Assessing race/ethnicity and socioeconomic status (SES) relationships with Attention-Deficit/Hyperactivity Disorder (ADHD) diagnosis, treatment, and access to care has yielded inconsistent results often based only on parent-report. In contrast, this study used broader ADHD diagnostic determination including case-definition to examine these relationships in a multisite elementary-school-based sample.
Secondary analysis of children with and without ADHD per parent and teacher-reported Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria evaluated SES, race/ethnicity, and other variables through simple bivariate/multivariable models within and across: parent-reported diagnosis, medication treatment, and meeting ADHD study case-definition.
The total sample included 51.9% male, 51.3% White, and 53.1% with private insurance; 10% had parent-reported ADHD diagnoses while 8.3% met ADHD study case-definition. In multivariable models, White children had higher odds of parent-reported diagnoses than Black, Hispanic, and Other Race/Ethnicity children (p < 0.05), but only Hispanic children had lower odds of being case-positive (<0.05); males and children in single-parent households had higher odds of parent-reported diagnoses and being case-positive (p < 0.05); and children who were White, male, and had health insurance had higher odds of taking medication (p < 0.05). Among children who were case-positive, those with Medicaid, White, and 2-parent statuses had higher odds of parent-reported diagnoses (p < 0.05).
Children with underlying ADHD appear more likely to have assessment/medication treatment access if they are White, male, have health insurance (particularly Medicaid), and live in 2-parent households. While boys and children raised by single parents may have higher rates of ADHD diagnoses, false-positive diagnostic risk also appeared higher, inviting further investigation.
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*Section on Developmental and Behavioral Pediatrics, Department of Pediatrics, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK;
†Department of Psychiatry, College of Medicine, University of Florida, Jacksonville, FL;
‡Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC.
Address for reprints: Ami C. Bax, MD, OU Child Study Center, 1100 NE 13th Street, Oklahoma City, OK 73117; e-mail: email@example.com.
Supported by the Centers for Disease Control and Prevention through cooperative agreements U50/CCU6223-02 & U84/CCU422516-02.
S. P. Cuffe received research funding from Otsuka, Alkermes, and Boehringer Ingelheim that has no direct relationship to the funding or outcomes of the research reported in this paper. The other authors have no other financial relationships or conflicts of interest relevant to this article to disclose.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.jdbp.org).
Received May 30, 2018
Accepted September 05, 2018