The incidence of cocaine use among pregnant women has been reported at about 10%, although in some areas it is as high as 28% (Singer, Garber, & Kliegman, 1991). Polydrug use has also become more frequent, with the majority of cocaine users also abusing marijuana, alcohol, or cigarettes, or a combination of these (Chasnoff, 1988; Gibson, Baghurst, & Colby, 1983). Cocaine use during pregnancy is associated with a number of perinatal complications, including premature birth, intrauterine growth retardation, diminished head circumference, and major congenital malformations (Burkett, Yasin, & Palow, 1990; Coles, Platzman, Smith, James, & Falek, 1991; Hadeed & Siegel, 1989; Porat & Brodsky, 1991; Rosenak, Diamont, Yaffe, & Hornstein, 1990). No specific cocaine syndrome has yet been described (cf. fetal alcohol syndrome), and the deficits that have been observed may relate to the higher incidence of SGA (small for gestational age), lower Apgar scores, lower birthweight, and smaller head circumference reported for cocaine-exposed infants. Nonetheless, the signs of fetal stress, including increased heart rate, lower vagal tone, and lower Apgar scores, do suggest central nervous system involvement (Richards, Kulkarni, & Bremner, 1990). Less subtle abnormalities include cerebral infarction and EEG, BAER, and ultrasonographic or pneumographic abnormalities (Chasnoff, Hevet, Kletter, & Kaplan, 1989; Dixon & Bejar, 1989; Doberczak, Shanzer, Senie, & Kandall, 1989).
Despite these less optimal neonatal outcomes, there is a paucity of developmental follow-up studies on cocaine-exposed infants. Those studies suggest the importance of using more sensitive measures than standardized tests, because the early delays/deficits are more subtle. For example, unlike other drug-exposed newborns, very few withdrawal symptoms have been reported for cocaine-exposed neonates, although some have reported tremulousness, irritability, wakefulness/restlessness, hypertonia, and abnormal reflexes (Livesay, Ehrlick, & Finnegan, 1987; Rosecan & Gross, 1986), highlighting the importance of observing sleep patterns and reflex behaviors. While neonates exposed to cocaine display fewer overt withdrawal signs than do infants exposed to heroin or methadone, aberrations in neurobehavioral status, motor tone, and crying, feeding, and cardiorespiratory patterns have been noted (Chasnoff, Burns, & Burns, 1987; Chasnoff, Burns, Schnoll, & Burns, 1985).
A recent observational study on the behavior of cocaine-exposed newborns noted more obstetric complications, smaller head circumference, and a greater number of withdrawal symptoms (Eisen, Field, Bandstra, Roberts, Morrow, Larson & Steele, 1991.). In addition, these polydrug-exposed infants were slower to habituate. In a pilot study by Larson and Field (1989), cocaine-exposed infants were found to have depressed vagal tone, suggesting a parasympathetic-sympathetic imbalance. Given the literature on the relationship between low vagal tone and low developmental scores later in infancy, this group may be at risk for delays in cognitive development. It is also noteworthy that dopamine levels were depressed in the cocaine-exposed newborns. Dopamine depletion has recently been implicated in habituation disturbances in the rat model (Simonik, Robinson, & Smotherman, 1994). It is interesting in that light that both dopamine depletion and habituation deficits were reported for cocaine-exposed infants.
In a recent study (Wheeden, Scafidi, Field, Ironson, Bandstra, Schanberg, & Valdeon, 1993), cocaine-exposed infants were massaged (30 minutes per day for 10 days). Compared with cocaine-exposed infants who were not massaged and preintervention baseline data, they gained more weight (8 grams more per day), they were less irritable, they showed superior habituation scores, their vagal tone was higher following massage, and their norepinephrine and dopamine levels significantly increased over the 10-day period (much like the normal developmental increase expected at this time). …