Vachon-Presseau Etienne
Department of Physiology, Northwestern University Feinberg School of Medicine, 710 N Lake Shore Drive, Room 1020, Chicago, IL 60611, USA.
Prog Neuropsychopharmacol Biol Psychiatry. 2018 Dec 20;87(Pt B):216-223. doi: 10.1016/j.pnpbp.2017.10.014. Epub 2017 Oct 25.
Stress has multifaceted effects on pain. On the one hand, it is a powerful inhibitor of nociception and inflammation; on the other hand, it contributes to enhanced pathological states including the establishment and continuation of chronic pain. These seemingly paradoxical effects can be better understood by investigating how stress-induced plasticity in particular brain circuitry contributes to the chronic pain state. This review presents the rationale and evidence for the interactions between stress and pain, emphasizing underlying mechanisms and putting forth the hypothesis that stress partly mediates the deleterious effects of pain on the corticolimbic system. First, a general description of the corticolimbic circuitry predisposing and amplifying chronic pain will be discussed, followed by an overview of the neurotoxic effects of stress hormones on this circuitry. Recent studies show that the resulting perturbations to these brain circuits have significant consequences both for chronic pain and for general regulation of the stress response, primarily through feedback mechanisms controlling the hypothalamic-pituitary-adrenal axis. This overlap in effected circuitry provides a key point of comparison between stress and pain, and the similarities between the plasticity induced by chronic pain and chronic stress will be examined here. Chronic pain patients have been shown to exhibit maladaptive stress responses in general and in response to pain; the cause of this response and its consequence on pain severity will then be reviewed. Finally, factors that have been shown to lead to resilience or vulnerability for chronic pain and maladaptive stress responses will be summarized.
压力对疼痛具有多方面的影响。一方面，它是伤害感受和炎症的强大抑制剂；另一方面，它会导致包括慢性疼痛的形成和持续在内的病理状态加剧。通过研究特定脑回路中压力诱导的可塑性如何导致慢性疼痛状态，可以更好地理解这些看似矛盾的影响。本综述阐述了压力与疼痛相互作用的基本原理和证据，强调了潜在机制，并提出了压力部分介导疼痛对皮质边缘系统有害影响的假说。首先，将讨论易患和加剧慢性疼痛的皮质边缘回路的一般描述，随后概述应激激素对该回路的神经毒性作用。最近的研究表明，这些脑回路由此产生的扰动对慢性疼痛和应激反应的一般调节都有重大影响，主要是通过控制下丘脑-垂体-肾上腺轴的反馈机制。受影响回路的这种重叠提供了压力与疼痛之间比较的关键点，本文将研究慢性疼痛和慢性压力诱导的可塑性之间的相似性。慢性疼痛患者通常表现出适应不良的应激反应，包括对疼痛的反应；随后将综述这种反应的原因及其对疼痛严重程度的影响。最后，将总结已被证明会导致慢性疼痛和适应不良应激反应的恢复力或易感性的因素。
