Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms

Abstract

Objective: We examined behavioral and neural markers of emotion competence in young children as predictors of psychopathology, and as mediators of the relation between hyperactivity/impulsivity (H/I) and psychopathology. Method: At Time 1 (T1), children (n = 49; ages 4–7 years) with and without H/I symptoms completed a frustration task. Frustration, observed emotion, and neural activity (P1, N2, and P3 event-related potentials) were measured. Symptoms of psychopathology were collected 18 months later (Time 2; T2). Results: T1 lability, negative affect, and frustration predicted T2 depression and aggression symptomatology, controlling for T1 symptoms. Children with difficulty allocating neural resources during and after frustration were at risk for depression, aggression, and anxiety symptoms, controlling for earlier symptoms. P3 amplitudes during recovery mediated the relation between H/I and later depression. Conclusion: Markers of emotion competence contribute to psychopathology symptoms, particularly in children at risk for attention-deficit/hyperactivity disorder (ADHD). Emotion competence skills may be useful intervention targets.

Keywords

emotion attention-deficit/hyperactivity disorder depression aggression neuroimaging

Emotion competence involves the ability to understand and regulate emotions appropriately and consists of three important components: (a) emotion understanding—knowledge of emotions, including the causes and effects of emotions; (b) emotion reactivity—arousal, observable expression of emotions, and emotion intensity; and (c) emotion regulation—employing physical, cognitive, or behavioral strategies to respond to emotional situations (Denham et al., 2007; Graziano & Garcia, 2016). These components draw on multiple systems, including cognitive, behavioral, physiological, and neural processes. Emotion competence difficulties are common among children with attention-deficit/hyperactivity disorder (ADHD; for example, Anastopoulos et al., 2011; Graziano & Garcia, 2016; Serrano et al., 2015), which is a neurodevelopmental disorder characterized by hyperactivity/impulsivity (H/I) and/or inattention. Deficits in emotion competence are also associated with other types of psychopathology, including depression (e.g., Lopez-Duran et al., 2013), aggression (e.g., Denham et al., 2002), and anxiety (e.g., Mathews et al., 2016). Conceptually, psychopathology and emotion competence are thought to be highly related but distinct phenomena. Some symptoms arise directly from emotion competence difficulties (Werner & Gross, 2010) as symptoms reflect chronic maladaptive emotion responses and strategies. However, emotion difficulties do not always indicate psychopathology, as impairing emotion difficulties may occur in the absence of a disorder (e.g., Stringaris & Goodman, 2009).

Emotion competence difficulties in children with ADHD symptoms may contribute to the development of co-occurring psychopathology (Steinberg & Drabick, 2015). However, literature on the relation between emotion competence, ADHD symptoms, and comorbid psychopathology is limited, and longitudinal research in this area is particularly sparse. Much of the literature on emotion competence has focused on behavioral measures of emotion competence; less is known about how neural indicators of emotion competence may predict the development of psychopathology. This study seeks to identify neural and behavioral indicators of emotion competence that predict later symptoms of psychopathology in young children with and without H/I symptoms. Furthermore, we examine whether these indicators mediate the relation between early H/I symptoms and later psychopathology symptoms.

Emotion Competence, ADHD Symptomatology, and Development of Psychopathology

ADHD is associated with impairment in recognizing and identifying emotions in others (e.g., Serrano et al., 2015), as well as emotion lability and dysregulation (e.g., Anastopoulos et al., 2011; Graziano & Garcia, 2016). Emotion regulation difficulties are evident according to parent report (e.g., Sjöwall et al., 2013), child report (e.g., Seymour et al., 2012), and observation during frustrating laboratory tasks (e.g., Scime & Norvilitis, 2006). Furthermore, there is some evidence that the H/I domain of ADHD is specifically related to emotion dysregulation compared with the inattentive domain (e.g., Maedgen & Carlson, 2000). These deficits in emotion competence may play a critical role in the development of comorbid psychopathology in children with ADHD (Steinberg & Drabick, 2015), but few studies have directly examined emotion competence as a mediator of the relation between ADHD and comorbid symptoms. In a cross-sectional study, parent-reported emotion lability partially mediated the relation between ADHD and other psychopathology (Anastopoulos et al., 2011). Seymour et al. (2012, 2014) found that school-age children with more ADHD (particularly H/I) symptoms experienced high emotion reactivity and poor emotion regulation, which in turn put them at risk for future symptoms of depression. There is also indirect evidence that emotion competence may mediate the relation between ADHD symptoms and other forms of psychopathology. For instance, children with high ADHD symptoms and emotion reactivity to anger showed more aggression with peers 3 years later (Thorell et al., 2016). Young adults with comorbid anxiety and ADHD have been found to have more difficulties regulating their emotions than those with anxiety or ADHD alone (Jarrett, 2016). Thus, difficulties with emotion competence are related to anxiety and aggression, particularly when co-occurring with ADHD. In sum, emotion competence has been linked with symptoms of ADHD and other psychopathology, but few studies have directly examined emotion competence as a mediator. The few studies that have done so have focused on older children and used behavioral measures of emotion competence.

Neural Indicators of Emotion Competence

It is important to build on existing research on early emotion competence to include neural markers of emotion competence because these may emerge prior to observable behavioral markers of emotion dysregulation. In particular, there is a need for longitudinal research on neural markers of emotion competence early in the development of emotion regulation skills when neural plasticity may allow for greater impact of intervention. Event-related potentials (ERPs) offer an important tool for measuring neural activity in emotional contexts, particularly among at-risk children. For instance, children with emotion dysregulation have been shown to exhibit altered ERPs on emotional tasks such as the affective Posner task, in which participants are given inaccurate feedback that their responses are incorrect on a simple computer game (e.g., Rich et al., 2005, 2007).

Three ERP components, the P1, N2, and P3, have been used to measure the impact of emotional burdens on cognitive processes, thereby making these components key neural markers of emotion competence. The P1 component is a positive deflection approximately 100 ms after stimulus onset that is thought to underlie early attention processing. Reduced P1 amplitude, suggesting deficits in initial attention, has been demonstrated in children with emotion dysregulation (Rich et al., 2007). The N2 component is a negative deflection about 200 ms after stimulus onset (Sur & Sinha, 2009) that is thought to measure inhibitory control and is larger (more negative) in dysregulated clinical populations following a negative mood induction (e.g., Stieben et al., 2007). Children with ADHD show larger N2 amplitudes while viewing emotional distractors, suggesting that emotion processing places a larger burden on cognitive resources for children with ADHD compared with typically developing children (López-Martín et al., 2013). The P3 component is a measure of attention allocation that occurs approximately 250 to 400 ms after stimulus onset (Sur & Sinha, 2009). This component was found to be reduced in children with bipolar disorder during the affective Posner task compared with typically developing children who showed increased P3 amplitudes, suggesting that difficulties regulating emotions interfere with attending to tasks when frustrated (Rich et al., 2005, 2007).

In the first wave of data collection in the present study, children with H/I symptoms showed little modulation in their allocation of neural resources (P3 and N2) during the affective Posner task compared with typically developing children (Lugo-Candelas, Flegenheimer, Harvey, & McDermott, 2017). Collectively, these studies suggest that children with psychopathology are less effective at modulating cognitive control and allocating attention, both during emotional situations and during nonemotional situations. It is important to understand whether these neural differences represent a risk factor for later psychopathology. To our knowledge, no longitudinal research has examined the predictive utility of neural markers of emotion competence for identifying children at risk for comorbid psychopathology, particularly in vulnerable populations such as children with ADHD symptoms.

The Present Study

The present study examines whether early markers of emotion competence predict later symptoms of anxiety, depression, and aggression and tests whether early emotion competence mediates the relation between early H/I and later symptoms of psychopathology. We examine emotion competence using multiple methods, including observations of behavior, child report of emotion, and neural markers. The sample includes young children (aged 4–7 years) who were oversampled for high H/I symptoms and, thus, at high risk for ADHD. We expected that young children with poor emotion competence would show greater anxiety, depression, and aggression symptoms approximately 18 months later (Time 2; T2), controlling for Time 1 (T1) symptoms. We expected that attenuated P1 and P3 and enhanced N2 during frustration would predict later symptoms. We also expected that emotion competence would mediate the relation between H/I and later psychopathology, such that greater symptoms of H/I would predict less emotion competence, which in turn would predict T2 psychopathology symptoms, controlling for T1 psychopathology symptoms.

Method

Participants

Participants were 49 children (33 boys¹) who took part in laboratory assessments when they were 4 to 7 years old (M = 6.41, SD = 0.87; T1) and again approximately 18 months later (T2) at 6 to 9 years old (M = 8.18, SD = 0.80; T2). Participants were drawn from a larger sample who participated at T1. The present sample included 32 of the original 37 control group children and 17 of the 31 children from the ADHD-risk group.² Two children were taking stimulant medication for ADHD at T1 (withheld for 48 hr). At T2, four children were taking (and withheld) stimulant medication for ADHD and two children were taking other medication (sertraline and nortriptyline; not withheld). At T2, nine children had diagnosed and three children had suspected ADHD. Children’s verbal skills were all at least average (standard scores: M = 111, SD = 11) on the National Institute of Health Toolbox Picture Vocabulary Test (Gershon et al., 2013) administered at T1. The sample was 80% European American, 18% multiethnic, and 2% Latinx. About half of the families had an income below US$80,000. All parents had at least a high school degree and most (88%) had at least a college degree.

Procedure

Participants were recruited via the university’s Child Studies Database, flyers sent through preschools, and advertisements in community centers and pediatrician offices. A phone interview assessing eligibility was conducted using the ADHD and oppositional defiant disorder sections of the National Institute of Mental Health Diagnostic Interview Schedule for Children-IV (DISC-IV; Shaffer et al., 2000). Children were eligible for the “ADHD-risk” group if they had six or more symptoms of H/I (at least three in two settings) and for the control group if they had two or fewer symptoms. Exclusionary diagnoses included intellectual disabilities, hearing or visual disabilities, language delays, cerebral palsy, epilepsy, autism spectrum disorder, or psychosis. At T1, parents completed questionnaires and children completed the affective Posner task to measure responses to frustration, while brain activity was measured using ERPs. At T2, children and families completed behavioral tasks, interviews, and questionnaires. This time lapse was selected to allow time for emotional and behavioral changes to occur but not so long that children were beginning to enter preadolescence, a period of rapid developmental changes. At each time point, families were paid US$20 for their participation and children received a prize. The study was approved at T1 and T2 by the university’s institutional review board.

T1 Measures

DISC-IV

The ADHD and oppositional defiant disorder sections of the DISC-IV interview were administered to parents via phone by a graduate student to recruit children into the ADHD-risk or control group. The DISC-IV is a structured diagnostic interview assessing psychopathology in children (Shaffer et al., 2000). Evidence suggests that the ADHD section of the DISC-IV is valid for use in children as young as 4 years old (Rolon-Arroyo et al., 2016). Scores range from 0 to 9 symptoms for H/I.

Emotion Regulation Checklist (ERC)

Parents completed the ERC, a 24-item questionnaire assessing parent perceptions of their child’s emotion regulation, with each item rated from 1 (rarely/never) to 4 (almost always). The emotion regulation subscale measures adaptive behaviors in emotion contexts, and the lability–negativity subscale measures mood lability. The ERC has good validity, and both subscales have shown good reliability (emotion regulation α = .83 and lability–negativity α = .96; Shields & Cicchetti, 1997). In the present sample, reliability of the lability–negativity subscale was good (α = .90) and reliability of the emotion regulation subscale was lower but adequate (α = .64). Scores were averaged to calculate each subscale, with a possible range of 1 to 4 for each subscale.

Frustration task

Children completed a modified affective Posner task (see Lugo-Candelas et al., 2017 for details), a frustration task in which children had to press a button corresponding to the location of a star on the computer screen and receive feedback regarding whether their response was correct or incorrect. Feedback was provided through a “thumbs up” or “thumbs down” icon after each of the 236 trials across four blocks. Children were told that they had to receive a stamp for each block to get a prize, and they were warned that the computer had been having problems. The first block (baseline; 40 trials) served as a reference for the subsequent blocks and consisted of trials in which children won points for every correct response and received a stamp at the end of each of these blocks. The second block (frustration; 78 trials), which assessed emotional reactivity to frustration, was rigged; on 40% of the trials, children were falsely told they answered incorrectly. The third block (regulation; 78 trials) assessed a form of emotion regulation (suppression). Children were told to mask their emotions as the incorrect feedback continued. After this block, children were told that they would still get stamps for Blocks 2 and 3 because the computer had been “malfunctioning.” The fourth and final block (recovery) was identical to baseline and assessed children’s ability to calm down after a frustrating experience.

Electroencephalography (EEG) was collected with a 64-channel Lycra Electro-Cap and segmented into ERP epochs that were time locked to stimulus presentation. Epochs were averaged separately for each type of the Posner trial: valid, invalid, and control and any epochs that exceeded ±150 uV were excluded from the analysis. The remaining usable epochs were then baseline corrected for each block using a 200-ms prestimulus baseline. The present study focuses on the P1, N2, and P3 ERP components. Both P1 (10–100 ms after stimulus onset) and N2 (50–220 ms after stimulus onset) mean amplitudes were assessed across the frontal region (collapsed across sites F3, F4, and FZ) as prior work suggests these components are evident in frontal regions when using similar types of tasks as the current study (Abundis-Gutiérrez et al., 2014; Rich et al., 2007). The P3 (130–400 ms after stimulus onset) mean amplitude was assessed at the frontocentral region (FC3, FC4, and FCZ). For additional details on waveform processing, see Lugo-Candelas et al. (2017) or Supplemental Materials. Note that because the N2 component is negative, higher values of this ERP component indicate less neural activity.

After each block (before receiving feedback on whether they earned a stamp), children self-reported how happy, sad, and frustrated they were. Children saw five images of a thermometer that ranged in fullness and indicated their level of each emotion by pointing to one of the five images, or stated if they were not feeling that emotion at all. Child-reported frustration was used in the present study, with scores ranging from 0 (no frustration) to 5 (highly frustrated) per block. Children’s negative affect (NA) expressions during 5-s epochs of each block were coded based on Davis’s (1995) dimensions of expressive behavior code. Undergraduate research assistants coded the presence/absence (0 = absent; 1 = present) of NA.³ When NA was present, they rated intensity (0 = mild; 1 = strong) every 5 s. Presence and intensity ratings were summed across 5-s intervals for each block and divided by the number of coded intervals per block. The possible range of scores was from 0 to 2 per block. To assess interrater reliability, 16 tapes were coded by two raters; first-order agreement coefficient (AC1; Wongpakaran et al., 2013) for presence/absence and intensity of NA was .89.

Emotion Matching Task

Children completed the 48-item Emotion Matching Task (EMT; Izard et al., 2003) to assess emotion understanding. In the first subscale, children selected an image with an emotion matching a target image. In the second subscale, children selected an image with an emotion matching a target situation. In the third subscale, children labeled the emotion in a target image, and in the fourth subscale, children selected an image that matched an emotion label. Performance was averaged across all four blocks. Scores could range from 0 to 12. Past studies have demonstrated good reliability (α = .81; Morgan et al., 2010). The present study showed adequate but lower reliability (α = .61), likely due to ceiling effects because children were slightly older than those in the reliability study (3–6 years old), in which age was related to EMT scores (Morgan et al., 2010).

T1 and T2 Measure

Behavior Assessment System for Children, Second Edition—Parent Rating Scale (BASC-2 PRS)

Parents completed the BASC-2 PRS (Reynolds & Kamphaus, 2004), a widely used scale measuring symptoms of psychopathology. This study used T-scores (using general age-based norms; T-scores have a mean of 50 and standard deviation of 10) from anxiety, depression, and aggression subscales from T2, with corresponding T1 scores included as control variables. These scales have good internal consistency, ranging from .84 to .88 (Reynolds & Kamphaus, 2004). BASC-2 PRS reliability in the present sample was good at T1 (anxiety α = .84, depression α =.86, aggression α = .90) and T2 (anxiety α = .87, depression α = .88, aggression α = .86).

T2 Measures

Behavior Assessment System for Children, Second Edition—Self-Report of Personality (BASC-2 SRP)

Children completed the BASC-2 SRP (Reynolds & Kamphaus, 2004). For children aged 6 to 7 years, the BASC-2 SRP-I was administered as an interview. Children indicate whether statements about their feelings and behavior are True or False. For children aged 8 to 11 years, the BASC-2 SRP-C was administered as an interview to maintain consistency. This study focuses on the anxiety and depression subscales. Internal consistency of the BASC-2 SRP-C is high (anxiety α = .86 and depression α = .84; Reynolds & Kamphaus, 2004). In the present study, BASC-2 SRP-C reliability was good for anxiety (α = .84) and moderate for depression (α = .60). Reliability was not calculated for the SRP-I because only 15 children completed this measure. T-scores (using general age-based norms) for depression and anxiety scales were used in the present study; there is no self-reported aggression scale to complement parent report.

Data Analysis

Descriptive statistics were calculated for all variables. Several variables were highly skewed (>2), so they were transformed (square root) and used in subsequent analyses: observed NA during baseline (skew = 2.58; transformed = 0.91) and recovery (skew = 3.12; transformed = 1.41); child-reported frustration during recovery (skew = 2.66; transformed = 0.99). All analyses were conducted in MPlus version 8 (Muthén & Muthén, 1998–2017), with full information maximum likelihood to account for missing data. Each T2 parent- and child-reported psychopathology measure was regressed on each T1 emotion competence variable and the corresponding T1 parent-reported psychopathology measure.⁴ Regressions were conducted separately for each psychopathology outcome and for each emotion competence variable. However, for variables from the affective Posner tasks (child-reported frustration, observed NA, P1 amplitudes, N2 amplitudes, and P3 amplitudes), scores from all four blocks of a single variable were entered together (e.g., the four P1 amplitude variables were entered together rather than in separate regressions) to control for performance on other blocks. T1 emotion competence variables were tested as mediators if they significantly predicted T2 psychopathology and were significantly correlated with T1 H/I. Mediation analyses utilized bootstrapping to determine confidence intervals. A power analysis in G*power for regression analyses indicated that with 49 participants, there was 80% power for detecting medium to large effects (β = .38). A second power analysis for mediation following a Monte Carlo approach (Thoemmes et al., 2010) in MPlus indicated that a sample of 49 participants was sufficient to detect indirect standardized effects of approximately .25 with 80% power. It has been argued that this is a large effect because two effects are multiplied (Kenny, 2018). Several variables tested as possible control variables were not related to outcome variables, including maternal education (all ps > .171), age at T1 (all ps > .070), gender (all ps > .209), and child verbal skills (all ps > .184), so they were not included as covariates.

Results

Descriptive Statistics

Descriptive statistics and intercorrelations between variables are provided in Supplemental Table 1. Group differences in symptoms were also examined. The control group had 0 to 3 H/I symptoms (M = 0.66, SD = 0.94) and the ADHD-risk group had 6 to 9 symptoms (M = 7.24, SD = 1.03) at T1, a significant difference, t (47) = −23.60, p < .001. At T2, the distribution was less bimodal because some children had 4 or 5 symptoms, but the control group (M = 0.75, SD = 1.24) still had significantly fewer H/I symptoms than the ADHD-risk group (M = 5.12, SD = 2.57), t (20.07) = −6.61, p < .001. Some of the psychopathology scales used in the study showed group differences. At T1, children in the H/I group exhibited more symptoms of aggression (M = 57.12, SD = 10.47) than those in the control group (M = 48.62, SD = 7.66), t (44) = −3.17, p = .003. At T2, children in the H/I group showed marginally more symptoms of parent-reported depression (M = 54.07, SD = 10.94) than those in the control group (M = 46.22, SD = 7.12), t (45) = −.90, p = .055, and more symptoms of aggression (M = 55.00, SD = 12.20) compared with the control group (M = 47.09, SD = 6.35), t (17.11) = −2.20, p = .042.

Children who completed T2 showed lower T1 H/I (M = 3.06, SD = 3.38) than children who did not return at T2 (M = 5.30, SD = 3.60), t (67) = −2.45, p = .017. Children who completed T2 showed lower T1 emotion lability (M = 1.77, SD = .50) than those who did not (M = 2.22, SD = .53), t (67) = −3.34, p = .001, and lower T1 parent-reported depression (M = 48.02, SD = 7.91) compared with children who did not (M = 55.50, SD = 13.18), t (58) = −2.62, p = .011. There was no significant difference between children who did and did not complete T2 across all other observational, child-reported, parent-reported, neural, and demographic measures at T1.

Does Emotion Competence Predict Later Symptoms of Psychopathology?

Behavioral markers of emotion competence

Full regression results are presented in Table 1 and are summarized here. The measure of emotion understanding at T1, the EMT, did not significantly predict symptoms of any type of psychopathology. Parents’ report of greater emotion lability at T1 predicted more symptoms of parent-reported depression and aggression at T2, controlling for T1 parent-reported symptoms. Higher observed NA during the frustration block predicted more symptoms of parent-reported aggression at T2, controlling for T1 symptoms and NA during other blocks. Lower observed NA during the recovery block predicted more symptoms of parent-reported depression at T2. Lower child-reported frustration after the frustration block at T1 predicted more symptoms of T2 parent-reported depression and aggression, controlling for T1 symptoms. Higher child-reported frustration after the regulation block at T1 predicted more T2 symptoms of parent-reported depression and aggression.

Table 1.

Summary of Regression Analysis for Behavioral and Neural Markers of Emotion Competence Predicting Psychopathology.

Emotion competence	Child-reported depression			Parent-reported depression			Parent-reported aggression			Parent-reported anxiety			Child-reported anxiety
Emotion competence	b (SE)	β	p	b (SE)	β	p	b (SE)	β	p	b (SE)	β	p	b (SE)	β	p
Lability	−1.06 (1.83)	−.10	.561	7.52 (2.50)	.41	0.001	7.81 (3.26)	.41	.013	4.40 (2.53)	.22	.076	−.73 (1.55)	−.07	.636
Emotion regulation	1.98 (2.21)	.13	.366	−5.82 (3.30)	−.23	0.072	−5.28 (3.75)	−.20	.153	−4.05 (3.62)	−.15	.259	1.71 (2.13)	.11	.421
Child-reported frustration
Baseline	−1.92 (0.96)	−.37	.046	0.44 (1.17)	.13	0.710	−0.34 (1.18)	−.04	.775	−1.26 (1.45)	−.13	.384	−1.09 (0.92)	−.21	.237
Frustration	0.07 (0.76)	.02	.930	−3.34 (0.98)	.17	<0.001	−2.73 (1.06)	−.47	.009	−0.09 (1.35)	−.01	.949	−0.09 (0.81)	−.03	.914
Regulation	0.63 (0.64)	.20	.323	3.00 (0.82)	.15	<0.001	2.64 (0.90)	.47	.003	0.11 (1.09)	.02	.923	0.62 (0.65)	.19	.342
Recovery	2.77 (1.70)	.31	.099	−0.00 (2.14)	.15	1.00	0.64 (2.25)	.04	.776	−1.76 (2.75)	−.11	.522	1.76 (1.64)	.19	.371
Observed NA
Baseline	−15.15 (6.78)	−.49	.022	1.98 (13.76)	.04	0.886	7.52 (12.75)	.14	.562	−4.52 (13.16)	−.08	.730	−10.45 (7.56)	−.34	.164
Frustration	−4.50 (6.91)	−.13	.515	20.12 (12.15)	.36	0.095	30.66 (11.11)	.56	.006	3.65 (12.30)	.06	.766	−7.82 (7.17)	−.24	.276
Regulation	11.73 (6.80)	.38	.078	−0.09 (11.74)	−.00	0.994	−14.10 (10.53)	−.27	.176	7.15 (11.30)	.13	.526	10.98 (6.83)	.36	.101
Recovery	−1.56 (4.54)	−.07	.732	−15.62 (7.50)	−.44	0.038	−1.35 (7.78)	.04	.862	−5.21 (7.99)	−.13	.512	−3.05 (4.64)	−.14	.512
P1 (F3, F4, FZ)
Baseline	−0.17 (0.28)	−.08	.541	−0.26 (0.38)	−.08	0.505	−0.14 (0.44)	−.04	.751	0.58 (0.54)	.16	.277	−0.15 (0.28)	−.08	.585
Frustration	1.13 (0.46)	.35	.010	−0.54 (0.61)	−.10	0.381	−0.98 (0.73)	−.17	.174	−0.75 (0.86)	−.13	.381	1.13 (0.46)	.35	.009
Regulation	−0.44 (0.30)	−.20	.140	0.26 (0.41)	.07	0.529	0.11 (0.47)	.03	.814	0.08 (0.59)	.02	.889	−0.38 (0.31)	−.17	.207
Recovery	−0.52 (0.27)	−.28	.045	−1.71 (0.37)	−.55	<0.001	−1.27 (0.40)	−.39	.001	−0.17 (0.49)	−.05	.728	−0.50 (0.25)	−.27	.044
N2 (F3, F4, FZ)
Baseline	−0.05 (0.24)	−.03	.845	0.20 (0.35)	.07	0.571	0.25 (0.41)	.09	.546	0.59 (0.47)	.20	.205	−0.05 (0.24)	−.03	.851
Frustration	1.06 (0.36)	.42	.001	−0.21 (0.48)	−.05	0.664	−0.35 (0.58)	−.08	.544	−0.68 (0.65)	−.15	.295	1.02 (0.35)	.41	.002
Regulation	−0.10 (0.29)	−.05	.736	0.91 (0.40)	.27	0.022	0.81 (0.46)	.23	.073	0.49 (0.53)	.13	.352	−0.12 (0.28)	−.06	.677
Recovery	−0.35 (0.22)	−.23	.095	−1.35 (0.30)	−.54	<0.001	−0.86 (0.34)	−.33	.009	−0.28 (0.39)	−.10	.483	−0.37 (0.21)	−.25	.069
P3 (FC3, FC4, FCZ)
Baseline	−0.01 (0.18)	−.01	.970	−0.14 (0.25)	−.06	0.593	−0.22 (0.30)	−.10	.455	0.23 (0.32)	.10	.469	−0.01 (0.18)	−.01	.964
Frustration	0.61 (0.27)	.33	.020	0.00 (0.35)	.00	0.991	−0.07 (0.42)	−.02	.866	−1.20 (0.47)	−.37	.009	0.53 (0.28)	.29	.048
Regulation	0.09 (0.23)	.05	.709	0.86 (0.20)	.32	0.004	0.69 (0.35)	.24	.045	0.45 (0.38)	.15	.242	0.05 (0.23)	.03	.819
Recovery	−0.50 (0.10)	−.40	.003	−1.05 (0.23)	−.51	<0.001	−0.63 (0.28)	−.29	.024	−0.19 (0.30)	−.08	.530	−0.50 (0.18)	−.41	.003
EMT	0.39 (0.83)	.07	.640	0.63 (1.23)	.07	0.605	−1.50 (1.25)	−.15	.225	1.77 (1.36)	.17	.190	0.15 (0.82)	.03	.860

Note. Controlled for the corresponding parent-reported BASC psychopathology score in each regression. Indented variables were entered as a group across all four affective Posner blocks. Significant results are in bold. NA = observed negative affect; EMT = Emotion Matching Task.

Neural markers of reactivity and regulation

P1. During the frustration block at T1, larger P1 amplitude predicted greater T2 child-reported depression and anxiety, controlling for P1 in other blocks and corresponding T1 symptoms. There were no associations between P1 amplitude in the regulation block at T1 and T2 psychopathology; however, attenuated P1 amplitude in the recovery block at T1 predicted higher parent-reported depression and aggression and higher child-reported depression and anxiety at T2.

N2

Attenuated (i.e., more positive amplitude) N2s during the frustration block at T1 predicted higher T2 child-reported depression and anxiety symptoms, controlling for N2 in other blocks and T1 symptoms. In the regulation block, attenuated N2s predicted greater T2 parent-reported depression. During the recovery block, larger (i.e., more negative amplitude) N2s predicted more symptoms of T2 parent-reported depression and aggression.

P3

Larger P3 amplitudes in the frustration block at T1 predicted higher child-reported depression and anxiety, but lower parent-reported anxiety at T2, controlling for P3 in other blocks and corresponding T1 symptoms. Larger P3 amplitude during the regulation block at T1 predicted more symptoms of parent-reported depression and aggression at T2. During the recovery block, attenuated P3 amplitude predicted more symptoms of parent-reported depression and aggression and child-reported depression and anxiety at T2.

Follow-up group analyses

We tested whether relations between emotion competence and psychopathology were driven by children with high H/I. All significant regressions were repeated with an interaction term of group with an emotion competence variable (e.g., Group × P3 during recovery). Several neural indicators, all during recovery, showed significant interactions and were followed up with separate regression analyses for each group. For children with high H/I, smaller P1 during recovery predicted higher parent-reported aggression (β = −.70, SE = .14, p < .001) and depression (β = −.81, SE = .10, p < .001), larger N2 during recovery predicted higher parent-reported aggression (β = −.70, SE = .14, p < .001) and depression (β = −.78, SE = .13, p < .001), and smaller P3 during recovery predicted higher parent-reported aggression (β = −.63, SE = .15, p < .001) and depression (β = −.74, SE = .12, p < .001) as well as child-reported depression (β = −.65, SE = .13, SE = .12, p < .001) and anxiety (β = −.74, SE = .12, p < .001). For children without H/I, these relations were not significant (ps from .103 to .629).

Does Emotion Competence Mediate the Relation Between Early H/I and Later Psychopathology?

Emotion competence variables that were significant predictors of psychopathology and related to H/I were tested as mediators between T1 H/I and T2 psychopathology symptoms (see Figure 1). P3 amplitude during the recovery block mediated the relation between T1 H/I symptoms and each T2 parent-reported depression, child-reported depression and anxiety, such that higher T1 H/I predicted attenuated T1 P3 amplitude, which in turn predicted greater T2 depression and anxiety, controlling for T1 symptoms and P3 amplitude during other blocks. P3 amplitude during the recovery block did not significantly mediate the relation between early H/I and later parent-reported aggression. Emotion lability did not mediate the relation between early H/I and later aggression or depression. Mediational analyses testing child-reported frustration after regulation as a mediator of H/I and parent-reported aggression and depression showed significant direct (a and b) paths in the expected direction, but indirect paths were not significant.

Figure 1.

Mediation models.

Discussion

This study examined whether early difficulties with emotion competence, indexed by behavioral and neural markers, play a role in the development of symptoms of psychopathology in young children with and without H/I symptoms. In addition, we examined whether emotion competence mediates the relation between early H/I symptoms and the development of comorbid psychopathology symptoms. Results indicated that early emotion lability, child-reported frustration, observed NA, and difficulties allocating neural resources both during and after frustration were predictive of later symptoms of depression, aggression, and anxiety, controlling for early symptoms. Neural findings during recovery were particularly driven by children with high H/I symptoms. Moreover, one neural component (the P3) mediated the relation between early H/I and later depression symptoms. Greater H/I was also associated with greater child-reported frustration when children were asked to regulate emotion expression, which in turn predicted later symptoms of aggression and depression. These findings suggest that difficulty with emotion regulation, particularly during recovery from frustrating situations, puts children at risk for psychopathology and may partially explain why young children with H/I symptoms are at risk for developing comorbid symptoms.

Emotion Understanding

The EMT, which measured identification of emotions, did not predict any symptoms of psychopathology at T2. Results for anxiety were consistent with a meta-analysis showing that children with anxiety symptoms do not show impairment in recognizing emotion in others (Mathews et al., 2016). However, past studies have found a link between emotion understanding and both aggression and depression (e.g., Denham et al., 2002; Lopez-Duran et al., 2013). It is possible that a ceiling effect on the EMT precluded finding relations with depression and aggression. Alternatively, other aspects of emotion understanding, such as deficits in understanding the causes of emotions, may be important to measure given prior associations with aggression (Bohnert et al., 2003) and anxiety (Mathews et al., 2016).

Emotion Reactivity and Regulation

Children with greater emotion lability later showed more parent-reported depression and aggression symptoms, controlling for earlier depression and aggression. In contrast to Seymour et al. (2014), emotion lability did not mediate the relation between earlier H/I and later depressive or aggressive symptoms. The indirect effect of H/I on depression via emotion lability in the present study was in the expected direction. Given the smaller sample size and the fact that H/I and lability were so strongly related in the present study, it may have been difficult to detect mediational effects, particularly small effects. In addition, the sample was younger than that in the study by Seymour et al. (2014), which might mean that lability plays less of a role in the development of psychopathology in children with H/I symptoms at younger ages.

Children’s observed and reported negative emotions predicted later symptoms of depression and aggression in unique ways across the task blocks. For the frustration block, lower child-reported frustration predicted more symptoms of parent-reported depression and aggression at T2. However, higher observed NA during this block predicted more parent-reported symptoms of aggression. We directly examined the discrepancy between observed and child-reported NA⁵ and found that children who showed a larger discrepancy were at greater risk for aggression. Perhaps children who are less aware of their emotion state are more vulnerable to aggression, similar to findings that children with aggression have difficulty identifying causes of negative emotions (e.g., Bohnert et al., 2003). In contrast, when asked to regulate their emotions (regulation block), higher child-reported frustration predicted higher parent-reported aggression and depression symptoms, suggesting that children who have difficulty reducing their own emotion distress are at greater risk for symptoms of both depression and aggression. Surprisingly, those children who showed less NA during the recovery block were reported by parents to show more symptoms of depression at T2. It is possible that children vulnerable to depression symptoms may be continuing to engage in outward emotion suppression even after the regulation block has ended.

Neural markers of emotion regulation during the frustration, regulation, and recovery blocks were important predictors of later psychopathology symptoms. During the frustration and regulation blocks, children who showed larger P1 and P3 amplitudes and smaller N2 amplitudes later showed higher parent-reported depression and child-reported anxiety symptoms. Smaller N2 amplitude during regulation also predicted higher T2 parent-reported aggression symptoms. Thus, children at risk for depression, aggression, and anxiety symptoms appeared to show altered patterns of cognitive processing during the emotionally challenging blocks of the task (i.e., frustration and regulation). In contrast, greater P3 during frustration predicted fewer parent-reported symptoms of anxiety. It is not clear whether parent or child report represents a more precise estimate of symptoms; however, different directions of findings underscore the need to collect ratings from both children and their parents.

Our results are consistent with findings showing that mood dysregulation in children is associated with heightened P3 amplitudes during frustrating tasks (e.g., Rich et al., 2007) and with previous work showing that neural markers of attention during frustration differ for children with symptoms of aggression and oppositional defiant disorder (e.g., Lamm et al., 2011; Rich et al., 2007). However, after the emotional challenge (i.e., during the recovery block), children at risk for depression, aggression, and anxiety symptoms exhibited a reduced P3, along with a reduced P1 and enhanced N2, suggesting that variations in cognitive processing during recovery from frustration can alter vulnerability to psychopathology. Further work is needed to elucidate the precise mechanisms reflected in the patterns for each component; however, the overall directional change in allocation of neural resources suggests that at-risk children engage with emotionally challenging tasks differently and that there are lasting differences after the emotional challenge is removed.

There was some evidence that children with more H/I symptoms are particularly vulnerable to the impact of emotion competence on psychopathology. For instance, several significant relations between neural measures during recovery and T2 psychopathology were evident in the ADHD-risk (i.e., high H/I symptoms) group only. P3 amplitude during recovery also mediated the relation between H/I and depression and anxiety symptoms; children with more H/I symptoms allocated fewer resources to attention allocation during recovery from the mood induction, which in turn predicted greater symptoms of parent- and child-reported depression, and child-reported anxiety. These results are consistent with studies showing that children with H/I symptoms may show difficulties modulating attention relative to typical peers during frustrating tasks, as measured by P3 amplitudes (e.g., Lugo-Candelas et al., 2017; Jonkman et al., 2000). However, in the present study, this difficulty was apparent when recovering from frustration and placed these children at risk for higher symptoms of depression and anxiety. Overall, the results suggest that children with elevated H/I symptoms who have difficulties modulating their cognitive resources, particularly after a frustrating situation, are more vulnerable to depression and aggression symptoms.

Limitations

Results should be interpreted in the context of several limitations. First, the sample was small, in part due to attrition. There was sufficient power to detect medium-large sized effects of early emotion competence on later psychopathology and large indirect effects of H/I via emotion competence. However, children who dropped out were more likely to have higher H/I and emotion lability at T1. With more high-risk children, we would have had greater variability in outcome measures, increasing our ability to detect effects. Relatedly, many statistical tests were conducted, increasing the likelihood of Type I error; however, given the power and small sample size, we did not correct for multiple tests. Second, the sample was not diverse enough to examine racial/ethnic differences in symptoms, which past studies have found (e.g., Nguyen et al., 2007). Third, neural measures were not collected at T2. Future research will be important to better understand whether these neural markers remain significant predictors of psychopathology as children age. Fourth, we cannot rule out other causal mechanisms for the relation between emotion competence and psychopathology, such as executive function deficits or heterotopic and homotopic continuity (e.g., Shevlin et al., 2017). Future research should examine other potential underlying processes. Finally, we examined psychopathology symptoms dimensionally; future studies should extend this to more severe samples with clinical diagnoses.

Implications and Future Directions

Results from the present study showed that children (with and without H/I) who have greater emotion lability, frustration, and difficulty recovering from a frustrating task are at risk for increasing symptoms of depression, anxiety, and aggression. These indicators of emotion competence predicted higher psychopathology symptoms 18 months later, above and beyond early symptoms, suggesting that findings were not a result of emotion competence serving as a proxy for early psychopathology. There was also some evidence that emotion competence deficits partially account for the relation between high H/I and co-occurring psychopathology symptoms. Altogether, the findings of this study demonstrate that behavioral and neural activity when children try to regulate emotions and recover from frustration is of particular importance to the later development of comorbid psychopathology symptoms. The present study underscores the need for intervention research. Specialized interventions to improve specific emotion competence skills may yield benefits for preventing the development of psychopathology symptoms, especially for children with high H/I symptoms.

Supplemental Material

Supplemental_Materials_ERP_Information1 – Supplemental material for Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms

Supplemental material, Supplemental_Materials_ERP_Information1 for Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms by Hallie R. Brown, Maya Hareli, Rosanna Breaux, Claudia I. Lugo-Candelas, Shannon L. Gair, Elizabeth A. Harvey and Jennifer M. McDermott in Journal of Attention Disorders

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Supplemental_Materials_Figures – Supplemental material for Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms

Supplemental material, Supplemental_Materials_Figures for Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms by Hallie R. Brown, Maya Hareli, Rosanna Breaux, Claudia I. Lugo-Candelas, Shannon L. Gair, Elizabeth A. Harvey and Jennifer M. McDermott in Journal of Attention Disorders

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Supplemental_Materials_Table – Supplemental material for Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms

Supplemental material, Supplemental_Materials_Table for Behavioral and Neural Markers of Emotion Competence as Predictors of Later Psychopathology in Children With and Without Hyperactive/Impulsive Symptoms by Hallie R. Brown, Maya Hareli, Rosanna Breaux, Claudia I. Lugo-Candelas, Shannon L. Gair, Elizabeth A. Harvey and Jennifer M. McDermott in Journal of Attention Disorders

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was partially funded by a University of Massachusetts Amherst Center for Research on Families Dissertation Fellowship Award, a University of Massachusetts Amherst Dissertation Research Grant, and a University of Massachusetts Amherst Graduate School Diversity Dissertation Fellowship, all awarded to the fourth author, as well as a University of Massachusetts Amherst Honors College Thesis Award to the second author.

ORCID iDs

Hallie R. Brown

Maya Hareli

Supplemental Material

Supplemental material for this article is available online.

Notes

Author Biographies

Hallie R. Brown, MS, is a doctoral student in the Department of Psychological and Brain Sciences at the University of Massachusetts Amherst. Her research interests are in the early identification of neurodevelopmental disorders.

Maya Hareli, BA, is a doctoral student in the Department of Psychology at Loyola University Chicago. Her research interests are in designing and evaluating interventions to promote well-being and success among at-risk youth.

Rosanna Breaux, PhD, is an assistant professor in the Department of Psychology at Virginia Tech. Her research focuses on the emotional and social functioning of children and adolescents with ADHD, with a focus on emotion regulation.

Claudia I. Lugo-Candelas, PhD is an assistant professor at Columbia University Medical Center/New York State Psychiatric Institute. Her research aims to develop a better understanding of how prenatal experiences and exposures impact early neurodevelopment in offspring and risk for ADHD.

Shannon L. Gair, MS, is a doctoral student in the Department of Psychological and Brain Sciences at the University of Massachusetts Amherst. Her research interests are in the early development of ADHD.

Elizabeth A. Harvey, PhD, is a professor in the Department of Psychological and Brain Sciences at the University of Massachusetts Amherst. She is active in training students in the Clinical Psychology graduate program and is affiliated with the Center for Research on Families. Her research interests are in the early development of ADHD and disruptive behavior disorders in preschool children and toddlers.

Jennifer M. McDermott, PhD, is an associate professor in the Department of Psychological and Brain Sciences at the University of Massachusetts Amherst. She is also faculty in the Neuroscience and Behavior graduate training program, and is affiliated with the Center for Research on Families and Rudd Adoption Research Program. Her research explores individual differences and the role of early experience in relation to cognitive development and socioemotional outcomes.

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