The Pathogenesis of Muscle Pain

Viktig studie fra S.Mense som nevner mange aspekter av muskelsmerter, som trykksensitivitet, sentral sensitering og referert smerte.

http://www.cfids-cab.org/cfs-inform/Neuroendocrin/mense03.pdf

The typical muscle nociceptor responds to noxious local pressure and injections of BKN; however, in animal experiments, receptors also can be found that are activated by one type of noxious stimulation (mechanical or chemical) only. This finding indicates that different types of nociceptors are present in skeletal muscle, similar to the skin in which mechano-, mechano-heat-, and poly-modal nociceptors have been reported to exist [12••].

The sensitization is associated with a decrease in the mechanical threshold of the receptor so that it responds to weak pressure stimuli. The sensitized muscle receptor still is connected to nociceptive central nervous neurons and thus elicits subjective pain when weak mechanical stimuli act on the muscle. This sensitization of muscle nociceptors is the best established peripheral mechanism explaining local tenderness and pain on movement of a pathologically altered muscle.

Of these neuropeptides, SP is of particular interest because, in experiments on fibers from the skin, SP has been shown to be predominantly present in nociceptive fibers [26]. The peptides are released during excitation of the ending and influence the chemical milieu of the tissue around the receptor. This means that a nociceptor is not a passive sensor for tissue-threatening stimuli, but actively changes the micromilieu in its vicinity by releasing neuropeptides. SP has a strong vasodilating and permeability increasing action on small blood vessels.

Mechanism of referral of muscle pain

The expansion of the input region of the inflamed GS muscle nerve likely underlies the spread and referral that is common in patients with muscle pain. The mechanisms mentioned previously can explain referral as follows: when a muscle is damaged, the patient will perceive local pain at the site of the lesion. If the nociceptive input from the muscle is strong or long-lasting, central sensitization in the dorsal horn neurons is induced, which opens silent synapses and leads to an expansion of the target area of that muscle in the spinal cord (or brain stem). As soon as the expansion reaches sensory neurons that supply peripheral areas other than the damaged muscle, the patient will feel pain in that area outside the initial pain site. In the area of pain referral, no nociceptor is active and the tissue is normal. The referral is simply caused by the excitation induced by the original pain source, which spreads in the central nervous system and excites neurons that supply the body region in which the referred pain is felt. This way, a trigger point in the temporalis muscle can induce pain in the teeth of the maxilla when the trigger point-induced central excitation spreads to sensory neurons that supply the teeth [43•].

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