**1. Introduction**

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with symptoms including sustained attention problems, impulsivity, and hyperactivity, a ffecting ~5% of children and adolescents [1]. Several studies have shown deficits of performance monitoring and adaptive adjustment in children and adults with ADHD [2–4]. While some ADHD symptoms may decline from childhood to adulthood in a subset of children [5], the developmental trajectory of performance monitoring and adaptive adjustment along with their underlying neural correlates of the deficits in youth with ADHD remain poorly understood.

Previous research has shown that children with ADHD perform poorly in a wide range of tasks involving conflict monitoring and inhibitory control (e.g., Go/No-go, flanker, and stop-signal tasks [6]).

In general, their behavioral responses in these high cognitive demand tasks tended to be slower, more variable, and more error-prone, and they showed deficits in adaptation to task demands and following error responses [7–9]. Post-error slowing, or an increase in RT on trials following an error, is a common behavioral indicator of adaptive control [10]. A failure to slow responding on post-error trials has been interpreted as reflecting a deficit in adaptive control. Diminished post-error slowing was found in children with ADHD, relative to controls [11,12]; however, other studies [13,14] reported intact post-error slowing in children with ADHD compared to typically developing children using a flanker task.

In studies using event-related potential (ERP) measures, children with ADHD have also shown deficits in neurocognitive processes of response inhibition and performance monitoring. Error-related negativity (ERN) and error positivity (Pe) are two reliable ERP indices of performance monitoring. Both components are time-locked to responses. The ERN has been observed in a variety of tasks; its onset coincides with response initiation, and it peaks 50–100 milliseconds (msec) thereafter [15]. The ERN has a fronto-central distribution, and is believed to be generated in the anterior cingulate cortex and nearby medial frontal regions involved in self-regulation and performance monitoring [15]. The ERN increases with age after early childhood and reflects the activity of a system that detects errors, increases cognitive control, and adjusts behaviors [15]. Following the ERN, the Pe occurs about 200–400 msec after an error and has a centro-parietal distribution, reflecting error awareness, motivational significance of errors, and initiation of adaptive control processes [16]. Some ADHD studies reported reduced ERN in children and adults with ADHD relative to healthy controls (HC) [17,18]; others reported null findings [19,20], and still another reported increased ERN in ADHD [21] (see review papers [6,22]). Pe results in ADHD studies are also mixed: some studies reported diminished Pe [11,13,23,24] (see review [6]), suggesting deficient error valuation or conscious error processing in ADHD, but others reported no di fference [21,25] between participants with ADHD and HC.

In addition to the response-locked ERN and Pe, the N2 and P3 are two main ERP components elicited during stimulus processing, reflecting processes involved in stimulus evaluation and response selection. Specifically, the N2 is a fronto-central negative voltage deflection peaking between 200 and 400 msec after stimulus onset; in cognitive control tasks, a larger N2 is elicited by high conflict trials (e.g., No-go trials in Go/No-go tasks, incongruent trials in flanker tasks) relative to low cognitive conflict trials (e.g., Go trials in Go/No-go tasks and congruen<sup>t</sup> trials in flanker tasks), reflecting adaptive conflict monitoring [26–28]. The P3 is a central-parietal positive voltage deflection peaking between 300 and 500 msec after stimulus onset, first observed in an auditory oddball task, which reflects processes related to attention and working memory [29]; it is also observed in cognitive control tasks, following the N2, relating to resource allocation necessary for task performance. Several studies have reported impairments of processes associated with N2 and P3 in ADHD, but the direction in which participants with ADHD di ffer from HC in these studies was inconsistent. For instance, some studies reported, compared to HC, participants with ADHD showed reduced N2 on successful inhibition trials in a stop-signal task [30] and a Go/No-go task [31], and reduced N2 congruency e ffect in a flanker task [25]; others did not find N2 di fferences in stop-signal tasks [32] or reported an increased N2 e ffect in No-go vs. Go trials in a Go/No-go task [33,34]. Reduced P3 in ADHD has been reported in Go/No-go tasks (see meta-analyses paper [34,35]), a flanker task [36], and an attention network test [37], but not in some other studies (see review paper [38]).

Variability of behavioral and ERP findings might be accounted for by several factors, including participant heterogeneity, sample size, age range, task paradigms and analysis strategies across laboratories [6]. Many studies have failed to report ADHD subtypes and comorbidity; some studies may have been underpowered to detect group di fferences in behavioral and ERP correlates of performance monitoring. More work is needed to explore whether the inconsistent results can be accounted for by sampling and methodological di fferences across studies. Moreover, examining how behavior and ERP correlates of performance monitoring correlate with ADHD symptomatology, and whether the relationship may change with age in youth with ADHD, may improve our understanding of performance monitoring processes and their development in ADHD [6]. Few studies have investigated the relationship of behavioral and ERP correlates with symptom severity in children with ADHD. In adults, Marquardt et al. [18] observed that P3 amplitude in high conflict trials was inversely correlated with symptom severity in the ADHD group; Wiersema et al. [20] reported reduced Pe in error trials and P3 amplitude in high conflict trials were associated with more ADHD symptoms; Herrmann et al. [8] compared individuals with low- and high-ADHD symptom scores in a non-clinical population, and observed lower Pe in the group with higher symptoms scores. In adolescents and adults, Michelini et al. [17] found that ADHD symptoms were correlated with congruen<sup>t</sup> errors, reaction time variability, and Pe. Using magnetic resonance imagining, a brain development study of ADHD suggested a brain structural developmental delay in ADHD; this structural development study may be associated with a functional delay [39]. While conflict processing and performance monitoring developed with age in healthy youth, few ERP studies have had a large enough sample size and age range to examine the developmental trajectory of performance monitoring in ADHD [25].

In the present study, we tested a relatively large (number of participants *n* = 77 in each group) sample of children and adolescents with ADHD with a broad age range (8–18 years), and ageand gender-matched HC in an arrow flanker task. Participants' behavioral performance and ERP correlates of performance monitoring and conflict processing were compared between groups, and these measures were related to ADHD symptom severity measured by the DSM-Oriented ADHD Problems Scale from the Child Behavior Checklist (CBCL) as a continuous measure within and across groups. We hypothesized that youth with ADHD would display slower reaction times, more reaction time variability (RTV), and reduced post-error slowing relative to healthy controls. Considering the inconsistent findings in the ERN, Pe, N2, and P3 in ADHD, we reported ERN and Pe on both error and correct trials and N2 and P3 on both congruen<sup>t</sup> and incongruent trials [6,34]. We focused on di fference scores between error and correct trials for the ERN and Pe error e ffects, along with di fference scores between incongruent and congruen<sup>t</sup> trials for N2 and P3 congruency e ffects, when discussing group di fferences and developmental alterations in ADHD. We hypothesized reductions in the ERN and Pe error e ffects and reduced N2 and P3 congruency e ffects in ADHD, compared to HC. We also hypothesized that behavioral and ERP impairments might be greater with increasing symptom severity within groups. In addition, we investigated whether behavioral and ERP alterations in ADHD vary with diagnostic subtype and age; we hypothesized that there might be a developmental delay in behavioral and ERP indices of performance monitoring in ADHD.

#### **2. Materials and Methods**
