Thyroid Disease and Mental Disorders: Cause and Effect or Only comorbidity?

Robertas Bunevičius; Arthur J. Prange Jr

Disclosures

Curr Opin Psychiatry. 2010;23(4):363-368. 

In This Article

Thyroid Hormones and the Developing Brain

Thyroid hormones are critical for the development of the brain during pregnancy and in the early postnatal period. Environmental factors (such as iodine deficiency), maternal thyroid dysfunction, and neonatal thyroid malformations may cause permanent neurological deficits with severe mental retardation and cretinism.

Timing and genetic factors contribute to the expression of neurological deficits.[6] The importance of timing may be illustrated by differences in neurological outcome in endemic cretinism and in congenital hypothyroidism.[2] In endemic cretinism, the resulting maternal iodine deficiency causes fetal brain hypothyroidism throughout gestation. Early fetal hypothyroidism, before the fetal thyroid gland is active, results in profound and irreversible mental retardation, deaf–mutism, spasticity, and ataxia, though thyroid function may be normal after birth. Endemic cretinism may be prevented by administration of iodine starting in the first trimester of pregnancy. Despite knowledge of this simple remedy, iodine deficiency remains the most prevalent preventable cause of mental retardation worldwide.[6]

In congenital hypothyroidism, fetal thyroid gland hypofunction is compensated by maternal thyroid hormone secretion. Untreated neonates with congenital hypothyroidism demonstrate symptoms of hypothyroidism and growth retardation together with mental retardation, spasticity, and language deficits. However, neurological deficits in congenital hypothyroidism are less severe than in endemic cretinism.[2] Early thyroid hormone replacement prevents most neurological symptoms in neonatal hypothyroidism, though mild deficits in cognitive functioning may persist.[7]

The importance of genetic factors may be illustrated by a study[8] performed in iodine-deficient areas in China. This study found an association between DIO2 polymorphisms and mental retardation in children. Individual differences in tolerance to low thyroid hormone concentrations during brain development may be explained by DIO2 variations that affect conversion of T4 to T3 in the brain.

Genetic factors, such as mutation in the MCT8 gene, may cause selective neuronal hypothyroidism with normal or even increased serum T3 concentrations. Intraneuronal hypothyroidism, similar to systemic hypothyroidism during fetal life, results in severe mental retardation, hypotonia, and absence of speech. This mutation provides a molecular basis for the Allan–Herndon–Dudley syndrome.[9]

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