Dissecting the neuropsychological structure of ADHD : inhibitory control and delay aversion
Dissecting the neuropsychological structure of ADHD : inhibitory control and delay aversion
Attention deficit/hyperactivity disorder (ADHD) has been characterised as a clinically and genetically heterogenous disorder. Over the past decades, researchers have studied the neuropsychological causal factors associated with this heterogeneity. Neuropsychological deficits such as inhibitory control (Barkley, 1997) and delay aversion (Sonuga-Barke et al., 1992) have been associated with ADHD. However, none of these unitary causal models can fully explain the aetiology of the disorder. In fact, there is a theoretical and empirical focus on identifying multiple causal pathways (Sonuga-Barke, 2002). Up to date, very few studies have been conducted to distinguish these different causal pathways to ADHD by using multiple indicators of these neuropsychological domains. In the present thesis 71 pairs of children with ADHD and their unaffected siblings and 50 children were examined on inhibitory control and delay aversion tasks as part of the Southampton site of the International Multicentre ADHD Genetics Study (IMAGE project). First, these two neuropsychological deficit domains were found to be two separate latent constructs. Secondly these latent factors of inhibitory control and delay aversion deficits were found to be associated with ADHD. Third, a comparison of probands and their siblings found little evidence of familial effects on either construct. Confounding effects such as age, gender, non-executive processes, IQ, and comorbid ODD were also investigated in a secondary analysis. The current thesis provides strong support for the dual pathway model of ADHD – but leaves open the question of whether these effects are familial or genetic in nature. Based on the present results, clinical and research implications on using neuropsychological subtypes, as part of the clinical diagnosis, are discussed.
University of Southampton
Bitsakou, Paraskevi
4f249dba-07a9-4dcc-a458-541658e95106
2007
Bitsakou, Paraskevi
4f249dba-07a9-4dcc-a458-541658e95106
Bitsakou, Paraskevi
(2007)
Dissecting the neuropsychological structure of ADHD : inhibitory control and delay aversion.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Attention deficit/hyperactivity disorder (ADHD) has been characterised as a clinically and genetically heterogenous disorder. Over the past decades, researchers have studied the neuropsychological causal factors associated with this heterogeneity. Neuropsychological deficits such as inhibitory control (Barkley, 1997) and delay aversion (Sonuga-Barke et al., 1992) have been associated with ADHD. However, none of these unitary causal models can fully explain the aetiology of the disorder. In fact, there is a theoretical and empirical focus on identifying multiple causal pathways (Sonuga-Barke, 2002). Up to date, very few studies have been conducted to distinguish these different causal pathways to ADHD by using multiple indicators of these neuropsychological domains. In the present thesis 71 pairs of children with ADHD and their unaffected siblings and 50 children were examined on inhibitory control and delay aversion tasks as part of the Southampton site of the International Multicentre ADHD Genetics Study (IMAGE project). First, these two neuropsychological deficit domains were found to be two separate latent constructs. Secondly these latent factors of inhibitory control and delay aversion deficits were found to be associated with ADHD. Third, a comparison of probands and their siblings found little evidence of familial effects on either construct. Confounding effects such as age, gender, non-executive processes, IQ, and comorbid ODD were also investigated in a secondary analysis. The current thesis provides strong support for the dual pathway model of ADHD – but leaves open the question of whether these effects are familial or genetic in nature. Based on the present results, clinical and research implications on using neuropsychological subtypes, as part of the clinical diagnosis, are discussed.
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Published date: 2007
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Local EPrints ID: 466370
URI: http://eprints.soton.ac.uk/id/eprint/466370
PURE UUID: b4d0ac14-49cd-4fef-819a-4ed5616f2c2c
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Date deposited: 05 Jul 2022 05:12
Last modified: 16 Mar 2024 20:40
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Author:
Paraskevi Bitsakou
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