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Continuing stories with discontinuity

When he broke the big news of anesthesia in the Ether Dome in 1846, William Morton probably did not think much about how you are supposed to tell a story. He did not start at the beginning with a carefully crafted tale including all of the characteristics of his miraculous lead character. He landed somewhere right in the middle with an agent that produced this amazing state of anesthesia and leaving others to try to work out the story in reverse. In this edition of the journal, we return to Boston as Cornelissen et al. report their work trying to provide some of the backstory by looking at the electroencephalogram (EEG) in infants undergoing anesthesia. More than 150 years later we are still firmly in the part of the story where there are more mysteries than certainties. In a follow-up analysis of data collected in an observational study (1) to explore age-dependent EEG patterns during sevoflurane anesthesia, the authors examined discontinuity events where there is a period of low amplitude activity lasting over 2 s across the cerebrum. Such discontinuity events are a background feature in the healthy premature infant during sleep–wake cycling but gradually leave the normal background of the EEG by term. Their presence in the awake sate by that age is abnormal and might be associated with critical illnesses like encephalopathy or complex heart disease. In this group of children between 0 and 40 months of age, they found that discontinuity events occurred during anesthesia in more than half of the patients studied. Such events were especially frequent in younger infants, in the first 30 min of anesthesia, and seemed to occur more often with higher concentrations of sevoflurane. These events may therefore be a marker of the ‘overanesthetized brain’. Discontinuity events are not a new finding in pediatric anesthesia. Davidson et al. have previously shown such events primarily during emergence rather than at higher volatile concentrations (2). However, Cornelissen et al. saw no cases of discontinuity during emergence. The reason for this discrepancy is not yet part of the story. Of course because anesthesia started with a demonstration aimed at producing a state where awareness and mobility during surgery were minimized, our practice was immediately influenced by these coupled goals even though they are separate things. Achieving immobility tends to require delivery of higher concentrations of volatile agent than those required for anesthesia. Now we have some new bits of information hinting at the possibility that we might be ‘overanesthetizing the brain’. What should the clinician do with this new knowledge? Are we looking at a biomarker of damage, a normal feature of anesthesia, or a complex mix of both? Discontinuity events may be associated with encephalopathy or adverse neurological outcomes in congenital heart disease. However, those are very distinct pathological states that produce their own disturbances when it comes to the brain. Is each unhappy cortex unhappy in its own way, or are they all alike? Could forms of discontinuity on the EEG be a different marker suggesting a risk of postoperative neurological issues after general anesthesia as has been suggested in some adult settings? That is a reasonable concern but in adult studies where some form of link has been suggested, the EEG did not just show discontinuity events but a distinctly different pattern of burst suppression (3). Maybe the EEG is trying to remind us that kids are not just little adults, particularly in neonates and infants, where the normal pattern of EEG activity is itself changing as the brain matures and develops. If a degree of discontinuity is part of normal brain maturation that resolves by term perhaps transient discontinuity events (as seen here and with use of barbiturates and some antiepileptics) are of minimal neurodevelopmental significance. So rigorous research such as this provides interesting new parts of the backstory of Morton’s miraculous character but there are many gaps to fill in. Some of those are not in the field of EEG monitoring, and may include areas such as cerebral perfusion, individual differences between anesthetic agents, and developmental neurology. The full story requires more information about the potential for neurodevelopmental impacts of anesthesia, although the most recent publications around neurotoxicity seem somewhat more reassuring than earlier animal work (4,5). We also need long-term follow-up of patients included in EEG research and work to establish if observed patterns are meaningfully associated with clinical outcomes for patients rather than being interesting monitoring artifacts. Then it might just be possible to start working out the link between the agents we use, the effects on the EEG with its suppressed bursts, pauses, waves, and oscillations, and the outcomes for the patient. William T. G. Morton may have introduced a very interesting character all that time ago but he did not