{"title":"The Evolving Paradigm for Identifying and Treating Patients With Acoustic Neuromas","authors":"S. Selesnick","doi":"10.11289/OTOLJPN.21.85","DOIUrl":"https://doi.org/10.11289/OTOLJPN.21.85","url":null,"abstract":"","PeriodicalId":19601,"journal":{"name":"Otology Japan","volume":"27 1","pages":"85-91"},"PeriodicalIF":0.0,"publicationDate":"2011-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86393278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Vestibular evoked myogenic potential in acoustic neuroma","authors":"Nakarin Angunsri, E. Omi, Y. Itasaka, K. Ishikawa","doi":"10.11289/OTOLJPN.20.735","DOIUrl":"https://doi.org/10.11289/OTOLJPN.20.735","url":null,"abstract":"","PeriodicalId":19601,"journal":{"name":"Otology Japan","volume":"9 1","pages":"735-742"},"PeriodicalIF":0.0,"publicationDate":"2010-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85521666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background A cochlear implant (CI) electrode is a neural interface to the excitable tissue of the inner ear. Small currents, driven through electrodes distributed within scala tympani, are able to synchronously depolarize small to large groups of afferent neurons depending on current intensity. Originally, CI electrodes were designed for profoundly deaf patients assuming that a mostly depleted neural population was present in the form of spiral ganglion cells and associated axons. No measurable residual hearing was present in the patient group, and it was often assumed that the dendrites were absent because of the duration of deafness and associated slow retrograde degeneration of unstimulated neurites. Retrograde degeneration of neurons begins at the first synapse in the organ of Corti and progresses toward the habenula perforata and the soma of the primary auditory afferent neurons located in the superior portion of the modiolus and in the Rosenthal’s canal of the basal turn. The unmyelinated spiral ganglion cell soma was widely believed to be the site of spike initiation under electrical stimulation. Because no dendrite survival was assumed and no residual hearing was present, the issue of electrode trauma was reduced to protecting the soma of sensory cells within the modiolus.
{"title":"New trends with cochlear implant electrodes","authors":"C. Jolly, J. Mueller, S. Helbig, S. Usami","doi":"10.11289/OTOLJPN.20.239","DOIUrl":"https://doi.org/10.11289/OTOLJPN.20.239","url":null,"abstract":"Background A cochlear implant (CI) electrode is a neural interface to the excitable tissue of the inner ear. Small currents, driven through electrodes distributed within scala tympani, are able to synchronously depolarize small to large groups of afferent neurons depending on current intensity. Originally, CI electrodes were designed for profoundly deaf patients assuming that a mostly depleted neural population was present in the form of spiral ganglion cells and associated axons. No measurable residual hearing was present in the patient group, and it was often assumed that the dendrites were absent because of the duration of deafness and associated slow retrograde degeneration of unstimulated neurites. Retrograde degeneration of neurons begins at the first synapse in the organ of Corti and progresses toward the habenula perforata and the soma of the primary auditory afferent neurons located in the superior portion of the modiolus and in the Rosenthal’s canal of the basal turn. The unmyelinated spiral ganglion cell soma was widely believed to be the site of spike initiation under electrical stimulation. Because no dendrite survival was assumed and no residual hearing was present, the issue of electrode trauma was reduced to protecting the soma of sensory cells within the modiolus.","PeriodicalId":19601,"journal":{"name":"Otology Japan","volume":"260 1","pages":"239-246"},"PeriodicalIF":0.0,"publicationDate":"2010-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77143757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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