The adequate functioning of both the maternal and fetal thyroid glands plays important roles to ensure that the fetal neuropsychointellectual development progresses normally. Three sets of clinical disorders ought to be envisaged, potentially leading to impaired brain development: defective glandular ontogenesis (leading to congenital hypothyroidism), maternal hypothyroidism (usually related to chronic autoimmune thyroiditis), and finally iodine deficiency (affecting both the maternal and fetal thyroid functions). The present review will be focused mainly on maternal hypothyroidism, where both the severity and temporal occurrence of maternal thyroid underfunction drive the resulting repercussions for an impaired fetal neuronal development: such clinical situations may take place during early gestation (in women with known but untreated hypothyroidism) or appear only during later gestational stages (in women with thyroid antibodies, who remain euthyroid during the first half of gestation). Recent available evidence and its implications are discussed, as well as our present concepts relating to the complexities of the fetomaternal thyroid relationships, and the potential impact of maternal thyroid function abnormalities on the ideal offspring's development.
Copyright 2001 S. Karger AG, Basel