Cerebrospinal Fluid and Plasma Beta-Endorphin Concentrations in Prolonged Infant Apnea (Near-Miss Sudden Infant Death Syndrome)

1986 ◽  
Vol 9 (4) ◽  
pp. 224-230 ◽  
Author(s):  
Koravangattu Sankaran ◽  
Kenneth Wayne Hindmarsh ◽  
Sylvia Mary Wallace ◽  
Rhonda Jane McKay ◽  
Maureen O’Donnell
PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 319-320
Author(s):  
CHRISTIAN GUILLEMINAULT

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.


1982 ◽  
Vol 101 (6) ◽  
pp. 911-917 ◽  
Author(s):  
Kristine McCulloch ◽  
Robert T. Brouillette ◽  
Anthony J. Guzzetta ◽  
Carl E. Hunt

PEDIATRICS ◽  
1979 ◽  
Vol 64 (6) ◽  
pp. 882-891 ◽  
Author(s):  
Christian Guilleminault ◽  
Ronald Ariagno ◽  
Rowena Korobkin ◽  
Lynn Nagel ◽  
Roger Baldwin ◽  
...  

Twenty-nine full-term near miss for sudden infant death syndrome (SIDS) and 30 normal control infants underwent 24-hour polygraphic monitoring. Several types of respiratory events during sleep (eg, central, mixed, and obstructive apnea, periodic breathing) were defined and tabulated. Analysis of these respiratory variables and comparison of groups of near miss and control infants indicated that between 3 weeks and 4½ months of age only one variable was consistently different at a statistically significant level: the number of mixed and obstructive apnea 3 seconds during total sleep time. This study also showed an increase in mixed and obstructive respiratory events during sleep at 6 weeks of age in control as well as in near miss infants.


PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 128-131
Author(s):  
Dorothy H. Kelly ◽  
Joseph Twanmoh ◽  
Daniel C. Shannon

Victims of sudden infant death syndrome (SIDS) have been shown to have pathologic abnormalities consistent with chronic hypoxia.1-7 Two groups of infants at high risk of dying of SIDS, near miss infants and subsequent siblings of SIDS victims, have been studied in attempts to demonstrate physiologic abnormalities that could account for these pathologic findings. Investigators have found abnormalities in breathing pattern and the respiratory control system in the former consisting of prolonged sleep apnea, excessive short apnea, periodic breathing, hypoventilation, and depressed response to hypercarbia.8-13 However, studies in the SIDS sibling group have demonstrated varying results of excessive periodic breathing in the home14 and decreased apnea in the laboratory.15


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