Cerebral Palsy and Intrauterine Growth

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The influence of gestational age

Judgment of the relative size of infants at birth must take into account gestational age, because this age has a profound effect on the risk for cerebral palsy (Fig. 1) [10]. Low birth weight infants (<2500 g) may have elevated risks of cerebral palsy because they are (1) of optimum weight for gestation but are born too early (eg, preterm only), (2) light for gestational age but born at term (small for gestational age [SGA] only), (3) both preterm and light for gestational age, or (4) heavy for

Birth weight for gestational age

When birth weight and gestational age data are both available, a more sophisticated account of relative size can be made using centile charts. Commonly, the attempt is made to define a “high-risk” subset of SGA and a similar high-risk group of large for gestational age (LGA) infants, leaving by exclusion a group who are considered an appropriate size for gestation (AGA). The actual centiles chosen to define these subgroups vary (eg, less than the 10th centile or less than the third centile for

Suitable growth standards

The size of preterm infants should be compared with that expected of their “healthy” peers. It is now clear that infants born before 37 weeks' gestation are not healthy in this sense but tend to be lighter [22] and slower growing [23] than fetuses of the same post conceptional age, presumably for reasons related to their preterm birth. Because conventional “neonatal” birth weight standards are based on the observed birth weights of infants born at different gestational ages, comparing the

Appropriate denominators

Because cerebral palsy is usually not described until well after the neonatal period, the infants used to form the denominator for rates have survived at least the first month of life, the period of highest postnatal mortality. If neonatal deaths are included, they artifactually decrease the estimated rate, because they could not be included in the numerator even if they had cerebral damage that would have resulted in cerebral palsy had they survived. Survival is strongly associated with size

Size versus growth/shape

Weight, at any gestation, is a snapshot of the infant's size. When compared with normative growth charts, a single reading at the 10th centile, especially if the chosen standard is carefully adjusted for factors such as gender, parity, and ethnicity, merely indicates that among 100 infants of this gestational age in the standard population, 10% will be lighter. To assess whether growth is proceeding as expected, two or more readings at least a month apart are required [1]. The difference

Do studies of abnormal growth or size give information about the timing of any intrauterine events associated with cerebral palsy?

If the increased risk of cerebral palsy associated with growth anomaly involved a single pathway, the striking pattern in Fig. 1 could be interpreted to mean that the growth disturbance associated with cerebral palsy has already occurred by 28 weeks of pregnancy. Nevertheless, there are likely to be many possible routes to cerebral palsy associated with growth anomaly, summarized diagrammatically in mechanisms A to D. In mechanisms A and B, cerebral palsy is the direct or indirect consequence

Acknowledgments

Fig. 1, Fig. 3, Fig. 4, Fig. 5, and associated analyses are based on data from the European Collaboration of Cerebral Palsy registers (SCPE). SCPE participants include C. Cans, J. Fauconnier (RHEOP, Grenoble, France), C. Arnaud (INSERM, Toulouse, France), J. Chalmers (ISDSHS, Edinburgh, United Kingdom), V. McManus (Lavanagh Centre, Cork, Ireland), J. Parkes, H. Dolk (Belfast, United Kingdom), G. Hagberg, B. Hagberg, P. Uvebrant (Gotenborg University, Gotenborg, Sweden), O. Hensey, V. Dowding

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References (56)

  • M.C. Petersen et al.

    Birthweight and risk for cerebral palsy

    Lancet

    (2003)
  • L.R. Leader et al.

    The assessment and significance of habituation to a repeated stimulus by the human fetus

    Early Hum Dev

    (1982)
  • D.C. Taylor

    Differential rates of cerebral maturation between sexes and between hemispheres: evidence from epilepsy

    Lancet

    (1969)
  • D. Altman et al.

    Assessment of fetal size and fetal growth

  • A.J. Wilcox et al.

    Birthweight and perinatal mortality. II. On weight specific mortality

    Int J Epidemiol

    (1983)
  • J. Liu et al.

    Cerebral palsy and multiple births in China

    Int J Epidemiol

    (2000)
  • J.H. Ellenberg et al.

    Birthweight and gestational age in children with cerebral palsy or seizure disorders

    Am J Dis Child

    (1979)
  • P. Uvebrant et al.

    Intrauterine growth in children with cerebral palsy

    Acta Paediatr

    (1992)
  • L. Palmer et al.

    Family patterns of gestational age at delivery and growth in utero in moderate and severe cerebral palsy

    Dev Med Child Neurol

    (1994)
  • P.M. Drummond et al.

    Analysis by gestational age of cerebral palsy in singleton births in northeast England 1970–1994

    Paediatr Perinat Epidemiol

    (2002)
  • E. Blair

    The undesirable consequences of controlling for birthweight in perinatal epidemiologic studies

    J Epidemiol Comm Health

    (1996)
  • P.O.D. Pharoah et al.

    Epidemiology of cerebral palsy in England and Scotland 1984–9

    Arch Dis Child Fetal Neonatal Ed

    (1998)
  • A. Colver et al.

    Increasing rates of cerebral palsy across the severity spectrum in North East England 1964–1993

    Arch Dis Child Fetal Neonatal Ed

    (2000)
  • F. Stanley et al.

    Cerebral palsies: epidemiology and causal pathways

    (2000)
  • Hemming K., Hutton J., Glinianaia S., et al. Differences between European birth weight standards: impact on small for...
  • S.R. Bonellie et al.

    Why are babies getting heavier? Comparison of Scottish births from 1980 to 1992

    BMJ

    (1997)
  • R. Skjaerven et al.

    Birthweight by gestational age in Norway

    Acta Obstet Gynecol Scand

    (2000)
  • A.J. Wilcox et al.

    Birth weight and perinatal mortality: the effect of gestational age

    Am J Public Health

    (1992)
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    Work for this article was supported by European Commission fund DGXII-BIOMED2-Contrat NBMH4-983701.

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