title: Deficient "sensory" beta synchronization in Parkinson's disease.
abstract: OBJECTIVE
  Beta rhythm movement-related synchronization (beta synchronization) reflects motor cortex deactivation and sensory afference processing. In Parkinson's disease (PD), decreased beta synchronization after active movement reflects abnormal motor cortex idling and may be involved in the pathophysiology of akinesia. The objectives of the present study were to (i) compare event-related synchronization after active and passive movement and electrical nerve stimulation in PD patients and healthy, age-matched volunteers and (ii) evaluate the effect of levodopa.
  
  
  METHODS
  Using a 128-electrode EEG system, we studied beta synchronization after active and passive index finger movement and electrical median nerve stimulation in 13 patients and 12 control subjects. Patients were recorded before and after 150% of their usual morning dose of levodopa.
  
  
  RESULTS
  The peak beta synchronization magnitude in the contralateral primary sensorimotor (PSM) cortex was significantly lower in PD patients after active movement, passive movement and electrical median nerve stimulation, compared with controls. Levodopa partially reversed the drop in beta synchronization after active movement but not after passive movement or electrical median nerve stimulation.
  
  
  CONCLUSIONS
  If one considers that beta synchronization reflects sensory processing, our results suggest that integration of somaesthetic afferences in the PSM cortex is abnormal in PD during active and passive movement execution and after simple electrical median nerve stimulation.
  
  
  CONCLUSIONS
  Better understanding of the mechanisms involved in the deficient beta synchronization observed here could prompt the development of new therapeutic approaches aimed at strengthening defective processes. The lack of full beta synchronization restoration by levodopa might be related to the involvement of non-dopaminergic pathways.
authors.affiliation: Department of Neurology, EA2683, Lille University Hospital, France.
authors.forename: A
authors.initials: A
authors.lastname: Degardin
authors.forename: E
authors.initials: E
authors.lastname: Houdayer
authors.forename: J-L
authors.initials: JL
authors.lastname: Bourriez
authors.forename: A
authors.initials: A
authors.lastname: Destée
authors.forename: L
authors.initials: L
authors.lastname: Defebvre
authors.forename: P
authors.initials: P
authors.lastname: Derambure
authors.forename: D
authors.initials: D
authors.lastname: Devos
mesh_terms: D000344:Afferent Pathways / Q000502:physiology; D000368:Aged; D000978:Antiparkinson Agents / Q000494:pharmacology; D001611:Beta Rhythm / Q000187:drug effects*; D003344:Cortical Synchronization / Q000187:drug effects*; D004185:Disability Evaluation; D004558:Electric Stimulation; D004569:Electroencephalography / Q000379:methods; D005260:Female; D006801:Humans; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D009044:Motor Cortex / Q000187:drug effects / Q000503:physiopathology*; D009068:Movement / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways / Q000503:physiopathology; D009460:Neurologic Examination; D010300:Parkinson Disease / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D010525:Peripheral Nerves / Q000502:physiology; D011237:Predictive Value of Tests; D012677:Sensation / Q000187:drug effects / Q000502:physiology*
chemical_list: D000978:Antiparkinson Agents; D007980:Levodopa