The Role of Neonatal Thyroxin In Neurodevelopmental Disabilities † 1257

Abstract

Recently, the concept that neonatal hypothyroxinemia (↓T4) is benign has been challenged and a link with cerebral palsy (CP) has been suggested. This study investigates a link between easily treatable ↓T4 and subsequent neurodevelopmental disorders. In this retrospective, case-control study data were collected in a regional university neonatal intensive care unit and its associated developmental high-risk follow-up clinic. Inclusion criteria for participation included: birth weight ≤1000 grams, born between January 1, 1992, and December 31, 1995, and survival-to-discharge. Eligible participants were selected based on availability of Thyroxin (T4) and accompanying developmental outcome data. Newborn screening procedures provided T4 and Thyroid Stimulating Hormone (TSH) data for the study. Neurodevelopmental assessments were performed at adjusted ages of 4, 12, and 24 months, by an interdisciplinary developmental team utilizing the Bayley Scales of Infant Development (BSID), the INFANIB assessment of neuromotor status and clinical assessment. Possession of T4 and developmental data provided inclusion of 60 subjects at 4 months, 82 at 12 months, and 53 at 24 months adjusted age. Analysis of data was done using Chi-square, contingency and stratified, and One-way Anova. Comparison of INFANIB results with thyroid function showed no significant association when controlling for the presence of Periventricular Leukomalacia (PVL) and Interventricular Hemorrhage (IVH). A similar conclusion was drawn for 12 month BSID results. Twenty-four month evaluations also suggested no significant relationship between T4 and developmental outcome as measured by BSID, however an association between the diagnosis of CP and Thyroid status was suggested (P≤.05). This study confirms the previously reported association between hypothyroxinemia and cerebral palsy, and fails to demonstrate an association with other abnormal neurological outcomes in this high risk population. A prospective interventional study will be needed to determine whether hypothyroxinemia is a contibuting factor in the development of CP or merely an early marker of cerebral injury.