Damage to prefrontal cortex associated with ADHD-like behavior; ADHD deficits on neuropsychological tests associated w. prefrontal lobe function; autonomic under-arousal (GSR, heart rate, etc);  decreased blood flow to prefrontal regions and striatum (globus pallidus, caudate nucleus, putamen); diminished metabolic activity in left anterior frontal correlates with severity of ADHD symptoms.

fMRI Findings: differences in size of temporal lobe (speech areas); corpus callosum; prefrontal cortex, and basal ganglia seen in ADHD versus normals. Differences in metabolic rate as indicated by blood flow during tasks requiring attention also seen.

Stimulants (amphetamines and related compounds) cause dopaminergic neurons that project to (among other structures) the basal ganglia to secrete more dopamine.  Basal ganglia structures have receptors for dopamine.  Basal ganglia are involved in control of learned motor sequences, repetitive behavior, and operant (reward-based) learning and performance.  Stimulants reduce symptoms of ADHD, presumably by increasing availability of dopamine.