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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Authors | M T Alkire, R J Haier, J H Fallon |
Journal | Consciousness and cognition
(Conscious Cogn)
Vol. 9
Issue 3
Pg. 370-86
(Sep 2000)
ISSN: 1053-8100 [Print] United States |
PMID | 10993665
(Publication Type: Journal Article)
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Copyright | Copyright 2000 Academic Press. |
Chemical References |
- Anesthetics, Inhalation
- Fluorodeoxyglucose F18
- Isoflurane
- Halothane
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Topics |
- Adolescent
- Adult
- Anesthesia, General
- Anesthetics, Inhalation
- Cerebral Cortex
(drug effects, physiopathology)
- Energy Metabolism
(drug effects, physiology)
- Female
- Fluorodeoxyglucose F18
- Halothane
- Humans
- Isoflurane
- Male
- Mesencephalon
(drug effects, physiopathology)
- Neural Pathways
(drug effects, physiopathology)
- Reticular Formation
(drug effects, physiopathology)
- Thalamus
(drug effects, physiopathology)
- Tomography, Emission-Computed
- Unconsciousness
(chemically induced, physiopathology)
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