Is there muscle pathology in fibromyalgia (FM) 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.

Simms RW

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