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

Abstract: 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

Abstract: feelings (brainstem, limbic system). The best scientific synchrony and consciousness.21,27 Anesthesiology, V 105, No 2, Aug 2006

Abstract: Empirical work is reviewed which correlates the presence or absence of various parts of the auditory evoked potential with the disappearance and reemergence of auditory sensation during induction of and recovery from anesthesia. As a result, the hypothesis is generated that the electrophysiological correlate of auditory sensation is whatever neural activity generates the middle latency waves of the auditory evoked potential. This activity occurs from 20 to 80 ms poststimulus in the primary and secondary areas of the auditory cortex. Evidence is presented suggesting that earlier or later waves in the auditory evoked potential do not covary with auditory sensation (as opposed to auditory perception) and it is therefore suggested that they are possibly not the electrophysiological correlates of sensation