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

Three-dimensional (3D) brain organoids derived from human pluripotent stem cells (hPSCs), including embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), appear to recapitulate the brain’s 3D cytoarchitectural arrangement and provide new opportunities to explore disease pathogenesis in the human brain. Human iPSC (hiPSC) reprogramming methods, combined with 3D brain organoid tools, may allow patient-derived organoids to serve as a preclinical platform to bridge the translational gap between animal models and human clinical trials. Studies using patient-derived brain organoids have already revealed novel insights into molecular and genetic mechanisms of certain complex human neurological disorders such as microcephaly, autism, and Alzheimer’s disease. Furthermore, the combination of hiPSC technology and small-molecule high-throughput screening (HTS) facilitates the development of novel pharmacotherapeutic strategies, while transcriptome sequencing enables the transcriptional profiling of patient-derived brain organoids. Finally, the addition of CRISPR/Cas9 genome editing provides incredible potential for personalized cell replacement therapy with genetically corrected hiPSCs. This review describes the history and current state of 3D brain organoid differentiation strategies, a survey of applications of organoids towards studies of neurodevelopmental and neurodegenerative disorders, and the challenges associated with their use as in vitro models of neurological disorders.

/pdf/3d-brain-organoids-derived-from-pluripotent-stem-cells-3k1wtygs4g.pdf

3D brain Organoids derived from pluripotent stem cells: promising experimental models for brain development and neurodegenerative disorders.

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.

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

Background. Studies of fetal cocaine exposure and newborn neurologic function have obtained conflicting results. Although some studies identify abnormalities, others find no differences between cocaine-exposed and cocaine-unexposed infants. To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function in infants, we prospectively evaluated 253 infants shortly after birth. Methods. Women who delivered a live singleton >36 weeks by dates were eligible for enrollment. Maternal exclusionary criteria were known parenteral drug use, alcoholism, and acquired immunodeficiency syndrome; infant exclusionary criteria were Apgar scores ≤4 at 5 minutes, obvious congenital malformations, seizures, or strokes. A total of 98% of infants were evaluated between 1 to 7 days of age. Newborns were assessed with the Neurological Examination for Children (NEC) by a pediatric neurologist (C.A.C.) who was blinded to exposure status. Gestational age was determined by Ballard9s examination. Cocaine exposure was determined for the last trimester by radioimmunoassay of maternal hair (RIAH). Exposure values ranged from 2 to 4457 ng/10 mg hair. Infants were excluded if a maternal hair sample was missing ( N = 13). The sample comprises 240 woman and infant pairs—104 cocaine-exposed and 136 cocaine-unexposed. Results. Compared with unexposed controls, cocaine-exposed infants exhibited higher rates of intrauterine growth retardation (24% vs 8%), small head circumference ([HC] 2 for trend); 1.0, 3.3, and 4.3 for global hypertonia (χ 2 for trend); 1.0, 3.4, and 7.4 for extensor leg posturing (χ 2 for trend); and 1.0, 3.8, and 3.8 for coarse tremor (χ 2 for trend). Significant associations between cocaine exposure and neurologic signs were found in logistic regression equations that controlled for 20 or more variables. Conclusion. We conclude that adverse neonatal effects associated with fetal cocaine exposure follow a dose–response relationship: newborns with higher levels of prenatal cocaine exposure show higher rates of impairments in fetal head growth and abnormalities of muscle tone, movements, and posture. Significant relationships between cocaine exposure and these outcomes remain in controlled analyses.

Dose–Response Effect of Fetal Cocaine Exposure on Newborn Neurologic Function

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

Dose–Response Effect of Fetal Cocaine Exposure on Newborn Neurologic Function