General Anesthesia and Human Brain Connectivity

Abstract

General anesthesia consists of amnesia, hypnosis, analgesia, and areflexia. Of these, the mechanism of hypnosis, or loss of consciousness, has been the most elusive, yet a fascinating problem. How anesthetic agents suppress human consciousness has been investigated with neuroimaging for two decades. Anesthetics substantially reduce the global cerebral metabolic rate and blood flow with a degree of regional heterogeneity characteristic to the anesthetic agent. The thalamus appears to be a common site of modulation by several anesthetics, but this may be secondary to cortical effects. Stimulus-dependent brain activation is preserved in primary sensory areas, suggesting that unconsciousness cannot be explained by cortical deafferentation or a diminution of cortical sensory reactivity. The effect of general anesthetics in functional and effective connectivity is varied depending on the agent, dose, and network studied. At an anesthetic depth characterized by the subjects' unresponsiveness, a partial, but not complete, reduction in connectivity is generally observed. Functional connectivity of the frontoparietal association cortex is often reduced, but a causal role of this change for the loss of consciousness remains uncertain. Functional connectivity of the nonspecific (intralaminar) thalamic nuclei is preferentially reduced by propofol. Higher-order thalamocortical connectivity is also reduced with certain anesthetics. The changes in functional connectivity during anesthesia induction and emergence do not mirror each other; the recovery from anesthesia may involve increases in functional connectivity above the normal wakeful baseline. Anesthetic loss of consciousness is not a block of corticofugal information transfer, but a disruption of higher-order cortical information integration. The prime candidates for functional networks of the forebrain that play a critical role in maintaining the state of consciousness are those based on the posterior parietal-cingulate-precuneus region and the nonspecific thalamus.

What insects can tell us about the origins of consciousness

“…Indeed, there is evidence of residual conscious awareness in patients with severe cortical damage who are otherwise unresponsive to the world, suggesting that preserved subcortical structures may continue to support subjective experience (23,24). Although the mechanism of anesthetic action is still debated (25), there is increasing evidence that the effect of anesthetics depends on the disconnection of cortical circuits from subcortical structures rather than on their direct cortical activity (26,27). Anesthetics (28) or electrical stimulation (19), which affect cortical midline structures without affecting subcortical structures, do not abolish consciousness; they instead produce unresponsive but conscious dreamlike states.…”

Cortico-centric effects of general anesthetics on cerebrocortical evoked potentials

“…Top-down cortico-centric proposals are based on the idea that anesthetics disrupt the cortical processing of incoming sensory information [7][8][9][10] , particularly impairing its capacity to represent complex information and/or integrate information across distributed cortical regions [11] .…”

The Hormesis of Thinking: A Deeper Quantum Thermodynamic Perspective?

“…Interestingly, some anaesthetics, at high concentrations, start to break up mitochondrial networks [115]; this would clearly alter the EM field pattern within the cell. During anaesthesia, the brains energy consumption drops dramatically from 30-70% [116]. This would suggest that electron flow in the brain is dramatically reduced and thus its ability to maintain electric fields.…”