Abstract：
Fibromyalgia (FM) is a condition characterized by chronic widespread pain whose pathogenesis is still not fully defined. Evidence based on structural and functional neuroimaging methods, electrophysiological, and morphological - skin biopsy - features demonstrated a central and peripheral nervous system involvement. A dysfunction in nociceptive inputs processing at the central level was highlighted as the primary cause of FM, but other data coming from different laboratories contributed to emphasize again the peripheral origin of FM. In fact, small fibers neuropathy (SFN) was observed in a large number of patients submitted to skin biopsy. The complex interaction between central and peripheral factors is opening a new scenario about the management of this neurological disorder. Whether proximal SFN is an initiating event leading to FM or is the consequence of stress-related insular hyper excitability remains unclear. Mild sufferance of peripheral afferents could function as a trigger for an exaggerated response of the so-called \"salience matrix\" in predisposed individuals. On the other side, the intriguing hypothesis rising from animal models could indicate that the cortical hyper function could cause peripheral small afferent damage. The research should go on the genetic origin of such peripheral and central abnormalities, the acquired facilitating factors, and the presence of different phenotypes in order to search for efficacious treatments, which are still lacking.
摘要：
纤维肌痛（FM）是一种以慢性广泛性疼痛为特征的疾病，其发病机理仍未完全确定。基于结构和功能神经影像学方法的证据，电生理学,形态学-皮肤活检-特征显示中枢和外周神经系统受累。强调中央级别的伤害性输入处理功能障碍是FM的主要原因，但是来自不同实验室的其他数据再次强调了FM的外围起源。事实上,在接受皮肤活检的大量患者中观察到小纤维神经病变（SFN）。中枢和外周因素之间的复杂相互作用正在为这种神经系统疾病的管理开辟新的方案。近端SFN是导致FM的始动事件，还是与压力相关的岛状高兴奋性的结果尚不清楚。周围传入的轻度痛苦可能会触发易感个体中所谓的“显著性矩阵”的过度反应。在另一边,从动物模型中得出的有趣的假设可能表明皮质功能亢进可能导致外周小的传入损伤。研究应该继续进行这种外周和中枢异常的遗传起源，获得的促进因素，以及不同表型的存在，以寻找有效的治疗方法，仍然缺乏。
