Liptan Ginevra L
Dept. of Medicine, Oregon Health & Science University, Portland, 97239, United States.
J Bodyw Mov Ther. 2010 Jan;14(1):3-12. doi: 10.1016/j.jbmt.2009.08.003.
Significant evidence exists for central sensitization in fibromyalgia, however the cause of this process in fibromyalgia-and how it relates to other known abnormalities in fibromyalgia-remains unclear. Central sensitization occurs when persistent nociceptive input leads to increased excitability in the dorsal horn neurons of the spinal cord. In this hyperexcited state, spinal cord neurons produce an enhanced responsiveness to noxious stimulation, and even to formerly innocuous stimulation. No definite evidence of muscle pathology in fibromyalgia has been found. However, there is some evidence for dysfunction of the intramuscular connective tissue, or fascia, in fibromyalgia. This paper proposes that inflammation of the fascia is the source of peripheral nociceptive input that leads to central sensitization in fibromyalgia. The fascial dysfunction is proposed to be due to inadequate growth hormone production and HPA axis dysfunction in fibromyalgia. Fascia is richly innervated, and the major cell of the fascia, the fibroblast, has been shown to secrete pro-inflammatory cytokines, particularly IL-6, in response to strain. Recent biopsy studies using immuno-histochemical staining techniques have found increased levels of collagen and inflammatory mediators in the connective tissue surrounding the muscle cells in fibromyalgia patients. The inflammation of the fascia is similar to that described in conditions such as plantar fasciitis and lateral epicondylitis, and may be better described as a dysfunctional healing response. This may explain why NSAIDs and oral steroids have not been found effective in fibromyalgia. Inflammation and dysfunction of the fascia may lead to central sensitization in fibromyalgia. If this hypothesis is confirmed, it could significantly expand treatment options to include manual therapies directed at the fascia such as Rolfing and myofascial release, and direct further research on the peripheral pathology in fibromyalgia to the fascia.
有大量证据表明纤维肌痛存在中枢敏化现象，然而，纤维肌痛中这一过程的原因以及它与纤维肌痛中其他已知异常情况的关系仍不明确。当中枢敏化现象发生时，持续的伤害性输入会导致脊髓背角神经元的兴奋性增加。在这种过度兴奋的状态下，脊髓神经元对有害刺激甚至对以前无害的刺激产生增强的反应。尚未发现纤维肌痛中肌肉病理学的确切证据。然而，有一些证据表明纤维肌痛中存在肌肉内结缔组织或筋膜功能障碍。本文提出，筋膜炎症是导致纤维肌痛中枢敏化的外周伤害性输入的来源。筋膜功能障碍被认为是由于纤维肌痛中生长激素分泌不足和下丘脑 - 垂体 - 肾上腺（HPA）轴功能障碍所致。筋膜有丰富的神经支配，并且筋膜的主要细胞成纤维细胞已被证明在受到拉伸时会分泌促炎细胞因子，特别是白细胞介素 - 6。最近使用免疫组织化学染色技术的活检研究发现，纤维肌痛患者肌肉细胞周围结缔组织中的胶原蛋白和炎症介质水平升高。筋膜炎症与足底筋膜炎和外侧上髁炎等病症中描述的炎症相似，可能更好地描述为功能失调的愈合反应。这可以解释为什么非甾体抗炎药和口服类固醇在纤维肌痛中未被发现有效。筋膜的炎症和功能障碍可能导致纤维肌痛中的中枢敏化。如果这一假设得到证实，它可能会显著扩大治疗选择范围，包括针对筋膜的手法治疗，如罗尔夫整脊法和肌筋膜松解术，并将对纤维肌痛外周病理学的进一步研究指向筋膜。
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