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纤维肌痛综合征的病因发病机制。

Etiopathogenetic mechanisms of fibromyalgia syndrome.

作者信息

Stisi S, Cazzola M, Buskila D, Spath M, Giamberardino M A, Sarzi-Puttini P, Arioli G, Alciati A, Leardini G, Gorla R, Marsico A, Ceccherelli F, Bazzichi L, Carignola R, Gracely R H, Salaffi F, Marinangeli F, Torta R, Di Franco M, Biasi G, Cassisi G, Casale R, Altomonte L, Atzeni F

机构信息

Rheumatology Unit, G.Rummo Hospital, Benevento, Italy.

出版信息

Reumatismo. 2008 Jul-Sep;60 Suppl 1:25-35.

PMID:18852906
Abstract

Fibromyalgia syndrome (FMS) is a common chronic condition of widespread pain with causal mechanisms that are largely unknown. It is characterized by moderate to severe musculoskeletal pain and allodynia, but its pathogenesis appears confined to the nociceptive structures of the central nervous system. FMS is often triggered by negative environmental influences, especially if they occur in childhood. In a fetus, these environmental triggers may influence the development of the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal axis (HPA). Increasing evidence supports the comorbidity of psychological conditions including depression, panic disorders, anxiety, and post-traumatic stress disorder (PTSD). Recent evidence suggests that genetic factors may play a role in the pathogenesis of FMS. Central sensitization has long been associated with FMS pain. It describes enhanced excitability of dorsal horn neurons, which leads to transmission of altered nociceptive information to the brain. Understanding of pathogenetic pathways in FMS has advanced beyond observing patient responses to neurophysiologically targeted therapies and basic research.

摘要

纤维肌痛综合征(FMS)是一种常见的慢性广泛性疼痛疾病,其病因机制大多不明。它的特征是中度至重度肌肉骨骼疼痛和痛觉过敏,但其发病机制似乎局限于中枢神经系统的伤害性结构。FMS通常由负面环境影响引发,尤其是在童年时期发生的影响。在胎儿期,这些环境触发因素可能会影响自主神经系统(ANS)和下丘脑 - 垂体 - 肾上腺轴(HPA)的发育。越来越多的证据支持包括抑郁症、惊恐障碍、焦虑症和创伤后应激障碍(PTSD)在内的心理疾病的共病现象。最近的证据表明,遗传因素可能在FMS的发病机制中起作用。中枢敏化长期以来一直与FMS疼痛相关。它描述了背角神经元兴奋性增强,这会导致改变的伤害性信息传递到大脑。对FMS发病途径的理解已经超越了观察患者对神经生理学靶向治疗的反应和基础研究。

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