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Dexmedetomidine produces more sleep-like brain activity compared to propofol
Preprint   Open access

Dexmedetomidine produces more sleep-like brain activity compared to propofol

Bryan M. Krause, Emily R. Dappen, Rashmi N. Mueller, Hiroto Kawasaki, Robert D. Sanders, Kirill V. Nourski and Matthew I. Banks
bioRxiv
Cold Spring Harbor Laboratory, 1.1
06/01/2025
DOI: 10.1101/2025.05.27.656383
PMCID: PMC12154880
PMID: 40502147
url
https://doi.org/10.1101/2025.05.27.656383View
Preprint (Author's original)This preprint has not been evaluated by subject experts through peer review. Preprints may undergo extensive changes and/or become peer-reviewed journal articles. Open Access

Abstract

Dexmedetomidine is a selective α2-adrenergic agonist used as an anesthesia adjunct to produce a state of sleep-like sedation. However, how brain activity compares quantitatively during dexmedetomidine anesthesia to that during natural sleep, and thus just how “sleep-like” dexmedetomidine anesthesia is, remains unclear. Previously, we showed that the general anesthetic propofol is associated with changes in connectivity and cortical network structure comparable to those observed during sleep. Here, we compare the effects on brain activity of dexmedetomidine, propofol, and sleep quantitatively using intracranial encephalographic (iEEG) recordings in human research participants. iEEG recordings were obtained in 34 epilepsy patients being evaluated for potential seizure resection surgery. Band power and functional connectivity (alpha weighted phase lag index, gamma envelope correlations) and network entropy were measured in recordings during task-free (“resting state”) periods just prior to surgery during anesthesia with either dexmedetomidine or propofol, and during overnight sleep. Anesthesia stage (wake, sedated, unresponsive) was determined using the Observer’s Assessment of Arousal and Sedation. Sleep was staged using standard polysomnography. As expected, significant differences in delta power were observed during dexmedetomidine and propofol as well as during sleep. However, the magnitude of changes in delta power were smaller and regionally heterogeneous for propofol compared to dexmedetomidine and sleep. Functional connectivity changes were comparable between dexmedetomidine, propofol, and natural sleep. Significant changes in network entropy were observed for dexmedetomidine, propofol, and sleep, but changes were larger for propofol compared to dexmedetomidine and sleep. Quantitative comparisons between changes in delta power and network entropy suggest that unresponsiveness under dexmedetomidine produces a similar brain state to that observed during N2 sleep. While delta power, functional connectivity, and network entropy all showed changes during propofol, dexmedetomidine, and sleep, the magnitudes of these changes suggest that dexmedetomidine is more similar than propofol to sleep, specifically to N2 sleep.
 Neuroscience

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