AbstractPrevious studies have indicated increased immunoreactivity of the endogenous opioid peptide β‐endorphin in the cerebrospinal fluid (CSF) of infants under 2 years of age with apnea. To assess the role of endogeneous opioids in the pathogenesis of apnea in children, the effect of oral treatment with the opioid antagonist naltrexone was studied in apneic infants, as well as in older apneic children, with demonstrated increases in CSF immunoreactive β‐endorphin (i‐BE). In the 8 apneic infants with elevated i‐BE in lumbar CSF (range, 55–155 pg/ml normal, 17–52 pg/ml), no further apnea occurred during natltrexone therapy (1 mg/kg/day, by mouth). Five children (2–8 years old) with apnea of unknown cause had elevated CSF i‐BE (range, 74–276 pg/ml) compared to 6 age‐matched nonapneic children (range, 15–48 pg/ml). No apneic events occurred during natlrexone therapy, except in 1 child during stressful events, but apnea recurred in some patients after attempts to discontinue natlrexone treatment. Adverse effects of natlrexone included complaints of headaches in 2 children and symptoms of a narcotic withdrawal syndrome during the first 3 days of treatment in 1 child. Three children with Leigh's syndrome had elevated CSF i‐BE (range, 104–291 pg/ml) and their apnea also responded to naltrexone. We conclude that elevated endogenous opioids contribute to the pathogenesis of apnea in children and may even re
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