The fetus requires thyroxine for normal brain and nerve development as well as other organ development. Fetal thyroid function does not become fully established until about the 20th week of gestation. Until then, the fetus is primarily maternally derived for thyroxine, especially in early gestation (before 12 weeks) when the fetus is almost completely dependent on the mother for thyroid hormones. It is well established that maternal clinical hypothyroidism is associated with neuropsychiatric developmental disorders in the offspring. Decreased thyroid hormones can cause incomplete differentiation and development of the parts of the developing fetal cortex that are responsible for speech, hearing and intelligence. Haddow et al. reported the IQ levels at 7-9 years of age in 62 offspring born to mothers with hypothyroidism (mean 13.2 mIU/L TSH) at 17 weeks of gestation and found that the mean IQ scores of children in the group not given maternal thyroxine treatment were 7 points lower than those of normal controls; the mean IQ scores of children in the group given maternal thyroxine treatment did not differ from those of normal controls [1]. Pop et al. conducted a two-year follow-up study of 62 offspring of women with hypothyroidism at 12 weeks of gestation and further confirmed that their offspring had IQ scores 10 points lower and motor scores 8 points lower than normal controls at age l, and IQ scores 8 points lower and motor scores 10 points lower than normal controls by age two.