"Although the specific cause of ADHD has been relatively elusive, recent advances in research methods and technology have helped us to find some of the neurobiological correlates with ADHD. This research into the cause of ADHD, is focus on neural circuits centered in the prefrontal cortex and striatum, as well as on the brain stem catecholamine systems that innervate this circuitry. Information from neural imaging studies suggest that impairments in these prefrontal-striatal regions may play a key role in determining the cause of ADHD.
Studies using magnetic resonance imaging (MRI) have identified subtle abnormal changes in the prefrontal cortex and basal ganglia unique to ADHD. Findings of a smaller right prefrontal cortex, in addition to a smaller caudate nucleus and globus pallidus, in children with ADHD suggest the possibility that there may be some association with fewer prefrontal corticostriatal fibers and less pallidal feedback to prefrontal regions of the brain. Also, the reduced area in the corresponding anterior genu region of the corpus callosum may indicate the presence of fewer interhemispheric fibers in prefrontal regions. Abnormalities have also been found in ADHD regions that project to the prefrontal cortex, including the parietal-occipital regions, and the cerebellum. These findings raise the possibility that brain abnormalities in ADHD extend beyond the prefrontal cortex and striatum to the posterior and subcortical regions that innervate these frontal circuits.
Some of these neuroimaging studies have provided some additional evidence of prefrontal-striatal impairment in ADHD. Research with single photon emission computerized tomography (SPECT) and positron emission tomography (PET) have reported that there may be lower basal activity in the prefrontal cortex and striatum of children and adults, but not adolescents with ADHD. More recent studies of the cause of ADHD employing functional MRI, have tentatively identified altered prefrontal-striatal activation with deficits in an individual?s control of inhibition. Reduced striatal activation during response inhibition tasks have been consistently reported in children and adolescents with this disease. However, prefrontal activation during the same tasks was enhanced in children with ADHD, but reduced in adolescents with this disorder.
The prefrontal cortex and striatum are believed to be very sensitive to catecholaminergic input from the brain stem nuclei, including noradrenaline (NA) from the locus coeruleus, and dopamine (DA) from the ventral tegmental area and substantia nigra. The fact that almost all medications which work in individuals with ADHD affect the levels of noradrenaline and dopamine transmission, suggests that perturbations of these systems may play a significant role in the cause of ADHD. However, a large group of studies of the catecholamine function in ADHD have continued to yield highly inconsistent findings. Only more recent studies that used central indices of catecholamine function that examined more homogenous subgroups of children with ADHD, have provided evidence of dopamine and noradrenaline dysfunction which is believed to possibly be a cause of ADHD."
Although they aren't sure what causes ADHD, I think that the presence of MRI features which are unique to individuals with ADHD implies that there is a biological basis for the condition.
MS is not well understood, nor Lupus. They don't get challenges to the biological basis of their existence.