Accepted wisdom that there is no physiologically important transport of thyroid hormones during development and that hormones would not be necessary to regulate fetal growth of the nervous system is likely to have contributed to a common lack of understanding and acceptance of the results of many epidemiological and clinical studies. A credible reason could not be proposed for the association between early maternal hypothyroxinemia result of the reduction of infant neurological development. It is difficult to solve the very serious and often permanent, injuries, neurological cretins (with normal thyroid function when iodine supply is complete), with the successful prevention of severe nervous system injuries early postnatal management of infants congenital hypothyroidism, counting children without the thyroid gland.

The lack of defensive actions maternal triiodothyronine (T3) compared to thyroxine (T4), shown in iodine-deficient regions deep, show many problems unresolved. Original held frequently purchased over the past 15 years in experimental animals and man, now evidently point to a function of the location of the mother of thyroid hormone in the mature nervous system for life fetal and suggest reasonable detail the above issues. Regardless of these new results and even with the increased recognition of a significant role in maternal T4 in the impediment of a serious nervous system damage in cases of congenital hypothyroidism, is still said that if thyroid hormone is needed throughout the 1st quarter is less certain, otherwise must be supplied by the mother, because nothing is released by the product until the second trimester.

Since this problem is fundamental to understanding the possible significance of thyroxine in the first quarter free (FT4) in fetal maturation of the nervous system, we must pay attention to the data currently available for experimental animals and humans. both T4 and T3 are available to the fetus early with very low amounts found in amounts that circulate in the mother are significantly low. As soon as this happens, changes in prenatal and postnatal development may be revealed. Nuclear receptors for thyroid hormones (TR) are also in the early stages of fetal development of the nervous system to some extent occupied by T3, in some animal models, with increasing levels at all times extremely vigorous birth of neurons in the cortex.

Several genes in the nervous system responds to thyroid hormone deficiency has been recognized frequently in the post-natal period, through a time of expansion of the nervous system corresponding to the last period of pregnancy and early postnatal period humans.