Department of Anesthesiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Brain Connect. 2012;2(6):291-302. doi: 10.1089/brain.2012.0107.
General anesthesia consists of amnesia, hypnosis, analgesia, and areflexia. Of these, the mechanism of hypnosis, or loss of consciousness, has been the most elusive, yet a fascinating problem. How anesthetic agents suppress human consciousness has been investigated with neuroimaging for two decades. Anesthetics substantially reduce the global cerebral metabolic rate and blood flow with a degree of regional heterogeneity characteristic to the anesthetic agent. The thalamus appears to be a common site of modulation by several anesthetics, but this may be secondary to cortical effects. Stimulus-dependent brain activation is preserved in primary sensory areas, suggesting that unconsciousness cannot be explained by cortical deafferentation or a diminution of cortical sensory reactivity. The effect of general anesthetics in functional and effective connectivity is varied depending on the agent, dose, and network studied. At an anesthetic depth characterized by the subjects' unresponsiveness, a partial, but not complete, reduction in connectivity is generally observed. Functional connectivity of the frontoparietal association cortex is often reduced, but a causal role of this change for the loss of consciousness remains uncertain. Functional connectivity of the nonspecific (intralaminar) thalamic nuclei is preferentially reduced by propofol. Higher-order thalamocortical connectivity is also reduced with certain anesthetics. The changes in functional connectivity during anesthesia induction and emergence do not mirror each other; the recovery from anesthesia may involve increases in functional connectivity above the normal wakeful baseline. Anesthetic loss of consciousness is not a block of corticofugal information transfer, but a disruption of higher-order cortical information integration. The prime candidates for functional networks of the forebrain that play a critical role in maintaining the state of consciousness are those based on the posterior parietal-cingulate-precuneus region and the nonspecific thalamus.
全身麻醉包括遗忘、催眠、镇痛和反射抑制。在这些作用中，催眠或意识丧失的机制一直是最难以捉摸的，但也是一个引人入胜的问题。麻醉剂如何抑制人类意识已经通过神经影像学研究了二十年。麻醉剂会显著降低大脑的整体代谢率和血流量，并且具有与麻醉剂特征相关的区域异质性。丘脑似乎是几种麻醉剂共同作用的调节部位，但这可能是皮质效应的结果。在初级感觉区域，刺激依赖性脑激活得以保留，这表明无意识不能用皮质去传入或皮质感觉反应性降低来解释。全身麻醉对功能和有效连接的影响因药物、剂量和研究网络而异。在以受试者无反应为特征的麻醉深度下，通常观察到连接的部分而非完全减少。额顶联合皮层的功能连接通常减少，但这种变化对意识丧失的因果作用尚不确定。异丙酚优先降低非特异性（层间）丘脑核的功能连接。某些麻醉剂也会降低高级丘脑皮质连接。麻醉诱导和苏醒期间的功能连接变化并不相互镜像；麻醉苏醒可能涉及到高于正常清醒基线的功能连接增加。麻醉引起的意识丧失不是皮质传出信息传递的阻断，而是高级皮质信息整合的破坏。在维持意识状态方面发挥关键作用的前脑功能网络的主要候选者是基于后顶叶-扣带回-楔前叶区域和非特异性丘脑的网络。
