Infants of diabetic mothers: late normalization of fetal cyclic motility persists after birth.

The prenatal development of cyclic motility (CM) in the human is disrupted by maternal diabetes, but appears normal by the end of gestation. To determine whether birth and adaptation to postnatal life reveal new or persisting abnormalities in CM, 24 newborn infants of insulin-dependent diabetic mothers (IDMs) and 24 normal newborns were studied for 2-4 hr in a controlled environment. Spectral analysis of spontaneous movement revealed that CM was common in both groups. Measures of its cyclic organization in each state did not differ between IDMs and controls. State differences were the same in the two groups, and replicated the pattern found in a previous study of normal newborns. For IDMs, there were no differences associated with neonatal evidence of increased glucose supply in utero (macrosomia, postnatal hypoglycemia), or with determinations of prenatal maternal hyperglycemia. IDMs had also been studied as fetuses, and the pattern of continuity and change in CM across birth replicated the pattern previously reported for normal fetuses. The results suggest that the development and control of CM is buffered from the prenatal metabolic insults suffered by IDMs, and support speculations that cyclic activation is a general and robust property of the developing motor system in the human.