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dc.contributor.authorMeeker, Timothy J.
dc.contributor.authorKeaser, Michael L.
dc.contributor.authorKhan, Shariq A.
dc.contributor.authorGullapalli, Rao P.
dc.contributor.authorSeminowicz, David A.
dc.contributor.authorGreenspan, Joel D.
dc.creatorMeeker, T.
dc.date.accessioned2019-07-30T18:25:29Z
dc.date.available2019-07-30T18:25:29Z
dc.date.issued2019-01-01
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85068572695&origin=inward
dc.identifier.urihttp://hdl.handle.net/10713/10135
dc.description.abstractCentral sensitization is a driving mechanism in many chronic pain patients, and manifests as hyperalgesia and allodynia beyond any apparent injury. Recent studies have demonstrated analgesic effects of motor cortex (M1) stimulation in several chronic pain disorders, yet its neural mechanisms remain uncertain. We evaluated whether anodal M1 transcranial direct current stimulation (tDCS) would mitigate central sensitization as measured by indices of secondary hyperalgesia. We used a capsaicin-heat pain model to elicit secondary mechanical hyperalgesia in 27 healthy subjects. In an assessor and subject-blind randomized, sham-controlled, crossover trial, anodal M1 tDCS decreased the intensity of pinprick hyperalgesia more than cathodal or sham tDCS. To elucidate the mechanism driving analgesia, subjects underwent fMRI of painful mechanical stimuli prior to and following induction of the pain model, after receiving M1 tDCS. We hypothesized that anodal M1 tDCS would enhance engagement of a descending pain modulatory (DPM) network in response to mechanical stimuli. Anodal tDCS normalized the effects of central sensitization on neurophysiological responses to mechanical pain in the medial prefrontal cortex, pregenual anterior cingulate cortex, and periaqueductal gray, important regions in the DPM network. Taken together, these results provide support for the hypothesis that anodal M1-tDCS reduces central sensitization-induced hyperalgesia through the DPM network in humans. Copyright © 2019 The Authorsen_US
dc.description.sponsorshipThis study was funded in part by The Essel Foundation. TM acknowledges support from NIH training grants (T32-NS063391 and T32-DE007309) as well as continuing support from the Johns Hopkins Neurosurgical Pain Research Institute and NIH R01-NS107602.en_US
dc.description.urihttps://doi.org/10.3389/fnins.2019.00467en_US
dc.language.isoen_USen_US
dc.publisherFrontiers Media S.A.en_US
dc.relation.ispartofFrontiers in Neuroscienceen_US
dc.subjectBold FMRIen_US
dc.subjectEvent-related FMRIen_US
dc.subjectHumanen_US
dc.subjectMotor cortex neuromodulationen_US
dc.subjectPainen_US
dc.subjectPain modelen_US
dc.subjectSecondary hyperalgesiaen_US
dc.subjectTranscranial direct current stimulationen_US
dc.titleNon-invasive motor cortex neuromodulation reduces secondary hyperalgesia and enhances activation of the descending pain modulatory networken_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fnins.2019.00467
dc.relation.volume13


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