Prenatal and concurrent cocaine, alcohol, marijuana, and tobacco effects on adolescent cognition and attention.
prospective_cohort · Level II
Where this comes from
- Record sourced from PubMed, PMID 30077054.
- Also identified by DOI 10.1016/j.drugalcdep.2018.06.022 and PMC identifier 10187465.
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Abstract
Prenatal cocaine/polydrug exposure (PCE) may increase vulnerability to substance use disorders due to associated cognitive deficits. We examined whether neurocognitive deficits in executive functions and attention observed in PCE children persisted to adolescence when compared to non-cocaine/polydrug (NCE) children, and whether adolescent substance use (tobacco, alcohol, marijuana) was also associated with neurocognitive deficits. 354 (180 PCE, 174 NCE) adolescents in a longitudinal study from birth were administered the Wechsler Intelligence Scales for Children - IV (WISC-IV), and the Integrated Visual and Auditory Continuous Performance Test (IVA/CPT) at age 15.5. Assessments of prenatal exposure to cocaine, alcohol, marijuana, and tobacco and measures of use at age 15.5 were taken. Confounding factors measured included lead, the caregiving environment, and violence exposure. Relationships between drug use and prenatal exposures on outcomes were assessed through multiple regression. Adolescents with PCE had deficits in Perceptual Reasoning IQ and visual attention. Prenatal alcohol exposure predicted verbal and working memory IQ and visual and auditory attention deficits. Adolescent tobacco, alcohol, and marijuana use predicted attention in addition to PCE, lead and the caregiving environment. Prenatal cocaine and alcohol exposure and adolescent use of substances are associated with neurocognitive deficits known to increase vulnerability to SUDs.
Medical subject headings
- Adolescent Behavior
- Attention
- Cognition
- Prenatal Exposure Delayed Effects
- Substance-Related Disorders