In the United States, more than 100,000 babies are exposed prenatally to cocaine each year (Office of the Inspector General, 1990). Increasing evidence indicates that prenatal cocaine exposure is associated with negative perinatal outcomes, including premature delivery, low birthweight, microcephaly, newborn behavioral abnormalities, and possible long-term cognitive and developmental difficulties (Singer et al., 2002). However, the impact of cocaine on the developing fetus is difficult to ascertain, because no confined, homogeneous, syndromic pattern of malformations has been identified, and because the mechanisms by which cocaine impacts on the unborn child are complex; maternal cocaine use may have both indirect and direct effects on a developing fetus (Vidaeff & Mastrobattista, 2003).
Indirect effects of maternal cocaine use include negative health consequences for mothers, which then impact their pregnancies. Women using cocaine are more likely to suffer arrhythmias, cardiac ischemias, and hemorrhagic strokes. In addition, they may develop pregnancy complications similar to preeclampsia, including hypertension, headaches, blurred vision, and placen-tal abruption, as well as vascular damage and uterine vasoconstriction, leading to problems such as spontaneous abortion and premature delivery (Church & Subramanian, 1997). Poor maternal weight gain and increased energy demands are another common effect of cocaine use in pregnant women, often leading to decreased birthweights and poorer prenatal nutrition (Church et al., 1991).
In addition to indirect effects, cocaine readily crosses the placental barrier and can thereby directly influence the unborn child (Moore, Sorg, Miller, Key, & Resnik, 1986; Volpe, 1992). Due to the fetus's immature metabolic systems, the drug is poorly metabolized, increasing its half-life (Chasnoff & Schnoll, 1987). Research has also shown that maternal intake of cocaine results in increased fetal systolic blood pressure, decreased uterine blood flow, and decreased fetal oxygenation (Moore et al., 1986), which may also negatively impact child outcomes.
Cocaine may directly affect early embryonic development by disrupting energy-producing mechanisms for cell metabolism and impact later fetal development by crossing the placenta, causing vascular disruption and changes in neurochemistry. Vascular disruption during a critical developmental period may be responsible for problems such as limb reduction deformities, intestinal atresia, fetal edema, necrotizing enterocolitis, intracranial hemorrhage, stroke, porencephaly, and other cocaine-related problems (Vidaeff & Mastrobasttista, 2003).
A stable, negative, cocaine-specific effect on language functioning was found through age 7, after controlling for sex, age, prenatal exposure to alcohol, marijuana and tobacco, and over 20 other medical and demographic factors (Bandstra et al., 2002). Similarly, Azuma and Chasnoff (1993) reported lower
IQ scores (though still in the normal range) on the Stanford-Binet for children prenatally exposed to cocaine in combination with other drugs; this study also identified mediating variables such as home environment, head circumference, and child behavior. In addition, a large study found that cocaine-exposed children were twice as likely to be significantly delayed developmentally throughout the first 2 years of life and were twice as likely to require intervention as the noncocaine polydrug-exposed comparison group. These cognitive delays were not due to exposure to other drugs or to covariates. Furthermore, poorer cognitive outcomes were related to higher levels of prenatal cocaine exposure (Singer et al., 2002). In addition to cognitive delays, 2-year-olds who had been prenatally exposed to both PCP and cocaine were found to utilize less mature play strategies and to evidence less sustained attention, more deviant behaviors, and poorer quality interactions with caregivers (Beckwith et al., 1994).
In summary, findings on the consequences of prenatal cocaine exposure relative to child development are inconsistent. Early concerns about severe, permanent neurobehavioral deficits appear to have been exaggerations; however, evidence remains that prenatal exposure to cocaine may contribute to the development of more mild or subtle neurobehavioral difficulties, such as poorer language functioning. In studying this population, it will be essential for researchers to control for confounding factors such as age, race, socioeconomic status, and other drug use; this is especially true, because some studies have found environmental factors to be equal even more important determinants of functioning.
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