👤 Macie Donahue

Examine whether neonatal neurobehavioral profiles are related to need for pharmacological treatment among infants with prenatal opioid exposure. Prospective cohort study of 217 infants with need for treatment determined using the Finnegan Neonatal Abstinence Tool (FNAST), Neonatal Withdrawal Inventory (NWI), or Eat Sleep Console (ESC). Neurobehavior was assessed with the NeoNatal Neurobehavioral Scale II (NNNS-II). Latent Profile Analysis (LPA) classified infants into neurobehavioral profiles, and logistic regression assessed the association between NNNS-II profiles and need for treatment. A 3-profile LPA solution best fit the NNNS-II data comprised of typical (67%), hyper-aroused (19%) and hypo-aroused groups (15%). Infants with atypical NNNS-II profiles were more likely to receive treatment (OR = 3.45, 95% CI 1.21-9.81) compared to infants with typical profiles (p < 0.05). Newborn neurobehavioral profiles may aid in early identification of infants requiring pharmacological treatment for opioid withdrawal, reducing length of stay and healthcare costs. Show less

Examine whether neonatal neurobehavioral profiles are related to need for pharmacological treatment among infants with prenatal opioid exposure. Prospective cohort study of 217 infants with need for treatment determined using the Finnegan Neonatal Abstinence Tool (FNAST), Neonatal Withdrawal Inventory (NWI), or Eat Sleep Console (ESC). Neurobehavior was assessed with the NeoNatal Neurobehavioral Scale II (NNNS-II). Latent Profile Analysis (LPA) classified infants into neurobehavioral profiles and logistic regression assessed the association between NNNS-II profiles and need for treatment. A 3-profile LPA solution best fit the NNNS-II data comprised of typical (67%), hyper-aroused (19%) and hypo-aroused groups (15%). Infants with atypical NNNS-II profiles were more likely to receive treatment (OR=3.45, 95% CI 1.21-9.81) compared to infants with typical profiles ( Newborn neurobehavioral profiles may aid in early identification of infants requiring pharmacological treatment for opioid withdrawal, reducing length of stay and healthcare costs. Show less

Juvenile-onset neuronal ceroid lipofuscinosis (JNCL; Batten disease) features hallmark membrane deposits and loss of central nervous system (CNS) neurons. Most cases of the disease are due to recessive inheritance of an approximately 1 kb deletion in the CLN3 gene, encoding battenin. To investigate the common JNCL mutation, we have introduced an identical genomic DNA deletion into the murine CLN3 homologue (Cln3) to create Cln3( Deltaex7/8) knock-in mice. The Cln3( Deltaex7/8) allele produced alternatively spliced mRNAs, including a variant predicting non-truncated protein, as well as mutant battenin that was detected in the cytoplasm of cells in the periphery and CNS. Moreover, Cln3( Deltaex7/8) homozygotes exhibited accrual of JNCL-like membrane deposits from before birth, in proportion to battenin levels, which were high in liver and select neuronal populations. However, liver enzymes and CNS development were normal. Instead, Cln3( Deltaex7/8) mice displayed recessively inherited degenerative changes in retina, cerebral cortex and cerebellum, as well as neurological deficits and premature death. Thus, the harmful impact of the common JNCL mutation on the CNS was not well correlated with membrane deposition per se, suggesting instead a specific battenin activity that is essential for the survival of CNS neurons. Show less