Effects Of Prenatal Cocaine Exposure Research Articles

Preadolescent Health Risk Behavior as a Function of Prenatal Cocaine Exposure and Gender

To examine the effect of prenatal cocaine exposure on health risk behaviors during preadolescence. The present study examined prenatal cocaine exposure, gender, and environmental risk as predictors of self-reported substance use, aggression, and a disregard for safety precautions on the Youth Risk Behavior Survey in a sample of 10.5 year olds (n = 154, including 60 who were prenatally exposed to cocaine). Gender tended to moderate the effects of prenatal cocaine exposure because exposure effects were found for boys but not girls. Boys who were prenatally exposed to cocaine reported engaging in more high-risk behavior. In examining individual outcomes, cocaine exposed boys had the highest scores for aggression, substance use, and a disregard for safety precautions, although these differences were significant only for the composite health risk behavior measure. The findings extend earlier work showing that prenatal cocaine exposure places boys at risk for problems of inhibitory control, emotional regulation, and antisocial behavior. Research is needed to examine whether the effects of prenatal cocaine on health risk behaviors persist into adolescence, when such behaviors tend to increase.

Effects of Prenatal Cocaine Exposure on Growth: A Longitudinal Analysis

There has been a limited amount of research on the long-term effects of prenatal cocaine exposure on growth of the infant, and there has been no use of longitudinal growth models. We investigated the effects of prenatal cocaine exposure on offspring growth from 1 through 10 years of age by using a repeated-measures growth-curve model. Women were enrolled from a prenatal clinic and interviewed at the end of each trimester of pregnancy about their cocaine, crack, alcohol, marijuana, tobacco, and other drug use. Fifty percent of the women were white, and 50% were black. Follow-up assessments occurred at 1, 3, 7, and 10 years of age. Cross-sectional analyses showed that children exposed to cocaine during the first trimester (n = 99) were smaller on all growth parameters at 7 and 10 years, but not at 1 or 3 years, than the children who were not exposed to cocaine during the first trimester (n = 125). The longitudinal analyses indicated that the growth curves for the 2 groups diverged over time: children who were prenatally exposed to cocaine grew at a slower rate than children who were not exposed. These analyses controlled for other factors associated with child growth. To our knowledge, this is the first study of the long-term effects of prenatal cocaine exposure to conduct longitudinal growth-curve analyses using 4 time points in childhood. Children who were exposed to cocaine during the first trimester grew at a slower rate than those who were not exposed. These findings indicate that prenatal cocaine exposure has a lasting effect on child development.

Vagal tone as a resilience factor in children with prenatal cocaine exposure

Studies have investigated the potential effects of prenatal cocaine exposure (CE) on children's development. However, few studies have examined predictors of resilient outcomes in this population. We examined vagal tone (VT) as a resilience factor in prenatal CE. Utilizing data from the Maternal Lifestyle Study, a cumulative risk index was derived for children with and without prenatal CE. Presence of CE and other prenatal drugs was summed with postnatal risks in infancy to yield a 15-item risk index. Preschool cognitive outcomes, problem behaviors, and adaptive behaviors were measured. VT was assessed during an infant exam at 1 month and toy exploration at 36 months. We included children with complete physiologic data (217 CE, 333 non-CE). Children were classified as having consistently high, consistently low, or fluctuating VT at 1 and 36 months. Children were also classified as high versus low risk. High-risk children had lower IQ scores, more problem behaviors, and lower ratings of adaptive behaviors than low-risk children. A significant risk by VT-stability interaction indicated that for high-risk children, those with stable low VT had higher ratings of adaptive behaviors at 36 months. This is consistent with theory linking reduced VT during tasks to adaptive regulation and indicates that such regulatory functioning may serve as a protective factor in prenatal CE.

Effects of prenatal cocaine exposure and lead on neuropsychological function using the CANTAB at 10 years

Effects of prenatal cocaine exposure and lead on neuropsychological function using the CANTAB at 10 years

Pre-natal exposures to cocaine and alcohol and physical growth patterns to age 8 years

Two hundred and two primarily African American/Caribbean children (classified by maternal report and infant meconium as 38 heavier, 74 lighter and 89 not cocaine-exposed) were measured repeatedly from birth to age 8 years to assess whether there is an independent effect of pre-natal cocaine exposure on physical growth patterns. Children with fetal alcohol syndrome identifiable at birth were excluded. At birth, cocaine and alcohol exposures were significantly and independently associated with lower weight, length and head circumference in cross-sectional multiple regression analyses. The relationship over time of pre-natal exposures to weight, height, and head circumference was then examined by multiple linear regression using mixed linear models including covariates: child's gestational age, gender, ethnicity, age at assessment, current caregiver, birth mother's use of alcohol, marijuana and tobacco during the pregnancy and pre-pregnancy weight (for child's weight) and height (for child's height and head circumference). The cocaine effects did not persist beyond infancy in piecewise linear mixed models, but a significant and independent negative effect of pre-natal alcohol exposure persisted for weight, height, and head circumference. Catch-up growth in cocaine-exposed infants occurred primarily by 6 months of age for all growth parameters, with some small fluctuations in growth rates in the preschool age range but no detectable differences between heavier versus unexposed nor lighter versus unexposed thereafter.

Autonomic Alterations in Cocaine-Exposed Neonates Following Orthostatic Stress

We investigated the effects of prenatal cocaine exposure (PCE) on heart rate (HR) and heart rate variability (HRV) in the presence of orthostatic stress among near- and full-term neonates. PCE infants (n = 21) and controls (n = 23) were enrolled within 120 h of birth. ECG was recorded for an hour during quiet sleep, 30 min in supine position and then 30 min in an inclined position. Linear mixed models were used to analyze HR and HRV in the time domain and wavelet and power spectrum analyses in the frequency domain. PCE infants had tachycardia both before (p = 0.091) and after tilting (p = 0.015), but with a clear interaction between PCE and orthostatic stress (p = 0.049). Compared with controls, PCE infants had a delayed and prolonged reaction to orthostatic stress. There was also a pronounced interaction with regard to log-transformed SDDRR, a measure of HRV (p = 0.049). Controls experienced an instantaneous increase in log (SDDRR) followed by a prompt return to normal levels, while PCE infants had a gradual increase that did not dissipate quickly. Frequency-domain analyses also distinguished between the cocaine-exposed infants and the controls. Results suggest that the effects of PCE on the development of sympathetic and parasympathetic systems could lead to altered cardiovascular function.

Impact of Prenatal Cocaine Exposure on Child Behavior Problems Through School Age

We examined the trajectory of childhood behavior problems after prenatal cocaine exposure. The Maternal Lifestyle Study, a longitudinal cohort study, enrolled children between 1993 and 1995 at 4 centers. Prenatal cocaine exposure was determined from mothers who admitted use and/or meconium results. Exposed children were matched with a group of nonexposed children within site and by gestational age, gender, race, and ethnicity. The study began at the 1-month corrected age with a total of 1388 children enrolled. A total of 1056 were assessed for internalizing, externalizing, and total behavior problems at ages 3, 5, and 7 years using the Child Behavior Checklist. Longitudinal hierarchical linear models were used to determine the effect of prenatal cocaine exposure on behavior problem trajectories while controlling for other prenatal exposures; time-varying covariates, including ongoing caregiver use of legal and illegal substances; demographic factors; family violence; and caregiver psychological distress. High prenatal cocaine exposure was associated with the trajectory of internalizing, externalizing, and total behavior problems; these effects were independent of and less than the significant combined effect of prenatal and postnatal tobacco and alcohol exposures. Caregiver depression and family violence had independent negative influence on all behavior outcomes. Prenatal cocaine exposure has a negative impact on the trajectories of childhood behavior outcomes. When they co-occur with prenatal cocaine exposure, prenatal and postnatal tobacco and alcohol exposures have added negative effects on behavior outcomes.

Early Intervention for Children Prenatally Exposed to Cocaine

This article brings together information from our experience of providing research-based intervention to more than 600 children who were prenatally exposed to cocaine and from the research literature on the effects of prenatal cocaine exposure. Based on our experience and this literature, it is now clear that there are no large negative independent effects of cocaine exposure and that there is no “crack baby” syndrome. However, many of these children who have been exposed to cocaine are at risk for poor developmental outcomes, particularly in the area of language development, primarily because of the environmental factors that are associated with parental substance abuse. As our intervention research shows, early intervention can be effective in ameliorating some of this risk. Suggestions are made regarding programmatic steps that should be taken next to further improve program effectiveness and enhance the knowledge base.

BTS Student Travel Award Winner Effects of prenatal cocaine exposure in DMTS task reversal on monkeys

BTS Student Travel Award Winner Effects of prenatal cocaine exposure in DMTS task reversal on monkeys

Effect of Prenatal Cocaine Exposure on D2 Receptors and DAT in Rhesus Macaques

Five adult rhesus monkeys with a history of prenatal cocaine exposure (PNCE) and two saline-exposed control animals were used to optimize positron emission tomography (PET) imaging methods and to gather preliminary data on the effects of PNCE on dopamine systems in the adult non-human primate central nervous system. Dynamic PET scans were performed on each monkey to measure the binding kinetics of PET ligands specific for dopamine D2/D3 receptors ([18F]fallypride) and dopamine transporter ([18F]FECNT). PET scans were coregistered to structural T1-weighted MR images to aid in identification of regions with significant dopamine innervation for tracer kinetic analysis. Brain regions of interest (ROI) included caudate, putamen, substantia nigra and anterior cingulate cortex. Kinetic modeling using a cerebellum reference region was implemented in the PMOD software package to determine ligand binding 
 potentials for D2/D3 receptors and dopamine transporters (DAT) in each of the ROIs to test whether fallypride and/or FECNT binding potentials, measures of D2/D3 and DAT levels respectively, were influenced by prenatal cocaine exposure. Preliminary results suggest a trend of reduced D2/D3 binding potential with increased PNCE, but future research is necessary.

Prenatal Exposure to Cocaine and Enriched Environment

Exposure to cocaine throughout gestation may produce several deleterious outcomes in the offspring that include effects on neurotransmitter systems and structure of the central nervous system. Such changes are most likely correlated with behavioral alterations. Environmental enrichment (EE) in early stages is a factor that affects structural and behavioral development. This article examines the effects, upon social interactions, of EE during the first month of life in rats prenatally exposed to cocaine. Wistar dams were subcutaneously exposed to 60 mg/kg of cocaine divided in two daily doses from gestational day (GD)8 to GD22. Pair-fed controls were given saline vehicle in the same protocol. Offspring were distributed to the different environments in four experimental groups. Group 1: offspring from dams prenatally exposed to cocaine as previously described and reared in EE from postnatal day (PND)1 to PND28; Group 2: pups from cocaine-exposed dams and reared in a standard environment (SE); Group 3: pups from pair-fed saline-exposed dams and reared in EE; Group 4: offspring from saline-exposed dams and reared in SE. On PND21, 24, and 28, rats were examined in several social behavioral categories (play fighting, social investigation, comfort behaviors, and solicitation to play) for 10 min. Animals reared in SE do not display any differences due to treatment in the behavioral categories analyzed. Control offspring reared in EE presented decreased play fighting, decreased solicitation to play, and decreased social investigation compared to the control SE group, while cocaine-exposed animals reared in EE did not present these variations. These results suggest that EE rearing may unmask hidden effects of prenatal cocaine exposure.

Prenatal cocaine exposure accelerates morphological changes and transient expression of tyrosine hydroxylase in the cochlea of developing rats

Prenatal cocaine exposure causes alterations in auditory brainstem response in children and experimental animals and has adverse effects on auditory information processing and language skills in children. These effects may result from lesions in the cochlea since this organ is particularly sensitive to chemical insults during the development. We have thus studied here the effect of prenatal cocaine exposure on the maturation of the rat cochlea using the transient non-catecholaminergic expression of tyrosine hydroxylase in spiral ganglion neurons as an index of cochlear maturation and morphometry to evaluate the maturation of primary auditory neurons and the organ of Corti. We showed that prenatal cocaine exposure accelerated the cochlear maturation. In the basal coil of cochleas from PND8 cocaine-treated pups, the Kölliker's organ had disappeared, the tunnel of Corti was opened, and the stria vascularis no longer contained undifferentiated marginal cells. The maximum expression of tyrosine hydroxylase in type I primary auditory neurons occurred at PND8 instead of PND12 in pair-fed controls. On the other hand, the prenatal cocaine exposure had no effect on the width and height of the organ of Corti, spiral ganglion volume and number and size of primary auditory neurons. In conclusion, our data suggest that prenatal cocaine exposure, though not lethal to primary auditory neurons, accelerates aspects of the cochlear sensorineural maturation. This accelerated cochlear maturation in cocaine-treated rat pups could cause auditory dysfunctions by desynchronizing the development of the whole auditory pathway.

Prenatal cocaine exposure specifically alters spontaneous alternation behavior

Our laboratory has previously characterized a rabbit model of gestational cocaine exposure in which permanent alterations in neuronal morphology, cell signaling and psychostimulant-induced behavior are observed. The cellular and molecular neuroadaptations produced by prenatal cocaine occur in brain regions involved in executive function and attention, such as the anterior cingulate and medial prefrontal cortices. Therefore, in the present study, we have measured the effects of prenatal cocaine exposure on specific behavioral tasks in adult offspring whose mothers were treated with cocaine (3 mg/kg, twice a day, E16–E25). We assessed non-spatial, short-term memory in a two-object recognition task and found no deficits in memory or exploratory behaviors in cocaine-exposed offspring in this paradigm. We also evaluated a different memory task with a more robust attentional component, using spontaneous alternation in a Y maze. In this task, young adult rabbits exposed to cocaine prenatally exhibited a significant deficit in performance. Deficits in spontaneous alternation can be induced by a wide variety of behavioral and cognitive dysfunctions, but taken together with previous findings in this and other animal models, we hypothesize that prenatal exposure to cocaine alters highly specific aspects of cognitive and emotional development.

Outcome from a Prospective, Longitudinal Study of Prenatal Cocaine Use: Preschool Development at 3 Years of Age

To determine the effects of prenatal cocaine exposure on child development. This prospective, longitudinal study recruited 154 pregnant cocaine users who were matched on race, parity, socioeconomic status, and perinatal risk to 154 noncocaine users. Drug use status was determined by maternal history and urine screening. At 3 years of age, the child subjects were assessed by an evaluator blinded to maternal drug use history. During a home visit at age 3, caregiver, family, and home assessments were administered. Structural equation modeling showed a direct effect of the amount of prenatal cocaine exposure on the adjusted birth head circumference which in turn directly affected preschool development. We could not demonstrate a direct effect of prenatal cocaine exposure on preschool development, a result that is consistent with that of earlier work and now extending findings to age 3. However, cocaine continued to exert an indirect effect on development through its direct effect on the head circumference at birth.

Postnatal consequences of prenatal cocaine exposure and myocardial apoptosis: does cocaine in utero imperil the adult heart?

Cocaine use is common among pregnant women with a history of substance abuse, and has been shown to cause abnormalities in the heart during fetal and postnatal development. However, mechanisms underlying the detrimental effects of cocaine on the developing heart are not fully understood. In this issue, Bae and Zhang show that prenatal cocaine exposure increases the susceptibility of the postnatal heart to ischemia and reperfusion injury. Their results suggest that myocardial apoptosis induced by cocaine during fetal development may represent one of the mechanisms by which prenatal cocaine exposure exerts its long-term, deleterious consequences on postnatal cardiac function.

Prenatal cocaine exposure alters spontaneous and cocaine-induced motor and social behaviors

The abuse of cocaine in pregnant women could affect emotional behaviors in their descendents. The aim of this work was to evaluate the effects of prenatal cocaine exposure on spontaneous and cocaine-induced motor and social behaviors in mice. Three kinds of prenatal treatment were used: non-treated animals; mice treated daily with physiological saline during the last week of pregnancy; and finally, those treated with cocaine (25 mg/kg) during the same period. Behavioral studies took place on adult males, which were housed in two different conditions: grouped (non-aggressive), or isolated (aggressive). Cocaine-pretreated animals exhibited slight differences in spontaneous motor activity, but alterations in their social relationship with conspecifics were presented, with decreases in isolated but increases in grouped mice. The cocaine challenge increased aggression specifically in grouped prenatally cocaine-treated mice, but increases in motor activity or avoidance and flee behavior were presented in those animals pretreated with either saline or cocaine. Isolated saline-or cocaine-treated animals exhibited greater concentrations of DA and DOPAC than those grouped. A decrease in 5-HIAA concentrations was presented in pretreated animals, irrespective of their housing conditions. In conclusion, cocaine administration during pregnancy induces long lasting effects on the offspring, for both behavioral abnormalities and cocaine response, which last to adult life.

Effect of Prenatal Cocaine Exposure on the Stress Axis in Young Adult Rats

Effect of Prenatal Cocaine Exposure on the Stress Axis in Young Adult Rats

Cognitive Outcomes of Preschool Children With Prenatal Cocaine Exposure

Cocaine passes the placental and fetal brain barriers and directly affects the developing brain. The few prospective studies reported that examined the long-term cognitive effects of prenatal cocaine exposure have given inconsistent results. The present trial was a prospective, longitudinal, blind comparison cohort study assessing the effects of in utero cocaine exposure and the quality of caregiving on cognitive function at age 4 years. Of 415 consecutively enrolled infants, all from a high-risk population, 376 (190 cocaine-exposed and 186 unexposed) were available for evaluation at age 4 using the Wechsler Preschool and Primary Scales of Intelligence-Revised. Caregivers completed the Home Observation of the Environment (HOME)-Preschool version that assesses the quality of the caregiving environment. A majority of women were low-income blacks. Cocaine users were older than nonusers, had more children, and were less likely to have received prenatal care. They also were less likely to be married and to have completed high school, and they experienced more psychologic distress. Cocaine users also used alcohol, tobacco, and marijuana more often (and in greater amounts) than nonusers of cocaine. Exposed infants were of lower gestational age, birth weight, length, and head circumference than unexposed infants. They were likelier than unexposed infants to be preterm, small for gestational age, and in nonmaternal care. Controlling for covariables, prenatal cocaine exposure was not associated with lower full-scale IQ scores or summary verbal IQ stores at age 4 years. It did, however, predict small but significant deficits in visual-spatial skills, general knowledge, and arithmetic skills. Children exposed to cocaine before birth were less likely to achieve an IQ above the normative mean. Exposed children in nonrelative foster or adoptive care lived in more stimulating environments and had IQ scores comparable to those of unexposed children who were in biologic maternal or relative care. Their scores were higher than those of cocaine-exposed children in biologic maternal or relative care. The latter children had lower full-scale and performance IQ scores than did unexposed children. The quality of the caregiving environment was the strongest independent predictor of cognitive outcomes. These findings are in accord with those from other studies of preschool cocaine-exposed children that identified specific but not global IQ deficits. Cocaine-exposed children do better cognitively when living in a favorable home environment.

Gender and alcohol moderate prenatal cocaine effects on teacher-report of child behavior

Prenatal cocaine exposure has been associated with behavior problems at school age. However, the correspondence between use of cocaine and alcohol during pregnancy is often high, making appropriate allocation of variance and control for other exposures and their interactions difficult. Additionally, gender-specific effects are not typically reported. The purpose of the current study was to determine the degree to which gender-specific effects of prenatal cocaine exposure on teacher-reported child externalizing behavior problems were evident when evaluated in relation to prenatal alcohol exposure. Subjects were singleton infants of mothers who were prospectively evaluated during pregnancy. At age seven, 499 children (214 exposed prenatally to cocaine) were evaluated in our laboratory and teacher reports were solicited. Analyses stratified by gender and prenatal alcohol exposure status, and controlled for significant pre- and postnatal confounders, revealed that among boys with prenatal alcohol exposure, those with persistent cocaine exposure throughout pregnancy had significantly higher levels of Delinquent Behavior compared to boys with no cocaine exposure. Boys with any prenatal cocaine exposure were twice as likely as unexposed boys to have clinically significant Externalizing Behavior scores. However, no association was found between prenatal cocaine exposure and scores on Externalizing Behavior and specific syndromes for boys with no prenatal alcohol exposure. Among girls with no prenatal alcohol exposure, those with persistent cocaine exposure had significantly higher levels of Externalizing Behaviors and Aggressive Behaviors compared to girls with no prenatal cocaine exposure after control for confounding, and were almost five times as likely to have clinically significant Externalizing Behavior scores. However, for girls with prenatal alcohol exposure, no association between prenatal cocaine exposure and scores on Externalizing Behavior and specific syndromes was found after control for confounding. The current findings support gender- and alcohol-moderated effects of prenatal cocaine exposure on school-age teacher-reported child behavior problems. These findings are similar to what we have reported for independent parent-reported behavioral evaluation.

Gender and alcohol moderate caregiver reported child behavior after prenatal cocaine

Objective The concurrence of prenatal alcohol exposure with other drug exposure, low socioeconomic status and environmental risk factors may obscure associations, if any, between prenatal cocaine exposure and child outcomes. This study evaluates the effects of prenatal cocaine exposure on child behavior in analyses stratified by gender and prenatal alcohol exposure status. Methods Maternal alcohol, cigarette, and illicit drug use were prospectively assessed by interview during pregnancy and postnatally. Maternal and neonatal urine were tested for drug exposure as clinically indicated. Caregiver report of child behavior was assessed with the Achenbach Child Behavior Checklist (CBCL). Dichotomous cocaine exposure was characterized as no (negative history and biologic markers), and any (positive history and/or biologic markers during pregnancy and/or positive urine screen at delivery from either mother or infant). Results Prenatal cocaine exposure was associated with adverse effects on offspring behavior that were moderated by the gender of the offspring as well as prenatal alcohol exposure. For girls without prenatal alcohol exposure, 6.5% of the unique variance in behavior was related to prenatal cocaine exposure. For these girls, the odds of scoring in the abnormal range for Aggression was 17 times control levels (95% confidence limits 1.4 to 203). These findings, though significant, have wide confidence intervals and need to be replicated in larger cohorts and on longitudinal follow-up.