Alterations in the Ventral Attention Network During the Stop-Signal Task in Children With ADHD: An Event-Related
Tieme W P Janssen1, Dirk J Heslenfeld1, Rosa van Mourik2
11 VU University Amsterdam, The Netherlands.
Insights
Children with ADHD show distinct brain activity differences, particularly in attention networks, challenging the idea that ADHD is solely an inhibitory control deficit. These findings highlight the role of attention in ADHD.
Area of Science:
- Neuroscience
- Developmental Psychology
- Cognitive Science
Background:
- Attention-Deficit/Hyperactivity Disorder (ADHD) is often modeled with response inhibition deficits.
- However, attentional deficiencies may offer a more comprehensive explanation for observed impairments.
Purpose of the Study:
- To investigate the neurophysiological underpinnings of response inhibition in ADHD.
- To test the hypothesis that attentional deficits, rather than solely inhibitory control issues, contribute to ADHD psychopathology.
Main Methods:
- Dense array electroencephalography (EEG) and event-related potentials (ERPs) were recorded during the stop-signal task (SST).
- 46 children with ADHD and 51 controls participated.
- N2 and P3 ERP components were analyzed and localized using the LAURA inverse solution.
Main Results:
- Children with ADHD exhibited reduced N2 and P3 amplitudes compared to controls.
- ADHD participants showed altered brain activation in regions including the right inferior frontal gyrus (rIFG), supplementary motor area (SMA), and anterior cingulate cortex (ACC) during inhibition tasks.
- A success-related N1 modulation was specific to the ADHD group.
Conclusions:
- Findings suggest that impairments in the ventral attention network are implicated in ADHD.
- This challenges the prevailing view of ADHD as primarily a disorder of impaired inhibitory control.
- Attentional network dysfunctions may be a more accurate explanation for ADHD symptoms.
Objective:
Deficits in response inhibition figure prominently in models of ADHD; however, attentional deficiencies may better explain previous findings of impaired response inhibition in ADHD. We tested this hypothesis at the neurophysiological level.
Method:
Dense array ERPs (event-related potentials) were obtained for 46 children with ADHD and 51 controls using the stop-signal task (SST). Early and late components were compared between groups. N2 and P3 components were localized with LAURA distributed linear inverse solution.
Results:
A success-related N1 modulation was only apparent in the ADHD group. N2 and P3 amplitudes were reduced in ADHD. During the successful inhibition N2, the ADHD group showed reduced activation in right inferior frontal gyrus (rIFG), supplementary motor area (SMA), and right temporoparietal junction (rTPJ), and during failed inhibition in the rIFG. During the successful inhibition P3, reduced activation was found in anterior cingulate cortex (ACC) and SMA.
Conclusion:
Impairments in the ventral attention network contribute to the psychopathology of ADHD and challenge the dominant view that ADHD is underpinned by impaired inhibitory control.
