Characterization of burst suppression. A. The spectrogram in fig. 6B from minute 4 to minute 20. Burst suppression in the spectrogram shows as periods of blue (isoelectric activity) interspersed with periods of red-yellow (slow-delta and alpha oscillations). The horizontal red line shows the principal period of burst suppression. B. Unprocessed electroencephalogram recordings corresponding to the spectrogram in A. The horizontal red lines at ±5 microvolts are the thresholds which separate burst events (amplitude ≥ 5 microvolts) from suppression events (amplitude
Fig. 9
Neurophysiology and electroencephalogram signatures of…
Fig. 9
Neurophysiology and electroencephalogram signatures of ketamine. A. At low doses, ketamine blocks preferentially…
Fig. 9 Neurophysiology and electroencephalogram signatures of ketamine. A. At low doses, ketamine blocks preferentially the actions of glutamate NMDA receptors on GABAergic inhibitory interneurons in the cortex and subcortical sites such as the 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 (PN) in the spinal cord. B. Spectrogram showing the beta-gamma oscillations in the electroencephalogram of a sixty-one year-old woman who received ketamine sedation for a vacuum dressing change. Blocking the inhibitory action of the interneurons in cortical and subcortical circuits helps explain why ketamine produces a high-frequency beta oscillation as its electroencephalogram signature. C. Ten-second electroencephalogram trace recorded at minute 5 from the spectrogram in B. Arrows indicates times of ketamine doses. Panel A is reproduced with permission from Brown, Lydic and Schiff, New England Journal of Medicine, 2010. Panels 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.
Fig. 10
Neurophysiology of dexmedetomidine. A. Dexmedetomidine…
Fig. 10
Neurophysiology of dexmedetomidine. A. Dexmedetomidine acts pre-synaptically to block the release of norepinephrine…
Fig. 10 Neurophysiology of dexmedetomidine. A. Dexmedetomidine acts pre-synaptically to block the release of norepinephrine (NE) from neurons projecting from the locus coeruleus (LC) to the basal forebrain (BF), the pre-optic area (POA) of the hypothalamus, the intralaminar nucleus (ILN) of the thalamus and the cortex. Blocking the release of NE in the POA leads to activation of its inhibitory GABAergic (GABA) and galanergic (Gal) projections to dorsal raphé (DR) which releases serotonin (5HT), the tuberomamillary nucleus (TMN) which releases histamine (His), the LC, the ventral periacqueductal gray (PAG) which releases dopamine, the lateral dorsal tegmental (LDT) nucleus and the pedunculopontine tegmental (PPT) nucleus which release acetylcholine (Ach). These actions lead to decreased arousal by inhibition of the arousal centers. B. Ten-second electroencephalogram segment showing spindles, intermittent 9 to 15 Hz oscillations (underlined in red), characteristic of dexmedetomidine sedation. C. The spindles are most likely produced by intermittent oscillations between the cortex and thalamus (light green region). Panel A is reproduced with permission from Brown, Purdon and Van Dort, Annual Review of Neuroscience, 2011.
Fig. 11
Spectrograms and time-domain electroencephalogram signatures…
Fig. 11
Spectrograms and time-domain electroencephalogram signatures of dexmedetomidine-induced sedation. A. Spectrogram of a 59…
Fig. 11 Spectrograms and time-domain electroencephalogram signatures of dexmedetomidine-induced sedation. A. Spectrogram of a 59 kg patient receiving a 0.65 mcg/kg/hour dexmedetomidine infusion to maintain sedation. The spectrogram shows spindles (9 to 15 Hz oscillations) and slow-delta oscillations. B. Ten-second electroencephalogram trace recorded at minute 60 from the spectrogram in A emphasizing spindles (red underlines). C. Spectrogram of a 65 kg patient receiving a 0.85 mcg/kg/hour dexmedetomidine infusion to maintain sedation. D. Ten-second electroencephalogram trace recorded at minute 40 from the spectrogram in C showing the slow-delta oscillations. Panels A–D were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission from the Partners Healthcare Office of Continuing Professional Development.
Fig. 12
Spectrograms and time-domain electroencephalogram signatures…
Fig. 12
Spectrograms and time-domain electroencephalogram signatures of sevoflurane, isoflurane and desflurane at surgical levels…
Fig. 12 Spectrograms and time-domain electroencephalogram signatures of sevoflurane, isoflurane and desflurane at surgical levels of unconsciousness. The inspired concentration of the anesthetics is the blue trace in the upper part of each panel. Green arrows below each panel are propofol bolus doses. A. At sub-MAC concentrations (minute 40 to minute 60) the spectrogram of sevoflurane resembles that of propofol (fig. 6, A and B). As the concentration of sevoflurane is increased (minute 100 to minute 120), theta (5 to 7Hz) oscillations appear. The theta oscillations dissipate when the sevoflurane concentration (blue curve) is decreased. B. Ten-second electroencephalogram trace of sevoflurane recorded at minute 39.8 of the spectrogram in A. C. The spectrogram of sevoflurane shows constant the alpha, slow, delta and theta oscillations at a constant concentration of 3%. D. Ten-second electroencephalogram trace of sevoflurane recorded at minute 30 of the spectrogram in C. E. At sub-MAC concentrations (minute 16 to minute 26) the spectrogram of isoflurane resembles that of propofol (fig. 6A, B) and sub-MAC sevoflurane (panel A). Theta oscillations strengthen as the isoflurane concentration increases towards MAC. F. Ten-second electroencephalogram trace of desflurane recorded at minute 40 of the spectrogram in E. G. At the sub-MAC concentrations shown here the spectrogram of desflurane resembles propofol with very low theta oscillation power. H. Ten-second electroencephalogram trace of desflurane recorded at minute 40 of the spectrogram in G. Panels A, C, E, and G were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission from the Partners Healthcare Office of Continuing Professional Development.
Fig. 13
Slow-delta and beta-gamma oscillations associated…
Fig. 13
Slow-delta and beta-gamma oscillations associated with nitrous oxide. A. In anticipation of emergence,…
Fig. 13 Slow-delta and beta-gamma oscillations associated with nitrous oxide. A. In anticipation of emergence, a patient was maintained on 0.5% isoflurane and 58% oxygen. At minute 82, the composition of the anesthetic gases was changed to 0.2% isoflurane (blue curve) in 75% nitrous oxide (green curve) and 24% oxygen. The total gas flow was increased from 3 to 7 liters per minute. The alpha, theta and slow oscillation power decreased between minutes 83 to 85. At minute 86 the power in the theta to beta bands decreased considerably (blue area) as the slow-delta oscillation power increased. At minute 88 the slow-delta oscillation power decreased and the beta-gamma oscillations appeared at minute 90. The flow rates and anesthetic concentrations were maintained constant between minutes 82 and 91. Isoflurane was turned off at minute 91. B. Ten-second electroencephalogram traces of the slow-delta oscillation at minute 86.7 and the beta-gamma oscillations at minute 90.8. Panels A and B were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission from the Partners Healthcare Office of Continuing Professional Development.
Fig. 14
Different anesthetics (propofol, sevoflurane, ketamine…
Fig. 14
Different anesthetics (propofol, sevoflurane, ketamine and dexmedetomidine), different electroencephalogram signatures and different molecular…
Fig. 14 Different anesthetics (propofol, sevoflurane, ketamine and dexmedetomidine), different electroencephalogram signatures and different molecular and neural circuit mechanisms. A. Anesthetic-specific differences in the electroencephalogram are difficult to discern in unprocessed electroencephalogram waveforms. B. In the spectrogram, it is clear that different anesthetics produce different electroencephalogram signatures. The dynamics the electroencephalogram signatures can be related to the molecular targets and the neural circuits at which the anesthetics act to create altered states of arousal. Panels A and B were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission from the Partners Healthcare Office of Continuing Professional Development.