{"title":"Suppressing consciousness: Mechanisms of general anesthesia","authors":"Anthony G. Hudetz BMD, PhD","doi":"10.1053/j.sane.2006.09.003","DOIUrl":null,"url":null,"abstract":"<div><p>Understanding the neuronal mechanism of general anesthesia<span><span><span> both helps and benefits from research into the neurobiological basis of consciousness. Although several theories have been proposed, current evidence from sensory electrophysiology, event-related potentials, and </span>functional brain imaging<span> suggests that the failure of conscious perception at a critical depth of anesthesia may best be interpreted as “information received but not perceived” due to the disintegration of cortical information processing. Cortico-cortical and thalamocortical information transfer may depend on the synchronization or coherence of gamma oscillations that may be suppressed by general anesthetic agents; however, the exact mechanism of these effects is yet unclear. The extent of thalamic involvement in the cortico-cortical disintegration of information processes in anesthesia needs further investigation. It is likely that different anesthetic agents affect different neuronal pathways in their action to produce </span></span>unconsciousness<span>. A common effect of several volatile anesthetic agents may be the suppression of recurrent feedback signaling between cortical sensory and higher association regions. Elucidation of the neurofunctional systems involved in anesthetic-induced unconsciousness is among the important future challenges for anesthesia research.</span></span></p></div>","PeriodicalId":82686,"journal":{"name":"Seminars in anesthesia","volume":"25 4","pages":"Pages 196-204"},"PeriodicalIF":0.0000,"publicationDate":"2006-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1053/j.sane.2006.09.003","citationCount":"72","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Seminars in anesthesia","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0277032606000547","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 72
Abstract
Understanding the neuronal mechanism of general anesthesia both helps and benefits from research into the neurobiological basis of consciousness. Although several theories have been proposed, current evidence from sensory electrophysiology, event-related potentials, and functional brain imaging suggests that the failure of conscious perception at a critical depth of anesthesia may best be interpreted as “information received but not perceived” due to the disintegration of cortical information processing. Cortico-cortical and thalamocortical information transfer may depend on the synchronization or coherence of gamma oscillations that may be suppressed by general anesthetic agents; however, the exact mechanism of these effects is yet unclear. The extent of thalamic involvement in the cortico-cortical disintegration of information processes in anesthesia needs further investigation. It is likely that different anesthetic agents affect different neuronal pathways in their action to produce unconsciousness. A common effect of several volatile anesthetic agents may be the suppression of recurrent feedback signaling between cortical sensory and higher association regions. Elucidation of the neurofunctional systems involved in anesthetic-induced unconsciousness is among the important future challenges for anesthesia research.