Department of Biophysics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Hum Brain Mapp. 2012 Oct;33(10):2487-98. doi: 10.1002/hbm.21385. Epub 2011 Sep 20.
Current theories suggest that disrupting cortical information integration may account for the mechanism of general anesthesia in suppressing consciousness. Human cognitive operations take place in hierarchically structured neural organizations in the brain. The process of low-order neural representation of sensory stimuli becoming integrated in high-order cortices is also known as cognitive binding. Combining neuroimaging, cognitive neuroscience, and anesthetic manipulation, we examined how cognitive networks involved in auditory verbal memory are maintained in wakefulness, disrupted in propofol-induced deep sedation, and re-established in recovery. Inspired by the notion of cognitive binding, an functional magnetic resonance imaging-guided connectivity analysis was utilized to assess the integrity of functional interactions within and between different levels of the task-defined brain regions. Task-related responses persisted in the primary auditory cortex (PAC), but vanished in the inferior frontal gyrus (IFG) and premotor areas in deep sedation. For connectivity analysis, seed regions representing sensory and high-order processing of the memory task were identified in the PAC and IFG. Propofol disrupted connections from the PAC seed to the frontal regions and thalamus, but not the connections from the IFG seed to a set of widely distributed brain regions in the temporal, frontal, and parietal lobes (with exception of the PAC). These later regions have been implicated in mediating verbal comprehension and memory. These results suggest that propofol disrupts cognition by blocking the projection of sensory information to high-order processing networks and thus preventing information integration. Such findings contribute to our understanding of anesthetic mechanisms as related to information and integration in the brain.
目前的理论表明，破坏皮质信息整合可能是全身麻醉抑制意识的机制。人类认知活动发生在大脑中分层结构的神经组织中。低阶神经对感觉刺激的表示在高阶皮质中整合的过程也称为认知绑定。通过结合神经影像学、认知神经科学和麻醉操作，我们研究了听觉言语记忆所涉及的认知网络在觉醒状态下如何维持，在异丙酚诱导的深度镇静中如何被破坏，以及在恢复过程中如何重新建立。受认知绑定概念的启发，我们利用功能磁共振成像引导的连接分析来评估任务定义的脑区不同层次之间和内部的功能相互作用的完整性。在深度镇静中，任务相关反应在初级听觉皮层（PAC）中持续存在，但在额下回（IFG）和运动前区消失。对于连接分析，代表记忆任务的感觉和高阶处理的种子区域在 PAC 和 IFG 中被识别。异丙酚阻断了从 PAC 种子到额叶区域和丘脑的连接，但没有阻断 IFG 种子到颞叶、额叶和顶叶广泛分布的脑区的连接（除了 PAC）。这些后来的区域被认为在介导言语理解和记忆方面起作用。这些结果表明，异丙酚通过阻断感觉信息到高阶处理网络的投射来破坏认知，从而阻止信息整合。这些发现有助于我们理解与大脑中的信息和整合相关的麻醉机制。
