Imaging insights of alterations and adaptations in the preterm and late preterm brain.

See related articles, p 882, p 889, and p 896 have increased, remained static, or decreased. In the United States alone, >60 000 infants weighing <1500 g are born annually. Magnetic resonance imaging (MRI) provides an opportunity to characterize the nature and timing of cerebral injury and alterations in cerebral development in preterm infants both during their intensive care unit stay and throughout childhood. This issue of The Journal presents 3 important articles that further delineate the impact of preterm birth on cerebral development. Adams et al use diffusion tensor (DT) MRI to identify alterations in cerebral white matter microstructure within the corticospinal tract in 55 preterm infants from 28 weeks postmenstrual age to term equivalency. They report 4 principal findings: (1) Infants with white matter injury on conventional MRI demonstrated the greatest diffusion abnormalities; (2) the greatest alterations were found in radial diffusivity, consistent with a selective vulnerability of oligodendrocytes; (3) postnatal infection was the strongest perinatal risk factor for altered white matter microstructure; and (4) abnormalities became more prominent as the infants grew toward term equivalency, suggesting an enhanced and lasting developmental impact of early white matter lesions. White matter injury is the most common neuropathological lesion in preterm infants. It appears to be mediated by the maturational vulnerability of immature oligodendroglia to free radicals and/or excitatory amino acids generated as a result of ischemia and inflammation. The study of Adams et al is consistent with previous work confirming vulnerability in the white matter of the corticospinal tract with greater technical elegance on DT-MRI, and extends our understanding of the impact of early injury by a greater developmental deficit in white matter development by term equivalency. The time course of an increased developmental deficit in white matter microstructure by term equivalency might be consistent with secondary axonal injury accompanying both primary oligodendroglial and neuronal injury. Diffuse axonal degeneration by apoptosis has been found throughout the white matter of preterm infants, often many weeks after birth. The finding of progressive abnormality also reinforces the concept of a more protracted period of vulnerability to cerebral white matter in-