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Electrophysiologic and Behavioral Responses to Ketamine Hydrochloride in the Rhesus Monkey

HE neural basis of general anesthesia is T not well understood. Descriptions of gross changes in electroencephalographic (EEG) and evoked potentials add little to this understanding.1 Longo and Silvestrini2 have shown that the anesthetic state is not necessarily related to the slowing of EEG activity, blocking of the ascending reticular activating system, or alteration of the evoked responses in the reticular formation. However, it is generally believed that general anesthet ic agents cause functional changes in some neuronal systems that impinge upon other systems, thus influencing the anesthetic state in the whole brain. Circulatory changes and depression of metabolism within neuronal systems also play an important role in the anesthetic state.3 Interaction of the above factors provides effective pain control via depression of the central nervous system (CNS) .4