Mayte Serrat, Sergi Estanyol, David Cifre, Andrea Lizama-Lefno, Felipe Araya-Quintanilla, Ruben Nieto, Carlos Suso-Ribera, Miriam Almirall
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引用次数: 0
Abstract
Fibromyalgia (FM) is a prevalent and highly complex disease associated with a substantial reduction in quality of life and functional capacity, as well as significant use of healthcare resources. It is characterized by widespread pain, fatigue, sleep disturbances, and cognitive symptoms, among other manifestations. The heterogeneity of this symptomatology challenges traditional linear clinical models focused on the identification of overt structural damage. Based on a critical review of the contemporary literature, we argue that FM may represent the clinical expression of chronic dysregulation across multiple interacting physiological systems. Within this perspective, the peripheral nervous, central nervous, endocrine, and immune systems may influence central processes involved in nociceptive amplification, potentially contributing to the persistence of nociplastic pain states and the emergence of nonpain symptoms such as fatigue and cognitive dysfunction. Rather than replacing existing models, this perspective aims to expand them into a broader, nonreductionist framework that emphasizes systemic interactions and the loss of adaptive physiological coordination. Evidence was identified through PubMed/MEDLINE, Scopus, and Web of Science (2000-2026).
纤维肌痛(FM)是一种普遍且高度复杂的疾病,与生活质量和功能能力的大幅下降以及医疗资源的大量使用有关。它的特点是广泛的疼痛、疲劳、睡眠障碍和认知症状,以及其他表现。这种症状的异质性挑战了传统的线性临床模型,重点是识别明显的结构损伤。基于对当代文献的批判性回顾,我们认为FM可能代表了多个相互作用的生理系统的慢性失调的临床表现。从这个角度来看,外周神经、中枢神经、内分泌和免疫系统可能影响涉及伤害性放大的中枢过程,可能导致伤害性疼痛状态的持续和疲劳和认知功能障碍等非疼痛症状的出现。这一观点的目的不是取代现有的模型,而是将它们扩展到一个更广泛的、非简化主义的框架,强调系统的相互作用和适应性生理协调的丧失。通过PubMed/MEDLINE、Scopus和Web of Science(2000-2026)确定证据。