Sleep and general anesthesia

Abstract

Purpose The mechanisms through which general anesthetics cause reversible loss of consciousness are characterized poorly. In this review, we examine the evidence that anesthetic-induced loss of consciousness may be caused by actions on the neuronal pathways that produce natural sleep. Principal findings It is clear that many general anesthetics produce effects in the brain (detected on electroencephalogram recordings) that are similar to those seen during non-rapid eye movement non-(REM) sleep. Gamma aminobutyric acid (GABA)ergic hypnogenic neurons are thought to be critical for generating non-REM sleep through their inhibitory projections to wake-active regions of the brain. The postsynaptic GABA A receptor is a major molecular target of many anesthetics and thus may be a point of convergence between natural sleep and anesthesia. Furthermore, we also present growing evidence in this review that modulating wake-active neurotransmitter (e.g., acetylcholine, histamine) release can impact on anesthesia, supporting the idea that this point of convergence is at the level of the brain arousal systems. Conclusions While it is clear that general anesthetics can have effects at various points in the sleep-wake circuitry, it remains to be seen which points are true anesthetic targets. It will be challenging to separate nonspecific effects on baseline arousal from a causal mechanism. Sophisticated experimental approaches are necessary to address basic mechanisms of sleep and anesthesia and should advance our understanding in both of these fields. RésuméObjectif Les me´canismes par lesquels les anesthe´siques ge´ne´raux induisent une perte de conscience re´versible sont mal caracte´rise´s. Dans ce compte-rendu, nous examinons les donne´es probantes qui soutiennent que la perte de conscience induite par l'anesthe´sie pourrait eˆtre provoque´e par des actions sur les voies neuronales qui produisent le sommeil naturel. Constatations principales Il est clair que plusieurs anesthe´siques ge´ne´raux produisent des effets sur le cerveau (tels que de´tecte´s lors de l'enregistrement d'e´lectroence´phalogrammes) qui ressemblent a`ceux observe´s pendant le sommeil lent. On pense que les neurones hypnoge`nes GABAergiques sont des e´le´ments cruciaux pour la ge´ne´ration du sommeil lent en raison de leurs projections inhibitrices dans les re´gions du cerveau actives a`l'e´veil. Le re´cepteur GABA A post-synaptique est une importante cible mole´culaire de plusieurs anesthe´siques et pourrait par conse´quent constituer un point de convergence entre le sommeil naturel et l'anesthe´sie. De plus, nous pre´sentons aussi dans ce compte-rendu des donne´es probantes de plus en plus nombreuses qui sugge`rent que la modulation de la libe´ration des neurotransmetteurs actifs a`l'e´veil (par ex., acetylcholine, histamine) pourrait avoir un impact sur l'anesthe´sie, ce qui corrobore l'hypothe`se selon laquelle ce point de convergence se situe au niveau des syste`mes d'e´veil du cerveau.

Dynamic Repertoire of Intrinsic Brain States Is Reduced in Propofol-Induced Unconsciousness

“…A reduction in the coherence and information transfer among select frontal, parietal, and occipital cortical regions has been found using electrophysiological techniques (Ku et al, 2011;Lee et al, 2009bLee et al, , 2013. More generally, anesthetics have been thought to target subcortical mechanisms (Brown et al, 2010;Guldenmund et al, 2013;Mhuircheartaigh et al, 2010) including the natural sleep promoting circuits (Franks and Zecharia, 2011;Zecharia and Franks, 2009), and the neocortex itself (Hentschke et al, 2005;Hudetz, 2006;Seth et al, 2005;Velly et al, 2007).…”

Sleep and Breathing the First Night After Adenotonsillectomy in Obese Children With Obstructive Sleep Apnea

“…30 Decreased REM has also been described under anesthesia. 31,32 Thus, the decreased REM sleep percentage on the first night after AT is perhaps evidence of the prolonged effect of anesthetics following surgery compounded by postsurgical stress. Our study also showed decreased periodic limb movement in sleep.…”

Endocannabinoid signaling in hypothalamic circuits regulates arousal from general anesthesia in mice

“…Arousal after cessation of general anesthesia provides an experimental model to investigate the neural mechanism that controls consciousness (3)(4)(5)(6), as yearly more than 312 million patients are placed under general anesthesia worldwide (7). Although the exact mechanism underlying arousal from anesthesia is unknown, ample evidence suggests a remarkable similarity between anesthesia-induced unconsciousness and deep sleep (1,3,4,6,8). The hypothalamus is a key brain region for regulation of sleep and wakefulness (9)(10)(11)(12)(13).…”