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Please use this identifier to cite or link to this item: http://hdl.handle.net/11055/1128
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dc.contributor.authorPullon, RMen_US
dc.contributor.authorWarnaby, CEen_US
dc.contributor.authorSleigh, JWen_US
dc.date2022-03-01-
dc.date.accessioned2022-04-20T01:27:13Z-
dc.date.available2022-04-20T01:27:13Z-
dc.identifier.citation136(3):420-433en_US
dc.identifier.issn0003-3022en_US
dc.identifier.urihttp://hdl.handle.net/11055/1128-
dc.description.abstractBackground: The wakeful brain can easily access and coordinate a large repertoire of different states-dynamics suggestive of "criticality." Anesthesia causes loss of criticality at the level of electroencephalogram waveforms, but the criticality of brain network connectivity is less well studied. The authors hypothesized that propofol anesthesia is associated with abrupt and divergent changes in brain network connectivity for different frequencies and time scales-characteristic of a phase transition, a signature of loss of criticality. Methods: As part of a previously reported study, 16 volunteers were given propofol in slowly increasing brain concentrations, and their behavioral responsiveness was assessed. The network dynamics from 31-channel electroencephalogram data were calculated from 1 to 20 Hz using four phase and envelope amplitude-based functional connectivity metrics that covered a wide range of time scales from milliseconds to minutes. The authors calculated network global efficiency, clustering coefficient, and statistical complexity (using the Jensen-Shannon divergence) for each functional connectivity metric and compared their findings with those from an in silico Kuramoto network model. Results: The transition to anesthesia was associated with critical slowing and then abrupt profound decreases in global network efficiency of 2 Hz power envelope metrics (from mean ± SD of 0.64 ± 0.15 to 0.29 ± 0.28 absolute value, P < 0.001, for medium; and from 0.47 ± 0.13 to 0.24 ± 0.21, P < 0.001, for long time scales) but with an increase in global network efficiency for 10 Hz weighted phase lag index (from 0.30 ± 0.20 to 0.72 ± 0.06, P < 0.001). Network complexity decreased for both the 10 Hz hypersynchronous (0.44 ± 0.13 to 0.23 ± 0.08, P < 0.001), and the 2 Hz asynchronous (0.73 ± 0.08 to 0.40 ± 0.13, P < 0.001) network states. These patterns of network coupling were consistent with those of the Kuramoto model of an order-disorder phase transition. Conclusions: Around loss of behavioral responsiveness, a small increase in propofol concentrations caused a collapse of long time scale power envelope connectivity and an increase in 10 Hz phase-based connectivity-suggestive of a brain network phase transition.en_US
dc.subjectAdulten_US
dc.subjectAnesthetics, Intravenous / pharmacologyen_US
dc.subjectBrain / drug effectsen_US
dc.subjectElectroencephalography / methodsen_US
dc.subjectNerve Net /drug effectsen_US
dc.subjectPropofol / pharmacologyen_US
dc.subjectUnconsciousness / chemically induceden_US
dc.titlePropofol-induced Unresponsiveness Is Associated with a Brain Network Phase Transitionen_US
dc.typeJournal Articleen_US
dc.type.contentTexten_US
dc.identifier.journaltitleAnesthesiologyen_US
dc.identifier.doi10.1097/ALN.0000000000004095.en_US
dc.description.affiliatesDepartment of Anesthesiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.en_US
dc.description.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/35120195/en_US
dc.type.studyortrialStudyen_US
dc.contributor.anzcaSleigh, JWen_US
Appears in Collections:Scholarly and Clinical

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