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Effect of medication on EMG patterns in individuals with Parkinson's disease

Authors

  • Julie A. Robichaud PT, PhD,

    Corresponding author
    1. School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois, USA
    2. Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA
    • School of Kinesiology (M/C 194), University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608
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  • Kerstin D. Pfann PhD,

    1. School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois, USA
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  • Cynthia L. Comella MD,

    1. Department of Neurological Sciences, Rush Medical Center, Chicago, Illinois, USA
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  • Daniel M. Corcos PhD

    1. School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois, USA
    2. Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA
    3. Department of Neurological Sciences, Rush Medical Center, Chicago, Illinois, USA
    4. Department of Psychology, University of Illinois at Chicago, Chicago, Illinois, USA
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Abstract

Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation. © 2002 Movement Disorder Society

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