Apnea and Sleep State in Infants with Nasopharyngitis

PEDIATRICS ◽  
1980 ◽  
Vol 65 (4) ◽  
pp. 713-717
Author(s):  
Jeffrey B. Gould ◽  
Austin F. S. Lee ◽  
Peter Cook ◽  
Suzette Morelock
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Infant Death ◽  
Sleep Time ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Upper Respiratory Tract ◽  
Sleep State ◽  
Upper Respiratory

Having a mild upper respiratory tract infection does not change the sleep state proportions or total sleep time of an infant. However, infants with colds exhibit some sleep state specific alterations in sleep apnea. At 40, 44, and 48 weeks postconception, the number of respiratory pauses of 2 to 4.9 seconds and of 5 to 9.9 seconds duration per 100 minutes of state, during rapid eye movement, and indeterminate sleep are decreased in infants with colds. The absence of this phenomenon at 52 weeks suggests that it is modified by maturation. We hypothesize that the reduction in rapid eye movement and indeterminate sleep apnea is a manifestation of an adaptive response in normal infants, but for infants at risk for the sudden infant death syndrome, this response may be overwhelmed, resulting in increased apnea and, in some instances, sudden infant death.

Sleep Apnea in Infants Who Succumb to The Sudden Infant Death Syndrome

PEDIATRICS ◽  
1991 ◽  
Vol 87 (6) ◽  
pp. 841-846
Author(s):  
Vicki L. Schechtman ◽  
Ronald M. Harper ◽  
Adrian J. Wilson ◽  
David P. Southall
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Matched Control ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Quiet Sleep

Previous studies have shown the frequency of respiratory pauses to be altered in groups of infants at risk for the sudden infant death syndrome (SIDS). In this study, we assess the frequency of apneic pauses during quiet sleep and rapid eye movement sleep in control infants and infants who subsequently died of SIDS. Sleep states were identified in 12-hour physiological recordings of SIDS victims and matched control infants, and the number of respiratory pauses from 4 to 30 seconds in duration was computed for quiet sleep and rapid eye movement sleep. SIDS victims 40 to 65 days of age showed significantly fewer apneic pauses than did age-matched control infants across the two sleep states. Fewer short respiratory pauses accounted for most of the reduction in number of apneic events in the SIDS victims during both sleep states. During the first month of life, SIDS victims did not differ significantly from control neonates on this measure. The finding that this respiratory difference exists during the second month of life, just before the period of maximal risk for SIDS, but not earlier, may have implications for the etiology of SIDS deaths.

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.

Muscimol dialysis in the rostral ventral medulla reduced the CO2 response in awake and sleeping piglets

2001 ◽  
Vol 90 (3) ◽  
pp. 971-980 ◽  
Author(s):  
Aidan K. Curran ◽  
Robert A. Darnall ◽  
James J. Filiano ◽  
Aihua Li ◽  
Eugene E. Nattie
Keyword(s):  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Arcuate Nucleus ◽  
Sudden Infant Death ◽  
Human Infant ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Ventral Medulla

Some victims of sudden infant death syndrome have arcuate nucleus abnormalities. The arcuate nucleus may be homologous with ventral medullary structures in the cat known to be involved in the control of breathing and the response to systemic hypercapnia. We refer to putative arcuate homologues in the piglet collectively as the rostral ventral medulla (RVM). We inhibited the RVM in awake and sleeping, chronically instrumented piglets by microdialysis of the GABAA receptor agonist muscimol. Muscimol dialysis (10 and 40 mM) had no effect on eupnea but caused a significant reduction in the response to hypercapnia during both wakefulness (34.8 ± 8.7 and 30.7 ± 10.1%, respectively) and sleep (36.7 ± 6.7 and 49.5 ± 8.9%, respectively). The effect of muscimol on the CO2 response was entirely via a reduction in tidal volume and appeared to be greater during non-rapid-eye-movement sleep. We conclude that the piglet RVM contains neurons of importance in the response to systemic CO2 during both wakefulness and non-rapid-eye-movement sleep. We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia, particularly during sleep, which could potentially be involved in the pathogenesis of sudden infant death syndrome.

Nasopharyngitis and the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1977 ◽  
Vol 60 (4) ◽  
pp. 531-533
Author(s):  
ALFRED STEINSCHNEIDER
Keyword(s):  
Respiratory Tract ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Clinical Symptoms ◽  
Sudden Infant Death ◽  
Epidemiological Studies ◽  
Sudden Infant ◽  
Upper Respiratory Tract ◽  
Inflammatory Processes ◽  
Upper Respiratory

Epidemiological studies repeatedly have demonstrated the importance of a number of variables in affecting the incidence of the sudden infant death syndrome (SIDS).1.2 Characteristically, the peak risk of SIDS is within the second to third month of life, with relatively few cases in the first month of life or after the first year. Another consistent observation is the association between minor upper respiratory tract inflammatory processes(nasopharyngitis) and SIDS: relatively more SIDS victims than controls have had clinical symptoms referable to the upper respiratory tract one to two weeks prior to death. Furthermore, histologic examinations have revealed upper respiratory tract

Nasopharyngitis and Prolonged Sleep Apnea

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 967-971
Author(s):  
Alfred Steinschneider
Keyword(s):  
Sleep Apnea ◽  
Respiratory Tract ◽  
Clinical Symptoms ◽  
Sudden Infant Death ◽  
Simultaneous Occurrence ◽  
Sudden Infant ◽  
Time Interval ◽  
Upper Respiratory Tract ◽  
Before And After ◽  
Upper Respiratory

The effect of nasopharyngitis on the simultaneous occurrence of prolonged sleep apnea (≥20 seconds in duration) was studied in 26 infants managed at home on an apnea monitor. During the observation period, these infants had a total of 69 illnesses which appeared to represent an upper respiratory tract inflammatory process. In general, the daily frequency of prolonged apneic episodes was significantly greater during nasopharyngitis when compared to comparable time intervals immediately prior to and following the illness. In addition, there was a decrease in the frequency of apneic episodes with increasing postnatal age until the episodes finally ceased to occur during the illnessreleted intervals. Apneic episodes ceased to occur at an earher age for the before- and after-illness intervals than for the time interval during which there were clinical symptoms. Thus, it would appear that infants go through an agerelated phase wherein prolonged apnea occurs during nasopharyngitis but not when free of illness. The implications of these results for the management of infants having prolonged sleep apnea are discussed. In view of the hypothesis that prolonged sleep apnea is part of the physiological process resulting in the sudden infant death syndrome, these results also provide for the prediction that infants who suddenly die in association with nasopharynqitis would do so, in general, at a later age than those who succumb when free of an upper respiratory tract inflammatory tory process.

The Uvula and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 319-320
Author(s):  
CHRISTIAN GUILLEMINAULT
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sleep Apnea Syndrome ◽  
Sudden Infant Death ◽  
Term Infant ◽  
Near Miss ◽  
Sudden Infant ◽  
Obstructive Sleep

In Reply.— Harpey and Renault postulate a relationship between the uvula, obstructive sleep apnea, and sudden infant death syndrome. Although I believe that obstructive sleep apnea syndrome may be one of the mechanisms leading to sudden infant death syndrome, this speculation is extremely controversial. I do concur with Harpey and Renault that obstructive sleep apnea can trigger esophageal reflux. A segment from a sleep recording of a 9-week-old, full-term infant with near-miss sudden infant death syndrome is presented in the Figure.

Neuronal Control of Neonatal Respiration - Sleep Apnea and the Sudden Infant Death Syndrome

1982 ◽  
Vol 13 (S 1) ◽  
pp. 3-14 ◽  
Author(s):  
F. Schulte ◽  
M. Albani ◽  
H. Schnizer ◽  
K. Bentele ◽  
R. Klingsporn
Keyword(s):  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Neuronal Control
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