From fibrositis to fibromyalgia to nociplastic pain: how rheumatology helped get us here and where do we go from here?

IF 20.3 1区 医学 Q1 RHEUMATOLOGY Annals of the Rheumatic Diseases Pub Date : 2024-10-21 DOI:10.1136/ard-2023-225327
Daniel J Clauw
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Abstract

Rheumatologists and rheumatology have had a prominent role in the conceptualisation of nociplastic pain since the prototypical nociplastic pain condition is fibromyalgia. Fibromyalgia had been previously known as fibrositis, until it became clear that this condition could be differentiatied from autoimmune disorders because of a lack of systemic inflammation and tissue damage. Nociplastic pain is now thought to be a third descriptor/mechanism of pain, in addition to nociceptive pain (pain due to peripheral damage or inflammation) and neuropathic pain. Nociplastic pain can occur in isolation, or as a co-morbidity with other mechanisms of pain, as commonly occurs in individuals with autoimmune disorders. We now know that the cardinal symptoms of nociplastic pain are widespread pain (or pain in areas not without evidence of inflammation/damage), accompanied by fatigue, sleep and memory issues. There is objective evidence of amplification/augmentation of pain, as well as of non-painful stimuli such as the brightness of lights and unpleasantness of sound or odors. Nociplastic pain states can be triggered by a variety of stressors such as trauma, infections and chronic stressors. Together these features suggest that the central nervous system (CNS) is playing a major role in causing and maintaining nociplastic pain, but these CNS factors may in some be driven by ongoing peripheral nociceptive input. The most effective drug therapies for nociplastic pain are non-opioid centrally acting analgesics such as tricyclics, serotonin-norepinephrine reuptake inhibitors and gabapentinoids. However the mainstay of therapy of nociplastic pain is the use of a variety of non-pharmacological integrative therapies, especially those which improve activity/exercise, sleep and address psychological co-morbidities.

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从纤维肌炎到纤维肌痛再到神经性疼痛:风湿病学如何帮助我们走到这一步,我们又该何去何从?
风湿病学家和风湿病学在非结节性疼痛的概念化方面发挥了重要作用,因为非结节性疼痛的典型病症是纤维肌痛。纤维肌痛以前被称为纤维肌炎,直到人们逐渐认识到,由于缺乏全身性炎症和组织损伤,这种病症可以与自身免疫性疾病区分开来。除了痛觉痛(外周损伤或炎症引起的疼痛)和神经病理性疼痛之外,现在人们认为非运动性疼痛是疼痛的第三种描述方法/机制。神经痉挛性疼痛可以单独发生,也可以与其他疼痛机制同时发生,常见于自身免疫性疾病患者。我们现在知道,非运动性疼痛的主要症状是广泛性疼痛(或疼痛部位没有炎症/损伤的证据),同时伴有疲劳、睡眠和记忆问题。有客观证据表明,疼痛以及非疼痛刺激(如灯光的亮度、声音或气味的难闻程度)会被放大/增强。外伤、感染和慢性压力等各种压力都可能引发非可塑性疼痛状态。这些特征共同表明,中枢神经系统(CNS)在引起和维持非痉挛性疼痛方面发挥着主要作用,但这些中枢神经系统因素在某些情况下可能是由持续的外周痛觉输入驱动的。治疗非痉挛性疼痛最有效的药物疗法是非阿片类中枢作用镇痛剂,如三环类、5-羟色胺-去甲肾上腺素再摄取抑制剂和加巴喷丁类。然而,治疗非痉挛性疼痛的主要方法是使用各种非药物综合疗法,尤其是那些能改善活动/运动、睡眠和解决心理并发症的疗法。
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来源期刊
Annals of the Rheumatic Diseases
Annals of the Rheumatic Diseases 医学-风湿病学
CiteScore
35.00
自引率
9.90%
发文量
3728
审稿时长
1.4 months
期刊介绍: Annals of the Rheumatic Diseases (ARD) is an international peer-reviewed journal covering all aspects of rheumatology, which includes the full spectrum of musculoskeletal conditions, arthritic disease, and connective tissue disorders. ARD publishes basic, clinical, and translational scientific research, including the most important recommendations for the management of various conditions.
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