Brain Mechanisms during Course of Anesthesia: What We Know from EEG Changes during Induction and Recovery

The mechanism of anesthesia remains unclear. We do understand, however, that the GABAA receptor, the NMDA receptor, and two-pore-domain K channels are the main targets of anesthetics (Franks, 2008), and several other receptors and ion channels are also influenced in different ways by anesthetics (Alkire et al., 2008). Propofol, barboturates, and volatile anesthetics, all potentiate GABAA receptor. During isoflurane, sevoflurane, and propofol anesthesia similar raw electroencephalogram (EEG) pattern sequences are observed. By contrast, ketamine, nitrous oxide, and xenon, which antagonize the NMDA receptor are characterized by patterns distinctive for each agent. My discussion here focuses on anesthetics that potentiate the GABAA receptor. Data in this experiment were obtained from Fp1–A1, or Fpz–At1, a hemi-frontal lead of the type commonly used with EEG-based anesthesia monitors. The relation between consciousness and EEG patterns has been extensively studied, and it is now well-known that EEG changes correlate well with anesthetic effect. Meanwhile, anesthesia is usually considered to be a reversible phenomenon. The question is, then, do the changes in the brain anesthesia mirror each other during induction and recovery, or are they independent phenomena? Here, based mainly on EEG evidence gathered during anesthesia, I will discuss this question.