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骨关节炎疼痛中安慰剂反应的机制。

Mechanisms of the placebo response in pain in osteoarthritis.

机构信息

Arthritis Research UK Pain Centre, Academic Rheumatology, University of Nottingham, Nottingham, United Kingdom.

出版信息

Osteoarthritis Cartilage. 2013 Sep;21(9):1229-35. doi: 10.1016/j.joca.2013.04.018.

Abstract

INTRODUCTION

Administration of a placebo associates with symptomatic improvement in many conditions--the so-called placebo response. In this review we explain the concept of placebo response, examine the data that supports existence in osteoarthritis (OA), and discuss its possible mechanisms and determinants.

METHODS

A Pubmed literature search was carried out. Key articles were identified, and their findings discussed in a narrative review.

RESULTS

Pain, stiffness, self-reported function and physician-global assessment in OA clearly improve in response to placebo. However, more objective measures such as quadriceps strength and radiographic progression appear less responsive. Although not directly studied in OA, contextual effects, patient expectation and conditioning are believed to be the main mechanisms. Neurotransmitter changes that mediate placebo-induced analgesia include increased endogenous opioid levels, increased dopamine levels, and reduced levels of cholecystokinin. Almost all parts of the brain involved in pain processing are influenced during placebo-induced analgesia. Determinants of the magnitude of placebo response include the patient-practitioner interaction, treatment response expectancy, knowledge of being treated, patient personality traits and placebo specific factors such as the route and frequency of administration, branding, and treatment costs.

CONCLUSION

Clearer understanding of the neurobiology of placebo response validates its existence as a real phenomenon. Although routine administration of placebo for symptomatic improvement is difficult to justify, contextual factors that enhance treatment response should be employed in the management of chronic painful conditions such as OA where available treatments have only modest efficacy.

摘要

简介

在许多情况下,给予安慰剂与症状改善相关,即所谓的安慰剂效应。在这篇综述中,我们解释了安慰剂效应的概念,考察了支持其在骨关节炎(OA)中存在的数据,并讨论了其可能的机制和决定因素。

方法

进行了 Pubmed 文献检索。确定了关键文章,并在叙述性综述中讨论了它们的发现。

结果

OA 患者的疼痛、僵硬、自我报告的功能和医生整体评估明显因安慰剂而改善。然而,更客观的措施,如股四头肌力量和放射学进展,似乎反应较小。尽管在 OA 中没有直接研究,但认为上下文效应、患者期望和条件作用是主要机制。介导安慰剂诱导镇痛的神经递质变化包括内源性阿片类物质水平增加、多巴胺水平增加和胆囊收缩素水平降低。在安慰剂诱导镇痛期间,大脑中几乎所有参与疼痛处理的部分都受到影响。安慰剂反应幅度的决定因素包括医患互动、治疗反应预期、治疗知情、患者人格特质以及安慰剂的特定因素,如给药途径和频率、品牌和治疗成本。

结论

对安慰剂反应的神经生物学的更清晰理解验证了其作为真实现象的存在。尽管常规给予安慰剂以改善症状难以证明其合理性,但应在管理慢性疼痛性疾病(如 OA)时利用增强治疗反应的上下文因素,而这些疾病的现有治疗方法仅具有适度的疗效。

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