Objective To identify associations between cocaine exposure during pregnancy and medical conditions in newborn infants from birth through hospital discharge. Design Multisite, prospective, randomized study. Setting Brown University, University of Miami, University of Tennessee (Memphis), and Wayne State University. Subjects A total of 717 cocaine-exposed infants and 7442 nonexposed infants. Main Outcome Measures Results of physical examination and conditions observed during hospitalization. Results Cocaine-exposed infants were about 1.2 weeks younger, weighed 536 g less, measured 2.6 cm shorter, and had head circumference 1.5 cm smaller than nonexposed infants (allP Conclusions Central and autonomic nervous system symptoms were more frequent in the exposed cohort and persisted in an adjusted analysis. They were usually transient and may be a true cocaine effect. Abnormal anatomic outcomes previously reported were not confirmed. Increased infections, particularly sexually transmitted diseases, pose a serious public health challenge. Exposure increased involvement of child protective services and out-of-home placement.

https://jamanetwork.com/journals/jamapediatrics/articlepdf/486109/poa50029.pdf

Acute Neonatal Effects of Cocaine Exposure During Pregnancy

BackgroundAlcohol and drug use by pregnant women are harmful to the developing embryo and fetus. Teasing apart the specific contributions of each substance to adverse child outcome, however, proves difficult in practice. The risks to the neonate include intrauterine growth retardation, birth defects

Fetal alcohol and drug effects.

Objective. This article was designed to investigate effects of prenatal cocaine exposure on motor development of young children from a predominately underprivileged, urban population. Methodology. A total of 260 infants and young children were initially recruited from either the newborn nursery or the at-risk pediatric clinic of an urban teaching hospital. Prenatal history and birth outcomes were collected from medical records. Demographic characteristics and additional drug histories were obtained from the mothers. The 199 subjects (98 cocaine-exposed and 101 unexposed) who returned at age 2 years were assessed by examiners blinded to drug exposure status using the Peabody Developmental Motor Scales. Results. Compared with control subjects, the cocaine-exposed group performed significantly less well on both the fine and the gross motor development indices. Mean scores for both groups were within the average range on the gross motor index, but greater than 1 standard deviation below average on the fine motor index. Differences were significant on the balance and the receipt and propulsion subscales of the gross motor scale, and on the hand use and the eye–hand coordination subscales of the fine motor scale. Cocaine status independently predicted poorer hand use and eye–hand coordination scores. There also was an effect of alcohol exposure on the receipt and propulsion subscale. Conclusions. Findings indicate that deficiencies in motor development remain detectable at 2 years of age in children exposed to drugs prenatally. Although other environmental variables may influence motor development, children exposed to cocaine and to alcohol in utero may encounter developmental challenges that impede later achievement.

Motor Development of Cocaine-exposed Children at Age Two Years

Background Behavioral teratology, particularly as it is applied to the evaluation of cognition and behavior of children beyond the toddler stage, has become an area of burgeoning activity. In the area of drug abuse, children exposed in utero are often at developmental peril because of non-drug pre- and postnatal risk factors that make a causal association between the drug of interest and a behavioral teratogenic outcome increasingly problematic as the child gets older. Methods In the first portion of this review, the strategies that behavioral teratologists have undertaken to investigate the putative consequences of in utero exposure are discussed in terms of research design, statistical methods and interpretative approaches. In the second part of the paper, the relatively limited literature dealing with the behavioral teratological consequences of prenatal marihuana exposure, particularly in school age offspring, is reviewed. Results An emergent theme arising from primarily two longitudinal investigations is that in utero cannabis exposure does not impact upon standardized derived IQ scores but is negatively associated with attentional behavior and visual analysis/hypothesis testing. These findings are interpreted as supporting the hypothesis that, among offspring beyond the toddler stage, prenatal marihuana exposure has a negative influence on aspects of executive function. Executive function is a 'top-down', multifaceted cognitive construct involved in organizing and integrating specific cognitive and output processes over a interval of time and is largely mediated by the late developing, prefrontal region of the brain. Conclusions The results and the interpretation of the prenatal marihuana findings are discussed in terms of the behavioral teratogenic effects (or lack of effects) during the various developmental stages of the offspring, the non-unitary nature of executive function, cannabis receptors, and the consequences of chronic marihuana use in the non-pregnant population.

Conceptual issues in behavioral teratology and their application in determining long-term sequelae of prenatal marihuana exposure.

The adult use of cocaine and nicotine has been linked to depression and/or anxiety. Changes in emotional behavior were assessed using behavioral paradigms developed as animal analogs of psychiatric disorders in 12-14 month old Sprague-Dawley rats exposed daily on gestational days 8-20 to cocaine and nicotine, either alone or in combination. Results from the elevated plus maze (EPM), used to assess anxiety-related behaviors, indicated that offspring prenatally exposed to either high-dose cocaine (40 mg/kg/day) or high-dose nicotine (5.0 mg/kg/day) were less timid/more impulsive. Animals from these two groups spent the most time on the open arms, and had the highest percentage of entries into the open arms of the EPM. Combined in utero exposure to cocaine and nicotine nullified these effects. Cocaine challenge (20 mg/kg) did not interact with prenatal treatment, but increased activity on all arms of the EPM in all groups. Sucrose preference was used as a measure of anhedonia, a cardinal symptom of depressive illness. Reduced sucrose preference was seen only in the group of offspring prenatally exposed to high-dose cocaine (40 mg/kg) plus low-dose nicotine (2.5 mg/kg/day). Exposure to a water-deprivation stress normalized sucrose preference in this group, without altering preference or intake in the other prenatal treatment groups. Transient hyperactivity was seen in the offspring of dams treated with high-dose nicotine, an effect that was again reversed in combined drug groups. Traditional gender differences in activity levels and sucrose intake, that is, females greater than males, were still evident in this population of aging rats. These data indicate that prenatal exposure to cocaine and/or nicotine has long-term effects on emotional behavior. Combined drug exposure contributed to the development of depressive symptoms, but not anxiety-like behavior, in a dose-dependent manner. In contrast, exposure to high doses of either drug alone reduced cautionary behavior. Data from this line of research could provide insight into the pathogenesis of emotional disorders, especially during the aging process.

Prenatal cocaine and/or nicotine exposure produces depression and anxiety in aging rats.

Objective. To assess whether prenatal cocaine exposure has any long-term effects on neuro-development. Design. A prospective cohort study with examiners blind to drug exposure and human immunodeficiency virus (HIV) status. Subjects. Of 144 high-risk infants enrolled in a perinatal HIV neurodevelopmental study, 119 (83%) infants with both neurological and urine toxicology measures were followed up to age 24 months. Methods. Neurological and developmental assessments were analyzed at 6-month intervals grouped according to the presence of cocaine in urine toxicology: 51 infants were cocaine-positive. Adjusted odds ratios (ORs) and 95% confidence interval (CI) were obtained by logistic regression equations that adjusted for perinatal variables, including measures of fetal growth, gestation, HIV status, and infant toxicology results. Setting. Harlem Hospital Center from 1988 to 1992. Results. At age 6 months, 21 of 51 (41%) cocaine-positive children exhibited hypentonia of any type (hypertonic tetraparesis, hypertonic diparesis, and hypertonic hemiparesis) compared with 17 of 68 (25%) cocaine-negative infants (OR = 2.1, CI = 1.0-4.6). Cocaine-positive infants were four times more likely to show hypertonic tetraparesis (HTP) than cocaine-negative infants (OR = 4.0; CI = 1.5-10.8). The association remained significant in multivariate analyses. Hypertonia, consistent with cerebral palsy, diminished over time in both groups. In 97% of affected infants hypertonia resolved by 24 months. Arm hypertonia abated first; leg hypertonia remained in some children up to age 18 months. No differences in development scores between cocaine-positive and cocaine-negative were noted at any age interval. However, among cocaine-positive infants those with early HTP showed significantly lower mean developmental scores at 6 and 12 month compared to infants without HTP. Conclusion. Cocaine positivity urine toxicology at birth is associated with hypertonia during infancy. Such cocaine-induced effects are usually symmetrical, transient, and the majority of exposed children outgrow hypertonia by 24 months of life. Among cocaine-positive infants, HTP may be a marker for later developmental impairments.

Neurological Correlates of Fetal Cocaine Exposure: Transient Hypertonia of Infancy and Early Childhood

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Neurological Correlates of Fetal Cocaine Exposure: Transient Hypertonia of Infancy and Early Childhood