title: Neurological and developmental outcomes of prenatally cocaine-exposed offspring from 12 to 36 months.
abstract: Second generation studies of prenatal cocaine exposure failed to find gross deficits after controlling for confounders. Concern remained that exposure could cause subtle deficits. This prospective, cohort study evaluated effects of cocaine on development at 12, 18, 24, and 36 months. From 1991-1993, 361 mother-infant pairs were recruited from the Children's Hospital of New York, Presbyterian Medical Center's prenatal clinic or delivery room suite. Mothers were assigned to the cocaine group based on report of prenatal cocaine use or positive urine toxicology. Control mothers were enrolled from the same clinic and matched for age and socioeconomic status (SES). Women with serious medical problems were excluded from either group. Of the retained cohort, at 12 months, 147 infants were exposed and 89 were unexposed case controls. Both groups were raised in impoverished environments with few supports. Developmental evaluations were conducted blinded to group. Cross-sectional analysis revealed cocaine-related deficits in neurological exams and speech across all time periods, in spite of catch up in weight, length, and head circumference. Overall analysis of development was evaluated using Generalized Estimating Equations regression analysis. Bayley Mental [Badj = -6.5 (CI--9.4, -3.5, p < or = 0.001)] and Psychomotor [Badj = -3.9 (CI--7.4, -0.5, p = 0.02)] Developmental Indices showed deficits after controlling for confounders. Males were more vulnerable to cocaine exposure for height, motor development, and emotional regulation. Dose-response relationships existed for abnormal neurological exams (Ptrends < 0.08), Mental Development Index (MDI) (Ptrend < 0.001), and Psychomotor Development Index (PDI) (Ptrend < 0.001) deficits. Although nonexposed children performed poorly, cocaine-exposed children showed worse performance. Both groups showed declines at 18 months in mental and psychomotor development from which only nonexposed children rebounded. Overall, cocaine exposure adds an additional risk to disadvantaged children's development. Cocaine-exposed children are less resilient to effects of these multiple risks.
authors.affiliation: Alcohol Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
authors.forename: Marilyn W
authors.initials: MW
authors.lastname: Lewis
authors.forename: Sonya
authors.initials: S
authors.lastname: Misra
authors.forename: Helen L
authors.initials: HL
authors.lastname: Johnson
authors.forename: Tove S
authors.initials: TS
authors.lastname: Rosen
mesh_terms: D001921:Brain / Q000503:physiopathology*; D016241:Child of Impaired Parents / Q000706:statistics & numerical data*; D019970:Cocaine-Related Disorders / Q000453:epidemiology*; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D002658:Developmental Disabilities / Q000453:epidemiology* / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007223:Infant; D008297:Male; D009035:Mothers / Q000706:statistics & numerical data*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D011596:Psychomotor Disorders / Q000453:epidemiology; D017678:Sex Distribution; D011795:Surveys and Questionnaires