dc.contributor.author | Pavone, Kara J. | |
dc.contributor.author | Akeju, Oluwaseun | |
dc.contributor.author | Sampson, Aaron L. | |
dc.contributor.author | Ling, Kelly | |
dc.contributor.author | Purdon, Patrick L. | |
dc.contributor.author | Brown, Emery Neal | |
dc.date.accessioned | 2016-05-02T16:53:39Z | |
dc.date.available | 2016-05-02T16:53:39Z | |
dc.date.issued | 2015-06 | |
dc.identifier.issn | 13882457 | |
dc.identifier.uri | http://hdl.handle.net/1721.1/102354 | |
dc.description.abstract | Objectives
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.sponsorship | National Institutes of Health (U.S.) (Grant DP1-OD003646) | en_US |
dc.description.sponsorship | National Institutes of Health (U.S.) (Grant TR01-GM104948) | en_US |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.relation.isversionof | http://dx.doi.org/10.1016/j.clinph.2015.06.001 | en_US |
dc.rights | Creative Commons Attribution-NonCommercial-NoDerivs License | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | en_US |
dc.source | Elsevier | en_US |
dc.title | Nitrous oxide-induced slow and delta oscillations | en_US |
dc.type | Article | en_US |
dc.identifier.citation | Pavone, 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 Neurophysiology | en_US |
dc.contributor.department | Massachusetts Institute of Technology. Institute for Medical Engineering & Science | en_US |
dc.contributor.department | Harvard University--MIT Division of Health Sciences and Technology | en_US |
dc.contributor.department | Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences | en_US |
dc.contributor.mitauthor | Brown, Emery N. | en_US |
dc.relation.journal | Clinical Neurophysiology | en_US |
dc.eprint.version | Final published version | en_US |
dc.type.uri | http://purl.org/eprint/type/JournalArticle | en_US |
eprint.status | http://purl.org/eprint/status/PeerReviewed | en_US |
dspace.orderedauthors | Pavone, Kara J.; Akeju, Oluwaseun; Sampson, Aaron L.; Ling, Kelly; Purdon, Patrick L.; Brown, Emery N. | en_US |
dc.identifier.orcid | https://orcid.org/0000-0003-2668-7819 | |
mit.license | PUBLISHER_CC | en_US |
mit.metadata.status | Complete | |