A plethora of terms - e.g., myalgia, myositis, myofibrositis, fibromyositis, fascitis, myofascitis, rheumatism, fibrositic nodule, myogelosis, fibropathic syndrome, myodysneufia - have been used to describe a myofascial pain syndrome that is now most commonly known as the myofascial trigger point. This is a hyper-irritable spot, usually within a taut band of skeletal muscle or in the muscle's fascia, that is painful on compression and that can give rise to characteristic referred pain, tenderness, and autonomic phenomena. A trigger point may be induced by trauma, local chilling, poor posture, or by muscle fatigue, strain, or tension. This phenomenon has been thoroughly described by Travell and Simons (1983).

Myofascial trigger points can be effectively treated through the application of focal deep pressure and massage over the trigger point (Travefl and Simons 1983:86). Although no quantitative studies of this treatment were located, it has been suggested that the applied pressure stimulates proprioceptive nerve endings which facilitate encephalin release and pain modulation. It is also thought that kneading of the tissues stretches musculotendinous structures that initiate reflex muscle relaxation via Golgi tendon organ and spindle receptors (Swezey 1983).

Danneskiold-Samsoe et al. (1982) studied 13 patients with regional muscle tension of the type now known as myofascial trigger points. Plasma myoglobin concentrations were measured throughout a course of therapy that consisted of 10 massage treatments of 30 to 40 minutes duration evenly distributed over a four-week period. a positive correlation was found between degree of muscle tension and increase in plasma myoglobin concentration following massage-, massage of non-tender, non-painful muscles did not increase myoglobin concentrations above non-nal. The rise in myoglobin became significant after the first massage treatment, and the effect on index of muscle tension became significant after the fourth treatment. Both effects plateaued after the seventh treatment, and plasma myoglobin concentrations were normal following the tenth treatment. The authors concluded that massage is effective in normalizing muscle tension.

A subsequent study (Danneskiold-Samsoe et al. 1986) of 26 patients with myofascial pain produced similar results. In the 21 patients for whom treatment was successful, massage again produced an increase in plasma myoglobin, and after repeated treatments, muscle tension and pain decreased, paralleled by a decline in the elevated myoglobin levels produced by massage. The authors suggest that the observed post-massage increase in plasma myoglobin indicated a leak of myoglobin from the muscle fibres, and further, that myofascial pain is a disease of the muscle fibres rather than of the connective tissue within the muscles.

They refer to a study of Fassbender et al. (1973), who examined biopsy material from fibrositic trapezium muscle under an electron microscope and found degenerated mitochondiia and increased glycogen deposits in the muscle fibres, which indicated that a state of hypoxia existed within the muscle. Hypoxia of the muscle might damage the muscle cell membrane, with a resultant loss of myoglobin.

According to this interpretation, the appearance of myoglobin in plasma following massage is a sign of the pathological process. It is not suggested that the presence of myoglobin gives rise to pairs or that the benefit of massage is related to its removal. The pain is considered to result from tissue aches, and massage works by allowing restoration of normal tissue blood supply.

In the five subjects in this study for whom treatment did not succeed in reducing muscle tension and pain, no increase in myoglobin was seen following massage, suggesting that these patients were suffering from a different muscle disease. If the above interpretation of the role of ischaeniia in myofascial pain is correct, this suggests that ischaemia was neither the cause nor the result of the muscle tension and pain in this group of patents.

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