Consciousness and anesthesia

Abstract

When we are anesthetized, we expect consciousness to vanish. But does it always? Although anesthesia undoubtedly induces unresponsiveness and amnesia, the extent to which it causes unconsciousness is harder to establish. For instance, certain anesthetics act on areas of the brain's cortex near the midline and abolish behavioral responsiveness, but not necessarily consciousness. Unconsciousness is likely to ensue when a complex of brain regions in the posterior parietal area is inactivated. Consciousness vanishes when anesthetics produce functional disconnection in this posterior complex, interrupting cortical communication and causing a loss of integration; or when they lead to bistable, stereotypic responses, causing a loss of information capacity. Thus, anesthetics seem to cause unconsciousness when they block the brain's ability to integrate information.

Figures

Fig. 1

Brain areas associated with anesthetic effects (references in the textand 2).

Fig. 2

Unconsciousness is associated with a loss of cortical integration. (A) The corticothalamic system is represented metaphorically as a large die having many faces, each corresponding to a different brain firing pattern. During conscious waking, the die rolls on a particular face, ruling out all the others and thus generating integrated information. If integration is lost (as in anesthesia or sleep), the die disintegrates into many two-faced dice, each generating 1 bit of information. (B) Anesthesia reduces cortical integration in the rat. (Top) During waking, transfer entropy, a measure of directional interactions among brain areas, is balanced in the feedforward (green) and feedback (red) directions. During anesthesia, feedback transfer entropy (red) is reduced, implying a decrease in front-toback interactions. (Bottom) Responses to a flashing light delivered at 0.2 Hz (arrow) from a representative rat when awake and under 1.1% isoflurane anesthesia (56). When the rat is awake, each flash evokes a sustained gamma frequency (20 to 60 Hz) response in visual occipital cortex (blue) and a later response in parietal association cortex (red). During anesthesia, the occipital response is preserved, although it is shorter (blue), and the parietal response is attenuated, indicating that anesthesia reduces cortical interactions and thus reduces integration. (C) Sleeping reduces cortical integration in humans. EEG voltages and current densities are shown from a representative subject in which the premotor cortex was stimulated with transcranial magnetic stimulation (TMS) (black arrow). During waking (top), stimulation evokes EEG responses first near the stimulation site (black circle; the white cross is the site of maximum evoked current) and then in sequence at other cortical locations. During deep sleep (bottom), the stimulus-evoked response remains local, indicating a loss of cortical integration.

Fig. 3

Unconsciousness is associated with a loss of information capacity. (A) As in Fig 2, the corticothalamic system is represented metaphorically as a large die having many faces, each corresponding to a different brain firing pattern. During conscious waking, the die rolls on a particular face, ruling out all the others and thus generating integrated information. If information is lost (as in anesthesia or sleeping), the die is flattened so that it has only two faces (firing patterns). Due to the loss of repertoire, it generates only 1 bit of information. (B) Anesthesia reduces information capacity in rat cortex. (Top) Field potentials recorded before and during light flashes (marks below each trace). During waking (left), flash-evoked field potentials (blue) (light flashes indicated by marks below each trace) are small and variable, being masked by spontaneous neuronal activity. During deep anesthesia (right), bursts of activity occur spontaneously and after each light flash. (Bottom) During anesthesia, the g-burst response is uniform across all three brain regions. Thus, responses are stereotypic and lack regional specificity, indicating a loss of information capacity. (C) Sleeping reduces cortical information carrying capacity in humans. (Top) During waking, stimulation over the mesial parietal cortex produces a specific, sequential pattern of activation. (Bottom) During sleep, stimulation produces a global, stereotypic response that spreads from the stimulation site to most of the cortex, indicating a loss of information capacity. Black traces represent averaged voltage potentials recorded at all electrodes and superimposed, while estimated current density is displayed in absolute scale (63, 64).