European Archives of Psychiatry and Clinical Neuroscience最新文献

Although previous studies have established the association between parental marital status and mental health problems in adolescents, however, the adverse effects of incomplete family settings and childhood maltreatment on adolescent anxiety symptoms have not been fully investigated. Moreover, whether childhood maltreatment can mediate the relationship between parental marital status and anxiety symptoms remains unclear. A population-based cross-sectional study was performed among 35,573 adolescents in elementary schools across 17 provinces in China. And childhood maltreatment, resilience, and anxiety symptoms were assessed among adolescents, respectively. The parental marital status was self-reported as having two married biological parents, divorced parents, stepparents, and single-parent. We found that the rates of anxiety symptoms among adolescents were 35.1% in intact families, 48.8% in divorced families, 49% in stepparent families, and 48% in single-parent families. Divorced parents (aOR = 1.191, 95% CI [1.060-1.337]) was an independent risk factor for adolescents' anxiety symptom while having stepparents and single-parent were not. In addition, emotional abuse (aOR = 1.300, 95% CI [1.285-1.316]), sexual abuse (aOR = 1.088, 95% CI [1.063-1.114]), and physical neglect (aOR = 1.019, 95% CI [1.007-1.031]) were all independent risk factors for anxiety symptoms in adolescents, while physical abuse and emotional neglect were not. The negative impacts of divorced and remarried parents on adolescent anxiety symptoms were mediated by childhood maltreatment partially (64.9% and 72.2%), while childhood maltreatment completely mediated the adverse impacts of single-parent on adolescent anxiety symptoms. Childhood maltreatment intervention strategies could be necessary for anxiety symptoms of adolescents in divorced/stepparent/single-parent families.

Most studies on antipsychotic efficacy and safety, including sex differences, focus on young schizophrenia patients. However, with an aging population, the number of older schizophrenia patients is increasing. This group faces challenges due to varying treatment responses and higher risks of adverse reactions, and guidelines often lack specific recommendations due to insufficient trials. Therefore, we investigated how age and sex influence antipsychotic prescribing practices in schizophrenia using the German Pharmacoepidemiological Research Database (GePaRD). We included patients diagnosed with schizophrenia (ICD-10 code F20.X) who had been prescribed at least one antipsychotic on an outpatient basis in at least two consecutive quarters in 2020, analyzing prescription data for 49,681 patients. Key findings include a notable preference for second-generation antipsychotics (SGAs) across all age groups, especially in younger patients, possibly due to their perceived better tolerability and efficacy. Treatment intensity with SGAs (expressed as the defined daily doses of SGAs per patient in 2020) initially increased with age, peaked among 35- to 44-year-olds, and then decreased, with the lowest treatment intensity in patients aged 65 years and older. The prescription patterns of specific SGAs and first-generation antipsychotics varied across age groups, highlighting the complexity of treatment decisions in schizophrenia management. Sex differences in prescription frequency and treatment intensity were also observed. The basic recommendation of the guideline to consider sex and age when prescribing antipsychotics therefore appears to be followed. Whether this prescribing practice is really optimal for older male and female schizophrenia patients, however, still needs to be proven in clinical trials.

Transient receptor potential canonical (TRPC) ion channels are expressed in areas of the brain responsible for processing emotion and mood and have been implicated in the pathophysiology of internalizing disorders such as major depressive disorder and anxiety disorders. This review outlines the rationale for targeting TRPC ion channels for drug development, with specific focus on TRPC4 and TRPC5. We provide preclinical evidence that the lack of TRPC4 and TRPC5 channels or its pharmacological inhibition attenuate fear and anxiety without impairing other behaviors in mice. We also report on clinical studies of BI 1358894, a small molecule inhibitor of TRPC4/5 ion channels, demonstrating reduced psychological and physiological responses to induced anxiety/panic-like symptoms in healthy volunteers. Furthermore, we highlight an imaging study that investigated the acute effects of BI 1358894 and showed reduced activation in several brain regions involved in emotional processing. We conclude that these findings demonstrate a critical role for TRPC4 and TRPC5 in emotional processing, even though it remains an open question if the biological signatures of TRPC4/5 inhibition reported here translate into clinical efficacy and indicate that a TRPC4/5 inhibitor might provide a more effective treatment of internalizing disorders.

The discovery of ketamine's rapid antidepressant action has generated intense interest in the field of neuropsychiatry. This discovery demonstrated that to alleviate the symptoms of depression, treatments do not need to elicit substantive alterations in neuronal circuitry or trigger neurogenesis, but rather drive synaptic plasticity mechanisms to compensate for the underlying pathophysiology. The possibility of a rapidly induced antidepressant effect makes therapeutic pursuit of fast-acting neuropsychiatric medications against mood disorders plausible. In the meantime, the accumulating clinical as well as preclinical observations raise critical questions on the nature of the specific synaptic plasticity events that mediate these rapid antidepressant effects. This work has triggered the current growing interest in alternative psychoactive compounds that are thought to have similar properties to ketamine and its action. This review covers our insight into these questions based on the work our group has conducted on this topic in the last decade.

Anhedonia, defined as a significant loss of interest or pleasure, is one of the core symptoms of treatment- resistant depression (TRD) and is often associated with poor prognosis. This article primarily investigates the changes in anhedonia symptoms, inflammatory markers, and cortisol levels in TRD patients after low-dose esketamine treatments. A total of sixty patients with TRD were enrolled in the clinical study of esketamine. We primarily assessed the severity of depressive symptoms and anhedonia using the Hamilton Rating Scale for Depression (HAMD) and the Snaith-Hamilton Pleasure Scal(SHAPS), respectively, before esketamine treatment and within 24 h after each treatment. Blood specimens were collected before the first treatment and within 1 h after the sixth treatment, measuring the levels of cortisol, interleukin-6(IL-6), interleukin-4(IL-4), and tumor necrosis factor-alpha(TNF-α) in plasma. We found that after six consecutive infusions of low-dose esketamine, patients' depressive symptoms and anhedonia showed improvement. After six treatments, plasma levels of cortisol, IL-6, and TNF-α decreased in patients with TRD, while the anti-inflammatory cytokine IL-4 increased. Multiple linear regression analysis revealed that baseline cortisol levels were correlated with anhedonia, while inflammatory factors showed no significant correlation. Add-on esketamine appears to be a good choice for the treament of the anhedonia in TRD. It has also shown promising effects on altering inflammatory markers in patients with TRD. Moreover, elevated plasma cortisol levels may serve as a potential biomarker for anhedonia in patients with TRD.

Impulsivity and emotion impairments have been noted in individuals with gambling disorder (GD). However, little research has investigated the influence of impulsivity and emotions on the severity of gambling in clinical populations. This study aimed to examine: (i) differences in emotions and impulsivity traits according to the severity of gambling in individuals with GD, (ii) the mediating effects of emotion in the relationship between impulsivity traits and gambling severity, and (iii) the predictive effects of emotion and impulsivity traits on GD severity. The study included 214 participants seeking treatment for GD who completed assessments for emotions (Patient Health Questionnaire-9 [PHQ-9], 7-item Generalized Anxiety [GAD-7]), impulsivity traits (Barratt Impulsiveness Scale [BIS], Self-control Scale [SCS]), and GD severity (DSM-5). Participants were categorized into mild (n = 78), moderate (n = 63), and severe (n = 73) gambling severity groups. Significant differences in emotions and impulsivity traits were observed across these groups. The severe GD group exhibited higher levels of depression, anxiety, and impulsivity traits, along with lower self-control, compared to the moderate and mild groups. Mediation analyses demonstrated that negative emotions mediated the association between impulsivity traits and the severity of gambling. More specifically, the indirect effects of impulsivity traits through PHQ-9 and GAD-7 were found to be significant, indicating a mediating role of emotions. Moreover, a predictive model incorporating emotion and impulsivity traits showed moderate accuracy in predicting the severity of gambling, with an area under the receiver operating characteristic curve of 0.714. This study highlights the distinct pathways through which impulsivity traits operate and emphasizes the need for prevention and treatment strategies that consider impulsivity traits and emotions for different levels of gambling severity.