| Summary: | Early brain abnormalities, including white matter injury, intraventricular hemorrhage and ventriculomegaly are associated with abnormalities of early motor functioning in premature neonates. Similarly, an increased risk of neurodevelopmental impairment is found in neonates with postnatal infections. The mechanism by which these factors impair motor functioning is largely unknown, but may result from altered development of white matter motor tracts. The purpose of this study was to evaluate the impact of brain abnormalities and neonatal illness on corticospinal tract (CST) development in premature neonates serially studied with diffusion tensor tractography (DTT). Fifty-five premature neonates between 24 and 32 weeks gestation at birth were scanned 2-4 weeks after birth, and again at term-equivalent age. Moderate to severe brain abnormalities (abnormal-MRI) were characterized by at least one of: moderate or severe white matter injury, moderate or severe intraventricular hemorrhage, or ventriculomegaly. CST DTT was performed using DTIStudio with seeding in the posterior limb of the internal capsule and filtering at the precentral gyrus and cerebral peduncle. This yielded CST diffusion parameters (fractional anisotropy; FA and average diffusivity; Dav), indicators of microstructural development. The effect of abnormal-MRI and neonatal illness on CST FA and Dav was assessed. Twenty-one neonates (38%) had abnormal-MRI on at least 1 of 2 scans. In neonates with normal MRIs, FA increased by 0.011 per week; Dav decreased by 1.9x10-⁵ mm²/sec (both P<0.001). In neonates with abnormal-MRI, however, FA increased at a significantly slower rate of 0.008 per week (interaction term P=0.05); Dav was 1.5x10-⁵ mm²/sec higher for any given age at scan (P<0.001). Changes in FA resulted from a decrease in radial, rather than axial, diffusivity. Radial diffusivity was higher in neonates with abnormal-MRI. Additionally, 23 neonates (42%) were exposed to a postnatal clinical infection. FA increased more slowly in neonates with postnatal infection (interaction term P=0.04), with a borderline slower rate of decrease in Dav (interaction term P=0.08). These results demonstrate that CST microstructural development, including maturation of the glial cells surrounding the axon, is impaired in premature neonates with abnormal-MRI. Maturation of the CST is also impaired in neonates with postnatal infections, independent of these abnormalities.
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