Pathophysiology of Active and Latent Myofascial Trigger Points

项目总结 由一系列健康问题引起的疼痛，包括头痛、腰痛、骨关节炎、腕管 综合征、手术后疼痛和癌症疼痛都与肌筋膜触发点(TRP)有关。这个 色氨酸是沿着紧绷的肌肉带的一个触痛的结节。已知Trp有两种状态：活动状态和潜伏状态。 在活动状态下，TRP是自发的疼痛，并引起模仿临床症状的疼痛转诊。 潜伏的Trp不是自发的疼痛，它在触诊时引起的任何牵涉性疼痛都与 临床疼痛主诉；潜在的TRP被认为是介于健康和活跃的TRP之间的中间状态。 来自超声波的证据表明，潜伏期TRP表现出血流减少，在活动期进一步减少 TRPs，提示代谢紊乱和细胞应激。根据这一观察结果，假想的TRP 模型预测TRP的血糖降低和乳酸升高，然而一项试点按摩干预试验表明 活动期Trp疼痛减轻后，血糖没有变化，乳酸增加。两者之间的差异 TRP模型和经验证据认为，TRP内的细胞新陈代谢可能不同于 公认的模型预测。乳酸也与伤害性感受器敏化有关，这可以解释 局部或牵涉疼痛体验的差异。此外，潜伏期和潜伏期血流速度的差异 活跃的TRP可导致代谢差异，这可能对肿瘤的形成、进展和 TRP的永久化。 本研究将使用靶向和非靶向代谢组学方法来了解代谢 两种类型的触发点和健康肌肉内的环境。来自健康个体的潜在TRP和 紧张型头痛患者的主动TRP将被调查。有针对性的方法将重点放在 以确定健康肌肉中碳水化合物能量平衡是否不同 和触发点位置。这种非靶向的方法将筛选出数千种代谢生物标记物 健康肌肉和TRP来识别代谢物的相对差异，从而识别哪些代谢物 导致潜在的Trp的发展，进展为活跃的Trp，或使活跃的Trp永久化。 这项提案中描述的实验将提供对TRP内部环境的洞察。应该 这项探索性研究揭示了碳水化合物能量平衡的破坏或确定了生物标记物的差异。 在潜在或活跃的TRP中，TRP的形成或进展的机制将变得清晰。这 信息可以用来优化干预技术，从而逆转或预防肌源性疼痛。 这项拟议的研究将解决关键目标，即开发和验证慢性疼痛或其他疾病的生物标记物 在精神和身体方法研究中使用的关键症状“来自资助机会 公告PA-18-322。

PROJECT SUMMARY Pain deriving from a range of health concerns including headache, low back pain, osteoarthritis, carpal tunnel syndrome, as well as post-surgical and cancer pain have been linked to myofascial trigger points (TrPs). The TrP is a tender nodule along a taut band of muscle. Two states of the TrP are known to exist: active and latent. In the active state, the TrP is spontaneously painful and elicits pain referral mimicking the clinical complaint. The latent TrP is not spontaneously painful and any referred pain it elicits upon palpation is not related to a clinical pain complaint; the latent TrP is thought to be an intermediary state between healthy and an active TrP. Evidence from ultrasound indicates latent TrPs exhibit reduced blood flow, which is further reduced in active TrPs, suggestive of metabolic disruption and cellular stress. In line with that observation, hypothesized TrP models predict reduced glucose and elevated lactate in TrPs, however a pilot massage intervention trial that reduced active TrP pain found no change in glucose and an increase in lactate. The discrepancy between the TrP model and empirical evidence argues that cellular metabolism within a TrP may behave differently than the well-accepted model predicts. Lactate has also been linked to nociceptor sensitization, which could explain differences in local or referred pain experience. Furthermore, the differences in blood flow between latent and active TrPs could result in metabolic differences that may be informative as to the formation, progression, and perpetuation of TrPs. The present study will use a targeted and non-targeted metabolomics approach to understand the metabolic environment within both types of trigger points and healthy muscle. Latent TrPs from healthy individuals and active TrPs from individuals with tension-type headache will be investigated. The targeted approach will focus on glucose and lactate to determine whether carbohydrate energy balance is different within healthy muscle and trigger point sites. The non-targeted approach will screen for thousands of metabolic biomarkers within healthy muscle and the TrPs to identify relative differences in metabolites that could identify which metabolites lead to development of a latent TrP, progression to an active TrP, or perpetuation of the active TrP. The experiments described in this proposal will provide insight into the internal environment of TrPs. Should this exploratory study reveal disruption to carbohydrate energy balance or identify differences in biomarkers within latent or active TrPs a mechanism for the formation or progression of the TrP will become clear. This information could be used to optimize intervention techniques that will reverse or prevent muscle-derived pain. This proposed study will address the key goal to “Develop and validate biomarkers for chronic pain or other key symptoms to be used in studies of mind and body approaches” from the Funding Opportunity Announcement PA-18-322.