Causal models of attention-deficit/hyperactivity disorder: from common simple deficits to multiple developmental pathways

Biol Psychiatry. 2005 Jun 1;57(11):1231-8. doi: 10.1016/j.biopsych.2004.09.008.


Until recently, causal models of attention-deficit/hyperactivity disorder (ADHD) have tended to focus on the role of common, simple, core deficits. One such model highlights the role of executive dysfunction due to deficient inhibitory control resulting from disturbances in the frontodorsal striatal circuit and associated mesocortical dopaminergic branches. An alternative model presents ADHD as resulting from impaired signaling of delayed rewards arising from disturbances in motivational processes, involving frontoventral striatal reward circuits and mesolimbic branches terminating in the ventral striatum, particularly the nucleus accumbens. In the present article, these models are elaborated in two ways. First, they are each placed within their developmental context by consideration of the role of person x environment correlation and interaction and individual adaptation to developmental constraint. Second, their relationship to one another is reviewed in the light of recent data suggesting that delay aversion and executive functions might each make distinctive contributions to the development of the disorder. This provides an impetus for theoretical models built around the idea of multiple neurodevelopmental pathways. The possibility of neuropathologic heterogeneity in ADHD is likely to have important implications for the clinical management of the condition, potentially impacting on both diagnostic strategies and treatment options.

Publication types

  • Review

MeSH terms

  • Animals
  • Attention Deficit Disorder with Hyperactivity / physiopathology*
  • Attention Deficit Disorder with Hyperactivity / psychology
  • Dopamine / metabolism
  • Humans
  • Mental Processes / physiology*
  • Models, Psychological
  • Motivation
  • Neural Networks, Computer*
  • Neural Pathways / physiopathology*


  • Dopamine