Abstract
Impairment of thyroid function early in life results in developmental defects. The prevention of the CNS damage caused by congenital hypothyroidism is the aim which is being successfully achieved by neonatal thyroid screening programs. But CNS damage may also result from maternal hypothyroxinemia alone. Especially severe CNS damage is found in the endemic cretin of the neurological type born to iodine deficient mothers: these women are hypothyroxinemic throughout pregnancy, and their fetus has an impaired thyroid function caused by the low iodine supply. The CNS damage increases in severity from that caused by maternal hypothyroxinemia alone, congenital hypothyroidism alone, or the combined maternal and fetal impairment of thyroid function found in areas of marked iodine deficiency. But whereas the mental retardation caused by congenital hypothyroidism may still be prevented by early treatment of the newborn, the CNS damage caused by maternal hypothyroxinemia is prevented by adequate treatment during pregnancy, and the birth of neurological cretins requires adequate iodization of the mothers before conception, or very early in pregnancy. These associations between thyroid failure and CNS damage, and the experimental models used to study them, have been previously reviewed by us 1–4. These reviews contain pertinent bibliography of the abundant work on the subject carried out by many investigators.
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de Escobar, G.M., Obregón, M.J., del Rey, F.E. (1989). Transfer of Thyroid Hormones from the Mother to the Fetus. In: Delange, F., Fisher, D.A., Glinoer, D. (eds) Research in Congenital Hypothyroidism. NATO ASI Series, vol 161. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7580-7_2
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DOI: https://doi.org/10.1007/978-1-4684-7580-7_2
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