Toward a unified theory of narcosis: brain imaging evidence for a thalamocortical switch as the neurophysiologic basis of anesthetic-induced unconsciousness.
M T Alkire, R J Haier, J H Fallon
Consciousness and Cognition September 2000 DOI: 10.1006/ccog.1999.0423 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational functional neuroimaging study Peer reviewed |
|---|---|
| Sample size | 11 |
| Population | Human volunteers undergoing general anesthesia |
| Key findings | Across two different volatile anesthetics, functional brain imaging showed specific suppression of regional thalamic and midbrain reticular formation activity. The authors hypothesize that the common mechanism of anesthetic-induced unconsciousness is a hyperpolarization block of thalamocortical neurons, as in sleep, and propose a model in which anesthetics' diverse cellular effects converge on this single system. |
Abstract
A unifying theory of general anesthetic-induced unconsciousness must explain the common mechanism through which various anesthetic agents produce unconsciousness. Functional-brain-imaging data obtained from 11 volunteers during general anesthesia showed specific suppression of regional thalamic and midbrain reticular formation activity across two different commonly used volatile agents. These findings are discussed in relation to findings from sleep neurophysiology and the implications of this work for consciousness research. It is hypothesized that the essential common neurophysiologic mechanism underlying anesthetic-induced unconsciousness is, as with sleep-induced unconsciousness, a hyperpolarization block of thalamocortical neurons. A model of anesthetic-induced unconsciousness is introduced to explain how the plethora of effects anesthetics have on cellular functioning ultimately all converge on a single neuroanatomic/neurophysiologic system, thus providing for a unitary physiologic theory of narcosis related to consciousness.
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