Abstract
Research on isometric contractions in subjects with Parkinson's disease (PD) has shown that anti-parkinsonian medication results in a greater increase in extensor strength than flexor strength. This finding is consistent with the hypothesis that there is a greater impairment in neural activation of extensor muscles as compared to flexor muscles in subjects with PD. Such a hypothesis is physiologically feasible given the known differences in the neural control of flexor and extensor muscles. If the above hypothesis is true for both phasic and tonic muscle activation, then differences between performance of rapid single-joint flexion and extension movements should exist in subjects with PD. Twelve subjects with PD, "off" and "on" medication, and 12 age-and sex-matched healthy control subjects performed rapid single-joint movements in flexion and extension over three distances. For neurologically healthy subjects, we did not identify any significant differences in either kinematic or EMG parameters between flexion and extension movements. In contrast, in the PD subjects extension movements were slower and associated with more agonist bursts when compared to flexion movements. The results are consistent with the hypothesis that there is a differential impairment of neural activation of extensor muscles of the arm as compared to flexor muscles in subjects with PD.
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