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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Shaquia Idlett
BME PhD Thesis Proposal Presentation
Date and Time: Thursday, March 2nd, 3pm
Location: Whitehead Biomedical Research Building, 600
Committee:
Shawn Hochman, Ph.D.(Advisor)
Robert Butera, Ph.D, P.E.
Lena Ting, Ph.D.
Sandra Garraway, Ph.D.
Timothy Cope, Ph.D
Title: Spinal Cord Stimulation(SCS)-mediated modulation of peripheral hyperexcitability following spinal cord injury
Abstract:
Neuropathic pain is a common complication following spinal cord injury (SCI). The emergence and long-term maintenance of this pain is thought to be the result of chronic spontaneous activity in pain transmitting Ad and C primary afferents. Pharmacological treatment methods are unfavorable options due to limited efficacy and possible negative side effects. Thus, spinal cord stimulation (SCS) has emerged as an alternative to traditional treatment. Early clinical trials of the technique in the spinal cord injury population find variable successful outcomes but suggest potential for the technique to relieve below-level pain for incomplete spinal lesions. The mechanisms underlying SCS modulation of SCI-neuropathic pain are unknown. One possibility is via central gating of ongoing spontaneous activity in pain transmitting primary afferents. Therefore, the primary objective of this proposal is to characterize changes in pain signaling during SCS, in a contusion SCI model with demonstrable spontaneous primary afferent activity. The central hypothesis of this proposal is that SCS inhibits central transmission of ongoing and spontaneous pain fiber activity in the injured spinal cord. A novel in vitro adult mouse spinal cord preparation will be developed to leverage its neural accessibility for studies that test the hypothesis. The proposed project aims to advance scientific knowledge by characterizing differences in SCS-mediated recruitment of dorsal axon tracts after SCI and investigating the role of presynaptic and postsynaptic inhibitory mechanisms in the observed effects of SCS.