The spectral exponent of the resting EEG indexes the presence of consciousness during unresponsiveness induced by propofol, xenon, and ketamine

During anesthesia, people may still be conscious even though they do not respond. A marker of consciousness based on the decay rate of the power spectral density (PSD) of resting EEG—measured by the spectral exponent β—was tested in healthy participants under xenon, propofol, or ketamine anesthesia (n=5 per group). Delayed reports indicated whether consciousness was present or absent. Xenon and propofol, which abolish consciousness, caused a steeper PSD decay (more negative β) compared to wakefulness. Ketamine, which preserves consciousness, showed a PSD decay similar to wakefulness overall but a flattening in high frequencies (20–40 Hz). The spectral exponent correlated strongly with the Perturbational Complexity Index (PCI), supporting its use as a marker of consciousness.

Study at a glance

Abstract

Despite the absence of responsiveness during anesthesia, conscious experience may persist. However, reliable, easily acquirable and interpretable neurophysiological markers of the presence of consciousness in unresponsive states are still missing. A promising marker is based on the decay-rate of the power spectral density (PSD) of the resting EEG. We acquired resting electroencephalogram (EEG) in three groups of healthy participants (n = 5 each), before and during anesthesia induced by either xenon, propofol or ketamine. Dosage of each anesthetic agent was tailored to yield unresponsiveness (Ramsay score = 6). Delayed subjective reports assessed whether conscious experience was present ('Conscious report') or absent/inaccessible to recall ('No Report'). We estimated the decay of the PSD of the resting EEG-after removing oscillatory peaks-via the spectral exponent β, for a broad band (1-40 Hz) and narrower sub-bands (1-20 Hz, 20-40 Hz). Within-subject anesthetic changes in β were assessed. Furthermore, based on β, 'Conscious report' states were discriminated against 'no report' states. Finally, we evaluated the correlation of the resting spectral exponent with a recently proposed index of consciousness, the Perturbational Complexity Index (PCI), derived from a previous TMS-EEG study. The spectral exponent of the resting EEG discriminated states in which consciousness was present (wakefulness, ketamine) from states where consciousness was reduced or abolished (xenon, propofol). Loss of consciousness substantially decreased the (negative) broad-band spectral exponent in each subject undergoing xenon or propofol anesthesia-indexing an overall steeper PSD decay. Conversely, ketamine displayed an overall PSD decay similar to that of wakefulness-consistent with the preservation of consciousness-yet it showed a flattening of the decay in the high-frequencies (20-40 Hz)-consistent with its specific mechanism of action. The spectral exponent was highly correlated to PCI, corroborating its interpretation as a marker of the presence of consciousness. A steeper PSD of the resting EEG reliably indexed unconsciousness in anesthesia, beyond sheer unresponsiveness.