慢性肌筋膜疼痛触发点发病机理的探索性研究

Myofascial trigger points (MTrPs) are main cause of chronic pain of soft tissues, which lead to a serial clinical symptom mainly for local pain, referred pain with dysfunctions of autonomic nerves system, neuromusculoskeletal system as well as adjacent viscera system. Our previous study implied muscle spindle possibly took part in the formation of MTrPs pain, and currently it is not clear of the relationship between the nerve endings and MTrPs muscle fibers which leads to an unclear pathogenic mechanism. Meanwhile, we hypothesize that the membrane of muscle fiber cells of MTrPs possibly has certain antigenicity, different from that of normal muscle fibers. Therefore, the present study is to explore an inner link between the discharge of muscle spindle and the formation of MTrPs, and to study if any connection exists between an abnormal contracture nodules and nerve endings utilizing micro immunofluorescence to stain silk fibroin of nerve at MTrPs. A virto culture of muscle fiber of MTrPs is part of study to observe any morphological changes of denervate contracture knot, which may help to understand the relationship between acetylcholine and contracture knots, also it is basis of finding membrane antigenicity of MTrPs for the future study. If this study can successfully be finished as our assumption, it will either indicate full new concepts of pathogenic mechanism for MTrPs which will provide new idea and mode on the aspects of clinical prevention, diagnosis and treatment of the muscle disease, and support the traditional hypotheses of pathogenic mechanism for MTrPs with real objective conditions.

肌筋膜疼痛触发点是造成慢性软组织疼痛的主要原因，主要表现为以局部疼痛和牵涉痛为主的自主神经和骨骼肌功能以及邻近内脏功能障碍的系列症状。前期研究怀疑肌梭可能参与肌筋膜疼痛触发点的形成，而且当前触发点处的神经末梢与挛缩结节关系不明确，因此导致疼痛触发点的发病机理仍不明确，同时假设触发点肌纤维处可能具有某种抗原性。因此，本项目拟以全新的模式从H反射和牵拉骨骼肌诱导肌梭探究肌梭放电与触发点形成之间的内在联系，并通过对触发点肌纤维处进行神经微丝蛋白免疫荧光染色精细观察触发点处的神经末梢与异常挛缩结节之间的联系，并对大鼠触发点处肌细胞进行离体培养,然后观察离神经后触发点挛缩结节的形态变化，同时也为今后发现触发点细胞抗原打下基础。此项研究的成功实现，将以全新的理念揭示慢性肌筋膜疼痛触发点的发病机理，和支持原有对肌筋膜疼痛触发点发病机理解释的假说，为临床预防、诊断和治疗该疾病提供新的治疗思路和模式。

一、项目背景：肌筋膜疼痛触发点是造成慢性软组织疼痛的主要原因，主要表现为以局部疼痛和牵涉痛为主的自主神经和骨骼肌功能以及邻近内脏功能障碍的系列症状。前期研究怀疑肌梭可能参与肌筋膜疼痛触发点的形成，而且当前触发点处的神经末梢与挛缩结节关系不明确，因此导致疼痛触发点的发病机理仍不明确。因此，本项目拟以全新的模式从H反射和牵拉骨骼肌诱导肌梭探究肌梭放电与触发点形成之间的内在联系，并通过对触发点肌纤维处进行神经微丝蛋白免疫荧光染色精细观察触发点处的神经末梢与异常挛缩结节之间的联系，并对大鼠触发点处肌细胞进行离体培养，然后观察离神经后触发点挛缩结节的形态变化。.二、研究内容：.（1）电生理学研究：（a）采用双极细针电极记录触发点处静息状态的自发性放电,分析这种电活动的特点。（b）采用神经电刺激方法，记录大鼠下肢股内侧肌的H反射。.（2）病理组织学研究：观察疼痛触发点处运动终板中是否会有运动神经支配，是否与异常的收缩结节有联系。.（3）细胞培养工程的探索：采用体外培养成肌细胞的方法，观察肌筋膜疼痛触发点处成肌细胞在离体条件下的培养情况。.三、重要结果：.（1）证实了肌筋膜触发点发生在运动终板。.（2）肌筋膜触发点大鼠脊髓中枢可能存在中枢敏化现象，Iα类传入神经兴奋性增高，肌梭敏感性增高。.（3）肌筋膜触发点严重影响了肌梭的形态结构和功能，也诱发了受累肌和多块关联肌肌梭内NT-3、受体TrkC蛋白和基因的显著性下调。.（4）肌筋膜触发点细胞可以在离体情况下继续维持挛缩形态。.四、科学意义：.（1）在基础研究方面：本研究为肌梭参与慢性肌筋膜触发点的电生理学、病理生理学和分子生物学基础奠定了坚实的理论基础，也为后续深入的肌筋膜触发点细胞的离体培养和肌筋膜触发点特异蛋白的筛选提供了丰富的理论依据。.（2）在临床研究方面：基于肌筋膜触发点理论的技术，可为临床上运动损伤的预防、诊断与康复提供一种科学的非手术处理方法。