Maternal and infant thyroid disorders and cerebral palsy

Abstract

Deficiency of thyroid hormone during critical periods of development can severely damage the nervous system, but the specific effects of thyroid hormones on neuromotor development are less certain. Nonetheless, evidence has accumulated to suggest that thyroid hormone deficiency might be one cause of cerebral palsy (CP). The evidence arises from three sets of observations: first, severely premature infants with transient hypothyroxinemia have elevated risks of CP; second, some children born with endemic cretinism in iodine-deficient areas of the world have motor findings compatible with the diagnosis of CP; and third, several studies of the antecedents of CP have encountered a higher than expected prevalence of maternal thyroidal disorders. The evidence thus far is insufficient to conclusively determine what role, if any, thyroid hormone deficiency plays in CP, although it seems clear that neuromotor abnormalities can be the result of insufficient supply of maternal thyroid hormone in utero. A major research priority should be to assess the effects on CP risk of thyroid supplementation in transient hypothyroxinemia of prematurity. Iodine deficiency can be addressed by inexpensive and well-established public health measures, and thyroid hormone deficiency can be addressed by inexpensive and well-established clinical measures. If a causal chain can be established that links iodine and thyroid hormone to risk of CP, the potential for introducing very cost-effective ways of reducing the burden of CP will be considerable.