Neurophysiology and electroencephalogram signatures of ketamine. (A) At low doses, ketamine blocks preferentially the actions of glutamate N-methyl-d-aspartate receptors on γ-aminobutyric acid (GABA)ergic inhibitory interneurons in the cortex and subcortical sites such as the thalamus, hippocampus, and the limbic system. The antinociceptive effect of ketamine is due in part to its blockade of glutamate release from peripheral afferent (PAF) neurons in the dorsal root ganglia (DRG) at their synapses on to projection neurons (PNs) in the spinal cord. (B) Spectrogram showing the beta-gamma oscillations in the electroencephalogram of a 61-yr-old woman who received ketamine administered in 30 mg and 20 mg doses (green arrows) for a vacuum dressing change. Blocking the inhibitory action of the interneurons in cortical and subcortical circuits helps explain why ketamine produces beta oscillations as its electroencephalogram signature. (C) Ten-second electroencephalogram trace recorded at minute 5 from the spectrogram in B. A is reproduced, with permission, from Brown, Purdon, and Van Dort: General anesthesia and altered states of arousal: A systems neuroscience analysis. Annu Rev Neurosci. 2011;324:601–28. B and C were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission, from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.
