The incidence of opioid abuse and subsequent drug withdrawal is exponentially on the rise in the United States for many populations including newborns who are born to drug-addicted mothers. These newborns often exhibit symptoms of neonatal abstinence syndrome (NAS) within 24 to 72 hours of birth. Treatment of NAS includes monitoring of withdrawal symptoms, managing physiological parameters, and the use of supportive and pharmacologic treatments. Although a few randomized controlled trials exist, studies on supportive intervention are generally limited by small sample sizes, case study reports, expert opinions, and descriptive design. Few studies address the safety of Reiki for newborns at risk for NAS using neonatal parameters. This pilot study addresses feasibility and demonstrates that Reiki is safe when administered to this high-risk population. Considerations for future studies are discussed.
Background: Lasting motor and cognitive impairments can be a consequence of hypoxic-ischemic (HI) injury to the immature brain. Functional deficits could be due to neuronal loss or altered synaptogenesis. Little is known about the effect of neonatal HI brain injury on synaptic indices, either in injured or unaffected brain tissue. Quantitation of dendritic morphology, e.g. dendritic spine density, branching and length in Golgi-stained tissue, is frequently used to evaluate the effects of brain injury on synaptic organization. We hypothesized that unilateral neonatal cerebral HI elicits distinct ipsilateral and contralateral dendritic abnormalities.Methods: We evaluated hippocampal dendritic trees in seven-day-old (P7) Long-Evans male rats (nϭ12) that underwent either unilateral cerebral HI (nϭ6, right carotid ligation followed by 1.5h in 8% O2) or a sham procedure (neck incision followed by 1.5h in 8% O2). These conditions elicit mild to moderate neuronal loss in ipsilateral striatum, cortex and hippocampus, with no visible contralateral abnormalities. Rats were weaned at P21 and were housed in standard cages until P60. Brains were perfused with saline followed by 1% paraformaldehyde, placed in Golgi-Cox solution for 2 wk, then sectioned at 200 m. Neurons (10 CA1 pyramidal neurons/side/rat ) were considered suitable for analysis if they were well impregnated and not obscured by blood vessels, astrocytes, or dendrites of other neurons, and their branching was intact within the section. Cells were drawn via camera lucida. Total dendritic length/neuron was estimated by counting dendritic intersections with a series of concentric spheres at 20 m intervals centered on the soma. Spine density was calculated by tracing a length of third order terminal basilar dendrite (Ն70 m long) at 2000X. The exact length of the dendritic segment was calculated, and the number of spines along the entire length counted and expressed as spines/10 m.Results: Bilateral hippocampal reductions in dendritic length, branch number and spine density were associated with HI. CA1 pyramidal spine density was reduced both ipsilaterally (Spines/10m, meanϮSD: Sham 10.6Ϯ0.6 vs. HI 8.4Ϯ0.3, pϽ0.001, t-test) and contralaterally (Sham 10.7Ϯ0.4 vs. HI 9.1Ϯ0.7, pϽ0.001,.Conclusion: These findings indicate that abnormalities of synaptic organization persist into adulthood after neonatal HI brain injury, and these abnormalities affect regions of the brain distant from the site of HI neuronal injury. Background: The forebrain subventricular zone (SVZ) contains oligodendroglial (OL) stem cells. Although some studies suggest acute loss of SVZ OL precursors after hypoxic-ischemic (HI) neonatal brain injury, recovery of myelin basic protein (MBP) immunostaining in the white matter 2 weeks after HI raises the possibility that OL stem cells in the SVZ might proliferate to repopulate injured white matter. As an alternative to using the HI model to study the SVZ response to neonatal brain injury, we developed a model of neonatal brain injury that focuses on a unique...
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