To investigate the link between infection-related risk factors for cerebral palsy subtypes in children born at term.
A case–control study was performed in a population-based series of children with cerebral palsy born at term (n=309) matched with a control group (n=618). The cases were divided into cerebral palsy subtypes: spastic hemiplegia, spastic diplegia, spastic tetraplegia, and dyskinetic cerebral palsy. All forms of spastic cerebral palsy were also analyzed together. All records were examined for maternal and neonatal signs of infection. Univariate and adjusted analyses were performed.
Infection-related risk factors were shown to be independent risk factors for spastic cerebral palsy in the adjusted analyses. This was especially pronounced in the subgroup with spastic hemiplegia in which bacterial growth in urine during pregnancy (n=11 [7.5%], odds ratio [OR] 4.7, 95% confidence interval [CI] 1.5–15.2), any infectious disease during pregnancy (n=57 [39.0%], OR 2.9, 95% CI 1.7–4.8), severe infection during pregnancy (n=12 [8.2%], OR 15.4, 95% CI 3.0–78.1), antibiotic therapy once during pregnancy (n=33 [22.6%], OR 6.3, 95% CI 3.0–15.2) as well as several times during pregnancy (n=9 [6.2%], OR 15.6, 95% CI 1.8–134.2) constituted strong independent risk factors. However, only neonatal infection (n=11 [9.1%], OR 14.7, 95% CI 1.7–126.5) was independently significantly associated with an increased risk of spastic diplegia and tetraplegia.
Infection-related factors are strong independent risk factors for the subgroup with spastic hemiplegia in children with cerebral palsy born at term. The finding is less pronounced in the subgroups with spastic diplegia or tetraplegia.
Infection-related factors are independent risk factors for the cerebral palsy subgroup spastic hemiplegia in children born at term, a finding less evident in other subgroups.
Perinatal Center, Department of Obstetrics and Gynaecology, Institute for Clinical Sciences, Sahlgrenska Academy, Sahlgrenska University Hospital/Östra, and the Department of Paediatrics, Institute for Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden; the Department of Obstetrics and Gynaecology, Charles University in Prague, Medical Faculty Hradec Kralove, Prague, Czech Republic; the Maternal Fetal Medicine Department, Hospital Clinic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain; and the Department of Genes and Environment, Division of Epidemiology, Institute of Public Health, Oslo, Norway.
Corresponding author: Bo Jacobsson, MD, PhD, Department of Obstetrics and Gynaecology, Perinatal Centre, Sahlgrenska University Hospital/East, SE-416 85 Gothenburg, Sweden; e-mail: firstname.lastname@example.org.
Supported by The Göteborg Medical Society, FOU-Unit in Södra Älvsborg, Swedish government grants (ALFGBG-136431), and the Swedish Medical Society (2008-21198).
Financial Disclosure The authors did not report any potential conflicts of interest.
The authors thank Mattias Molin at Statistiska Konsultgruppen, Göteborg, for assistance with statistics and Dr. Elisabet Hentz for expert advice on neonatal issues.