抑制意识:全身麻醉的机制

Anthony G. Hudetz BMD, PhD
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引用次数: 72

摘要

了解全身麻醉的神经元机制有助于意识的神经生物学基础的研究。虽然已经提出了几种理论,但目前来自感觉电生理学、事件相关电位和功能性脑成像的证据表明,在麻醉的临界深度,意识知觉的失败可能最好地被解释为由于皮质信息处理的解体而“接收但未感知的信息”。皮质-皮质和丘脑皮质的信息传递可能依赖于可能被全身麻醉剂抑制的伽马振荡的同步或相干性;然而,这些影响的确切机制尚不清楚。丘脑参与麻醉中皮质-皮质信息过程解体的程度有待进一步研究。这可能是不同的麻醉剂影响不同的神经通路在他们的行动产生无意识。几种挥发性麻醉剂的共同作用可能是抑制皮层感觉区和高级关联区之间的反复反馈信号。阐明参与麻醉诱导无意识的神经功能系统是麻醉研究未来的重要挑战之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Suppressing consciousness: Mechanisms of general anesthesia

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.

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