Wireless peripheral nerve stimulation increases pain threshold in two neuropathic rat models

Rosellini, Will; Casavant, Reema; Beall, Patrick; Pierce, David M.; Jain, Ravi; Dougherty, Patrick M.

doi:10.1016/j.expneurol.2012.03.016

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…When pharmacological therapies fail to relieve chronic pain, or side effects associated with these therapies substantially impair quality of life, spinal cord stimulation (SCS) or peripheral nerve stimulation (PNS) are considered as alternative strategies for pain management (Long et al, 1981; Weiner, 2003; Kumar et al, 2008). SCS and PNS with parameters similar to those used in the clinic (e.g., 50–60 Hz, 0.2 ms) attenuate behavioural hypersensitivity to mechanical and thermal stimuli in nerve-injured rats (Maeda et al, 2008; Yang et al, 2011; Rosellini et al, 2012). In addition to initiating a feed forward inhibition of spinal nociceptive transmission (Melzack and Wall, 1965), synchronized electrical stimulation may also induce inhibitory postsynaptic potentials in dorsal horn neurons (Foreman et al, 1976; Narikawa et al, 2000), facilitate primary afferent depolarization to elicit presynaptic inhibition of incoming afferent inputs, activate descending pain modulation (Barchini et al, 2012; Song et al, 2013) and change afferent conduction properties (Campbell, 1981; Shechter et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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

Yang

Cheong

et al. 2014

European Journal of Pain

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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.

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Section: Introductionmentioning

confidence: 99%

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

Yang

Cheong

et al. 2014

European Journal of Pain

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“…Mechanisms engaged by lower stimulation at Aβ fiber strength in chronic pain models have not been studied. Although preliminary research has been done to investigate the effects of PNS on chronic models of pain , no animal model of SQS exists, and definitive mechanisms for pain relief are unknown.…”

Section: Introductionmentioning

confidence: 99%

Differential Effects of Subcutaneous Electrical Stimulation (SQS) and Transcutaneous Electrical Nerve Stimulation (TENS) in Rodent Models of Chronic Neuropathic or Inflammatory Pain

Vera–Portocarrero

Cordero

Billstrom

et al. 2013

Neuromodulation: Technology at the Neural Interface

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“…In agreement with these findings, PNS at 40–100 Hz and low density showed its strong ability to relieve multiple types of pain in the clinic; 10 – 12 meanwhile, 50 Hz PNS attenuated behavioral hypersensitivity to mechanical and thermal stimuli in nerve-injured rats. 26 In this study, the effect of PNS at >120 Hz was not explored because at that frequency it may induce reversible movement dysfunction resulting from motor nerve damage. Secondly, intrathecal administration of Arc shRNA inhibited the anti-nociceptive effect of PNS.…”

Section: Discussionmentioning

confidence: 99%

“… 34 Therefore, there is a possibility that SCS and DRGS could relieve pain by inducing Arc expression and decreasing AMPAR expression, which will be explored in future research. With the development of advanced techniques, including voltage-controlled capacitive discharge enabling wireless neuromodulation 26 and less-invasive ultrasound-guided implantation technique, 35 neuromodulation could be expanded in clinic.…”

Section: Discussionmentioning

confidence: 99%

Electrical peripheral nerve stimulation relieves bone cancer pain by inducing Arc protein expression in the spinal cord dorsal horn

Sun

Feng

Liu

et al. 2018

JPR

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ObjectiveThe analgesic effect on chronic pain of peripheral nerve stimulation (PNS) has been proven, but its underlying mechanism remains unknown. Therefore, this study aimed to assess the analgesic effect of PNS on bone cancer pain in a rat model and to explore the underlying mechanism.Materials and methodsPNS on sciatic nerves with bipolar electrode was performed in both naïve and bone cancer pain model rats. Then, the protein levels of activity-regulated cytoskeleton-associated protein (Arc), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid–type glutamate receptor 1 (GluA1), and phosphate N-methyl-d-aspartic acid-type glutamate receptor subunit 2B (pGluNR2B) in spinal cord were evaluated by immunohistochemistry and Western blotting. Thermal paw withdraw latency and mechanical paw withdraw threshold were used to estimate the analgesic effect of PNS on bone cancer pain. Intrathecal administration of Arc shRNA was used to inhibit Arc expression in the spinal cord.ResultsPNS at 60 and 120 Hz for 20 min overtly induced Arc expression in the spinal cord, increased thermal pain thresholds in naïve rats, and relieved bone cancer pain; meanwhile, 10 Hz PNS did not achieve those results. In addition, PNS at 60 and 120 Hz also reduced the expression of GluA1, but not pGluNR2B, in the spinal cord. Finally, the anti-nociceptive effect and GluA1 downregulation induced by PNS were inhibited by intrathecal administration of Arc shRNA.ConclusionPNS (60 Hz, 0.3 mA) can relieve bone-cancer-induced allodynia and hyperalgesia by upregulating Arc protein expression and then by decreasing GluA1 transcription in the spinal cord dorsal horn.

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Wireless peripheral nerve stimulation increases pain threshold in two neuropathic rat models

Cited by 6 publications

References 22 publications

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

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

Differential Effects of Subcutaneous Electrical Stimulation (SQS) and Transcutaneous Electrical Nerve Stimulation (TENS) in Rodent Models of Chronic Neuropathic or Inflammatory Pain

Electrical peripheral nerve stimulation relieves bone cancer pain by inducing Arc protein expression in the spinal cord dorsal horn

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