Farasyn Andre
Vrije Universiteit Brussel, Physiotherapy Science and Human Physiology, Faculty of Physical Education, Laar Beeklaan 103, B-1090 Brussels, Belgium.
Med Hypotheses. 2007;68(1):144-50. doi: 10.1016/j.mehy.2006.05.063. Epub 2006 Aug 8.
The mechanisms leading to the frequent occurrence of referred muscle pain (RP) are largely unknown. It is possible that RP is caused by the increased sensitivity of local muscle nociceptors and/or by a central sensitisation. When deep pressure by palpation is used on a subject with smooth fibrotic lesions (myofibrosis) in a muscle, RP can originate as a hyperalgesic cutaneous area, adjacent to, or totally apart from the pressure pain locus. It is currently postulated that a chain reaction is activated implicating triggering of an ever-increasing number of afferent neurons and facilitation of the synaptic connection at the level of the spinal cord, causing more distally a distributed RP via convergent efferent pathways. The human interpretation of this phenomenon can be misleading when the tested person positions, after a few seconds, his RP distally from the site of pressure to the distally located RP area. As a result of what we have found in our experimentally induced RP probes, we hypothesize that deep pressure on a myofibrosis will, in the first place, within a few seconds, increase the nociceptive excitability of the afferent sensitive nerves from the RP area to the local spot of pressure on the muscle, which in return will, in the second place, excite the whole dependent RP area. The mechanism for referred muscle pain proposed in this article is linked to the "pre-local hyper-excitability theory" or "barrier-dam theory". The afferent sensitive peripheral nerves might be entrapped in local muscle hardenings (barrier-dam) with the consequence of the hyper-excitation of pre-local nerves between the distally referred pain area and the local muscular zone of tenderness. The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa. Clinical and fundamental studies with experimentally induced RP are nevertheless needed to examine the hypothesis.
导致牵涉性肌肉疼痛（RP）频繁发生的机制在很大程度上尚不清楚。RP可能是由局部肌肉伤害感受器的敏感性增加和/或中枢敏化引起的。当对肌肉中存在平滑纤维化病变（肌纤维化）的受试者进行触诊深压时，RP可起源于与压痛部位相邻或完全分开的痛觉过敏皮肤区域。目前推测，一种连锁反应被激活，这涉及触发越来越多的传入神经元，并促进脊髓水平的突触连接，通过汇聚的传出通路在更远端引起分布性RP。当被测试者在几秒钟后将其RP从施压部位向远端的RP区域定位时，人类对这种现象的解读可能会产生误导。根据我们在实验诱导的RP探针中发现的结果，我们假设对肌纤维化进行深压首先会在几秒钟内增加从RP区域到肌肉上局部施压点的传入敏感神经的伤害性兴奋性，反过来，这又会在第二步激发整个相关的RP区域。本文提出的牵涉性肌肉疼痛机制与“局部前高兴奋性理论”或“屏障 - 损伤理论”有关。传入敏感的外周神经可能被困在局部肌肉硬化（屏障 - 损伤）中，结果是在远端牵涉痛区域和局部肌肉压痛区之间的局部前神经出现高兴奋性。牵涉性肌肉疼痛的主要发病机制可能是外周敏化，此外还有中枢调节，而非相反。然而，仍需要进行实验诱导RP的临床和基础研究来检验这一假设。
