Objective: To determine if apneic preterm infants currently treated with methylxanthines develop evidence of sleep deprivation from cumulative arousal and motor activational effects.Study Design: Sleep, wake, arousal and actigraphic movements were monitored in extubated clinically stable premature infants (N ¼ 37). Neonates were free of other medications for >72 h and were grouped based on methylxanthine exposure: >5 days with caffeine (n ¼ 14), >5 days theophylline (n ¼ 13) or no prior exposure (n ¼ 10).Result: Duration of methylxanthine treatment predicted increased arousals, wakefulness and actigraphic movements, and decreased active sleep. Recording from 1200 to 0500 hours, methylxanthine-treated groups showed reductions in all arousal parameters: waking state, number of wake epochs, brief arousals and composite arousal index, and shorter fast-burst, sleep-related motility than untreated controls. Conclusion:In apneic preterms, chronic methylxanthine treatment appears to produce sleep deprivation secondary to the stimulatory action of methylxanthines on arousal and motor systems.
Infancy and early childhood sleep-wake behaviours from current and retrospective parental reports were used to explore the relationship between sleeping arrangements and parent-child nighttime interactions at both time points. Children (N ¼ 45) from educated, middle-class families, mostly breastfed in infancy, composed a convenience sample that was recruited from a university preschool in the Northeast US. Parents responded to the Sleep Habits Inventory, a 19-item Likert-style inventory measuring sleep-related behaviours during the last week, and the Sleeping Arrangements Questionnaire, a 30-question, openended, short-answer-style instrument which queries both retrospective infancy and current sleep location, bedtime routine, night waking and parent-child interactions during the sleep period. Co-sleeping in early childhood was associated with sleep location in infancy (i.e. proximity to the mother's bed) during wake-sleep transitions and night feedings. Security object use during infancy was inversely related to early childhood cosleeping (calling for the parents, night waking, poor bedtime routine and fear of the dark). Results showed that early childhood co-sleeping in this sample was reactive, i.e. associated with current parent-seeking, night waking and social contact during wake-sleep transitions. These findings suggest that co-sleeping in early childhood is related to social experiences during infancy, particularly the amount of parent social contact and security object use.
Developmental features of the P2 auditory ERP in a change detection paradigm were examined in infants prenatally exposed to methadone. Opiate dependent pregnant women maintained on methadone replacement therapy were recruited during pregnancy (N = 60). Current and historical alcohol and substance use, SES, and psychiatric status were assessed with a maternal interview during the third trimester. Medical records were used to collect information regarding maternal medications, monthly urinalysis, and breathalyzer to confirm comorbid drug and alcohol exposures. Between birth and 4 months infant ERP change detection performance was evaluated on one occasion with the oddball paradigm (.2 probability oddball) using pure-tone stimuli (standard = 1 kHz and oddball = 2 kHz frequency) at midline electrode sites, Fz, Cz, Pz. Infant groups were examined in the following developmental windows: 4-15, 16-32, or 33-120 days PNA. Older groups showed increased P2 amplitude at Fz and effective change detection performance at P2 not seen in the newborn group. Developmental maturation of amplitude and stimulus discrimination for P2 has been reported in developing infants at all of the ages tested and data reported here in the older infants are consistent with typical development. However, it has been previously reported that the P2 amplitude difference is detectable in neonates; therefore, absence of a difference in P2 amplitude between stimuli in the 4-15 days group may represent impaired ERP performance by neonatal abstinence syndrome or prenatal methadone exposure.
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