Neurobehavioral deficits in neonatal rhesus monkeys exposed to cocaine in utero.

In spite of significant efforts, the neurobehavioral deficits in infants born from cocaine-abusing mothers have not been clearly defined. In the present study, we examined the presence of these abnormalities in a rhesus monkey model of prenatal cocaine exposure using a nonhuman primate adaptation of the Neonatal Behavioral Assessment Scale (NBAS). Pregnant monkeys (n = 14) received 10 mg/kg cocaine twice a day orally (in fruit treats) from the 40th through 102nd postconception days (PCD40-PCD102), which is the period of cerebral cortical neuronogenesis (approximately second trimester). The control consisted of pregnant monkeys (n = 14) receiving fruit treats only. The animals were allowed to deliver vaginally at term (approximately PCD165). The first testing session was conducted on PCD171 (within the first week after birth); the second testing session was conducted on PCD177 (within the second week after birth); the third test was conducted on PCD183 (within the third week after birth); and the fourth testing session was conducted on PCD189 (within the fourth week after birth). The prenatally cocaine-exposed infants showed deficits in orientation, state control, and motor maturity, which were detectable during the second, third, and fourth testing sessions. The same testing sessions also revealed a significant reduction in the time devoted to toy manipulation, which points to impaired attention. None of these abnormalities were seen during the first testing session. The first session, however, revealed increased tremulousness (one of the indicators of autonomic stability) in the prenatally cocaine-exposed infants. This impairment disappeared by the third testing session. The present findings demonstrate the potential of prenatal cocaine exposure to induce neurobehavioral deficits detectable by NBAS-like testing in primate infants.