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High-frequency gamma activity to propofol

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Anesthesia is a unique tool for examining the relationship between slow waves and effective connectivity. A recent report on another anesthetic, midazolam, showed that effective connectivity was reduced during anesthesia. In propofol induced LOC, a similar phenomenon occurs when high ampli

When people wake up from NREM sleep early in the night, they rarely report having dreams. The EEG recorded during this period contains high amplitude slow waves that are not found when awake. During non rapid eye movement sleep and anesthesia, cortical and thalamic neurons oscillate between the low polarization state and the depolarized upper state, and there is almost no peak in the low polarization state, when the discharge rate exceeds the awake state. Slow wave is an electro physiological phenomenon that millions of neurons switch between upper and lower states. Recently, researchers used transcranial magnetic stimulation (TMS) and hd-EEG to measure effective connectivity (the ability of brain regions to interact). They found that effective connectivity was disrupted during non REM sleep compared to waking. The decrease of effective connections during sleep may reflect the impairment of the brain's ability to integrate information, which may lead to a decrease in the level of consciousness. In early non rapid eye movement sleep, cortical bistability, which widely exists between upper and lower states, eventually forms large slow waves, which may be the reason for the decline of effective connectivity.


Anesthesia is a unique tool for examining the relationship between slow waves and effective connectivity. A recent report on another anesthetic, midazolam, showed that effective connectivity was reduced during anesthesia. In propofol induced LOC, a similar phenomenon occurs when high amplitude EEG slow wave occurs. Further studies using TMS-EEG should confirm that the bistable dynamics established in propofol induced LOC will also lead to the loss of effective connectivity.


It should be pointed out that many studies have reported that muscarinic agonists and antagonists can produce slow waves of EEG in conscious behavioral animals. However, many of these reports include very limited behavioral assessments. In addition, the author can only achieve this "separation" between EEG and behavior when the slow wave is relatively small and limited to the frontal electrode. When slow waves expand to include the posterior cortex, animals will transition to sleep behavior. In addition, human studies have shown that the EEG effects of these drugs cannot be separated from their sedative effects. In our paper, we purposely chose the large slow wave containing most of our scalp electrodes


Gamma and Theta's activities are not enough to generate consciousness


Power, synchronization and synchronization are all believed to contribute to conscious awareness. Some reports suggest that the gamma power may be reduced during non REM sleep and anesthesia compared to awake. However, animal studies have found that gamma power increases during anesthesia. In addition, studies of intracranial recordings showed no difference in gamma coherence between REM and non REM sleep. In addition, the gamma coherence of semi intracerebral EEG may even be higher in slow wave sleep than in wakefulness. Here, we have proved that the power of gamma and theta will not decrease with LOC. In fact, the gamma power of the default network components has increased. This shows that when slow waves appear, the gamma activity in this network is not enough to maintain consciousness. We also found that after LOC, γ or θ Functional connectivity has not changed. Contrary to previous reports, gamma functional connectivity decreased during anesthesia and sedation. This divergence may be related to the differences between these previous studies and our research in the choice of anesthesia, the depth of anesthesia (unconscious vs. surgical anesthesia) and animal models (rat vs. human). In addition, in these previous reports, the decline in gamma power and functional connectivity occurred at a faster frequency than the gamma we analyzed. This may be due to the different responses of high-frequency gamma activity to propofol, although at these faster frequencies, muscle and eye related EEG artifacts may complicate the interpretation of the results. Therefore, we limit our analysis to slower, relatively clean frequency bands where we can show a significant increase in gamma power and functional connectivity, most likely due to changes in brain activity. We found that compared with the conscious state, the gamma power in the unconscious state induced by propofol increased θ The fact that synchronization increases challenges the use of these parameters as neural related parameters of consciousness. This is clinically relevant, as these parameters may be poor markers of consciousness in patients with NCBI.

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