Pathophysiological mechanisms involved in genesis and spread of muscular tension in occupational muscle pain and in chronic musculoskeletal pain syndromes: a hypothesis.

This paper introduces a pathophysiological model for the cause of muscular tension and pain in occupational pain syndromes and chronic muskuloskeletal pain syndromes, which also might clarify why these conditions have a tendency to perpetuate themselves and spread from one muscle to another. The model can briefly be described as follows. Metabolites produced by (static) muscle contractions stimulate group III and IV muscle afferents, which activate gamma-motoneurones projecting to both homonymous and heteronymous muscles. The gamma-motoneurones influence the stretch sensitivity and discharges of secondary and primary spindle afferents. Increased activity in the primary muscle spindle afferents enhances the muscle stiffness, which leads to further production of metabolites in both homo- and heteronymous muscles. Increased activity in secondary spindle afferents, which project back to the gamma system, constitutes a 'built in' second positive feedback loop which may perpetuate the condition with less 'support' from activity in group III and IV muscle afferents.