Prenatal Alcohol Exposure Affects Frontal–Striatal BOLD Response During Inhibitory Control

Authors


  • Research supported by NIAAA: R01 AA10417, T32 AA013525 to EPR, R01 AA10820 and U01 AA14834 to SNM, and F31 AA016051 to SLF.

Reprint requests: S. L. Fryer, MS, 6363 Alvarado Court, Suite 200 San Diego, CA 92120; Fax: 619-594-1895; E-mail: sfryer@ucsd.edu

Abstract

Background: Prenatal alcohol exposure can lead to widespread cognitive impairment and behavioral dysregulation, including deficits in attention and response inhibition. This study characterized the neural substrates underlying the disinhibited behavioral profile of individuals with fetal alcohol spectrum disorders (FASD).

Methods: Children and adolescents (ages 8–18) with (n=13) and without (n=9) histories of heavy prenatal alcohol exposure underwent functional magnetic resonance imaging while performing a response inhibition (go/no-go) task.

Results: Despite similar task performance (mean response latency, performance accuracy, and signal detection), blood oxygen level-dependent (BOLD) response patterns differed by group. Region-of-interest analyses revealed that during portions of the behavioral task that required response inhibition, alcohol-exposed participants showed greater BOLD response across prefrontal cortical regions (including the left medial and right middle frontal gyri), while they showed less right caudate nucleus activation, compared with control participants.

Conclusions: These data provide an account of response inhibition-related brain functioning in youth with FASD. Furthermore, results suggest that the frontal–striatal circuitry thought to mediate inhibitory control is sensitive to alcohol teratogenesis.

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