-specific neural alterations in MDD and ANX as well as the comorbid condition (COM) have not been reviewed systematically. Following PRISMA guidelines, the literature was screened and N = 247 articles were checked according to the PICOS criteria: MRI studies investigating transdiagnostic (across MDD, ANX, COM compared to healthy controls) and/or disorder-specific (between MDD, ANX, COM) neural alterations. N = 35, thereof n = 13 structural MRI and diffusion-tensor imaging studies and n = 22 functional MRI studies investigating emotional, cognitive deficits and resting state were included and quality coded. Results indicated transdiagnostic structural/functional alterations in the orbitofrontal cortex/middle frontal cortex and in limbic regions (amygdala, cingulum, hippocampus). Few and inconsistent disorder-specific alterations were reported. However, depression-specific functional alterations were reported for the inferior frontal gyrus and dorsolateral prefrontal cortex during emotional tasks, and limbic regions at rest. Preliminary results for anxiety-specific functional alterations were found in the insula and frontal regions during emotional tasks, in the inferior parietal lobule, superior frontal gyrus and superior temporal gyrus during cognitive tasks, and (para)limbic alterations at rest. This review provides evidence to support existing transdiagnostic fronto-limbic neural models in MDD and ANX. On top, it expands existing knowledge taking into account comorbidity and comparing MDD with ANX. Heterogeneous evidence exists for disorder-specific alterations. Research focusing on ANX sub-types, and the consideration of COM would contribute to a better understanding of basic neural underpinnings. • Depression (MDD) and anxiety disorders (ANX) are highly co-morbid conditions (COM). • There is a gap in transdiagnostic research of comparing MDD, ANX and considering COM. • Transdiagnostic research allows exploring general and disorder-specific underpinnings. • Studies results suggest general fronto-limbic alterations supporting existing models. • Studies results presented heterogeneous disorder-specific findings. [ABSTRACT FROM AUTHOR]

Background: Alexithymia is a risk factor for major depressive disorder (MDD) and has been associated with diminished treatment response. Neuroimaging studies have revealed structural aberrations of the anterior cingulate cortex and the fusiform gyrus in healthy controls with high levels of alexithymia. The present study tried to corroborate and extend these results to patients with MDD compared with healthy controls. Methods: We investigated the relationship between alexithymia, depression and grey matter volume in 63 patients with MDD (mean age ± standard deviation = 42.43 yr ± 11.91; 33 female) and 46 healthy controls (45.35 yr ± 8.37; 22 female). We assessed alexithymia using the Toronto Alexithymia Scale. We conducted an alexithymia x group analysis of covariance; we used a region-of-interest approach, including the fusiform gyrus and anterior cingulate cortex, and conducted whole brain analysis using voxelbased morphometry. Results: Our analysis revealed a significant alexithymia x group interaction in the fusiform gyrus (left, pFWE = 0.031; right, pFWE = 0.010). Higher alexithymia scores were associated with decreased grey matter volume in patients with MDD (pFWE = 0.009), but with increased grey matter volume of the fusiform gyrus in healthy controls (pFWE = 0.044). We found no significant main effects in the region-of-interest analysis. Limitations: Owing to the naturalistic nature of our study, patients with MDD and healthy controls differed significantly in their alexithymia scores. Conclusion: Our results showed the fusiform gyrus as a correlate of alexithymia. We also found differences related to alexithymia between patients with MDD and healthy controls in the fusiform gyrus. Our study encourages research related to the transition from risk to MDD in people with alexithymia. [ABSTRACT FROM AUTHOR]