The popular media and initial clinical reports have focused on the catastrophic associations of prenatal cocaine exposed infants. This compound has been said to be the cause of microcephaly, growth retardation, malformations, strokes, seizures, and a wide range of behavior changes. Clinical disturbances in the neonate due to prenatal drug exposure are thought to represent a continuing behavioral and learning disability in the older child. However, a firm scientific bias for many of the ominous conclusions is not established. Most of these children have confounding factors present. Commonly they born into poverty and are exposed to other drugs, particularly ethanol. Current surveys indicate that the high risk drug exposed pregnancies will continue in the future. While studies of infants exposed to drugs are provocative, there is a publication bias for those reporting dramatic positive effects. In contrast, animal studies allow a more direct examination of drug action but many do not reflect the multifactorial nature of influences impinging on fetal development. Clinicians are then faced with the prospect of making assessments and clinical decisions without benefit of adequate understanding of the underlying pathophysiological mechanisms. The recent expansion of the clinical and scientific literature provides an opportunity for a review of studies evaluating the prenatal factors which may predict outcome of cocaine exposed infants. The purpose of this symposium is to integrate basic science and clinical studies on prenatal cocaine exposure as a basis for informed decisions in medical practice. This symposium should facilitate exchange and sharing of scientific and clinical data on this continuing medical problem. Therefore, it should be of interest to both clinicians and scientists with an interest in developmental toxicology. Areas of emphasis will include drug use epidemiology, molecular genetics, neuroanatomy, clinical neuroimaging and pharmacology of cocaine. Clinical observations will be compared to experimental animal models evaluating vascular, epileptogenic and short- and long-term behavior changes attributed to cocaine.