Acta Neuropsychiatrica最新文献

Objective: To assess satisfaction and pain-related knowledge levels following an inclusive Pain Neuroscience Education (PNE) programme in improving pain-related knowledge and perceived satisfaction among adolescents with and without intellectual disabilities, and to assess its applicability in digital health education settings. Methods: A multicentre, cross-sectional study was conducted in 15 public schools. A total of 373 students (5th-6th grade), including those with intellectual disabilities, participated in a hybrid-format PNE programme delivered in two 90-minute sessions. Satisfaction and knowledge were assessed using an adapted, easy-to-read questionnaire, with exploratory factor analysis identifying three core domains: activity format, teacher evaluation, and SDG-related training. Results: Overall satisfaction and knowledge gains were high across all participants. No significant differences were found between students with and without intellectual disabilities or between urban and rural schools in satisfaction and teacher evaluation. However, rural students reported greater awareness of the SDG-related content (p < 0.05). Conclusion: The adapted PNE programme was well-received and associated with high levels of pain-related knowledge across diverse educational contexts. Its inclusive and hybrid design supports its potential scalability through digital health strategies, promoting equity in pain education.

Introduction: Autoimmune psychosis (AP) and other autoimmune psychiatric syndromes (APS) are associated with central nervous system antibodies. This study investigated related magnetic resonance spectroscopic imaging (MRSI) signatures and their correlations with electroencephalography (EEG), cerebrospinal fluid (CSF), and psychometric/neuropsychological measures.

Methods: Twenty-eight adults with suspected antibody-positive AP spectrum syndromes were compared with 28 matched healthy controls. Inclusion in the patient group was based on the APS concept, resulting in a heterogeneous group with uniform autoimmunity. MRSI was performed using a spiral-encoded Mescher-Garwood localised adiabatic selective refocusing 3D-MRSI sequence. Glutamate+glutamine (Glx), gamma-aminobutyric acid (GABA), total N-acetylaspartate (tNAA), and total creatine (tCr) were reported as ratios to tNAA and/or tCr. EEG was analysed for intermittent rhythmic delta/theta activity (IRDA/IRTA) using independent component analysis.

Results: No significant differences in Glx, GABA, tNAA, or tCr ratios were observed between patients and controls. Correlation analyses in patients showed a trend for a negative association of the IRDA/IRTA rate before hyperventilation with the GABA/tCr ratio in both hippocampi and with the GABA/tNAA ratio in the left hippocampus and Glx/tCr ratio in the right putamen and pallidum. Significant positive correlations were observed between inflammatory CSF markers (white blood cell count and IgG Index) and GABA/tCr and GABA/tNAA ratios in the left caudate nucleus and right isthmus cingulate and thalamus, as well as between negative symptoms in PANSS and higher GABA/tCr ratios in the right putamen.

Discussion: No group differences were identified; however, correlations suggest a link between neuroinflammatory CSF markers and negative symptoms with GABAergic signalling in patients. Multimodal diagnostic approaches may provide a better understanding of the link between neuroinflammation, neurochemistry, and EEG slowing.

Objective: Amisulpride, a substituted benzamide derivative, has a unique pharmacological profile characterised by a high affinity for dopaminergic D₂/D₃ receptors, as well as an affinity for 5-HT₇ receptors. Its effectiveness and safety surpass those of traditional antipsychotic drugs and multi-receptor antipsychotic medications in improving global symptoms, including both positive and negative symptoms. This makes it a compelling subject for study. However, the molecular mechanisms that contribute to its clinical efficacy in treating schizophrenia remain largely unexplored.

Methods: We assessed cell viability following amisulpride treatment using the MTT and a real-time cell viability assay. Subsequently, we conducted RNA-seq and LC-MS/MS analyses to identify differentially expressed genes and proteins in SH-SY5Y neuroblastoma cells treated with amisulpride.

Results: In the present study, we used RNA-seq analysis to identify downregulated expression of a transcriptional factor, FOSB, in amisulpride-treated SH-SY5Y neuroblastoma cells, while using LC-MS/MS analysis to identify multiple differentially expressed proteins in these cells. Among these differentially expressed proteins, we confirmed four proteins (ACTG1, ANP32E, CLTC, IPO8) that are differentially expressed under the administration of amisulpride.

Conclusion: Our data reveal novel insights into the role of amisulpride in modulating the differential expression of genes and proteins. These findings, which involve genes/proteins related to AP-1 transcription factor family gene regulation, cytoskeleton, histone binding activity, the intracellular trafficking of receptors and endocytosis of a variety of macromolecules, and nuclear localisation signal, are particularly significant as they shed light on the molecular underpinnings of the clinical efficacy of amisulpride and the pathogenesis of schizophrenia.

Progress in the development of new and improved medications for psychosis has been notably slow and disappointing. The first treatment for schizophrenia was introduced in early 1950s and the majority of medications available today exclusively function through dopamine antagonism. The search for a new drug treatment with a different mechanism of action was extremely slow-paced mainly due to the limited understanding of the aetiology, pathophysiology and genetics of schizophrenia. Given the fact that a third of people do not respond to dopamine antagonists, there is a clear need for an antipsychotic with a different mechanism of action. In 2024, FDA approved a new medication for psychosis branded as Cobenfy. This xanomeline-trospium combination works via cholinergic pathway and the dual M1 and M4 receptor activation helps regulates dopaminergic and glutaminergic neurotransmission as well, thereby restoring balance in these circuits. Acetylcholine also helps improve cognitive processing including attention, learning and sensory gating. In this article, we try to understand the place of this unique drug in the antipsychotic ladder. We also explore the clinical scenarios where this medication can be effective as well as the potential future outlook when it comes to the treatment of schizophrenia.

Introduction: Extant literature indicated that glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may potentially reduce risk of opioid overdose in persons with opioid use disorders (OUDs). Herein, we conducted a comprehensive synthesis of the effects of GLP-1 and GLP-1 RAs on OUDs.

Methods: We examined preclinical and clinical paradigms examining the effects of GLP-1 and GLP-1 RAs on OUD and OUD-associated behaviours (i.e. opioid self-administration, opioid-seeking behaviour). Relevant articles were retrieved from OVID (MedLine, Embase, AMED, PsychINFO, and JBI EBP Database), PubMed, and Web of Science from database inception to 1 May 2025. Primary studies (n = 10) examining the aforementioned effects associated with GLP-1 and GLP-1 RA administration were retrieved for analysis.

Results: GLP-1 RAs (i.e. exenatide, liraglutide) reduced opioid-seeking behaviour (p < 0.05) and self-administration of opioid drugs (p < 0.05) in preclinical paradigms. In addition, results from human studies indicate that GLP-1 administration was associated with reducing the risk of opioid overdose in human studies (aIRR = 0.60, 95% CI [0.43, 0.83]).

Conclusion: GLP-1 RAs may affect opioid self-administration as well as the risk for overdose as evidenced by both preclinical and clinical data. There is a need for adequate well-controlled studies to determine whether GLP-1 RAs may provide clinically meaningful improvement and risk reduction in persons living with OUDs.

Objective: Cortisol is a well-established biomarker of stress, assessed through salivary or blood samples, which are intrusive and time-consuming. Speech, influenced by physiological stress responses, offers a promising non-invasive, real-time alternative for stress detection. This study examined relationships between speech features, state anger, and salivary cortisol using a validated stress-induction paradigm.

Methods: Participants (N = 82) were assigned to cold (n = 43) or warm water (n = 39) groups. Saliva samples and speech recordings were collected before and 20 minutes after the Socially Evaluated Cold Pressor Test (SECPT), alongside State-Trait Anger Expression Inventory (STAXI) ratings. Acoustic features from frequency, energy, spectral, and temporal domains were analysed. Statistical analyses included Wilcoxon tests, correlations, linear mixed models (LMMs), and machine learning (ML) models, adjusting for covariates.

Results: Post-intervention, the cold group showed significantly higher cortisol and state anger. Stress-related speech changes occurred across domains. Alpha ratio decreased and MFCC3 increased post-stress in the cold group, associated with cortisol and robust to sex and baseline levels. Cortisol-speech correlations were significant in the cold group, including sex-specific patterns. LMMs indicated baseline cortisol influenced feature changes, differing by sex. ML models modestly predicted SECPT group membership (AUC = 0.55) and showed moderate accuracy estimating cortisol and STAXI scores, with mean absolute errors corresponding to ∼ 24-38% and ∼16-28% of observed ranges, respectively.

Conclusion: This study demonstrates the potential of speech features as objective stress markers, revealing associations with cortisol and state anger. Speech analysis may offer a valuable, non-invasive tool for assessing stress responses, with notable sex differences in vocal biomarkers.

Background: Major depressive disorder (MDD) is a significant public health concern, and current treatments often have limitations in effectiveness and adherence. Psilocybin, a psychedelic compound found in certain mushrooms, is being explored as a potential treatment for depression. It primarily acts through the serotonin 5-HT2A receptor but interacts with 5-HT1A and 5-HT2C receptors. Its precise mechanisms remain under investigation.

Objectives: (1) To consolidate evidence on psilocybin’s efficacy and safety for depression and the role of 5HT2a, (2) to identify limitations in the literature, and (3) to highlight areas needing further research.

Methods: This systematic review follows PRISMA guidelines and analyses 22 studies, including randomised controlled trials (RCTs) and open-label studies. The studies cover various populations, including individuals with treatment-resistant depression, different dosing regimens, and adjunctive therapies.

Results: Psilocybin therapy shows substantial and rapid antidepressant effects, often after one or two sessions with psychological support. Improvements are sustained for weeks or months in many cases. Psilocybin is generally well-tolerated, with mild adverse effects such as anxiety during administration and transient headaches, which are manageable in controlled settings.

Conclusions: Psilocybin demonstrates promise as a novel treatment for depression, especially for individuals unresponsive to conventional antidepressants. Further research is needed to refine dosing, explore long-term effects, and understand its mechanisms of action.

Objectives: There are differences in IgA responses to tryptophan catabolites (TRYCATs) in major neurocognitive psychosis (MNP) versus simple neurocognitive psychosis (SNP) and normal controls. MNP and SNP are distinct schizophrenia classes which are differentiated by neurocognitive deficits, phenome features, and biomarker pathways. Nevertheless, there is no data on serum concentrations of those TRYCATs in MNP and SNP. The aim of the present study is to examine serum concentrations of tryptophan and TRYCATs in MNP versus SNP and controls.

Methods: This case-control study examines serum levels of tryptophan and TRYCATs in 52 MNP patients, 68 SNP patients and 60 controls in association with overall severity of schizophrenia (OSOS).

Results: MNP patients show lower tryptophan, kynurenic acid (KA), 3-OH-anthranilic acid (3HAA), and higher anthranilic acid (AA) and quinolinic acid (QA) than SNP patients and controls. There were no differences between SNP and controls in these TRYCATs. Kynurenine (KYN) was lower in MNP+SNP than in controls. We found that 36.5% of the variance in OSOS was explained by the combined effects of lowered tryptophan, KA, and 3-HK, and increased QA and AA. The most important biomarkers of MNP and OSOS were the QA/KA ratio followed by the QA/3HAA ratio.

Conclusions: The alterations in serum TRYCAT levels further emphasize that MNP and SNP represent two biologically distinct subtypes of schizophrenia. The reductions in TRYCATs diminish the antioxidant and immunoregulatory functions of the TRYCAT pathway. Elevated QA levels may exacerbate the disruption of the blood-brain barrier and the immune-related and oxidative neurotoxicity in MNP.

Background: Autoimmune thyroid disease (AITD) and major depressive disorder (MDD) are common genetic diseases. The comorbidity of AITD and MDD has been widely demonstrated by large amounts of epidemiological studies. However, the genetic architectures of the comorbidity remain unknown.

Methods: We use large-scale GWAS summary data and novel genetic statistical methods to assess the genetic correlation and potential causality between AITD and MDD disorders. We perform cross-trait GWAS meta-analyses to identify genetic risk variants not previously associated with the individual traits. And we use summary-data-based mendelian randomisation to identify putative functional genes shared between diseases.

Results: Both global and local genetic correlation study confirmed the genetic correlation of AITD and MDD. Through multi-trait analysis of GWAS (MTAG), we identified 112 SNPs associated with the conjoint phenotype, but not with individual traits. Mendelian randomisation confirmed the causal relationship between MDD (exposure) and AITD (outcome). The summary-based mendelian randomisation study found two plausible functional genes for AITD and MDD comorbidity.

Conclusions: AITD and MDD are genetically correlated in global and local chromosomal regions. MR analyses support a putative casual effect of MDD on AITD risk, though residual pleiotropy or confounding cannot be fully excluded. These findings highlight the need for triangulation with experimental and longitudinal studies to confirm causality.

Objective: Patient-Initiated Brief Admission (PIBA) is an intervention designed to provide constructive crisis management for patients. The purpose of this study was to evaluate outcomes in healthcare utilisation and self-inflicted injuries at one Swedish Hospital where PIBA was implemented in late 2017.

Methods: Patients who signed a PIBA-contract between 2017 and 2023 were included in the study. Data on inpatient care, contacts with the psychiatric emergency department and self-inflicted injuries that resulted in contact with medical care were collected from patients' medical records. Effects of PIBA were assessed using paired t-tests, comparing pre-post changes 0.5, 1 and 2 years, from initiation of PIBA-contract, respectively.

Results: Data from a total of 38 patients were analysed. There was a marked decrease in inpatient care from voluntary admissions in the first six months after initiation of PIBA. There was also a significant decrease in number of contacts with the psychiatric emergency department (for all patients) in the 1-year pre-post comparison, but not for the 0.5- and 2-year pre-post comparisons. There were no significant reductions in compulsory inpatient care or self-inflicted injuries in our cohort. Patients with contracts extending over several years appeared stable, on average, in their use of care and prevalence of intoxications.

Conclusion: The main effect on inpatient care after initiation of PIBA was a reduction in voluntary admissions, coinciding with a shift from voluntary admissions in favour of PIBA. The results support a more widespread utilisation of PIBA from a health-economic perspective.