Little is known about the neurophysiologic effects of prenatal cocaine/crack use. The aim of this study, designed to overcome methodologic limitations of previous research, was to investigate the effects of prenatal cocaine use on electroencephalographic (EEG) sleep patterns, a marker of central nervous system development.
In a longitudinal study of prenatal cocaine/crack exposure, women were interviewed at the end of each trimester about cocaine, crack, alcohol, tobacco, marijuana, and other drug use. Two-hour paper- and computer-generated EEG sleep recordings were obtained on a sample of the full-term infants on the second day of life and at 1 year postpartum. Eligible newborns were full-term, had received no general anesthesia, and had a 5-minute Apgar score >5. All infants whose mothers used one or more lines of cocaine during their first trimester or any crack (n = 37) were selected. A comparison group was chosen randomly from the group of women who did not use cocaine or crack during their pregnancy (n = 34).
Women who used cocaine/crack during the first trimester were older, less educated, less likely to be working, and used more tobacco, alcohol, marijuana, and other illicit drugs than women who did not use cocaine/crack during the first trimester. There were no differences in infant birth weight, length, head circumference, or gestational age between the two exposure groups. After controlling for the significant covariates, prenatal cocaine exposure was associated with less well developed spectral correlations between homologous brain regions at birth, and with lower spectral EEG power values at 1 year of age. Prenatal alcohol, marijuana, and tobacco use were found to affect state regulation and cortical activities.
These results indicate that the neurotoxic effects of prenatal cocaine/crack use can be detected with quantitative EEG measures.