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

• Published in: Alcoholism, clinical and experimental research Vol. 34; no. 4; pp. 617 - 627
• Main Authors: Burden, Matthew J., Jacobson, Joseph L., Westerlund, Alissa, Lundahl, Leslie H., Morrison, Audrey, Dodge, Neil C., Klorman, Rafael, Nelson, Charles A., Avison, Malcolm J., Jacobson, Sandra W.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.04.2010
• Subjects: Alcohol Drinking - adverse effects; Alcohol Drinking - physiopathology; Attention Deficit Disorder with Hyperactivity - diagnosis; Attention Deficit Disorder with Hyperactivity - physiopathology; Attention Deficit Disorder with Hyperactivity - psychology; Attention Deficit Hyperactivity Disorder; Cohort Studies; Event-Related Potentials; Evoked Potentials - physiology; Female; Fetal Alcohol Spectrum Disorders; Follow-Up Studies; Humans; Inhibition (Psychology); Male; Pregnancy; Prenatal Alcohol Exposure; Prenatal Exposure Delayed Effects - diagnosis; Prenatal Exposure Delayed Effects - physiopathology; Prenatal Exposure Delayed Effects - psychology; Prospective Studies; Reaction Time - physiology; Response Inhibition; Young Adult
• ISSN: 0145-6008; 1530-0277
• DOI: 10.1111/j.1530-0277.2009.01130.x

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.