This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Executive function is a term used to refer to the processes of inhibition, maintenance of set/preparedness to act, and planning of sequences of actions. Executive function impairments are often observed in children with Attention Deficit Hyperactivity Disorder (ADHD) and High Functioning Autism (HFA). Executive function impairments have been related to abnormal functioning of the frontal lobes either due to frontal lobe impairment or because of malfunctioning of another cortical or subcortical system having direct connections to the frontal lobes. Executive function impairments in childhood neuropsychiatric disorders may arise from deviations in a variety of cortical and subcortical systems during development.
Aims of this proposal are: 1. Executive function impairments in HFA and ADHD may be characterized by different neuropsychological profiles, 2. Deficits in executive function in HFA and ADHD are related to impairments in neuronal circuitry involving the prefrontal cortex. On behavioral paradigms, children with High Functioning Autism are predicted to show impairments in planning, set-shifting, and spatial working memory with sparing of response inhibition. In contrast, children with ADHD are predicted to show impairments in inhibition, planning, and spatial working memory with sparing of set-shifting ability. We will use structural MR scans to test the hypotheses that dorsolateral prefrontal brain region volumes are smaller in children with autism and that medial and orbital prefrontal brain volumes are smaller in children with ADHD. If these hypotheses are correct, then: a) smaller dorsolateral prefrontal volumetric measures will be correlated with abnormalities in planning, set shifting, and spatial working memory in children with HFA and b) smaller medial and orbital prefrontal brain regions will be correlated with abnormalities in inhibition in children with ADHD. We will use fMRI to test the hypotheses that the medial and orbital prefrontal brain regions involved in response inhibition are a) impaired in ADHD and b) spared in autism. We predict that compared to control subjects, children with ADHD will demonstrate anomalous activation of medial and orbital prefrontal areas during a response inhibition task. In contrast, we predict that children with HFA will demonstrate normal activation of medial and orbital prefrontal areas during the same task.
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