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Cortical muscle coupling in Parkinson’s disease (PD) bradykinesia

  • Conference paper
Parkinson’s Disease and Related Disorders

Part of the book series: Journal of Neural Transmission. Supplementa ((NEURALTRANS,volume 70))

Summary

Objectives: To determine if novel methods establishing patterns in EEG-EMG coupling can infer subcortical influences on the motor cortex, and the relationship between these subcortical rhythms and bradykinesia. Background: Previous work has suggested that bradykinesia may be a result of inappropriate oscillatory drive to the muscles. Typically, the signal processing method of coherence is used to infer coupling between a single channel of EEG and a single channel of rectified EMG, which demonstrates 2 peaks during sustained contraction: one, ∼10 Hz, which is pathologically increased in PD, and a ∼30 Hz peak which is decreased in PD, and influenced by pharmacological manipulation of GABAA receptors in normal subjects. Materials and methods: We employed a novel multiperiodic squeezing paradigm which also required simultaneous movements. Seven PD subjects (on and off L-Dopa) and five normal subjects were recruited. Extent of bradykinesia was inferred by reduced relative performance of the higher frequencies of the squeezing paradigm and UPDRS scores. We employed Independent Component Analysis (ICA) and Empirical Mode Decomposition (EMD) to determine EEG/EMG coupling. Results: Corticomuscular coupling was detected during the continually changing force levels. Different components included those over the primary motor cortex (ipsilaterally and contralaterally) and over the midline. Subjects with greater bradykinesia had a tendency towards increased ∼10 Hz coupling and reduced ∼30 Hz coupling that was erratically reversed with L-dopa. Conclusions: These results suggest that lower ∼10 Hz peak may represent pathological oscillations within the basal ganglia which may be a contributing factor to bradykinesia in PD.

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Authors and Affiliations

  1. Pacific Parkinson’s Research Centre, University of British Columbia, Vancouver, Canada

    Dr. M. J. McKeown & W.-L. Au

  2. Brain Research Centre, University of British Columbia, Vancouver, Canada

    Dr. M. J. McKeown & R. Abu-Gharbieh

  3. Department of Medicine (Neurology), University of British Columbia, Vancouver, Canada

    Dr. M. J. McKeown

  4. Program in Neuroscience, University of British Columbia, Vancouver, Canada

    S. J. Palmer

  5. Department of Electrical and Computer Engineering, University of British Columbia, Vancouver, Canada

    R. G. McCaig, R. Saab & R. Abu-Gharbieh

  6. Department of Medicine, Pacific Parkinson’s Research Centre, University of British Columbia, University Hospital, M31, Purcy Pavilion, UBC Site, 2221, Wesbrook Mall, Vancouver, BC, V6T 2B5, Canada

    Dr. M. J. McKeown

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  1. Dr. M. J. McKeown
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  2. S. J. Palmer
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  3. W.-L. Au
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  4. R. G. McCaig
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  5. R. Saab
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  6. R. Abu-Gharbieh
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Editor information

Editors and Affiliations

  1. Klinik und Poliklinik für Psychiatrie und Psychotherapie, Würzburg, Germany

    P. Riederer  & M. Gerlach  & 

  2. Universitätsklinikum der TU Dresden, Dresden, Germany

    H. Reichmann

  3. Israel Institute of Technology, Haifa, Israel

    M. B. H. Youdim

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© 2006 Springer-Verlag

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McKeown, M.J., Palmer, S.J., Au, WL., McCaig, R.G., Saab, R., Abu-Gharbieh, R. (2006). Cortical muscle coupling in Parkinson’s disease (PD) bradykinesia. In: Riederer, P., Reichmann, H., Youdim, M.B.H., Gerlach, M. (eds) Parkinson’s Disease and Related Disorders. Journal of Neural Transmission. Supplementa, vol 70. Springer, Vienna . https://doi.org/10.1007/978-3-211-45295-0_7

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  • DOI: https://doi.org/10.1007/978-3-211-45295-0_7

  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-211-28927-3

  • Online ISBN: 978-3-211-45295-0

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