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Author Notes:

Address for Correspondence: Sarah N. Mattson, Ph.D., 6330 Alvarado Court, Suite 100, San Diego, CA 92120 USA, Phone: 619-594-7228, FAX: 619-594-1895, smattson@sunstroke.sdsu.edu

The authors thank the families who graciously participate in our studies and the members of the Center for Behavioral Teratology for ongoing assistance and support.

We also acknowledge the efforts in data collection of Kristina Hubbard, Delilah Bolo, and Heather Holden in San Diego; Suzanne Houston, Ariel Starr, and Genevieve Rodriguez in Los Angeles; Sharron Paige-Whitaker in Atlanta; and Alfredo Aragon, Ethan White, and Stephanie Rueda in Albuquerque; and Tania Pomario, Claire Corbett, Dominique Brand, Gosia Lipinska and Karen van Eden in Cape Town.


Research Funding:

Research described in this paper was supported by NIAAA grant numbers U01 AA014834 (Mattson), U24 AA014811 (Riley), U24 AA014818 (Barnett), and U24 AA014815 (Jones).

All or part of this work was done in conjunction with the Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD), which is funded by grants from the National Institute on Alcohol and Alcohol Abuse (NIAAA). Additional information about CIFASD can be found at www.cifasd.org.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Substance Abuse
  • Fetal Alcohol Syndrome (FAS)
  • Prenatal Alcohol Exposure
  • Neurobehavioral Profile
  • Attention-Deficit
  • Hyperactivity Disorder (ADHD)
  • Latent Profile Analysis (LPA)

Further Development of a Neurobehavioral Profile of Fetal Alcohol Spectrum Disorders

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Journal Title:

Alcoholism: Clinical and Experimental Research


Volume 37, Number 3


, Pages 517-528

Type of Work:

Article | Post-print: After Peer Review


Background: Heavy prenatal alcohol exposure (AE) results in a broad array of neurobehavioral deficits. Recent research has focused on identification of a neurobehavioral profile or profiles that will improve the identification of children affected by AE. This study aimed to build on our preliminary neurobehavioral profile to improve classification accuracy and test the specificity of the resulting profile in an alternate clinical group. Methods: A standardized neuropsychological test battery was administered to 3 groups of children: subjects with AE (n = 209), typically developing controls (CON, n = 185), and subjects with attention-deficit/hyperactivity disorder (ADHD, n = 74). We assessed a large sample from 6 sites in the United States and South Africa, using standardized methodology. Data were analyzed using 3 latent profile analyses including (i) subjects with fetal alcohol syndrome (FAS) and controls, (ii) subjects with AE without FAS and controls, and (iii) subjects with AE (with or without FAS) and subjects with ADHD. Results: Classification accuracy was moderate but significant across the 3 analyses. In analysis 1, overall classification accuracy was 76.1% (77.2% FAS, 75.7% CON). In the second analysis, overall classification accuracy was 71.5% (70.1% AE/non-FAS, 72.4% CON). In the third analysis, overall classification accuracy was 73.9% (59.8% AE, 75.7% ADHD). Subjects that were misclassified were examined for systematic differences from those that were correctly classified. Conclusions: The results of this study indicate that the neuropsychological effects of AE are clinically meaningful and can be used to accurately distinguish alcohol-affected children from both typically developing children and children with ADHD. Further, in combination with other recent studies, these data suggest that approximately 70% of children with heavy prenatal alcohol exposure are neurobehaviorally affected, while the remaining 30% are spared these often-devastating consequences, at least those in the domains under study. Refining the neurobehavioral profile will allow improved identification and treatment development for childr en affected by prenatal alcohol exposure.

Copyright information:

© 2012 by the Research Society on Alcoholism.

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