Reversal of sensory deficit through sacral neuromodulation in an animal model of fecal incontinence

DC FieldValueLanguage
dc.contributor.authorEvers, Judith-
dc.contributor.authorDevane, L.-
dc.contributor.authorCarrington, E. V.-
dc.contributor.authorScott, S. M.-
dc.contributor.authorKnowles, C. H.-
dc.contributor.authorO'Connell, P. R.-
dc.contributor.authorJones, James F. X.-
dc.date.accessioned2021-11-19T15:59:53Z-
dc.date.available2021-11-19T15:59:53Z-
dc.date.copyright2016 Wileyen_US
dc.date.issued2016-05-
dc.identifier.citationNeurogastroenterology and Motilityen_US
dc.identifier.issn1350-1925-
dc.identifier.urihttp://hdl.handle.net/10197/12663-
dc.description.abstractBackground: Sacral neuromodulation (SNM) is a treatment option for intractable fecal incontinence. The mechanism of action is unclear, however, increasing evidence for afferent somatosensory effects exists. This study's aim was to elucidate effects of acute SNM on the cerebral cortex in a rodent model of pudendal nerve injury. Methods: The effects of 14 Hz and 2 Hz SNM on sensory cortical activation were studied. In 32 anesthetized rats, anal canal evoked potentials (EPs) were recorded over the primary somatosensory cortex. Pudendal nerve injury was produced by 1-hour inflation of two intra-pelvic balloons. Four groups were studied: balloon injury, balloon injury plus either 14 Hz or 2 Hz SNM, sham operation. Immunohistochemistry for the neural plasticity marker polysialylated neural cell adhesion molecule (PSA-NCAM) positive cells (numerical density and location) in the somatosensory cortex was performed. Key Results: Anal EP amplitudes diminished during balloon inflation; 14 Hz SNM restored diminished anal EPs to initial levels and 2 Hz SNM to above initial levels. Evoked potential latencies were prolonged during balloon inflation. The numerical density of PSA-NCAM positive cells increased in the SNM groups, but not in sham or balloon injury without SNM. Stimulated cortices showed clusters of PSA-NCAM positive cells in layers II, IV, and V. Post SNM changes were similar in both SNM groups. Conclusions & Inferences: Sacral neuromodulation augments anal representation in the sensory cortex and restores afferent pathways following injury. PSA-NCAM positive cell density is increased in stimulated cortices and positive cells are clustered in layers II, IV, and V.en_US
dc.description.sponsorshipScience Foundation Irelanden_US
dc.format.mediumPrint-Electronic-
dc.language.isoenen_US
dc.publisherWileyen_US
dc.rightsThis is the peer reviewed version of the following article: Evers, J., Devane, L., Carrington, E.V., Scott, S.M., Knowles, C.H., O'Connell, P.R. and Jones, J.F.X. (2016), Reversal of sensory deficit through sacral neuromodulation in an animal model of fecal incontinence. Neurogastroenterol. Motil., 28: 665-673., which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1111/nmo.12762. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.en_US
dc.subjectSacrumen_US
dc.subjectSomatosensory cortexen_US
dc.subjectAnimalsen_US
dc.subjectRatsen_US
dc.subjectWistar ratsen_US
dc.subjectFecal incontinenceen_US
dc.subjectAnimal disease modelsen_US
dc.subjectElectric stimulation therapyen_US
dc.subjectSomatosensory evoked potentialsen_US
dc.subjectFemaleen_US
dc.titleReversal of sensory deficit through sacral neuromodulation in an animal model of fecal incontinenceen_US
dc.typeJournal Articleen_US
dc.internal.authorcontactotherjudith.evers@ucd.ieen_US
dc.statusPeer revieweden_US
dc.identifier.volume28en_US
dc.identifier.issue5en_US
dc.identifier.startpage665en_US
dc.identifier.endpage673en_US
dc.identifier.doi10.1111/nmo.12762-
dc.neeo.contributorEvers|Judith|aut|-
dc.neeo.contributorDevane|L.|aut|-
dc.neeo.contributorCarrington|E. V.|aut|-
dc.neeo.contributorScott|S. M.|aut|-
dc.neeo.contributorKnowles|C. H.|aut|-
dc.neeo.contributorO'Connell|P. R.|aut|-
dc.neeo.contributorJones|James F. X.|aut|-
dc.date.updated2021-05-13T11:19:44Z-
dc.identifier.grantid11/RFP.1/NES/3115-
dc.rights.licensehttps://creativecommons.org/licenses/by-nc-nd/3.0/ie/en_US
item.fulltextWith Fulltext-
item.grantfulltextopen-
Appears in Collections:Electrical and Electronic Engineering Research Collection
Medicine Research Collection
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