There is controversy about the use of electrical stimulation in muscular dystrophy. The muscular dystrophy reference list includes publications that are clinically relevant to the improvement of muscle performance. The chronological order reveals the 1979-1981 enthusiasm for the Luthert, Vrbova and Wards’ work [10 Hz, 30 min, 6 times/day for 14 days] in dystrophic mouse leg muscles. The authors reported that “clinical use of the leg was improved” and tension developed by ES was greater. Not only were oxidative enzymes increased in the stimulated muscles but there were more muscle fibers than in the un-stimulated muscles. In the next few years, Vrbova reported that “low frequency” ES changed passive membrane properties of dystrophic muscle to “normal” and suggested that ES induced maturation of dystrophic muscle fibers. In 1989 Dangain and Vrbova reported that the changes induced by ES in dystrophic mouse muscle were not permanent.
The few clinical studies reported between 1986 and 1993 involved small sample sizes and the abstracts do not give enough information to allow a thorough evaluation of the outcomes. Scott, Vrbova and Zupan did report “significant” improvements in the muscle groups studied after lengthy ES protocols [ie 9 months] but no values were given for the isometric efforts. Edwards reported that longitudinal follow-up demonstrated no change in the disease process. The discussion of resection of the Achilles’ tendon in combination with ES of the ankle dorsiflexors would have no clinical application.
Of particular interest, none of the abstracts reported actual torque values or addressed the differences between a “statistically significant” change in muscle force and clinically useful improvement in muscle force or performance. For example, if the improvement was from a Trace [1/5] manual muscle test [MMT] equivalent to a Poor [2/5] that would reflect a change from 1 to 5% of expected force production. A change from Poor to Fair [3/5] would represent improvement of 10% to 15% of expected force production. A change from Fair to Good [4/5] would represent approximately 25% improvement and unless the Good MMT equivalent contraction could be repeated over enough repetitions to address function, it would not be clinically useful for function such as walking.
The Yoshida report in 1997 does raise the question of safety of ES in dystrophic muscle. If ES induces “excessive calcium accumulation in muscle fibers” and this does lead to premature degeneration with ES induced tetanic contractions, it would appear that ES may not only be of minimal to no clinical value but could be contraindicated.
Based upon this review, it appears that the jury is out in regard to this limited body of research. Some animal studies report increased force and number of mature fibers in dystrophic muscle. One study reports increased muscle fiber degeneration with tetanic ES. The clinical studies listed can be counted on one hand and statistical improvements in “strength” or “torque” may be academically encouraging but not related to the functional demands that must be met to stand, transfer and walk.
Contributor: J.M. Campbell, Ph.D., P.T., 2002
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