From the Department of Anesthesia, Critical Care and Pain Medicine (J.J.B., Y.I.) the Department of Neurology (S.R.P.), Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts the Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California (P.H.) the Departments of Neurological Surgery, Neuroscience, Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, Bronx, New York (E.N.E.).
Anesthesiology. 2020 Apr;132(4):750-762. doi: 10.1097/ALN.0000000000003159.
Ketamine is a noncompetitive N-methyl-D-aspartate antagonist and is known for unique electrophysiologic profiles in electroencephalography. However, the mechanisms of ketamine-induced unconsciousness are not clearly understood. The authors have investigated neuronal dynamics of ketamine-induced loss and return of consciousness and how multisensory processing is modified in the primate neocortex.
The authors performed intracortical recordings of local field potentials and single unit activity during ketamine-induced altered states of consciousness in a somatosensory and ventral premotor network. The animals were trained to perform a button holding task to indicate alertness. Air puff to face or sound was randomly delivered in each trial regardless of their behavioral response. Ketamine was infused for 60 min.
Ketamine-induced loss of consciousness was identified during a gradual evolution of the high beta-gamma oscillations. The slow oscillations appeared to develop at a later stage of ketamine anesthesia. Return of consciousness and return of preanesthetic performance level (performance return) were observed during a gradual drift of the gamma oscillations toward the beta frequency. Ketamine-induced loss of consciousness, return of consciousness, and performance return are all identified during a gradual change of the dynamics, distinctive from the abrupt neural changes at propofol-induced loss of consciousness and return of consciousness. Multisensory responses indicate that puff evoked potentials and single-unit firing responses to puff were both preserved during ketamine anesthesia, but sound responses were selectively diminished. Units with suppressed responses and those with bimodal responses appeared to be inhibited under ketamine and delayed in recovery.
Ketamine generates unique intracortical dynamics during its altered states of consciousness, suggesting fundamentally different neuronal processes from propofol. The gradually shifting dynamics suggest a continuously conscious or dreaming state while unresponsive under ketamine until its deeper stage with the slow-delta oscillations. Somatosensory processing is preserved during ketamine anesthesia, but multisensory processing appears to be diminished under ketamine and through recovery.
氯胺酮是一种非竞争性 N-甲基-D-天冬氨酸拮抗剂，其脑电图具有独特的电生理特征。然而，氯胺酮诱导意识丧失的机制尚不清楚。作者研究了氯胺酮诱导的意识丧失和恢复过程中的神经元动力学，以及多感觉处理在灵长类新皮层中的变化。
作者在体感和腹侧运动前网络中进行了氯胺酮诱导的意识状态改变时的皮层内局部场电位和单细胞活动的记录。动物接受训练以执行按钮保持任务来表示警觉。在每个试验中，空气喷射到面部或发出声音是随机的，与它们的行为反应无关。氯胺酮输注 60 分钟。
氯胺酮诱导的意识丧失是在高β-γ振荡逐渐演变过程中确定的。慢振荡似乎在氯胺酮麻醉的后期阶段发展。在γ振荡逐渐向β频率漂移期间，观察到意识恢复和术前性能水平的恢复（性能恢复）。氯胺酮诱导的意识丧失、意识恢复和性能恢复都是在动力学逐渐变化过程中确定的，与异丙酚诱导的意识丧失和恢复时的突然神经变化不同。多感觉反应表明，在氯胺酮麻醉期间，吹气诱发的电位和吹气的单细胞放电反应都被保留，但声音反应被选择性地减弱。对氯胺酮抑制和恢复延迟的反应受到抑制的单元和具有双模态反应的单元似乎被抑制。
氯胺酮在其意识状态改变时产生独特的皮层内动力学，这表明与异丙酚的神经元过程根本不同。逐渐变化的动力学表明，在氯胺酮作用下，存在持续的意识或做梦状态，而在深度慢δ振荡阶段则无反应。氯胺酮麻醉期间保留了躯体感觉处理，但多感觉处理似乎在氯胺酮作用下减弱，并在恢复过程中恢复。
