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Please use this identifier to cite or link to this item: http://hdl.handle.net/11055/613
Title: Suppression of underlying neuronal fluctuations mediates EEG slowing during general anaesthesia.
Authors: Hutt, A
Lefebvre, J
Hight, D
Sleigh, J
Anzca Brief Name: Sleigh, J
Keywords: Alpha-activity
Functional fragmentation
noise
Issue Date: 16-Jun-2018
Citation: 10.1016/j.neuroimage.2018.06.043. [Epub ahead of print]
Abstract: 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.
URI: http://hdl.handle.net/11055/613
DOI: 10.1016/j.neuroimage.2018.06.043
PubMed URL: https://www.ncbi.nlm.nih.gov/pubmed/29920378
ISSN: 1053-8119
Journal Title: NeuroImage
Type: Journal Article
Appears in Collections:Scholarly and Clinical

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