Cerebral palsy and neonatal thyroid function

Research Findings

Scientists have linked low levels of a thyroid hormone in premature infants to the development of disabling cerebral palsy. They examined more than 400 premature infants screened for blood levels of the hormone thyroxine during the first week of life. They found that infants with low levels of thyroxine at birth had a 3- to 4-fold increase in the incidence of disabling cerebral palsy at age 2.

The study is the most comprehensive to date that explores the relationship between low levels of thyroid hormone (called hypothyroxinemia) at birth and neurodevelopment in preterm infants. The work was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute of Child Health and Human Development.

Investigators also found lowered mental development scores at age 2 in the affected children, who had a gestational age of 33 weeks or less.

Cerebral palsy is a group of chronic disorders characterized by impaired body movement. Faulty development or damage to motor areas in the brain disrupts the brain's ability to adequately control movement and posture. Over 500,000 Americans have the disorder, and 4,500 American infants are diagnosed each year.

Thyroid hormone is indispensable to cerebral development. Babies in the United States are routinely screened for abnormal thyroid function.

Premature infants often go through a period of transient hypothyroxinemia. They are already at risk for cerebral palsy and account for approximately one-third of cerebral palsy cases. In most cases, thyroid function returns to normal within a period of months. Rarely, a premature child will have permanently low thyroid hormone levels.

References

• Some of the original contents of this article appeared in the March 28, 1996 issue of the New England Journal of Medicine.
• The research for this article was conducted by the National Institute of Neurological Disorders and Stroke