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Abstract：
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.
摘要：
复杂区域疼痛综合征（CRPS）是一种慢性疼痛障碍，其特征是各种症状，包括与初始触发事件不成比例的疼痛，伴随着自主神经，感官,电机,和sudomotor紊乱。两种类型的CRPS的主要病理（I型，也被称为反射性交感神经营养不良，RSD；II型，也称为灼痛）的特征是异常性疼痛，水肿,皮肤颜色和温度的变化，营养不良,主要影响四肢。最近的研究开始揭示CRPS的复杂致病机制，特别是从自身免疫和神经免疫相互作用的角度来看。CRPS现在被认为是一种全身性疾病，源于炎症的复杂相互作用，免疫学,神经性，遗传,和心理因素。随着时间的推移，这些因素的相对贡献可能在患者之间变化，甚至在单个患者中变化。临床表现的主要机制包括外周和中枢致敏，交感神经失调,和体感加工的改变。增强对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的机械理解仍然不完整，本文更新了最近的研究进展，并对病因进行了展望，发病机制，和CRPS的分子基础。
