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Introduction: The purpose of this study was to compare agonist and antagonist electromyography (EMG) during an isokinetic fatigue protocol in subjects with cerebral palsy (CP) and typical development (TD).Methods: Nine individuals with CP and 11 with TD completed 50 repetitions of maximum concentric knee extensions (KE) and flexions (KF) at 60°/second.Results: Rate of decline in peak torque for KE was significantly less in CP compared with TD. Rate of decline in agonist EMG was not significantly different between groups, but the rate of decline in antagonist EMG was significantly greater in CP. There were no differences between groups for KF.Conclusions: Declining agonist EMG occurred in parallel with declining antagonist hamstring activity in CP, decreasing the relative opposing force and resulting in a lesser decline in net torque. This finding illustrates a potential mechanism by which net torque is preserved in those with CP who are inherently weaker. [ABSTRACT FROM AUTHOR]

Introduction: In this study of spastic hemiparesis we evaluated cocontraction during sustained agonist/antagonist efforts, before and after botulinum toxin (BoNT) injection in 1 agonist. Methods: Nineteen hemiparetic subjects performed maximal isometric elbow flexion/extension efforts with the elbow at 100° (extensors stretched). Using flexor and extensor surface electromyography we calculated agonist recruitment/cocontraction indices from 500-ms peak voluntary agonist recruitment, before and 1 month after onabotulinumtoxinA injection (160 U) into biceps brachii. Results: Before injection, agonist recruitment and cocontraction indices were higher in extensors than flexors [0.74 ± 0.15 vs. 0.59 ± 0.10 ( P < 0.01) and 0.43 ± 0.25 vs. 0.25 ± 0.13 ( P < 0.05), respectively]. Biceps injection decreased extensor cocontraction index (−35%, P < 0.05) while increasing flexor agonist recruitment and cocontraction indices. Conclusions: In spastic hemiparesis, stretch may facilitate agonist recruitment and spastic cocontraction. In the non-injected antagonist, cocontraction may be reduced by enhanced reciprocal inhibition from a more relaxed, and therefore stretched, agonist, or through decreased recurrent inhibition from the injected muscle. Muscle Nerve, 2012 [ABSTRACT FROM AUTHOR]