The Appropriate Use of Neurostimulation: New and Evolving Neurostimulation Therapies and Applicable Treatment for Chronic Pain and Selected Disease States

Deer, Timothy R.; Krames, Elliot S.; Mekhail, Nagy; Pope, Jason E.; Leong, Michael S.; Stanton‐Hicks, Michael; Golovac, Stan; Kapural, Leo; Alo, Ken; Anderson, Jack; Foreman, Robert D.; Caraway, David; Narouze, Samer; Linderoth, Bengt; Buvanendran, Asokumar; Feler, Claudio A.; Poree, Lawrence; Lynch, Paul; McJunkin, Tory; Swing, Edward L.; Staats, Peter S.; Liem, Liong; Williams, Kayode

doi:10.1111/ner.12204

Cited by 106 publications

(94 citation statements)

References 245 publications

(248 reference statements)

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“…14,15,30,32,42 Moreover, the inhibition of C-LFP and neuropathic pain behavior by SCS is brief and diminishes quickly after stimulation. Previous findings suggested that SCS inhibits pain through multiple neurochemical mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Activation of cannabinoid CB1 receptor contributes to suppression of spinal nociceptive transmission and inhibition of mechanical hypersensitivity by Aβ-fiber stimulation

Yang¹,

Shu

et al. 2016

Pain

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Activation of Aβ-fibers by is an intrinsic feature of spinal cord stimulation (SCS) pain therapy. Cannabinoid receptor type 1 (CB1) is important to neuronal plasticity and pain modulation, but its role in SCS-induced pain inhibition remains unclear. Here, we showed that CB1 receptors are expressed in both excitatory and inhibitory interneurons in substantia gelatinosa (SG). Patch-clamp recording of the evoked excitatory postsynaptic currents (eEPSCs) in mice after spinal nerve ligation (SNL) showed that electrical stimulation of Aβ-fibers (Aβ-ES) using clinical SCS-like parameters (50 Hz, 0.2 millisecond, 10 μA) induced prolonged depression of eEPSCs to C-fiber inputs in SG neurons. Pretreatment with CB1 receptor antagonist AM251 (2μM) reduced the inhibition of C-eEPSCs by Aβ-ES in both excitatory and inhibitory SG neurons. We further determined the net effect of Aβ-ES on spinal nociceptive transmission in vivo by recording spinal local field potential (LFP) in SNL rats. Epidural SCS (50 Hz, Aβ-plateau, 5 minutes) attenuated C-fiber-evoked LFP. This effect of SCS was partially reduced by spinal topical application of AM251 (25 μg, 50 μl), but not CB2 receptor antagonist AM630 (100 μg). Finally, intrathecal pretreatment with AM251 (50 μg, 15 μl) in SNL rats blocked the inhibition of behavioral mechanical hypersensitivity by SCS (50 Hz, 0.2 millisecond; 80% of motor threshold, 60 minutes). Our findings suggest that activation of spinal CB1 receptors may contribute to synaptic depression to high-threshold afferent inputs in SG neurons after Aβ-ES and may be involved in SCS-induced inhibition of spinal nociceptive transmission after nerve injury.

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Section: Discussionmentioning

confidence: 99%

Activation of cannabinoid CB1 receptor contributes to suppression of spinal nociceptive transmission and inhibition of mechanical hypersensitivity by Aβ-fiber stimulation

Yang¹,

Shu

et al. 2016

Pain

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“…Traditional SCS produces tonic waveforms in which pulses are delivered at a consistent frequency, pulse width, and amplitude. New technological developments using alternate waveforms to stimulate the dorsal column and/or aim at new stimulation targets show promising results [2]. Burst stimulation, in particular, is a waveform that delivers groups of pulses at a high frequency and at amplitudes much lower than tonic stimulation; these groups of pulses are separated by a pulse-free period called an interburst interval during which passive repolarization occurs prior to the next burst.…”

Section: Introductionmentioning

confidence: 99%

Tonic and burst spinal cord stimulation waveforms for the treatment of chronic, intractable pain: study protocol for a randomized controlled trial

Slavin

North

Deer³

et al. 2016

Trials

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BackgroundBurst stimulation is a novel form of neurostimulation for the treatment of chronic pain which has demonstrated promise in small uncontrolled studies, but has not yet gained approval for use in the U.S. We report the study methods for an ongoing multicenter, randomized, controlled, cross-over study designed to gain United States Food and Drug Administration (FDA) approval for burst stimulation.MethodsParticipants who are candidates for a currently approved neurostimulation device were enrolled and screened. Participants who fail a tonic trial evaluation, have significant depressive symptoms, or evidence lack of compliance with study procedures by failing to complete 7 days of a Pain Diary are excluded. Participants receiving a permanent implant are randomized to receive: (1) 12 weeks of tonic followed by 12 weeks of burst stimulation or (2) 12 weeks of burst stimulation followed by 12 weeks of tonic stimulation. Assessments occur at 6, 12, 18, and 24 weeks. After 24 weeks, participants choose their preferred therapy and are assessed every 6 months for up to 2 years. All patients had the device leads inserted at the site of a successful tonic stimulation trial. Assessments include: a Pain Diary using a Visual Analog Scale (VAS) for overall, trunk, and limb pain, the Beck Depression Inventory, the Pain Catastrophizing Scale, the Oswestry Disability Index, paresthesia, satisfaction, and therapy preference. Reported adverse events are collected throughout the study. The primary endpoint is the noninferiority of burst stimulation compared to tonic measured by the within-subject difference in the mean overall VAS score at the end of each 12-week stimulation period.DiscussionThis trial represents the largest controlled trial of burst stimulation to date, and is expected to yield important information regarding the safety and efficacy of burst stimulation.Trial registrationClinicalTrials.gov, NCT02011893. Registered on 10 December 2013.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-016-1706-5) contains supplementary material, which is available to authorized users.

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“…Device-related FDA approvals have been performed largely by the acquisition of level 1 data, regarded as the most robust and scientifically valid evidence available [4][5][6]. Understandably, it is the foremost position of the FDA to approve products that have proven efficacy and safety and to protect the public while allowing access to the best care possible and innovation.…”

Section: The Drg Storymentioning

confidence: 99%

Dorsal root ganglion stimulation approval by the Food and Drug Administration: advice on evolving the process

Deer

Pope²

2016

Expert Review of Neurotherapeutics

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The Appropriate Use of Neurostimulation: New and Evolving Neurostimulation Therapies and Applicable Treatment for Chronic Pain and Selected Disease States

Cited by 106 publications

References 245 publications

Activation of cannabinoid CB1 receptor contributes to suppression of spinal nociceptive transmission and inhibition of mechanical hypersensitivity by Aβ-fiber stimulation

Activation of cannabinoid CB1 receptor contributes to suppression of spinal nociceptive transmission and inhibition of mechanical hypersensitivity by Aβ-fiber stimulation

Tonic and burst spinal cord stimulation waveforms for the treatment of chronic, intractable pain: study protocol for a randomized controlled trial

Dorsal root ganglion stimulation approval by the Food and Drug Administration: advice on evolving the process

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