Cerebral palsy is the most common severe motor disability in childhood, but its etiology is incompletely understood. Studies have suggested that prenatal thyroid hormone disturbances affect child neurodevelopment and may alter motor function.

To investigate the association between maternal thyroid disorder in pregnancy and risk of cerebral palsy in the child in two large study populations in Denmark and Norway.

We conducted a population-based cohort study using two study populations. (1) 1,270,079 children born in Denmark 1979–2007 identified in nationwide registers, and (2) 192,918 children born 1996–2009 recruited into the Danish National Birth Cohort and The Norwegian Mother and Child Cohort study, combined in the MOthers and BAbies in Norway and Denmark (MOBAND) collaboration cohort. Register based and self-reported information on maternal thyroid disorder were studied in relation to risk of cerebral palsy and its unilateral and bilateral spastic subtypes using multiple logistic regression. Information on CP was derived from the Danish and Norwegian National Cerebral Palsy Registries, and all CP cases registered from age one to age six years, which were verified by neuro-pediatricians, were included.

In register data, hypothyroidism was recognized in 12,929 (1.0%), hyperthyroidism in 9943 (0.8%), and unclassifiable thyroid disorder in 753 (< 0.1%) of the mothers. The odds ratio for an association between maternal thyroid disorder and bilateral spastic cerebral palsy was 1.0 (95% CI: 0.7–1.5). Maternal thyroid disorder identified during pregnancy was associated with elevated risk of unilateral spastic cerebral palsy [odds ratio 3.1 (95% CI: 1.2–8.4)]. In MOBAND, 3042 (1.6%) of the mothers reported a thyroid disorder in pregnancy, which was not associated with cerebral palsy overall [odds ratio 1.2 (95% CI: 0.6–2.4)].

Maternal thyroid disorder was not related in this study to bilateral spastic CP, which is the predominant CP subtype, but we do find a higher risk of unilateral spastic CP in children of mothers whose thyroid disorders were identified in pregnancy. The offspring of such women are more likely to have been exposed to abnormal thyroid hormone levels in utero than the offspring of women whose thyroid disorders were diagnosed and treated prior to conception. A useful extension of our findings would be to see whether they can be replicated in studies making use of maternal blood samples.