复杂区域疼痛综合征的发病机制

Jagan Devarajan, Shayla Mena, Jianguo Cheng
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摘要

复杂性区域疼痛综合征(CRPS)是一种慢性疼痛疾病,其特点是症状多种多样,包括与最初诱发事件不相称的疼痛,并伴有自主神经、感觉、运动和渗出性运动障碍。这两种 CRPS(I 型,又称反射性交感神经营养不良,RSD;II 型,又称因果痛)的主要病理特征是异动症、水肿、皮肤颜色和温度的变化,以及主要影响四肢的营养不良。最近的研究开始揭示 CRPS 复杂的致病机制,尤其是从自身免疫和神经免疫相互作用的角度。CRPS 现在被认为是一种系统性疾病,源于炎症、免疫、神经源、遗传和心理因素的复杂相互作用。这些因素的相对作用可能因患者而异,甚至在同一患者体内也会随着时间的推移而变化。临床表现的关键机制包括外周和中枢敏化、交感神经失调和躯体感觉处理的改变。加强对 CRPS 机制的了解对于开发有效的治疗干预措施至关重要。虽然我们对 CRPS 的机理认识仍不全面,但本文更新了最新的研究进展,并阐明了 CRPS 的病因、发病机制和分子基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanisms of complex regional pain syndrome
Complex Regional Pain Syndrome (CRPS) is a chronic pain disorder characterized by a diverse array of symptoms, including pain that is disproportionate to the initial triggering event, accompanied by autonomic, sensory, motor, and sudomotor disturbances. The primary pathology of both types of CRPS (Type I, also known as reflex sympathetic dystrophy, RSD; Type II, also known as causalgia) is featured by allodynia, edema, changes in skin color and temperature, and dystrophy, predominantly affecting extremities. Recent studies started to unravel the complex pathogenic mechanisms of CRPS, particularly from an autoimmune and neuroimmune interaction perspective. CRPS is now recognized as a systemic disease that stems from a complex interplay of inflammatory, immunologic, neurogenic, genetic, and psychologic factors. The relative contributions of these factors may vary among patients and even within a single patient over time. Key mechanisms underlying clinical manifestations include peripheral and central sensitization, sympathetic dysregulation, and alterations in somatosensory processing. Enhanced understanding of the mechanisms of CRPS is crucial for the development of effective therapeutic interventions. While our mechanistic understanding of CRPS remains incomplete, this article updates recent research advancements and sheds light on the etiology, pathogenesis, and molecular underpinnings of CRPS.
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