ADHD is among the most frequently diagnosed disorders of childhood and is defined by developmentally inappropriate levels of inattention, hyperactivity, and impulsivity (American Psychiatric Association, 2000). Research strongly suggests children with ADHD have significant neuropsychological dysfunction (Barkley, 1997; Faraone & Biederman, 1998) that persists into adulthood (Hervey, Epstein, & Curry, 2004). Children with ADHD exhibit a wide range of performance deficits across a range of neuropsychological domains including response inhibition, working memory, planning, sense of time, sustained attention, and verbal learning ( Barkley, Grodzinsky, & DuPaul, 1992; Martinussen, Hayden, Hogg-Johnson, & Tannock, 2005; Nigg, Blaskey, Huang-Pollock, & Rappley, 2002; Nigg, Butler, Huang-Pollock, & Henderson, 2002; Nigg, Willcutt, Doyle, & Sonuga-Barke, 2005; Seidman, 2006; Seidman, Benedict et al., 1995; Seidman, Biederman, Faraone, Weber, & Ouellette, 1997; Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). Despite the considerable evidence documenting the presence of neuropsychological deficits in individuals with ADHD, questions still exist regarding the persistence and course of these deficits over time. The current study begins to address this gap in the literature by examining the trajectory of specific neuropsychological deficits as measured by outcomes on a continuous performance test (CPT).
Understanding the developmental course of neuropsychological functioning in individuals with ADHD has descriptive as well as theoretical implications. Descriptively, ADHD-related neuropsychological deficits have been documented across the lifespan, albeit using primarily cross-sectional samples (Barkley et al., 1992; Seidman, Biederman et al., 1995; Seidman et al., 1997; Seidman, Biederman, Weber, Hatch, & Faraone, 1998). Although research has documented improvement in neuropsychological performance through adolescence into young adulthood (Biederman, Petty, Fried, Doyle, Spencer, Seidman et al., 2007; Fischer, Barkley, Smallish, & Fletcher, 2005), little is known regarding the effects of such neuropsychological improvements in terms of the presence or magnitude of deficits especially in relation to developmentally-related changes in core ADHD symptomatology.
Theoretically, investigators have hypothesized that the developmental course of ADHD-related neuropsychological deficits may provide insights into which neuropsychological deficits are core to the disorder and which are epiphenomenal (Carr, Nigg, & Henderson, 2006; Halperin & Schulz, 2006). Some have suggested that attenuation in neuropsychological deficits, specifically when this attenuation parallels reductions in ADHD symptomatology, may be indicative of epiphenomenal rather than core ADHD deficits (Carr et al., 2006; Halperin, Trampush, Miller, Marks, & Newcorn, 2008). Recently, Halperin and Schulz (2006) proposed that developmentally-related attenuation in executive functioning deficits among patients with ADHD is likely caused by prefrontal cortex maturation which promotes compensatory cognitive and neural mechanisms in patients. In support, they cite the parallel developmental course of prefrontal cortex during late childhood and adolescence and the typical attenuation in ADHD symptomatology during this same span (Biederman, Mick, & Faraone, 2000; Hill & Schoener, 1996). Halperin and Schulz (2006) further argue that core ADHD deficits are more likely linked to non-cortical structures (e.g., striatum, cerebellum); hence, neuropsychological measures that assess function in these structures should remain relatively constant throughout the lifespan irrespective of ADHD symptom status.
In order to examine the developmental course of ADHD symptoms and neuropsychological deficits, longitudinal studies including children with and without ADHD with repeated assessment of neuropsychological function are necessary. However, few such longitudinal studies with ADHD samples exist (Biederman et al., 2008; Drechsler, Brandeis, Foldenyi, Imhof, & Steinhausen, 2005; Fischer et al., 2005; Halperin et al., 2008; Hinshaw, Carte, Fan, Jassy, & Owens, 2007). Of the existing longitudinal studies, most have collected neuropsychological data with groups of children with and without ADHD using a follow-up assessment in late adolescence or young adulthood. The typical lag between assessments ranges from 5 to 9 years. In summary, these studies demonstrated that 1) children with ADHD have poorer neuropsychological performance across a range of measures compared to normal controls; 2) neuropsychological performance improves from childhood to adolescence/young adulthood among both ADHD and normal control samples; and 3) despite time-related improvements in neuropsychological performance, patients diagnosed with ADHD in childhood continue to demonstrate poorer neuropsychological performance in adolescence/young adulthood than normal controls (Drechsler et al., 2005; Fischer et al., 2005; Halperin et al., 2008; Hinshaw et al., 2007). Results also suggested that individuals meeting criteria for a diagnosis of ADHD at both time points had the poorest levels of neuropsychological performance (Biederman et al., 2007; Hinshaw et al., 2007). One criticism of these studies is the lengthy lag between assessment points.
One study (Drechsler et al., 2005) using a shorter time lag between neuropsychological assessments examined a small group (n=28) of children with ADHD aged 8–13 and a group of age-matched normal controls (n=25) yearly over 2 years. The only neuropsychological outcome on which the ADHD group performed more poorly than the normal controls was variability in reaction time. However, this between-group effect was present only at the Time 1 and Time 2 assessments. At the third assessment, between-group differences were no longer present with both groups improving from the Time 2 to Time 3 assessment. There was an interesting interaction effect indicating that improvement was more pronounced for children with ADHD than was demonstrated for normal controls. Their results suggested that neuropsychological development appeared to be non-linear and possibly differentially non-linear across ADHD and normal control groups. Indeed, data exist for both normal control and ADHD samples demonstrating that brain development progresses at different rates especially in the teenage years (Barnea-Goraly et al., 2005; Krain & Castellanos, 2006) and that these rates of brain development may be different in ADHD samples versus normal controls (Castellanos et al., 2002; Shaw et al., 2007). These results suggest that research examining shorter intervals within critical developmental periods (e.g., early adolescence) is necessary to clarify the developmental course of neuropsychological functioning.
In addition to examining changes in neuropsychological performance over targeted developmental periods, it is equally relevant to examine how these developmentally-related neuropsychological changes correspond to changes in ADHD symptoms. As noted earlier, the relationship between neuropsychological performance and behavior has implications for determining core versus epiphenomenal neuropsychological deficits (Carr et al., 2006; Halperin et al., 2008). In regards to developmental changes in ADHD symptoms, despite high rates of documented persistence (Biederman et al., 2006), studies have shown that the actual presentation of ADHD symptoms tends to change over time (Barkley, Fischer, Edelbrock, & Smallish, 1990; Biederman et al., 1996; Hart, Lahey, Loeber, Applegate, & Frick, 1995). Significant declines (i.e., improvement) over time in hyperactive/impulsive symptoms have been shown with more stable trends in inattentive symptoms over the same period (Fischer et al., 2005; Hart et al., 1995). However, despite these documented decreases of hyperactivity and impulsivity with age, children with ADHD continue to exhibit non-normative levels of ADHD symptomatology (Barkley et al., 1990; Biederman et al., 1998; Molina et al., 2009).
A hypothesized relation between developmental trends in neuropsychological performance and trends in ADHD symptom change over time is not well-established. All research to date attempting to address this issue has examined ADHD symptoms dichotomously (i.e., either the patient meets ADHD criteria or not) and unitarily (i.e., examining ADHD symptom domains collectively). For example, Halperin and colleagues (Halperin et al., 2008) found that only individuals with a persistent diagnosis of ADHD continued to have difficulties with effortful executive processes over time; whereas, children failing to meet criteria for ADHD were no longer different from controls. The use of diagnostic stability may fail to accurately account for the heterotypic continuity in the developmental course of ADHD symptoms that is commonly observed in patients with ADHD (Biederman et al., 2000; Hart et al., 1995; Hinshaw, Owens, Sami, & Fargeon, 2006; Larsson, Lichtenstein, & Larsson, 2006; Larsson, Larsson, & Lichtenstein, 2004). That is, there seems to be significant attenuation in hyperactivity/impulsivity symptoms and maintenance of inattention symptoms from childhood to adolescence.
While the majority of findings suggest that ADHD symptoms and neuropsychological dysfunction are correlated (Nigg, 2005; Seidman, 2006), questions remain unanswered. For example, are observed improvements in neuropsychological functioning selectively related to hyperactivity/impulsivity, as would be expected given the observed improvements in this symptom domain, or are these improvements in neuropsychological functioning also related to inattentive symptoms? Also, are the relations between neuropsychological and behavioral improvements specific to particular neuropsychological outcomes? According to the hypothesis offered by Halperin and Schulz (2006), neuropsychological deficits on task outcomes measuring effortful processing (e.g., commission errors on a go/no-go task) should attenuate with maturation paralleling attenuation in ADHD symptomatology. On the other hand, neuropsychological deficits on outcomes measuring less conscious control (e.g., reaction time variability) should largely persist over time remaining unrelated to ADHD symptom presentation.
The purpose of the present study is threefold. First, we examined the trajectory of neuropsychological deficits, as measured by outcomes on a CPT task, in children with and without ADHD over a 1 year period. Second, we examined the trajectory of ADHD symptoms in each domain over the same period. Third, as no research has examined directly the relations among developmental changes in neuropsychological functioning and ADHD symptomatology, we examined the correspondence between developmental changes in performance on a CPT and in ADHD symptomatology over the same period.
Children in the Multimodal Treatment Study of Children with ADHD (MTA) sample completed the Conners’ CPT (i.e., a Go/No-Go task) twice with an approximate 1 year lag. Results from the first test administration demonstrated that children with ADHD responded more slowly, more variably, and with more errors when compared to a matched control group (Hervey et al., 2006). Consistent with previous longitudinal studies, albeit over a shorter course of time, we predict that children with ADHD as well as a matched normative comparison group will exhibit improved neuropsychological performance as evidenced by decreased reaction time, reaction time variability and errors of commission and omission with development (Fischer et al., 2005). As raw scores on the CPT task (e.g., errors, reaction time) are the primary dependent variable, age-related improvements across both groups are expected. A similar pattern would be observed if raw scores were used on achievement tests. The majority of previous research has not shown rates of improvement to be different across ADHD and normal control groups thus only a main effect, not an interaction effect, is predicted. Also consistent with previous research, we expect to confirm that hyperactive and impulsive symptoms will improve with development while inattention symptoms will remain stable. Finally, in respect to correspondences between neuropsychological function, we predict correlations between CPT outcomes and ADHD symptoms at each time point (Nigg, 2005; Seidman, 2006). Further, consistent with Halperin and Schulz’s hypothesis (2006) we expect that changes in CPT outcomes measuring effortful control processes (i.e., omission and commission errors) will be related to ADHD symptom domain trajectories while other CPT outcomes measuring processes with little conscious control (i.e., reaction time variability) will demonstrate no relation to ADHD symptom trajectories.