Study Of Prenatal Cocaine Exposure Research Articles

Pathways from prenatal cocaine exposure to adult substance use and behavior

This is a report from the most recent adult follow-up of the longest running cohort study of prenatal cocaine exposure (PCE), in which women were enrolled prenatally and offspring were assessed in infancy, childhood, adolescence, and young adulthood. In previous studies, PCE was linked to offspring behavior problems such as early substance use and externalizing behavior problems. The current analyses examine pathways from PCE to behavioral outcomes in offspring at the 25-year assessment. Prenatal cocaine exposure was moderate in this cohort; most women decreased or discontinued use after the first trimester. During the first and third trimesters, 38% and 11% used cocaine, respectively. This represents the most common pattern of PCE in non-treatment samples. At this phase, the adult offspring were, on average, 27.3 years old (range = 25–30), had 13.4 years of education, 83% were employed, 55% were Black, and 55% were female. Offspring who were exposed to cocaine during the first trimester were significantly more likely to use marijuana in the past year, report more arrests, and have poorer scores on a decision-making task, controlling for other prenatal substance exposure, demographic, and socioeconomic factors. In mediation analyses, there were indirect pathways from PCE to current marijuana use through early initiation of marijuana use and 21-year marijuana use, and through 15-year status offenses and 21-year marijuana use. There was also an indirect pathway from PCE to lifetime arrests through early initiation of marijuana use and 21-year Conduct Disorder, although the direct pathway from PCE to arrests also remained significant. These findings are consistent with those from previous phases and are an indication that there are detrimental associations with PCE that persist across developmental stages and into adulthood.

Family Risk Exposure Profiles During Early Childhood: Developmental Processes and Adolescent Well-Being.

Although prior work indicates that exposure to multiple family risk factors negatively impacts adjustment in childhood and adolescence, few studies have examined whether children in high-risk families transition in and out of adversity during early childhood and whether patterns of change matter for adjustment in adolescence. Using data from a sample of 216 caregiver-child dyads participating in a study of prenatal cocaine exposure (116 exposed and 100 non-exposed; 50.9% girls), we used latent transition analysis to identify distinct profiles of early exposure to caregiver substance use (SU) and SU-related familial risk (caregiver psychological distress, exposure to violence, harshness, and low sensitivity) and the association between these profiles and adolescent well-being (i.e., hope, happiness, and life satisfaction). Assessments occurred when children were 13, 24, 36, and 48 months and during kindergarten (Mmonths = 66.16, SD = 4.47) and early adolescence (Myears = 13.26, SD = 0.88). Caregivers self-identified as 72.09% Black, 15.81% White, 10.23% Hispanic/Latinx, 1.40% other, and 0.47% American Indian. Four profiles of varying levels of exposure to caregiver SU and SU-related risks were identified from infancy to kindergarten: SU/family risks, no SU/low family risks, SU/negative parenting, and SU/low family risks. Most children stayed in the same profile (64.2%), while the rest transitioned between profiles. Children exposed to caregiver SU and family adversity had lower positive outcomes in adolescence. Stable membership in the SU/family risks profile had significant maladaptive consequences on adolescent well-being. Implications for research and the design of tailored interventions to promote well-being among at-risk youth are discussed.

Prenatal cocaine exposure: The role of cumulative environmental risk and maternal harshness in the development of child internalizing behavior problems in kindergarten

This study examined the associations between prenatal exposure to cocaine and other substances and child internalizing behavior problems at kindergarten. We investigated whether maternal harshness or cumulative environmental risk mediated or moderated this association. Participants consisted of 216 (116 cocaine exposed, 100 non-cocaine exposed) mother–infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that, as hypothesized, maternal harshness moderated the association between prenatal cocaine exposure to child internalizing in kindergarten such that prenatal cocaine exposure increased risk for internalizing problems at high levels of maternal harshness from 7 to 36months and decreased risk at low levels of harshness. Contrary to hypothesis, the association between prenatal cocaine exposure and child internalizing in kindergarten was not mediated by maternal harshness or cumulative environmental risk. However, cumulative environmental risk (from 1month of child age to kindergarten) was predictive of child internalizing behavior problems at kindergarten. Results have implications for parenting interventions that may be targeted toward reducing maternal harshness in high risk samples characterized by maternal substance use in pregnancy.

Effects of prenatal cocaine exposure on child behavior and growth at 10 years of age

We examined physical growth and behavioral outcomes in 226 10-year-old children who were participants in a longitudinal study of prenatal cocaine exposure (PCE), while controlling for other factors that affect development. During the first trimester, 42% of the women used cocaine, with use declining across pregnancy. At the 10-year follow-up, the caregivers were 37years old, had 12.8years of education, and 50% were African American. First trimester cocaine exposure predicted decreased weight, height, and head circumference at 10years. First trimester cocaine use also predicted maternal ratings of less sociability on the EAS Temperament Survey and more withdrawn behavior problems on the Child Behavior Checklist, more anxious/depressed behaviors on the Teacher Report Form, and more self-reported depressive symptoms on the Children's Depression Inventory. In addition, exposure to violence mediated the effect of PCE on child and teacher reports of depressive symptoms, but not of maternal reports of sociability and withdrawn behaviors. These behaviors may be precursors of later psychiatric problems.

Prenatal Cocaine Exposure and Gray Matter Volume in Adolescent Boys and Girls: Relationship to Substance Use Initiation

Studies of prenatal cocaine exposure have primarily examined childhood populations. Studying adolescents is especially important because adolescence is a time of changing motivations and initiation of substance use. Using magnetic resonance imaging and whole-brain voxel-based morphometry, we assessed gray matter volume (GMV) differences in 42 prenatally cocaine exposed (PCE) and 21 noncocaine-exposed (NCE) adolescents, aged 14 to 17 years. Associations between GMV differences in significant clusters and the probability of substance use initiation were examined. PCE relative to NCE adolescents demonstrated three clusters of lower GMV involving a limbic and paralimbic (p < .001, family-wise error [FWE] corrected), superior frontal gyrus (p = .001, FWE corrected), and precuneus (p = .019, FWE corrected) cluster. GMVs in the superior frontal and precuneus clusters were associated with initiation of substance use. Each 1-mL decrease in GMV increased the probability of initiating substance use by 69.6% (p = .01) in the superior frontal cluster and 83.6% (p = .02) in the precuneus cluster. PCE is associated with structural differences in cortical and limbic regions. Lower GMVs in frontal cortical and posterior regions are associated with substance use initiation and may represent biological risk markers for substance use.

Adolescents with prenatal cocaine exposure show subtle alterations in striatal surface morphology and frontal cortical volumes

BackgroundPublished structural neuroimaging studies of prenatal cocaine exposure (PCE) in humans have yielded somewhat inconsistent results, with several studies reporting no significant differences in brain structure between exposed subjects and controls. Here, we sought to clarify some of these discrepancies by applying methodologies that allow for the detection of subtle alterations in brain structure.MethodsWe applied surface-based anatomical modeling methods to magnetic resonance imaging (MRI) data to examine regional changes in the shape and volume of the caudate and putamen in adolescents with prenatal cocaine exposure (n = 40, including 28 exposed participants and 12 unexposed controls, age range 14 to 16 years). We also sought to determine whether changes in regional brain volumes in frontal and subcortical regions occurred in adolescents with PCE compared to control participants.ResultsThe overall volumes of the caudate and putamen did not significantly differ between PCE participants and controls. However, we found significant (P <0.05, uncorrected) effects of levels of prenatal exposure to cocaine on regional patterns of striatal morphology. Higher levels of prenatal cocaine exposure were associated with expansion of certain striatal subregions and with contraction in others. Volumetric analyses revealed no significant changes in the volume of any subcortical region of interest, but there were subtle group differences in the volumes of some frontal cortical regions, in particular reduced volumes of caudal middle frontal cortices and left lateral orbitofrontal cortex in exposed participants compared to controls.ConclusionsPrenatal cocaine exposure may lead to subtle and regionally specific patterns of regional dysmorphology in the striatum and volumetric changes in the frontal lobes. The localized and bidirectional nature of effects may explain in part the contradictions in the existing literature.

Maternal cocaine use and mother–toddler aggression

This study examined the direct and indirect associations between maternal cocaine use during pregnancy and mother–toddler aggression in an interactive context at 2 years of child age. We hypothesized that in addition to direct effects of cocaine exposure on maternal and child aggression, the association between maternal cocaine use and mother–toddler aggression may be indirect via higher maternal psychiatric symptoms, negative affect, or poor infant autonomic regulation at 13 months. Participants consisted of 220 (119 cocaine exposed, 101 non-cocaine exposed) mother–toddler dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher levels of aggression toward their toddlers compared to mothers in the control group. Results from model testing indicated significant indirect associations between maternal cocaine use and maternal aggression via higher maternal negative affect as well as lower infant autonomic regulation at 13 months. Although there were no direct associations between cocaine exposure and toddler aggression, there was a significant indirect effect via lower infant autonomic regulation at 13 months. Results highlight the importance of including maternal aggression in predictive models of prenatal cocaine exposure examining child aggression. Results also emphasize the important role of infant regulation as a mechanism partially explaining associations between cocaine exposure and mother–toddler aggression.

Maternal cocaine use and mother–infant interactions: Direct and moderated associations

This study examined the associations between prenatal cocaine exposure and quality of mother–infant play interactions at 13 months of infant ages. We investigated whether maternal psychological distress and infant reactivity mediated or moderated this association. Participants consisted of 220 (119 cocaine exposed and 101 non-cocaine exposed) mother–infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher negative affect and lower sensitivity toward their infant during play interactions at 13 months, and that their infants were less responsive toward them. Contrary to hypothesis, this association was not mediated by maternal psychological distress or by infant reactivity. However, results for both the cocaine and non-cocaine exposed infants were supportive of a transactional model where lower maternal sensitivity at 1 month was predictive of higher infant reactivity at 7 months, which in turn was predictive of lower maternal warmth/sensitivity at 13 months, controlling for potential stability in maternal behavior. Results also indicated that as hypothesized, infant reactivity moderated the association between maternal cocaine use during pregnancy and maternal warmth/sensitivity at 13 months of age. Cocaine-using mothers who experienced their infants as being more reactive in early infancy were less warm/sensitive toward them in later infancy. Results have implications for parenting interventions that may be targeted toward improving maternal sensitivity among cocaine-using mothers with more reactive infants.

Prenatal cocaine exposure: Effects on mother- and teacher-rated behavior problems and growth in school-age children

In this longitudinal study of prenatal cocaine exposure (PCE), school-age physical and cognitive development and behavioral characteristics were examined, while controlling for other factors that affect child development. At this follow-up phase, children were on average 7.2 years old, and their caregivers were 33.7 years old, had 12.5 years of education, and 48% were African American. During the first trimester, 20% of the women were frequent cocaine users (≥1 line/day). First trimester cocaine exposure predicted decreased weight and height at 7 years. There was no significant relationship between PCE and the cognitive and neuropsychological measures. Third trimester cocaine use predicted more total and externalizing behavior problems on the Child Behavior Checklist (Achenbach, 1991 [3]) and the Teacher Report Form (Achenbach, 1991 [4]), and increased activity, inattention, and impulsivity on the Routh Activity (Routh et al., 1974 [67]) and SNAP scales (Pelham and Bender, 1982 [55]). Children who were exposed to cocaine throughout pregnancy had more mother- and teacher-rated behavior problems compared to children of women who stopped using early in pregnancy or who never used cocaine prenatally. These detrimental effects of PCE on behavior are consistent with other reports in the literature and with the hypothesis that PCE affects development through changes in neurotransmitter systems. These school-age behaviors may be precursors of later adolescent behavior problems.

Effects of prenatal cocaine exposure on infant reactivity and regulation

The purpose of this study was to examine the role of prenatal cocaine exposure and associated risk factors on infant reactivity and regulation at 7 months of infant age. Participants consisted of 167 mother–infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure, who completed the arm restraint procedure at the 7-month assessment (87 cocaine exposed, 80 non-cocaine exposed). We hypothesized that cocaine exposed infants would display higher arousal or reactivity and lower regulation during a procedure designed to arouse anger/frustration. Results indicated that cocaine exposed infants were more reactive to increases in the level of stress from trial 1 to trial 2 but exhibited no change in the number of regulatory strategies as stress increased, unlike the control group infants. Infant birth weight moderated the association between cocaine exposure and infant regulation. Among cocaine exposed infants, those with lower birth weight displayed higher reactivity compared to those with higher birth weight. Contrary to expectations, there were no indirect effects between cocaine exposure and infant reactivity/regulation via environmental risk, parenting, or birth weight. Results are supportive of a teratological model of prenatal cocaine exposure for infant reactivity/regulation in infancy.

Suicidal Ideation Among Urban Nine and Ten Year Olds

Little is known about rates and correlates of suicidal ideation among nonclinical samples of preadolescents from low-income urban backgrounds. Using the Children's Depression Inventory, we measured suicidal ideation in 131 preadolescent urban children (49% female, 90% African American/Caribbean) participating in an ongoing prospective longitudinal study of prenatal cocaine exposure and children's outcome. Suicidal ideation was reported by 14.5% of the children in this sample at 9 to 10 years of age. Children's reports of depressive symptoms, exposure to violence, and distress symptoms in response to witnessing violence were associated with suicidal ideation, but prenatal cocaine exposure, parent-rated child behavior, and caregivers' psychological distress symptoms were not. Suicidal ideation may be more prevalent among preadolescents from urban, low-income backgrounds than clinicians suspect, particularly among children exposed to violence.

Neurological and Developmental Outcomes of Prenatally Cocaine‐Exposed Offspring from 12 to 36 Months

Second generation studies of prenatal cocaine exposure failed to find gross deficits after controlling for confounders. Concern remained that exposure could cause subtle deficits. This prospective, cohort study evaluated effects of cocaine on development at 12, 18, 24, and 36 months. From 1991–1993, 361 mother‐infant pairs were recruited from the Children's Hospital of New York, Presbyterian Medical Center's prenatal clinic or delivery room suite. Mothers were assigned to the cocaine group based on report of prenatal cocaine use or positive urine toxicology. Control mothers were enrolled from the same clinic and matched for age and socioeconomic status (SES). Women with serious medical problems were excluded from either group. Of the retained cohort, at 12 months, 147 infants were exposed and 89 were unexposed case controls. Both groups were raised in impoverished environments with few supports. Developmental evaluations were conducted blinded to group. Cross‐sectional analysis revealed cocaine‐related deficits in neurological exams and speech across all time periods, in spite of catch up in weight, length, and head circumference. Overall analysis of development was evaluated using Generalized Estimating Equations regression analysis. Bayley Mental [Badj = − 6.5 (CI—9.4 − 3.5, p ≤ 0.001)] and Psychomotor [Badj = − 3.9 (CI—7.4, − 0.5, p = 0.02)] Developmental Indices showed deficits after controlling for confounders. Males were more vulnerable to cocaine exposure for height, motor development, and emotional regulation. Dose‐response relationships existed for abnormal neurological exams (ptrend < 0.08), Mental Development Index (MDI) (ptrend < 0.001), and Psychomotor Development Index (PDI) (ptrend < 0.001) deficits. Although nonexposed children performed poorly, cocaine‐exposed children showed worse performance. Both groups showed declines at 18 months in mental and psychomotor development from which only nonexposed children rebounded. Overall, cocaine exposure adds an additional risk to disadvantaged children's development. Cocaine‐exposed children are less resilient to effects of these multiple risks.

Do "we just know"? Masked assessors' ability to accurately identify children with prenatal cocaine exposure.

This study evaluated perceptions of masked assessors to determine whether there are subtle differences in cocaine-exposed and unexposed children who might be identified by those interacting with children. As part of a longitudinal study, developmental assessors were masked to 163 4-year-old children's actual in utero cocaine exposure status and developmental history. After each battery, assessors documented their guesses of the child's cocaine exposure. Thirty-seven percent of the children who were exposed were misclassified as unexposed, whereas 74% of those unexposed were incorrectly classified as exposed. Although the sample did not differ on assessment scores when results were analyzed by actual cocaine exposure status ( >.3), children who did less well on assessments were more likely to be labeled by assessors as cocaine-exposed ( <.001). Results highlight the potential of stereotyping and negative attributions that might distort observations, both in unmasked studies of prenatal cocaine exposure and in clinical settings.

Cocaine exposure and developmental outcome from birth to 6 months

The theoretical framework for many of the early studies of prenatal cocaine exposure has been rooted in the basic concepts of teratology/developmental toxicology. Few have published longitudinal analyses of the complex interplay between the relative effects of prenatal cocaine exposure and perinatal and environmental factors on development. The purpose of this paper was to use structural equation modeling to describe the direct and indirect effects of prenatal drug exposure on developmental outcome from birth to age 6 months. Key variables considered for study include prenatal drug exposure, perinatal medical characteristics, maternal/caregiver/family characteristics, the home environment, and neurobehavioral outcomes. We prospectively enrolled 154 predominantly crack-using women. A priori exclusion criteria included: <18 years old, major illnesses diagnosed prior to pregnancy, chronic use of legal drugs, and any use of illicit drugs other than cocaine and marijuana. From the pool of noncocaine users, 154 subjects were matched to users on pregnancy risk, parity, race, and socioeconomic status. At the end of each trimester, experienced staff conducted private interviews prompting memory of amount and timing of past drug use. Urine specimens were collected at two unanticipated times; positive screens were confirmed by gas chromatography/mass spectroscopy. Measures analyzed include medical (birth) and developmental (birth, 1 month, 6 months) assessments, all performed by blinded evaluators, as well as caregiver characteristics and environmental factors (birth, 1 month). A series of four theoretical models was tested, one for each time point (birth, 1 month, 6 months) and a longitudinal model spanning birth to 6 months. Key findings include direct effects of prenatal cocaine exposure on development at birth in the birth model and on development at birth and 6 months in the longitudinal model. In addition, indirect effects of prenatal cocaine exposure were identified on development at birth, 1 month, and 6 months, mediated through the prenatal use of alcohol and tobacco and the birth head circumference. Implications of these and other findings, including the advantages and limitations of structural equation modeling, are discussed.

Studies of Prenatal Cocaine Exposure: Assessing the Influence of Extraneous Variables

Using data from a longitudinal study of prenatal cocaine exposure, we demonstrate that women who use cocaine during pregnancy differ in demographic, substance use, and environmental characteristics from women who do not use cocaine. Each of these characteristics affects the child's development independent of cocaine exposure, and it is not appropriate to draw conclusions regarding the effects of cocaine use per se without taking into consideration the ways in which women who use cocaine differ from women who do not use. We present statistical examples where the effect of prenatal cocaine use was not significant after control for extraneous variables and examples where the effects remained significant after control. Thus, it is necessary to identify which variables are extraneous variables and to explore the effects of these variables on the findings. Failure to control for these variables can lead to inaccurate conclusions regarding the effects of prenatal cocaine exposure.

Prenatal Coke: What's Behind the Smoke?: Prenatal Cocaine/Alcohol Exposure and School-Age Outcomes: The SCHOO-BE Experiencea.

Despite media reports and educators' concerns, little substantive data have been published to document or refute the emerging reports that children prenatally exposed to cocaine have serious behavioral problems in school. Recent pilot data from this institution have indeed demonstrated teacher-reported problem behaviors following prenatal cocaine exposure after controlling for the effects of prenatal alcohol use and cigarette exposure. Imperative in the study of prenatal exposure and child outcome is an acknowledgment of the influence of other control factors such as postnatal environment, secondary exposures, and parenting issues. We report preliminary evaluation from a large ongoing historical prospective study of prenatal cocaine exposure on school-age outcomes. The primary aim of this NIDA-funded study is to determine if a relationship exists between prenatal cocaine/alcohol exposures and school behavior and, if so, to determine if the relationship is characterized by a dose-response relationship. A secondary aim evaluates the relationship between prenatal cocaine/alcohol exposures and school achievement. Both relationships will be assessed in a black, urban sample of first grade students using multivariate statistical techniques for confounding as well as mediating and moderating prenatal and postnatal variables. A third aim is to evaluate the relationship between a general standardized classroom behavioral measure and a tool designed to tap the effects thought to be specific to prenatal cocaine exposure. This interdisciplinary research team can address these aims because of the existence of a unique, prospectively collected Perinatal Database, funded in part by NIAAA and NICHD. The database includes repeated measures of cocaine, alcohol, and other substances for over 3,500 births since 1986. Information from this database is combined with information from the database of one of the largest public school systems in the nation. The final sample will be composed of over 600 first grade students for whom the independent variables, prenatal cocaine/alcohol exposures, were prospectively assessed and quantified at the university maternity center. After informed consent, the primary dependent variable, school behavior, is assessed, using the PROBS-14 (a teacher consensus developed instrument), the Child Behavior Check List, and the Conners' Teacher Rating Scale. The secondary dependent measure, school achievement, is measured by the Metropolitan Achievement Text and the Test of Early Reading Ability. Control variables, such as the environment and parenting, are measured by several instruments aimed at capturing the child and family ecology since birth. All analyses will be adjusted as appropriate for prospectively gathered control variables such as perinatal risk, neonatal risk, and other prenatal drug and cigarette exposures. Further adjustment will be made for postnatal social risk factors which may influence outcome. Of particular concern are characteristics of the home (adaptation of HOME), parent (depression, stress), and neighborhood (violence exposure). Finally, postnatal exposure to lead and other drugs is being considered.

Longitudinal Growth Patterns in Cocaine-Exposed Children † 1132

Almost all studies of prenatal cocaine exposure document negative growth effects on the fetus. Few studies report a dose-response relationship or report data beyond birth. We report growth data from birth-18 months on children participating in a longitudinal study of the effects of prenatal cocaine exposure. Women were prospectively enrolled from rural health departments as they came in for prenatal care or arrived at the hospital for delivery. Of 2,526 women approached, 85% consented to the study's interviews and urine screens, from which 154 were identified as cocaine users and matched on prenatal risk, race, parity, and socioeconomic status to 154 consenters verified as non-users. Women were >18 y/o, had no prenatally diagnosed chronic illness, no use of other illicit drugs except marijuana, and no chronic use of prescription drugs or other medications. Urine toxicology screening was done at two unanticipated times. Histories were taken at the end of each trimester and along with child growth measures at 1, 6, 12, 18, 24, and 36 months of age. Cocaine use was quantified using drug history. Four categories of use were analyzed: high (≥ $2/day), low, non-admitters (urine+;history -), and non-users. Analyses based on amount of drug usage used one-way ANOVA with comparison of means using a Multiple F Test. Analyses of growth, adjusting for prenatal exposure to alcohol, nicotine, and marijuana, race, gender, gestational age, and time were made using multiple regression with two-way interaction terms for all the variables. At birth, cocaine was significantly related to lower WT and smaller HC. The non-admitters differed significantly from the non-users with lower WT and smaller HC and from the high users with smaller HC. By 1 month, cocaine no longer had a significant effect on WT or HC. There was no relationship between cocaine exposure and growth from birth to 18 months, however alcohol had strong, significant effects on WT and LT. Our study shows catch-up growth in WT for the cocaine-exposed infants by 1 month of age. Unlike previous studies, we demonstrated catch-up growth in HC by 1 month, as well. We were unable to show a relationship between amount of cocaine exposure and growth. These findings are meaningful given our low attrition, resulting in a sample size large enough to show differences if they existed, and provide guarded optimism for the outcome of these children.

New evidence for neurobehavioral effects of in utero cocaine exposure

Most studies of prenatal cocaine exposure have found gestational age or intrauterine growth deficits but few, if any, cognitive effects. In a large, well-controlled study we detected cognitive deficits in relation to heavy cocaine exposure. These findings demonstrate that prenatal exposure to cocaine at sufficiently high doses early in pregnancy has the potential to produce cognitive changes in infants and that more focused, narrow-band tests may be necessary to detect these subtle neurobehavioral effects. A total of 464 inner-city, black infants whose mothers were recruited prenatally on the basis of pregnancy alcohol and cocaine use were tested at 6.5, 12, and 13 months of age. Standard analyses, based on presence or absence of cocaine use during pregnancy, confirmed effects on gestational age but failed to detect cognitive effects. A new approach to identifying heavy users found that heavy exposure early in pregnancy was related to faster responsiveness on an infant visual expectancy test but to poorer recognition memory and information processing, deficits consistent with prior human and animal findings. These persistent neurobehavioral effects of heavy prenatal cocaine exposure appear to be direct effects of exposure and independent of effects on gestational age. (J P EDIATR 1996;129:581-90)

Mothers, babies, and cocaine: the role of toxins in development

Contents: C.L. Jones, Foreword. Preface. Part I:Models. D.L. Dow-Edwards, Developmental Toxicity of Cocaine: Mechanisms of Action. B.M. Lester, K. Freier, L. LaGasse, Prenatal Cocaine Exposure and Child Outcome: What Do We Really Know? B. Weiss, Incipient Hazards of Cocaine: Lessons from Environmental Toxicology. D.E. Hutchings, A.C. Zmitrovich, Methadone During Pregnancy: A Brief Review of Clinical Outcome and a New Animal Model. Part II:Methods. C.V. Vorhees, A Review of Developmental Exposure Models for CNS Stimulants: Cocaine. D.R. Neuspiel, The Problem of Confounding in Research on Prenatal Cocaine Effects on Behavior and Development. J.L. Jacobson, S.W. Jacobson, Strategies for Detecting the Effects of Prenatal Drug Exposure: Lessons from Research on Alcohol. H.C. Olson, T.M. Grant, J.C. Martin, A.P. Streissguth, A Cohort Study of Prenatal Cocaine Exposure: Addressing Methodological Concerns. M. Bendersky, S.M. Alessandri, M.W. Sullivan, M. Lewis, Measuring the Effects of Prenatal Cocaine Exposure. E.M. Ostrea, Jr., Meconium Drug Analysis. Part III:Outcomes. L.P. Spear, Alterations in Cognitive Function Following Prenatal Cocaine Exposure: Studies in an Animal Model. R. Needlman, D.A. Frank, M. Augustyn, B.S. Zuckerman, Neurophysiological Effects of Prenatal Cocaine Exposure: Comparison of Human and Animal Investigations. L.C. Mayes, M.H. Bornstein, Developmental Dilemmas for Cocaine-Abusing Parents and Their Children. S.M. Alessandri, M.W. Sullivan, M. Bendersky, M. Lewis, Temperament in Cocaine-Exposed Infants. L. Beckwith, S. Crawford, J.A. Moore, J. Howard, Attentional and Social Functioning of Preschool-Age Children Exposed to PCP and Cocaine in Utero. N.S. Woods, M. Behnke, F.D. Eyler, M. Conlon, K. Wobie, Cocaine Use Among Pregnant Women: Socioeconomic, Obstetrical, and Psychological Issues. Part IV:Intervention. A. Baxter, L.S. Butler, R.P. Brinker, W.A. Frazier, D.M. Wedgeworth, Effective Early Intervention for Children Prenatally Exposed to Cocaine in an Inner-City Context. T. Field, Cocaine Exposure and Intervention in Early Development.

A longitudinal study of prenatal cocaine exposure: 3-year outcome

A longitudinal study of prenatal cocaine exposure: 3-year outcome