Prenatal Alcohol Exposure Alters Biobehavioral Reactivity to Pain in Newborns
Article first published online: 27 JAN 2010
Copyright © 2010 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 34, Issue 4, pages 681–692, April 2010
How to Cite
Oberlander, T. F., Jacobson, S. W., Weinberg, J., Grunau, R. E., Molteno, C. D. and Jacobson, J. L. (2010), Prenatal Alcohol Exposure Alters Biobehavioral Reactivity to Pain in Newborns. Alcoholism: Clinical and Experimental Research, 34: 681–692. doi: 10.1111/j.1530-0277.2009.01137.x
- Issue published online: 23 MAR 2010
- Article first published online: 27 JAN 2010
- Received for publication April 22, 2009; accepted November 13, 2009.
- Prenatal Alcohol Exposure;
- Neonatal Pain;
- Stress Reactivity;
- Brazelton Behavioral Assessment
Objectives: To examine biobehavioral responses to an acute pain event in a Cape Town, South Africa, cohort consisting of 28 Cape Colored (mixed ancestry) newborns (n = 14) heavily exposed to alcohol during pregnancy (exposed), and born to abstainers (n = 14) or light (≤0.5 oz absolute alcohol/d) drinkers (controls).
Methods: Mothers were recruited during the third trimester of pregnancy. Newborn data were collected on postpartum day 3 in the maternity obstetrical unit where the infant had been delivered. Heavy prenatal alcohol exposure was defined as maternal consumption of at least 14 drinks/wk or at least 1 incident of binge drinking/mo. Acute stress-related biobehavioral markers [salivary cortisol, heart rate (HR), respiratory sinus arrhythmia (RSA), spectral measures of heart rate variability (HRV), and videotaped facial actions] were collected thrice during a heel lance blood collection (baseline, lance, and recovery). After a feeding and nap, newborns were administered an abbreviated Brazelton Neonatal Behavioral Assessment Scale.
Results: There were no between-group differences in maternal age, marital status, parity, gravidity, depression, anxiety, pregnancy smoking, maternal education, or infant gestational age at birth (all ps > 0.15). In both groups, HR increased with the heel lance and decreased during the postlance period. The alcohol-exposed group had lower mean HR than controls throughout, and showed no change in RSA over time. Cortisol levels showed no change over time in controls but decreased over time in exposed infants. Although facial action analyses revealed no group differences in response to the heel lance, behavioral responses assessed on the Brazelton Neonatal Scale showed less arousal in the exposed group.
Conclusions: Both cardiac autonomic and hypothalamic–pituitary–adrenal stress reactivity measures suggest a blunted response to an acute noxious event in alcohol-exposed newborns. This is supported by results on the Brazelton Neonatal Scale indicating reduced behavioral arousal in the exposed group. To our knowledge, these data provide the first biobehavioral examination of early pain reactivity in alcohol-exposed newborns and have important implications for understanding neuro-/biobehavioral effects of prenatal alcohol exposure in the newborn period.