Search

• Ketamine is an anesthetic drug with dissociative properties. • Ketamine induces highly structured oscillations that may be used to monitor drug-induced altered arousal. • Surface electroencephalogram oscillations are unlikely to underly ketamine-induced dissociation. Ketamine is an anesthetic drug associated with dissociation. Decreased electroencephalogram alpha (8–13 Hz) and low-beta (13–20 Hz) oscillation power have been associated with ketamine-induced dissociation. We aimed to characterize surface electroencephalogram signatures that may serve as biomarkers for dissociation. We analyzed data from a single-site, open-label, high-density surface electroencephalogram study of ketamine anesthesia (2 mg/kg, n = 15). We assessed dissociation longitudinally using the Clinician Administered Dissociation States Scale (CADSS) and administered midazolam to attenuate dissociation and enable causal inference. We analyzed electroencephalogram power and global coherence with multitaper spectral methods. Mixed effects models were used to assess whether power and global coherence signatures of ketamine could be developed into dissociation-specific biomarkers. Compared to baseline, ketamine unresponsiveness was associated with increased frontal power between 0.5 to 9.3 Hz, 12.2 to 16.6 Hz, and 24.4 to 50 Hz. As subjects transitioned into a responsive but dissociated state (mean CADSS ± SD, 22.1 ± 17), there was a decrease in power between 0.5 to 10.3 Hz and 11.7 to 50 Hz. Midazolam reduced dissociation scores (14.3 ± 11.6), decreased power between 4.4 to 11.7 Hz and increased power between 14.2 to 50 Hz. Our mixed-effects model demonstrated a quadratic relationship between time and CADSS scores. When models (frontal power, occipital power, global coherence) were reanalyzed with midazolam and electroencephalogram features as covariates, only midazolam was retained. Ketamine is associated with structured electroencephalogram power and global coherence signatures that may enable principled anesthetic state but not dissociation monitoring. A neurophysiological biomarker for dissociation may lead to a better understanding of neuropsychiatric disorders. [ABSTRACT FROM AUTHOR]

Highlights • Intraoperative electroencephalogram burst-suppression is associated with post-operative delirium. • Decreased alpha and beta power was evident in the EEG prior to the occurrence of burst-suppression. • Decreased EEG alpha and beta power predicted the later incidence and duration of burst-suppression. Abstract Objective Electroencephalogram burst-suppression during general anesthesia is associated with post-operative delirium (POD). Whether burst-suppression causes POD or merely reflects susceptibility to POD is unclear. We hypothesized decreased intraoperative alpha (8–12 Hz) and beta (13–33 Hz) power prior to the occurrence of burst-suppression in susceptible patients. Methods We analyzed intraoperative electroencephalogram data of cardiac surgical patients undergoing cardiopulmonary bypass (CPB). We detected the incidence and duration of CPB burst-suppression with an automated burst-suppression detection algorithm. We analyzed EEG data with multitaper spectral estimation methods. We assessed associations between patient characteristics and burst-suppression using Binomial and Zero-inflated Poisson Regression Models. Results We found significantly decreased alpha and beta power (7.8–22.95 Hz) in the CPB burst-suppression cohort. The odds ratio for the association between point estimates for alpha and beta power (7.8–22.95 Hz) and the incidence of burst-suppression was 0.88 (95% CI: 0.79–0.98). The incidence rate ratio for the association between point estimates for power between the alpha and beta range and the duration of burst-suppression was 0.89 (95% CI: 0.84–0.93). Conclusion Decreased intra-operative power within the alpha and beta range was associated with susceptibility to burst-suppression during CPB. Significance This dynamic may be used to develop principled neurophysiological-based approaches to aid the preemptive identification and targeted care of POD vulnerable patients. [ABSTRACT FROM AUTHOR]