Contribution to the study of the mechanisms of the loss of consciousness induced by general anesthesia: A brain mapping and electrophysiology approach

In the present thesis, the results of three studies aimed at further elucidating the mechanisms by which anesthetic agents suppress consciousness are reported. The first study contributes to a better understanding of the mechanisms by which propofol, a commonly used intravenous anesthetic agent, can affect cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET), we demonstrated that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus. The second study validates the bispectral index (BIS) of the electroencephalogram and the auditory steady-state response (ASSR) as monitors of the level of consciousness during propofol-induced sedation. The ability of those parameters to predict consciousness was excellent. In the third study, we investigated the effect of altering central cholinergic transmission on the loss of consciousness produced by propofol. We concluded from this study that the loss of consciousness produced by propofol is mediated at least in part via interruption of central cholinergic muscarinic transmission.