{'fraction_non_alphanumeric': 0.023485784919653894, 'fraction_numerical': 0.0, 'mean_word_length': 5.532258064516129, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Rapid eye movement sleep, apnea, and cardiac slowing influenced by phenobarbital administration in the neonate.

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.