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慢性应激、皮质醇功能障碍与疼痛:疼痛康复中压力管理的心理神经内分泌原理

Chronic stress, cortisol dysfunction, and pain: a psychoneuroendocrine rationale for stress management in pain rehabilitation.

作者信息

Hannibal Kara E, Bishop Mark D

机构信息

K.E. Hannibal, PT, DPT, Rehabilitation Science Doctoral Program, University of Florida, PO Box 100154, Gainesville, FL 32610-0154 (USA).

M.D. Bishop, PT, PhD, Department of Physical Therapy, University of Florida, Gainesville.

出版信息

Phys Ther. 2014 Dec;94(12):1816-25. doi: 10.2522/ptj.20130597. Epub 2014 Jul 17.

Abstract

Pain is a primary symptom driving patients to seek physical therapy, and its attenuation commonly defines a successful outcome. A large body of evidence is dedicated to elucidating the relationship between chronic stress and pain; however, stress is rarely addressed in pain rehabilitation. A physiologic stress response may be evoked by fear or perceived threat to safety, status, or well-being and elicits the secretion of sympathetic catecholamines (epinephrine and norepinepherine) and neuroendocrine hormones (cortisol) to promote survival and motivate success. Cortisol is a potent anti-inflammatory that functions to mobilize glucose reserves for energy and modulate inflammation. Cortisol also may facilitate the consolidation of fear-based memories for future survival and avoidance of danger. Although short-term stress may be adaptive, maladaptive responses (eg, magnification, rumination, helplessness) to pain or non-pain-related stressors may intensify cortisol secretion and condition a sensitized physiologic stress response that is readily recruited. Ultimately, a prolonged or exaggerated stress response may perpetuate cortisol dysfunction, widespread inflammation, and pain. Stress may be unavoidable in life, and challenges are inherent to success; however, humans have the capability to modify what they perceive as stressful and how they respond to it. Exaggerated psychological responses (eg, catastrophizing) following maladaptive cognitive appraisals of potential stressors as threatening may exacerbate cortisol secretion and facilitate the consolidation of fear-based memories of pain or non-pain-related stressors; however, coping, cognitive reappraisal, or confrontation of stressors may minimize cortisol secretion and prevent chronic, recurrent pain. Given the parallel mechanisms underlying the physiologic effects of a maladaptive response to pain and non-pain-related stressors, physical therapists should consider screening for non-pain-related stress to facilitate treatment, prevent chronic disability, and improve quality of life.

摘要

疼痛是促使患者寻求物理治疗的主要症状,疼痛减轻通常被视为治疗成功的标志。大量证据致力于阐明慢性应激与疼痛之间的关系;然而,疼痛康复中很少涉及应激因素。生理应激反应可能由对安全、地位或幸福的恐惧或感知到的威胁引发,会促使交感儿茶酚胺(肾上腺素和去甲肾上腺素)和神经内分泌激素(皮质醇)分泌,以促进生存并激发成功动力。皮质醇是一种强效抗炎物质,其作用是调动葡萄糖储备以提供能量并调节炎症。皮质醇还可能促进基于恐惧的记忆巩固,以利于未来生存和避免危险。虽然短期应激可能具有适应性,但对疼痛或与疼痛无关的应激源的适应不良反应(如放大、反复思考、无助感)可能会加剧皮质醇分泌,并形成一种易于引发的敏感生理应激反应。最终,长期或过度的应激反应可能会使皮质醇功能紊乱、炎症扩散和疼痛持续存在。生活中的应激可能无法避免,挑战是成功所固有的;然而,人类有能力改变他们所认为的应激因素以及应对方式。对潜在应激源进行适应不良的认知评估,将其视为威胁后产生的过度心理反应(如灾难化思维),可能会加剧皮质醇分泌,并促进对疼痛或与疼痛无关的应激源的基于恐惧的记忆巩固;然而,应对、认知重新评估或直面应激源可能会使皮质醇分泌降至最低,并预防慢性复发性疼痛。鉴于对疼痛和与疼痛无关的应激源的适应不良反应所产生的生理效应具有相似机制,物理治疗师应考虑筛查与疼痛无关的应激因素,以促进治疗、预防慢性残疾并提高生活质量。

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