Abstract
Ketamine is a dissociative anesthetic with proconvulsant properties that acts by noncompetitively blocking the N-methyl-d-aspartate receptors (NMDARs) in the central nervous system (CNS). In general, scalp electroencephalography (EEG) demonstrates low amplitude paroxysmal fast activity (PFA) at low doses, associated with mild sedation, and slow waves as well as burst suppression (BS) pattern associated with unconsciousness at higher doses. Intracranial EEG studies support initial changes of burst suppression pattern occurring in the parieto-occipital regions before frontal propagation suggesting that initial anesthetic effects are associated with activation in the posterior hemispheres, especially the occipital lobes. Initially in people predisposed to epilepsy, ketamine may lower seizure thresholds and increase interictal epileptiform discharges (IEDs) within minutes of administration. In this chapter, we will discuss EEG changes encountered with ketamine administration and compare its anesthetic and proconvulsant effects on EEG with other anesthetics.
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