Congenital cocaine syndrome

Daniel J Bonthius MD PhD (Dr. Bonthius of the University of Iowa has no relevant financial relationships to disclose.)
Dylan Todd MD (Dr. Todd of the University of Iowa has no relevant financial relationships to disclose.)
Michael V Johnston MD, editor. (Dr. Johnston of Johns Hopkins University School of Medicine and Chief Medical Officer at Kennedy Krieger Institute has no relevant financial relationships to disclose.)
Originally released November 28, 1994; last updated March 20, 2017; expires March 20, 2020

Overview

Cocaine is one of the most addictive and frequently abused illicit drugs. Maternal abuse of cocaine during pregnancy is common and is associated with a host of neurologic and developmental abnormalities in offspring. In this updated article, the authors describe the many adverse effects that cocaine can have on the fetus and the newborn, and they discuss the various mechanisms by which cocaine induces disturbances in the structure and function of the developing brain.

Key points

 

• Maternal cocaine abuse during pregnancy is common and is associated with a host of neurologic and developmental abnormalities in the offspring.

 

• Cocaine is a potent vasoconstrictor, and many of the medical and neurologic problems of children exposed to cocaine in utero are due to compromised blood flow through placental and cerebral vasculature.

 

• Cocaine can interact with the monoaminergic synapses in the developing brain to induce short-term and long-term changes in neurophysiology and anatomy.

Historical note and terminology

Cocaine is benzoylmethylecgonine, an alkaloid derived from the leaves of the coca shrub (Erythroxylon coca), which grows wild and is cultivated in South American and Central American countries (Farrar and Kearns 1989). Cocaine is available either as cocaine hydrochloride or as the highly purified (free base form) cocaine alkaloid. Cocaine hydrochloride is water soluble but heat labile and is most commonly administered by nasal insufflation (“snorting”). In contrast, cocaine alkaloid is water insoluble but heat stable and is typically administered by inhalation (smoking). Because the alkaloid preparation produces a popping sound when the crystals are heated, it has acquired the name “crack.”

In light of cocaine's widespread use among pregnant women, the effect of the drug on the fetus is an issue of major public health importance. It is widely accepted that cocaine can be deleterious to the fetus and that the fetal brain is particularly vulnerable. However, several factors have made the study of cocaine's effects on the human fetus difficult to conduct and interpret.

Foremost among these difficulties is the inescapable fact that a cocaine-exposed fetus is often exposed to many additional deleterious confounding variables during prenatal and postnatal life (Lutiger et al 1991; Mayes et al 1992). A pregnant woman who abuses cocaine may also drink alcohol, smoke cigarettes, and abuse other illicit drugs. She may transmit to the fetus a congenital infection, such as HIV or syphilis. Following birth, the child of a cocaine-abusing mother may receive inadequate nutrition and grow up in a poor social environment (Streissguth et al 1991).

During the 1980s, a plethora of papers described wide ranging and highly negative outcomes among children exposed to cocaine in utero. The alarm sounded in the medical literature and lay press that an entire generation of deeply disabled “crack babies” was being produced. It later became evident that physicians, scientists, journalists, and politicians had overreacted in the face of the data and that cocaine did not necessarily have as profound and far reaching consequences for the fetus as had been feared. This overreaction was due, in large part, to the failure of the physicians and scientists to appreciate the many confounding variables accompanying fetal cocaine exposure. It is now appreciated that cocaine can damage a fetus, sometimes with permanent consequences, but that the damage is typically either circumscribed in nature or subtle in severity, and the impending onslaught of multiply injured crack babies is a myth (Church 1993; Coles 1993).

A second issue that has complicated the study of fetal cocaine exposure relates to the choice of outcome measure. Cocaine may adversely affect neural systems involved in complex neurologic and behavioral functions, such as motivation, attention, social interaction, and intelligence, which are difficult to measure, particularly during infancy. Because many children prenatally exposed to cocaine are in chaotic home environments, locating the children for long-term follow-up studies is often difficult.

A third methodological difficulty relates to accurately identifying the exposed fetuses and children and determining the degree and timing of the exposure. Because cocaine use is illegal and carries moral implications when used during pregnancy, women lie about their use of the drug. Testing for cocaine metabolites in urine, meconium, amniotic fluid, umbilical cord tissue, and brain identifies some, but not all, exposed fetuses, and the issues of dose and timing of exposure remain. The nature and severity of the teratogenic and destructive effects of cocaine on the fetus probably depend on the gestational timing and magnitude of exposure (Volpe 1992; Eyler et al 1998). Thus, the imprecise measure of these crucial variables has limited the ability to determine cocaine's effect on the developing brain.

Although cocaine's adverse fetal effects are real, these methodologic issues lead to overestimation of the incidence and impact of prenatal cocaine. It is important for clinicians and others to avoid unjustified negative conclusions and assumptions about children who were prenatally exposed to cocaine as these false inferences can enhance harmful and unwarranted stigma against them (McAllister and Hart 2015).

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