The pathogenesis of muscle pain.

Abstract

Nociceptive nerve endings in muscles and other tissues are equipped with a multitude of receptor molecules for endogenous pain-producing and sensitizing agents. Particularly interesting molecules are the purinergic receptors, which can be activated by adenosine triphosphate (ATP), and the vanilloid receptor, which is sensitive to protons (low pH). The purinergic receptors are activated by tissue damage because cell necrosis is associated with the release of ATP. A low pH is present in many pathologic conditions such as ischemia and inflammation. At the spinal and medullar level, painful muscle lesions induce marked neuroplastic changes that result in hyperexcitability and hyperactivity of nociceptive neurons. This central sensitization is the basis for the spontaneous pain and hyperalgesia of patients. The transition from acute to chronic muscle pain is complete when the initially functional changes are transformed into structural ones. Patients with morphologic alterations in their nociceptive system are difficult to treat because the changes need time to normalize.