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Background: Multiple traumata such as child sexual and/or physical abuse often result in complex psychopathologies and a range of associated dysfunctional behaviors. Although evidence-based interventions exist, some therapists are concerned that trauma-focused psychotherapy with exposure-based elements may lead to the deterioration of associated dysfunctional behaviors in adolescents and young adults. Therefore, we examined the course of suicidal ideation, self-injury, aggressive behavior and substance use in a group of abuse-related posttraumatic stress disorder (PTSD) patients during phase-based, trauma-focused PTSD treatment.
Methods: Daily assessments from a randomized controlled trial (RCT) of Developmentally adapted Cognitive Processing Therapy (D-CPT) were analyzed to test for differences in the stated dysfunctional behaviors between the four treatment phases. We conducted multilevel modeling and repeated measure ANOVAs.
Results: We did not find any significant differences between the treatment phases concerning the stated dysfunctional behaviors, either at the level of urge or at the level of actual actions. On the contrary, in some primary outcomes (self-injury, aggressive behavior), as well as secondary outcomes (distress caused by trauma, joy), we observed significant improvements.
Discussion: Overall, during D-CPT, adolescents and young adults showed no deterioration in dysfunctional behaviors, while even showing improvements in some, suggesting that trauma-focused treatment preceded by skills building was not deleterious to this population. Hence, the dissemination of effective interventions such as D-CPT should be fostered, whilst the concerns of the therapists regarding exposure-based components need to be addressed during appropriate training. Nevertheless, further studies with momentary assessment, extended measurement methods, a control group and larger sample sizes are needed to confirm our preliminary findings.
Trial registration: The trial was registered at the German Clinical Trial Registry (GCTR), DRKS00004787, 18 March 2013, https://www.drks.de/DRKS00004787.
Conduct Disorder (CD) is an impairing psychiatric disorder of childhood and adolescence characterized by aggressive and dissocial behavior. Environmental factors such as maternal smoking during pregnancy, socio-economic status, trauma, or early life stress are associated with CD. Although the number of females with CD is rising in Western societies, CD is under-researched in female cohorts. We aimed at exploring the epigenetic signature of females with CD and its relation to psychosocial and environmental risk factors. We performed HpaII sensitive genome-wide methylation sequencing of 49 CD girls and 50 matched typically developing controls and linear regression models to identify differentially methylated CpG loci (tags) and regions. Significant tags and regions were mapped to the respective genes and tested for enrichment in pathways and brain developmental processes. Finally, epigenetic signatures were tested as mediators for CD-associated risk factors. We identified a 12% increased methylation 5’ of the neurite modulator SLITRK5 (FDR = 0.0046) in cases within a glucocorticoid receptor binding site. Functionally, methylation positively correlated with gene expression in lymphoblastoid cell lines. At systems-level, genes (uncorr. P < 0.01) were associated with development of neurons, neurite outgrowth or neuronal developmental processes. At gene expression level, the associated gene-networks are activated perinatally and during early childhood in neocortical regions, thalamus and striatum, and expressed in amygdala and hippocampus. Specifically, the epigenetic signatures of the gene network activated in the thalamus during early childhood correlated with the effect of parental education on CD status possibly mediating its protective effect. The differential methylation patterns identified in females with CD are likely to affect genes that are expressed in brain regions previously indicated in CD. We provide suggestive evidence that protective effects are likely mediated by epigenetic mechanisms impairing specific brain developmental networks and therefore exerting a long-term effect on neural functions in CD. Our results are exploratory and thus, further replication is needed.