Persistent negative symptoms (PNS), defined as negative symptoms of at least moderate severity that endure over time and are not attributable to other psychopathological dimensions such as depression or parkinsonism, have been associated with poor functional outcomes in schizophrenia, in both chronic stages and in the early phases of the disorder. This post-hoc analysis of a large cohort of schizophrenia spectrum disorder patients within their first 7 years of illness, enrolled in the European Long-acting Antipsychotics in Schizophrenia Trial (EULAST), aimed to: 1) confirm prior findings about the prevalence and clinical impact of unconfounded persistent negative symptoms (PNS) on dropout rates and psychosocial functioning after 12 and 18 months of treatment; and 2) explore the prevalence of enduring negative symptoms (E-NS), defined as persistent negative symptoms either confounded or unconfounded by depression or parkinsonism, and their influence on functional outcome. At week 0, 60.6% of patients exhibited at least one negative symptom of moderate severity. Among them, 42.8% met criteria for unconfounded negative symptoms. After 1 year, the frequency of PNS and E-NS was 7.9% and 15%, respectively, with a prospective consistency around 32%. PNS subjects had similar levels of functioning at week 0 (d = -0.179, p = 0.194), but worse functioning after 12 (d = -0.697, p = 0.028) and 18 (d = -0.676, p = 0.024) months of treatment, as compared to those with negative symptoms of similar severity at baseline that did not persist (non-persistent negative symptoms, N-PNS). No difference among groups was observed in drop-out rates. The comparison between the E-NS and N-PNS groups revealed the same functional outcome differences observed in the PNS versus N-PNS comparison. Our findings confirm that long-term persistence of negative symptoms, both primary and secondary, contributes to poor functional outcome. Future research should focus on identifying predictors of symptom persistence to guide the development of targeted interventions aimed at improving long-term functional outcomes in this patient population.

Working memory (WM) deficits are commonly observed across the depression spectrum and may represent a modifiable cognitive mechanism. This systematic review and meta-analysis evaluated the effects of WM training (WMT) on depressive symptoms and WM performance, and examined potential moderators and the association between WM gains and symptom change. Systematic searches of PsycINFO, Embase, and PubMed were conducted in December 2022 and updated in January 2025. Eligible studies were randomized controlled trials (RCTs) using WMT as the sole cognitive intervention with depressive symptoms as outcomes. Two-level random-effects models were used for depressive symptoms and three-level models for WM outcomes. Risk of bias was assessed by the Cochrane Risk of Bias Tool. Twenty-seven RCTs involving 1692 participants were included. WMT produced a small but significant reduction in depressive symptoms at post-training (Hedges' g = 0.20, 95% CI [0.04, 0.35]), though effect was not maintained at follow-up. Moderate improvements in WM were observed at post-training (g = 0.61, 95% CI [0.24, 0.98]) and follow-up (g = 0.72, 95% CI [0.07, 1.38]). Post-training WM gains were positively associated with symptom reductions at follow-up. Moderator analyses indicated that baseline symptom severity and training material valence may influence outcomes, though subgroup effects were not statistically significant and warrant cautious interpretation. These findings suggest that WMT targets a potentially modifiable mechanism in depression, but its clinical utility remains uncertain. Larger RCTs, particularly in clinical populations and with extended follow-ups, are needed to establish more definitive evidence regarding its preventive and therapeutic value. (Protocol registration: PROSPERO, CRD42023400213.).

Despite decades of research, the underlying mechanism of auditory verbal hallucinations (AVH), a core symptom of schizophrenia, remain unclear. Previous studies have tried to capture the neural activity during AVH episodes, whereas trait features of AVH have been less investigated. To address this gap, we employed functional Near-Infrared Spectroscopy (fNIRS) to investigate the neuroimaging patterns in healthy controls (HCs), patients with schizophrenia with a history of AVH (AVHh+) and those without a history of AVH history (AVHh-). We hypothesized that significant differences of functional connectivity (FC) changes would be observed in AVHh+.

We recruited 23 AVHh+, 16 AVHh-, and 17 matched HCs. Participants underwent an 8-minute resting-state fNIRS scanning. Data processing and analysis were conducted by the NirSpark software (HuiChuang, China) package and R Studio.

Compared to the AVHh-, the AVHh+ showed significantly lower FC between the Broca's area and the left supplementary motor area (SMA).

The hypoconnectivity of Broca-left SMA circuit might serve as a trait-like marker of vulnerability to AVH.

The contemporary characteristics of mental health disorders (MHDs) among liver transplant (LT) survivors are not well understood. We aimed to describe the prevalence of post-LT anxiety, depression or post-traumatic (PTS) diagnoses and symptoms before and after LT and explore their association with post-LT health-related quality of life (HRQOL). In a cross-sectional study, participants presenting for post-LT care completed surveys measuring HRQOL (PROMIS-29), anxiety/depression (Hospital Anxiety and Depression Scale, HADS) and PTS (Impact of Event Scale-Revised, IES-R). Participants self-reported sociodemographics and a history of MHD diagnoses and treatment and clinical data on transplant course and prior MHDs and treatment were collected. Overall, 202 patients [58% male, 89% white, median age 63 years (IQR: 54-69)] consented to participate. Median time from LT was 4.4 years (IQR: 1.4-10.0). The prevalence of anxiety or depression after LT was 30% and PTS was 7%. There was a significant difference in HRQOL in those 5+ years vs. 0-1 years post-LT (MCS scores: 49.5 ± 8.8 vs. 45.8 ± 9.3, p = 0.03 and PCS scores: 44.7 ± 9.2 vs. 40.6 ± 8.8, p = 0.02). Active symptoms of anxiety, depression or PTS after LT were noted in 25.6% LT survivors; of these, 55% patients did not have a mental health diagnosis at the time of transplant. Active symptoms of anxiety, depression or PTS after transplant were associated with significantly worse HRQOL across multiple domains after adjusting for sociodemographic and clinical variables. Anxiety, depression or post-traumatic stress are common in LT survivors and associated with poor HRQOL. MHDs represent modifiable factors to improve patient-reported outcomes in LT survivors, including in patients without MHDs at the time of transplant.

In prisons, the issue of assessing the risk of violence is often a major point of disagreement between correctional authorities and healthcare professionals. Mental health professionals must prioritize a clinical approach that is independent and non-stigmatizing with regard to the patient's criminal history, viewing violence as a vulnerability in crisis situations from a recovery perspective.

Gait impairments remain a major therapeutic challenge in Parkinson's disease (PD). Apomorphine is gaining renewed clinical attention with the expanding use of pump infusion systems. Yet the specific role of apomorphine on the neural regulation of gait has remained poorly characterized, limiting its targeted use for symptom-specific therapy in PD. Here, we examined the neurobehavioral effects of apomorphine on runway locomotion in the unilateral 6-hydroxydopamine (6-OHDA) rat model. Therapeutic drug doses significantly increased total walking distance, related to reduced akinesia and prolonged gait episodes. Conversely, 3D kinematic analysis revealed reduced limb velocities under medication. At the neural level, therapy doses selectively enhanced cortical high-gamma rhythms without substantially altering beta or low-gamma activity. Instead, beta and low-gamma oscillations were consistently suppressed during motor activity in both medication ON and OFF conditions. Neurobehavioral correlations showed that transitions into gait were facilitated by reductions in beta and low-gamma activity, whereas transitions to akinesia were primarily suppressed when high-gamma activity was elevated. Our findings highlight that cortical oscillations can serve as state specific biomarkers for gait impairments in PD. We further propose that the complex therapy effects of apomorphine are best explained by a shift in motor-state equilibrium that is defined by the transitions of akinesia, stationary movements and gait. Together, these insights establish a mechanistic framework to guide the development of targeted gait therapies in PD.

Suicidal ideation and self-injurious behaviors (SISIB) in children and adolescents are a major concern in clinical practice. Yet, little is known about the prevalence rates of SISIB in outpatient clinics and its response to routine psychotherapy. Therefore, the present study aims to assess the prevalence of SISIB and the changes in SISIB in a heterogeneous clinical outpatient sample of children and adolescents undergoing cognitive behavioral therapy in Germany.

The sample consists of N = 5730 child and adolescent outpatients, 54.05% female, mean age = 12.16 years (SD = 3.51). As metrics of SISIB, two items (Item 18 on self-injurious behavior and Item 91 on suicidal ideation) of the Youth Self Report (YSR/11-18R) and the Child Behavior Checklist (CBCL/6-18R) as caregiver report were used.

Pretreatment, suicidal ideation was reported by 33.45% of patients and 15.39% of caregivers. Self-injurious behavior was reported pretreatment by 35.35% of patients and 20.16% of caregivers. Posttreatment, suicidal ideation was reported by 11.32% of patients and 5.25% of caregivers. Self-injurious behavior was reported posttreatment by 19.00% of patients and 9.43% of caregivers.

SISIB are very common in children and adolescents in outpatient settings. Prevalence rates are higher in self-reports than in caregiver reports, indicating the importance of assessing SISIB in children and adolescents themselves. After routine-care psychotherapy, a substantial proportion of patients report an amelioration of SISIB. These results indicate the importance of monitoring SISIB during treatment and of therapists being aware of risk assessment techniques and psychotherapy interventions targeting SISIB.

Vasopressin, a key molecular regulator of social behavior, is implicated in promoting self-protective responses to threats against physical safety and resources. However, its role in defending against self-view threats-common in social interactions and critical to well-being-remains unclear. This study investigates the neural mechanisms through which vasopressin modulates self-protective responses to spontaneous social comparison. In a double-blind, placebo-controlled neuroimaging study, 48 healthy male participants were randomized to receive intranasal vasopressin or placebo. Participants then underwent fMRI while rating their satisfaction with social evaluations and monetary outcomes assigned to a stranger, friend, or themselves. Compared to placebo, vasopressin selectively intensified contrastive emotional responses to social evaluations of the stranger, decreasing satisfaction with positive evaluations and increasing satisfaction with negative evaluations, relative to those of the self or friend. At the neural level, vasopressin reduced the neural distinction between the stranger and the self/friend in medial prefrontal cortex (mPFC), an effect that was stronger in more socially dominant individuals. Complementing this regional effect, vasopressin attenuated whole-brain multivariate differentiation and reduced functional connectivity from ventral mPFC to the temporoparietal junction and precuneus. Together, these converging neuroimaging findings suggest that vasopressin may increase the psychological salience of strangers and thereby modulate their neural representations, potentially engaging self-protective affective processes. Our findings elucidate novel neuropsychological mechanisms through which vasopressin amplifies emotional defense against social threats and offer insights into potential clinical applications for psychiatric conditions characterized by impaired self-protection.

This World Federation of Societies of Biological Psychiatry (WFSBP) consensus paper aims to summarise and evaluate the published study results on objectively measurable biological markers associated with anorexia nervosa (AN).

The relevant literature was reviewed by the WFSBP Task Forces on Eating Disorders and on Biological Markers, and a consensus regarding the significance of the published evidence was reached.

Candidate biological markers that have been associated with AN include clinical (e.g. body weight), molecular (e.g. genetic, epigenetic, hormonal, immunological, metabolomic), cellular (e.g. leukocytes), neuroimaging (e.g. structure, function, connectivity), digital, cardiac and neurophysiological parameters. Some clinical and laboratory parameters are risk markers in clinical practice. Biological markers have pathophysiological relevance in understanding the biological and metabolic pathophysiology of AN and its physical health consequences. Few studies have examined pharmacogenetics or therapeutic drug monitoring as tools to monitor and guide the treatment of AN.

Biological markers will hopefully soon enable clinicians to intervene earlier in a more targeted manner to mitigate treatment resistance. However, the current scientific basis for most biological markers are group comparisons only. Studies on sensitivity, specificity and the prognostic value of these markers are lacking.