Abstract
The burst-suppression pattern is well recognized as a distinct feature of the mammalian electroencephalogram (EEG) waveform. Consisting of alternating periods of high amplitude oscillatory and isoelectric activity, it can be induced in health by deep anesthesia as well as being evoked by a range of pathophysiological processes that include coma and anoxia. While the electroencephalographic phenomenon and clinical implications of burst suppression have been studied extensively, the physiological mechanisms underlying its emergence remain unresolved and obscure. Because electroencephalographic bursting phenomenologically resembles the bursting observed in single neurons, it would be reasonable to assume that the theoretical insights developed to understand bursting at the cellular (“microscopic”) level would enable insights into the dynamical genesis of bursting at the level of the whole brain (“macroscopic”). In general action potential bursting is the result of the interplay of two time scales: a fast time scale responsible for spiking, and a slow time scale that modulates such activity. We therefore hypothesize that such fast-slow systems dynamically underpin electroencephalographic bursting. Here we show that a well-known mean field dynamical model of the electroencephalogram, the Liley model, while unable to produce burst suppression unmodified, is able to give rise to a wide variety of burst-like activity by the addition of one or more slow systems modulating model parameters speculated to be major “targets” for anesthetic action. The development of a physiologically plausible theoretical framework to account for burst suppression will lead to a more complete physiological understanding of the EEG and the mechanisms that serve to modify ongoing brain activity necessary for purposeful behavior and consciousness.
Highlights
Prior to the development of the modern intensive care unit in the early 1960s, that featured intubation, artificial respiration, and comprehensive physiological monitoring, reports of the electroencephalographic pattern of burst suppression (BS) were confined to animal studies involving deep anesthesia and the occasional case of psychosurgery (Niedermeyer, 2009)
Since the burstsuppression pattern has become well recognized as a major diagnostic feature of the EEG waveform that is encountered in a range of encephalopathic conditions, in addition to its appearance in health during deep anesthesia
First identified during deep anesthesia with tribromoethanol in cats (Derbyshire et al, 1936), labeled burst-suppression pattern by Swank and Watson (1949) during barbiturate and ether anesthesia in dogs, it is associated with cortical deafferentation (Henry and Scoville, 1952), cerebral anoxia and hypoxia, various types of intracortical lesions (Fischer-Williams and Cooper, 1963), deep coma, various infantile encephalopathies, the final stages of deteriorated status epilepticus (Treiman et al, 1990), hypothermia, and high levels of many sedative and anesthetic agents (Schwartz et al, 1989; Akrawi et al, 1996)
Summary
Prior to the development of the modern intensive care unit in the early 1960s, that featured intubation, artificial respiration, and comprehensive physiological monitoring, reports of the electroencephalographic pattern of burst suppression (BS) were confined to animal studies involving deep anesthesia and the occasional case of psychosurgery (Niedermeyer, 2009). In adult populations while an anoxic/hypoxic BS pattern signals a serious pathophysiological event the outcome is not necessarily fatal and recovery with or without severe neurological damage is possible (Niedermeyer, 2009). Consistent with this are results of experimental work with EEG monitoring in rats revealing that animals with greater rates of high amplitude bursts have a better survival and neurological outcome compared to those with lower rates of low amplitude bursts (Geocadin et al, 2002)
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