The reactivity of an electroencephalogram (EEG) to external stimuli is impaired in comatose patients showing burst-suppression (BS) patterns following hypoxic–ischemic brain injury (HIBI). We explored the reactivity of BS induced by isoflurane in rat models of HIBI and controls using intermittent photic stimulation (IPS) delivered to one eye. The relative time spent in suppression referred to as the suppression ratio (SR) was measured on the contralateral fronto-occipital cortical EEG channel. The BS reactivity (BSR) was defined as the decrease in the SR during IPS from the baseline before stimulation (SR_PRE). We found that BSR increased with SR_PRE. To standardize by anesthetic depth, we derived the BSR index (BSRi) as BSR divided by SR_PRE. We found that the BSRi was decreased at 3 days after transient global cerebral ischemia in rats, which is a model of brain injury after cardiac arrest. The BSRi was also reduced 2 months after experimental perinatal asphyxia in rats, a model of birth asphyxia, which is a frequent neonatal complication in humans. Furthermore, Oxytocin attenuated BSRi impairment, consistent with a neuroprotective effect in this model. Our data suggest that the BSRi is a promising translational marker in HIBI which should be considered in future neuroprotection studies.

During deep anesthesia, the EEG becomes discontinuous. Burst-suppression is often an intended target during deep sedation or medically induced coma. Within this state, anesthetic depth is commonly monitored by the suppression ratio (SR), which expresses the fraction of time spent in suppression. However, accumulating evidence suggests that SR remains reactive to external stimulation. We tested whether ambient music commonly played in operating theaters alters the SR in male Wistar rats under sevoflurane, chloral hydrate, or isoflurane anesthesia. To this end, the first 60 s of the Stayin’ Alive audio track by the Bee Gees were played to examine auditory-induced burst-suppression reactivity in an experimental model previously established for intermittent photic stimulation. SR and the burst-suppression reactivity index (BSRi, derived as the decrease in SR during stimulation normalized to pre-stimulation SR) were measured in repeated trials. Auditory stimulation transiently decreased SR under all three anesthetics. This was associated with an increase in the rate of burst occurrence without increased burst duration. The BSRi changes depended on the anesthetic type, comparable to photic stimulation. Our experimental data suggest that the suppression ratio used to monitor targeted burst-suppression reflects both anesthetic depth and the level of ambient stimulation. Ambient sound in the operating theater or intensive care settings could influence EEG-based measures used for anesthesia monitoring.