This systematic dependence on anesthetic level can be utilized in the treatment of status epilepticus ( Kalviainen et al., 2005) and the management of brain trauma in the intensive care setting ( Doyle and Matta, 1999) by defining an endpoint in which more than 50% of an EEG recording consists of suppressions.
In contrast, in deep anesthesia bursts are typically separated by clear isoelectric periods, the duration (relative and absolute) of which increases systematically with increasing anesthetic level.
For example, in the case of infantile hypoxic-ischemic encephalopathy the burst suppression pattern can be quite complex and due to significant variability in the amplitude of individual bursts a clear transition to suppression may not readily be apparent ( Lamblin et al., 2013). The burst suppression pattern can show a significant degree of variation depending on its aetiology. Consisting of quasi-periodic alternations of high amplitude periods of spiking activity with low amplitude periods that are near isoelectric, the burst suppression pattern is associated with a range of central insults or interventions that include cortical deafferentation ( Henry and Scoville, 1952 Kellaway et al., 1966 Lukatch and MacIver, 1996), cerebral ischaemia ( Bauer et al., 2013), deep coma ( Young, 2000), various infantile encephalopathies ( Grigg-Damberger et al., 1989), the final stages of deteriorated status epilepticus ( Treiman et al., 1990), hypothermia ( Stecker et al., 2001), and high levels of many anesthetic and sedative drugs ( Schwartz et al., 1989 Akrawi et al., 1996). In the case of the deeply inactivated brain, whether through trauma or medical intervention, a burst suppression pattern is typically observed ( Niedermeyer, 2009 Ching et al., 2012). Over the many years since its discovery in humans ( Berger, 1929, 1930 Adrian and Matthews, 1934), the electroencephalogram (EEG) has been shown to be a sensitive, and often specific, indicator of brain state and function ( Schomer and Lopes da Silva, 2010). We have taken a first step in this direction by showing that a neural field model can qualitatively match recent experimental data that indicate spatial differentiation of burst suppression activity across cortex. Because burst suppression corresponds to a dynamical end-point of brain activity, theoretically accounting for its spatiotemporal emergence will vitally contribute to efforts aimed at clarifying whether a common physiological trajectory is induced by the actions of general anesthetic agents. Simulations reveal heterogeneous bursting over the model cortex and complex spatiotemporal dynamics during simulated anesthetic action, and provide forward predictions of neuroimaging signals for subsequent empirical comparisons and more detailed characterization. Here we outline a realistic neural field model for burst suppression by adding a slow process of synaptic resource depletion and recovery, which is able to reproduce qualitatively the empirically observed features during general anesthesia at the whole cortex level. Not only does it appear that burst suppression activity is highly asynchronous across cortex, but also that it may occur in isolated regions of circumscribed spatial extent. However, its characterization as a “global brain state” has been challenged by recent results obtained with intracranial electrocortigraphy. Classically it is thought of as spatially synchronous, quasi-periodic bursts of high amplitude EEG separated by low amplitude activity. 2Brain and Psychological Sciences Research Centre, School of Health Sciences, Swinburne University of Technology, Hawthorn, VIC, Australiaīurst suppression in the electroencephalogram (EEG) is a well-described phenomenon that occurs during deep anesthesia, as well as in a variety of congenital and acquired brain insults.1Systems Neuroscience Research Group, School of Systems Engineering, University of Reading, Reading, UK.