Optimal cutoff scores of the Chinese version of 15-item negative symptom assessment that indicate prominent negative symptoms of schizophrenia.

Objective: The Chinese version of 15-item negative symptom assessment (NSA-15) is an instrument with a three-factor structure specifically validated for assessing negative symptoms of schizophrenia. To provide a reference for future practical applications in the recognition of schizophrenia patients with negative symptoms, this study aimed to determine an appropriate NSA-15 cutoff score regarding negative symptoms to identify prominent negative symptoms (PNS). Methods: A total of 199 participants with schizophrenia were recruited and divided into the PNS group (n = 79) and non-PNS group (n = 120) according to scale for assessment of negative symptoms (SANS) scores. Receiver-operating characteristic (ROC) curve analysis was used to determine the optimal NSA-15 cutoff score for identifying PNS. Results: The optimal cutoff NSA-15 score for identifying PNS was 40. Communication, emotion and motivation factors in the NSA-15 had cutoffs of 13, 6, and 16, respectively. The communication factor score had slightly better discrimination than scores on the other two factors. The discriminant ability of the global rating of the NSA-15 was not as good as that of the NSA-15 total score (area under the curve (AUC): 0.873 vs. 0.944). Conclusion: The optimal NSA-15 cutoff scores for identifying PNS in schizophrenia were determined in this study. The NSA-15 provides a convenient and easy-to-use assessment for identifying patients with PNS in Chinese clinical situations. The communication factor of the NSA-15 also has excellent discrimination.

Anterior cingulate glutamate levels associate with functional activation and connectivity during sensory integration in schizophrenia: a multimodal 1H-MRS and fMRI study.

BACKGROUND: Glutamatergic dysfunction has been implicated in sensory integration deficits in schizophrenia, yet how glutamatergic function contributes to behavioural impairments and neural activities of sensory integration remains unknown. METHODS: Fifty schizophrenia patients and 43 healthy controls completed behavioural assessments for sensory integration and underwent magnetic resonance spectroscopy (MRS) for measuring the anterior cingulate cortex (ACC) glutamate levels. The correlation between glutamate levels and behavioural sensory integration deficits was examined in each group. A subsample of 20 pairs of patients and controls further completed an audiovisual sensory integration functional magnetic resonance imaging (fMRI) task. Blood Oxygenation Level Dependent (BOLD) activation and task-dependent functional connectivity (FC) were assessed based on fMRI data. Full factorial analyses were performed to examine the Group-by-Glutamate Level interaction effects on fMRI measurements (group differences in correlation between glutamate levels and fMRI measurements) and the correlation between glutamate levels and fMRI measurements within each group. RESULTS: We found that schizophrenia patients exhibited impaired sensory integration which was positively correlated with ACC glutamate levels. Multimodal analyses showed significantly Group-by-Glutamate Level interaction effects on BOLD activation as well as task-dependent FC in a 'cortico-subcortical-cortical' network (including medial frontal gyrus, precuneus, ACC, middle cingulate gyrus, thalamus and caudate) with positive correlations in patients and negative in controls. CONCLUSIONS: Our findings indicate that ACC glutamate influences neural activities in a large-scale network during sensory integration, but the effects have opposite directionality between schizophrenia patients and healthy people. This implicates the crucial role of glutamatergic system in sensory integration processing in schizophrenia.

Neurocognitive trajectories and their clinical implications in first-episode schizophrenia after one year of antipsychotic treatment.

Neurocognitive impairment is a core feature of schizophrenia, and patients with first-episode schizophrenia (FES) are optimal candidates for cognitive remediation, but we do not know enough about the incidence, severity and longitudinal changes in neurocognitive impairment in those with FES. This study aimed to assess the neurocognitive trajectories of patients with FES and to compare the clinical and functional outcomes among those with different trajectories. A total of 562 untreated patients with FES completed a neurocognitive test battery and psychopathological and functional assessment. A total of 373 patients attended the follow-up. Group-based trajectory modelling (GBTM) was applied to identify neurocognitive trajectories. Analysis of variance and chi-square tests were conducted to compare demographic characteristics, multiple neurocognitive domains, and clinical and functional outcomes among the different subgroups. We identified three neurocognitive subgroups: preserved (n = 133), mildly to moderately impaired (n = 187) and severely impaired (n = 53). Neurocognitive function in the two impaired subgroups improved within a year but failed to reach the normal level. The processing speed followed trajectories similar to those of overall cognition. The three subgroups did not significantly differ in antipsychotic usage or clinical remission rate. The severely impaired subgroup had poorer functional outcomes than the preserved subgroup, but the mildly to moderately impaired subgroup did not. Patients with FES followed distinct neurocognitive trajectories during the first year of treatment. Patients with severe neurocognitive impairment have poorer functional outcomes, which require and are more likely to benefit from cognitive remediation. Processing speeding is a potential indicator for screening overall cognition.

Hub-connected functional connectivity within social brain network weakens the association with real-life social network in schizophrenia patients.

Hubs in the brain network are the regions with high centrality and are crucial in the network communication and information integration. Patients with schizophrenia (SCZ) exhibit wide range of abnormality in the hub regions and their connected functional connectivity (FC) at the whole-brain network level. Study of the hubs in the brain networks supporting complex social behavior (social brain network, SBN) would contribute to understand the social dysfunction in patients with SCZ. Forty-nine patients with SCZ and 27 healthy controls (HC) were recruited to undertake the resting-state magnetic resonance imaging scanning and completed a social network (SN) questionnaire. The resting-state SBN was constructed based on the automatic analysis results from the NeuroSynth. Our results showed that the left temporal lobe was the only hub of SBN, and its connected FCs strength was higher than the remaining FCs in both two groups. SCZ patients showed the lower association between the hub-connected FCs (compared to the FCs not connected to the hub regions) with the real-life SN characteristics. These results were replicated in another independent sample (30 SCZ and 28 HC). These preliminary findings suggested that the hub-connected FCs of SBN in SCZ patients exhibit the abnormality in predicting real-life SN characteristics.

Social brain network correlates with real-life social network in individuals with schizophrenia and social anhedonia.

Social behaviour requires the brain to efficiently integrate multiple social processes, but it is not clear what neural substrates underlie general social behaviour. While psychosis patients and individuals with subclinical symptoms are characterized by social dysfunction, the neural mechanisms underlying social dysfunctions in schizophrenia spectrum disorders remains unclear. We first constructed a general social brain network (SBN) using resting-state functional connectivity (FC) with regions of interest based on the automatic meta-analysis results from NeuroSynth. We then examined the general SBN and its relationship with social network (SN) characteristics in 30 individuals with schizophrenia (SCZ) and 33 individuals with social anhedonia (SA). We found that patients with SCZ exhibited deficits in their SN, while SA individuals did not. SCZ patients showed decreased segregation and functional connectivity in their SBN, while SA individuals showed a reversed pattern with increased segregation and functional connectivity of their SBN. Sparse canonical correlation analysis showed that both SCZ patients and SA individuals exhibited reduced correlation between SBN and SN characteristics compared with their corresponding healthy control groups. These preliminary findings suggest that both SCZ and SA participants exhibit abnormality in segregation and functional connectivity within the general SBN and reduced correlation with SN characteristics. These findings could guide the development of non-pharmacological interventions for social dysfunction in SCZ spectrum disorders.

Validation of the Questionnaire of Cognitive and Affective Empathy in patients with schizophrenia, major depressive disorder and bipolar disorder.

INTRODUCTION: Alteration of empathy is common in patients with psychiatric disorders. Reliable and valid assessment tools for measuring empathy of clinical samples is needed. The Questionnaire of Cognitive and Affective Empathy (QCAE) is a newly-developed instrument to capture cognitive and affective components of empathy. This study aimed to validate the QCAE and compared self-reported empathy between clinical groups with varied psychiatric diagnoses and healthy sample. METHODS: The present study performed factor analysis for the QCAE on clinical samples in the Chinese setting (n = 534), including patients with schizophrenia (n = 158), bipolar disorder (n = 213) and major depressive disorder (n = 163). Internal consistency, internal correlation and convergent validity was examined in the subsample (n = 361). Group comparison among patients with schizophrenia, bipolar disorder, major depressive disorder and healthy controls (n = 107) was conducted to assess the discriminant validity. RESULTS: Our results indicated acceptable factor model, good reliability and validity of the QCAE. Impaired cognitive empathy was found in clinical samples, especially in patients with schizophrenia, while higher affective empathy was found in patients with bipolar disorder and major depressive disorder. CONCLUSION: The QCAE is a useful tool in assessing empathy in patients with varied psychiatric diagnoses.

Validation of the Chinese Version of the 16-Item Negative Symptom Assessment.

PURPOSE: The Negative Symptom Assessment-16 (NSA-16) is an instrument with significant validity and utility for assessing negative symptoms associated with schizophrenia. This study aimed to validate the Chinese version of the NSA-16. PATIENTS AND METHODS: A total of 172 participants with schizophrenia were assessed with the NSA-16, Scale for Assessment of Negative Symptoms (SANS), Positive and Negative Syndrome Scale (PANSS), Calgary Depression Scale for Schizophrenia (CDSS) and Rating Scale for Extrapyramidal Side Effects (RSESE). The factor structure of the NSA-16 was evaluated via exploratory and confirmatory factor analysis. Cronbach's α and intraclass correlation coefficients were computed. Correlations were evaluated via Spearman correlation coefficient. RESULTS: The original five-factor model of the NSA-16 did not fit our sample. Exploratory factor analysis followed by confirmatory factor analysis suggested a three-factor structure, consisting of communication, emotion and motivation, with 15 items. The NSA with 15 items was termed as the NSA-15. The NSA-15 showed excellent convergent validity by high correlations with the SANS and PANSS total and negative factor scores and good divergent validity by independence from the PANSS positive factor, CDSS and RSESE. The NSA-15 showed good internal consistency, interrater reliability and test-retest reliability. CONCLUSION: The NSA-15 is best characterized by a three-factor structure and is valid for assessing negative symptoms of schizophrenia in Chinese individuals.

MiRNA-365 and miRNA-520c-3p respond to risperidone treatment in first-episode schizophrenia after a 1 year remission.

BACKGROUND: MicroRNAs (miRNAs) control gene expression by destabilizing target transcripts and inhibiting their translation. Aberrant expression of miRNAs has been described in many human diseases, including schizophrenia. However, the effects on miRNA expression in response to antipsychotic treatment in peripheral circulation have not been thoroughly examined. METHODS: Using quantitative real-time PCR (qRT-PCR), We quantified the expression of seven candidate miRNAs in plasma samples of 40 first-episode schizophrenics before and after antipsychotic treatment. The patients were all treated with risperidone and achieved remission in 1 year. RESULTS: Compared with the baseline, the expression levels of miR-365 and miR-520c-3p were significantly down-regulated after 1 year of risperidone treatment (P < 0.001). There were no significant correlations between the clinical symptoms and the expression levels of these two miRNAs (P > 0.05). CONCLUSIONS: This study analyzed possible circulating miRNAs in response to antipsychotic monotherapy for schizophrenia, the further mechanism need to be confirmed.