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dc.contributor.authorWang, Kaieren_NZ
dc.contributor.authorSteyn-Ross, Moira L.en_NZ
dc.contributor.authorSteyn-Ross, D. Alistairen_NZ
dc.contributor.authorWilson, Marcus T.en_NZ
dc.contributor.authorSleigh, James W.en_NZ
dc.coverage.spatialSwitzerlanden_NZ
dc.date.accessioned2016-02-18T03:53:29Z
dc.date.available2014en_NZ
dc.date.available2016-02-18T03:53:29Z
dc.date.issued2014en_NZ
dc.identifier.citationWang, K., Steyn-Ross, M. L., Steyn-Ross, D. A., Wilson, M. T., & Sleigh, J. W. (2014). EEG slow-wave coherence changes in propofol-induced general anesthesia: experiment and theory. Front Syst Neurosci, 8, article no. 215. http://doi.org/10.3389/fnsys.2014.00215en
dc.identifier.urihttps://hdl.handle.net/10289/9930
dc.description.abstractThe electroencephalogram (EEG) patterns recorded during general anesthetic-induced coma are closely similar to those seen during slow-wave sleep, the deepest stage of natural sleep; both states show patterns dominated by large amplitude slow waves. Slow oscillations are believed to be important for memory consolidation during natural sleep. Tracking the emergence of slow-wave oscillations during transition to unconsciousness may help us to identify drug-induced alterations of the underlying brain state, and provide insight into the mechanisms of general anesthesia. Although cellular-based mechanisms have been proposed, the origin of the slow oscillation has not yet been unambiguously established. A recent theoretical study by Steyn-Ross et al. (2013) proposes that the slow oscillation is a network, rather than cellular phenomenon. Modeling anesthesia as a moderate reduction in gap-junction interneuronal coupling, they predict an unconscious state signposted by emergent low-frequency oscillations with chaotic dynamics in space and time. They suggest that anesthetic slow-waves arise from a competitive interaction between symmetry-breaking instabilities in space (Turing) and time (Hopf), modulated by gap-junction coupling strength. A significant prediction of their model is that EEG phase coherence will decrease as the cortex transits from Turing-Hopf balance (wake) to Hopf-dominated chaotic slow-waves (unconsciousness). Here, we investigate changes in phase coherence during induction of general anesthesia. After examining 128-channel EEG traces recorded from five volunteers undergoing propofol anesthesia, we report a significant drop in sub-delta band (0.05-1.5 Hz) slow-wave coherence between frontal, occipital, and frontal-occipital electrode pairs, with the most pronounced wake-vs.-unconscious coherence changes occurring at the frontal cortex.en_NZ
dc.format.mimetypeapplication/pdf
dc.language.isoenen_NZ
dc.publisherFrontiers Research Foundationen_NZ
dc.rights© 2014 Wang, Steyn-Ross, Steyn-Ross, Wilson and Sleigh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.subjectTuring–Hopf instabilitiesen_NZ
dc.subjectgap-junctionen_NZ
dc.subjectmean-field cortical modelen_NZ
dc.subjectphase-coherence measureen_NZ
dc.subjectslow-wave sleepen_NZ
dc.titleEEG slow-wave coherence changes in propofol-induced general anesthesia: experiment and theory.en_NZ
dc.typeJournal Article
dc.identifier.doi10.3389/fnsys.2014.00215en_NZ
dc.relation.isPartOfFront Syst Neuroscien_NZ
pubs.begin-page215en_NZ
pubs.elements-id117006
pubs.issueOctoberen_NZ
pubs.volume8en_NZ
dc.identifier.eissn1662-5137en_NZ
uow.identifier.article-no215


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