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Auditory verbal hallucination (AVH) is a pathological hallmark of schizophrenia; however, their neural basis is unclear. Voice identity is an important phenomenological feature of AVHs. Certain voice identity recognition deficits are specific to schizophrenic patients with AVHs. We tested our hypothesis that among schizophrenia patients with hallucination, dysfunctional voice identity recognition is associated with poor functional integration in the neural networks involved in the evaluation of voice identity. Using functional magnetic resonance imaging (fMRI) during a voice recognition task, we examined the modulation of neural network connectivity in 26 schizophrenic patients with or without AVHs, and 13 healthy controls. Our results showed that the schizophrenic patients with AVHs had altered frontotemporal connectivity compared to the schizophrenic patients without AVHs and healthy controls. The latter two groups did not show any differences in functional connectivity. In addition, the strength of frontotemporal connectivity was correlated with the accuracy of voice recognition. These findings provide preliminary evidence that impaired functional integration may contribute to the faulty appraisal of voice identity in schizophrenic patients with AVHs.

Objective: Auditory hallucinations (AVHs), like real auditory perceptions, are often perceived as familiar voices. Given that neural correlates of AVHs involve the auditory cortex, it is likely that those brain regions responsible for recognition of voice identity are invoked during AVHs. Method: Schizophrenic patients with (n = 13) and without (n = 13) auditory hallucinations, and 13 healthy subjects performed a voice recognition task during functional magnetic resonance imaging at 1.5 T. In the task using prerecorded vocal stimuli, they classified voice as familiar and unfamiliar. Results: Under the familiar minus unfamiliar contrasts, cerebral activation pattern is different in the three groups and patients with auditory hallucinations showed less activation in the right temporal lobe than controls. Conclusion: Voice recognition was impaired in patients with AVHs. Our results support that auditory association cortices play a role in the perception of AVHs.

Antipsychotic drug-induced sexual dysfunction is an important and problematic side effect. We have investigated the effect of chronic antipsychotic treatment on sexual behaviour, sex hormones and genital organ size in the male rat. The following sexual functions were significantly impaired in both risperidone (2 mg/kg) and haloperidol (2 mg/kg) groups at 3 weeks: Libido (assessed in mounting frequency and intromission), sexual arousability/motivation (in terms of Latencies for mounting and intromission) and orgasm (in terms of Latency for ejaculation). At 6 weeks, haLoperidol also suppressed the `hit ratio' (intromissions/mounts) as well as the above-mentioned parameters indicating erectile dysfunction. Risperidone had no significant effect on sexual function at 6 weeks. Compared with the control group, haLoperidol and risperidone decreased the serum Level of testosterone after 6 weeks but not after 3 weeks. The two drugs did not influence the serum Level of Leutenizing hormone (LH). At 3 weeks, the epididymis was significantly decreased beLow controls in both risperidone and haloperidol groups. At 6 weeks, the epididymis, seminal vesicle and prostate weights were significantLy reduced in the haLoperidol group, but not in the risperidone group. The serum concentration of testosterone significantly correLated with sex organ weight, but not with sexual behaviours. These results suggest that sexual function, testosterone Levels and genital tissue size in male rats were affected to different degrees by risperidone and haloperidol. These findings contribute to our understanding of antispsychotic drug-induced male sexual dysfunction.

Background Weight gain and type 2 diabetes mellitus (DM) are often linked to antipsychotics treatment. The aim of the study is to investigate serum free fatty acids (FFA) levels in schizophrenic patients who received long-term antipsychotics treatment, and to explore the associations between serum FFA and fasting blood glucose, and insulin resistance. Methods 308 inpatients with schizophrenia who met with the criteria of DSM-IV were recruited into this study, and were divided into four groups: control subjects, single obesity, impaired glucose tolerance (IGT) and type 2 DM according to different body mass index, fasting blood glucose level and 2-hour postprandial blood glucose. Serum FFA was measured with colorimetry. Serum insulin and leptin were measured with radioimmunoassay respectively. Results There was a significant elevation in serum FFA levels in schizophrenic patients who received long-term antipsychotics treatment, especially in single obesity, IGT, and DM groups. The elevated serum FFA was remarkably positive correlated with fasting blood glucose and insulin resistance. Conclusions The study suggested the elevated serum FFA in schizophrenic patients with long-term antipsychotics treatment affected the blood glucose metabolism, may have played an important role in insulin resistance and type 2 DM, and was also an important trait of metabolic syndromes.