Anesthesiology, University of Michigan, Ann Arbor, Michigan, USA
Ann Rheum Dis. 2024 Oct 21;83(11):1421-1427. doi: 10.1136/ard-2023-225327.
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.
风湿学家和风湿病学在概念化病理性疼痛方面发挥了突出作用，因为典型的病理性疼痛病症是纤维肌痛。纤维肌痛以前被称为纤维组织炎，直到人们清楚地认识到，由于缺乏系统性炎症和组织损伤，这种疾病可以与自身免疫性疾病区分开来。病理性疼痛现在被认为是除伤害性疼痛（由于外周损伤或炎症引起的疼痛）和神经性疼痛之外的第三种疼痛描述符/机制。病理性疼痛可以单独发生，也可以与其他疼痛机制共存，这种情况在患有自身免疫性疾病的个体中很常见。我们现在知道，病理性疼痛的主要症状是广泛疼痛（或在没有炎症/损伤证据的区域疼痛），伴有疲劳、睡眠和记忆问题。有客观证据表明疼痛会放大/增强，以及非疼痛刺激，如灯光亮度、声音或气味的不愉快。病理性疼痛状态可以由多种应激源引发，如创伤、感染和慢性应激源。所有这些特征表明，中枢神经系统（CNS）在引起和维持病理性疼痛方面起着重要作用，但这些 CNS 因素在某些情况下可能是由持续的外周伤害性输入驱动的。治疗病理性疼痛最有效的药物是中枢作用的非阿片类镇痛药，如三环类抗抑郁药、5-羟色胺去甲肾上腺素再摄取抑制剂和加巴喷丁类药物。然而，病理性疼痛的主要治疗方法是使用各种非药物性综合疗法，特别是那些能改善活动/运动、睡眠和解决心理共病的疗法。
