Self Comes to Mind

millions of people who otherwise could not have had surgery. One often thinks of general anesthesia as a painkiller, since its effects preclude the pain that surgical wounds would cause, but the truth is that anesthesia precludes pain in the most radical way possible: it suspends consciousness altogether, not merely pain but all aspects of the conscious mind.
    Superficial levels of anesthesia reduce consciousness lightly, leaving room for some unconscious learning and the occasional “breakthrough” of conscious processing. Deep levels of anesthesia cut deep into the conscious process and are, in point of fact, pharmacologically controlled variations on the vegetative state or even coma. That is what your surgeon needs if he is to work in peace inside your heart or your hip joint. You must be far, far away from it all, so deeply asleep that your muscular tone is as tough as jelly and you are not able to move. Stage III anesthesia is the ticket, and at that stage you will hear nothing, feel nothing, and think of nothing. When the surgeon talks to you, you will not respond.
    The history of anesthesia has provided surgeons with numerous pharmacological agents to work with, and the search for the molecules that can do the most efficient job with minimal risks and little toxicity is an ongoing effort. By and large, anesthetics do their job by increasing inhibition in neural circuits. This can be achieved by strengthening the action of GABA (gamma-aminobutyric acid), the leading inhibitory transmitter in the brain. Anesthetics act by hyperpolarizing neurons and blocking acetylcholine, an important molecule in normal neuron-to-neuron communication. It was commonly thought that anesthetic agents worked by depressing brain function across the board, bringing down the activity of neurons most everywhere. But recent studies have shown that some anesthetics work very selectively, exerting their action at specific brain sites. A case in point is propofol. As shown in functional neuroimaging studies, it does its splendid job by working principally at three sites: the posteromedial cortices, the thalamus, and the brain-stem tegmentum. While the relative importance of each site in the production of unconsciousness is unknown, the decreases in level of consciousness are correlated with the decrease of regional blood flow in the posteromedial cortices. 5 But the evidence goes well beyond propofol. Other anesthetic agents seem to have comparable effects, as a comprehensive review demonstrates. Three paramedian brain territories instrumental in building consciousness are selectively depressed by propofol anesthesia.
SLEEP RESEARCH
    Sleep is a natural setting for the study of consciousness, and sleep studies were early contributors to the understanding of the problem. It has been well established that electroencephalographic rhythms, the distinct patterns of electrical activity generated by the brain, are associated with specific stages of sleep. It is notoriously difficult to peg the origin of electroencephalographic patterns to particular brain regions, and that is where the spatial localization of functional neuroimaging techniques has come in handy to complete the picture. Using imaging techniques, it has been possible, over the past decade, to take a closer look at specific brain regions during varied stages of sleep.
    For example, consciousness is deeply depressed during slow-wave sleep, also known as non–rapid eye movement sleep or N-REM. This is the deep slumber of the kind and the just, the slumber from which only the unkind and unjust alarm clock will wake us up. This is “dreamless sleep,” although the complete absence of dreams appears to apply only to the first part of the night. Functional neuroimaging studies show that in slow-wave sleep, activity is reduced in a number of brain regions, most prominently in parts of the brain-stem tegmentum (at the pons and midbrain), the diencephalon (the thalamus and the hypothalamus/basal forebrain), the medial and lateral parts of the prefrontal cortex, the anterior cingulate cortex, the lateral parietal cortex, and the PMCs. The pattern of functional reduction in slow-wave sleep is less selective than in general anesthesia (there is no reason why the pattern should be the same), but as in anesthesia, it does not suggest an across-the-board depression of function. The pattern does include, prominently, the three correlates of consciousness-making (brain stem, thalamus, and