title: Comparison of intensity-dependent inhibition of spinal wide-dynamic range neurons by dorsal column and peripheral nerve stimulation in a rat model of neuropathic pain.
abstract: BACKGROUND
  Spinal cord stimulation (SCS) and peripheral nerve stimulation (PNS) are thought to reduce pain by activating a sufficient number of large myelinated (Aβ) fibres, which in turn initiate spinal segmental mechanisms of analgesia. However, the volume of neuronal activity and how this activity is associated with different treatment targets is unclear under neuropathic pain conditions.
  
  
  METHODS
  We sought to delineate the intensity-dependent mechanisms of SCS and PNS analgesia by in vivo extracellular recordings from spinal wide-dynamic range neurons in nerve-injured rats. To mimic therapeutic SCS and PNS, we used bipolar needle electrodes and platinum hook electrodes to stimulate the dorsal column and the tibial nerve, respectively. Compound action potentials were recorded to calibrate the amplitude of conditioning stimulation required to activate A-fibres and thus titrate the volume of activation.
  
  
  RESULTS
  Dorsal column stimulation (50 Hz, five intensities) inhibited the windup (a short form of neuronal sensitization) and the C-component response of wide-dynamic range neurons to graded intracutaneous electrical stimuli in an intensity-dependent manner. Tibial nerve stimulation (50 Hz, three intensities) also suppressed the windup in an intensity-dependent fashion but did not affect the acute C-component response.
  
  
  CONCLUSIONS
  SCS and PNS may offer similar inhibition of short-term neuronal sensitization. However, only SCS attenuates spinal transmission of acute noxious inputs under neuropathic pain conditions. Our findings begin to differentiate peripheral from spinal-targeted neuromodulation therapies and may help to select the best stimulation target and optimum therapeutic intensity for pain treatment.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, School of Medicine, Johns Hopkins University, Baltimore, USA.
authors.forename: F
authors.initials: F
authors.lastname: Yang
authors.forename: Q
authors.initials: Q
authors.lastname: Xu
authors.forename: Y-K
authors.initials: YK
authors.lastname: Cheong
authors.forename: R
authors.initials: R
authors.lastname: Shechter
authors.forename: A
authors.initials: A
authors.lastname: Sdrulla
authors.forename: S-Q
authors.initials: SQ
authors.lastname: He
authors.forename: V
authors.initials: V
authors.lastname: Tiwari
authors.forename: X
authors.initials: X
authors.lastname: Dong
authors.forename: P W
authors.initials: PW
authors.lastname: Wacnik
authors.forename: R
authors.initials: R
authors.lastname: Meyer
authors.forename: S N
authors.initials: SN
authors.lastname: Raja
authors.forename: Y
authors.initials: Y
authors.lastname: Guan
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000698:Analgesia / Q000379:methods; D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D009437:Neuralgia / Q000628:therapy*; D009474:Neurons / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D059408:Pain Management; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000503:physiopathology*; D062187:Spinal Cord Stimulation / Q000379:methods; D004561:Transcutaneous Electric Nerve Stimulation / Q000379:methods