Burst and Tonic Spinal Cord Stimulation Differentially Activate GABAergic Mechanisms to Attenuate Pain in a Rat Model of Cervical Radiculopathy

Crosby, Nathan D.; Weisshaar, Christine L.; Smith, Jenell R.; Zeeman, Martha E.; Goodman-Keiser, Melanie D.; Winkelstein, Beth A.

doi:10.1109/tbme.2015.2399374

Cited by 77 publications

(71 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The motor thresholds necessary to evoke contractions of the hind paws of the animals were lower for Burst‐DRGS than Con‐DRGS in our study, albeit not significant. This is in line with preclinical findings that Burst‐SCS requires significantly lower amplitudes to obtain a motor response when compared to Con‐SCS . The latter has important consequences for the stimulation amplitude, which is generally lower with Burst‐SCS when compared to Con‐SCS .…”

Section: Discussionsupporting

confidence: 89%

Dorsal Root Ganglion Stimulation in Experimental Painful Diabetic Peripheral Neuropathy: Burst vs. Conventional Stimulation Paradigm

Franken

Debets

Joosten

2019

Neuromodulation: Technology at the Neural Interface

View full text Add to dashboard Cite

Objectives Painful diabetic peripheral neuropathy (PDPN) is a long‐term complication of diabetes mellitus (DM). Dorsal Root Ganglion Stimulation (DRGS) has recently emerged as a neuromodulation modality in the treatment of chronic neuropathic pain. The objective of this study was to compare the effect of burst DRGS (Burst‐DRGS) and conventional DRGS (Con‐DRGS) in an experimental model of PDPN. Materials and Methods DM was induced in female Sprague–Dawley rats by intraperitoneal injection of streptozotocin (STZ, n = 48). Animals were tested for mechanical hypersensitivity (50% hind paw withdrawal threshold on Von Frey test) before, and 4 weeks after STZ injection. PDPN rats were then implanted with a unilateral bipolar lead at the L5 DRG (n = 22) and were stimulated for 30 min at days 2 and 3 postimplantation. Animals received Con‐DRGS and Burst‐DRGS in a randomized crossover design (n = 10), or received Sham‐DRGS (n = 7) for 30 min, and were tested for mechanical hypersensitivity at baseline, 15 and 30 min during DRGS, and 15 and 30 min following DRGS. Five animals were withdrawn from the study due to electrode‐related technical problems. Results Con‐DRGS and Burst‐DRGS normalized STZ‐induced mechanical hypersensitivity at 15 and 30 min during stimulation. A significant difference in terms of mechanical hypersensitivity was observed between both of the stimulated groups and the Sham‐DRGS group at 15 and 30 min during stimulation. Interestingly, Burst‐DRGS showed signs of a residual effect at 15 min after cessation of stimulation, while this was not the case for Con‐DRGS. Conclusions Under the conditions tested, Con‐DRGS and Burst‐DRGS are equally effective in attenuating STZ‐induced mechanical hypersensitivity in an animal model of PDPN. Burst‐DRGS showed signs of a residual effect at 15 min after cessation of stimulation, which requires further investigation.

show abstract

Section: Discussionsupporting

confidence: 89%

Dorsal Root Ganglion Stimulation in Experimental Painful Diabetic Peripheral Neuropathy: Burst vs. Conventional Stimulation Paradigm

Franken

Debets

Joosten

2019

Neuromodulation: Technology at the Neural Interface

View full text Add to dashboard Cite

show abstract

“…More recent data indicate that the effects of burst SCS do not rely on activation of GABA‐B receptors as has been claimed for conventional SCS .…”

Section: Burst Scsmentioning

confidence: 84%

Conventional and Novel Spinal Stimulation Algorithms: Hypothetical Mechanisms of Action and Comments on Outcomes

Linderoth

Foreman

2017

Neuromodulation: Technology at the Neural Interface

170

184

View full text Add to dashboard Cite

“…Compression was applied for 15 min and then removed. Microclips have been commonly used in other animal models of radiculopathy (49, 50, 53). Sham procedures were performed in separate groups of rats and involved all surgical procedures except that the nerve or root was not disturbed.…”

Section: Methodsmentioning

confidence: 99%

“…This avoids potential interactions of ligation with nerve growth during early development and has not been tested in infants. In adult rodents, cervical root compression, a transient one-time event, induces long-term thermal and mechanical hyperalgesia (49, 50). In humans, the comparable injury is brachial plexus avulsion.…”

Section: Introductionmentioning

confidence: 99%

Developmental Changes in Pain and Spinal Immune Gene Expression after Radicular Trauma in the Rat

et al. 2016

Self Cite

View full text Add to dashboard Cite

Neuropathic pain is chronic pain that develops after nerve injury and is less frequent in infants and children than in adults. Likewise, in animal models of neuropathic pain, allodynia and hyperalgesia are non-existent or attenuated in the infant, with a “switch” during development by which acute nerve injury transitions to chronic pain. Concomitant with the delay in neuropathic pain, there is a parallel delay in the ability of nerve injury to activate the immune system. Models of neuropathic pain in the infant have used various ligation methods and find that neuropathic pain does not occur under after postnatal days 21–28 (PN21–PN28), linked to activation of immune processes and developmental regulation of anti-inflammatory cytokines. We applied a model of neuropathic pain in the adult using a transient compression of the cervical nerve or nerve root in infant rats (injured at 10, 14, 21, or 28 days of age) to define transition periods during which injury results in no change in thermal and mechanical pain sensitivity or in short-term changes in pain. There was little to no hyperalgesia when the injury was imposed at PN10, but significant thermal hyperalgesia and mechanical allodynia 1 day after compression injury when performed at PN14, 21, or 28. Thermal withdrawal latencies returned to near baseline by 7 days postsurgery when the injuries were at PN14, and lasted up to 14 days when the injury was imposed at PN28. There was mechanical allodynia following injury at 1 day postinjury and at 14 days after injury at PN14. Measurements of mRNA from spinal cord at 1, 7, and 14 days postinjury at PN14, 21, and 28 showed that both the magnitude and duration of elevated immune markers and chemokines/cytokines were greater in the older animals, corresponding to the development of hyperalgesia. Thus, we confirm the late onset of neuropathic pain but found no evidence of emergent hyperalgesia if the injury was before PN21. This may be due to the use of a transient, and not sustained, compression ligation model.

show abstract

Burst and Tonic Spinal Cord Stimulation Differentially Activate GABAergic Mechanisms to Attenuate Pain in a Rat Model of Cervical Radiculopathy

Cited by 77 publications

References 58 publications

Dorsal Root Ganglion Stimulation in Experimental Painful Diabetic Peripheral Neuropathy: Burst vs. Conventional Stimulation Paradigm

Dorsal Root Ganglion Stimulation in Experimental Painful Diabetic Peripheral Neuropathy: Burst vs. Conventional Stimulation Paradigm

Conventional and Novel Spinal Stimulation Algorithms: Hypothetical Mechanisms of Action and Comments on Outcomes

Developmental Changes in Pain and Spinal Immune Gene Expression after Radicular Trauma in the Rat

Contact Info

Product

Resources

About