Changes in information integration and brain networks during propofol-, dexmedetomidine-, and ketamine-induced unresponsiveness.
Zhenhu Liang, Yu Chang, Xiaoge Liu, Shumei Cao, Yali Chen, Tingting Wang, Jianghui Xu, Duan Li, Jun Zhang
British journal of anaesthesia March 1, 2024 DOI: 10.1016/j.bja.2023.11.033 via PubMed
Summary
AI-generated from the abstractInformation integration and brain network measures derived from EEG can distinguish conscious from unconscious states induced by three different anaesthetics. In 72 participants given propofol, dexmedetomidine, or ketamine until they lost responsiveness, permutation cross mutual information (PCMI) within frontal, parietal, and occipital regions decreased during unresponsiveness—for example, frontal within-area PCMI fell from 0.54 to 0.46. Alpha-band PCMI in the frontal region and gamma-band PCMI in posterior areas also dropped. Network analyses showed reduced clustering coefficients and nodal efficiency in frontal, parietal, and occipital areas, while normalized path length increased in delta, theta, and gamma bands, indicating impaired global integration. The three drugs produced similar changes, suggesting a common EEG signature of anaesthesia-induced unconsciousness.
Study at a glance
| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 72 |
| Population | Participants receiving propofol, dexmedetomidine, or ketamine |
| Interventions | Propofol Dexmedetomidine Ketamine |
| Duration | Consciousness transition from eye-closed baseline to unresponsiveness state and then to recovery of responsiveness state |
| Topics | Ketamine |
| Keywords | Brain network Dexmedetomidine Electroencephalography Propofol |
| Citations | 10 |
| Key finding | Permutation cross mutual information and brain network measures showed state-related decreases in information integration and network efficiency during anaesthesia-induced unresponsiveness across three different drugs. |
Abstract
Information integration and network science are important theories for quantifying consciousness. However, whether these theories propose drug- or conscious state-related changes in EEG during anaesthesia-induced unresponsiveness remains unknown. A total of 72 participants were randomised to receive i.v. infusion of propofol, dexmedetomidine, or ketamine at a constant infusion rate until loss of responsiveness. High-density EEG was recorded during the consciousness transition from the eye-closed baseline to the unresponsiveness state and then to the recovery of the responsiveness state. Permutation cross mutual information (PCMI) and PCMI-based brain networks in broadband (0.1-45 Hz) and sub-band frequencies were used to analyse drug- and state-related EEG signature changes. PCMI and brain networks exhibited state-related changes in certain brain regions and frequency bands. The within-area PCMI of the frontal, parietal, and occipital regions, and the between-area PCMI of the parietal-occipital region (median [inter-quartile ranges]), baseline vs unresponsive were as follows: 0.54 (0.46-0.58) vs 0.46 (0.40-0.50), 0.58 (0.52-0.60) vs 0.48 (0.44-0.53), 0.54 (0.49-0.59) vs 0.47 (0.42-0.52) decreased during anaesthesia for three drugs (P<0.05). Alpha PCMI in the frontal region, and gamma PCMI in the posterior area significantly decreased in the unresponsive state (P<0.05). The frontal, parietal, and occipital nodal clustering coefficients and parietal nodal efficiency decreased in the unresponsive state (P<0.05). The increased normalised path length in delta, theta, and gamma bands indicated impaired global integration (P<0.05). The three anaesthetics caused changes in information integration patterns and network functions. Thus, it is possible to build a quantifying framework for anaesthesia-induced conscious state changes on the EEG scale using PCMI and network science.