Absence of pain and loss of consciousness are the most striking characteristics of anesthesia and anesthesia-like states such as concussion, reversible coma, syncope (fainting). These states also exhibit movement inhibition, amnesia, a shift to delta-wave EEG pattern, and depressed cerebral metabolism. It is generally presumed that this constellation of signs reflects widely distributed suppression of neuronal excitability and synaptic action due to ubiquitous drug action, or oxygen or nutrient starvation. I will present evidence for a radically different architecture; that a small group of neurons in the mesopontine tegmentum has executive control over the alert status of the entire cerebrum and spinal cord, and can generate loss of pain and loss of consciousness through specific neural circuitry.
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