A neurophysiological-metabolic model for burst suppression
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Author(s)
Ching, ShiNung
Purdon, Patrick Lee
Vijayan, Sujith
Kopell, Nancy J.
Brown, Emery N.
Date Issued
February 2012
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Ching, S., P. L. Purdon, S. Vijayan, N. J. Kopell, and E. N. Brown. “A Neurophysiological-Metabolic Model for Burst Suppression.” Proceedings of the National Academy of Sciences 109, no. 8 (February 7, 2012): 3095–3100.
Version
Final published version
Abstract
Burst suppression is an electroencepholagram (EEG) pattern in which high-voltage activity alternates with isoelectric quiescence. It is characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia, hypothermia, and in pathological conditions such as coma and early infantile encephalopathy. We propose a unifying mechanism for burst suppression that accounts for all of these conditions. By constructing a biophysical computational model, we show how the prevailing features of burst suppression may arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of ATP-gated potassium channels, leads to the characteristic epochs of suppression. Consequently, the model makes a number of specific predictions of experimental and clinical relevance.
MIT Department
Harvard University--MIT Division of Health Sciences and Technology
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1073/pnas.1121461109
