This application is based on the hypothesis that at least partially distinct neural and cognitive mechanisms are involved in the etiology of and recovery from Attention-deficit/Hyperactivity Disorder - combined type (ADHD-C). We posit that ADHD-C is due to a primary deficit in a neural system emerging from the reticular formation within the hindbrain/midbrain region that is present early in ontogeny and remains relatively static throughout the lifetime. Further, we posit that the diminution of symptoms frequently seen throughout development is related to the degree to which frontostriatal systems are able to compensate for these early deficits through the use of effort or """"""""top-down"""""""" executive control. To test this hypothesis, we propose to use functional magnetic resonance imaging (fMRI) along with neurocognitive measures in three groups of young adults. Two groups consist of patients from a longitudinal sample, all of whom met criteria for ADHD-C during childhood. Among these, many can be clearly identified either as ADHD persisters (ADHD-P) or ADHD remitters (ADHD-R). In addition, we have well-matched controls who never met criteria for any subtype of ADHD. Thus, we will evaluate the neural correlates of diverse developmental pathways in ADHD-C. If our hypotheses are correct, behavioral and fMRI indices of the system emerging the reticular formation should differ from controls in those who had childhood ADHD-C irrespective of adult clinical status. In contrast, measures of frontostriatal function should vary as a function of adult status such that more severe ADHD symptoms in adulthood are associated with poorer efficiency on these measures while those no longer having significant ADHD symptoms should perform more similarly to never-ADHD controls. ? ? ?
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