Phosphorus (31P) spectra from the brains of severely birth-asphyxiated human infants are commonly normal on the first day of life. Later, cerebral energy failure develops, which carries a serious prognosis. The main purpose of this study was to test the hypothesis that this delayed ("secondary'') energy failure could be reproduced in the newborn piglet after a severe acute reversed cerebral hypoxicischemic insult. Twelve piglets were subjected to temporary occlusion of the common carotid arteries and hypoxemia [mean arterial Po, 3.1 (SD 0.6) magnetic resonance spectra from the brains of gas exchange ("birth asphyxia") were commonly normal babies with evidence of critically impaired intrapartum o n the first day of life (1,2). Subsequently, impairment of cerebral energy metabolism developed in some of the Received February 8, 1994; accepted JUIY 7, 1994.
US accurately predicted the presence of GLH, IVH, and hemorrhagic parenchymal infarction on MRI. However, its ability to predict the presence of DEHSI and small petechial hemorrhages in the WM on T2 weighted images is not as good, but improves on scans performed at >/=7 days after birth. In addition, normal WM echogenicity on US is not a good predictor of normal WM signal intensity on MRI.
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