Practice guidelines are presented for diagnosis and treatment of patients with thyroid-related medical issues just before and during pregnancy and in the postpartum interval. These include evidence-based approaches to assessing the cause of the condition, treating it, and managing hypothyroidism, hyperthyroidism, gestational hyperthyroidism, thyroid autoimmunity, thyroid tumors, iodine nutrition, postpartum thyroiditis, and screening for thyroid disease. Indications and side effects of therapeutic agents used in treatment are also presented.

The original concept of the critical period of thyroid hormone (TH) action on brain development was proposed to identify the postnatal period during which TH supplement must be provided to a child with congenital hypothyroidism to prevent mental retardation. As neuropsychological tools have become more sensitive, it has become apparent that even mild TH insufficiency in humans can produce measurable deficits in very specific neuropsychological functions, and that the specific consequences of TH deficiency depends on the precise developmental timing of the deficiency. Models of maternal hypothyroidism, hypothyroxinaemia and congential hyperthyroidism have provided these insights. If the TH deficiency occurs early in pregnancy, the offspring display problems in visual attention, visual processing (i.e. acuity and strabismus) and gross motor skills. If it occurs later in pregnancy, children are at additional risk of subnormal visual (i.e. contrast sensitivity) and visuospatial skills, as well as slower response speeds and fine motor deficits. Finally, if TH insufficiency occurs after birth, language and memory skills are most predominantly affected. Although the experimental literature lags behind clinical studies in providing a mechanistic explanation for each of these observations, recent studies confirm that the specific action of TH on brain development depends upon developmental timing, and studies informing us about molecular mechanisms of TH action are generating hypotheses concerning possible mechanisms to account for these pleiotropic actions.Clinical and experimental studies demonstrate thyroid hormone (TH) is essential for normal brain development. This was documented initially in children with congenital hypothyroidism (1-5), followed by animal studies focused on cerebellar development, which occurs largely postnatally (6-9). However, recent observations in humans (10-13) provide important new evidence that TH is also important in early (foetal) brain development, and that the timing and severity of TH insufficiency predicts the type and severity of the neurological deficits. Because these deficits presumably reflect the impact of a loss of TH on different aspects of brain development, this clinical research provides clues as to when and where TH exerts its actions in developing brain.Animal models of developmental TH insufficiency are beginning to provide mechanistic explanations for these observations in humans. The use of genetic models of TH insufficiency, of TH receptor deletion and mutation, and of cofactor deletion (14-17), are showing us how different brain regions may exhibit different sensitivity to TH during development. Moreover, these studies show that TH exerts different effects in different brain areas at different times during development. However, despite advances in our understanding of TH action, the specific developmental events affected by TH remain poorly understood. Several recent comprehensive reviews on TH actions in brain development have appeared (6,7,14). Thus, our go...

Exposure to tricyclic antidepressants or fluoxetine throughout gestation does not appear to adversely affect cognition, language development, or the temperament of preschool and early-school children. In contrast, mothers' depression is associated with less cognitive and language achievement by their children. When needed, adequate antidepressant therapy should be instituted and maintained during pregnancy and postpartum.