One necessary assumption of this approach is that ADHD (or even its clinical subtypes) represents a homogenous patient population. However, there is now considerable justification suggesting that multiple developmental and pathophysiological pathways inform ADHD symptomatology (Fair et al., 2012; Nigg et al., 2004; Sonuga-Barke et al., 2003). The implications of this premise are considerable. Including multiple etiologically distinct subgroups as a unitary sample in any study is likely to produce muted effects and could be why only modest effect sizes are often seen for large genetic and behavioral studies, and why neuroimaging studies yield difficult to replicate effects (Hyman, 2007). Of course, overcoming the limitations of conventional research in mental disorders is not straightforward and may require new approaches to understanding complex disease (Hyman, 2007). Nevertheless, understanding the neurobiology underlying the disease phenotypes is essential for improving treatment and consequently for the wellbeing of individuals with ADHD.
