Interstitial myofibrositis, described by Smythe as a rubric, pain amplification syndrome, is referred to by Simon as a muscle pain syndrome. Both tend to agree on the diagnostic criteria of local exquisite pain tenderness, circumscribed painful hardening (fibrous nodules), and referred pain caused by pressure on the fibrous nodules. They describe heparin and histamine being released by action on mast cells resulting in vasodilation; local platelets release serotonin, a vasoconstrictor. If trauma is involved in the history, a mucoid substance infiltrates the interfascial and intercellular spaces resulting in local edema which is the antecedent to fibrous adhesion formation.
In keeping with the clinical precepts of Kraft, Maigne, and Wolfe, there is suspected interstitial myofibrositis when the patient complains of pain, fatigue, and nonrestful sleep, with multiple tender points and, commonly, normal laboratory test results.
Shortwave diathermy is applied to the area of the lesion for a period of time sufficient to obtain maximum blood flow which may be determined by induction of patient perspiration. At this point removal of toxin catabolites will be enhanced and the application of continuous ultrasonic energy will then irritate the mast cells and contribute to degranulation. Interferential current therapy may then be applied employing the Davis procedure (Dynamic Chiropractic issue dated November 15, 1988) to inhibit the pain-spasm cycle and contribute to vasodilation. Travell also recommends spraying the fibrous painful points with a cutaneous refrigerant spray (ethyl chloride or fluoroethyl) until cooled, not frosted. This author has not found this necessary with the previous regimen.
The pain-spasm cycle in interstitial myofibrositis is recognized as due to muscle twitches which last longer than the duration of the action potential. With repeated action potentials resulting from the pain-spasm cycle, tetanus results with a constant, smooth contraction. The regimen described here interferes with this twitch/action potential mechanism and tends to stabilize the reflex arc.
Considering the pathology described and the mechanism of its action, it is probable that individuals with this diagnosis will experience amelioration and exacerbation in their histories. This will be to the frustration of both the patient and the treating chiropractic physician. However, the patient will gain transient relief employing this regimen and it may be possible to enhance this benefit by employing specific nutritional agents of the free-form amino acid group in order to aid in achieving an improved sleeping pattern. This information, however, is properly referred to another specialty subject for greater detail.
References
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