Prenatal Alcohol Exposure Affects Frontal–Striatal BOLD Response During Inhibitory Control
Article first published online: 9 JUN 2007
DOI: 10.1111/j.1530-0277.2007.00443.x
Issue

Alcoholism: Clinical and Experimental Research
Volume 31, Issue 8, pages 1415–1424, August 2007
Additional Information
How to Cite
Fryer, S. L., Tapert, S. F., Mattson, S. N., Paulus, M. P., Spadoni, A. D. and Riley, E. P. (2007), Prenatal Alcohol Exposure Affects Frontal–Striatal BOLD Response During Inhibitory Control. Alcoholism: Clinical and Experimental Research, 31: 1415–1424. doi: 10.1111/j.1530-0277.2007.00443.x
Publication History
- Issue published online: 9 JUN 2007
- Article first published online: 9 JUN 2007
- Received for publication October 3, 2006; accepted March 30, 2007.
- Abstract
- Article
- References
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Keywords:
- Fetal Alcohol Spectrum Disorders;
- Response Inhibition;
- Functional Neuroimaging;
- Fetal Alcohol Syndrome
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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