Document Type

Honors Thesis

Publication Date

Spring 5-2015


Neonatal Abstinence Syndrome (NAS) is a neonatal medical condition of prenatal opioid withdrawal, secondary to prenatal exposure. NAS increases mortality and morbidity through seizure risk, and excessive sympathetic autonomic tone; which affects respiration and dysregulates sleep and feeding. Our laboratory has recruited more than 200 pregnant women who are in treatment for opiate dependence with methadone maintenance treatments. We have found that NAS severity is modulated by the presence of allelic variants of OPRM1 118A>G (μ-opiate receptor) and COMT 158 A>G (catechol-o-methyl transferase) genes, revealing a positive correlation between minor alleles of these two genes and severity reflected in length of hospitalization and treatment.

In neonates, in this thesis, it is predicted that SNPs protective for NAS will be associated with improved sleep-wake regulation, including movement arousals (MAs), periodic movement bursts during sleep, whereas those infants without the protective alleles may show increased sleep fragmentation and resulting sleep deprivation, providing psychobiological markers of neurodevelopmental risk. In this thesis, I propose that the allelic variants of OPRM1 118A>G, and COMT, that have been associated with NAS severity, will similarly associate with early markers of withdrawal in sleep and arousal before withdrawal has begun. Further, we had examined several genes from the ABCB1 cassette, MDRa, MDRb, MDRc, which are associated with multi-drug resistance (Levran, et al., 2008), for relation to NAS severity. Although there had been no prior research on the ABCB1 cassette (Wachman et al., 2013), I examined MDR genes as well for potential association with pre-withdrawal sleep and wake.

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