Developmental Imaging and Psychopathology Lab, Department of Psychiatry, School of Medicine, University of Geneva, David Dufour, Geneva, Switzerland.
Center for Contextual Psychiatry, Department of Neurosciences, KU Leuven, Leuven, Belgium.
Schizophr Bull. 2018 Oct 15;44(suppl_2):S525-S535. doi: 10.1093/schbul/sby025.
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.
越来越多的证据表明，精神分裂症是由遗传和环境因素的复杂相互作用引起的。生活应激事件（SLEs）与应对策略以及功能失调的下丘脑-垂体-肾上腺轴（HPAA）一起起着突出的作用。有人提出，精神分裂症倾向的框架可能有助于理清遗传和环境因素在精神分裂症发病机制中的相互作用。同样，22q11.2 缺失综合征（22q11DS）被认为是精神分裂症易感性的遗传模型。然而，SLE 和应对策略在 22q11DS 中仍在很大程度上未被探索。此外，在该人群中尚未系统地研究 HPAA。在这里，我们在 43 名健康对照者（HCs）与 59 名 22q11DS 个体的样本中探讨了 SLE、情绪应对策略、精神分裂症人格特质、阈下精神病症状之间的相关性。在后者中，我们还探索了与垂体体积的相关性，该体积是通过结构磁共振成像估计的。我们发现，SLE 和消极应对策略与 HCs 和 22q11DS 中的精神分裂症人格特质相关，并且仅与 22q11DS 组中的精神病症状相关，而垂体体积减少与一般精神病理学相关。此外，功能失调的应对方式介导了 SLE 对 22q11DS 中精神分裂症人格特质和精神病症状的影响。我们的研究结果再现了非综合征患者的证据，并证实了应激和应对在精神病发病机制中的核心作用。更广泛地说，它们强调了环境因素在 22q11DS 精神分裂症发病途径中的重要性，这表明在该人群中实施应激特别是应对导向干预具有很强的理由。
