The thyroid hormone is important to the functional development and maturation of the central nervous system; the association between the absence of thyroid hormones and congenital hypothyroidism and profound mental retardation has been recognized for more than a century. It is thought that the administration of supplementary iodine prior to conception in human mothers is effective in preventing the significant neuropsychological effects of thyroid gland dysfunction.3 Results from magnetic resonance imaging scans of cerebral morphologic features and myelination in infants diagnosed as having congenital hypothyroidism through neonatal screening reveal findings ranging from delayed and abnormal white matter myelination patterns4,5 to normal brain myelination and circumvolutions.6 The latter finding of no detectable morphological brain abnormalities has been attributed to the lingering neuroprotective effects of maternal thyroid hormones introduced to fetal transport by the placenta. However, there is evidence7 that very little thyroxine actually crosses the placental barrier, compelling the fetus to depend almost exclusively on its own thyroid gland, which, if underdeveloped, constitutes an imminent risk for congenital hypothyroidism. The story, however, is still not that simple: evidence from animal studies8,9 suggests a critical perinatal period during which deficiencies in thyroid gland function result in permanent morphological, histopathological, and behavioral abnormalities. While this window of opportunity has not been clearly delineated in humans, there are reports of normal intellectual function in patients with hypothyroidism who underwent thyroid replacement therapy (TRT) prior to 3 or even 7 months of age.10- 12 Despite these findings, the lack of a comprehensive evaluation of a wide variety of cognitive domains other than general intelligence (eg, attention, language, learning and memory skills) necessitates restraint in inferring that early intervention with TRT results in normal neurocognitive functioning. Evoked potential studies of auditory brainstem responses in children with congenital hypothyroidism who received postnatal TRT as early as 3 weeks of age showed significant audiometric deficits well into midchildhood.13 Consistent with these audiometric deficits are findings of hearing impairment14 and expressive language deficits,15 including difficulties with naming,16 in young children, which together call for more a comprehensive assessment of neurocognitive functioning across a broad range of domains in children with congenital hypothyroidism. Recent retrospective Canadian data17 report mild binaural conduction and sensorineural hearing loss in 20% of children with congenital hypothyroidism identified at neonatal screening, with strong indications that early treatment (within 2 weeks after birth) may reduce the incidence of hearing impairment. Although the children with congenital hypothyroidism and hearing impairment scored in the normal range on most general language tests, subtle impairments in their auditory speech-sound discriminations17 and reading skills18 were evident. Psychometric evidence of average IQ scores in children with hypothyroidism is not necessarily evidence that those children have normal cognitive abilities. For example, a Belgian study19 found notable deficits in the attention spans and cognitive information processing skills of children whose average IQ was a normal 100.1 (range, 87.6-113.8).