Breakdown of consciousness: Neuronal oscillations during distinct levels of human anesthesia

Abstract

Event Abstract Back to Event Breakdown of consciousness: Neuronal oscillations during distinct levels of human anesthesia Gernot G. Supp1*, M. Siegel2, M. Hauck1, G. N. Schmidt3 and A.K Engel1 1 University Medical Center Hamburg-Eppendorf, Department of Neurophysiology and Pathophysiology, Germany 2 Massachusetts Institute of Technology, Picower Institute for Learning and Memory, Department of Brain and Cognitive Science, United States 3 Department of Anesthesiology, University Medical Center Hamburg-Eppendorf, Germany A primary goal of clinical anesthesia is to suppress consciousness. Although anesthesia has become standard clinical procedure, the neural mechanisms underlying the concomitant loss of consciousness remain poorly understood on the system-level. We thus investigated changes in macroscopic brain signals during the loss of consciousness under step-wise anesthesia. We recorded the 128-channel EEG in 10 healthy male volunteers during intravenous application of the short-acting anesthetic agent propofol (target-controlled infusions of 0.5, 1.0, 1.5, 2.0, 2.5, 3.0, 5.0 μg/ml). During each period, subjects received median nerve stimulation at their left wrist and electric intracutaneous pain stimulation at the tip of their left middle finger. We continuously measured vital parameters, subjective pain ratings, vigilance and sedation level. We classified periods for which subjects were able or not able to verbally rate painfulness as “conscious” or “unconscious”, respectively. We found that propofol anesthesia profoundly altered ongoing neural activity and stimulus-related cortical oscillations. For ongoing neural activity, propofol anesthesia induced strong 8-18 Hz (peak: 13 Hz) oscillations that increased in a dose-dependent manner up to 1000 % relative to the pre-medication baseline. Distributed source reconstruction revealed that this activity originated bilaterally from prefrontal and temporal cortical regions. Median nerve stimulation elicited an early (20-50 ms) power increase in the gamma band (> 30 Hz) that originated from contralateral primary somatosensory cortex and remained unchanged during increasing levels of propofol anesthesia. In addition, propofol induced a late (100-500 ms) decrease of gamma-band activity during the post-stimulation interval. This late decrease in gamma power was located in the left and right prefrontal gyrus, and the right superior and middle frontal gyrus. Directly contrasting conscious and unconscious periods, we found a stronger gamma decrease for unconscious periods in left prefrontal brain areas, especially in the left medial frontal and cingulate cortex. Our results indicate that propofol anesthesia alters the global processing mode of the brain by inducing spindle-like low-frequency oscillations similar to those observed during regular sleep. Additionally, our data suggest that anesthesia affects somatosensory processing in a stage-specific manner. While during anesthesia, sensory processing in primary somatosensory cortex was preserved, processing at later stages presumably was impaired. This suggests that anesthesia may specifically block the routing of sensory information from primary to subsequent cortical processing stages. Furthermore, during unconscious somatosensory processing activation of the anterior parts of the medial frontal cortex was reduced, which may reflect a blocked transmission of sensory input to cortical parts of the limbic system. Conference: 10th International Conference on Cognitive Neuroscience, Bodrum, Türkiye, 1 Sep - 5 Sep, 2008. Presentation Type: Oral Presentation Topic: Symposium 12: Gamma-band responses in the brain: A general Mechanism subserving cortical information processing? Citation: Supp GG, Siegel M, Hauck M, Schmidt GN and Engel A (2008). Breakdown of consciousness: Neuronal oscillations during distinct levels of human anesthesia. Conference Abstract: 10th International Conference on Cognitive Neuroscience. doi: 10.3389/conf.neuro.09.2009.01.055 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 28 Nov 2008; Published Online: 28 Nov 2008. * Correspondence: Gernot G Supp, University Medical Center Hamburg-Eppendorf, Department of Neurophysiology and Pathophysiology, Geneva, Germany, g.supp@uke.uni-hamburg.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Gernot G Supp M. Siegel M. Hauck G. N Schmidt A.K Engel Google Gernot G Supp M. Siegel M. Hauck G. N Schmidt A.K Engel Google Scholar Gernot G Supp M. Siegel M. Hauck G. 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