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 × 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.
Key Words
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Article info
Publication history
Published online: November 11, 2004
Accepted:
September 14,
2004
Received in revised form:
August 30,
2004
Received:
May 26,
2004
Identification
Copyright
© 2004 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
