SUMMARYResearch on animal models demonstrates that fetal cocaine exposure results in neurologic deficits in memory and learning. Although drug effects on human infants are difficult to separate from other environmental influences of a drug-using lifestyle, studies suggest that infants exposed to cocaine in utero have reduced growth, delays in sensory-motor development, attentional deficits, and depressed responsivity to social stimulation. Standard interventions to promote behavioral state regulation in affected infants may be helpful when parents are capable of participating.The history of research on the effects of in utero cocaine exposure has been both short and turbulent. In the 10 years since the "crack baby" was first identified and birth outcomes reported, findings have been controversial and at times contradictory. Perinatal epidemiologic studies in the late 1980s documented the large numbers of infants born after fetal exposure to cocaine. Estimates of the proportion of babies born in urban teaching hospitals who test positive for cocaine range from 5-45%. [1][2][3][4] Early alarming reports about pronounced neurobehavioral abnormalities in neonates exposed to cocaine in utero 5-7 raised subsequent concerns about potential long-term neurodevelopmental effects on fetal and infant outcome. Recent reports, however, indicate that the effects may be subtle and could be masked and/or confounded by environmental factors, such as amount of prenatal care 8 or socioeconomic status. 9 Part of the ambiguity in results might be attributed to the initial lack of information regarding effects of cocaine on human development. With little else to go on, investigators interested in studying the effects of cocaine on the human fetus had two potential bodies of research on which to draw, the known effects of cocaine on adults and on animals. As the volume of literature grew, several issues central to the further study of prenatal exposure to a potentially neurotoxic agent became evident: (a) whether any pre-or perinatal neurologic effect could be attributed to cocaine, (b) whether identified effects could be related to specific neurobehavioral outcomes, and (c) the long-term consequences. An examination, therefore, of the evidence pertaining to the neurologic development of infants exposed to cocaine follows. Additionally, some considerations concerning intervention are offered.