title: Functional reorganization of sensorimotor cortex in early Parkinson disease.
abstract: OBJECTIVE
  Compensatory reorganization of the nigrostriatal system is thought to delay the onset of symptoms in early Parkinson disease (PD). Here we sought evidence that compensation may be a part of a more widespread functional reorganization in sensorimotor networks, including primary motor cortex.
  
  
  METHODS
  Several neurophysiologic measures known to be abnormal in the motor cortex (M1) of patients with advanced PD were tested on the more and less affected side of 16 newly diagnosed and drug-naive patients with PD and compared with 16 age-matched healthy participants. LTP-like effects were probed using a paired associative stimulation protocol. We also measured short interval intracortical inhibition, intracortical facilitation, cortical silent period, and input/output curves.
  
  
  RESULTS
  The less affected side in patients with PD had preserved intracortical inhibition and a larger response to the plasticity protocol compared to healthy participants. On the more affected side, there was no response to the plasticity protocol and inhibition was reduced. There was no difference in input/output curves between sides or between patients with PD and healthy participants.
  
  
  CONCLUSIONS
  Increased motor cortical plasticity on the less affected side is consistent with a functional reorganization of sensorimotor cortex and may represent a compensatory change that contributes to delaying onset of clinical symptoms. Alternatively, it may reflect a maladaptive plasticity that provokes symptom onset. Plasticity deteriorates as the symptoms progress, as seen on the more affected side. The rate of change in paired associative stimulation response over time could be developed into a surrogate marker of disease progression in PD.
authors.affiliation: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, UK.
authors.forename: M
authors.initials: M
authors.lastname: Kojovic
authors.forename: M
authors.initials: M
authors.lastname: Bologna
authors.forename: P
authors.initials: P
authors.lastname: Kassavetis
authors.forename: N
authors.initials: N
authors.lastname: Murase
authors.forename: F J
authors.initials: FJ
authors.lastname: Palomar
authors.forename: A
authors.initials: A
authors.lastname: Berardelli
authors.forename: J C
authors.initials: JC
authors.lastname: Rothwell
authors.forename: M J
authors.initials: MJ
authors.lastname: Edwards
authors.forename: K P
authors.initials: KP
authors.lastname: Bhatia
mesh_terms: D000328:Adult; D000368:Aged; D003342:Corpus Striatum / Q000503:physiopathology; D004292:Dominance, Cerebral / Q000502:physiology; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D006801:Humans; D007537:Isometric Contraction / Q000502:physiology; D017774:Long-Term Potentiation / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000503:physiopathology*; D009415:Nerve Net / Q000503:physiopathology; D009433:Neural Inhibition / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D010153:Paired-Associate Learning / Q000502:physiology; D010300:Parkinson Disease / Q000175:diagnosis* / Q000503:physiopathology*; D011712:Pyramidal Tracts / Q000503:physiopathology; D011930:Reaction Time / Q000502:physiology; D012016:Reference Values; D012684:Sensory Thresholds / Q000502:physiology; D013003:Somatosensory Cortex / Q000503:physiopathology*; D013378:Substantia Nigra / Q000503:physiopathology