European Archives of Psychiatry and Clinical Neuroscience最新文献

There is a growing interest in the potential benefits of attentional bias modification (ABM) training in chronic pain patients. However, studies examining the effectiveness of ABM programs in fibromyalgia patients have demonstrated inconclusive effects on both behavioral indices and clinical symptoms. Additionally, underlying neural dynamics of ABM effects could yield new insights but remain yet unexplored. Current study, therefore, aims to investigate the effects of ABM training on known neural electrophysiological indicators of attentional bias to pain (P2, N2a). Thirty-two fibromyalgia patients were enrolled and randomly assigned to an ABM training (N = 16) or control (N = 16) condition (2 weeks duration). Within the ABM training condition participants performed five sessions consisting of a modified version of the dot-probe task in which patients were trained to avoid facial pain expressions, whereas in the control group participants performed five sessions consisting of a standard version of the dot-probe task. Potential ABM training effects were evaluated by comparing a single pre- and post-treatment session, in which event-related potentials (ERPs) were recorded in response to both facial expressions and target stimuli. Furthermore, patients filled out a series of self-report questionnaires assessing anxiety, depression, pain-related worrying, fear of pain, fatigue and pain status. After training, results indicated an overall reduction of the amplitude of the P2 component followed by an enhancement of N2a amplitude for the ABM condition compared to control condition. In addition, scores on anxiety and depression decreased in patients assigned to the training condition. However, we found no effects derived from the training on pain-related and fatigue status. Present study offers new insights related to the possible neural mechanisms underlying the effect of ABM training in fibromyalgia. Clinical trial (TRN: NCT05905159) retrospectively registered (30/05/2023).

Suicide is considered one of the major public health problems worldwide, being the second leading cause of death in the 15-29 age group. It is estimated that every 40s someone in the world commits suicide. The social taboo surrounding this phenomenon as well as the fact that suicide prevention measures currently fail to avoid deaths from this cause, means that more research is needed to understand its mechanisms. The present narrative review on suicide tries to point out several important aspects, such as risk factors or the dynamics of suicide, as well as the current findings in the field of physiology that could offer advances in the understanding of suicide. Subjective measures of risk such as scales and questionnaires are not effective alone, whereas the objective measures can be addressed from physiology. Thus, an increased neuroinflammation in people who take their own lives has been found, with an increase in inflammatory markers such as interleukin-6 and other cytokines in plasma or cerebrospinal fluid. Also, the hyperactivity of the hypothalamic-pituitary-adrenal axis and a decrease in serotonin or in vitamin D levels seems to also be involved. In conclusion, this review could help to understand which factors can trigger an increased risk of dying by suicide, as well as pointing out those alterations that occur in the body when someone attempt to commit suicide or succeeds in taking their own life. There is a need for more multidisciplinary approaches that address suicide to help to raise awareness of the relevance of this problem that causes the death of thousands of people every year.

Background: The scientific literature shows some gender differences in the clinical course of schizophrenia. The aim of this study is to identify gender differences in clinical and biochemical parameters in subjects affected by schizophrenia. This would allow for the implementation of individualized treatment strategies.

Methods: We examined a large set of clinical and biochemical parameters. Data were obtained from clinical charts and blood analyses from a sample of 555 schizophrenia patients consecutively admitted for exacerbation of symptoms to the inpatient clinic of Fondazione IRCCS Policlinico (Milan) or ASST Monza in Italy from 2008 to 2021. Univariate analyses, binary logistic regression, and a final logistic regression model were performed with gender as dependent variable.

Results: The final logistic regression models showed that male patients (compared to females) were more prone to lifetime substance use disorders (p = 0.010). However, they also had higher GAF (global functioning) mean scores (p < 0.001) at the time of hospitalization. Univariate analyses showed that male patients (with respect to females) had an earlier age at onset (p < 0.001), a more frequent family history of multiple psychiatric disorders (p = 0.045), were more often smokers (p < 0.001), had a more frequent comorbidity with at least one psychiatric disorder (p = 0.001), and less often suffered from hypothyroidism (p = 0.011). In addition, men had higher levels of albumin (p < 0.001) and bilirubin (t = 2.139, p = 0.033), but lower levels of total cholesterol (t = 3.755, p < 0.001).

Conclusions: Our analyses indicate a less severe clinical profile in female patients. This is evident especially in the early years of the disorder, as suggested by less comorbidity with psychiatric disorders or later age at onset; this is consistent with the related literature. In contrast, female patients seem to be more vulnerable to metabolic alterations as demonstrated by more frequent hypercholesterolemia and thyroid dysfunction. Further studies are needed to confirm these results in the framework of precision medicine.

Many individuals have been suffering from consistent neurological and neuropsychiatric manifestations even after the remission of coronavirus disease (COVID-19). Brain-derived neurotrophic factor (BDNF) is a protein involved in the regulation of several processes, including neuroplasticity, neurogenesis, and neuronal differentiation, and has been linked to a range of neurological and psychiatric disorders. In this study, we aimed to synthesize the available evidence on the profile of BDNF in COVID-19. A comprehensive search was done in the Web of Science core collection, Scopus, and MEDLINE (PubMed), and Embase to identify relevant studies reporting the level of BDNF in patients with COVID-19 or those suffering from long COVID. We used the NEWCASTLE-OTTAWA tool for quality assessment. We pooled the effect sizes of individual studies using the random effect model for our meta-analysis. Fifteen articles were included in the systematic review. The sample sizes ranged from 16 to 183 participants. Six studies compared the level of BDNF in COVID-19 patients with healthy controls. The pooled estimate of the standardized mean difference in BDNF level between patients with COVID-19 and healthy individuals was - 0.84 (95% CI - 1.49 to - 0.18, p = 0.01, I2 = 81%) indicating a significantly lower BDNF level in patients with COVID-19. Seven studies assessed BDNF in different severity statuses of patients with COVID-19. The pooled estimate of the standardized mean difference in BDNF level was - 0.53 (95% CI - 0.85 to - 0.21, p = 0.001, I2 = 46%), indicating a significantly lower BDNF level in patients with more severe COVID-19. Three studies evaluated BDNF levels in COVID-19 patients through different follow-up periods. Only one study assessed the BDNF levels in long COVID patients. Sensitivity analyses did not alter the significance of the association. In this study, we showed a significant dysregulation of BDNF following COVID-19 infection. These findings may support the pathogenesis behind the long-lasting effects of this disease among infected patients. PROSPERO: CRD42023413536.

There is growing evidence of disproportionate retinal thinning in schizophrenia, but doubts are still raised regarding its significance in the context of the neurobiology of the disease. Therefore, we examined whether these abnormalities are significantly associated with neurological soft signs (NSS) which are closely related to the risk of schizophrenia. This cross-sectional study analyzing linear correlations between variables involved 56 schizophrenia inpatients and 60 controls. The results confirmed such relationships, and only in the patient sample. In addition, retinal abnormalities and NSS were significantly correlated with duration of illness. These findings provide further evidence for linked neurodevelopmental and neurodegenerative aspects of schizophrenia.

This study aims to explore the link between Apo-E, brain white matter, and suicide in patients with major depressive disorder (MDD) to investigate the potential neuroimmune mechanisms of Apo-E that may lead to suicide. Thirty-nine patients with MDD (22 patients with suicidality) and 57 age, gender, and education-matched healthy controls participated in this study, provided plasma Apo-E samples, and underwent diffusion tensor imaging scans. Plasma Apo-E levels and white matter microstructure were analyzed among the MDD with suicidality, MDD without suicidality, and HC groups using analysis of variance with post hoc Bonferroni correction and tract-based spatial statistics (TBSS) with threshold-free cluster enhancement correction. Mediation analysis investigated the relationship between Apo-E, brain white matter, and suicidality in MDD. The MDD with suicidality subgroup had higher depressive and suicide scores, longer disease course, and lower plasma Apo-E levels than MDD without suicidality. TBSS revealed that the MDD non-suicide subgroup showed significantly increased mean diffusivity in the left corticospinal tract and body of the left corpus callosum, as well as increased axial diffusivity in the left anterior corona radiata and the right posterior thalamic radiation compared to the suicidal MDD group. The main finding was that the increased MD of the left corticospinal tract contributed to the elevated suicide score, with Apo-E mediating the effect. Preliminary result that Apo-E's mediating role between the left corticospinal tract and the suicide factor suggests the neuroimmune mechanism of suicide in MDD. The study was registered on ClinicalTrials.gov (NCT03790085).

Psychiatric disorders frequently co-occur and share common symptoms and genetic backgrounds. Previous research has used genome-wide association studies to identify the interrelationships among psychiatric disorders and identify clusters of disorders; however, these methods have limitations in terms of their ability to examine the relationships among disorders as a network structure and their generalizability to the general population. In this study, we explored the network structure of the polygenic risk score (PRS) for 13 psychiatric disorders in a general population (276,249 participants of European ancestry from the UK Biobank) and identified communities and the centrality of the network. In this network, the nodes represented a PRS for each psychiatric disorder and the edges represented the connections between nodes. The psychiatric disorders comprised four robust communities. The first community included attention-deficit hyperactivity disorder, autism spectrum disorder, major depressive disorder, and anxiety disorder. The second community consisted of bipolar I and II disorders, schizophrenia, and anorexia nervosa. The third group included Tourette's syndrome and obsessive-compulsive disorder. Cannabis use disorder, alcohol use disorder, and post-traumatic stress disorder make up the fourth community. The PRS of schizophrenia had the highest values for the three metrics (strength, betweenness, and closeness) in the network. Our findings provide a comprehensive genetic network of psychiatric disorders and biological evidence for the classification of psychiatric disorders.

Electroconvulsive therapy (ECT) is an effective, safe, and mostly well-tolerated treatment for patients with severe or difficult to treat depression or psychotic disorders. However, a relevant number of patients experience subjective and/or objective cognitive side-effects. The mechanism of these transient deficits is not yet clear. Thus, our study prospectively investigated neurofilament light chain (NfL) concentrations as a highly sensitive biomarker for neuroaxonal damage along with cognitive performance during a course of ECT. Serum NfL concentrations from 15 patients with major depressive disorder receiving ECT were analyzed (1) 24 h before the first ECT, (2) 24 h and (3) 7 days after the last ECT (45 measurements in total). Neuropsychological testing including memory, executive functions and attention was performed at each time-point. NfL concentrations did not change between the three time-points, while a temporary cognitive impairment was found. Even in the subset of patients with the strongest impairment, NfL concentrations remained unchanged. Neuropsychological testing revealed the common pattern of transient cognitive side-effects with reduced performance 24 h post-ECT (global cognition score: p < 0.001; memory: p = 0.043; executive functions: p = 0.002) and return to baseline after 7 days (all p < 0.001). Our study adds to the evidence that neither ECT per se nor the transient cognitive side-effects seem to be associated with an increase of NfL as a marker of neuroaxonal damage. In contrast, we discuss cognitive side effects to be potentially interpreted as a byproduct of ECT's neuroplastic effects.

The role of the complement system in schizophrenia (Sz) is inconclusive due to heterogeneity of the disease and study designs. Here, we assessed the levels of complement activation products and functionality of the classical pathway in acutely ill unmedicated Sz patients at baseline and after 6 weeks of treatment versus matched controls. The study included analyses of the terminal complement complex (sTCC) and C5a in plasma from 96 patients and 96 controls by enzyme-linked immunosorbent assay. Sub-group analysis of serum was conducted for measurement of C4 component and activity of the classical pathway (28 and 24 cases per cohort, respectively). We found no differences in levels of C5a, C4 and classical pathway function in patients versus controls. Plasma sTCC was significantly higher in patients [486 (392-659) ng/mL, n = 96] compared to controls [389 (304-612) ng/mL, n = 96] (p = 0.027, δ = 0.185), but not associated with clinical symptom ratings or treatment. The differences in sTCC between Sz and controls were confirmed using an Aligned Rank Transformation model considering the covariates age and sex (p = 0.040). Additional analysis showed that sTCC was significantly associated with C-reactive protein (CRP; p = 0.006). These findings suggest that sTCC plays a role in Sz as a trait marker of non-specific chronic immune activation, as previously described for CRP. Future longitudinal analyses with more sampling time points from early recognition centres for psychoses may be helpful to better understand the temporal dynamics of innate immune system changes during psychosis development.

Previous studies reported that peripheral inflammation was associated with cognitive performance and brain structure in schizophrenia. However, the moderating effect of inflammation has not been extensively studied. This study investigated whether inflammation markers moderated the association between negative symptoms and neurocognition in schizophrenia. This cross-sectional study included 137 drug-naïve schizophrenia patients (DNS) and 67 healthy controls (HC). We performed the Measurements and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) for cognitive assessment and the Positive and Negative Syndrome Scale (PANSS) for psychiatric symptoms. Plasma concentrations of interferon-gamma (IFN-γ), neutrophil gelatinase-associated lipocalin (NGAL), and nuclear factor kappa B (NF-κB) were measured. The MCCB neurocognition score, social cognition score, and total score; the plasma concentrations of NGAL, IFN-γ, and NF-κB were significantly decreased in DNS than in HC (all P's < 0.001). PANSS negative subscale (PNS), PANSS reduced expressive subdomain (RES) negatively correlated with neurocognition score (P = 0.007; P = 0.011, respectively). Plasma concentrations of IFN-γ and NGAL positively correlated with neurocognition score (P = 0.043; P = 0.008, relatively). The interactions of PNS × NGAL; PNS × IFN-γ; RES × IFN-γ accounted for significant neurocognition variance (P = 0.025; P = 0.029, P = 0.007, respectively). Simple slope analysis showed that all the above moderating effects only occurred in patients with near normal IFN-γ and NGAL levels. Plasma concentrations of IFN-γ and NGAL moderated the relationship between negative symptoms (especially RES) and neurocognition in schizophrenia. Treatment targeting inflammation may contribute to neurocognition improvement in schizophrenia.