Behavioral and neurofunctional profiles of delay aversion in children with attention-deficit hyperactivity disorder.

IF 5.8 1区 医学 Q1 PSYCHIATRY
Pilar Fernández-Martín, Daniela Tovar-Suárez, Rocío Rodríguez-Herrera, José J León, Rosa Cánovas, Pilar Flores
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引用次数: 0

Abstract

Despite substantial efforts to unravel cognitive heterogeneity in ADHD, the examination of motivational variability, particularly delay aversion, remains limited. This study aimed to identify homogeneous delay-averse profiles in children with ADHD to understand motivational deficits. Delay-averse profiles were examined in a clinically well-characterized sample of 43 children with ADHD and 47 control participants using cluster analyses on an experiential delay discounting task. External validation analyses included parents' and teachers' clinical ratings, and fNIRS-based resting-state functional connectivity (rsFC) from the frontoparietal (FPN) and the default mode (DMN) networks. A five-profile solution best fit the data. Two clusters, labeled Conventional and Conventional-steeper, exhibited a conventional reward discount with increased delay but differed in the discounting slope. Three clusters demonstrated altered discounting: Steep discounting (abrupt devaluation of the reward), Shallow discounting (shallow discounting), and Zero discounting (no devaluation across delay durations). 77.78% of ADHD-C children clustered into steep discounting profiles, while 41.67% of ADHD-IN children were found in Shallow and Zero profiles, showing a significant disparity in the distribution of categorical presentations. External validation showed no differences in clinical ratings. However, clusters showing Zero and Shallow discounting demonstrated hypoconnectivity within and between FPN and DMN nodes. Delay aversion in ADHD spans a continuum from decreased to increased discounting rather than being solely defined by steeper discounting. These findings highlight the relevance of dimensional approaches in capturing ADHD's motivational heterogeneity and identifying distinct neurobiological substrates, with implications for improving diagnostic protocols and intervention strategies through the incorporation of behavioral measures of reward processing.

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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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