An Event-Related Potential Study of Response Inhibition in ADHD With and Without Prenatal Alcohol Exposure

Authors

  • Matthew J. Burden,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Joseph L. Jacobson,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Alissa Westerlund,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Leslie H. Lundahl,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Audrey Morrison,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Neil C. Dodge,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Rafael Klorman,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Charles A. Nelson,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Malcolm J. Avison,

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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  • Sandra W. Jacobson

    1. From the Wayne State University School of Medicine (MJB, JLJ, LHL, AM, NCD, SWJ), Detroit, Michigan; Children’s Hospital Boston, Harvard Medical School (AW, CAN), Boston, Massachusetts; University of Rochester (RK), Rochester, New York; and Vanderbilt University (MJA), Nashville, Tennessee.
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Reprint requests: Sandra W. Jacobson, PhD, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, 2751 E. Jefferson, Ste. 460, Detroit, MI 48207; Fax: 313-993-3427; E-mail: sandra.jacobson@wayne.edu

Abstract

Background:  The attention and cognitive problems seen in individuals with a history of prenatal alcohol exposure often resemble those associated with attention deficit hyperactivity disorder (ADHD), but few studies have directly assessed the unique influence of each on neurobehavioral outcomes.

Methods:  We recorded event-related potentials (ERPs) during a Go/No-go response inhibition task in young adults with prospectively obtained histories of prenatal alcohol exposure and childhood ADHD.

Results:  Regardless of prenatal alcohol exposure, participants with childhood ADHD were less accurate at inhibiting responses. However, only the ADHD group without prenatal alcohol exposure showed a markedly diminished P3 difference between No-go and Go, which may reflect a more effortful strategy related to inhibitory control at the neural processing level.

Conclusion:  This finding supports a growing body of evidence suggesting that the manifestation of idiopathic ADHD symptoms may stem from a neurophysiologic process that is different from the ADHD symptomatology associated with prenatal alcohol exposure. Individuals who have been prenatally exposed to alcohol and present with ADHD symptomatology may represent a unique endophenotype of the disorder, which may require different treatment approaches from those found to be effective with idiopathic ADHD.

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