Adverse effects of fetal cocaine exposure on neonatal auditory informationprocessing

Background. Studies with animals have shown that in utero exposure to cocai ne interferes with fetal brain development by disrupting the processes of n euronal proliferation, differentiation, and migration, often leading to sub sequent neurobehavioral deficits. However, studies with humans have produce d inconsistent findings. Although neurobehavioral abnormalities have been o bserved among cocaine-exposed infants in several studies and in some cases dose-response effects have been found, the specific neurobehaviors affected vary from one study to the next. Researchers studying the effects of fetal cocaine-exposure are faced with many difficult challenges. For example, wo men who use cocaine typically use other substances in addition to cocaine, many of the methods available for identifying cocaine-exposed neonates are not reliable, and the available methods for assessing cocaine-exposed newbo rns may not be sufficiently sensitive to detect the subtle effects of cocai ne on the developing central nervous system. Despite these difficulties, th ere is a growing body of research that suggests that fetal cocaine exposure is associated with subsequent language deficits among children exposed in utero. However, it is virtually impossible to disentangle the effects of th e impoverished environments in which these children are often raised from t he effect, if any, of fetal cocaine exposure. To determine the effects of f etal cocaine exposure independent of postnatal environmental effects, cocai ne-exposed neonates would ideally be tested within the first few weeks of b irth, and to identify early risks for subsequent language delay, well-resea rched auditory information processing measures could be used. Objective. The purpose of the present study was to assess the effects of fe tal cocaine exposure on neonatal auditory information processing ability. T o overcome limitations of some previous studies on the neuroteratogenic eff ects of cocaine, such as unreliable subject identification techniques, inad equate control over confounding variables, and questionable measures of cen tral nervous system integrity, a valid measure of auditory information proc essing was used in a rigorous, case-control design. Method. Newborn information processing was assessed using habituation and r ecovery of head-turning toward an auditory stimulus across the 3 phases of the procedure: familiarization, novelty, and dishabituation. During the fam iliarization phase, the infant orients and habituates to a repeated word; d uring the novelty phase, the infant recovers head-turning to a novel word a nd subsequently habituates to this word; and during the dishabituation phas e the infant displays renewed head-turning to the return of the original st imulus. Testing takes similar to 20 minutes. This procedure has been shown previously to discriminate among infants at high-, moderate-, and low-risk for subsequent developmental delay. Twenty-five cocaine-exposed and 25 none xposed control neonates, identified by meconium analysis, urine analysis, a nd/or maternal self-report, were tested on the auditory information process ing procedure. The majority of infants were tested within the first few day s of birth. Cocaine-exposed and control neonates were matched on birth weig ht, gestational age, Apgar scores, age at testing, and socioeconomic status as reflected by household income. Mothers were matched on age, weight gain , cigarette smoking, and alcohol consumption. Results. Fetal cocaine exposure was associated with impaired auditory infor mation processing. Both cocaine-exposed and nonexposed control neonates ori ented to the familiarization stimulus, but cocaine-exposed neonates display ed impaired habituation. Moreover, cocaine-exposed neonates did not recover or habituate to the novel stimulus or dishabituate to the return of the fa miliarization stimulus. Whereas nonexposed, control infants exhibited high levels of turning away from the familiarization stimulus during habituation (implying boredom), followed by high levels of turning toward the novel st imulus, indicating recovery of attention, the cocaine-exposed infants turne d randomly. Clearly, auditory information processing of cocaine-exposed inf ants was impaired, despite the fact that they exhibited the same overall nu mber of head-turns and the same high level of positive state as the nonexpo sed infants. Conclusions. The results imply that cocaine is a neuroteratogenic agent tha t impairs auditory information processing ability during the newborn period . Cocaine-exposed neonates exhibited a response pattern that is consistent with slower speed of auditory information processing. These deficits were o bserved within the first few days of birth, before adverse postnatal enviro nmental influences could exert their effect. Moreover, the case-control des ign increased the probability that the observed information processing defi cits were due primarily to the direct effects of fetal exposure to cocaine and not other prenatal factors. However, the long-term implications of thes e findings for the development of the infant/child are not known and must b e addressed in follow-up studies.