A new neurological focus in neonatal intensive care.

Department of Pediatrics, UCSF School of Medicine, UCSF Benioff Children's Hospital, Box 0410, 513 Parnassus Avenue, S211, San Francisco, CA 94143-0410, USA.
Nature Reviews Neurology (Impact Factor: 14.1). 08/2011; 7(9):485-94. DOI: 10.1038/nrneurol.2011.119
Source: PubMed

ABSTRACT Advances in the care of high-risk newborn babies have contributed to reduced mortality rates for premature and term births, but the surviving neonates often have increased neurological morbidity. Therapies aimed at reducing the neurological sequelae of birth asphyxia at term have brought hypothermia treatment into the realm of standard care. However, this therapy does not provide complete protection from neurological complications and a need to develop adjunctive therapies for improved neurological outcomes remains. In addition, the care of neurologically impaired neonates, regardless of their gestational age, clearly requires a focused approach to avoid further injury to the brain and to optimize the neurodevelopmental status of the newborn baby at discharge from hospital. This focused approach includes, but is not limited to, monitoring of the patient's brain with amplitude-integrated and continuous video EEG, prevention of infection, developmentally appropriate care, and family support. Provision of dedicated neurocritical care to newborn babies requires a collaborative effort between neonatologists and neurologists, training in neonatal neurology for nurses and future generations of care providers, and the recognition that common neonatal medical problems and intensive care have an effect on the developing brain.

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    ABSTRACT: Research evidence is limited regarding developmentally appropriate care. Variations exits with respect to test procedure type, infant age at testing, and test relatedness. To assess developmental continuity using multiple developmental measures from birth to 12 months in a single cohort of term infants. A secondary analysis, longitudinal, correlational design was used to assess developmental continuity in a single cohort of infants (n 27). Measures included: sleep, using the Motility Monitoring System (first 48 hours of life); temperament, using the Infant Characteristics Questionnaire (ICQ, 6 months) and the Revised Infant Temperament Questionnaire (RITQ, 12 months); problem-solving, using the Willatts Infant Planning Test (PS, 9 and 12 months); and the Fagan Test of Infant Intelligence (FTII, 6 and 9 months). Using Spearmen correlation, significant correlations included: (1) Sleep and ICQ: transitional sleep and "unpredictable" (r 0.455, P .017), "unadaptable" (r 0.420, P .026), and "dull" (r 0.416, P .028); (2) ICQ and FTII 6 months (r -0.512, P .008); (3) RITQ "approachability" and quiet sleep (r 0.662, P .005); (4) arousals in active sleep and PS at 9 months (r -0.528, P .016). Given our reported continuity between early sleep and later developmental measures, sleep-wake state should be considered in caregiving and environmental control to support sleep. Parental education on facilitating sleep-wake regulation in the home environment is essential. These data support the existence of continuity between early sleep and later developmental milestones warranting a larger-scale investigation. Specific focus on development of care strategies for facilitating sleep immediately following birth is warranted.
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    ABSTRACT: Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), which results in infant cerebral palsy due to the effects on myelination. The origin of OPC vulnerability in HIBD, however, remains controversial. In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity (DEHSI) in postnatal 7-day rats. The electrophysiological functional properties of OPCs in HIBD were recorded by patch clamp in acute cerebral cortex slices. The slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibody to identify local OPCs. Passive membrane properties and K(+) channel functions in OPCs were analyzed to estimate the onset of vulnerability in HIBD. The resting membrane potential (RMP), membrane resistance (Rin) and membrane capacitance (Cm) of OPCs were increased both in the grey and white matter of the cerebral cortex. OPCs in both the grey and white matter exhibited voltage-dependent K(+) currents, which consisted of the initiated rectified potassium currents (IA) and the sustained rectified currents (IK). The significant alternation in membrane resistance was influenced by the diversity of potassium channel kinetics. These findings suggest that the rectification of IA and IK channels may play a significant role in OPC vulnerability in HIBD.
    Journal of Neurophysiology 10/2014; 113(2):jn.00144.2014. DOI:10.1152/jn.00144.2014 · 3.04 Impact Factor
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    ABSTRACT: We examined two potential biomarkers of brain damage in hypoxic-ischemic encephalopathy (HIE) neonates: glial fibrillary acidic protein (GFAP; a marker of gliosis) and ubiquitin C-terminal hydrolase L1 (UCH-L1; a marker of neuronal injury). We hypothesized that the biomarkers would be measurable in cord blood of healthy neonates and could serve as a normative reference for brain injury in HIE infants. We further hypothesized that higher levels would be detected in serum samples of HIE neonates and would correlate with brain damage on magnetic resonance imaging (MRI) and later developmental outcomes.? Serum UCH-L1 and GFAP concentrations from HIE neonates (n = 16) were compared to controls (n = 11). The relationship between biomarker concentrations of HIE neonates and brain damage (MRI) and developmental outcomes (Bayley-III) was examined using Pearson correlation coefficients and a mixed model design. Both biomarkers were detectable in cord blood from control subjects. UCH-L1 concentrations were higher in HIE neonates (p < 0.001), and associated with cortical injury (p < 0.055) and later motor and cognitive developmental outcomes (p < 0.05). The temporal change in GFAP concentrations during (from birth to 96 h of age) predicted motor developmental outcomes (p < 0.05) and injury to the basal ganglia and white matter. Ubiquitin C-terminal hydrolase L1 and GFAP should be explored further as promising serum biomarkers of brain damage and later neurodevelopmental outcomes in neonates with HIE.
    Frontiers in Neurology 12/2014; 5:273. DOI:10.3389/fneur.2014.00273

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