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Jonah’s mother was a heroin addict. Shortly after birth, it was obvious Jonah was in withdrawal. His jittery movements and crying persisted for the next 2 days and there was little anyone could do to console him. He scratched his face trying to get his hands to his mouth. His knees and elbows were rubbed raw from his agitated movements, and the muscles in his tiny legs were so stiff that it was difficult to straighten his legs to diaper him.
Source: www.cmiproject.net
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The full extent of the effects of prenatal drug exposure on a child is not known, however studies show that various drugs of abuse may result in premature birth, miscarriage, low birth weight, and a variety of behavioral and cognitive problems.
| Drugs that may have adverse prenatal effects: |
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| Selected Research Findings on the Prenatal Effects of Drug Abuse |
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Prenatal Methamphetamine Use and Neonatal Neurobehavioral Outcome
Neurobehavioral effects of prenatal methamphetamine exposure were examined in this study conducted by Dr. Barry Lester and his colleagues from the Infant Development, Environment and Lifestyle (IDEAL) study. Of 13,808 subjects screened, 1632 were eligible and consented and 166 (n=74 exposed) were enrolled in a longitudinal follow-up. Exposure was determined by meconium assay and self-report with alcohol, marijuana, and tobacco present in both groups. The NICU Network Neurobehavioral Scale (NNNS) was administered within the first 5 days of life. Analyses conducted on NNNS summary scores included exposure group effects, heavy MA use effects, association with frequency of use by trimester, and dose-response relationships with amphetamine metabolites. After adjusting for covariates, exposure to MA was associated with increased physiological stress. Heavy MA use was related to lower arousal, more lethargy, and increased physiological stress. First trimester MA use was related to elevated stress abstinence. Third trimester use was related to poorer quality of movement. Higher level of amphetamine metabolites in meconium was associated with increased CNS stress. Prenatal MA exposure was associated with neurobehavioral patterns of decreased arousal, increased stress, and poor quality of movement. The dose-response relationships may represent neurotoxic effects from MA. Smith, L.M., Lagasse, L.L., Derauf, C., Grant, P., Shah, R., Arria, A., Huestis, M., Haning, W., Strauss, A., Grotta, S.D., Fallone, M., Liu, J., and Lester, B.M., Prenatal Methamphetamine Use and Neonatal Neurobehavioral Outcome. Neurotoxicology and Teratology. Oct 3, 2007 (e-pub ahead of print).
Prenatal Cocaine Exposure, Gender, and Preadolescent Substance Use and Other Health Risk Behaviors
Dr. Michael Lewis and his colleagues 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. Bennett, D., Bendersky, M., and Lewis, M. Preadolescent Health Risk Behavior as a Function of Prenatal Cocaine Exposure and Gender. Journal of Behavioral Pediatrics, 28(6), pp. 467- 472, 2007.
Longitudinal Analysis of the Effects of Prenatal Cocaine Exposure on Growth
Dr. Gale Richardson and her colleagues at the University of Pittsburgh investigated the effects of prenatal cocaine exposure on offspring growth from 1 through 10 years of age using a repeated-measures growth-curve model. 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. This is the first study of the long-term effects of prenatal cocaine exposure to conduct longitudinal growth-curve analyses using four 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. Richardson, G.A., Goldschmidt, L., and Larkby, C. Effects of Prenatal Cocaine Exposure on Growth: A Longitudinal Analysis. Pediatrics, 120(4), pp. e1017-1027, 2007.
Smoking During Teenage Pregnancies and Offspring Behavioral Problems
Dr. Nancy Day and her colleagues at the University of Pittsburgh prospectively examined the relationship between prenatal tobacco exposure (PTE) and child behavior in a birth cohort of 357 offspring of teenage mothers. PTE was defined as any exposure across pregnancy and, in separate analyses, exposure within each trimester. Outcomes included measures of behavior problems, activity, and attention. On average, the children were 6.4 years of age, 48% were females, and 69% were Black. Data on maternal tobacco and other substance use were collected prenatally and postnatally: 46% of the mothers smoked in the first trimester and 58% smoked 6 years later. Child urinary cotinine measured exposure to environmental tobacco smoke (ETS). PTE predicted significantly increased offspring activity; impulsivity; and aggression, externalizing, and total behavior problems in step 1. PTE remained a significant predictor of increased activity when maternal psychological characteristics, home environment, and ETS were added. The results were similar when PTE was examined by trimesters, although later pregnancy tobacco exposure predicted the most behavioral outcomes. In the final model, PTE (all three trimesters) and PTE (second trimester) were significant predictors of increased activity and attention problems, respectively. Other predictors of child behavior included maternal anxiety, depression, hostility, and home environment. ETS was not a significant predictor of child behavior when PTE was considered. Smoking during pregnancy among adolescents is a significant predictor of increased activity and attention problems in their offspring after controlling for covariates in the prenatal and current environments. Smoking cessation interventions are recommended for this population to avoid the effects of PTE on the offspring of pregnant adolescents. This is particularly important because these mothers will likely become pregnant again and many will increase their level of tobacco use as they mature. Cornelius, M.D., Goldschmidt, L., DeGenna, N., and Day, N.L. Smoking During Teenage Pregnancies: Effects on Behavioral Problems in Offspring. Nicotine and Tobacco Research, 9(7), pp. 739-750, 2007.
Impact of Prenatal Cocaine Exposure on Attention and Response Inhibition as Assessed by Continuous Performance Tests
This longitudinal study examined the influence of prenatal cocaine exposure on attention and response inhibition measured by continuous performance tests (CPTs) at ages 5 and 7 years. The sample included 415 children from the Miami Prenatal Cocaine Study (219 cocaine-exposed, 196 non-cocaine-exposed as determined by maternal self-report and infant bioassays). Children were enrolled prospectively at birth and assessed comprehensively through age 7 years. Deficits in attention and response inhibition were estimated in relation to prenatal cocaine exposure using generalized estimating equations within the general linear model. Results indicate cocaine-associated increases in omission errors at ages 5 and 7 as well as increases in response times for target tasks (i.e., slower reaction times) and decreased consistency in performance at age 7. There were no demonstrable cocaine-associated deficits in commission errors. Estimates did not change markedly with statistical adjustment for selected prenatal and postnatal covariates. Evidence supports cocaine-associated deficits in attention processing through age 7 years. Accornero, V.H., Amado, A.J., Morrow, C.E., Xue, L., Anthony, J.C., and Bandstra, E.S. Impact of Prenatal Cocaine Exposure on Attention and Response Inhibition as Assessed by Continuous Performance Tests. Journal of Developmental Behavioral Pediatrics, 28(3), pp. 195-205, 2007.
Resting Cerebral Blood Flow in Adolescents with In Utero Cocaine Exposure
The aim of this study was to explore effects of in utero cocaine exposure on resting cerebral activation patterns in the brains of adolescents. The investigators employed arterial spin labeling (ASL) perfusion functional MRI (fMRI) to measure resting cerebral blood flow (CBF) in two groups of adolescents, one group that had been exposed to cocaine prenatally (N = 25), and one not prenatally-exposed (N = 24). A priori regions of interest of frontal lobe and limbic structures were defined, including the cingulate cortex, caudate, insula, and amygdala. The occipital lobe and thalamus were included as the lower-order sensory processing regions for compassion with the frontal lobe. Perfusion fMRI was combined with optimized voxel-based morphometry, a quantitative morphometric analysis of structural MRI, to compare gray matter between the two groups. Relative to the comparison group, cocaine-exposed adolescents showed significantly reduced global CBF, seen mainly in posterior and inferior brain regions, including the occipital cortex and thalamus. After adjusting for global CBF, a significant increase in relative CBF in cocaine-exposed adolescents was found in anterior and superior brain regions, including the prefrontal, cingulate, insular, amygdala, and superior parietal cortex. The investigators conclude that in utero cocaine exposure may reduce global CBF, which may persist into adolescence. They also point out that the relative increase in CBF in anterior and superior brain regions in cocaine-exposed adolescents suggests that compensatory mechanisms for reduced global CBF may develop during neurodevelopment. Rao, H., Wang, J., Giannetta, J., et al. Altered Resting Cerebral Blood Flow in Adolescents with in Utero Cocaine Exposure Revealed by Perfusion Functional MRI. Pediatrics, 120(5), pp. e1245-1254, 2007.
Prenatal and Adolescent Exposure to Tobacco Smoke Modulates the Development of White Matter Microstructure
Smoking during pregnancy is related to elevated risks of cognitive and auditory processing deficits. Preclinical studies have revealed that disruption in neurodevelopment by exposure to nicotine is likely linked to the disruption of the trophic actions of acetylcholine at nicotinic acetylcholine receptors. This study utilized diffusion tensor anisotropy and anatomical magnetic resonance images to examine white matter microstructure in 67 adolescent smokers and nonsmokers with and without prenatal exposure to maternal smoking. Auditory attention was assessed in all subjects. Adolescents with prenatal and/or adolescent exposure demonstrated increases in regional white matter fractional anisotropy (FA) primarily in anterior cortical and subcortical regions. Increased FA of regions of the internal capsule that contain auditory thalamocortical and corticofugal fibers was associated with adolescent smoking. Performance on the auditory performance task in smokers was positively correlated with FA of the posterior limb of the left internal capsule, but not in nonsmokers. The magnitude of tobacco exposure during adolescence was positively related to the FA of the genu of the corpus callosum further supporting the notion that the effects of nicotine on white matter maturation may be particularly significant during this developmental period. The results suggest that nicotine may disrupt the development of auditory corticofugal fibers which ultimately leads to reduced efficiency in the neurocircuitry that supports auditory processing. Jacobsen, L., Picciotto, M., Heath, C., Frost, S., Tsou, K., Dwan, R., Jackowski, M., Constable, R., and Menel, W. Prenatal and Adolescent Exposure to Tobacco Smoke Modulates the Development of White Matter Microstructure. The Journal of Neuroscience, 27(49) pp. 13491-13498, 2007.
| Relevant NIDA Meetings |
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The National Institute on Drug Abuse (NIDA), in collaboration with the National Institute of Mental Health (NIMH), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the National Institutes of Health Office of Behavioral and Social Sciences Research (OBSSR), the Substance Abuse and Mental Health Services Administration (SAMHSA), and the Administration for Children and Families (ACF) Office of Planning, Research and Evaluation (OPRE) organized Intervening Early: Progress and Opportunities in Child Service Settings meeting, September 18-19, 2007, Gaithersburg, MD. The purpose of this meeting was to review existing prevention programs for children ages 0-5 years and their families that are designed to improve child, parent, and family outcomes in a variety of domains (e.g., parenting, education, family functioning, substance use, mental health), with a particular focus on programs delivered within child service settings. In addition, the speakers discussed opportunities for advancing the science of prevention for young children through the translation of basic research—particularly on self-regulatory processes—into novel interventions, and research on the translation of evidence-based interventions into practice.
NIDA, in collaboration with the American Psychological Association, held the Science of Addiction: Translating New Insights into Better Psychiatric Practice meeting May 19-24, 2007, San Diego, CA. During this meeting, the symposium, Prenatal Nicotine Exposure: How Does it Relate to Developmental Vulnerabilities?, co-chaired by Nicolete Borek and Allison Chausmer, was also held. Impressive advances have been made in examining relationships between prenatal nicotine exposure and developmental vulnerabilities among the exposed offspring. For example, a strong association has been reported between maternal smoking during pregnancy and disruptive behavior disorders in childhood. This symposium: (1) examines associations between prenatal nicotine exposure and neurobiological and behavioral vulnerabilities in the developmental period from birth into adolescence, (2) considers possible mechanisms underlying these relationships, and (3) examines implications of the research for clinical practice. Using focused presentations and interactions between the speakers and the attendees, the symposium addresses multiple developmental outcome areas, reflects findings from clinical and preclinical studies, and includes neurobiological, behavioral, and neuroimaging data. This symposium is intended for individuals with clinical and/or research interest in the effects of prenatal risk factors on the development of clinical disorders.
CAPT Steve Oversby, Psy.D., DPMCDA, convened a workshop on March 8-9, 2007 on Pharmacotherapy Research for the Treatment of In Utero Substance Exposed Neonates: Advances and Future Directions. The workshop brought together experts in the field to develop ideas, concepts, and research questions addressing new pharmacotherapy research for the treatment of in utero substance exposed neonates. Ivan Montoya, M.D., DPMCDA, gave a presentation on "The Public Health Scope of In Utero Drug Exposure" and Jamie Biswas, Ph.D., DPMCDA, gave a presentation on "In Utero Substance Exposure and the Division Portfolio".
Allison Chausmer (NIDA), Cora Lee Wetherington (NIDA), Nicolette Borek (NIDA), Cathy Backinger (NCI) and Michele Bloch (NCI) co-chaired the Drug Abuse Vulnerability and Neurodevelopmental Effects of Early Exposure to Secondhand Tobacco Smoke: Methodological Issues and Research Priorities - Workshop held January 2009, Rockville, MD. The purpose of this one-day workshop was to convene an expert panel to address (1) methodological issues related to the measurement of SHS exposure and (2) the identification of neurodevelopmental effects of early SHS exposure including executive function, problem solving, decision making and early predictors of vulnerability to drug use or abuse, with the ultimate goal of identifying research priorities for the NIH and extramural research communities.
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