The article discusses the clinical and neurophysiological features of general anesthesia, focusing on its relationship to sleep and coma. General anesthesia is a reversible condition characterized by unconsciousness, amnesia, analgesia, and akinesia, with stable autonomic, cardiovascular, respiratory, and thermoregulatory systems. The EEG patterns during general anesthesia can be categorized into induction, maintenance, and emergence periods. During induction, patients experience sedation, paradoxical excitation, and loss of consciousness. In the maintenance period, the EEG patterns reflect different stages of anesthesia, from light to deep anesthesia, with burst suppression in the most profound state. During emergence, patients gradually regain consciousness, with physiological and behavioral signs indicating a return to normal function. The mechanisms of unconsciousness induced by anesthetic drugs involve altering neurotransmission in the cerebral cortex, brain stem, and thalamus, particularly through GABA_A and NMDA receptors. The article also explores the role of the central thalamus in arousal regulation and the active brain states associated with unconsciousness, such as those induced by ketamine. Understanding these mechanisms may lead to new approaches in anesthesia and consciousness manipulation.The article discusses the clinical and neurophysiological features of general anesthesia, focusing on its relationship to sleep and coma. General anesthesia is a reversible condition characterized by unconsciousness, amnesia, analgesia, and akinesia, with stable autonomic, cardiovascular, respiratory, and thermoregulatory systems. The EEG patterns during general anesthesia can be categorized into induction, maintenance, and emergence periods. During induction, patients experience sedation, paradoxical excitation, and loss of consciousness. In the maintenance period, the EEG patterns reflect different stages of anesthesia, from light to deep anesthesia, with burst suppression in the most profound state. During emergence, patients gradually regain consciousness, with physiological and behavioral signs indicating a return to normal function. The mechanisms of unconsciousness induced by anesthetic drugs involve altering neurotransmission in the cerebral cortex, brain stem, and thalamus, particularly through GABA_A and NMDA receptors. The article also explores the role of the central thalamus in arousal regulation and the active brain states associated with unconsciousness, such as those induced by ketamine. Understanding these mechanisms may lead to new approaches in anesthesia and consciousness manipulation.