Abstract
Burst suppression is an EEG pattern characterized by alternating periods of high-amplitude activity (bursts) and relatively low amplitude activity (suppressions). Burst suppression can arise from several different pathological conditions, as well as from general anesthesia. Here we review current algorithms that are used to quantify burst suppression, its various etiologies, and possible underlying mechanisms. We then review clinical applications of anesthetic-induced burst suppression. Finally, we report the results of our new study showing clear electrophysiological differences in burst suppression patterns induced by two common general anesthetics, sevoflurane and propofol. Our data suggest that the circuit mechanisms that generate burst suppression activity may differ among general anesthetics.
Highlights
Burst suppression is an EEG pattern characterized by quasiperiodic high amplitude activity and relativity low amplitude activity
We found that the durations, peak-to-peak amplitudes, and spectral power of the bursts and suppressions differed substantially between the two anesthetics at equivalent burst suppression probability (BSP) levels, suggesting that at least some aspects of the mechanisms underlying burst suppression induced by sevoflurane and propofol may be distinct
Previous studies on burst suppression induced by general anesthetics have found differences between burst and suppression durations and peak-to-peak amplitudes between propofol, etomidate, thiopental, and isoflurane in rodents, and between propofol and isoflurane in rabbits
Summary
Burst suppression is an EEG pattern characterized by quasiperiodic high amplitude activity (bursts) and relativity low amplitude activity (suppressions; Amzica, 2009; Brown et al, 2010). The phenomenon was first observed while recording EEG from the motor cortex of cats under tribromoethanol and pentobarbitalinduced general anesthesia (Derbyshire et al, 1936). Early work on burst suppression focused on general anesthesia, burst suppression can be induced by several different etiologies (Martin et al, 1959). We describe clinical applications of burst suppression induced by general anesthetics. In the second part of this article, we present original research findings from our laboratory that demonstrate the distinct electrophysiological characteristics of burst suppression induced by the inhaled anesthetic sevoflurane and the intravenous anesthetic propofol
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