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Background To assess the reliability and validity of Patient Health Questionnaire-9 (PHQ-9) for patients with major depressive disorder (MDD) and to assess the feasibility of its use in psychiatric hospitals in China. Methods One hundred nine outpatients or inpatients with MDD who qualified the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria completed PHQ-9 and Hamilton Depression Scale (HAMD-17). Two weeks after the initial evaluation, 54 randomly selected patients underwent repeat assessment using PHQ-9. For validity analysis, the construct validity and criterion validity were assessed. The internal concordance coefficient and the test-retest correlation coefficients were used for reliability analysis. The correlation between total score and scores for each item and the correlation between scores for various items were evaluated using Pearson correlation coefficient. Results Principal components factor analysis showed good construct validity of the PHQ-9. PHQ-9 total score showed a positive correlation with HAMD-17 total score ( r  = 0.610, P  < 0.001). With HAMD as the standard, PHQ-9 depression scores of 7, 15, and 21 points were used as cut-offs for mild, moderate, and severe depression, respectively. Consistency assessment was conducted between the depression severity as assessed by PHQ-9 and HAMD (Kappa = 0.229, P  < 0.001). Intraclass correlation coefficient between PHQ-9 total score and HAMD total score was 0.594 (95% confidence interval, 0.456–0.704, P  < 0.001). The Cronbach’s α coefficient of PHQ-9 was 0.892. Correlation coefficients between each item score and the total score ranged from 0.567–0.789 ( P  < 0.01); the correlation coefficient between various item scores ranged from 0.233–0.747. The test-retest correlation coefficient for total score was 0.737. Conclusions PHQ-9 showed good reliability and validity, and high adaptability for patients with MDD in psychiatric hospital. It is a simple, rapid, effective, and reliable tool for screening and evaluation of the severity of depression.

To compare the safety and efficacy of adjunctive aripiprazole versus placebo for antipsychotic-induced hyperprolactinemia. adult patients presenting with antipsychotic-induced hyperprolactinemia diagnosed by prolactin level with or without prolactin-related symptoms. adjunctive aripiprazole vs. adjunctive placebo. adverse events and efficacy of treatment. randomized controlled trials. Five randomized controlled trials with a total of 639 patients (326 adjunctive aripiprazole, 313 adjunctive placebo) met the inclusion criteria. Adjunctive aripiprazole was associated with a 79.11% (125/158) prolactin level normalization rate. Meta-analysis of insomnia, headache, sedation, psychiatric disorder, extrapyramidal symptom, dry mouth, and fatigue showed no significant differences in the adjunctive aripiprazole treatment group compared with the placebo group (risk difference (Mantel-Haenszel, random or fixed) -0.05 to 0.04 (95% confidence interval -0.13 to 0.16); I(2) =0% to 68%, P=0.20 to 0.70). However, sedation, insomnia, and headache were more frequent when the adjunctive aripiprazole dose was higher than 15 mg/day. Meta-analysis of the prolactin level normalization indicated adjunctive aripiprazole was superior to placebo (risk difference (Mantel-Haenszel, random) 0.76 (95% confidence interval 0.67 to 0.85); I(2) =43%, P<0.00001). The subgroup analysis confirmed that the subjects who received adjunctive aripiprazole 5 mg/day showed a degree of prolactin normalization similar to that of all participants. No significant differences between groups in discontinuation and improvements of psychiatric symptoms. Adjunctive aripiprazole is both safe and effective as a reasonable choice treatment for patients with antipsychotic-induced hyperprolactinemia. The appropriate dose of adjunctive aripiprazole may be 5 mg/day.

Background Theoretical and empirical evidence indicates the critical role of the default mode network (DMN) in the pathophysiology of the bipolar disorder (BD). This study aims to identify the specific brain regions of the DMN that is impaired in patients with BD. Methods A total of 56 patients with BD and 71 healthy controls (HC) underwent resting-state functional magnetic resonance imaging. Three commonly used functional indices, i.e., fractional amplitude of low-frequency fluctuation (fALFF), regional homogeneity (ReHo), and degree centrality (DC), were utilized to identify the brain region showing abnormal spontaneous brain activity in patients with BD. Then, this region served as the seed region for resting-state functional connectivity (rsFC) analysis. Results Compared to the HC group, the BD group showed reduced fALFF, ReHo, and DC values in the left precuneus. Moreover, patients exhibited decreased rsFCs within the left precuneus and between the left precuneus and the medial prefrontal cortex. Additionally, there was diminished negative connectivity between the left precuneus and the left putamen, extending to the left insula (putamen/insula). The abnormalities in DMN functional connectivity were confirmed through various analysis strategies. Conclusions Our findings provide convergent evidence for the abnormalities in the DMN, particularly located in the left precuneus. Decreased functional connectivity within the DMN and the reduced anticorrelation between the DMN and the salience network are found in patients with BD. These findings suggest that the DMN is a key aspect for understanding the neural basis of BD, and the altered functional patterns of DMN may be a potential candidate biomarker for diagnosis of BD.

Clinicians need to remember that (1) systemic inflammations can increase clozapine level; (2) clozapine, by itself, can cause inflammation, particularly during titration that is too rapid for that patient; (3) clozapine may increase the risk of infection; and (4) more specifically, clozapine may be particularly strongly associated with the risk of pneumonia. Pneumonia appears to be associated with high mortality in clozapine patients around the world. Clinicians who are alert to the risk of pneumonia in clozapine patients may significantly decrease mortality in clozapine patients. There is no data on COVID-19 infections in clozapine patients, but based on what we know about clozapine pharmacology, we can hypothesise that clozapine, possibly by impairing immunological mechanisms, may increase the risk of pneumonia in infected patients. More importantly, once fever and/or pneumonia develops, the clozapine dose should be cut in half to decrease the risk of clozapine intoxication. If there is any doubt that in spite of halving the dose there are still signs of clozapine intoxication, completely stopping clozapine may be indicated. Once the signs of inflammation and fever have disappeared, the clozapine dose can be increased to the prior dosage level.

The Measurement and Treatment Research to Improve Cognition Schizophrenia Consensus Cognitive Battery (MCCB) has also been proposed for use in clinical trials to assess cognitive deficits in patients with bipolar disorder (BD). The aim of this study was to evaluate cognitive function assessed by the MCCB in BD. A literature search of the PubMed, Embase, PsycINFO, SCI, Cochrane Library databases and the Cochrane Controlled Trials Register was conducted. Case reports, reviews and meta-analyses were excluded and a systematic review of the remaining studies of cognitive function in BD was carried out. The cognitive outcome measure was the MCCB, including 7 domains and overall cognition. A random-effects model was applied. Eighty eight studies were initially identified. Seven clinical studies comprising a total of 487 patients and 570 healthy controls (HC) were included in the meta-analysis. Patients with BD performed worse than HC in overall cognition and processing speed with a large effect size of >0.8; with a medium effect size (0.5-0.8) in attention, working memory, verbal learning and visual learning; and with a small effect size (0.2-0.5) in reasoning and problem solving and social cognition. Patients with BD performed worse than HC in overall cognition and all cognitive domains of the MCCB. Cognitive deficits in domains of processing speed and working memory are prominent in patients with BD. Our findings suggest that MCCB can be usefully applied in BD.

Background This is a cross-sectional study comparing the degree of subjective quality of life (QOL) impairment and its predictive factors in first-episode schizophrenia (FES) and individuals at clinical high-risk (CHR) for psychosis. Methods Seventy-seven FES, 59 CHR, and 64 healthy controls (HC) were included. The QOL of all participants was assessed using the World Health Organization Quality of Life (WHOQOL)-Brief Form (BREF). Psychiatric symptoms of individuals with FES were assessed with the Positive and Negative Syndrome Scale (PANSS), five factors were further identified through factor analysis; for individuals with CHR and HC, the Scale of Prodromal Symptoms (SOPS) was used. Results The total and four sub-domain scores of the WHOQOL-BREF in the FES and CHR groups were lower than those of the HC group. The overall and psychological health scores in the CHR group were lowest. In the FES group, after applying Bonferroni’s correction, there is a negative correlation between the total QOL scores and anxiety/depressive symptom scores ( r  = –0.34, P  = 0.003). The stepwise multiple regression analysis showed that the QOL of both FES and CHR group were negatively affected by anxiety/depressive symptoms and unemployment ( P  < 0.05). Conclusions Compared with FES, CHR individuals are more dissatisfied with their QOL. Although diagnostic assessment of FES and CHR relies heavily on positive symptoms, the QOL is more affected by anxiety/depressive symptoms and social functioning.

BackgroundCognitive dysfunction is acknowledged as one of the most pivotal symptoms in schizophrenia. Although many studies have assessed cognitive functioning in first-episode schizophrenia (FES), the pattern and severity of impairment across cognitive domains remain unclear. Moreover, few studies have directly compared the pattern of cognitive performance between FES and subjects at clinical high risk for psychosis (CHR). The objective of the study was to examine the cognitive profile of Chinese patients with FES and to compare that to the profile of patients with subjects at CHR and healthy controls (HC).MethodsWe applied the MATRICS Consensus Cognitive Battery to evaluate the cognitive function of 56 first-episode patients with schizophrenia aged between 19–32 years old), 42 cases of clinical high risk for psychosis (aged between 18–28 years old) and 62 healthy controls (aged between 21–29 years old).All data were analyzed using SPSS 20.0 statistical software.ResultsFES showed impaired performance across all MCCB domains relative to HC（P＜0.05）. With the exception of relative preservation of reasoning and problem solving (P=0.21) and social cognition （P=0.16）in CHR, the MCCB domain scores were similar in CHR and FES.DiscussionThe findings suggest that the pattern, magnitude, and distribution of severity of impairment in CHR were similar to that observed in FES. However, early in the illness, there may be relative sparing of reasoning and problem solving and social cognition.

Background Bipolar disorder (BD) is a complex mental illness characterized by different mood states, including depression, mania/hypomania, and euthymia. This study aimed to comprehensively evaluate dynamic changes in intrinsic brain activity by using dynamic fractional amplitude of low-frequency fluctuations (dfALFF) and dynamic degree centrality (dDC) in patients with BD euthymia or depression and healthy individuals. Methods The resting-state functional magnetic resonance imaging data were analyzed from 37 euthymic and 28 depressed patients with BD, as well as 85 healthy individuals. Using the sliding-window method, the dfALFF and dDC were calculated for each participant. These values were compared between the 3 groups using one-way analysis of variance (ANOVA). Additional analyses were conducted using different window lengths, step width, and window type to ensure the reliability of the results. Results The euthymic group showed significantly lower dfALFF and dDC values of the left and right cerebellum posterior lobe compared with the depressed and control groups (cluster level P FWE < 0.05), while the latter two groups were comparable. Brain regions showing significant group differences in the dfALFF analysis overlapped with those with significant differences in the dDC analysis. These results were consistent across different window lengths, step width, and window type. Conclusions These findings suggested that patients with euthymic BD exhibit less flexibility of temporal functional activities in the cerebellum posterior lobes compared to either depressed patients or healthy individuals. These results could contribute to the development of neuropathological models of BD, ultimately leading to improved diagnosis and treatment of this complex illness. Highlights This study highlights the importance of investigating dynamic intrinsic brain activity in patients with bipolar disorder (BD) during different mood states. The patients with euthymic BD showed significantly less flexibility of temporal functional activities in the left and right cerebellum posterior lobe compared to patients with depressed BD or healthy individuals. The use of dynamic fractional amplitude of low-frequency fluctuations and dynamic degree centrality allowed for a comprehensive analysis of brain activity, providing reliable and objective results.

Background Prepulse inhibition (PPI) is a measurement method for the sensory gating process, which helps the brain adapt to complex environments. PPI may be reduced in patients with bipolar disorder (BD). This study investigated PPI deficits in BD and pooled the effect size of PPI in patients with BD. Methods We conducted a literature search on PPI in patients with BD from inception to July 27, 2019 in PubMed, Embase, Cochrane Library databases, and Chinese databases. No age, sex, and language restriction were set. The calculation formula was PPI = 100 - [100*((prepulse - pulse amplitude) / pulse amplitude)]. The Newcastle-Ottawa Scale (NOS) was used to assess the quality of studies. Results Ten eligible papers were identified, of which five studies including a total of 141 euthymic patients and 132 healthy controls (HC) were included in the meta-analysis. Compared with HC, euthymic patients with BD had significantly lower PPI at the 60 ms interstimulus interval (ISI) between pulse and prepulse ( P  = 0.476, I 2  = 0.0%, SMD = − 0.32, 95% CI = − 0.54 - -0.10). Sensitivity analysis shows no significant change in the combined effect value after removing any single study. There was no publication bias using the Egger’s test at 60 ms ( P  = 0.606). The meta-analysis of PPI at the 60 ms ISI could have significant clinical heterogeneity in mood episode state, as well as lack of data on BD I or II subtypes. Conclusions Euthymic patients with BD show PPI deficits at the 60 ms, suggesting a deficit in the early sensory gate underlying PPI. The PPI inhibition rate at a 60 ms interval is a stable index. More research is needed in the future to confirm this outcome, and to delve deeper into the mechanisms behind deficits.

Tourette syndrome (TS) is a childhood-onset neuropsychiatric disorder characterized by repetitive motor movements and vocal tics. The clinical manifestations of TS are complex and often overlap with other neuropsychiatric disorders. TS is highly heritable; however, the underlying genetic basis and molecular and neuronal mechanisms of TS remain largely unknown. We performed whole-exome sequencing of a hundred trios (probands and their parents) with detailed records of their clinical presentations and identified a risk gene, ASH1L, that was both de novo mutated and associated with TS based on a transmission disequilibrium test. As a replication, we performed follow-up targeted sequencing of ASH1L in additional 524 unrelated TS samples and replicated the association (P value = 0.001). The point mutations in ASH1L cause defects in its enzymatic activity. Therefore, we established a transgenic mouse line and performed an array of anatomical, behavioral, and functional assays to investigate ASH1L function. The Ash1l+/− mice manifested tic-like behaviors and compulsive behaviors that could be rescued by the tic-relieving drug haloperidol. We also found that Ash1l disruption leads to hyper-activation and elevated dopamine-releasing events in the dorsal striatum, all of which could explain the neural mechanisms for the behavioral abnormalities in mice. Taken together, our results provide compelling evidence that ASH1L is a TS risk gene.