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G Mirabella, AM Perron, CA Westall, K Perlman, D Feig, W Wolfman, J Rovet; Deficits in the Development of Contrast Sensitivity in Infants with Prenatal and Neonatal Thyroid Hormone Insufficiencies . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4687.
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Purpose: Human and animal research suggests thyroid hormone is essential for normal fetal and neonatal neurodevelopment of the primary visual pathway. We assessed functioning and development of the visual system by measuring contrast sensitivity in infants who had a prenatal or neonatal thyroid hormone insufficiency, and compared them to infants with normal thyroid hormone exposure. Methods: Each infant was tested at 3, 4.5, and 6 months of age. Two differerent thyroid insufficient groups were tested: The first included 17 infants whose mothers were hypothyroid during pregnancy. The second included 8 infants born with congenital hypothyroidism (an absent or dysfunctional thyroid gland). These infants were compared to 32 normal controls. Contrast sensitivity was measured using sweep visual evoked potentials (PowerDiva). A contrast sensitivity function was fit to obtained thresholds for three contrast sweeps and two acuity sweeps using a negative exponential model. From the model, estimates of maximum sensitivity and high frequency roll-off parameter were determined at each age of testing. A coefficient of determination (r2) was also calculated to determine how well the model fit the obtained thresholds measured at each age. Results: There was a significant difference in log maximum sensitivity between control and maternal hypothyroid groups (2.00 versus 1.82, p=.003). There was also a significant group by age interaction for the coeffient of determination (p=.02). Contrast thresholds for both congenital and maternal hypothyroid groups fit the model more poorly at 3 months compared to controls (.85 and .85, versus .92, p=.001), but there were no differences at 4.5 or 6 months of age. Poor fit in the clinical groups was associated with reduced contrast sensitivity at the lowest spatial frequencies. There were no group differences in roll-off. Conclusion: Loss of contrast sensitivity is related to insufficient thyroid hormone prenatally and neonatally, suggesting that thyroid hormone is essential for normal visual pathway development. The overall loss of sensitivity seen in the maternal hypothyroid group appears to be related to a fetal thyroid insufficiency during early pregnancy, while a transient deficit seen in both thyroid insufficient groups may be related to a deficiency during late gestation and early life.
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