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Dexamethasone treatment and cerebral palsy
  1. P O D PHAROAH
  1. University of Liverpool, UK
  2. p.o.d.pharoah{at}liv.ac.uk

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Editor—Referring to the paper entitled Early postnatal dexamethasone treatment and increased incidence of cerebral palsy by Shinwell et al 1, both its title and the first paragraph of the Discussion imply that the use of postnatal dexamethasone may lead to cerebral palsy. However, it is the misuse of the term “incidence” that gives rise to this interpretation. The authors did not, neither could they, provide incidence data. What they presented was cerebral palsy prevalence data.

If it is accepted that prevalence and not incidence data are provided, then a very different interpretation of the findings can be made. Supposing the cerebral impairment of cerebral palsy occurred prepartum, then the use of dexamethasone may have allowed these children to survive, whereas, had they received the placebo, they would have died before a diagnosis of cerebral palsy could be made. This would account for the higher prevalence of cerebral palsy in the dexamethasone compared with the placebo group. Support for this interpretation comes from the authors' statement “Eleven (22%) of the 51 children with cerebral palsy had normal neonatal ultrasound scans. All 11 of these infants were treated with dexamethasone”. This suggests that the cerebral impairment was prenatal in timing. Further support comes from the observation that there were fewer cases of IVH in the dexamethasone group, although the difference did not quite attain the conventional level of statistical significance.

It needs to be appreciated that prevalence = incidence × duration of disease. The duration of the disease is affected by how long the child (or fetus) survives. Unless it is known what happens to the fetus from the time of conception, it is not possible to determine incidence in those diseases that have their origin during uterine development.

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