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Neuroimage. 2018 Oct 1;179:414-428. doi: 10.1016/j.neuroimage.2018.06.043. Epub 2018 Jun 18.

Suppression of underlying neuronal fluctuations mediates EEG slowing during general anaesthesia.

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Department FE 12 - Data Assimilation, Deutscher Wetterdienst, 63067, Offenbach am Main, Germany; Department of Mathematics and Statistics, University of Reading, Reading, RG6 6AX, UK. Electronic address:
Krembil Research Institute, University Health Network, Toronto, Ontario, M5T 2S8, Canada; Department of Mathematics, University of Toronto, Toronto, Ontario, M5T 2S8, Canada; Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, M5T 2S8, Canada.
Department of Anaesthesiology, Waikato Clinical Campus, University of Auckland, Hamilton, 3240, New Zealand; Department of Anaesthesiology and Pain Therapy, University Hospital Bern, Inselspital, Bern, Switzerland.
Department of Anaesthesiology, Waikato Clinical Campus, University of Auckland, Hamilton, 3240, New Zealand. Electronic address:


The physiological mechanisms by which anaesthetic drugs modulate oscillatory brain activity remain poorly understood. Combining human data, mathematical and computational analysis of both spiking and mean-field models, we investigated the spectral dynamics of encephalographic (EEG) beta-alpha oscillations, observed in human patients undergoing general anaesthesia. The effect of anaesthetics can be modelled as a reduction of neural fluctuation intensity, and/or an increase in inhibitory synaptic gain in the thalamo-cortical circuit. Unlike previous work, which suggested the primary importance of gamma-amino-butryic-acid (GABA) augmentation in causing a shift to low EEG frequencies, our analysis demonstrates that a non-linear transition, triggered by a simple decrease in neural fluctuation intensity, is sufficient to explain the clinically-observed appearance - and subsequent slowing - of the beta-alpha narrowband EEG peak. In our model, increased synaptic inhibition alone, did not correlate with the clinically-observed encephalographic spectral changes, but did cause the anaesthetic-induced decrease in neuronal firing rate. Taken together, our results show that such a non-linear transition results in functional fragmentation of cortical and thalamic populations; highly correlated intra-population dynamics triggered by anaesthesia decouple and isolate neural populations. Our results are able to parsimoniously unify and replicate the observed anaesthetic effects on both the EEG spectra and inter-regional connectivity, and further highlight the importance of neural activity fluctuations in the genesis of altered brain states.


Alpha-activity; Anaesthesia; Functional fragmentation; Noise

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