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Obstet Gynecol. 2013 Oct;122(4):869-77. doi: 10.1097/AOG.0b013e3182a265ab.

Antecedents of cerebral palsy and perinatal death in term and late preterm singletons.

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University of Sydney, Cerebral Palsy Alliance, University of Notre Dame Australia, Darlinghurst, New South Wales, the Centre for Child Health Research, University of Western Australia at the Telethon Institute for Child Health Research, Perth, and the Cerebral Palsy Alliance, University of Notre Dame Australia, Grace Centre for Newborn Care, the Children's Hospital at Westmead, the University of Sydney, and the University of Sydney, Sydney Adventist Hospital, Sydney, Australia; the Department of Neurology, Children's National Medical Centre, Washington, DC; and the National Institute of Neurological Disorder and Stroke, National Institutes of Health, Bethesda, Maryland.



To examine the antecedents of cerebral palsy and of perinatal death in singletons born at or after 35 weeks of gestation.


From a total population of singletons born at or after 35 weeks of gestation, we identified 494 with cerebral palsy and 508 neonates in a matched control group, 100 neonatal deaths, and 73 intrapartum stillbirths (all deaths in selected birth years). Neonatal death and cerebral palsy were categorized as without encephalopathy, after neonatal encephalopathy, or after neonatal encephalopathy considered hypoxic-ischemic. We examined the contribution of potentially asphyxial birth events, inflammation, fetal growth restriction, and birth defects recognized by age 6 years to each of these outcomes and to intrapartum stillbirths.


The odds of total cerebral palsy after potentially asphyxial birth events or inflammation were modestly increased (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.2 and OR 2.2, 95% CI 1.0-4.2, respectively). However, potentially asphyxial birth events occurred in 34% of intrapartum stillbirths and 21.6% of cerebral palsy after hypoxic-ischemic encephalopathy. Inflammatory markers occurred in 13.9% and 11.9% of these outcomes, respectively. Growth restriction contributed significantly to all poor outcome groups. Birth defects were recognized in 5.5% of neonates in the control group compared with 60% of neonatal deaths and more than half of cases of cerebral palsy without hypoxic-ischemic encephalopathy. In children with cerebral palsy, a potentially asphyxial birth event, inflammation, or both were experienced by 12.6%, whereas growth restriction, a birth defect, or both were experienced by 48.6% (P<.001).


Fetal growth restriction and birth defects recognized by age 6 years were more substantial contributors to cerebral palsy and neonatal death than potentially asphyxial birth events and inflammation.


: II.

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