METHODS: The study enrolled 110 participants (age: M = 46.85, SD = 11.23; female: 55.45%) undergoing hospital treatment, of whom 87 were included in the pre-post analysis. Participants completed a German translation of MAIA-2 and the Beck Depression Inventory-II (pre-/post-treatment). Internal consistency reliability was determined by Cronbach's α/McDonalds's ω, sensitivity to change was determined by effect sizes, and MIDs were determined by distribution- (0.5*SD) and anchor-based approaches (mean change method; ROC curve cut-points).
RESULTS: Depression severity reduced over the course of treatment (Median = -65.22%), and 34.48% of patients achieved remission. Reliability was appropriate for post-treatment (range of ω: .70-.90), but questionable for two pre-treatment scales (Noticing: ω = .64; Not-Distracting: ω = .66). The eight dimensions of MAIA-2 were sensitive to change (standardized response mean: .32-.81; Cohen's effect size: .30-.92). Distribution-based MIDs (.38-.61) and anchor-based mean change MIDs (remission vs. partial response: .00-.85; partial response vs. nonresponse: .08-.88) were established on the group level. For six scales, ROC cut-points (remission: .00-1.33; response: -.20-1.00) demonstrated accurate classification to treatment response groups on the individual level.
CONCLUSIONS: This study demonstrated the applicability of the MAIA-2 questionnaire in MDD. The updated version may have led to reliability improvements regarding the revised scales, but subthreshold reliability was evident prior to treatment. The measure's dimensions were sensitive to change. MIDs were established that corresponded with antidepressive treatment outcomes. Our findings are consistent with a growing area of research which considers somatic feelings as key contributors to mental health.
METHODS: Data were combined from 3024 MDD cases and 2741 control subjects from nine cohorts contributing to the MDD Working Group of the Psychiatric Genomics Consortium. MDD-PRS were based on a discovery sample of ∼110,000 independent individuals. CT was assessed as exposure to sexual or physical abuse during childhood. In a subset of 1957 cases and 2002 control subjects, a more detailed five-domain measure additionally included emotional abuse, physical neglect, and emotional neglect.
RESULTS: MDD was associated with the MDD-PRS (odds ratio [OR] = 1.24, p = 3.6 × 10-5, R2 = 1.18%) and with CT (OR = 2.63, p = 3.5 × 10-18 and OR = 2.62, p = 1.4 ×10-5 for the two- and five-domain measures, respectively). No interaction was found between MDD-PRS and the two-domain and five-domain CT measure (OR = 1.00, p = .89 and OR = 1.05, p = .66).
CONCLUSIONS: No meta-analytic evidence for interaction between MDD-PRS and CT was found. This suggests that the previously reported interaction effects, although both statistically significant, can best be interpreted as chance findings. Further research is required, but this study suggests that the genetic heterogeneity of MDD is not attributable to genome-wide moderation of genetic effects by CT.
METHODS: We analysed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders in 33,332 cases and 27,888 controls of European ancestory. To characterise allelic effects on each disorder, we applied a multinomial logistic regression procedure with model selection to identify the best-fitting model of relations between genotype and phenotype. We examined cross-disorder effects of genome-wide significant loci previously identified for bipolar disorder and schizophrenia, and used polygenic risk-score analysis to examine such effects from a broader set of common variants. We undertook pathway analyses to establish the biological associations underlying genetic overlap for the five disorders. We used enrichment analysis of expression quantitative trait loci (eQTL) data to assess whether SNPs with cross-disorder association were enriched for regulatory SNPs in post-mortem brain-tissue samples.
FINDINGS: SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10(-8)) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2. Model selection analysis supported effects of these loci for several disorders. Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity. Polygenic risk scores showed cross-disorder associations, notably between adult-onset disorders. Pathway analysis supported a role for calcium channel signalling genes for all five disorders. Finally, SNPs with evidence of cross-disorder association were enriched for brain eQTL markers.
INTERPRETATION: Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology. These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.
FUNDING: National Institute of Mental Health.
METHODS: In this cross-sectional study, 101 TBI patients were interviewed using the Structured Clinical Interview for DSM-IV Axis I Disorders to assess the rates of depressive and anxiety disorders after TBI. The association of socio-demographic and clinical factors with depressive and anxiety disorders were determined using Pearson's Chi-Square test.
RESULTS: A total of 25% of TBI patients (n = 25/101) were diagnosed with depressive disorders, of which 15% had major depressive disorder (n = 15/101) and 10% had minor depression (n = 10/101). Fourteen percent of TBI patients had anxiety disorders (n = 14/101), of which post-traumatic stress disorder (PTSD) was the commonest anxiety disorder (9%, n = 9/101). Seven percent of TBI patients (n = 7/101) had comorbid depressive and anxiety disorders. The only factor associated with depressive disorder was the duration of TBI (≥ 1 year) while the only factor associated with anxiety disorder was the mechanism of trauma (assault).
CONCLUSION: Major depressive disorder, minor depression and PTSD are common psychiatric complications of TBI. Clinicians should screen for depressive and anxiety disorders in TBI patients, particularly those with ≥1 year of injury and had sustained TBI from assault.