Pathophysiology of Active and Latent Myofascial Trigger Points

项目摘要 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 综合征以及手术后和癌症疼痛与肌筋膜触发点（TrP）有关。的 TrP是一个沿着肌肉绷紧带的沿着压痛结节。已知TrP存在两种状态：活跃和潜伏。 在活动状态下，TrP是自发性疼痛和模仿临床主诉的诱发性疼痛。 潜伏性TrP不是自发性疼痛，触诊时引起的任何牵涉性疼痛都与疼痛无关。 临床疼痛主诉;潜伏性TrP被认为是健康和活性TrP之间的中间状态。 来自超声的证据表明，潜伏性TrPs表现出血流量减少，这在活性TrPs中进一步减少。 TrPs，提示代谢紊乱和细胞应激。根据这一观察，假设TrP 模型预测TrPs中葡萄糖降低和乳酸升高，然而， 活动性TrP疼痛的减少没有发现葡萄糖的变化和乳酸的增加。之间的差异 TrP模型和经验证据认为，TrP内的细胞代谢可能表现得不同于 公认的模型预测。乳酸盐也与伤害感受器敏感化有关，这可以解释 局部或牵涉疼痛体验的差异。此外，潜伏期和潜伏期之间的血流量差异 活性TrPs可能导致代谢差异，这可能是关于形成、进展和 TrPs的延续。 本研究将使用靶向和非靶向代谢组学方法来了解代谢 这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TrPs， 将研究来自患有紧张型头痛的个体的活性TrPs。有针对性的方法将侧重于 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。这种非靶向方法将筛选出数千种代谢生物标志物， 健康肌肉和TrPs，以确定代谢物的相对差异， 导致潜伏性TrP的发展、进展为活性TrP或活性TrP的永久存在。 本提案中描述的实验将提供对TrPs内部环境的深入了解。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志物的差异， 在潜伏或活性TrP中，TrP形成或进展的机制将变得清楚。这 这些信息可用于优化干预技术，从而逆转或预防肌肉源性疼痛。 这项拟议的研究将解决关键目标，“开发和验证慢性疼痛或其他疾病的生物标志物， 关键症状将用于身心方法的研究”从资助机会 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.