[Mechanisms of transition from acute to chronic muscle pain]

The present article presents an overview of neurophysiological and neuroanatomical mechanisms that may be involved in the transition from acute to chronic muscle pain. The report is based on data that were obtained in studies on anaesthetised rats in which an acute or chronic myositis was induced experimentally. The inflamed muscle tissue was evaluated using histochemical and immunohistochemical methods, and the impulse activity of single muscle nociceptors or dorsal horn neurones was recorded in electrophysiological experiments in vivo. Chronic myositis was associated with a higher innervation density of the tissue with putative nociceptive free nerve endings that contain the neuropeptide substance P (SP). The nociceptive information from muscle to the spinal cord was largely carried by unmyelinated fibres with tetrodotoxin-resistant Na(+)-channels. At the spinal level, myositis caused changes in the connectivity of dorsal horn neurones which were reflected in an expansion of the input (target) region of the muscle nerve. The central sensitisation can explain the hyperalgesia and spread of pain in patients. Chronic spontaneous muscle pain, however, appears to be due to a lack of NO. The final step in the transition from acute to chronic pain involves structural changes that perpetuate the functional changes. In rat experiments employing nerve lesions or muscle inflammation, such morphological changes become apparent within a few hours after the lesion.