European Archives of Psychiatry and Clinical Neuroscience最新文献

Ecological momentary assessment (EMA), a structured diary assessment technique, has shown feasibility to capture psychotic(-like) symptoms across different study groups. We investigated whether EMA combined with unsupervised machine learning can distinguish groups on the continuum of genetic risk toward psychotic illness and identify individuals with need for extended healthcare. Individuals with psychotic disorder (PD, N = 55), healthy individuals (HC, N = 25) and HC with first-degree relatives with psychosis (RE, N = 20) were assessed at two sites over 7 days using EMA. Cluster analysis determined subgroups based on similarities in longitudinal trajectories of psychotic symptom ratings in EMA, agnostic of study group assignment. Psychotic symptom ratings were calculated as average of items related to hallucinations and paranoid ideas. Prior to EMA we assessed symptoms using the Positive and Negative Syndrome Scale (PANSS) and the Community Assessment of Psychic Experience (CAPE) to characterize the EMA subgroups. We identified two clusters with distinct longitudinal EMA characteristics. Cluster 1 (N_PD = 12, N_RE = 1, N_HC = 2) showed higher mean EMA symptom ratings as compared to cluster 2 (N_PD = 43, N_RE = 19, N_HC = 23) (p < 0.001). Cluster 1 showed a higher burden on negative (p < 0.05) and positive (p < 0.05) psychotic symptoms in cross-sectional PANSS and CAPE ratings than cluster 2. Findings indicate a separation of PD with high symptom burden (cluster 1) from PD with healthy-like rating patterns grouping together with HC and RE (cluster 2). Individuals in cluster 1 might particularly profit from exchange with a clinician underlining the idea of EMA as clinical monitoring tool.

This study aimed to explore the pathway from childhood trauma to nonsuicidal self-injury (NSSI) in adolescents with major depressive disorder (MDD) and to examine the chain-mediating role of psychological resilience and depressive symptoms in this pathway. A total of 391 adolescents with MDD were recruited in the present study. The Chinese version of the Childhood Trauma Questionnaire-Short Form (CTQ-SF), the Chinese version of the Symptoms Check List-90 (SCL-90), the Chinese version of the Conner-Davidson Resilience Scale (CD-RISC), and the Ottawa Self-Injury Inventory Chinese Revised Edition (OSIC) were used to evaluate childhood trauma, depressive symptoms, psychological resilience and NSSI, respectively. Our results showed that 60.87% of adolescents with MDD had NSSI in the past month. Childhood trauma frequency was negatively correlated with psychological resilience but positively correlated with depressive symptoms and NSSI severity in adolescents with MDD. The stepwise logistic regression analysis identified that age, childhood trauma and depressive symptoms could independently predict the occurrence of NSSI, and the three-step hierarchical regression showed that childhood trauma, psychological resilience and depressive symptoms were all significantly associated with NSSI frequency in adolescents with MDD. Furthermore, the chain-mediation analysis revealed that psychological resilience and depression serially mediated the relationship between childhood trauma and NSSI in adolescents with MDD. Interventions targeted at improving resilience and depression may mitigate the impact of childhood trauma severity on NSSI risk in adolescents with MDD.

Temporal coordination of communicative behavior is not only located between but also within interaction partners (e.g., gaze and gestures). This intrapersonal synchrony (IaPS) is assumed to constitute interpersonal alignment. Studies show systematic variations in IaPS in individuals with autism, which may affect the degree of interpersonal temporal coordination. In the current study, we reversed the approach and mapped the measured nonverbal behavior of interactants with and without ASD from a previous study onto virtual characters to study the effects of the differential IaPS on observers (N = 68), both with and without ASD (crossed design). During a communication task with both characters, who indicated targets with gaze and delayed pointing gestures, we measured response times, gaze behavior, and post hoc impression formation. Results show that character behavior indicative of ASD resulted in overall enlarged decoding times in observers and this effect was even pronounced in observers with ASD. A classification of observer's gaze types indicated differentiated decoding strategies. Whereas non-autistic observers presented with a rather consistent eyes-focused strategy associated with efficient and fast responses, observers with ASD presented with highly variable decoding strategies. In contrast to communication efficiency, impression formation was not influenced by IaPS. The results underline the importance of timing differences in both production and perception processes during multimodal nonverbal communication in interactants with and without ASD. In essence, the current findings locate the manifestation of reduced reciprocity in autism not merely in the person, but in the interactional dynamics of dyads.

Patients with mood disorders commonly manifest comorbid psychiatric disorders, including attention-deficit/hyperactivity disorder (ADHD). However, few studies have evaluated ADHD symptoms in this population. The current study aimed to explore the network structure of ADHD symptomology and identify central symptoms in patients with mood disorders. The Korean version of the Adult ADHD Self-Report Scale was used to assess the overall ADHD symptoms in 1,086 individuals diagnosed with mood disorders (major depressive disorder [n = 373], bipolar I disorder [n = 314], and bipolar II disorder [n = 399]). We used exploratory graph analysis to detect the number of communities, and the network structure was analyzed using regularized partial correlation models. We identified the central ADHD symptom using centrality indices. Network comparison tests were conducted with different subgroups of patients with mood disorders, including three mood diagnosis groups, between the patients who met the diagnostic criteria for ADHD [ADHD-suspected, n = 259] in their self-report and the others [ADHD-non-suspected, n = 827], and groups with high [n = 503] versus low [n = 252] levels of depressive state. The network analysis detected four communities: disorganization, agitation/restlessness, hyperactivity/impulsivity, and inattention. The centrality indices indicated that "feeling restless" was the core ADHD symptom. The result was replicated in the subgroup analyses within our clinically diverse population of mood disorders, encompassing three presentations: Patients with suspected ADHD, patients without suspected ADHD, and patients with a high depressive state. Our findings reveal that "feeling restless" is the central ADHD symptom. The treatment intervention for "feeling restless" may thus play a pivotal role in tackling ADHD symptoms in adult patients with mood disorders.

In patients with psychosis, rates of tobacco smoking and childhood trauma are significantly higher compared to the general population. Childhood trauma has been proposed as a risk factor for tobacco smoking. However, little is known about the relationship between childhood trauma and smoking in psychosis. In a subsample of the Genetic Risk and Outcome of Psychosis study (760 patients with psychosis, 991 unaffected siblings, and 491 healthy controls), tobacco smoking was assessed using the Composite International Diagnostic Interview and childhood trauma was measured with the Childhood Trauma Questionnaire. Logistic regression models were used to assess associations between trauma and smoking, while correcting for confounders. Positive associations were found between total trauma, abuse, and neglect, and an increased risk for smoking in patients, while correcting for age and gender (OR_trauma 1.77, 95% CI 1.30-2.42, p < 0.001; OR_abuse 1.69, 95% CI 1.23-2.31, p = 0.001; OR_neglect 1.48, 95% CI 1.08-2.02, p = 0.014). In controls, total trauma and abuse were positively associated with smoking, while correcting for age and gender (OR_trauma 2.40, 95% CI 1.49-3.88, p < 0.001; OR_abuse 2.02, 96% CI 1.23-3.32, p = 0.006). All associations lost their significance after controlling for additional covariates and multiple testing. Findings suggest that the association between childhood trauma and tobacco smoking can be mainly explained by confounders (gender, cannabis use, and education) in patients with psychosis. These identified aspects should be acknowledged in tobacco cessation programs.

Schizophrenia diagnosis and admission history were associated with a polygenic score (PGS) for schizophrenia based on a subset of variants that act by modifying the expression of genes whose expression is also modified by antipsychotics. This gene set was enriched in cytokine production. Interleukin-6 (IL-6) is the only cytokine whose plasma levels were associated both with schizophrenia diagnosis and with acute decompensations in the largest meta-analysis. Therefore, we hypothesized that an IL-6 PGS, but not other cytokines PGSs, would be associated with schizophrenia chronicity/psychiatric admissions. Using the IL-6 PGS model from The PGS Catalog, IL-6 PGS was calculated in 427 patients with schizophrenia and data regarding admission history. Association between IL-6 PGS and chronicity, measured as number and duration of psychiatric admissions, or ever readmission was analyzed by multivariate ordinal and logistic regression, respectively. Specificity of results was assessed by analysis of PGSs from the other cytokines at The PGS Catalog with meta-analytic evidence of association with schizophrenia diagnosis or acute decompensations, IL-1RA, IL-4, IL-8, and IL-12. IL-6 PGS was associated with schizophrenia chronicity, explaining 1.51% of variability (OR = 1.29, 95% CI 1.07-1.55, P = 0.007). There was no association with ever readmission. Other cytokines PGSs were not associated with chronicity. Association with IL-6 PGS was independent of association with schizophrenia PGS. Our results provide evidence that genetically regulated higher levels of IL-6 are involved in schizophrenia chronicity, highlighting the relevance of immunity processes for a subgroup of patients.

Reward processing impairments are a key factor associated with negative symptoms in those with severe mental illnesses. However, past findings are inconsistent regarding which reward processing components are impaired and most strongly linked to negative symptoms. The current study examined the hypothesis that these mixed findings may be the result of multiple reward processing pathways (i.e., equifinality) to negative symptoms that cut across diagnostic boundaries and phases of illness. Participants included healthy controls (n = 100) who served as a reference sample and a severe mental illness-spectrum sample (n = 92) that included psychotic-like experiences, clinical high-risk for psychosis, bipolar disorder, and schizophrenia participants. All participants completed tasks measuring four RDoC Positive Valence System constructs: value representation, reinforcement learning, effort-cost computation, and hedonic reactivity. A k-means cluster analysis of the severe mental illness-spectrum samples identified three clusters with differential reward processing profiles that were characterized by: (1) global reward processing deficits (22.8%), (2) selective impairments in hedonic reactivity alone (40.2%), and (3) preserved reward processing (37%). Elevated negative symptoms were only observed in the global reward processing cluster. All clusters contained participants from each clinical group, and the distribution of these groups did not significantly differ among the clusters. Findings identified one pathway contributing to negative symptoms that was transdiagnostic and transphasic. Future work further characterizing divergent pathways to negative symptoms may help to improve symptom trajectories and personalized treatments.

The prevalence of pain and dementia increases with age, affecting a significant percentage of the population due to aging. Both pathologies are connected through the inflammatory process, specifically through the tumor necrosis factor. The effect of this cytokine is mediated through the modulation of its TNFRI and TNFRII receptors, which are linked to the dementia process. In addition, immunoglobulins such as secretory immunoglobulin A (sIgA) have been recognized as one of the main biomarkers of pain in saliva. sTNFRII and sIgA levels were determined in saliva samples by ELISA from healthy people and patients with dementia in GDS stages 5-7. The concentrations of these markers were also correlated with the GDS stage and sex. We observed a significant decrease (*** p ≤ 0.001) in the levels of sTNFRII (pg/mL) and a significant increase (** p ≤ 0.01) in the levels of sIgA (ng/mL) in the saliva of patients with dementia compared to the healthy control group. We did not observe a correlation with the data of the biomarkers regarding the GDS stage and sex. The results obtained for sTNFRII are consistent with those obtained by other authors on brain tissue, who conclude that unopposed neuronal TNFRI signaling, when TNFRII is selectively downregulated, leads to a more severe course of AD pathogenesis. Regarding sIgA, the elevated values of sIgA may reflect the immune status of these patients. Therefore, these biomarkers can provide us with relevant information through a non-invasive method such as saliva analysis.

In addition to higher-order executive functions, underlying sensory processing ability is also thought to play an important role in Attention-Deficit/Hyperactivity Disorder (AD/HD). An event-related potential feature, the mismatch negativity, reflects the ability of automatic sensory change processing and may be correlated with AD/HD symptoms and executive functions. This study aims to investigate the characteristics of visual mismatch negativity (vMMN) in adults with AD/HD. Twenty eight adults with AD/HD and 31 healthy controls were included in this study. These two groups were matched in age, IQ and sex. In addition, both groups completed psychiatric evaluations, a visual ERP task used to elicit vMMN, and psychological measures about AD/HD symptoms and day-to-day executive functions. Compared to trols, the late vMMN (230-330 ms) was significantly reduced in the AD/HD group. Correlation analyses showed that late vMMN was correlated with executive functions but not AD/HD symptoms. However, further mediation analyses showed that different executive functions had mediated the relationships between late vMMN and AD/HD symptoms. Our findings indicate that the late vMMN, reflecting automatic sensory change processing ability, was impaired in adults with AD/HD. This impairment could have negative impact on AD/HD symptoms via affecting day-to-day executive functions.

Major depressive disorder (MDD) is strongly associated with type 2 diabetes mellitus (T2DM). The kynurenine and serotonin pathways, as well as chronic low-grade inflammation, are being considered potential links between them. MDD associated with T2DM is less responsive to treatment than that without T2DM; however, the underlying mechanism remains unknown. We aimed to investigate the effects of inflammatory cytokines on the kynurenine and serotonin pathways in patients with comorbid MDD and T2DM and those with only MDD. We recruited 13 patients with comorbid MDD and T2DM and 27 patients with only MDD. We measured interleukin-6 and tumor necrosis factor-α (TNF-α) levels as inflammatory cytokines and metabolites of the kynurenine pathway and examined the relationship between the two. TNF-α levels were significantly higher in patients with comorbid MDD and T2DM than in those with only MDD in univariate (p = 0.044) and multivariate (adjusted p = 0.036) analyses. TNF-α showed a statistically significant effect modification (interaction) with quinolinic acid/tryptophan and serotonin in patients from both groups (β = 1.029, adjusted p < 0.001; β =  - 1.444, adjusted p = 0.047, respectively). Limitations attributed to the study design and number of samples may be present. All patients were Japanese with mild to moderate MDD; therefore, the generalizability of our findings may be limited. MDD with T2DM has more inflammatory depression components and activations of the kynurenine pathway by inflammatory cytokines than MDD without T2DM. Hence, administering antidepressants and anti-inflammatory drugs in combination may be more effective in patients with comorbid MDD and T2DM.