Neurological correlates of fetal cocaine exposure.
Cocaine is a highly psychoactive substance with numerous effects that readily crosses the placenta, achieving variables levels in the fetus. Determining whether prenatal exposure to cocaine and its metabolites damages the developing human nervous system is hindered by the multiple intervening factors (confounders) that plague clinical settings, which warrant consideration in controlled studies. Prenatal cocaine exposure has been linked to numerous adverse neonatal outcomes, affecting fetal growth (i.e., low birth weight, intrauterine growth retardation, and small head size) and neurobehavior. These neurobehavior effects span the gamut from no abnormalities to impairments in arousal, neurological function, neurophysiological function, and state regulation. Strokes and possibly seizures are also noted. Dose-response effects of fetal cocaine exposure on fetal growth and neonatal neurobehavior are reported using quantitative methods of ascertainment. In early infancy, irritability and hypertonia are also described. Most cocaine associations are transient and resolve in infancy and early childhood. Whether such transient abnormalities place infants at increased risk for later neurodevelopmental impairments is not known. Controlled studies have found no cognitive differences related to prenatal cocaine exposure among toddlers or school age children, except as mediated through effects on head growth. Anecdotally, cocaine-exposed children seem to suffer from neurobehavioral abnormalities, but to date controlled studies have not established an association between cocaine and behavioral disorders, except for inattentiveness. Despite encouraging reports, the question of whether cocaine exerts long-term adverse effects on the developing human nervous system has not yet been resolved, largely because of the limitations of existing studies that rely on inadequate, mostly qualitative ascertainment of cocaine exposure as well as the dearth of studies in older children. Such methodological limitations may have compromised our ability to identify cocaine-exposed children at most risk.
Chiriboga
C A
CA
Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA. cac3@columbia.edu
D003042:Cocaine / Q000009:adverse effects / Q000493:pharmacokinetics; D002658:Developmental Disabilities / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D005317:Fetal Growth Retardation; D005333:Fetus / Q000187:drug effects*; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D008431:Maternal-Fetal Exchange; D001523:Mental Disorders / Q000209:etiology / Q000503:physiopathology*; D010920:Placenta / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
D003042:Cocaine