These studies are based on the assumption that prenatal cocaine exposure disrupts central arousal mechanisms as manifested through altered state development and postnatal respiratory control and may increase the risk for SIDS. To test these hypotheses, we will evaluate the fetus, newborn, and infant of mothers who abuse cocaine and compare two control populations; a drug and tobacco-free group, and a drug-free but tobacco- using group for the following measures in the fetus, neonate and older infant to 6 months: physical growth (by standard morphometric measures), state development with focus on differentiation, integration, and regulation and respiratory control. Fetal state organization will be assessed by fetal ultrasound. Postnatally, state development will be evaluated behaviorally and by 12 hour overnight polysomnographic recordings for sleep architecture and occurrence of short arousals (defined by behavioral, physiologic, and EEG criteria). Respiratory pattern abnormalities during sleep states will be assessed by evaluating the presence of apnea (central, obstructive, mixed) and periodic breathing with and without desaturations; hypoxic and hypercarbic arousal and ventilatory tests will also be administered. The extent of cardiorespiratory interactions will be examined by estimates of respiratory variation of heart rate. Mothers will be enrolled prenatally and mother-child pairs followed to the child's 6th month. Infant and maternal charts will be reviewed for medical complications that could also influence outcome measures. biological markers for prenatal exposure will be determined by maternal and newborn urine screens and by newborn meconium screens. Intake and subsequent serial interviews will assess known biological and caregiving confounders of cocaine use as well as add to our ability to address pattern and timing of cocaine use. These studies will increase our understanding of prenatal cocaine exposure effects on respiration and state development. Another benefit may be identification of early fetal and neonatal markers of risk making possible early interventions for these and other high risk infants.
| Zeskind, Philip Sanford; Gingras, Jeannine L (2006) Maternal cigarette-smoking during pregnancy disrupts rhythms in fetal heart rate. J Pediatr Psychol 31:5-14 |
| Gaultney, Jane F; Gingras, Jeannine L; Martin, Mindy et al. (2005) Prenatal cocaine exposure and infants' preference for novelty and distractibility. J Genet Psychol 166:385-406 |
| Gaultney, Jane F; Gingras, Jeannine L (2005) Fetal rate of behavioral inhibition and preference for novelty during infancy. Early Hum Dev 81:379-86 |
| Gingras, J L; Mitchell, E A; Grattan, K E (2005) Fetal homologue of infant crying. Arch Dis Child Fetal Neonatal Ed 90:F415-8 |
| Gingras, J L; Mitchell, E A; Grattan, K J et al. (2004) Effects of maternal cigarette smoking and cocaine use in pregnancy on fetal response to vibroacoustic stimulation and habituation. Acta Paediatr 93:1479-85 |
