Central motor control failure in fibromyalgia: a surface electromyography study.

Fibromyalgia (FM) is characterised by diffuse musculoskeletal pain and stiffness at multiple sites, tender points in characteristic locations, and the frequent presence of symptoms such as fatigue. The aim of this study was to assess whether the myoelectrical manifestations of fatigue in patients affected by FM are central or peripheral in origin.Eight female patients aged 55.6 +/- 13.6 years (FM group) and eight healthy female volunteers aged 50.3 +/- 9.3 years (MCG) were studied by means of non-invasive surface electromyography (s-EMG) involving a linear array of 16 electrodes placed on the skin overlying the biceps brachii muscle, with muscle fatigue being evoked by means of voluntary and involuntary (electrically elicited) contractions. Maximal voluntary contractions (MVCs), motor unit action potential conduction velocity distributions (mean +/- SD and skewness), and the mean power frequency of the spectrum (MNF) were estimated in order to assess whether there were any significant differences between the two groups and contraction types.The motor pattern of recruitment during voluntary contractions was altered in the FM patients, who also showed fewer myoelectrical manifestations of fatigue (normalised conduction velocity rate of changes: -0.074 +/- 0.052\%/s in FM vs -0.196 +/- 0.133\%/s in MCG; normalised MNF rate of changes: -0.29 +/- 0.16\%/s in FM vs -0.66 +/- 0.34\%/s in MCG). Mean conduction velocity distribution and skewnesses values were higher (p < 0.01) in the FM group. There were no between-group differences in the results obtained from the electrically elicited contractions.The apparent paradox of fewer myoelectrical manifestations of fatigue in FM is the electrophysiological expression of muscle remodelling in terms of the prevalence of slow conducting fatigue-resistant type I fibres. As the only between-group differences concerned voluntary contractions, they are probably more related to central motor control failure than muscle membrane alterations, which suggests pathological muscle fibre remodelling related to altered suprasegmental control.