From epidemiology to physiology and pathology: apnea and arousal deficient theories in sudden infant death syndrome (SIDS)--with particular reference to hypoxic brainstem gliosis.

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age. They included 26 cases of sudden infant death syndrome (SIDS). Five infants who died from congenital cardiac abnormalities, two from infected pulmonary dysplasia, two from septic shock with multi-organ failure, one during a prolonged seizure, one from a prolonged neonatal hypoxemia, one from meningitis with brain infarction. All the infants had been recorded during one night in a pediatric sleep laboratory some 3-12 weeks before death. The frequency and duration of sleep apneas were analyzed. The infants' brain stem material was collected and immunohistochemistry of glial fibrillary acidic protein (GFAP) was carried out. The density of GFAP-positive reactive astrocytes was measured in the cardiorespiratory and arousal pathway. Akaike information criterion statistics (AIC) were calculated to elucidate the relationship between the epidemiological data on sleep position, the physiological data and the pathological data in SIDS victims. The duration of obstructive apnea was the most significant variable to differentiate between SIDS victims and control infants. In conclusion, the present study sustains the possibility of an organic fragility within the arousal pathway in SIDS victims with repetitive sleep apneas.