Walker E F, Diforio D
Department of Psychology, Emory University, Atlanta, Georgia 30322, USA.
Psychol Rev. 1997 Oct;104(4):667-85. doi: 10.1037/0033-295x.104.4.667.
There is a substantive literature on the behavioral effects of psychosocial stressors on schizophrenia. More recently, research has been conducted on neurohormonal indicators of stress responsivity, particularly cortisol release resulting from activation of the hypothalamic-pituitary-adrenal (HPA) axis. This article integrates the psychosocial and biological literatures on stress in schizophrenia, and it offers specific hypotheses about the neural mechanisms involved in the effects of stressors on the diathesis. Both the behavioral and biological data indicate that stress worsens symptoms and that the diathesis is associated with a heightened response to stressors. A neural mechanism for these phenomena is suggested by the augmenting effect of the HPA axis on dopamine (DA) synthesis and receptors. Assuming the diathesis for schizophrenia involves an abnormality in DA receptors, it is proposed that the HPA axis acts as a potentiating system by means of its effects on DA. At the same time, DA receptor abnormality and hippocampal damage render the patient hypersensitive to stress. This neural diathesis-stress model is consistent with findings on prenatal factors and brain abnormalities in schizophrenia, and it provides a framework for explaining some key features of the developmental course and clinical presentation.
关于心理社会应激源对精神分裂症行为影响的文献颇为丰富。最近，人们针对应激反应性的神经激素指标展开了研究，尤其是下丘脑 - 垂体 - 肾上腺（HPA）轴激活导致的皮质醇释放。本文整合了关于精神分裂症应激的心理社会和生物学文献，并针对应激源对素质产生影响所涉及的神经机制提出了具体假设。行为学和生物学数据均表明，应激会使症状恶化，且素质与对应激源的反应增强有关。HPA轴对多巴胺（DA）合成及受体的增强作用提示了这些现象的一种神经机制。假设精神分裂症的素质涉及DA受体异常，那么有人提出HPA轴通过其对DA的作用充当一个增强系统。同时，DA受体异常和海马体损伤使患者对应激高度敏感。这种神经素质 - 应激模型与精神分裂症产前因素及脑异常的研究结果相符，并为解释其发展过程和临床表现的一些关键特征提供了一个框架。
