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Published on: October 24, 2019
Rapid eye movement sleep, apnea, and cardiac slowing influenced by phenobarbital administration in the neonate
Insights
Phenobarbital (phenobarbitone) reduced active sleep and neurogenic apnea/bradycardia in preterm infants. As drug levels decreased, these symptoms returned, supporting a neurophysiologic link between active sleep and apnea.
Area of Science:
- Neonatal Medicine
- Neurophysiology
- Pharmacology
Background:
- Neonatal apnea and bradycardia are significant concerns in preterm infants.
- The neurophysiological mechanisms underlying these events are not fully understood.
- Phenobarbital is a commonly used medication in neonatal care.
Purpose of the Study:
- To evaluate the effect of phenobarbital on neonatal sleep behavior.
- To assess the impact of phenobarbital on the incidence of neurogenic apnea and/or bradycardia.
- To investigate the relationship between phenobarbital serum levels, active sleep, and apnea/bradycardia.
Main Methods:
- Polygraphic recordings were conducted in seven preterm infants.
- Infants received phenobarbital to achieve therapeutic serum levels.
- Sleep patterns and the occurrence of apnea/bradycardia were monitored.
Main Results:
- Therapeutic phenobarbital levels decreased active sleep and the incidence of apnea/bradycardia.
- Apnea and bradycardia predominantly occurred during active sleep.
- As phenobarbital levels declined, active sleep rebounded, and apnea/bradycardia recurred.
Conclusions:
- Phenobarbital effectively reduces active sleep and associated apnea/bradycardia in preterm infants.
- The findings support the hypothesis that active sleep facilitates neonatal apnea.
- Active sleep-inhibitory brain mechanisms may play a role in the pathophysiology of neonatal apnea.
Abstract:
Polygraphic recordings were performed in seven preterm infants who had been given phenobarbital (phenobarbitone) to evaluate its effect on neonatal sleep behavior and on the incidence of neurogenic apnea and/or bradycardia. The amount of active sleep, as well as the incidence of apnea and/or cardiac slowing occurring predominantly in active sleep, were decreased at therapeutic serum levels of phenobarbital. With declining serum drug levels, active sleep showed a rebound effect; at the same time, apnea and/or cardiac slowing relapsed. Thus, our previously proposed neurophysiologic concept that neonatal apnea is facilitated by active sleep-inhibitory brain mechanisms seems to be confirmed.
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