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dc.contributor.authorAhmad, Hena
dc.contributor.authorRoberts, Ed
dc.contributor.authorPatel, Mitesh
dc.contributor.authorLobo, Rhannon
dc.contributor.authorSeemungal, Barry M.
dc.contributor.authorArshad, Qadeer
dc.contributor.authorBronstein, Adolfo M.
dc.date.accessioned2019-02-15T12:33:54Z
dc.date.available2019-02-15T12:33:54Z
dc.date.issued2017-08-16
dc.identifier.citationAhmad H., Roberts RE., Patel M., Lobo R., Seemungal B., Arshad Q., Bronstein A. (2017) 'Downregulation of early visual cortex excitability mediates oscillopsia suppression', Neurology 89 (11) pp. 1179-1185; doi: 10.1212/WNL.0000000000004360en
dc.identifier.issn0028-3878en
dc.identifier.doi10.1212/WNL.0000000000004360
dc.identifier.urihttp://hdl.handle.net/2436/622092
dc.description.abstractObjective: To identify in an observational study the neurophysiologic mechanisms that mediate adaptation to oscillopsia in patients with bilateral vestibular failure (BVF). Methods: We directly probe the hypothesis that adaptive changes that mediate oscillopsia suppression implicate the early visual-cortex (V1/V2). Accordingly, we investigated V1/V2 excitability using transcranial magnetic stimulation (TMS) in 12 avestibular patients and 12 healthy controls. Specifically, we assessed TMS-induced phosphene thresholds at baseline and cortical excitability changes while performing a visual motion adaptation paradigm during the following conditions: baseline measures (i.e., static), during visual motion (i.e., motion before adaptation), and during visual motion after 5 minutes of unidirectional visual motion adaptation (i.e., motion adapted). Results: Patients had significantly higher baseline phosphene thresholds, reflecting an underlying adaptive mechanism. Individual thresholds were correlated with oscillopsia symptom load. During the visual motion adaptation condition, no differences in excitability at baseline were observed, but during both the motion before adaptation and motion adapted conditions, we observed significantly attenuated cortical excitability in patients. Again, this attenuation in excitability was stronger in less symptomatic patients. Conclusions: Our findings provide neurophysiologic evidence that cortically mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with BVF.en
dc.formatapplication/PDFen
dc.language.isoenen
dc.publisherAcademic Academy of Neurologyen
dc.relation.urlhttp://n.neurology.org/content/89/11/1179en
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subjectbilateral vestibular failureen
dc.subjecttranscranial magnetic stimulationen
dc.subjecteye-head coordinationen
dc.subjectfunctional connectivityen
dc.subjectvestibuloocular reflexen
dc.subjectcortical excitabilityen
dc.subjectmotionsen
dc.subjectmechanismsen
dc.subjectadaptationsen
dc.titleDownregulation of early visual cortex excitability mediates oscillopsia suppressionen
dc.typeJournal article
dc.identifier.journalNeurologyen
dc.date.accepted2017-06-06
rioxxterms.funderThe research was funded by the UK Medical Research Council (MR/J004685/1) and supported by the National Institute for Health Research (NIHR) Imperial Biomedical Research Centreen
rioxxterms.identifier.projectUOW150219MPen
rioxxterms.versionVoRen
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/en
rioxxterms.licenseref.startdate2019-02-15en
refterms.dateFCD2019-02-15T12:33:55Z
refterms.versionFCDVoR
refterms.dateFOA2019-02-15T12:33:55Z


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