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Translating electrophysiological signatures of awareness into thalamocortical mechanisms by inverting systems-level computational models across arousal states

Vicente Medel, Eli J Müller, Brandon R Munn, Cameron P Casey, Robert D. Sanders, James M Shine

bioRxiv October 16, 2023 preprint DOI: 10.1101/2023.10.11.561970 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Observational study using computational modeling of EEG data
Intervention Dexmedetomidine
Key findings The authors report that declining conscious experience and sensory awareness under dexmedetomidine sedation was associated with reduced engagement of excitatory thalamocortical loop resonances and increased inhibitory intrathalamic loop gains. They propose this as a systems-level thalamocortical mechanism underlying how consciousness fades across arousal states.

Abstract

While consciousness never fades during wakefulness, there is a paradoxical coexistence of consciousness during dreaming states. It’s also possible for sensory awareness to be either present or absent when awakened from seemingly-identical states of sedation and anaesthesia. Traditionally, these states have been characterised in terms of their electroencephalographic neural correlates, however, without clear underlying neurobiological mechanisms. To bridge this gap, we invert a validated neural mass model of the corticothalamic system using scalp EEG collected during nonlinear transitions in conscious experience and sensory awareness across varying depths of dexmedetomidine sedation. We found that a decline in conscious experience and sensory awareness with dexmedetomidine was associated with a decrease in the engagement of excitatory thalamocortical loop resonances, along with an increase in inhibitory intrathalamic loop gains. These findings shed light into the neural mechanisms of conscious experience and sensory awareness, and explain how it fades across arousal states, bridging the gap between the neural correlates of consciousness and its underlying systems-level thalamocortical mechanisms.

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