Sleep State Organization in Normal Infants and Victims of the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 865-870 ◽  
Author(s):  
Vicki L. Schechtman ◽  
Ronald M. Harper ◽  
Arian J. Wilson ◽  
David P. Southall
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Early Morning ◽  
Sudden Infant ◽  
Sleep State ◽  
Quiet Sleep ◽  
Increased Risk ◽  
State Organization

Infants at increased risk of the sudden infant death syndrome (SIDS) show abnormal patterning of sleep-waking states. It was hypothesized that infants who were to die of SIDS would show abnormalities of sleep state distribution prior to their deaths. Twenty-two 12-hour recordings were obtained from infants who subsequently died of SIDS, and sleep state patterns were compared in these records and 66 records of age-matched control infants. Each 1-minute epoch was classified as quiet sleep, rapid eye movement (REM) sleep, waking, indeterminate state, or artifact-contaminated. Victims of SIDS showed less waking and more sleep than control infants during the early-morning hours. Victims of SIDS younger than 1 month of age showed significantly more epochs classified as REM sleep across the night and significantly fewer epochs contaminated by artifacts relative to control infants. Further analysis indicated that the increased number of REM epochs resulted from fewer artifact-contaminated epochs, suggesting reduced motility during REM sleep in the SIDS victims compared with the control infants. The finding of decreased waking time during the early morning is of particular importance since most SIDS deaths occur during this portion of the day. The findings of altered sleep patterns in SIDS victims suggest that central neural changes are associated with SIDS risk.

Sudden Infant Death Syndrome: Sleep Apnea and Respiration in Subsequent Siblings

PEDIATRICS ◽  
1980 ◽  
Vol 66 (2) ◽  
pp. 205-214
Author(s):  
Toke Hoppenbrouwers ◽  
Joan E. Hodgman ◽  
Dennis McGinty ◽  
R. M. Harper ◽  
M. B. Sterman
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Study Groups ◽  
Sudden Infant Death ◽  
High Risk Group ◽  
Sudden Infant ◽  
Sleep State ◽  
Quiet Sleep ◽  
Increased Risk ◽  
High Degree

Subsequent siblings of infants who died of the Sudden Infant Death Syndrome are at a four- to six-times increased risk to die of this syndrome. This study compares the respiratory development during sleep state of this epidemiologic high risk group with that of normal infants during the first six months of life. Subsequent siblings exhibited higher respiratory rates in all states at 3 months of age. Quiet sleep and indeterminate respiratory rates were elevated at 1 week of age compared to control infants. Indeterminate respiratory rates remained higher at 6 months of age. These differences were accompanied by a reduced incidence of total breathing pauses of two to five seconds and six to nine seconds duration in siblings. Study groups could not be differentiated on the basis of either breathing pauses of more than ten seconds or central apnea of six seconds or more. Obstructive and mixed apnea (6 seconds or more) were infrequently observed in these study groups. A high degree of intersubject variability characterized all data on breathing pauses.

scholarly journals Active sleep unmasks apnea and delayed arousal in infant rat pups lacking central serotonin

2017 ◽  
Vol 123 (4) ◽  
pp. 825-834 ◽  
Author(s):  
Jacob O. Young ◽  
Aron Geurts ◽  
Matthew R. Hodges ◽  
Kevin J. Cummings
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Tryptophan Hydroxylase ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Rat Pups ◽  
Infant Rat ◽  
Increased Risk

Sudden infant death syndrome (SIDS), occurring during sleep periods, is highly associated with abnormalities within serotonin (5-HT) neurons, including reduced 5-HT. There is evidence that future SIDS cases experience more apnea and have abnormal arousal from sleep. In rodents, a loss of 5-HT neurons is associated with apnea in early life and, in adulthood, delayed arousal. As the activity of 5-HT neurons changes with vigilance state, we hypothesized that the degree of apnea and delayed arousal displayed by rat pups specifically lacking central 5-HT varies with state. Two-week-old tryptophan hydroxylase 2-deficient ( TPH2−/−) and wild-type (WT) rat pups were placed in plethysmographic chambers supplied with room air. At the onset of active (AS) or quiet (QS) sleep, separate groups of rats were exposed to hypercapnia (5% CO2) or mild hypoxia (~17% O2) or maintained in room air. Upon arousal, rats received room air. Apnea indexes and latencies to spontaneous arousal from AS and QS were determined for pups exposed only to room air. Arousal latencies were also calculated for TPH2−/− and WT pups exposed to hypoxia or hypercapnia. Compared with WT, TPH2−/− pups hypoventilated in all states but were profoundly more apneic solely in AS. TPH2−/− pups had delayed arousal in response to increasing CO2, and AS selectively delayed the arousal of TPH2−/− pups, irrespective of the gas they breathed. Thus infants who are deficient in CNS 5-HT may be at increased risk for SIDS in AS because of increased apnea and delayed arousal compared with QS. NEW & NOTEWORTHY Sudden infant death syndrome (SIDS) occurs during sleep and is associated with central serotonin (5-HT) deficiency. We report that rat pups deficient in central 5-HT ( TPH2−/−) are profoundly more apneic in active sleep (AS) but not quiet sleep (QS). Unlike control pups, the arousal of TPH2−/− pups in air, CO2, and hypoxia was delayed in AS compared with QS. Thus for infants deficient in central 5-HT, the risk of SIDS may be higher in AS than in QS.

scholarly journals Association between monoamine oxidase A promoter polymorphism and the risk of sudden infant death syndrome: a meta-analysis

2021 ◽  
Author(s):  
Qiaoxia Zhou ◽  
Daoyin Gong ◽  
Yu Zhang ◽  
Feijun Huang
Keyword(s):  
Monoamine Oxidase ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Protective Factor ◽  
Meta Analysis ◽  
Variable Number Tandem Repeat ◽  
Sudden Infant Death ◽  
Monoamine Oxidase A ◽  
Sudden Infant ◽  
Increased Risk

Abstract Introduction The etiology of sudden infant death syndrome (SIDS) remains an unsolved problem. The aim of this meta-analysis is to investigate the potential association between monoamine oxidase A (MAOA) promoter variable number tandem repeat (VNTR) polymorphism and SIDS risk. Methods A systematic review and meta-analysis were conducted on studies from accessible electronic databases. Each VNTR variant was examined in each gender independently by comparing with the pooled results of other alleles. Results A total of six independent case–control studies including 1022 SIDS cases and 1839 controls were enrolled in this meta-analysis. In both of the whole populations and Caucasian populations, male infants with the low-MAOA-expression alleles (2R+3R) were found to exhibit a statistically significant increased risk of SIDS, whereas those with a 4R allele exhibited a reduced risk of SIDS. Besides, an increased risk of SIDS was detected in male Caucasian infants with 2R or 3R alleles. However, none of the allele or genotype variants was associated with SIDS in female victims. Conclusion In male Caucasian infants, the low expression of MAOA promoter VNTR alleles (2R and 3R) is associated with an increased risk of SIDS, and the existence of the 4R allele could be regarded as a protective factor.

Smoking and the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1993 ◽  
Vol 91 (5) ◽  
pp. 893-896 ◽  
Author(s):  
E. A. Mitchell ◽  
R. P. K. Ford ◽  
A. W. Stewart ◽  
B. J. Taylor ◽  
D. M. O. Becroft ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Risk Of Death ◽  
Increased Risk ◽  
Wide Range ◽  
Household Members ◽  
Control Study

Objective. Maternal smoking has been shown to be a risk factor for sudden infant death syndrome (SIDS). The effect of smoking by the father and other household members has not previously been examined. Methods. A large nationwide case-control study. Four hundred eighty-five SIDS deaths in the postneonatal age group were compared with 1800 control infants. Results. Infants of mothers who smoked during pregnancy had a 4.09 (95% confidence interval [CI] = 3.28, 5.11) greater risk of death than infants of mothers who did not smoke. Infants of mothers who smoked postnatally also had an increased risk of SIDS compared with infants of nonsmokers and, furthermore, the risk increased with increasing levels of maternal smoking. Smoking by the father and other household members increased the risk (odds ratio [OR] = 2.41, 95% CI = 1.92, 3.02 and OR = 1.54, 95% CI = 1.20, 1.99, respectively). Smoking by the father increased the risk of SIDS if the mother smoked, but had no effect if she did not smoke. In analyses controlled for a wide range of potential confounders, smoking by the mother and father was still significantly associated with an increased risk of SIDS. Conclusion. Passive tobacco smoking is causally related to SIDS.

Prolongation of the laryngeal chemoreflex after inhibition of the rostral ventral medulla in piglets: a role in SIDS?

2003 ◽  
Vol 94 (5) ◽  
pp. 1883-1895 ◽  
Author(s):  
Liesbeth van der Velde ◽  
Aidan K. Curran ◽  
James J. Filiano ◽  
Robert A. Darnall ◽  
Donald Bartlett ◽  
...  
Keyword(s):  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Nrem Sleep ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Ventral Medulla ◽  
Before And After

We tested the hypothesis that inhibition of neurons within the rostral ventral medulla (RVM) would prolong the laryngeal chemoreflex (LCR), a putative stimulus in the sudden infant death syndrome (SIDS). We studied the LCR in 19 piglets, age 3–16 days, by injecting 0.05 ml of saline or water into the larynx during wakefulness, non-rapid eye movement (NREM) sleep, and REM sleep, before and after 1 or 10 mM muscimol dialysis in the RVM. Muscimol prolonged the LCR ( P < 0.05), and the prolongation was greater when the LCR was stimulated with water compared with saline ( P < 0.02). The LCR was longer during NREM sleep than during wakefulness and longest during REM sleep (REM compared with wakefulness). Muscimol had no effect on the likelihood of arousal from sleep after LCR stimulation. We conclude that the RVM provides a tonic facilitatory drive to ventilation that limits the duration of the LCR, and loss of this drive may contribute to the SIDS when combined with stimuli that inhibit respiration.

Sudden Infant Death Syndrome in Twins and Singletons

2007 ◽  
Vol 10 (4) ◽  
pp. 644-648 ◽  
Author(s):  
Peter O. D. Pharoah ◽  
Mary J. Platt
Keyword(s):  
Risk Factor ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Low Birthweight ◽  
Sudden Infant Death ◽  
Multiple Births ◽  
Sudden Infant ◽  
Microscopical Examination ◽  
Increased Risk ◽  
Opposite Sex

AbstractTwins compared with singletons and monozygous (MZ) compared with dizygous (DZ) twins are at increased risk of fetal and infant death, cerebral palsy and many congenital anomalies. The aim of this study is to investigate whether zygosity is a risk factor for the sudden infant death syndrome (SIDS). Birth registration data and draft infant death certificates for all multiple births in England and Wales 1993 to 2003 were provided by the Office for National Statistics. As a partial proxy for zygosity, same-sex was compared with opposite-sex twins for birthweight-specific mortality and mortality attributed to SIDS. Data on singleton infants were obtained by subtraction of multiple births from routinely published population births and infant deaths. SIDS mortality among low birthweight infants was significantly less in twins than singletons. The twin-singleton relative risk was reversed in infants of normal birthweight. Among infants of normal birthweight, neonatal SIDS was significantly more common in same- compared with opposite-sex pairs. Among infants of low birthweight, postneonatal SIDS was significantly more common in same- compared with opposite-sex pairs. The difference in birthweight distribution of same- compared with opposite-sex twins for neonatal SIDS suggests that zygosity is a risk factor for SIDS. As congenital cerebral anomalies are a feature of many monozygous twin conceptions, a detailed macro- and microscopical examination of the brain in twin SIDS may indicate an otherwise unrecognised pathology.

Incidence of Recurrence of Sudden Infant Death Syndrome

1993 ◽  
Vol 14 (3) ◽  
pp. 94-116
Keyword(s):  
United States ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
South Australia ◽  
Sudden Infant Death ◽  
The United States ◽  
Sudden Infant ◽  
Specific Population ◽  
Live Births ◽  
Increased Risk

Incidence figures for sudden infant death syndrome (SIDS) are affected by the specific population being studied, the method of data collection, the way in which the diagnosis is determined, and other variables. The occurrence of SIDS per 100 live births has been estimated to be 1.3 in Norway, 2.1 in South Australia, and 2 to 3 in the United States. Subsequent siblings are at increased risk of SIDS, with estimates ranging from 3.7 times that of the general population to as high as 10 times. Beal et al found that families in South Australia who lost a child older than 12 months of age to SIDS were 11 times more likely to have a subsequent child with SIDS than were families in which the SIDS victim was younger than 1 year of age.

Sleep Parameters and Respiratory Variables in ‘Near Miss’ Sudden Infant Death Syndrome Infants

PEDIATRICS ◽  
1981 ◽  
Vol 68 (3) ◽  
pp. 354-360
Author(s):  
Christian Guilleminault ◽  
Ronald Ariagno ◽  
Rowena Korobkin ◽  
Susan Coons ◽  
Margaret Owen-Boeddiker ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sleep Onset ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Sudden Infant ◽  
Normal Infant ◽  
Respiratory Events ◽  
Increased Risk ◽  
Sleep Parameters

Twenty-nine near miss for sudden infant death syndrome and thirty normal infants between the ages of 3 weeks and 6 months were monitored polygraphically for 24 hours. The distribution of sleep and abnormal respiratory events were analyzed for both groups. On the basis of mixed and obstructive apnea, 12-hour nocturnal segments (8 pm to 8 am) consistently distinguished near miss from normal infant groups between the ages of 3 weeks and 4.5 months. Daytime naps do not provide statistical differences sufficient to differentiate between the two groups. During sleep, abnormal respiratory events are more likely to occur between 1 am and 6 am, at least 40 minutes after sleep onset. Respiratory pauses show a significant increase just prior to waking (a strong respiratory stimulus). Any impairment of the arousal threshold during sleep will place near miss infants at increased risk.

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