Clinicopathological correlation between brainstem gliosis using GFAP as a marker and sleep apnea in the sudden infant death syndrome

2004 ◽  
Vol 10 (3-4) ◽  
pp. 149-153 ◽  
Author(s):  
Toshiko Sawaguchi ◽  
Patricia Franco ◽  
Hazim Kadhim ◽  
Jose Groswasser ◽  
Martine Sottiaux ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Clinicopathological Correlation

Clinicopathological correlation between brainstem gliosis using GFAP as a marker and sleep apnea in the sudden infant death syndrome

2003 ◽  
Vol 75 ◽  
pp. 3-11 ◽  
Author(s):  
Toshiko Sawaguchi ◽  
Franco Patricia ◽  
Hazim Kadhim ◽  
Jose Groswasser ◽  
Martine Sottiaux ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Clinicopathological Correlation

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

Statistics and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1987 ◽  
Vol 79 (3) ◽  
pp. 486-487
Author(s):  
SUSAN K. CUMMINS
Keyword(s):  
Risk Factors ◽  
Cohort Study ◽  
Relative Risk ◽  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Color Change ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Recent Cohort

To the Editor.— The recent cohort study by Oren et al1 examined risk factors for sudden infant death syndrome (SIDS) in infants with prolonged unexplained sleep apnea with color change (severe apnea of infancy). This analysis revealed three possible risk factors for SIDS death: having a subsequent monitored apnea episode needing resuscitation or vigorous stimulation, being a sibling of a SIDS victim, or developing a seizure disorder after monitoring began. Unfortunately, there are two serious problems with the authors' analysis: the misrepresentation of relative risk and the use of the χ2 statistic to test associations in small subgroups.

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.

scholarly journals SLEEP APNEA AND THE SUDDEN INFANT DEATH SYNDROME (SIDS)

1982 ◽  
Vol 10 (s2) ◽  
pp. 32-32 ◽  
Author(s):  
F.J. Schulte ◽  
M. Albani ◽  
K.H.P. Bentele ◽  
H. Schnizer
Keyword(s):  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant

Phenothiazines and Sudden Infant Death Syndrome

PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 75-78 ◽  
Author(s):  
André Kahn ◽  
Denise Blum
Keyword(s):  
Sleep Apnea ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Upper Airway ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Sudden Infant ◽  
Present Observation ◽  
Airway Infections ◽  
A Prospective Study

A relationship between sudden infant death syndrome (SIDS), sleep apnea, and upper airway infections has been reported. The present observation stresses the possible influence of phenothiazine-containing medications and the occurrence of SIDS. The drug is commonly used for the treatment of infants with nasopharyngitis in Belgium and in some other European countries. In a prospective study, 52 SIDS victims, 36 near miss infants, and 175 control infants were compared for the coexistence of nasopharyngitis and phenothiazine treatment in the days preceding death or hospitalization. The incidence of nasopharyngitis was comparable in the three groups (approximately 31%), but phenothiazines were used significantly more frequently in SIDS victims (23%) and near miss infants (22%) than in control subjects (2%). It is postulated that phenothiazines, as CNS depressors, may contribute to the occurrence of SIDS.

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