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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Curr Opin Neurobiol. 2014 Jan 21;25:116–122. doi: 10.1016/j.conb.2013.12.011

Figure 3.

Figure 3

Secondary effects of propofol lead to anteriorization and burst suppression. (A) The differential structure and cell types (in particular, high-threshold thalamocortical neurons) of fronto-thalamic versus posterior-thalamic networks leads to the phenomenon of Anteriorization ■[23,46,47]. (B) At very high doses, propofol leads to secondary effects on cerebral metabolism which can be modeled as a disruption to the rate of ATP regeneration in local circuits. (C) This disruption causes periodic cessation of neuronal activity when ATP levels drop below threshold-levels. This cessation, in turn, manifests as the phenomenon of EEG burst suppression ■[6]. Figure adapted from ■[6,46].