The Taut Band and Other Mysteries of the Trigger Point: An Examination of the Mechanisms Relevant to the Development and Maintenance of the Trigger Point

Abstract

Objective: To examine the mechanisms that underlie the development of the myofascial trigger point [TrP].

Results: The TrP represents chronically dysfunctional muscle, but initiation and persistence of the TrP taut band have not been fully explained. Studies suggest that the initiating factors are excessive mechanical forces generated by muscle. Supramaximal muscle contraction, overloaded eccentric contraction, or repetitive activity are consistent with Simons' hypothesis of an energy crisis as a critical event. Ischemia, hypoxia, and cell damage occur, leading to the release of cytokines, bradykinin, substance P, and calcitonin-gene-related peptide, all of which activate peripheral nociceptors. The taut band, chronically contracted, displays a sympathetic nervous system [SNS] modulated, localized, excessive endplate potential activity that produces a localized, nonpropagated contraction. The net effect is an excess of acetylcholine [ACh] at the motor end plate. This results from a combination of excess spontaneous release of ACh modulated by calcitonin-gene-related peptide and the SNS, inhibition of acetylcholinesterase, and upregulation of ACh receptors in the endplate zone. Postsynaptic events in the muscle cell that promote prolonged contraction are those that increase the concentration of calcium in the cytosol. Excessive release of calcium from the sarcoplasmic reticulum through a dysfunctional Ryanidine Receptor calcium channel, by a second messenger system mediated by the SNS, or by mitochondria could result in persistent muscle fiber contraction.

Conclusion: Pre- and postsynaptic modulation of ACh release and intracellular Ca^{2 +} can explain many of the features of the TrP.

KEYWORDS:

• Trigger points
• taut band
• sympathetic nervous system
• muscle contraction
• calcium channels