Attention-Deficit/Hyperactivity Disorder (ADHD) is thought to affect approximately 5-10% of all school-age children and nearly 5% of adults (1
). Cardinal symptoms of ADHD include inattention, impulsivity, and hyperactivity. The DSM-IV-TR categorizes ADHD into three subtypes: ADHD-Predominantly Hyperactive/Impulsive (ADHD-H/I), ADHD-Predominantly Inattentive (ADHD-PI), and ADHD-Combined Type (ADHD-C; i.e., meeting criteria for both ADHD-H/I and ADHD-PI).
Foundational theories connect the symptoms of ADHD to impairments in executive functioning (EF) (2
). Based on this work, meta-analytic reviews representing approximately 109 studies on EF in children with ADHD found significant impairments in planning ability, response inhibition, and in particular, working memory (3
). Furthermore, EF tasks are thought to be modulated by the prefrontal cortex and the associated neural networks of the basal ganglia and cerebellum (5
). These neural networks are thought to be altered in children with ADHD.
The cause of ADHD is unknown. Current etiological theories of ADHD, however, suggest impairments in fronto-striatal neurocircuitry are at the core of ADHD symptomotology (2
). Support for this hypothesis comes from both neuropsychological and neuroimaging studies of ADHD.
Investigations using magnetic resonance imaging (MRI) and functional MRI (fMRI), implicate fronto-striatal-cerebellar neural circuit deficits in ADHD. Specifically, research has found that abnormalities in brain structure and function are key components of the ADHD phenotype. For example, Castellanos, Giedd, Hamburger, Marsh, & Rapoport, (1996; 11
) reported that the volume of the frontal cortex was significantly smaller in boys with ADHD compared to boys without. Similarly, it appears that caudate volume (9
) as well as cerebellar volume and area are smaller in children with ADHD (14
). For example, numerous studies observed smaller cerebellar volume and area with a particular reduction in the posterior inferior vermis (Lobules XIII-V) (14
). Other studies, using fMRI, found dysfunctions (i.e., hypoactivation) in the anterior cingulate cortex (ACC; 20). This finding is significant given the importance of the ACC in the monitoring of attention and in error processing. The prefrontal cortex (PFC), an area responsible for a host of executive functions, has also been found to be impaired in children with ADHD (21
). Thus, many neural systems are impaired in children with ADHD, which likely contributes to the vast heterogeneity of the disorder.
Stimulant medication is often prescribed for children with ADHD given its effects on the fronto-striatal dopaminergic system (24
). Stimulants, such as methylphenidate, block the re-uptake of dopamine and norepinephrine, allowing for improved neurochemical transmission between neurons. In animal studies, chronic stimulant use has been linked to changes in the density of dopamine transporters (26
). For this reason researchers have also been interested in the effects of stimulant medication on the development of brain structures in humans.
A 5-year longitudinal study looking at the effects of stimulant medication on brain development found that unmedicated ADHD children (compared to medicated) had smaller total white matter volume (7
). Thus, it appears that stimulant medication may normalize white matter development. Researchers have also observed volumetric differences in the ACC in medicated versus unmedicated children with ADHD (27
). The right ACC was significantly smaller in unmedicated children compared to both chronically medicated ADHD children and typically developing control children. Therefore, it is hypothesized that chronic medication may also normalize ACC development.
These studies collectively suggest that chronic medication treatment is related to the normalization of brain structures associated with symptoms of ADHD. The results of only two studies, however, should be interpreted with caution given inconsistent findings, limited sample sizes and decision to control or not control for comorbid disorders or ADHD subtypes which may reflect qualitatively different populations. Further, while these studies provide important information about the effects of chronic stimulant treatment on the development of cerebral white matter and the ACC, it is unclear how/if stimulant medication affects the development of the cerebellum. Because numerous studies found differences in cerebellar volume and area in ADHD children (14
), the question regarding chronic treatment and cerebellar development remains.
The current study looked at the effects of chronic medication on the development of the cerebellar vermis in children with ADHD. We hypothesized that reductions in vermal area would be found in treatment-naïve children with ADHD but not chronically-treated ADHD or typically developing controls. Further, we hypothesized that chronically-treated children with ADHD would have similar vermal area as controls.