title: Cortical muscle coupling in Parkinson's disease (PD) bradykinesia.
abstract: OBJECTIVE
  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, approximately 10 Hz, which is pathologically increased in PD, and a approximately 30 Hz peak which is decreased in PD, and influenced by pharmacological manipulation of GABAA receptors in normal subjects.
  
  
  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 approximately 10 Hz coupling and reduced approximately 30 Hz coupling that was erratically reversed with L-dopa.
  
  
  CONCLUSIONS
  These results suggest that lower approximately 10 Hz peak may represent pathological oscillations within the basal ganglia which may be a contributing factor to bradykinesia in PD.
authors.affiliation: Pacific Parkinson's Research Centre, University of British Columbia, University Hospital, Vancouver, Canada. mmckeown@interchange.ubc.ca
authors.forename: M J
authors.initials: MJ
authors.lastname: McKeown
authors.forename: S J
authors.initials: SJ
authors.lastname: Palmer
authors.forename: W L
authors.initials: WL
authors.lastname: Au
authors.forename: R G
authors.initials: RG
authors.lastname: McCaig
authors.forename: R
authors.initials: R
authors.lastname: Saab
authors.forename: R
authors.initials: R
authors.lastname: Abu-Gharbieh
mesh_terms: D000978:Antiparkinson Agents / Q000627:therapeutic use; D003625:Data Collection; D004569:Electroencephalography; D004576:Electromyography; D006801:Humans; D018476:Hypokinesia / Q000503:physiopathology*; D007980:Levodopa / Q000627:therapeutic use; D009044:Motor Cortex / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology*; D010300:Parkinson Disease / Q000503:physiopathology*; D011597:Psychomotor Performance / Q000502:physiology
chemical_list: D000978:Antiparkinson Agents; D007980:Levodopa