Cystic periventricular leukomalacia (cPVL), the principal ischemic brain injury in premature infants, is characterized by necrosis of the white matter in the periventricular region and the major neuropathology for spastic motor deficits in cerebral palsy or epilepsy. Recent reports strongly suggest that the brain injury associated with cPVL may have already occurred in utero. In this study we searched retrospectively for possible clinical situations related to cPVL to facilitate assessment of optimal management. A total of 201 babies born at gestational ages from 24 to 33 weeks were entered into the study (1992–1997) and examined for involvement of 18 factors in cPVL retrospectively. And psychomotor development was examined at least until 18 months of corrected age. Among 201 premature babies 35 cases were diagnosed as cPVL later developed spastic diplegia. There are 23 cases of preeclampsia, no infant suffering from cPVL. In the univariate analysis, exposure to antenatal indomethacin, cord length ≥40 cm, and a low Apgar score were significantly associated with a 2–3 risk increased of cPVL occurrence, while antenatal magnesium sulfate reduced the risk. Chorioamnionitis was positively correlated with the risk, but did not reach statistical significance. In the multivariate analysis we found the statistical significance in exposure to antenatal indomethacin, a low Apgar score, and antenatal magnesium sulfate. Our results suggested that preeclampsia and antenatal exposure of magnesium sulfate reduced the risk while antenatal exposure of indomethacin and low Apgar score associated with the occurrence of cPVL. These findings support a growing consensus that cPVL is often the result of maternal and fetal factors as well as antenatal treatment.
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Maternal and Child Health Division, Children and Families Bureau, Ministry of Health and Welfare, Japan. Maternal and child health statistics of Japan, Tokyo: Kaneda I, Mothers and Children and Family Health Education Group Representative; 2003.
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Accepted: February 19, 2004
Received in revised form: February 9, 2004
Received: October 7, 2003
© 2004 Elsevier B.V. Published by Elsevier Inc. All rights reserved.