Abstract
Anesthetic drugs are typically administered to induce altered states of arousal that range from sedation to general anesthesia (GA). Systems neuroscience studies are currently being used to investigate the neural circuit mechanisms of anesthesia-induced altered arousal states. These studies suggest that by disrupting the oscillatory dynamics that are associated with arousal states, anesthesia-induced oscillations are a putative mechanism through which anesthetic drugs produce altered states of arousal. However, an empirical clinical observation is that even at relatively stable anesthetic doses, patients are sometimes intermittently responsive to verbal commands during states of light sedation. During these periods, prominent anesthesia-induced neural oscillations such as slow-delta (0.1–4 Hz) oscillations are notably absent. Neural correlates of intermittent responsiveness during light sedation have been insufficiently investigated. A principled understanding of the neural correlates of intermittent responsiveness may fundamentally advance our understanding of neural dynamics that are essential for maintaining arousal states, and how they are disrupted by anesthetics. Therefore, we performed a high-density (128 channels) electroencephalogram (EEG) study (n = 8) of sevoflurane-induced altered arousal in healthy volunteers. We administered temporally precise behavioral stimuli every 5 s to assess responsiveness. Here, we show that decreased eyes-closed, awake-alpha (8–12 Hz) oscillation power is associated with lack of responsiveness during sevoflurane effect-onset and -offset. We also show that anteriorization—the transition from occipitally dominant awake-alpha oscillations to frontally dominant anesthesia induced-alpha oscillations—is not a binary phenomenon. Rather, we suggest that periods, which were defined by lack of responsiveness, represent an intermediate brain state. We conclude that awake-alpha oscillation, previously thought to be an idling rhythm, is associated with responsiveness to behavioral stimuli.
Highlights
Anesthetic drugs are typically administered to induce altered states of arousal that range from sedation to general anesthesia (GA), a reversible state comprised of unconsciousness, amnesia, analgesia and immobility with maintenance of physiological stability (Brown et al, 2010)
We studied EEG correlates of intermittent responsiveness to behavioral stimuli during sevoflurane anesthesia-induced altered arousal states that clinically correspond to light sedation
Decreased awake-alpha power (Figure 3, Table 1; frontal and occipital), increased beta power (Figure 3, frontal and occipital), and decreased gamma power (Figures 3D–F, Table 1; occipital) distinguished when volunteers did not respond to behavioral stimuli, compared to when they responded during sevoflurane anesthesia effect-onset
Summary
Anesthetic drugs are typically administered to induce altered states of arousal that range from sedation to general anesthesia (GA), a reversible state comprised of unconsciousness, amnesia, analgesia and immobility with maintenance of physiological stability (Brown et al, 2010). Studies of anesthesia-induced neural oscillations provide a framework that currently guide investigations of the neural circuit mechanisms of anesthesiainduced altered arousal states (McCarthy et al, 2008; Ching et al, 2010; Murphy et al, 2011; Supp et al, 2011; Boly et al, 2012; Vijayan and Kopell, 2012; Lee et al, 2013; Ní Mhuircheartaigh et al, 2013; Purdon et al, 2013; Vijayan et al, 2013; Hashemi et al, 2015). Slow oscillations may result from decreased excitatory cortical inputs from brainstem arousal nuclei, and from simultaneous drug action in the thalamus and cortex (Brown et al, 2010; Hashemi et al, 2015)
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