Functional imaging studies of attention-deficit hyperactivity disorder (ADHD) tend to follow a dimensional rather than a categorical approach and focus on a combination of behavioral- and circuit-specific paradigms to elucidate neural abnormalities specific to behavioral subtypes. A much needed approach is the application of methods designed to examine functional interactions between various brain regions such as prefrontal cortex, caudate nuclei, putamen and globus pallidus to delineate more closely the neural circuits underlying the psychopathology. The authors hypothesized that ADHD is a progressive neurodevelopmental disorder in which the initial deficit is at the site of dopaminergic cell bodies. A step in investigating ADHD using neuroimaging involves the use of cognitive/behavioral activation tasks that place demands on the neurobiochemical systems that are putatively dysfunctional in ADHD. Continuous performance tasks (CPTs) are used frequently in research to assess deficits in sustained attention in individuals with ADHD.

Functional magnetic resonance imaging (fMRI) allows neuroscientists to examine the function of the human brain, especially the developing human brain, in a relatively noninvasive manner. The significance of studying functional brain changes in a developmental context becomes more apparent when aspects of brain development are considered. Several neuroimaging studies have examined developing sensorimotor systems in infants and young children. The prefrontal cortex supports representations of information against interference over time or from competing sources. A number of classic developmental studies have demonstrated that memory-related processes develop throughout childhood and adolescence. This chapter addresses the important themes of the development of age-appropriate behavioral paradigms and appropriate task designs in the context of four developmental fMRI studies. These empirical studies revolve around two central themes: maintenance of information in prefrontal cortex over time and suppression of competing responses in prefrontal cortex.