A theoretical basis for assessing muscle dysfunction due to sprain/strain injuries is presented. We propose that muscle tissue trauma results in an alteration in the patterns of neural recruitment, a reduction in the force-generating capability of the injured muscle, and/or pain sensations. Furthermore, a lower than normal recruitment of motoneuron pools in the injured area can result in elevated recruitment levels from compensating motoneuron pools for a given motor task. It is proposed that these changes in motoneuron recruitment can be readily apparent in the ratios of EMG amplitudes among multiple pairs of muscles associated kinesiologically with the affected muscle. Chronic compensating actions, such as those resulting from faulty neural feedback of the force-length-velocity relationships for a stretched tendon or muscle unit, could cause further injuries. It is proposed that consistent and valid measures of ratios of EMG amplitudes between many muscle pairs acquired for well-defined motor tasks can be used to facilitate diagnoses and direct treatment strategies for sprain/strain injuries and pain.
Department of Physiological Sciences, University of California at Los Angeles, Los Angeles, CA 90095-1527; Department of Rehabilitation Medicine, Emory University School of Medicine, Atlanta, GA 30322; Brain Research Institute, University of California at Los Angeles, Los Angeles, CA 90095-1761; and Myo Diagnostics Inc., Culver City, CA 90232
Submitted for publication March 1995.
Accepted for publication February 1996.
The authors thank H. Bud Clark for his assistance in preparing the figures.
Funding for the development of this theory and the associated clinical studies was provided by Myo Diagnostics, Inc., and Daniel J. Levendowski is the Director of Research.
Address for correspondence: Daniel J. Levendowski, B.S., Director of Research, Myo Diagnostics Inc., 3710 S. Robertson Blvd., Suite 212, Culver City, CA 90232.