Effects Of Cocaine Exposure Research Articles

Conjuring a New Category of Disability from Prenatal Cocaine Exposure

The paper reviews the available literature on the biological mechanisms and effects of cocaine exposure impacting pregnant women, the fetus, the neonate, and the infant. The potential causal mechanisms for neural damage to the fetus are quite robust; however, the empirical literature does not support an inevitable developmental consequence for infants exposed in utero to cocaine. The most impaired of the cocaine-exposed infants do not seem to differ, behaviorally, from other groups of neurologically impaired infants. However, the infant exposed to cocaine in utero may have the added disadvantage of a dysfunctional caregiving environment focused more on drug habit maintenance than on caretaking. This combination of biological vulnerability and caretaking inadequacy increases the odds that a child will be a “caretaking casualty.” Classifications of children are useful only if they organize and name individuals with the same biological or behavioral characteristics. The classification of infants and young children as prenatally cocaine-exposed does not constitute a coherent cluster of either biological or behavioral characteristics. Hence, the construct of “cocaine babies” that has received considerable attention in the popular and professional press is neither descriptive nor predictive of behavior. Recommendations are offered for classification of behavior rather than labeling of the child. In addition, an overview of types of early intervention appropriate for various kinds of behavior exhibited by some children exposed to cocaine is presented. Finally, the development of empowerment strategies and professional partnerships with families of infants exposed to cocaine in utero is discussed.

Cocaine exposure in utero: perinatal development and neonatal manifestations--review.

The question of whether cocaine exposure in utero increases the risk of major structural malformations remains controversial. Most animal studies have demonstrated that cocaine can have a teratogenic effect. The ultimate association between cocaine exposure and fetal development must be inferred from human data. The relative effects of cocaine exposure, exposure to other illicit drugs and alcohol and deficient prenatal care are difficult to assess. Little specific information is available about the amount, duration, and timing of cocaine use during the nine months of pregnancy. Unlike the case with many other teratogens, cocaine exposure at any point in pregnancy can result in some abnormality. The extent of damage and the organ involved depend on the particular stage of morphogenesis. A large scale prospective human study is needed to confirm the suggested teratogenic effects. Since it involves an illicit drug such a study is obviously difficult to perform.

Maternal cocaine use and infant behavior

We hypothesized that prenatal cocaine exposure results in less optimal infant behavior and more impaired maternal-infant interaction in healthy term infants. Infants were evaluated with the Neonatal Behavioral Assessment Scale (NBAS) at days 1–3 and 11–30 of age, and mother-infant pairs with the Nursing Child Assessment of Feeding Scale (NCAFS) at 7–16 weeks of age. Drug use was determined from confidential interviews, urine assays and medical records. Cocaine-exposed infants ( N=51) were no different than unexposed comparison infants ( N=60) on the first NBAS exam. On the second NBAS exam, 20 cocaine-exposed infants had slightly lower motor cluster scores compared with those of 32 unexposed infants ( p=0.01), but this difference was reduced after control for several confounding variables. The NCAFS detected no differences between groups in maternal or infant behavior. Infants in this population showed no clinically meaningful effects of cocaine exposure on behavior or maternal-infant interaction.

Structural and functional effects of prenatal cocaine exposure in adult rat brain

The long-term effects of cocaine exposure early in development on the metabolic function of major central neuronal systems in the rat are reported in this study. Pregnant Wistar rats were administered either 60 mg/kg cocaine or the vehicle from gestation day (G) 8 through 22 via daily gastric incubation. Sixty-day-old male offspring were examined using the quantified deoxyglucose autoradiographic method. Of the 45 structures examined, 2 cortical and 14 subcortical structures showed statistically significant alterations in glucose metabolism compared to controls. The primary somatosensory and motor cortices showed significant decreases. The hypothalamus contained the greatest concentration of nuclei showing significant changes in activity. All of these changes were decreases. The nigrostriatal pathway, the medial forebrain bundle, the hippocampus, septum and amygdala were all significantly less metabolically active in the exposed offspring. The subcortical sensory systems did not appear to be affected at the dose of cocaine studied. Adjacent sections incubated in 1nM [ 3H]SCH 23390 showed an increase in the concentration of D 1 receptors in the substantia nigra, pars reticulata. Forebrain dopaminergic regions which showed decreased glucose metabolism did not appear to have altered SCH 23390 binding. Although size determinations were made on several cortical and subcortical structures, none were significantly affected by prenatal cocaine. Effects of chronic prenatal cocaine exposure on adult brain metabolism in several neuronal systems were identified at doses which had no significant effects on adult brain or body size. These data support the hypothesis that cocaine use during pregnancy produces permanent neurological effects at doses below those which produce growth retardation and terata.

The effect of cocaine on oocyte development and the follicular microenvironment in the rabbit

We examined the effects of cocaine exposure in the rabbit on in vitro oocyte development and on steroidal content of follicular fluid (FF) and serum progesterone (P). Cocaine hydrochloride (0, 10, 20, 40, or 80 mg/kg) was administered daily subcutaneously for 5 days to New Zealand White female rabbits before superovulation. On the last day of cocaine administration, animals were given human chorionic gonadotropin intravenously, and laparotomy was performed 6 to 8 hours later. During laparotomy, ovaries were removed, the number of follicles recorded, oocytes retrieved, and FF was obtained. In vitro fertilization (IVF) was then performed on the oocytes and the rate of cleavage observed. For all cocaine dosage groups, no differences were observed in the number of follicles present, number of oocytes retrieved, or IVF and cleavage rates. Cocaine did, however, decrease periovulatory serum P, and FF P, whereas FF estradiol concentrations increased. This suggests that short-term cocaine exposure affects the follicular steroid milieu, possibly by delaying granulosa cell luteinization.

Cocaine: A maternal, fetal, and neonatal risk

The effects of cocaine exposure in utero are not well understood. Studies have alluded to respiratory irregularities, tremors, tachycardia, and congenital malformations in neonates of cocaine-using mothers. Women using cocaine during pregnancy have a higher incidence of spontaneous abortion and abruptio placentae related to cocaine-induced transient hypertension. Cocaine abstinence during pregnancy is essential for optimal neonatal outcome.

Integration of the NBAS into routine maternity nursing care

We hypothesized that prenatal cocaine exposure results in less optimal infant behavior and more impaired maternal-infant interaction in healthy term infants. Infants were evaluated with the Neonatal Behavioral Assessment Scale (NBAS) at days 1–3 and 11–30 of age, and mother-infant pairs with the Nursing Child Assessment of Feeding Scale (NCAFS) at 7–16 weeks of age. Drug use was determined from confidential interviews, urine assays and medical records. Cocaine-exposed infants (N=51) were no different than unexposed comparison infants (N=60) on the first NBAS exam. On the second NBAS exam, 20 cocaine-exposed infants had slightly lower motor cluster scores compared with those of 32 unexposed infants (p=0.01), but this difference was reduced after control for several confounding variables. The NCAFS detected no differences between groups in maternal or infant behavior. Infants in this population showed no clinically meaningful effects of cocaine exposure on behavior or maternal-infant interaction.