Differential Dynamic of Action on Cortical and Subcortical Structures of Anesthetic Agents during Induction of Anesthesia

Velly, Lionel; Rey, Marc; Bruder, Nicolas; Gouvitsos, F.; Witjas, Tatiana; Régis, Jean; Péragut, Jean-Claude; Gouin, F

doi:10.1097/01.anes.0000270734.99298.b4

Cited by 192 publications

(143 citation statements)

References 55 publications

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“…Besides decreasing activity in the higher-order brain areas of the cortex, increase of connectivity has also been observed in other brain regions during sedation [66], as already observed in patients with DOC. Mild sedation with propofol increased thalamic excitability [65] and increased connectivity between the pontine tegmental area and the insulae [64].…”

Section: Unconsciousness In General Anesthesiasupporting

confidence: 65%

Functional neuroanatomy of disorders of consciousness

Perri

Stender

Laureys

et al. 2014

Epilepsy & Behavior

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This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. Our understanding of the mechanisms of loss and recovery of consciousness, following severe brain injury or during anesthesia, is changing rapidly. Recent neuroimaging studies have shown that patients with chronic disorders of consciousness and subjects undergoing general anesthesia present a complex dysfunctionality in the architecture of brain connectivity. At present, the global hallmark of impaired consciousness appears to be a multifaceted dysfunctional connectivity pattern with both within-network loss of connectivity in a widespread frontoparietal network and between-network hyperconnectivity involving other regions such as the insula and ventral tegmental area. Despite ongoing efforts, the mechanisms underlying the emergence of consciousness after severe brain injury are not thoroughly understood. Important questions remain unanswered: What triggers the connectivity impairment leading to disorders of consciousness? Why do some patients recover from coma, while others with apparently similar brain injuries do not? Understanding these mechanisms could lead to a better comprehension of brain function and, hopefully, lead to new therapeutic strategies in this challenging patient population.This article is part of a Special Issue entitled Epilepsy and Consciousness.

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Section: Unconsciousness In General Anesthesiasupporting

confidence: 65%

Functional neuroanatomy of disorders of consciousness

Perri

Stender

Laureys

et al. 2014

Epilepsy & Behavior

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“…Of notice, the opposite phenomenon (i.e., the cortex being deactivated before the thalamus) has been claimed recently to occur during anesthesia induction (33,34). This precedence in the decrease in thalamic activity is unlikely to be related to antiepileptic treatment or a patient's clinical condition.…”

Section: Discussionmentioning

confidence: 98%

Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans

Magnin

Rey

Bastuji

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

196

147

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Thalamic and cortical activities are assumed to be time-locked throughout all vigilance states. Using simultaneous intracortical and intrathalamic recordings, we demonstrate here that the thalamic deactivation occurring at sleep onset most often precedes that of the cortex by several minutes, whereas reactivation of both structures during awakening is synchronized. Delays between thalamus and cortex deactivations can vary from one subject to another when a similar cortical region is considered. In addition, heterogeneity in activity levels throughout the cortical mantle is larger than previously thought during the descent into sleep. Thus, asynchronous thalamocortical deactivation while falling asleep probably explains the production of hypnagogic hallucinations by a still-activated cortex and the common self-overestimation of the time needed to fall asleep.A bundant electrophysiological and functional imaging data have revealed that sleep-related brain activity is not the result of a global deactivation of cerebral structures but rather is a multifocal process associated with local changes in brain activities (1-10). Examples of such functional heterogeneities are, among others, the fronto-occipital gradient in cortical activity during sleep (1, 2), the preponderant fronto-parietal localization of sleep spindles (3, 4), and interhemispheric imbalanced activity (5, 6). So far, very few studies have addressed the time course of these regional differences during transitions between vigilance states (11)(12)(13)(14), and most of these studies were based on scalp recordings performed during stable periods of wakefulness or sleep. Although reports that favor some asynchrony of sleep-onset activity between the different cortical areas are accumulating, there still is a firm belief that thalamic and cortical activities are tightly coupled, at both the cellular and integrative level, during wakefulness and sleep (15)(16)(17)(18). Recent intracranial data in humans, however, indicate that, during both paradoxical (rapid eye movement) sleep and sleep stage 2, thalamic and cortical activities may alternate periods of coupling and decoupling (19,20). In this context, the question is whether the dynamics of the neuronal deactivation that characterizes the transition from wakefulness to sleep is identical in thalamus and cortex, or, conversely, whether transient decoupling may occur at this transition time that would suggest different sleep-onset timing in these two structures. The opportunity to record thalamic and cortical activities simultaneously in epileptic patients chronically implanted with intracerebral electrodes allowed us to address this issue. In contrast to the generally accepted view that thalamic and cortical activities are tightly locked along the different vigilance states, we found that the thalamic activity most often decreased to sleep levels several minutes before the cortical activity started to abate. This finding suggests that the cortex remains neurophysiologically awake but decoupled from thalamic i...

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“…Although thalamus is very likely involved in PI-LOC, observed changes in connectivity may be attributed to direct effects of propofol on thalamic nuclei or indirect effects via thalamocortical feedback loops. A study in Parkinson's patients reported that propofol-induction lead to slowing in cortical before subcortical electrophysiologic patterns, which may indicate a potentially secondary role of thalamus in initiating loss of consciousness (Velly et al, 2007). In contrast, for the onset of NREM sleep, deactivation of thalamus was found to precede that of cortex (Magnin et al, 2010).…”

Section: Effects Of Pi-loc On Subcortical and Cortical Functional Conmentioning

confidence: 99%

Spatiotemporal Reconfiguration of Large-Scale Brain Functional Networks during Propofol-Induced Loss of Consciousness

et al. 2012

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Applying graph theoretical analysis of spontaneous BOLD fluctuations in functional magnetic resonance imaging (fMRI), we investigated whole-brain functional connectivity of 11 healthy volunteers during wakefulness and propofol-induced loss of consciousness (PI-LOC). After extraction of regional fMRI time series from 110 cortical and subcortical regions, we applied a maximum overlap discrete wavelet transformation and investigated changes in the brain's intrinsic spatiotemporal organization. During PI-LOC, we observed a breakdown of subcortico-cortical and corticocortical connectivity. Decrease of connectivity was pronounced in thalamocortical connections, whereas no changes were found for connectivity within primary sensory cortices. Graph theoretical analyses revealed significant changes in the degree distribution and local organization metrics of brain functional networks during PI-LOC: compared with a random network, normalized clustering was significantly increased, as was small-worldness. Furthermore we observed a profound decline in long-range connections and a reduction in whole-brain spatiotemporal integration, supporting a topological reconfiguration during PI-LOC. Our findings shed light on the functional significance of intrinsic brain activity as measured by spontaneous BOLD signal fluctuations and help to understand propofol-induced loss of consciousness.

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Differential Dynamic of Action on Cortical and Subcortical Structures of Anesthetic Agents during Induction of Anesthesia

Abstract: These data suggest that in humans, unconsciousness mainly involves the cortical brain, but that suppression of movement in response to noxious stimuli is mediated through the effect of anesthetic agents on subcortical structures.

Cited by 192 publications

References 55 publications

Functional neuroanatomy of disorders of consciousness

Functional neuroanatomy of disorders of consciousness

Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans

Spatiotemporal Reconfiguration of Large-Scale Brain Functional Networks during Propofol-Induced Loss of Consciousness

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