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

Abstract

Background: Chronic hypoxia, leading to brainstem gliosis, has been postulated as a factor in the sudden infant death syndrome (SIDS), which is still the main cause of postneonatal infant death. Gliosis detected by immunohistochemistry of glial fibrillary acidic protein (GFAP) is a marker of apoptosis. The correlation between GFAP-positive reactive astrocytes in the brainstem and sleep apnea in SIDS was investigated. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry of GFAP carried out. The density of GFAP-positive reactive astrocytes was measured quantitatively. Correlation analyses were carried out between the data on gliosis and the physiological data of sleep apnea. Results: A SIDS-specific negative correlation between the density of gliosis in the dorsal vagus nucleus in the medulla oblongata and the frequency of obstructive apnea ( P=0.022) was found. Conclusions: A significant SIDS-specific correlation with gliosis in the dorsal vagus nucleus and the characteristics of sleep apnea might invite the cardiorespiratory changes in SIDS.