| Popis: |
This chapter summarizes the available clinical data on neurological, neuropathological and neuroimaging abnormalities due to various hypothyroid syndromes in children. This information will help to consider the possible consequences of iodine deficiency occurring during the critical period of brain development. Iodine deficiency interferes with the prenatal and postnatal neurointellectual development of children through maternal, fetal and neonatal hypothyroxinemia. In addition, recent advances in molecular and cell biology have led to an improved understanding of normal thyroid physiology and of the genes involved in thyroid gland development. Iodine is a constituent of THs; therefore, iodine deficiency impacts on thyroid function in pregnant women, their fetuses and neonates. TH is required for normal brain development beginning in the first trimester, before the onset of fetal TH secretion.Even during the early months of postnatal life, TH is necessary for brain development; however, it is unclear when this critical period is completed. The effects of TH are restricted to a subset of neuroanatomical events occurring at that time in different areas of the brain. The impairment of specific neuropsychological functions depends on the timing of TH deficiency. Infant-onset hypothyroidism can also cause irreversible neurological deficits similar to CH and EC. Patients with severe cases of EC, CH, or juvenile hypothyroidism can demonstrate irreversible motor, intellectual impairments and hearing problems. Neuropathology and neuroimaging cannot be distinguished among children with hypothyroid diseases. Specific distributions of intracranial calcifications are common in hypothyroid diseases. |
