The Electroencephalogram in Anesthesia: Fundamentals, Practical Applications, Examples

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Bottom panel. Power spectra from one animal for the cortex and thalamus. Segments of the original recordings from one animal are shown in Fig 3. Our criterion for considering that the attenuation of power within a frequency band is related to the hypnotic effect is that the highest level of power within this frequency band observed during the periods when the animal is unconscious i.

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For cortical power, only the — Hz range satisfied this condition. Recovery recordings were obtained to confirm a return towards baseline power values to rule out other possible causes for the observed power changes duration of experiment, equipment malfunction. Accurate electrode placement was confirmed by microscopy in the four brains available Fig 4. The filled circles denote the end of the electrode tracks on an overlay from the Paxinos atlas [ 22 ] and confirm correct electrode placement in the 4 available specimens.

Distances are relative to bregma.

The main finding of this study is that propofol causes a more extensive and pronounced attenuation of high-frequency rhythms in the sensory thalamus than in the sensory cortex. The attenuation of power of the high-frequency rhythms occurred over a wider frequency range in the thalamus where all four frequency bands were affected than in the cortex where only the 76— Hz and — Hz bands were affected.

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Another important finding of this study is that the attenuation of thalamic power appears to provide a more consistent marker of unconsciousness than cortical power. Thalamic power the 51— Hz range passed a fairly stringent test requiring that there be a significant difference between the highest level of power observed during the periods when the animal is unconscious i.

For cortical power, only the — Hz range met these criteria. Further work on these rhythms appears warranted to assess their usefulness as potential markers of anesthetic-induced unconsciousness. In regard to the issue of whether anesthetic-induced unconsciousness primarily results for impairment of the cortex, thalamus or both, [ 1 ] the present findings support the view that both structures are affected. This conclusion is in line with our recent report showing, on the basis of EEG recordings from the motor cortex and sensory thalamus in three patients, that induction of anesthesia with propofol is associated with concurrent alterations of cortical and thalamic activity [ 32 ].

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Hudetz et al [ 12 ] had showed in rats that isoflurane attenuates spectral power in the 70— Hz range in neocortical and hippocampal recordings in a concentration-dependent manner. The present report confirms and extends these observations by showing that propofol exerts a similar effect on neocortical recordings. Breashears et al [ 14 ] had reported that propofol anesthesia is associated with a decrease of power in the 75— Hz range in human electrocorticograms. The present report shows that the same can be observed in an animal model. The importance of providing such confirmatory observations should not be underestimated.

There is an increasing awareness of the need for replication in biomedical science in view of the alarmingly high proportion of findings that cannot be reproduced even though they were published in good faith by honest and competent investigators [ 33 ]. It is easy to forget that the results described above were obtained on data after logarithmic transform base Our observation of a greater effect of propofol on the thalamus is in line the report of Ying et al [ 34 ]. These authors measured the concentration of propofol required to decrease synaptic responsiveness of thalamocortical relay neurons in the ventrobasal complex VB mouse brain slices and noted that this concentration was much less than for potentiation of GABA A receptor-elicited responses in the hippocampus or olfactory cortex, suggesting that the ventro-basal thalamic neurons are more sensitive to propofol.

The attenuation of the power of high-frequency rhythms by propofol likely reflects a decrease of neuronal firing rates. Concurrent recordings of both LFPs and of action potentials with the same electrode would allow verification of this interpretation. Propofol exerted a puzzling effect on power in the 30—50 Hz range. It caused a concentration-dependent attenuation of thalamic, but not cortical, power in this range Table 1.

During unconsciousness, however, cortical power in the 30—50 Hz range was significantly increased compared with the period of consciousness with lowest power Table 3. This is a clear indication that power in this band does not provide a good reflection of anesthetic effect, as noted by others [ 12 ]. The inconsistent effects of general anesthetics of the 30—50 Hz band may perhaps be justified to some extent by the fact that this frequency band occupies the border zone between the low frequency range where anesthetics increase power and the high-gamma range where anesthetics decrease power [ 38 ].

Furthermore, this effect is also concentration-dependent [ 3 , 42 , 43 ]. The effects of isoflurane on these responses have been documented in the rat and are similar to those seen in humans [ 45 ]. This confirms that there are important differences between spontaneous and evoked gamma oscillations [ 46 ]. We acknowledge two main limitations. First, we did not assay the propofol concentrations in blood to confirm the accuracy of the target controlled infusion protocol.

We believe that collecting sequential arterial blood samples for each propofol concentration was not compatible with our testing protocol. Instead, we relied on predicted concentrations based on the Stanpump software and are thus dependent on the accuracy of the kinetic model [ 24 ]. In the worst-case scenario, we can conclude that we have demonstrated a dose-dependent as opposed to concentration-dependent effect since the dose of propofol and the rate of administration were similar across animals.

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While we are aware of prior use of target controlled infusion of propofol in rodents [ 47 ], we found no such studies where blood concentrations were measured. Second, histological confirmation of proper electrode placement is only available in four animals. Problems with tissue processing made the other specimens unusable. We nevertheless feel confident that the electrodes were properly positioned in all animals because we used electrophysiological guidance for fine adjustment of the antero-posterior position of the cortical electrode by measuring the cortical field excitatory post-synaptic potentials in response to electrical stimulation of the VPM.

We conclude that propofol causes a concentration-dependent attenuation of the spectral power of thalamocortical rhythms in the 51— Hz range and that this attenuation is of sufficient magnitude to cause statistically significant reductions of power during unconsciousness. This effect is more consistent and more pronounced for the thalamus than for the cortex, suggesting greater thalamic sensitivity to propofol.

Further work is warranted to determine to what extent and how this attenuation could contribute to the hypnotic action of propofol. Surgery and testing: SJR. Assisted surgery and testing: GP.

EEG monitoring of brain states under general anesthesia and sedation- Emery Brown - Porto 2018

Wrote first draft: SJR. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field.

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Abstract Background Thalamocortical EEG rhythms in gamma Hz and high-gamma Hz ranges have been linked to arousal and conscious processes. Methods Adult male Long-Evans rats were chronically implanted with electrodes in somatosensory barrel cortex and ventroposteromedial thalamus. Conclusions Propofol causes a concentration-dependent attenuation of the power of thalamocortical rhythms in the Hz range and this effect is far more pronounced for the thalamus, where the attenuation provides a robust correlate of the hypnotic action of propofol.

This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Data Availability: Data are available at the Harvard Dataverse Network, with the following DOI: doi: Introduction The mechanisms by which general anesthetics suppress consciousness remain elusive [ 1 , 2 ]. Design The experimental sessions were preceded by a forty-minute acclimation session, which occurred daily for three days, allowing the animals to explore the testing chamber.

Electrophysiological Recording Local field potentials from the cortical and thalamic contacts were recorded with a common reference on the contralateral parietal bone referential montage , amplified 0. Statistical Analysis All power values were transformed with log base Results Behavioral Observations Propofol had a consistent effect on behavior.

Concentration-effect relationships Fig 1 shows that propofol caused a significant, linear decrease of logarithmic power as a function of propofol concentration for the cortex in the 76— Hz and — Hz frequency ranges as well as for the thalamus in all frequency ranges. Download: PPT. Fig 1. Power as a function of propofol concentration for each frequency band for the cortex and thalamus.

Table 2. Fig 3. Segments of the original recordings from the same animal as Fig 2. Relationship with level of consciousness Our criterion for considering that the attenuation of power within a frequency band is related to the hypnotic effect is that the highest level of power within this frequency band observed during the periods when the animal is unconscious i.

Table 4. Histology Accurate electrode placement was confirmed by microscopy in the four brains available Fig 4. Discussion The main finding of this study is that propofol causes a more extensive and pronounced attenuation of high-frequency rhythms in the sensory thalamus than in the sensory cortex. Limitations We acknowledge two main limitations. Conclusions We conclude that propofol causes a concentration-dependent attenuation of the spectral power of thalamocortical rhythms in the 51— Hz range and that this attenuation is of sufficient magnitude to cause statistically significant reductions of power during unconsciousness.

Supporting Information. S1 Histology. A histology slide showing the electrode tracks for cortex matched to middle cut on Fig 4 and VPM corresponding to the most posterior cut on Fig 4.

Multimodal General Anesthesia: Theory and Practice : Anesthesia & Analgesia

References 1. Consciousness and anesthesia. Science ; — Franks NP. General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal. Nat Rev Neurosci ;9: — Sensory information processing during general anaesthesia: Effect of isoflurane on auditory evoked neuronal oscillations. Br J Anaesth ; 81— Plourde G. Depth of anesthesia. Clinical use of the Hz auditory steady state response. Int Anesthesiol Clin ; — The anesthetic cascade: a theory of how anesthesia suppresses consciousness.

Anesthesiology ; — One example increased the frequency of the alpha peak to 15 Hz and simultaneously developed a separate beta peak during emergence. Another example from the same study showed an increase in the frequency of the alpha peak to about 18 Hz and no other peak in the beta range A few patients never demonstrated slow wave anesthesia and possibly could be considered to be in the indeterminate state during surgery and emergence. Anesthetized patients that did not have alpha or delta EEG waves have been observed. Natural sleep produces its characteristic EEG phenomena as a result of a reduction of brainstem induced depolarization of the thalamus and cortex McCormick, ; McCormick et al.

There are multiple brainstem nuclei which project depolarizing neuromodulators to the thalamus and cerebral cortex. There is a nucleus in the brainstem that can affect the activity of all of these nuclei. This nucleus is the ventrolateral preoptic VLPO nucleus. Studies have been conducted to determine whether the VLPO nucleus is involved in mechanisms of anesthesia Lu et al.


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In a study using rats as subjects, isoflurane increased activity in VLPO neurons but only one third as much as natural sleep Lu et al. The membrane potential of cortical or thalamic neurons i. If additional anesthetic agents such as opioids or dexmedetomidine could reduce the influence of the brainstem arousal system to the levels similar to that which occur in natural sleep, less anesthetic agent would be required to achieve the same degree of hyperpolarization of the thalamus and cortex.

If the brainstem arousal system was active during emergence the spindle mechanism would stop as the anesthetic agent level was reduced because the active brainstem arousal system would depolarize the thalamus and cortex.