Premium
Naltrexone therapy of apnea in children with elevated cerebrospinal fluid β‐endorphin
Author(s) -
Myer Edwin C.,
Morris Dale L.,
Brase David A.,
Dewey William L.,
Zimmerman Andrew W.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410270112
Subject(s) - apnea , medicine , naltrexone , endogenous opioid , cerebrospinal fluid , anesthesia , opioid , opioid peptide , lumbar puncture , pathogenesis , headaches , surgery , receptor
Previous 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 result in physical dependence.