Key result
Sudden infant death syndrome was not associated with significant differences in age-adjusted mean 3H-naloxone binding to opioid receptors in 21 brainstem sites compared to controls.
Why the study?
Is Sudden Infant Death Syndrome (SIDS) associated with altered opioid receptor binding in brainstem nuclei related to respiratory and autonomic control?
Case-Control (n=74)
Is Sudden Infant Death Syndrome (SIDS) associated with altered opioid receptor binding in brainstem nuclei related to respiratory and autonomic control?
p-value: p=NS
This study suggests there is no defect in opioid receptor binding in cardiorespiratory nuclei in the brainstems of infants with Sudden Infant Death Syndrome.
Altered brainstem opioid binding in SIDS is hypothesis-generating; prospective studies needed before any clinical implications.
The sudden infant death syndrome (SIDS) is defined as the sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation, including a complete autopsy. We hypothesized that SIDS is associated with altered 3H - naloxone binding to opioid receptors in brainstem nuclei related to respiratory and autonomic control. We analyzed 3H - naloxone binding in 21 regions in SIDS and control brainstems using quantitative tissue receptor autoradiography. Three groups were analyzed: SIDS (n = 45); acute controls (n = 14); and a chronic group with oxygenation disorders (n = 15). Opioid binding was heavily concentrated in the caudal nucleus of the solitary tract, nucleus parabrachialis medialis, spinal trigeminal nucleus, inferior olive, and interpeduncular nucleus in all cases analyzed (n = 74). The arcuate nucleus on the ventral medullary surface contained negligible binding in all cases (n = 74), and therefore binding was not measurable at this site. We found no significant differences among the three groups in the age-adjusted mean 3H - naloxone binding in 21 brainstem sites analyzed. The only differences we have found to date between SIDS and acute controls are decreases in 3H - quinuclidinyl benzilate binding to muscarinic cholinergic receptors and in 3H - kainate binding to kainate receptors in the arcuate nucleus in alternate sections of this same data set. The present study suggests that there is not a defect in opioid receptor binding in cardiorespiratory nuclei in SIDS brainstems.
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Kinney et al. (1998) conducted a case-control in Sudden infant death syndrome (SIDS) (n=74). Sudden infant death syndrome vs. Acute controls and chronic oxygenation disorders was evaluated on Age-adjusted mean 3H-naloxone binding in 21 brainstem sites (p=NS). Sudden infant death syndrome was not associated with significant differences in age-adjusted mean 3H-naloxone binding to opioid receptors in 21 brainstem sites compared to controls.
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