Attention and executive functions in ADHD and treatment with methylphenidate: An fMRI and behavioral investigation

Many studies have documented cognitive and executive functioning deficits associated with Attention-Deficit/Hyperactivity Disorder (ADHD). These deficits have been indirectly linked to dysfunction in a number of regions within the attention system of the brain, but the exact nature of the neural mechanisms leading to the disruptive and disinhibited behavior in ADHD remains largely unknown. Moreover, the manner in which stimulant medication, the most common treatment for ADHD, alters the neural circuitry involved is poorly understood. Two studies were conducted to further elucidate the neural underpinnings of ADHD and its treatment with methylphenidate (MPH). The primary investigation used fMRI to investigate the neural correlates of selective and divided attention on- and off-MPH in adolescents with ADHD or reading disorder, and to compare neural activity to a group of non-impaired adolescents. Executive functioning was also assessed through the Tower of Hanoi and Wisconsin Card Sorting Test. Results indicated that neural activation was remarkably similar for all groups of subjects, with the exception of reduced activation of the left basal ganglia and right inferior parietal cortex in ADHD adolescents off-drug. Results from executive functioning tests revealed that MPH led to better performance, but only during the second testing session. In addition, better performance on the Wisconsin Card Sorting Test in the second session was correlated with increased activation in the basal ganglia. A second study used fMRI to create a novel paradigm for the study of parietal lobe functioning in ADHD and to determine the role of the parietal cortex in visual feature integration. Results indicated that regions of the parietal lobe involved in spatial attention are more engaged when multiple objects are presented simultaneously at different spatial locations, but not when they are shown sequentially at the same location. Results of both studies are discussed in terms of a possible neural model for ADHD.