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. (shrink)

Following the pragmatic practices of anesthesiologists an individual is defined to be in a state of consciousness empirically by the behavioral ability to respond to simple stimuli and the loss of consciousness is defined by the loss of that facility. Several brain activities are proposed as properties of the state of consciousness. Baseline brain energy consumption has been shown by 13C MRS to be almost completely used for neuronal signaling. PET measurements of glucose or oxygen consumption, from several laboratories, show (...) a widespread ~45% reduction in cerebral energy during anesthesia-induced loss of consciousness. We propose that the high level of brain energy consumption of the awake state is a necessary property of the state of consciousness. Two additional neuronal properties are drastic changes in the patterns of fMRI activation and neuronal population activity at deep vs. light levels of anesthesia, which correspond to low vs. high energy states, respectively. The brain-wide fMRI activity patterns with rat sensory stimulation at the higher energy state collapses to contralateral somatosensory response at the lower energy state. Firing rates of an ensemble of neurons in the rat somatosensory cortex show that most of the energy in light anesthesia is consumed in the spiking frequency range of 20-40 Hz, which include γ-band electrical signals. In deep anesthesia the frequency range shifts to below 10 Hz. The high brain energy consumption, characteristic of the state of consciousness, supports elevated levels of high frequency neuronal firing observed in the resting, awake brain. In our model, necessary brain properties of the state of consciousness create our physical understanding of that state rather than the converse, popular in neuroimaging, in which subjective mental processes are identified to be necessary and sufficient correlates of the state of consciousness. (shrink)