Disentangling Deficits in Adults With Attention-Deficit/Hyperactivity Disorder

Bekker, Evelijne M.; Overtoom, C.C.E.; Kooij, J. J. Sandra; Buitelaar, Jan K.; Verbaten, Marinus N.; Kenemans, J. Leon

doi:10.1001/archpsyc.62.10.1129

Cited by 102 publications

(86 citation statements)

References 49 publications

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“…Moreover, the P3 is altered in clinical groups such as those with schizophrenia and ADHD (Bekker et al, 2005;Groom et al, 2008;Groom et al, 2010;Hughes, Fulham, Johnston, & Michie, 2012;Wiersema & Roeyers, 2009) and the NGA described by Fallgatter et al is also reduced in these groups (Fallgatter, 2001;Fallgatter et al, 2004;Fallgatter & Muller, 2001). …”

Section: The P3 Event-related Potentialmentioning

confidence: 99%

“…In particular, reduced N2 amplitude has often been hailed as a marker of impaired inhibitory control in ADHD (Barry et al, 2003;Brandeis et al, 1998;Groom et al, 2010;Liotti et al, 2005). However, this population also tend to show reduced P3 amplitude (Bekker et al, 2005;Groom et al, 2008;Groom et al, 2010;Hughes et al, 2012;Wiersema & Roeyers, 2009) and altered P3 topography (Fallgatter et al, 2004) as well as a much wider range of deficits in action control (Johnson et al, 2007;Kuntsi & Klein, 2012;Simmonds et al, 2007). Establishing the parameters that modulate the N2 and P3 will improve the measurement of action control in ADHD and other clinical populations, potentially leading to a more refined understanding of the particular neural systems that underlie in specific disorders or symptom dimensions.…”

Section: Implications and Limitationsmentioning

confidence: 99%

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Differential modulation of the N2 and P3 event-related potentials by response conflict and inhibition

Groom

Cragg

2015

Brain and Cognition

156

127

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Background: Developing reliable and specific neural markers of cognitive processes is essential to improve understanding of healthy and atypical brain function. Despite extensive research there remains uncertainty as to whether two electrophysiological markers of cognitive control, the N2 and P3, are better conceptualised as markers of response inhibition or response conflict. The present study aimed to directly compare the effects of response inhibition and response conflict on the N2 and P3 event-related potentials, withinsubjects. Method:A novel hybrid go/no-go flanker task was performed by 19 healthy adults aged 18 to 25 years while EEG data were collected. The response congruence of a central target stimulus and 4 flanking stimuli was manipulated between trials to vary the degree of response conflict. Response inhibition was required on a proportion of trials. N2 amplitude was measured at two frontal electrode sites; P3 amplitude was measured at 4 midline electrode sites.Results: N2 amplitude was greater on incongruent than congruent trials but was not enhanced by response inhibition when the stimulus array was congruent. P3 amplitude was greater on trials requiring response inhibition; this effect was more pronounced at frontal electrodes. P3 amplitude was also enhanced on incongruent compared with congruent trials. Discussion:The findings support a role for N2 amplitude as a marker of response conflict and for the frontal shift of the P3 as a marker of response inhibition. This paradigm could be applied to clinical groups to help clarify the precise nature of impaired action control in disorders such as attention deficit/hyperactivity disorders (ADHD).3

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Section: The P3 Event-related Potentialmentioning

confidence: 99%

Section: Implications and Limitationsmentioning

confidence: 99%

Differential modulation of the N2 and P3 event-related potentials by response conflict and inhibition

Groom

Cragg

2015

Brain and Cognition

156

127

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“…The no-go N2-P3 complex is consistently seen over fronto-central scalp sites on trials requiring response inhibition, 200-600 msec after no-go stimulus onset. Although their functions are debated, there is consensus that the N2 component probably indexes aspects of response selection or conflict detection that signal the need for response inhibition (Falkenstein, 2006;Kok, Ramautar, De Ruiter, Band, & Ridderinkhof, 2004) while the latency and amplitude of the P3 have been shown to predict successful inhibitions in keeping with Logan's (1994) race model of inhibition (Bekker, Overtoom, et al, 2005;Bekker, Kenemans, & Verbaten, 2004;Falkenstein, Hoomann, & Hohnsbein, 1999). Hence, the findings of Dockree et al suggest a reduced requirement for response inhibition in the SART fixed .…”

Section: Introductionmentioning

confidence: 95%

Two Types of Action Error: Electrophysiological Evidence for Separable Inhibitory and Sustained Attention Neural Mechanisms Producing Error on Go/No-go Tasks

O’Connell

Dockree

Bellgrove

et al. 2009

Journal of Cognitive Neuroscience

113

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Abstract& Disentangling the component processes that contribute to human executive control is a key challenge for cognitive neuroscience. Here, we employ event-related potentials to provide electrophysiological evidence that action errors during a go/ no-go task can result either from sustained attention failures or from failures of response inhibition, and that these two processes are temporally and physiologically dissociable, although the behavioral error-a nonintended response-is the same. Thirteen right-handed participants performed a version of a go/no-go task in which stimuli were presented in a fixed and predictable order, thus encouraging attentional drift, and a second version in which an identical set of stimuli was presented in a random order, thus placing greater emphasis on response inhibition. Electrocortical markers associated with goal maintenance (late positivity, alpha synchronization) distinguished correct and incorrect performance in the fixed condition, whereas errors in the random condition were linked to a diminished N2-P3 inhibitory complex. In addition, the amplitude of the error-related negativity did not differ between correct and incorrect responses in the fixed condition, consistent with the view that errors in this condition do not arise from a failure to resolve response competition. Our data provide an electrophysiological dissociation of sustained attention and response inhibition. &

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“…The contribution of non-inhibitory processes is still largely neglected in the 'reactive' inhibitory control literature, even though computational work indicates that most of SSRT is occupied by afferent processes Logan et al, 2014Logan et al, , 2015Salinas & Stanford, . Other studies have shown that stopping deficits in certain clinical populations could be due to impairments in signal detection rather than in inhibition per se (e.g., Bekker et al, 2005). Thus, a failure to detect the signal quickly can have important consequences and lead to 'stopping' deficits.…”

Section: Cortical-basal Ganglia Modelmentioning

confidence: 99%

Control in Response Inhibition

Verbruggen

Logan

2017

The Wiley Handbook of Cognitive Control

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Disentangling Deficits in Adults With Attention-Deficit/Hyperactivity Disorder

Abstract: Disturbed attentional processing of the stop signal contributed to impaired stopping in adults with ADHD. This finding may have implications for treatment.

Cited by 102 publications

References 49 publications

Differential modulation of the N2 and P3 event-related potentials by response conflict and inhibition

Differential modulation of the N2 and P3 event-related potentials by response conflict and inhibition

Two Types of Action Error: Electrophysiological Evidence for Separable Inhibitory and Sustained Attention Neural Mechanisms Producing Error on Go/No-go Tasks

Control in Response Inhibition

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