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dc.contributor.authorPavone, Kara J.
dc.contributor.authorAkeju, Oluwaseun
dc.contributor.authorSampson, Aaron L.
dc.contributor.authorLing, Kelly
dc.contributor.authorPurdon, Patrick L.
dc.contributor.authorBrown, Emery Neal
dc.date.accessioned2016-05-02T16:53:39Z
dc.date.available2016-05-02T16:53:39Z
dc.date.issued2015-06
dc.identifier.issn13882457
dc.identifier.urihttp://hdl.handle.net/1721.1/102354
dc.description.abstractObjectives Switching from maintenance of general anesthesia with an ether anesthetic to maintenance with high-dose (concentration >50% and total gas flow rate >4 liters per minute) nitrous oxide is a common practice used to facilitate emergence from general anesthesia. The transition from the ether anesthetic to nitrous oxide is associated with a switch in the putative mechanisms and sites of anesthetic action. We investigated whether there is an electroencephalogram (EEG) marker of this transition. Methods We retrospectively studied the ether anesthetic to nitrous oxide transition in 19 patients with EEG monitoring receiving general anesthesia using the ether anesthetic sevoflurane combined with oxygen and air. Results Following the transition to nitrous oxide, the alpha (8–12 Hz) oscillations associated with sevoflurane dissipated within 3–12 min (median 6 min) and were replaced by highly coherent large-amplitude slow-delta (0.1–4 Hz) oscillations that persisted for 2–12 min (median 3 min). Conclusions Administration of high-dose nitrous oxide is associated with transient, large amplitude slow-delta oscillations. Significance We postulate that these slow-delta oscillations may result from nitrous oxide-induced blockade of major excitatory inputs (NMDA glutamate projections) from the brainstem (parabrachial nucleus and medial pontine reticular formation) to the thalamus and cortex. This EEG signature of high-dose nitrous oxide may offer new insights into brain states during general anesthesia.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant DP1-OD003646)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant TR01-GM104948)en_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.clinph.2015.06.001en_US
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.sourceElsevieren_US
dc.titleNitrous oxide-induced slow and delta oscillationsen_US
dc.typeArticleen_US
dc.identifier.citationPavone, Kara J., Oluwaseun Akeju, Aaron L. Sampson, Kelly Ling, Patrick L. Purdon, and Emery N. Brown. “Nitrous Oxide-Induced Slow and Delta Oscillations.” Clinical Neurophysiology 127, no. 1 (January 2016): 556–564. © 2015 International Federation of Clinical Neurophysiologyen_US
dc.contributor.departmentMassachusetts Institute of Technology. Institute for Medical Engineering & Scienceen_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technologyen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.mitauthorBrown, Emery N.en_US
dc.relation.journalClinical Neurophysiologyen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsPavone, Kara J.; Akeju, Oluwaseun; Sampson, Aaron L.; Ling, Kelly; Purdon, Patrick L.; Brown, Emery N.en_US
dc.identifier.orcidhttps://orcid.org/0000-0003-2668-7819
mit.licensePUBLISHER_CCen_US
mit.metadata.statusComplete


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