Akinci A.KarakaŞ H.M.2024-08-042024-08-0420099780123741356https://doi.org/10.1016/B978-0-12-374135-6.00065-0https://hdl.handle.net/11616/92186Most studies show that iodine deficiency and maternal-fetal hypothyroxinemia have negative effects on fetal neural maturation, dendritic arborization and synaptic formation. They delay the myelinization process and gliogenesis, which start in the second half of gestation and continue in postnatal life. Altered levels of iodine are correlated with defective brain development and neuronal maturation. Various degrees of irreversible neurocognitive defects that are caused by severe iodine deficiency, and subsequent maternal and fetal hypothyroxinemia are wellknown. Recent studies further showed that, even in cases without clinical hypothyroidism, maternal hypothyroxinemia due to mild-to-moderate iodine deficiency would lead to fetal brain damage that could be reversed with early thyroxine therapy. Magnetic resonance spectroscopy (MRS) is a sensitive technique that detects alterations in brain metabolite levels in various neurodevelopmental disorders. The most prominent MRS change in congenital hypothyrodism due to iodine deficiency is decreased NAA level. Decreased NAA level that is caused by maternal and fetal hypothyroxinemia due to iodine deficiency implies the adverse effect of intrauterine hypothyroxinemia on fetal neuronal development. Iodine deficiency at any degree of severity causes maternal and fetal hypothyroxinemia. As thyroid hormones of the mother and the fetus must be kept at optimal levels, iodine prophylaxis should be provided, especially in iodine deficient areas. To establish normal fetal brain development, iodine supplementation must be started before pregnancy and should be continued during the gestational period. © 2009 Elsevier Inc. All rights reserved.eninfo:eu-repo/semantics/closedAccess[No Keyword]Book Chapter62563410.1016/B978-0-12-374135-6.00065-02-s2.0-85137234776N/A