Jafri M Saleet
Krasnow Institute for Advanced Study, George Mason University, 4400 University Drive, MNS 2A1, Fairfax, VA 22030, USA.
Int Sch Res Notices. 2014;2014. doi: 10.1155/2014/523924.
Myofascial pain syndrome is an important health problem. It affects a majority of the general population, impairs mobility, causes pain, and reduces the overall sense of well-being. Underlying this syndrome is the existence of painful taut bands of muscle that contain discrete, hypersensitive foci called myofascial trigger points. In spite of the significant impact on public health, a clear mechanistic understanding of the disorder does not exist. This is likely due to the complex nature of the disorder which involves the integration of cellular signaling, excitation-contraction coupling, neuromuscular inputs, local circulation, and energy metabolism. The difficulties are further exacerbated by the lack of an animal model for myofascial pain to test mechanistic hypothesis. In this review, current theories for myofascial pain are presented and their relative strengths and weaknesses are discussed. Based on new findings linking mechanoactivation of reactive oxygen species signaling to destabilized calcium signaling, we put forth a novel mechanistic hypothesis for the initiation and maintenance of myofascial trigger points. It is hoped that this lays a new foundation for understanding myofascial pain syndrome and how current therapies work, and gives key insights that will lead to the improvement of therapies for its treatment.
肌筋膜疼痛综合征是一个重要的健康问题。它影响着大多数普通人群,损害活动能力,引发疼痛,并降低整体幸福感。该综合征的潜在原因是存在疼痛的肌肉紧张带,其中包含离散的、超敏感的病灶,称为肌筋膜触发点。尽管对公众健康有重大影响,但目前对该疾病尚无清晰的机制性认识。这可能是由于该疾病的复杂性,它涉及细胞信号传导、兴奋 - 收缩偶联、神经肌肉输入、局部循环和能量代谢的整合。由于缺乏用于测试机制假说的肌筋膜疼痛动物模型,这些困难进一步加剧。在本综述中,介绍了目前关于肌筋膜疼痛的理论,并讨论了它们的相对优缺点。基于将活性氧信号的机械激活与不稳定的钙信号联系起来的新发现,我们提出了一个关于肌筋膜触发点起始和维持的新机制假说。希望这为理解肌筋膜疼痛综合征以及当前治疗方法的作用机制奠定新的基础,并提供关键见解,从而推动其治疗方法的改进。