Maternal hypothyroxinemia: psychoneurological deficits of progeny

E B Man1, J F Brown, S A Serunian

  • 1Yale University School of Medicine, New Haven, CT.

Maternal thyroid function was evaluated clinically, by reproductive history, and by serial measurements of serum butanol-extractable iodine (thyroxine-like iodine), two before and two after 24 gestational weeks during 1,349 pregnancies. Three percent of the women were hypothyroxinemic. Developmental, intellectual, and motor abilities of progeny born to (Group I) 210 euthyroxinemic, (Group II) 15 hypothyroxinemic given adequate thyroid replacement therapy, and (Group III) 21 inadequately treated hypothyroxinemic women were compared. The groups of mothers exhibited no significant differences in intelligence, years of education, or chronological age. Mean developmental and intellectual scores at eight months, four and seven years of Group II progeny evidenced remarkably consistent similarity to scores of siblings and controls. At each age, mean developmental and intellectual scores were lower for Group III progeny, and motor scores of the latter were lowest. Some progeny of Group II mothers, treated only after 12 or 29 weeks, failed the ball catch and line walk tests; some had strabismus and other ocular disturbances. Could these deficits have originated with maternal hypothyroxinemia during first semester weeks before the thyroid-pituitary axis matures? Now in 1990-1991, early findings fit into the modern concepts of significant maternal gestational transfer of thyroxine to the fetus. The authors encourage prenatal and/or early gestational screening for maternal hypothyroxinemia and urge prescription of adequate thyroid replacement therapy for hypothyroxinemic women.

Related Concept Videos

Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
Meiosis vs. Mitosis02:57

Meiosis vs. Mitosis

Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is...
Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...