Objective: To evaluate cerebrovascular autoregulation as a function of arterial blood pressure (ABP) in the critically ill, premature infant.Study Design: A prospective observational pilot study was conducted in two tertiary care Neonatal Intensive-Care Units. Premature infants (n ¼ 23, p30 weeks estimated gestational age with invasive ABP monitoring) were enrolled and received routine care while undergoing continuous autoregulation monitoring, using the cerebral oximetry index (COx). The COx is a moving, linear correlation coefficient between cortical reflectance oximetry and ABP. COx values were stratified as a function of ABP for individual subject recordings and for the cohort.Result: The mean duration of autoregulation monitoring was 3.2 days (median: 2.97, range: 0.61-3.99). A total of 10 of 23 (43%) developed intraventricular hemorrhage and 1 of 23 (4%) developed periventricular leukomalacia by head ultrasound. No association was found between neurologic injury and percentage of the monitoring periods with autoregulation impairment (defined as COx>0.5). Lower ABP was associated with dysautoregulation (higher COx values, P<0.01). The percentage of time with impaired autoregulation was greater with lower ABP (P ¼ 0.013, Spearman r ¼ 0.51).Conclusion: All infants studied had periods with intact and periods with impaired cerebrovascular autoregulation, measured with the COx. Low ABP was associated with impaired autoregulation.
Objective-Clinical MR studies show delayed and ongoing neurodegeneration following neonatal hypoxia-ischemia (HI), but the mechanisms and timing of this neurodegeneration remain unclear. We use ex vivo Diffusion Tensor Imaging (DTI) and brain neuropathology to determine if selective injury to white matter tracts occurs following neonatal HI in mice resulting in neural system associated attrition in remote regions and at delayed time points. Methods-TheRice Vannucci model (unilateral carotid ligation + 45 minutes of hypoxia FIO2=0.08) was used to cause brain injury in postnatal (p)7 C57BL6 mice and ex vivo DTI and correlative neuropathology were performed at p8,p11,p15,p21,p28, and p42.Results-DTI provides excellent contrast visualization of unmyelinated white matter in the immature mouse brain. Acute severe ipsilateral injury to the hippocampus is seen with both histopathology and diffusion-weighted MRI 24 hours post injury. Injury to axons is evident 24 hours after HI in the hippocampal alveus. By p11 and continuing until p28, the ipsilateral fimbria fornix degenerates. Beginning at p15, there is injury and loss of axons entering the ipsilateral septal nucleus followed by ipsilateral septal atrophy. Volume loss in the hippocampus is rapid and severe but is subacute and significantly slower in the ipsilateral septum. Neonatal HIE, also interrupts the normal developmental increase in fractional anisotropy in the ipsilateral fimbria but not in the contralateral fimbria from p8 to p42.Interpretation-In the neonatal brain there is a progressive systems-preferential injury following HI. DTI allows unparalleled visualization of this neural-network associated attrition so that it can be followed longitudinally in the developing brain.
Background: Diffusion tensor imaging (DTI) can be used to predict outcome following perinatal arterial ischemic stroke (PAIS), though little is known about white matter changes over time. Methods: Infants with PAIS were serially scanned in the neonatal period (n=15), at 3 months (n=16), and at 24 months (n=8). FA-values in five regions of interest (anterior and posterior limb of the internal capsule, corpus callosum, optic radiation and posterior thalamic radiation) were obtained and compared with FA- values of healthy controls and neurodevelopmental outcome. Results: In the neonatal period, no differences in FA were found. At three months, the six infants who ultimately developed motor deficits showed lower FA-values in all affected regions. Four infants developed a visual field defect and showed lower FA-values in the affected optic radiation at three months (0.22 vs 0.29,p=0.03). Finally, a correlation between FA-values of the corpus callosum at three months and the Griffiths’s developmental quotients was found (r =.66 p=0.03). At 24 months a similar pattern was observed. Conclusion: Neonatal FA measurements may underestimate the extent of injury following PAIS. FA measurements at three months could be considered a more reliable predictor of neurodevelopmental outcome and correlate with DTI findings at 24 months.
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