Myofascial pain syndrome: Here we are, where must we go

Objective: To present the current state of knowledge of myofascial pain syndrome MPS and to point the direction for new research. Findings: MPS was first defined clinically by Janet Travell, MD, and later by David Simons, MD. Pain neurophysiology has only recently provided the basis for understanding the sensorimotor manifestations of MPS. This article reviews the current state of knowledge concerning MPS. MPS is a form of myalgia characterized by local regions of muscle hardness and tenderness that cause referred pain. The signature feature is the trigger point, a tender, taut band of muscle that can be painful spontaneously or when stimulated. The active trigger point has identifiable pathophysiologic changes. Levels of substance P, calcitonin gene related peptide, bradykinin, and assorted cytokines, are elevated, indicating a chemical inflammation. Trigger point milieu pH is low, about pH 5, consistent with hypoxia and ischemia. Persistent, low-amplitude, high-frequency electrical discharges that look like endplate potentials characteristic. The taut band can be visualized using high definition ultrasonograpy and magnetic resonance sonography. Central sensitization in MPS has been documented in humans by functional magnetic resonance image scanning. The role of MPS in headache and pelvic pain has been extensively studied in the last few years. Conclusion: Although great progress has been made, studies are still needed to substantiate the energy crisis hypothesis of trigger point formation, to understand the nature of sustained muscle contraction that forms the taut band and of referred pain in humans, and to develop a more rationale and effective treatment.