When an adverse pregnancy outcome occurs, one considers the prenatal factors that may have contributed to the outcome. When drugs such as cocaine and amphetamines are discovered to be associated with the pregnancy, the infant frequently is labeled as a “cocaine baby,” “crack baby,” or “speed baby.” Such infants carry these distinctions for life and are expected to have behavioral deficiencies and learning disabilities that will never be overcome because of the “teratogenic exposure it received in utero.” Despite the fact that many women who use cocaine or amphetamines during pregnancy deliver normal infants developing within normal parameters, there are many maternal and fetal risks associated with the use of cocaine or amphetamines during pregnancy. This article reviews the effects of amphetamines on pregnancy and their respective effects on the fetus.

Often, the effects of cocaine and amphetamines are considered to be identical, because both drugs have essentially similar pharmacologic effects as central nervous system (CNS) stimulants. However, as demonstrated in this review, these compounds produce different developmental effects as well. This article reviews the background effects of amphetamines, their respective effects on human pregnancy, and the effects demonstrated in animal studies.

Several components of prenatal drug abuse in humans may affect the fetus or newborn. The following text outlines those described by Brooks-Gunn and co-workers<sup>8 Brooks-Gunn J., McCarton C., Hawley T. Effects of in utero drug exposure on children's development: Review and recommendations Arch Pediatr Adolesc Med 1994 ;  148 : 33-39

Cliquez ici pour aller à la section Références</sup>; several others are added for completeness. The first component is the drug effect on the developing neural system. The second component is drug exposure resulting in prematurity and fetal growth retardation. The third involves exposures of the drug after birth occurring via passive inhalation and breast-feeding. The fourth involves characteristics of the mother, including other abused drugs such as alcohol and nicotine, education, and mental health. The fifth mechanism focuses on how the affected child influences the behavior of its mother, that is, a drug-abusing mother may not care for her premature or low-birth-weight infant in the same manner as a drug-free mother. The sixth and final mechanism outlined by Brooks-Gunn and colleagues is the social environment in which the child is raised. All of these mechanisms are important factors contributing to the development of the prenatally drug-exposed child.

Several other issues must be considered in a discussion of drug abuse in pregnancy. One of these is the gestational period in which the drug exposure occurs, because damage to structures occurs at critical developmental time windows. Toxicologic issues are also important and involve exposure concentration of the drug and how the drug is handled by the body. Because drug disappearance depends on metabolic machinery and enzymatic capability, the toxicity and thus teratogenicity of a drug are likewise dependent on such enzymatic capacity. In both the fetus and the mother, the genetic composition that determines this enzymatic capacity influences and defines the concentration of the drug at the critical fetal site of action. If drug concentrations exceed the effect threshold, damage may occur.

The fact that a woman takes a drug during pregnancy does not mean she will deliver a malformed infant or behaviorally compromised child, because cause and effect are not always clearly defined. Malformations and behavioral effects in humans are not all-or-none phenomena, and whether damage occurs depends upon a multitude of different factors, including environmental, nutritional, genetic differences, and polydrug abuse. It can be concluded, however, that the use of certain drugs during pregnancy will increase the risks of adverse outcomes.