The University of Southampton
University of Southampton Institutional Repository

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

Causal models of attention-deficit/hyperactivity disorder: from common simple deficits to multiple developmental pathways
Causal models of attention-deficit/hyperactivity disorder: from common simple deficits to multiple developmental pathways
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.
attention-deficit-hyperactivity disorder, causal models, executive function, delay aversion, development, dopamine
0006-3223
1231-1238
Sonuga-Barke, Edmund J.S.
bc80bf95-6cf9-4c76-a09d-eaaf0b717635
Sonuga-Barke, Edmund J.S.
bc80bf95-6cf9-4c76-a09d-eaaf0b717635

Sonuga-Barke, Edmund J.S. (2005) Causal models of attention-deficit/hyperactivity disorder: from common simple deficits to multiple developmental pathways. Biological Psychiatry, 57 (11), 1231-1238. (doi:10.1016/j.biopsych.2004.09.008).

Record type: Article

Abstract

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.

This record has no associated files available for download.

More information

Published date: 2005
Additional Information: Advancing the neuroscience of ADHD
Keywords: attention-deficit-hyperactivity disorder, causal models, executive function, delay aversion, development, dopamine

Identifiers

Local EPrints ID: 40518
URI: http://eprints.soton.ac.uk/id/eprint/40518
ISSN: 0006-3223
PURE UUID: 4713179c-6c69-45b7-b6e9-d7894e857183

Catalogue record

Date deposited: 04 Jul 2006
Last modified: 15 Mar 2024 08:20

Export record

Altmetrics

Contributors

Author: Edmund J.S. Sonuga-Barke

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×