Anesthesia, neural information processing, and conscious awareness

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. Neuronal-specificity theories postulate that activity in particular neural populations is sufficient for conscious awareness, while process-coherence theories postulate that particular organizations of neural activity are sufficient. Accounts of anesthetic narcosis, on the other hand, explain losses of consciousness in terms of neural signal-suppressions, transmission blocks, and the disruptions of signal interpretation. While signal-suppression may account for the actions of some anesthetic agents, the existence of anesthetics, such as choralose, that cause both loss of consciousness and elevated discharge rates, is problematic for a general theory of narcosis that is based purely on signal suppression and transmission-block. 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.