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Foundational Research

Prenatal Cocaine Exposures and Dose-Related Effects on Infant Tone and Behavior

Chiriboga CA, Kuhn L, Wasserman GA. Neurotoxicol Teratol. 
First Published: 08 December 2006 DOI: 10.1016/


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In experimental models, prenatal cocaine exposure has been found to perturb monoaminergic development. In humans, numerous studies have sought clinical correlates, but few have focused on dose-related effects, especially as regards neurologic function beyond the neonatal period.


To assess whether prenatal cocaine exposure has adverse effects on infant neurologic, developmental, and behavioral outcomes and whether any effects are dose-dependent.


Infants (398) were enrolled at birth from an urban hospital. Drug exposure was ascertained with biomarkers in hair (n=395), urine (n=170), and meconium (n=109). Children were followed prospectively, and 286 (72%) were evaluated blind to drug exposure at 6 months of age with the Bayley scales, Fagan Scale of Infant Intelligence, and a standardized neurological examination.


Specific neurological findings increased significantly by the amount of cocaine detected in maternal hair, e.g., abnormality of tone, as indicated by extensor posture, was detected among 28% of cocaine-unexposed infants, 43% of infants exposed to lower and 48% exposed to higher cocaine levels in maternal hair (p<0.009). Persistent fisting increased in a similar dose-dependent manner. These associations persisted in adjusted analyses. Prenatal cocaine exposure was not associated with developmental scores (mental, motor, or novelty preference) but was associated with lower orientation scores in adjusted analyses.


At 6 months of age, prenatal cocaine exposure was associated with abnormalities of tone and posture and with lower orientation scores. Perturbations in monoaminergic systems by cocaine exposure during fetal development may explain the observed neurological and behavioral symptoms. Whether such findings in infancy increase the risk of later neurobehavioral problems requires further study.

Keywords: perinatal, cocaine exposure, drug use, hypertonia, child development


Although cocaine use has declined since the height of the epidemic in the 1980s, it remains a major public health problem in urban centers in the United States, where a high level of use continues. Earlier studies of in-utero cocaine-exposed infants, which exaggerated risks to exposed offspring, were limited by a lack of controlled analyses and by the lack of biological markers that quantified exposure in a cumulative manner (i.e., meconium or hair analyses). Over the last 10 years, numerous controlled studies have identified developmental and behavioral differences associated with prenatal cocaine exposure. Developmental delays linked with prenatal cocaine exposure have included cognitive differences and language delays. Motor delays are the most consistently reported finding among cocaine-exposed children, with prenatal cocaine exposure predicting poorer fine motor development skills at age 2, particularly in hand use and eye-hand coordination. Others, however, have failed to identify developmental or cognitive effects associated with prenatal cocaine exposure after controlling for confounders.

From a behavioral perspective, a convergence of experimental and clinical studies suggests that prenatal cocaine exposure disrupts the development of arousal and attention. Cocaine-exposed infants exhibit a preference for higher rates of stimuli, excessive irritability and dose-related perturbations in orientation and state regulation. Exposed toddlers and grade school children show differences in task persistence and sustained attention, problems with impulse control, temperamental differences, and aggressive/hyperactive behaviors.

A handful of studies have prospectively assessed neurological function among cocaine-exposed children beyond the newborn period, and even fewer have quantified fetal exposure. Lewis et al. describe higher rates of a suspect or abnormal neurological examination among cocaine-exposed toddlers, but the authors did not further define the nature of neurological abnormalities. Others have described muscle tone abnormalities, hypertonia in particular, among cocaine-exposed infants and toddlers. We described hypertonia among infants at risk for HIV with cocaine exposure that resolved by 24 months but was unable to control for confounding exposures, especially tobacco exposure, which has been linked to hypertonus.

The current study was designed to assess the effect of cocaine exposure on neurological, developmental, and behavioral outcomes. The primary hypothesis was that children with prenatal cocaine exposure would exhibit higher rates of neurological, developmental, and behavioral impairments compared to cocaine-unexposed children of comparable demographic backgrounds after controlling for confounding factors. We also hypothesized that risks would be dose-dependent with higher rates of abnormalities observed with higher levels of cocaine exposure. We report on the neurologic, developmental, and behavioral outcomes of infants enrolled prospectively at delivery in a longitudinal study in whom prenatal exposure to cocaine and other drugs of abuse was determined at the time of birth with multiple biomarkers.


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