An update on medication management of women with schizophrenia in pregnancy

Introduction: Women with schizophrenia and their babies are at high risk of adverse outcomes in pregnancy and childbirth. A better understanding of the specific risks conferred by the illness itself and by the treatment provided will help guide more effective care of these women.

Areas covered: Herein, the authors review genetic, demographic, socioeconomic, nutritional and lifestyle risks associated with schizophrenia in pregnancy. They also cover specific risks associated with typical antipsychotic medications, specific risks associated with atypical antipsychotic medications, risks associated with polypharmacy and risks of developmental delay in children exposed to antipsychotic medications in utero.

Expert opinion: Our understanding of the risks that women with schizophrenia face in pregnancy from their illness and from the treatment they receive continues to evolve. As our ability to analyze data progresses, the risks conferred by antipsychotic medication treatment appear to lessen in clinical and statistical significance, whilst the true risks to these women and their babies from their experience of disadvantage continue to set them aside from the general population. Reducing polypharmacy and providing comprehensive and supportive care can minimize harm to women with schizophrenia and their babies.     

HTR2C polymorphisms,olanzapine-induced weight gain and antipsychotic-induced metabolic syndrome in schizophrenia patients: A meta-analysis

Objective. To conduct meta-analyses of all published association studies on the HTR2C -759C/T (rs3813829) polymorphism and olanzapine-induced weight gain in schizophrenia patients and on the HTR2C -759C/T, -697G/C (rs518147) and rs1414334:C> G polymorphisms and olanzapine/clozapine/risperidone-induced metabolic syndrome in schizophrenia patients. Methods. Eligible studies were identified by searching PubMed and Web of Science databases. Meta-analyses were performed using Cochrane Review Manager (RevMan, version 5.2) to calculate the pooled odds ratio (OR) and its corresponding 95% confidence interval (CI). Results. Our meta-analyses revealed both a significant positive association between the rs1414334 C allele and olanzapine/clozapine/risperidone-induced metabolic syndrome and a marginally significant positive association between the -697C allele and the induced metabolic syndrome in schizophrenia patients, but no significant association between the -759C/T polymorphism and the induced metabolic syndrome in schizophrenia patients. Our analysis further revealed a pronounced trend toward a significant negative association between the -759T allele and high olanzapine-induced weight gain and a trend toward a significant positive association between the -759C allele and high olanzapine-induced weight gain in Caucasian schizophrenia patients. Conclusions. Our results support that HTR2C polymorphisms play a role in antipsychotic-induced metabolic disturbance. More association studies are needed to further elucidate association of different HTR2C polymorphisms and antipsychotic-induced metabolic disturbance.     

Dominant negative DISC1 mutant mice display specific social behaviour deficits and aberration in BDNF and cannabinoid receptor expression

Objectives. Disrupted in schizophrenia 1 (DISC1) is considered the most prominent candidate gene for schizophrenia. In this study, we aimed to characterize behavioural and brain biochemical traits in a mouse expressing a dominant negative DISC1mutant (DN-DISC1). Methods. DN-DISC1 mice underwent behavioural tests to evaluate object recognition, social preference and social novelty seeking. ELISA was conducted on brain tissue to evaluate BDNF levels. Western blot was employed to measure BDNF receptor (TrkB) and cannabinoid receptor CB1. Results. The mutant DISC1 mice displayed deficits in preference to social novelty while both social preference and object recognition were intact. Biochemical analysis of prefrontal cortex and hippocampus revealed a modest reduction in cortical TrkB protein levels of male mice while no differences in BDNF levels were observed. We found sex dependent differences in the expression of cannabinoid-1 receptors. Conclusions. We describe novel behavioural and biochemical abnormalities in the DN-DISC1 mouse model of schizophrenia. The data shows for the first time a possible link between DISC1 mutation and the cannabinoid system.     

Genes and schizophrenia: a pseudoscientific disenfranchisement of the individual

The biological model of schizophrenia remains the dominant model within mental health services. It has a powerful influence on the culture of mental health services; providing the structure for the delivery and selection of mental health treatments. There is widespread acceptance of a genetic cause for schizophrenia. Acceptance of a genetic cause is inconsistent with a person-centred recovery-orientated approach. The following paper provides a rigorous review of the underpinning research that supports the genetic argument. Appraisal of family, twin and adoption studies uncovers serious flaws in the methodologies and statistical analyses used in studies. These flaws not only artificially inflate the genetic contribution to schizophrenia but also invalidate many of the findings. More recent micro-imaging techniques have also failed to find replicable and consistent findings indicating a clear genetic pathway to schizophrenia. Freed from the implied pessimism of an unmodifiable genetic cause for schizophrenia, mental health nurses can confidently work to instil hope with people that have a diagnosis of schizophrenia.     

精神分裂症的抑郁症状

为了探讨精神分裂症抑郁症状发生率及其相关因素,对159例精神分裂症患者在疗前和疗后8周进行了阳性症状量表(SAPS)、阴性症状量表(SANS)和Hamilton抑郁量表(HAMD)评定,并对抑郁症状的相关因素进行了分析。结果显示,精神分裂症患者的抑郁症状发生率为60.38%;抑郁症状与阳性症状(SAPS总分)、住院次数和自杀未遂发生率有显著相关,而与阴性症状(SANS总分)和疗效无明显相关。作者认为抑郁症状是精神分裂症症状的组成部分,一般不需合并抗抑郁剂治疗。