title: Conventional and kilohertz-frequency spinal cord stimulation produces intensity- and frequency-dependent inhibition of mechanical hypersensitivity in a rat model of neuropathic pain.
abstract: BACKGROUND
  Spinal cord stimulation (SCS) is a useful neuromodulatory technique for treatment of certain neuropathic pain conditions. However, the optimal stimulation parameters remain unclear.
  
  
  METHODS
  In rats after L5 spinal nerve ligation, the authors compared the inhibitory effects on mechanical hypersensitivity from bipolar SCS of different intensities (20, 40, and 80% motor threshold) and frequencies (50, 1 kHz, and 10 kHz). The authors then compared the effects of 1 and 50 Hz dorsal column stimulation at high- and low-stimulus intensities on conduction properties of afferent Aα/β-fibers and spinal wide-dynamic-range neuronal excitability.
  
  
  RESULTS
  Three consecutive daily SCS at different frequencies progressively inhibited mechanical hypersensitivity in an intensity-dependent manner. At 80% motor threshold, the ipsilateral paw withdrawal threshold (% preinjury) increased significantly from pre-SCS measures, beginning with the first day of SCS at the frequencies of 1 kHz (50.2 ± 5.7% from 23.9 ± 2.6%, n = 19, mean ± SEM) and 10 kHz (50.8 ± 4.4% from 27.9 ± 2.3%, n = 17), whereas it was significantly increased beginning on the second day in the 50 Hz group (38.9 ± 4.6% from 23.8 ± 2.1%, n = 17). At high intensity, both 1 and 50 Hz dorsal column stimulation reduced Aα/β-compound action potential size recorded at the sciatic nerve, but only 1 kHz stimulation was partially effective at the lower intensity. The number of actions potentials in C-fiber component of wide-dynamic-range neuronal response to windup-inducing stimulation was significantly decreased after 50 Hz (147.4 ± 23.6 from 228.1 ± 39.0, n = 13), but not 1 kHz (n = 15), dorsal column stimulation.
  
  
  CONCLUSIONS
  Kilohertz SCS attenuated mechanical hypersensitivity in a time course and amplitude that differed from conventional 50 Hz SCS, and may involve different peripheral and spinal segmental mechanisms.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
authors.forename: Ronen
authors.initials: R
authors.lastname: Shechter
authors.forename: Fei
authors.initials: F
authors.lastname: Yang
authors.forename: Qian
authors.initials: Q
authors.lastname: Xu
authors.forename: Yong-Kwan
authors.initials: YK
authors.lastname: Cheong
authors.forename: Shao-Qiu
authors.initials: SQ
authors.lastname: He
authors.forename: Andrei
authors.initials: A
authors.lastname: Sdrulla
authors.forename: Alene F
authors.initials: AF
authors.lastname: Carteret
authors.forename: Paul W
authors.initials: PW
authors.lastname: Wacnik
authors.forename: Xinzhong
authors.initials: X
authors.lastname: Dong
authors.forename: Richard A
authors.initials: RA
authors.lastname: Meyer
authors.forename: Srinivasa N
authors.initials: SN
authors.lastname: Raja
authors.forename: Yun
authors.initials: Y
authors.lastname: Guan
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D009437:Neuralgia / Q000628:therapy*; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000503:physiopathology*; D062187:Spinal Cord Stimulation / Q000379:methods*