Fig. 7.

Spatio-temporal characterization of electroencephalogram alpha and slow oscillations observed during induction of and recovery from propofol-induced unconsciousness. A. In the volunteer subject lying awake with eyes closed, spatially coherent alpha oscillations are observed over the occipital area. The alpha oscillations shift to the front of the head with loss of consciousness (LOC) where they intensify and become spatially coherent during unconsciousness. The alpha oscillations dissipate anteriorly and return to the occipital area during return of consciousness (ROC) where they re-intensify and are spatially coherent in the eyes-closed awake state. B. During consciousness there is broadband communication between the thalamus and the frontal cortex with beta and gamma activity in the electroencephalogram. Modeling studies suggest during propofol-induced unconsciousness that the spatially coherent alpha oscillations are highly-structured rhythms in thalamocortical circuits.⁵⁷ C. Slow oscillations recorded from grid electrodes implanted in a patient with epilepsy, 30 seconds after bolus induction of general anesthesia with propofol. The slow oscillations at nearby electrodes (red and green dots) are in phase (red and green traces) whereas the slow oscillation recorded at an electrode 2 centimeters away (blue dot) is out of phase (blue trace) with those at the other two locations. Neurons spike only (histograms) in a limited time window governed by the phase of the local slow oscillations. These slow oscillations are a marker of intracortical fragmentation with propofol as communication through spiking activity is restricted to local areas. The spatially coherent alpha oscillations and the disruption of neural spiking activity associated with the slow oscillations are likely to be two of the mechanisms through which propofol induces unconsciousness. Panel A is reproduced from Purdon et al. PNAS, 2013 and Panel B is adapted from Lewis et al. PNAS, 2012 with permission.