Fewer spontaneous arousals during prone sleep in preterm infants at 1 and 3 months corrected age

Ariagno, Ronald L.; Liempt, Saskia van; Mirmiran, M.

doi:10.1038/sj.jp.7211490

Cited by 36 publications

(10 citation statements)

References 34 publications

(51 reference statements)

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“…One study [30] demonstrated less frequent arousals in premature infants when lying prone at 1-3 months of age, corrected for prematurity. The second study [31] demonstrated that although subcortical arousals were unchanged regardless of sleep position in healthy infants, the number of cortical arousals was decreased when lying prone.…”

Section: Sleep In Sudden Infant Death Syndromementioning

confidence: 97%

Sudden infant death syndrome: another year of new hope but no cure

Loghmanee

Weese‐Mayer

2007

Current Opinion in Pulmonary Medicine

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The cause of sudden infant death syndrome remains elusive. Recent studies, however, suggest that improved culturally sensitive educational programs, increased diagnostic specificity, and further clarification of the link between genetics and developmental stage might further decrease the number of infants lost to this devastating disease and elucidate the mechanism(s) responsible for this syndrome.

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Section: Sleep In Sudden Infant Death Syndromementioning

confidence: 97%

Sudden infant death syndrome: another year of new hope but no cure

Loghmanee

Weese‐Mayer

2007

Current Opinion in Pulmonary Medicine

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“…Physiologic studies have found that infants are less likely to arouse when they are sleeping in the prone position. [87][88][89][90][91][92][93][94][95] The ability to arouse from sleep is an important protective physiologic response to stressors during sleep, [96][97][98][99][100] and the infant's ability to sleep for sustained periods might not be physiologically advantageous.…”

Section: Figurementioning

confidence: 99%

SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment

Moon¹

2011

Pediatrics

219

115

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Despite a major decrease in the incidence of sudden infant death syndrome (SIDS) since the American Academy of Pediatrics (AAP) released its recommendation in 1992 that infants be placed for sleep in a nonprone position, this decline has plateaued in recent years. Concurrently, other causes of sudden unexpected infant death occurring during sleep (sleep-related deaths), including suffocation, asphyxia, and entrapment, and ill-defined or unspecified causes of death have increased in incidence, particularly since the AAP published its last statement on SIDS in 2005. It has become increasingly important to address these other causes of sleep-related infant death. Many of the modifiable and nonmodifiable risk factors for SIDS and suffocation are strikingly similar. The AAP, therefore, is expanding its recommendations from being only SIDS-focused to focusing on a safe sleep environment that can reduce the risk of all sleep-related infant deaths including SIDS. The recommendations described in this report include supine positioning, use of a firm sleep surface, breastfeeding, room-sharing without bed-sharing, routine immunization, consideration of a pacifier, and avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and illicit drugs. The rationale for these recommendations is discussed in detail in this technical report. The recommendations are published in the accompanying “Policy Statement—Sudden Infant Death Syndrome and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment,” which is included in this issue (www.pediatrics.org/cgi/doi/10.1542/peds.2011-2220).

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“…Spontaneous arousals and those in response to exogenous stimuli are affected by many factors: sleep position (3,29,37), sleep efficiency (30), prenatal exposure to cigarette smoking (28,38), and stage of development (39). It has been hypothesized that arousal impairment may play an important role in the etiology of sudden infant death syndrome (SIDS) (32,40,43,46).…”

mentioning

confidence: 99%

Arousal from sleep in response to intermittent hypoxia in rat pups is modulated by medullary raphe GABAergic mechanisms

Darnall¹,

Schneider²,

Tobia³

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Darnall RA, Schneider RW, Tobia CM, Zemel BM. Arousal from sleep in response to intermittent hypoxia in rat pups is modulated by medullary raphe GABAergic mechanisms. Am J Physiol Regul Integr Comp Physiol 302: R551-R560, 2012. First published December 7, 2011; doi:10.1152/ajpregu.00506.2011Arousal is an important defense against hypoxia during sleep. Rat pups exhibit progressive arousal impairment (habituation) with multiple hypoxia exposures. The mechanisms are unknown. The medullary raphe (MR) is involved in autonomic functions, including sleep, and receives abundant GABAergic inputs. We hypothesized that inhibiting MR neurons with muscimol, a GABA A receptor agonist, or preventing GABA reuptake with nipecotic acid, would impair arousal and enhance arousal habituation and that blocking GABA A receptors with bicuculline would enhance arousal and attenuate habituation. Postnatal day 15 (P15) to P25 rat pups were briefly anesthetized, and microinjections with aCSF, muscimol, bicuculline, or nipecotic acid were made into the MR. After a ϳ30-min recovery, pups were exposed to four 3-min episodes of hypoxia separated by 6 min of normoxia. The time to arousal from the onset of hypoxia (latency) was determined for each trial. Latency progressively increased across trials (habituation) in all groups. The overall latency was greater after muscimol and nipecotic acid compared with aCSF, bicuculline, or noninjected controls. Arousal habituation was reduced after bicuculline compared with aCSF, muscimol, nipecotic acid, or noninjected pups. Increases in latency were mirrored by decreases in chamber [O2] and oxyhemoglobin saturation. Heart rate increased during hypoxia and was greatest in muscimol-injected pups. Our results indicate that the MR plays an important, not previously described, role in arousal and arousal habituation during hypoxia and that these phenomena are modulated by GABAergic mechanisms. Arousal habituation may contribute to sudden infant death syndrome, which is associated with MR serotonergic and GABAergic receptor dysfunction.␥-aminobutyric acid; sudden infant death syndrome; GABAA receptor; habituation IN HUMAN INFANTS, AROUSAL is an important protective mechanism against hypoxia during sleep. Spontaneous arousals and those in response to exogenous stimuli are affected by many factors: sleep position (3, 29, 37), sleep efficiency (30), prenatal exposure to cigarette smoking (28, 38), and stage of development (39). It has been hypothesized that arousal impairment may play an important role in the etiology of sudden infant death syndrome (SIDS) (32,40,43,46). Moreover, many SIDS infants have repeated episodes of apnea and hypoxia in the days or weeks prior to death (44,56). We propose that repeated exposure to hypoxia during sleep leads to progressive lengthening of the time to arousal in response to hypoxia that might contribute to sudden death.We and others have shown in newborn and infant rodents (17, 18, 21), lambs (25,41,42), and piglets (71) that repeated brief exposures to mild hypoxia result in...

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Fewer spontaneous arousals during prone sleep in preterm infants at 1 and 3 months corrected age

Cited by 36 publications

References 34 publications

Sudden infant death syndrome: another year of new hope but no cure

Sudden infant death syndrome: another year of new hope but no cure

SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment

Arousal from sleep in response to intermittent hypoxia in rat pups is modulated by medullary raphe GABAergic mechanisms

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