Effects of maternal cigarette smoking and cocaine use in pregnancy on fetal response to vibroacoustic stimulation and habituation
Article first published online: 2 JAN 2007
Volume 93, Issue 11, pages 1479–1485, November 2004
How to Cite
Gingras, J., Mitchell, E., Grattan, K. and Stewart, A. (2004), Effects of maternal cigarette smoking and cocaine use in pregnancy on fetal response to vibroacoustic stimulation and habituation. Acta Paediatrica, 93: 1479–1485. doi: 10.1111/j.1651-2227.2004.tb02633.x
- Issue published online: 2 JAN 2007
- Article first published online: 2 JAN 2007
- Received Mar. 4, 2004; revision received May 25, 2004; accepted June 10, 2004
- auditory stimulation;
Background: Cigarette smoking and cocaine use in pregnancy are common in the US and both are risk factors for sudden infant death syndrome (SIDS). Although the cause of SIDS is not known, one postulated mechanism involves abnormalities of arousal and arousal regulation. Cigarette smoking and cocaine use may cause deficits of arousal. Many believe arousal deficits occur prenatally. Aims: The aim of this study was to assess the effects of cigarette smoke and cocaine exposure during pregnancy on measures of fetal arousal and arousal competency: 1) the fetal response to vibroacoustic stimulation (VAS) and 2) habituation to VAS. Hypothesis: Maternal cigarette smoking and cocaine use in pregnancy are associated with altered arousal and arousal regulation in the fetus. Methods: Three groups of mother-fetal dyads were enrolled: 1) cigarette smokers (n= 54), 2) cocaine users (n= 30), and 3) controls (n= 60). One hundred eight fetuses were tested at 29–31 wk gestation, 119 at 32–35 wk, and 118 at 36+ wk. The fetal response to VAS was assessed using real-time ultrasound and a paradigm of arousal responsiveness. Responders were tested with repeated VAS to assess habituation. Also, the quality of fetal reactivity to repeated stimuli was assessed as a measure of arousal and arousal regulation competence (Behavioral Reactivity Scale). Results: The control group had a larger proportion of fetuses who were too active to initiate testing (“too active to test”) (p= 0.013); the proportion of fetuses too active to test decreased with increasing gestational age. The majority of the fetuses who could be tested responded to the initial VAS, and there were no group differences. The proportion of fetuses that habituated and the rate of habituation did not differ between the groups. Behavioral reactivity did not differ between groups.
Conclusions: The original hypotheses were not confirmed. However, the chosen assessment paradigms may have lacked sensitivity. The proportion of fetuses that were “too active to test” decreased with gestational age. The control group had a larger proportion of fetuses that were “too active to test” compared with the exposure groups. We speculate that these findings indicate that prenatal exposure to these neuroteratogens may have produced an acceleration of the behavioral response to vibroacoustic stimulation.