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

TitleCortical muscle coupling in Parkinson's disease (PD) bradykinesia
Publication TypeJournal Article
Year of Publication2006
AuthorsMcKeown, M. J., S. J. Palmer, W. L. Au, R. G. McCaig, R. Saab, and R. Abu-Gharbieh
JournalJournal of Neural Transmission-Supplement
Pagination31–40
ISSN0303-6995
Abstract

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, similar to 10 Hz, which is pathologically increased in PD, and a similar to 30 Hz peak which is decreased in PD, and influenced by pharmacological manipulation of GABA(A) 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 similar to 10 Hz coupling and reduced -30 Hz coupling that was erratically reversed with L-dopa. Conclusions: These results suggest that lower similar to 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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