title: Subthalamic deep brain stimulation at individualized frequencies for Parkinson disease.
abstract: OBJECTIVE
  The oscillation model of Parkinson disease (PD) states that, in the subthalamic nucleus (STN), increased θ (4-10 Hz) and β (11-30 Hz) frequencies were associated with worsening whereas γ frequencies (31-100 Hz) were associated with improvement of motor symptoms. However, the peak STN frequency in each band varied widely from subject to subject. We hypothesized that STN deep brain stimulation (DBS) at individualized γ frequencies would improve whereas θ or β frequencies would worsen PD motor signs.
  
  
  METHODS
  We prospectively studied 13 patients with PD. STN local field potential (LFP) was recorded after electrode implantations, in the OFF and then in ON dopaminergic medication states while patients performed wrist movements. Six individual peak frequencies of the STN LFP power spectra were obtained: the greatest decrease in θ and β and greatest increase in γ frequencies in the ON state (MED) and during movements (MOVE). Eight DBS frequencies were applied including 6 MED and MOVE frequencies, high frequency (HF) used for chronic stimulation, and no stimulation. The patients were assessed using the motor Unified Parkinson's Disease Rating Scale (mUPDRS).
  
  
  RESULTS
  STN DBS at γ frequencies (MED and MOVE) and HF significantly improved mUPDRS scores compared to no stimulation and both γ frequencies were not different from HF. DBS at θ and β frequencies did not worsen mUPDRS scores compared to no stimulation.
  
  
  CONCLUSIONS
  Short-term administration of STN DBS at peak dopamine-dependent or movement-related γ frequencies were as effective as HF for reducing parkinsonian motor signs but DBS at θ and β frequencies did not worsen PD motor signs.
  
  
  METHODS
  This study provides Class III evidence that STN DBS at patient-specific γ frequencies and at usual high frequencies both improved mUPDRS scores compared to no stimulation and did not differ in effect.
authors.affiliation: Division of Brain Imaging & Behaviour Systems–Neuroscience, Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada.
authors.forename: E W
authors.initials: EW
authors.lastname: Tsang
authors.forename: C
authors.initials: C
authors.lastname: Hamani
authors.forename: E
authors.initials: E
authors.lastname: Moro
authors.forename: F
authors.initials: F
authors.lastname: Mazzella
authors.forename: U
authors.initials: U
authors.lastname: Saha
authors.forename: A M
authors.initials: AM
authors.lastname: Lozano
authors.forename: M
authors.initials: M
authors.lastname: Hodaie
authors.forename: R
authors.initials: R
authors.lastname: Chuang
authors.forename: T
authors.initials: T
authors.lastname: Steeves
authors.forename: S Y
authors.initials: SY
authors.lastname: Lim
authors.forename: B
authors.initials: B
authors.lastname: Neagu
authors.forename: R
authors.initials: R
authors.lastname: Chen
mesh_terms: D000328:Adult; D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D046690:Deep Brain Stimulation / Q000379:methods*; D005260:Female; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009068:Movement / Q000502:physiology; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D057285:Precision Medicine; D012642:Selegiline / Q000627:therapeutic use; D020531:Subthalamic Nucleus / Q000503:physiopathology / Q000601:surgery*; D016896:Treatment Outcome
chemical_list: D000978:Antiparkinson Agents; D012642:Selegiline; D007980:Levodopa