Mechanisms in the lesioned muscle:The peripheral mechanism underlying the t
enderness and pain during movement of a damaged muscle is the sensitization
of muscle nociceptors. Ongoing activity of nociceptors causes spontaneous
pain in addition to tenderness. Muscle pain (particularly that originating
in myofascial trigger points) is often mislocalized because it is referred
to other deep somatic tissues. The development of trigger points is a purel
y peripheral event, whereas the referral of muscle pain is based on central
nervous mechanisms.
Mechanisms at the spinal level: The input from muscle nociceptors induces n
europlastic changes in the spinal cord and higher centres of the central ne
rvous system. These changes are associated with an overexcitability of neur
ones (central sensitization) and contribute to hyperalgesia of patients. Re
sting activity of spinal neurones (and hence spontaneous pain) is strongly
dependent on nitric oxide (NO). A muscle lesion is likely to lead to an inh
ibition of the homonymous muscle, it can, however, elicit spasm in another
muscle.
Supraspinal mechanisms: Spinal neurones that mediate muscle pain are subjec
ted to a strong descending inhibitory influence. The inhibitory tracts orig
inate in the mesencephalon and medulla oblongata. A dysfunction of this inh
ibitory system might be involved in the pathogenesis of fibromyalgia.