Consciousness and cognition
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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. ⋯ 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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Possible systemic effects of general anesthetic agents on neural information processing are discussed in the context of the thalamocortical suppression hypothesis presented by Drs. Alkire, Haier, and Fallon (this issue) in their PET study of the anesthetized state. Accounts of the neural requisites of consciousness fall into two broad categories. ⋯ However, anesthetic agents also alter relative firing rates and temporal discharge patterns that may disrupt the coherence of neural signals and the functioning of the neural networks that interpret them. It is difficult at present, solely on the basis of regional brain metabolic rates, to test process-coherence hypotheses regarding organizational requisites for conscious awareness. While these pioneering PET studies have great merit as panoramic windows of mind-brain correlates, wider ranges of theory and empirical evidence need to be brought into the formulation of truly comprehensive theories of consciousness and anesthesia.