Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013 Oct;122(4):869-877.
doi: 10.1097/AOG.0b013e3182a265ab.

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

Sarah McIntyre  1 , Eve Blair, Nadia Badawi, John Keogh, Karin B Nelson
Affiliations
Free article

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

Sarah McIntyre et al. Obstet Gynecol. 2013 Oct.
Free article

Abstract

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

Methods: 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.

Results: 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).

Conclusion: 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.

Level of evidence: : II.

PubMed Disclaimer

References

    1. Himmelmann K, Hagberg G, Uvebrant P. The changing panorama of cerebral palsy in Sweden. X. Prevalence and origin in the birth-year period 1999–2002. Acta Paediatr 2010;99:1337–43.
    1. Korzeniewski SJ, Birbeck G, DeLano MC, Potchen MJ, Paneth N. A systematic review of neuroimaging for cerebral palsy. J Child Neurol 2008;23:216–27.
    1. Himmelmann K, Ahlin K, Jacobsson B, Cans C, Thorsen P. Risk factors for cerebral palsy in children born at term. Acta Obstet Gynecol Scand 2011;90:1070–81.
    1. Blair E. Epidemiology of the cerebral palsies. Orthop Clin North Am 2010;41:441–55.
    1. McIntyre S, Badawi N, Brown C, Blair E. Population case-control study of cerebral palsy: neonatal predictors for low risk term singletons. Pediatrics 2011;127:e667–73.

Publication types