Myofascial pain dysfunction is a dysfunction of a muscle that occurs due to its overload and manifests itself in muscle spasm, the presence of painful muscle seals in tense muscles or local muscle hypertonicity, and trigger points. It is a syndrome, the origin of which is associated with the occurrence of tonic muscle tension (muscular protective spasm) that occurs in response to pain impulses emanating from various sources (internal organs, the spine and related structures, joints, ligaments).
The goal of treating myofascial dysfunction is to eliminate pain in the acute period and the effect of the initial pathogenic factor, correct the impaired biomechanics of the spine and motor stereotype, against which muscle overload develops, as well as eliminate the maximum number of trigger points. The last two provisions are important since the preservation of the effect of the initial pathogenic factor contributes to the formation of secondary triggers and an increase in the zone of pain syndrome. The preservation of latent areas with appropriate provoking factors can cause an exacerbation of the disease. Thus, timely diagnosis and pathogenetic approach to treatment significantly improve the prognosis of myofascial dysfunction.
Pathophysiology: the role of nitrous oxide
In the future, the potential of safe NO synthase inhibitors with a long half-life is to be evaluated. Another critical question remains whether the described approach will be effective in other forms of pain syndrome. Data from experimental models of chronic HDN indicate that nitric oxide is involved in the mechanisms of the primary pain of various types, and the central sensitization associated with it is an essential common denominator of the latter. It would be interesting to evaluate the possible sensitization of second-order neurons in long-term cephalgias using quantitative methods. The study of neuropeptides’ role indicates that plasma levels of calcitonin gene-associated peptide (CGRP), substance P, neuropeptide B, and vasoactive intestinal polypeptide (VIP) in these patients are normal and not associated with pain as such. The study of neuropeptides in other tissues, for example, in the cerebrospinal fluid or pericranial muscles, using new sensitive analytical methods is necessary to clarify their role in the pathogenesis of this disease.
Microdialysis studies indicate that central sensitization can aggravate vasoconstriction mediated by the sympathetic nervous system, which, in turn, is responsible for a decrease in blood flow in painful skeletal muscles under static tension in patients.
It is also possible that central neuroplastic changes affect the regulation of peripheral mechanisms and therefore exacerbate painfulness and increase the risk of chronicity.
The research conducted to date has greatly improved our understanding of the complex mechanisms of the myofascial syndrome. It is likely to continue to provide us with new information relevant to the development of promising treatment approaches.