, 2002, Schrouff et al , 2011 and Veselis et al , 2004) ( Figure 

, 2002, Schrouff et al., 2011 and Veselis et al., 2004) ( Figure 9). Consistent with these views, Velly et al. (2007) found that during induction of anesthesia by sevofurane and propofol in human patients with Parkinson disease, cortical EEG complexity decreased dramatically at the precise time where consciousness was lost, while for several minutes there was little change in subcortical signals, and eventually a slow decline ( Figure 9). These data suggest that in humans, the early stage of anesthesia correlates with cortical disruption, and that the effects on the thalamus are indirectly driven

by cortical feedback ( Alkire et al., 2008). Indeed, in the course of anesthesia induction, there is a decrease in EEG AC220 nmr coherence in the 20 to 80 Hz frequency range between right and left frontal cortices and between frontal and occipital territories ( John and Prichep, R428 clinical trial 2005). Quantitative analysis of EEG under propofol induction further indicates a reduction of mean information integration, as measured

by Tononi’s Phi measure, around the γ-band (40 Hz) and a breakdown of the spatiotemporal organization of this particular band ( Lee et al., 2009b). In agreement with experiments carried out with rats ( Imas et al., 2005 and Imas et al., 2006), quantitative EEG analysis in humans under propofol anesthesia induction noted a decrease of directed feedback connectivity with loss of consciousness and a return with responsiveness to verbal command ( Lee et al., 2009a). Also, during anesthesia induced by the benzodiazepine midazolam, an externally induced transcranial pulse evoked reliable initial activity monitored by ERPs in humans, but the subsequent late phase of propagation to distributed areas was abolished ( Ferrarelli et al., Ketanserin 2010). These observations are consistent with the postulated role of top-down frontal-posterior amplification in

conscious access (see also Supèr et al., 2001). Coma and vegetative state. The clinical distinctions between coma, vegetative state ( Laureys, 2005), and minimal consciousness ( Giacino, 2005) remain poorly defined, and even fully conscious but paralyzed patients with locked-in syndrome can remain undetected. It is therefore of interest to see whether objective neural measures and GNW theory can help discriminate them. In coma and vegetative state, as with general anesthesia, global metabolic activity typically decreases to ∼50% of normal levels ( Laureys, 2005). This decrease is not homogeneous, however, but particularly pronounced in GNW areas including lateral and mesial prefrontal and inferior parietal cortices ( Figure 9). Spontaneous recovery from VS is accompanied by a functional restoration of this broad frontoparietal network ( Laureys et al.

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