Abstract

This chapter deals with peripheral mechanisms that lead to local muscle pain and describes diseases that exhibit this type of pain. Local muscle pain is due to excitation of muscle nociceptors (so-called nociceptive pain; other forms of muscle pain such as radiculopathic pain or pain due to CNS lesions can occur without activation of muscle nociceptors). Nociceptors in muscle are sensitive to strong mechanical stimuli and pain-producing substances, some of which are released from muscle tissue during pathological alterations. Substances such as bradykinin and prostaglandin E2 have a sensitizing rather than excitatory action and increase the sensitivity of nociceptors to other stimuli. This sensitization of muscle nociceptors is assumed to be the peripheral mechanism of the tenderness of lesioned muscle (there are also CNS mechanisms causing tenderness). Clinical examples of local muscle pain include trauma, acute inflammation, and intermittent claudication. ATP, protons (H+ ions), bradykinin, and other substances are known to be released from inflamed tissue. Ischemic contractions elicit strong muscle pain but excite just a small subpopulation of nociceptive free nerve endings. Non-nociceptive free nerve endings in muscle are likely to have an important function in the adjustment of respiration and circulation during muscular exercise.

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