Electrophysiologic Effects of Propofol Sedation

Comparison of spontaneous frontal EMG, EEG power spectrum and bispectral index to monitor propofol drug effect and emergence

“…1. This is caused by the well-known biphasic EEG response of propofol at concentrations sufficient to induce unconsciousness (35). In our study, the target-controlled effect-site concentration at loss of consciousness was 1.9-tO.6 pg/ml.…”

“…This was obtained by the use of a target-controlled infusion (TCI) system. Blood concentrations of propofol were not measured but were calculated using a pharmacokinetic model (13)(14)(15)(16) However, in previous studies (35), using a TCI system with the same pharmacokinetic model (36), discrepancies between calculated and actual blood concentrations were small, even in a long infusion regimen and regardless of weight and gender (16).…”

Midlatency median nerve evoked responses during recovery from propofol/sufentanil total intravenous anaesthesia Note

“…However, anaesthetic effects are not uniformly distributed in different brain areas, as it could be demonstrated for propofol by neuroimaging techniques in volunteers or limbic evoked potentials in rats, for example ( 21, 22). In conscious subjects it was shown that sedation induced by low doses of propofol was reflected by an increase in β1 activity (12.75–20 Hz frequency band of the spontaneous electroencephalogram [EEG]) primarily located at frontal and central brain areas ( 23). The generators of MnSSER component N20 are supposed to be located in the primary sensory projection area of the brain, reflecting the afferent somatosensory input from thalamic structures.…”

Consciousness and Complexity during Unresponsiveness Induced by Propofol, Xenon, and Ketamine

“…The finding of high brain complexity (PCI) observed during unresponsiveness induced by ketamine anesthesia is interesting in the context of previous studies employing sensory-evoked potentials and functional connectivity analyses. For example, the late positive P3b evoked by auditory stimuli is equally suppressed during both propofol [41] and ketamine [42,43], even at sub-anesthetic concentrations, and can be absent in awake subjects who do not pay attention to the stimulus [44]. Similarly, front-to-back functional connections were found to be selectively reduced both during propofol-and ketamine-induced unresponsiveness (though coherence is preserved [45,46]) at dosages comparable to the ones employed in the present study and in the presence of a similar background EEG.…”