Statisticians at the National Institutes of Health (NINCDS), Bethesda, MD have compared the follow-up neurologic status of full-term infants whose birth was complicated but who were free of signs of hypoxic-ischemic encephalopathy (HIE) in the nursery period with asymptomatic infants whose births were uncomplicated. The rate of CP was 2.3/1000 in asymptomatic infants with one or more birth complications and 2.4/1000 among asymptomatic infants whose births were uncomplicated. A total of 41,012 patients was evaluated at 7 years of age in the National Collaborative Perinatal Project. The full-term infant whose birth was complicated but who was free from abnormal signs of HIE in the newborn period was not at increased risk of CP. The neonatal signs judged indicative of HIE were (1) decreased activity after the first day of life, (2) need for incubator care for three or more days, (3) feeding problems, (4) poor suck, (5) respiratory difficulty, and/or (6) neonatal seizure. 
COMMENT. Term infants whose brains have been injured during delivery show signs of damage in the neonatal period. Children with sustained neurologic abnormality in the newborn period are at a higher risk of CP than those with transient abnormalities. The. risk increases directly with the number of abnormal signs. Neonatal seizures are the most reliable evidence of intrapartum asphyxia. The Apgar score is not the best indicator. In the NCPP, the proportion of CP attributable to asphyxia - as defined by a 5-min Apgar score score of <6-was about 25%. Most children with CP do not have low Apgars at birth. Only about 12% of surviving children with Apgar scores of 0-3 developed CP . For babies over 2500 gm, irrespective of birth complication, most achieved 5-min Apgar scores of 7 or higher, and the risk of CP was not significantly higher than in children whose births were uncomplicated. The risk of CP attending low Apgars was conditioned on low birth weight, and 25% of CP cases are attributable to premature delivery (Freeman JM, Editor, Prenatal and perinatal factors associated with brain disorders. NIH Publication 1985; No 85-1149).