Ketamine Across the Dose–State Continuum: EEG Signatures, Network Dynamics, and Implications for Brain-State Monitoring in Anesthesia and Critical Care

Ketamine produces clinical states ranging from subanesthetic analgesia and dissociation to anesthetic-dose behavioral unresponsiveness. Its electroencephalographic (EEG) effects differ from the slow-delta and frontal-alpha patterns commonly observed with GABAergic-dominant anesthetics and vary with exposure, administration kinetics, and co-administered agents. After anesthetic bolus dosing, ketamine may produce alternating slow-delta and gamma activity; at lower exposures, spectral and connectivity findings are more heterogeneous. When ketamine is added to propofol or volatile anesthesia, bispectral index and spectral-entropy values may remain elevated or increase, limiting their interpretation as stand-alone measures of hypnotic state. Prior syntheses have largely addressed molecular, cellular, and cortical-circuit mechanisms of dissociation; this narrative review instead synthesizes human EEG, connectivity, imaging, and selected mechanistic evidence using a dose–state framework. We distinguish behavioral responsiveness, environmental connectedness, and conscious experience; assess which network measures are technically derivable from clinical scalp recordings; and consider implications for operating-room and critical-care monitoring. Available evidence supports a cautious interpretation of processed indices and greater attention to the raw EEG, spectrogram, background hypnotic, administration pattern, and clinical context. Validated ketamine-specific EEG biomarkers and prospective monitoring algorithms are not yet available. Potential links between acute EEG effects and antidepressant mechanisms are discussed as shared upstream pathways rather than a single electrophysiological state.