Is there muscle pathology in fibromyalgia syndrome?

A number of studies have reported abnormalities in the muscles of fibromyalgia patients. The early studies, some of which indicated morphologic abnormalities, had major problems with patient selection and lacked adequate control groups. More recent studies of morphology have shown only nonspecific or mild changes, perhaps consistent with subtle metabolic abnormalities, especially at tender point sites. Studies of muscle metabolism, however, particularly the more rigorous studies using MR spectroscopy, have failed to confirm abnormalities in muscle metabolism, both at tender and nontender point locations. The abnormalities detected in earlier studies appear to have been confounded by subtle metabolic changes resulting from muscle deconditioning. Studies of muscle blood flow also demonstrate abnormalities that can be explained by deconditioning alone. Studies of muscle strength that show differences between patients and controls can be explained by lack of voluntary effort. A popular theory of the genesis of pain in fibromyalgia syndrome was that excessive muscle tension led to increased excitability of nociceptors in muscle leading to muscle hypertension and chronic pain. Furthermore, defective sympathetic control was proposed to result in disturbed microcirculation and nociceptor excitation. In aggregate, however, studies using EMG techniques show no evidence of excessive muscle tension or defective sympathetic nervous function. Therefore, although muscular pain has been a central feature of fibromyalgia syndrome, controlled studies of muscle fail to support a convincing role for muscle in the pathophysiology of the condition. Muscle tenderness in fibromyalgia cannot be explained on the basis of primary muscle abnormalities, either structural or functional. Future pathophysiologic studies in fibromyalgia should focus on central mechanisms.