Date of Degree

9-2016

Document Type

Dissertation

Degree Name

Ph.D.

Program

Psychology

Advisor

Jeffrey Halperin

Committee Members

Sarah O'Neill

Joel Sneed

Keywords

ADHD, children, executive function, neurodevelopmental

Abstract

Background: Attention-deficit/hyperactivity disorder (ADHD) is a highly prevalent neurodevelopmental disorder marked by developmentally inappropriate levels of inattention and hyperactivity/impulsivity. ADHD typically emerges during the preschool years, though the developmental course is highly variable across individuals (American Psychological Association, 2013; Faraone et al., 2006). Individuals with ADHD have been shown to have a number of structural and functional brain differences (Bush, Valera, & Seidman, 2005; Castellanos et al., 1996; Durston et al., 2004; Krain & Castellanos, 2006) as well as an array of neurocognitive deficits (Pennington and Ozonoff, 1996; Wilcutt et al., 2005) relative to typically developing peers. Considerable attention has been given to executive functions (EFs) and their role in the etiology of the disorder (Alderson et al., 2010; Barkley, 1997, 2006; Pennington & Ozonoff, 1996). However, there is compelling research to suggest that EFs are not the primary contributors to ADHD symptomatology; rather, deficits in more basic, lower-order cognitive functions may drive executive dysfunction in ADHD (Halperin & Schulz, 2006; Marks et al., 2005; Rommelse et al., 2007). Halperin and Schulz (2006) proposed a model of ADHD etiology wherein subcortical deficits underlie the disorder and improvements in EFs over the course of development compensate for those deficits. In order to properly evaluate this model and EF-based models of ADHD, rigorous research designs are essential to distinguish EF performance from basic, lower-order cognitive performance (Rommelse et al., 2007). The Delis-Kaplan Executive Function System (D-KEFS; Delis, Kaplan, & Kramer, 2001) is a battery of EF tests that contain multiple conditions of increasing complexity, moving from lower to higher-order processing. Using selected subtests from the D-KEFS, the current study examined EFs and non-EF cognitive performance in a sample of children at-risk for ADHD and typically developing children from ages 8 to 12 years.

Methods: 160 children (96 labeled as at-risk for ADHD in early childhood) were assessed annually from age 8 to 12 with a selection of D-KEFS measures and their parents filled out ADHD rating forms and completed a clinical interview to assess symptomatology at each year.

Results: Overall, children at-risk for ADHD performed more poorly on tests of higher-order processing and to a lesser extent, approaching significance, on lower-order processing as well. Trajectory analysis on the entire sample, using hierarchical linear modeling, indicated that 1) poorer higher-order functioning at age 8 significantly predicted greater ADHD symptom severity at age 12; 2) poorer lower-order functioning at age 8 was associated with higher ADHD symptom severity at age 12; and 3) improvements in higher-order functioning from ages 8 to 12 significantly predicted lower ADHD symptom severity scores at age 12. Trajectory analysis conducted in the at-risk children only, found that poorer lower-order functioning at age 8 significantly predicted higher ADHD symptom severity at age 12.

Conclusions: Taken together, these results suggest that improvement in higher-order processing is associated with the diminution of symptoms seen across childhood and poorer lower- order processing may be associated with greater symptom severity. As the Halperin and Schulz model suggests, more optimal neural development appears to be associated with greater symptom reduction. Additionally, there is considerable variability in trajectories of neuropsychological functioning as well as symptomatology across childhood, suggesting that ADHD is a highly heterogeneous disorder with likely diverse etiologies. Future research should include moving away from exclusively EF-based models to incorporate a wider range of neuropsychological weaknesses. This, in turn, could facilitate the development of a wider array of treatment alternatives for ADHD.

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