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首页> 美国卫生研究院文献>Schizophrenia Bulletin >Coping Strategies Mediate the Effect of Stressful Life Events on Schizotypal Traits and Psychotic Symptoms in 22q11.2 Deletion Syndrome
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Coping Strategies Mediate the Effect of Stressful Life Events on Schizotypal Traits and Psychotic Symptoms in 22q11.2 Deletion Syndrome

机译：应对策略介导应激性生活事件对22q11.2缺失综合征的精神分裂症特征和精神症状的影响

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Converging evidence suggests that psychosis emerges from the complex interaction of genetic and environmental factors. Stressful life events (SLEs) play a prominent role in combination with coping strategies and with a dysfunctional hypothalamus-pituitary-adrenal axis (HPAA). It has been proposed that the framework of schizotypy might help disentangle the interaction between genetic and environmental factors in the pathogenesis of psychosis. Similarly, 22q11.2 deletion syndrome (22q11DS) is considered as a genetic model of psychosis vulnerability. However, SLE and coping strategies remain largely unexplored in 22q11DS. Moreover, the HPAA has not been systematically investigated in this population. Here, we explored the correlation between SLE, emotional coping strategies, schizotypal personality traits, subthreshold psychotic symptoms in a sample of 43 healthy controls (HCs) compared with 59 individuals with 22q11DS. In the latter, we also explored the correlation with pituitary volume as estimated from structural magnetic resonance imaging. We found that SLE and negative coping strategies were correlated with schizotypal personality traits in both HCs and 22q11DS, and with psychotic symptoms in the 22q11DS group only, whereas reduced pituitary volume correlated with general psychopathology. Moreover, dysfunctional coping mediated the effect of SLE on schizotypal personality traits and psychotic symptoms in 22q11DS. Our findings recapitulate evidence in nonsyndromic patients and confirm the central role of stress and coping in the pathogenesis of psychosis. More broadly, they highlight the importance of environmental factors in the pathway to psychosis in 22q11DS, suggesting a strong rationale for the implementation of stress and particularly coping-oriented interventions in this population.
机译：越来越多的证据表明，精神病是由遗传和环境因素之间复杂的相互作用引起的。应激性生活事件（SLE）与应对策略和功能异常的下丘脑-垂体-肾上腺轴（HPAA）一起起着重要作用。有人提出，精神分裂症的框架可能有助于弄清精神病发病机理中遗传因素和环境因素之间的相互作用。同样，22q11.2缺失综合征（22q11DS）被认为是精神病易感性的遗传模型。但是，SLE和应对策略在22q11DS中仍未开发。而且，尚未对该人群中的HPAA进行过系统的调查。在这里，我们探讨了43名健康对照（HCs）与59名22q11DS个体相比，SLE，情绪应对策略，精神分裂型人格特质，亚阈精神病症状之间的相关性。在后者中，我们还探讨了根据结构磁共振成像估计的与垂体体积的相关性。我们发现，SLE和消极应对策略在HCs和22q11DS中均与精神分裂型人格特征相关，而在22q11DS组中仅与精神病症状相关，而垂体体积的减少与一般精神病理学相关。此外，功能障碍的应对介导了SLE对22q11DS中精神分裂症人格特质和精神病症状的影响。我们的发现概括了非综合征患者的证据，并证实了压力和应对在精神病发病机理中的核心作用。更广泛地说，它们突显了环境因素在22q11DS患精神病的途径中的重要性，表明了对这一人群实施压力特别是应对压力的干预措施的强烈理由。

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