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Emotion dysregulation is cross-diagnostic and impairing. Most research has focused on dysregulated expressions of negative affect, often measured as irritability, which is associated with multiple forms of psychopathology and predicts negative outcomes. However, the Research Domain Criteria (RDoC) include both negative and positive valence systems. Emerging evidence suggests that dysregulated expressions of positive affect, or excitability, in early childhood predict later psychopathology and impairment above and beyond irritability. Typically, irritability declines from early through middle childhood; however, the developmental trajectory of excitability is unknown. The impact of excitability across childhood on later emotion dysregulation is also yet unknown. In a well-characterized, longitudinal sample of 129 children studied from ages 3 to 5.11 years through 14 to 19 years, enriched for early depression and disruptive symptoms, we assessed the trajectory of irritability and excitability using multilevel modeling and how components of these trajectories impact later emotion dysregulation. While irritability declines across childhood, excitability remains remarkably stable both within and across the group. Overall levels of excitability (excitability intercept) predict later emotion dysregulation as measured by parent and self-report and predict decreased functional magnetic resonance imaging activity in cognitive emotion regulation regions during an emotion regulation task. Irritability was not related to any dysregulation outcome above and beyond excitability.

Exposure to adversity is a well-documented risk factor for cognitive, behavioral, and mental health problems. In fact, the consequences of adversity may be intergenerational. A growing body of research suggests that maternal exposures to adversity, including those prior to childbirth, are associated with offspring biobehavioral development. In a sample of 36 mothers and their preschool-age children (mean child age = 4.21 ± 0.92 years), we used functional near-infrared spectroscopy to replicate and extend this work to include brain activation during inhibitory control in young children. We found that measures of maternal exposure to adversity, including cumulative, childhood, and preconception exposures, were significantly and positively associated with activation in the right frontopolar prefrontal cortex (PFC) and in the left temporal and parietal clusters during inhibitory control. In addition, and consistent with previous findings, children's increased negative affect and decreased effortful control were associated with increased right PFC activation during inhibitory control. These findings provide preliminary evidence that maternal and dispositional risk factors are linked to alterations in PFC functioning during the preschool years. Children of mothers with a history of exposure to adversity, as well as children who are less temperamentally regulated, may require increased neural resources to meet the cognitive demands of inhibitory control.

While substantial research supports the role of parent–child interactions on the emergence of psychiatric symptoms, few studies have explored biological mechanisms for this association. The current study explored behavioral and neural parent–child synchronization during frustration and play as predictors of internalizing and externalizing behaviors across a span of 1.5 years. Parent–child dyads first came to the laboratory when the child was 4–5 years old and completed the Disruptive Behavior Diagnostic Observation Schedule: Biological Synchrony (DB-DOS: BioSync) task while functional near-infrared spectroscopy (fNIRS) data were recorded. Parents reported on their child's internalizing and externalizing behaviors using the Child Behavior Checklist (CBCL) four times over 1.5 years. Latent growth curve (LGC) modeling was conducted to assess neural and behavioral synchrony as predictors of internalizing and externalizing trajectories. Consistent with previous investigations in this age range, on average, internalizing and externalizing behaviors decreased over the four time points. Parent–child neural synchrony during a period of play predicted rate of change in internalizing but not externalizing behaviors such that higher parent–child neural synchrony was associated with a more rapid decrease in internalizing behaviors. Our results suggest that a parent–child dyad's ability to coordinate neural activation during positive interactions might serve as a protective mechanism in the context of internalizing behaviors.

The ongoing stream of sensory experience is so complex and ever-changing that we tend to parse this experience at “event boundaries”, which structures and strengthens memory. Memory processes undergo profound change across early childhood. Whether young children also divide their ongoing processing along event boundaries, and if those boundaries relate to memory, could provide important insight into the development of memory systems. In Study 1, 4-7-year-old children and adults segmented a cartoon, and we tested their memory. Children’s event boundaries were more variable than adults’ and differed in location and consistency of agreement. Older children’s event segmentation was more adult-like than younger children’s, and children who segmented events more like adults had better memory for those events. In Study 2, we asked whether these developmental differences in event segmentation had their roots in distinct neural representations. A separate group of 4-8-year-old children watched the same cartoon while undergoing an fMRI scan. In the right hippocampus, greater pattern dissimilarity across event boundaries compared to within events was evident for both child and adult behavioral boundaries, suggesting children and adults share similar event cognition. However, the boundaries identified by a data-driven Hidden Markov Model found that a different brain region—the left and right angular gyri—aligned only with event boundaries defined by children. Overall, these data suggest that children’s event cognition is reasonably well-developed by age 4 but continues to become more adult-like across early childhood.

Social deficits in autism spectrum disorder (ASD) have been linked to atypical activation of the mentalizing network. This work, however, has been limited by a focus on the brain activity of a single person during computerized social tasks rather than exploring brain activity during in vivo interactions. The current study assessed neural synchronization during a conversation as a mechanism for social impairment in adults with ASD (n = 24) and matched controls (n = 26). Functional near-infrared spectroscopy (fNIRS) data were collected from the prefrontal cortex (PFC) and tempoparietal junction (TPJ). Participants self-reported on their social communication and videos of the interaction were coded for utterances and conversational turns. As expected, controls showed more neural synchrony than participants with ASD in the TPJ. Also as expected, controls showed less social communication impairment than participants with ASD. However, participants with ASD did not have fewer utterances compared with control subjects. Overall, less neural synchrony in the TPJ was associated with higher social impairment and marginally fewer utterances. Our findings advance our understanding of social difficulties in ASD by linking them to decreased neural synchronization of the TPJ. LAY SUMMARY: The coordination of brain responses is important for efficient social interactions. The current study explored the coordination of brain responses in neurotypical adults and adults with ASD to investigate if difficulties in social interactions are related to difficulties coordinating brain responses in ASD. We found that participants with ASD had more difficulties coordinating brain responses during a conversation with an interacting partner. Additionally, we found that the level of coordination in brain responses was linked to problems with social communication.

The vast individual differences in the developmental origins of risk and resilience pathways combined with sophisticated capabilities of big data science increasingly point to the imperative of large, neurodevelopmental consortia to capture population heterogeneity and key variations in developmental trajectories. At the same time, such large-scale population-based designs involving multiple independent sites also must weigh competing demands. For example, the need for efficient, scalable assessment strategies must be balanced with the need for nuanced, developmentally sensitive phenotyping optimized for linkage to neural mechanisms and specification of common and distinct exposure pathways. Standardized epidemiologic batteries designed for this purpose such as PhenX (consensus measures for Phenotypes and eXposures) and the National Institutes of Health (NIH) Toolbox provide excellent "off the shelf" assessment tools that are well-validated and enable cross-study comparability. However, these standardized toolkits can also constrain ability to leverage advances in neurodevelopmental measurement over time, at times disproportionately advantaging established measures. In addition, individual consortia often expend exhaustive effort "reinventing the wheel," which is inefficient and fails to fully maximize potential synergies with other like initiatives. To address these issues, this paper lays forth an early childhood neurodevelopmental assessment strategy, guided by a set of principles synthesizing developmental and pragmatic considerations generated by the Neurodevelopmental Workgroup of the HEALthy Brain and Child Development (HBCD) Planning Consortium. These principles emphasize characterization of both risk- and resilience-promoting processes. Specific measurement recommendations to HBCD are provided to illustrate application. However, principles are intended as a guiding framework to transcend any particular initiative as a broad neurodevelopmentally informed, early childhood assessment strategy for large-scale consortia science.

Standardized developmentally based assessment systems have transformed the capacity to identify transdiagnostic behavioral markers of mental disorder risk in early childhood, notably, clinically significant irritability and externalizing behaviors. However, behavior-based instruments that both differentiate risk for persistent psychopathology from normative misbehavior, and are feasible for community clinicians to implement, are in nascent phases of development. Young children’s facial expressions during frustration challenges may form the basis for novel assessments tools that are flexible, quick, and easy to implement as markers of psychopathology to complement validated questionnaires. However, the accuracy of facial expressions to correctly classify young children falling above and below clinical cut-offs is unknown. Our goal was to test how facial expressions during frustration, defined by different facial muscular movements, related to individual differences in irritability and externalizing behaviors and discriminated children with clinically significant levels from peers. Participants were 79 children (ages 3–7) who completed a short, moderately frustrating computer task while facial expressions were recorded. Only negative facial expressions that included eye constriction related to irritability and externalizing behaviors and were clinically discriminating. Moreover, these expressions significantly discriminated children with and without clinically significant irritability and externalizing symptoms with high Area Under the Curve (AUC) values (> .75) indicating good clinical utility. In contrast, expressions without eye constriction showed no clinical utility. The presence of negative expressions with eye constriction in response to a short frustration prompt may serve as an indicator of early psychopathology, raising the potential for novel assessment tools that may enhance precision of early identification.

Irritability is a substrate of more than one dozen clinical syndromes. Thus, identifying when it is atypical and interfering with functioning is crucial to the prevention of mental disorder in the earliest phase of the clinical sequence. Advances in developmentally based measurement of irritability have enabled differentiation of normative irritable mood and tantrums from indicators of concern, beginning in infancy. However, developmentally sensitive assessments of irritability-related impairment are lacking. We introduce the Early Childhood Irritability-Related Impairment Interview (E-CRI), which assesses impairment associated with irritable mood and tantrums across contexts. Reliability and validity are established across two independent samples varied by developmental period: the Emotional Growth preschool sample (EmoGrow; N = 151, M = 4.82 years) and the When to Worry infant/toddler sample (W2W; N = 330, M = 14 months). We generated a well-fitting two-factor E-CRI model, with tantrum- and irritable mood-related impairment factors. The E-CRI exhibited good interrater, test–retest, and longitudinal reliability. Construct and clinical validity were also demonstrated. In both samples, E-CRI factors showed association to internalizing and externalizing problems, and to caregiver-reported concern in W2W. Tantrum-related impairment demonstrated stronger and more consistent explanatory value across outcomes, while mood-related impairment added explanatory utility for internalizing problems. The E-CRI also showed incremental utility beyond variance explained by the Family Life Impairment Scale (FLIS) survey indicator of developmental impairment. The E-CRI holds promise as an indicator of impairment to inform identification of typical versus atypical patterns reflecting early emerging irritability-related syndromes in the initial phase of the clinical sequence.

The intergenerational transmission of psychopathology is one of the strongest known risk factors for childhood disorder and may be a malleable target for prevention and intervention. Anxious parents have distinct parenting profiles that impact socioemotional development, and these parenting effects may result in broad alterations to the biological and cognitive functioning of their children. Better understanding the functional mechanisms by which parental risk is passed on to children can provide (1) novel markers of risk for socioemotional difficulties, (2) specific targets for intervention, and (3) behavioral and biological indices of treatment response. We propose a developmental model in which dyadic social dynamics serve as a key conduit in parent-to-child transmission of anxiety. Dyadic social dynamics capture the moment-to-moment interactions between parent and child that occur on a daily basis. In shaping the developmental trajectory from familial risk to actual symptoms, dyadic processes act on mechanisms of risk that are evident prior to, and in the absence of, any eventual disorder onset. First, we discuss dyadic synchrony or the moment-to-moment coordination between parent and child within different levels of analysis, including neural, autonomic, behavioral, and emotional processes. Second, we discuss how overt emotion modeling of distress is observed and internalized by children and later reflected in their own behavior. Thus, unlike synchrony, this is a more sequential process that cuts across levels of analysis. We also discuss maladaptive cognitive and affective processing that is often evident with increases in child anxiety symptoms. Finally, we discuss additional moderators (e.g., parent sex, child fearful temperament) that may impact dyadic processes. Our model is proposed as a conceptual framework for testing hypotheses regarding dynamic processes that may ultimately guide novel treatment approaches aimed at intervening on dyadically linked biobehavioral mechanisms before symptom onset.

Social information processing is vital for inferring emotional states in others, yet affective neuroscience has only begun to scratch the surface of how we represent emotional information in the brain. Most previous affective neuroscience work has used isolated stimuli such as static images of affective faces or scenes to probe affective processing. While this work has provided rich insight to the initial stages of emotion processing (encoding cues), activation to isolated stimuli provides limited insight into later phases of emotion processing such as interpretation of cues or interactions between cues and established cognitive schemas. Recent work has highlighted the potential value of using complex video stimuli to probe socio-emotional processing, highlighting the need to develop standardized video coding schemas as this exciting field expands. Toward that end, we present a standardized and open-source coding system for complex videos, two fully coded videos, and a video and code processing Python library. The EmoCodes manual coding system provides an externally validated and replicable system for coding complex cartoon stimuli, with future plans to validate the system for other video types. The emocodes Python library provides automated tools for extracting low-level features from video files as well as tools for summarizing and analyzing the manual codes for suitability of use in neuroimaging analysis. Materials can be freely accessed at https://emocodes.org/. These tools represent an important step toward replicable and standardized study of socio-emotional processing using complex video stimuli. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s42761-021-00100-7.

The integration of neurodevelopmental perspectives into clinical science has identified irritability as an early dimensional marker of lifespan mental health risk. Elucidating the developmental patterning of irritable behavior is key to differentiating normative variation from risk markers. Accounting for dysregulation and contextual features of irritability is useful for differentiation at preschool age, laying the groundwork for even earlier characterization. We provide initial evidence for the validity of the Multidimensional Assessment Profile of Disruptive Behavior Temper Loss Scale, Infant-Toddler version in two independent samples of 12-18-month-olds from the US. We calibrated the measure using item response theory in a large representative sample, then validated within an independent sample. We characterized the developmental patterning of irritable behaviors and their dimensional spectrum, and demonstrated test-retest reliability, and convergent validity. The MAP-DB-IT is a standardized, dimensional survey assessing irritability that serves as a tool for characterizing the developmental expression of early mental health risk.

Children reared in socioeconomically disadvantaged environments are at risk for academic, cognitive, and behavioral problems. Mounting evidence suggests that childhood adversities, encountered at disproportionate rates in contexts of socioeconomic risk, shape the developing brain in ways that explain disparities. Circuitries that subserve neurocognitive functions related to memory, attention, and cognitive control are especially affected. However, most work showing altered neural function has focused on middle childhood and adolescence. Understanding alterations in brain development during foundational points in early childhood is a key next step. To address this gap, we examined functional near-infrared-spectroscopy-based neural activation during a working memory (WM) task in young children aged 4-7 years (N = 30) who varied in socioeconomic risk exposure. Children who experienced greater disadvantage (lower income to needs ratio and lower Hollingshead index) exhibited lower activation in the lateral prefrontal cortex than children who experienced less to no disadvantage. Variability in prefrontal cortex activation, but not behavioral performance on the WM task, was associated with worse executive functioning in children as reported by parents. These findings add to existing evidence that exposure to early adversity, such as socioeconomic risk, may lead to foundational changes in the developing brain, which increases risk for disparities in functioning across multiple cognitive and social domains.

Background Research to date has largely conceptualized irritability in terms of intraindividual differences. However, the role of interpersonal dyadic processes has received little consideration. Nevertheless, difficulties in how parent-child dyads synchronize during interactions may be an important correlate of irritably in early childhood. Innovations in developmentally sensitive neuroimaging methods now enable the use of measures of neural synchrony to quantify synchronous responses in parent-child dyads and can help clarify the neural underpinnings of these difficulties. We introduce the Disruptive Behavior Diagnostic Observation Schedule: Biological Synchrony (DB-DOS:BioSync) as a paradigm for exploring parent-child neural synchrony as a potential biological mechanism for interpersonal difficulties in preschool psychopathology. Methods Using functional near-infrared spectroscopy (fNIRS) 4- to 5-year-olds (N = 116) and their mothers completed the DB-DOS:BioSync while assessing neural synchrony during mild frustration and recovery. Child irritability was measured using a latent irritability factor that was calculated from four developmentally sensitive indicators. Results Both the mild frustration and the recovery contexts resulted in neural synchrony. However, less neural synchrony during the recovery context only was associated with more child irritability. Conclusions Our results suggest that recovering after a frustrating period might be particularly challenging for children high in irritability and offer support for the use of the DB-DOS:BioSync task to elucidate interpersonal neural mechanisms of developmental psychopathology.

There is surprisingly little empirical evidence supporting theoretical and anecdotal claims regarding the spontaneous production of prototypic facial expressions used in numerous emotion recognition studies. Proponents of innate prototypic expressions believe that this lack of evidence may be due to ethical restrictions against presenting powerful elicitors in the lab. The current popularity of internet platforms designed for public sharing of videos allows investigators to shed light on this debate by examining naturally-occurring facial expressions outside the laboratory. An Internet prank (“Scary Maze”) has provided a unique opportunity to observe children reacting to a consistent fear- and surprise-inducing stimulus: The unexpected presentation of a “scary face” during an online maze game. The purpose of this study was to examine children’s facial expressions in this naturalistic setting. Emotion ratings of non-facial behaviour (provided by untrained undergraduates) and anatomically-based facial codes were obtained from 60 videos of children (ages 4–7) found on YouTube. Emotion ratings were highest for fear and surprise. Correspondingly, children displayed more facial expressions of fear and surprise than for other emotions (e.g. anger, joy). These findings provide partial support for the ecological validity of fear and surprise expressions. Still prototypic expressions were produced by fewer than half the children.

The ability to detect differences among similar events in our lives is a crucial aspect of successful episodic memory performance, which develops across early childhood. The neural substrate of this ability is supported by operations in the medial temporal lobe (MTL). Here, we used representational similarity analysis (RSA) to measure neural pattern similarity in hippocampus, perirhinal cortex, and parahippocampal cortex for 4- to 10-year-old children and adults during naturalistic viewing of clips from the same compared to different movies. Further, we assessed the role of prior exposure to individual movie clips on pattern similarity in the MTL. In both age groups, neural pattern similarity in hippocampus was lower for clips drawn from the same movies compared to those drawn from different movies, suggesting that related content activates processes focused on keeping representations with shared content distinct. However, children showed this only for movies with which they had prior exposures, whereas adults showed the effect regardless of any prior exposures to the movies. These findings suggest that children require repeated exposure to stimuli to show adult-like MTL functioning in distinguishing among similar events.

Although emotion dysregulation has been defined as a maladaptive process of emotional experiences, there is no specific reference to the emotional valence of the dysregulation. To date, child psychiatry has focused primarily on dysregulation of negative affect. Here, we suggest that positive emotion dysregulation requires additional clinical and research attention.First, we present a developmental approach to the study of positive emotion regulation within a temperament framework. Second, we describe emerging research findings regarding dysregulation of positive emotion in early childhood. Third, we integrate neuroscientific approaches to positive emotion regulation and introduce a framework for future investigations and clinical applications.Dysregulation in positive affect can be examined from temperamental, developmental, clinical, and neuroscientific perspectives. Both temperamental surgency, which includes positive affect, and the proposed clinical extension, excitability, are associated with increased risk of externalizing symptoms and clinical impairment in youth.Studying the role of both temperamental surgency and clinically impairing positive affect, or excitability, in developmental psychopathology will help to elucidate the full spectrum of emotion dysregulation and to clarify the neural basis of dysregulation. A more comprehensive conceptualization of positively valanced emotion dysregulation will provide a more nuanced understanding of developmental risk and potential targets for intervention.One or more of the authors of this paper self-identifies as a member of one or more historically underrepresented sexual and/or gender groups in science.

Developmental studies have identified differences in prefrontal and subcortical affective structures between children and adults, which correspond with observed cognitive and behavioral maturations from relatively simplistic emotional experiences and expressions to more nuanced, complex ones. However, developmental neurocognitive affective changes have not yet been well explored. It stands to reason that adults and children may demonstrate observable differences in the representation of affect within key neurological structures implicated in affective cognition. Forty-five participants (25 children; 20 adults) passively viewed positive, negative, and neutral clips from popular films while undergoing functional magnetic resonance imaging. Using representational similarity analysis to measure variability in neural pattern similarity, we found developmental differences between children and adults in the amygdala, nucleus accumbens, and ventromedial prefrontal cortex, such that children generated contrasting patterns between subcortical structures and the ventromedial prefrontal cortex; a phenomenon not replicated among their older counterparts. Furthermore, children generated valence-specific differences in representational patterns across regions while adults failed to demonstrate similar valence-specific responses. These results may suggest that affective representations grow increasingly dissimilar over development as individuals mature from visceral affective responses to more evaluative analyses. Further research is required to determine how these differences correspond with affective expression and behavior.

Irritability is a transdiagnostic psychiatric symptom that spans the internalizing- externalizing divide and places children at greater risk for common mental health problems. There is evidence for disrupted affect-biased attention processing in children with high levels of irritability, but the underlying mechanisms supporting this dysfunction are not well understood. 24 children with clinical irritability (IRR) and 25 typically-developing comparison children (TD) ages 6-10 years old completed a modified visual Oddball task, which is optimized for probing the attention system, during functional magnetic resonance imaging (fMRI). Influence of happy, angry, or neutral distractor stimuli were analyzed using two methods. One analysis compared the two groups within each condition using voxel-wise whole brain t-tests. A second analysis examines dimensional irritability (assessed using the Multidimensional Assessment Profile of Disruptive Behavior or MAP-DB) predicting neural functioning across the sample within each condition. Both analytical approaches revealed increased activity in sensorimotor cortex with increased irritability in the affective conditions. In the Neutral condition, there were negative associations between primary sensory and parietal cortex activation and MAP-DB irritability scores. Our findings suggest maladaptive integration of visual-spatial information during sustained attention in clinically irritable children that may underlie disruptions in emotion processing.

Disruptive behavior in childhood is common. It spans from normative child misbehaviors to clinically-significant and impairing problems. While there are many rating scales evaluating such behaviors, historically, measurement has emphasized counting the number of symptoms present rather than assessing the normal-abnormal spectrum of behavioral expression. This study uses data from 644 early school age children aggregated from two data sources to statistically link a commonly used symptom count measure, the Child Behavior Checklist (CBCL), to a more developmentally-sensitive measure, the Multidimensional Assessment Profile of Disruptive Behavior (MAP-DB). Two links between conceptually similar scales on each measure were developed: CBCL Conduct Problems and MAP-DB Aggression; and CBCL Oppositional Defiant Problems and MAP-DB Temper Loss. We compared two innovative methods-Item Response Theory (IRT) and Deming regression-to determine the optimal linking relationship. Results suggest IRT methods were superior in reducing linking error compared to Deming regression. While Deming regression accurately modeled the mean scores (thus minimizing linking bias), this method could not adequately address the floor effect for scores on the CBCL. For practical purposes, this study provides a crosswalk of score conversions between the CBCL and MAP-DB, such that data aggregation and group comparisons can be made across the two measures; this enables longitudinal analyses with historically-collected CBCL data to transition to the more innovative dimensional scales of the MAP-DB without undo loss of extant data. This study furthers efforts to shift from historical symptom counts to more developmentally-sensitive measurement across the disruptive behaviors spectrum.

We aimed to identify markers of future affective lability in youth at bipolar disorder risk from the Pittsburgh Bipolar Offspring Study (BIOS) (n = 41, age = 14, SD = 2.30), and validate these predictors in an independent sample from the Longitudinal Assessment of Manic Symptoms study (LAMS) (n = 55, age = 13.7, SD = 1.9). We included factors of mixed/mania, irritability, and anxiety/depression (29 months post MRI scan) in regularized regression models. Clinical and demographic variables, along with neural activity during reward and emotion processing and gray matter structure in all cortical regions at baseline, were used to predict future affective lability factor scores, using regularized regression. Future affective lability factor scores were predicted in both samples by unique combinations of baseline neural structure, function, and clinical characteristics. Lower bilateral parietal cortical thickness, greater left ventrolateral prefrontal cortex thickness, lower right transverse temporal cortex thickness, greater self-reported depression, mania severity, and age at scan predicted greater future mixed/mania factor score. Lower bilateral parietal cortical thickness, greater right entorhinal cortical thickness, greater right fusiform gyral activity during emotional face processing, diagnosis of major depressive disorder, and greater self-reported depression severity predicted greater irritability factor score. Greater self-reported depression severity predicted greater anxiety/depression factor score. Elucidating unique clinical and neural predictors of future-specific affective lability factors is a step toward identifying objective markers of bipolar disorder risk, to provide neural targets to better guide and monitor early interventions in bipolar disorder at-risk youth.

Shared intentionality, or collaborative interactions in which individuals have a shared goal and must coordinate their efforts, is a core component of human interaction. However, the biological bases of shared intentionality and, specifically, the processes by which the brain adjusts to the sharing of common goals, remain largely unknown. Using functional near infrared spectroscopy (fNIRS), coordination of cerebral hemodynamic activation was found in subject pairs when completing a puzzle together in contrast to a condition in which subjects completed identical but individual puzzles (same intention without shared intentionality). Interpersonal neural coordination was also greater when completing a puzzle together compared to two control conditions including the observation of another pair completing the same puzzle task or watching a movie with a partner (shared experience). Further, permutation testing revealed that the time course of neural activation of one subject predicted that of their partner, but not that of others completing the identical puzzle in different partner sets. Results indicate unique brain-to-brain coupling specific to shared intentionality beyond what has been previously found by investigating the fundamentals of social exchange.

Despite high heritability, no research has followed children with ADHD to parenthood to study their offspring and parenting behaviors. Given greater prevalence of ADHD in males and lack of research involving fathers, this study evaluated offspring of fathers with and without ADHD histories for ADHD and disruptive behavior and compared fathers' parenting behaviors. Male fathers (N = 29) from the Pittsburgh ADHD Longitudinal Study (PALS) participated with their preschool-aged offspring. Fathers completed self-reported measures, and father-child dyads completed an interaction task. ADHD offspring had elevated ADHD symptoms and behavior dysregulation. All fathers displayed positive parenting. ADHD fathers reported lower supportive responses to their child's negative emotions than comparison fathers, yet rated their parenting as more efficacious. ADHD offspring were distinguishable as early as age 3; thus, earlier diagnosis and intervention may be feasible for this at-risk population. Future research should investigate the acceptability and efficacy of parent training for fathers with ADHD.

Background The DSM-5 separates the diagnostic criteria for mood and behavioral disorders. Both types of disorders share neurocognitive deficits of executive function and reading difficulties in childhood. Children with dyslexia also have executive function deficits, revealing a role of executive function circuitry in reading. The aim of the current study is to determine whether there is a significant relationship of functional connectivity within the fronto-parietal and cingulo-opercular cognitive control networks to reading measures for children with mood disorders, behavioral disorders, dyslexia, and healthy controls (HC). Method Behavioral reading measures of phonological awareness, decoding, and orthography were collected. Resting state fMRI data were collected, preprocessed, and then analyzed for functional connectivity. Differences in the reading measures were tested for significance among the groups. Global efficiency (GE) measures were also tested for correlation with reading measures in 40 children with various disorders and 17 HCs. Results Significant differences were found between the four groups on all reading measures. Relative to HCs and children with mood disorders or behavior disorders, children with dyslexia as a primary diagnosis scored significantly lower on all three reading measures. Children with mood disorders scored significantly lower than controls on a test of phonological awareness. Phonological awareness deficits correlated with reduced resting state functional connectivity MRI (rsfcMRI) in the cingulo-opercular network for children with dyslexia. A significant difference was also found in fronto-parietal global efficiency in children with mood disorders relative to the other three groups. We also found a significant difference in cingulo-opercular global efficiency in children with mood disorders relative to the Dyslexia and Control groups. However, none of these differences correlate significantly with reading measures. Conclusions/significance Reading difficulties involve abnormalities in different cognitive control networks in children with dyslexia compared to children with mood disorders. Findings of the current study suggest increased functional connectivity of one cognitive control network may compensate for reduced functional connectivity in the other network in children with mood disorders. These findings provide guidance to clinical professionals for design of interventions tailored for children suffering from reading difficulties originating from different pathologies., Highlights • Significant differences were found between children with mood vs those with behavioral disorders and children with dyslexia • Phonological awareness correlated with reduced connectivity in both the fronto-parietal and the cingulo-opercular networks in dyslexia • Differences in fronto-parietal global efficiency in children with mood disorders vs the other three groups

The Journal’s 175th anniversary combined with recent advances in research provides an ideal opportunity to present a neurodevelopmental roadmap for understanding, preventing, and treating psychiatric disorders. Such a roadmap is particularly relevant for early childhood onset neurodevelopmental conditions, which emerge when experience-dependent neuroplasticity is at its peak. Employing a novel developmental specification approach, this review places recent neurodevelopmental research on early childhood disruptive behavior within the historical context of The Journal. We highlight irritability and callous behavior as two core exemplars of early disruptive behavior. Both phenotypes can be reliably differentiated from normative variation as early as the first years of life. Both link to discrete pathophysiology: irritability with disruptions in prefrontal regulation of emotion, and callous behavior with abnormal fear processing. Each phenotype also possesses clinical and predictive utility. Based on a nomologic net of evidence, we conclude that early disruptive behavior is neurodevelopmental in nature, and should be reclassified as an early childhood-onset neurodevelopmental condition in DSM 5. Rapid translation from neurodevelopmental discovery to clinical application has transformative potential for psychiatric approaches of the millennium.

BACKGROUND: A major challenge in prenatal drug exposure research concerns the balance of measurement quality with sample sizes necessary to address confounders. To inform the selection of optimal exposure measures for the HEALthy Brain and Child Development (HBCD) Study, we employed integrated analysis to determine how different methods used to characterize prenatal tobacco exposure influence the detection of exposure-related risk, as reflected in normal variations in birth weight. METHODS: Participants were N=2323 mother-infant dyads derived from 7 independent developmental cohorts harmonized on measures of exposure, outcome (birthweight), and covariates. We compared estimates of PTE-related effects on birthweight derived from linear regression models when PTE was categorized dichotomously based on any fetal exposure (30% exposed; 69% not exposed); versus categorically, based on common patterns of maternal smoking during pregnancy (never smoked 69%; quit smoking 16%; smoked intermittently 2%; smoked persistently 13%). We secondarily explored sex differences in PTE-birthweight associations across these categorization methods. RESULTS: When PTE was categorized dichotomously, exposure was associated with a −125-gram difference in birthweight (95% C.I. −173.7 – −76.6, p

Few studies have investigated the neural systems involved in decreasing behavioral reactivity to emotional stimuli as children age. It has been suggested that this process may interact with temperament-linked variations in neurodevelopment to better explain individual differences in the maturation of emotion regulation. In this investigation, children ages 4 to 12 (n = 30, mean age = 7.62 years, SD = 1.71 years) and adults (n = 21, mean age = 26.67 years) watched clips from popular children's films containing positive, negative, or neutral emotional content during functional magnetic resonance imaging. Compared to adults, children demonstrated greater activation in subcortical and visual regions (hippocampus, thalamus, visual cortex, fusiform) during negative clips and greater activation of subcortical and prefrontal regions during positive clips (hippocampus, thalamus, caudate, ACC, OFC, superior frontal cortex). In children only, we found an age by temperament interaction in frontal and subcortical regions indicating that activation increased as a function of age in the most irritable children, but decreased as a function of age in the least irritable children. Findings were not present in the temperament domain of fear. Findings replicate and extend the existing irritability literature, indicating that healthy children highest in irritability may develop comparatively greater activation of the lateral prefrontal cortex in order to support adaptive regulation during emotional challenges. These results are discussed within the context of the emerging literature on the utility of complex, multidimensional, and naturalistic stimuli, which present a complementary alternative to understanding ecologically valid and sustained neural responses to emotionally evocative stimuli. Hum Brain Mapp 38:5307-5321, 2017. © 2017 Wiley Periodicals, Inc.

Background Changes in neural circuitry function may be associated with longitudinal changes in psychiatric symptom severity. Identification of these relationships may aid in elucidating the neural basis of psychiatric symptom evolution over time. We aimed to distinguish these relationships using data from the Longitudinal Assessment of Manic Symptoms cohort. Methods Forty-one youth completed two study visits (interscan mean = 21.3 months). Elastic net regression (multiple-response Gaussian family) identified emotional regulation neural circuitry that changed in association with changes in depression, mania, anxiety, affect lability, and positive mood and energy dysregulation, accounting for clinical and demographic variables. Results Nonzero coefficients between change in the previously mentioned symptom measures and change in activity over the interscan interval were identified in right amygdala and left ventrolateral prefrontal cortex. Differing patterns of neural activity change were associated with changes in each of the previously mentioned symptoms over time. Specifically, from scan 1 to scan 2, worsening affective lability and depression severity were associated with increased right amygdala and left ventrolateral prefrontal cortical activity. Worsening anxiety and positive mood and energy dysregulation were associated with decreased right amygdala and increased left ventrolateral prefrontal cortical activity. Worsening mania was associated with increased right amygdala and decreased left ventrolateral prefrontal cortical activity. These changes in neural activity between scans accounted for 13.6% of the variance; that is, 25% of the total explained variance (39.6%) in these measures. Conclusions Distinct neural mechanisms underlie changes in different mood and anxiety symptoms over time.

Burgeoning interest in early childhood irritability has recently turned toward neuroimaging techniques to better understand normal versus abnormal irritability using dimensional methods. Current accounts largely assume a linear relationship between poor frustration management, an expression of irritability, and its underlying neural circuitry. However, the relationship between these constructs may not be linear (i.e., operate differently at varying points across the irritability spectrum), with implications for how early atypical irritability is identified and treated. Our goal was to examine how the association between frustration-related lateral prefrontal cortex (LPFC) activation and irritability differs across the dimensional spectrum of irritability by testing for non-linear associations. Children (N = 92; ages 3–7) ranging from virtually no irritability to the upper end of the clinical range completed a frustration induction task while we recorded LPFC hemoglobin levels using fNIRS. Children self-rated their emotions during the task and parents rated their child’s level of irritability. Whereas a linear model showed no relationship between frustration-related LPFC activation and irritability, a quadratic model revealed frustration-related LPFC activation increased as parent-reported irritability scores increased within the normative range of irritability but decreased with increasing irritability in the severe range, with an apex at the 91st percentile. Complementarily, we found children’s self-ratings of emotion during frustration related to concurrent LPFC activation as an inverted U function, such that children who reported mild distress had greater activation than peers reporting no or high distress. Results suggest children with relatively higher irritability who are unimpaired may possess well-developed LPFC support, a mechanism that drops out in the severe end of the irritability dimension. Findings suggest novel avenues for understanding the heterogeneity of early irritability and its clinical sequelae.

Mood disorders and behavioral are broad psychiatric diagnostic categories that have different symptoms and neurobiological mechanisms, but share some neurocognitive similarities, one of which is an elevated risk for reading deficit. Our aim was to determine the influence of mood versus behavioral dysregulation on reading ability and neural correlates supporting these skills in youth, using diffusion tensor imaging in 11- to 17-year-old children and youths with mood disorders or behavioral disorders and age-matched healthy controls. The three groups differed only in phonological processing and passage comprehension. Youth with mood disorders scored higher on the phonological test but had lower comprehension scores than children with behavioral disorders and controls; control participants scored the highest. Correlations between fractional anisotropy and phonological processing in the left Arcuate Fasciculus showed a significant difference between groups and were strongest in behavioral disorders, intermediate in mood disorders, and lowest in controls. Correlations between these measures in the left Inferior Longitudinal Fasciculus were significantly greater than in controls for mood but not for behavioral disorders. Youth with mood disorders share a deficit in the executive-limbic pathway (Arcuate Fasciculus) with behavioral-disordered youth, suggesting reduced capacity for engaging frontal regions for phonological processing or passage comprehension tasks and increased reliance on the ventral tract (e.g., the Inferior Longitudinal Fasciculus). The low passage comprehension scores in mood disorder may result from engaging the left hemisphere. Neural pathways for reading differ mainly in executive-limbic circuitry. This new insight may aid clinicians in providing appropriate intervention for each disorder., Highlights • Mood disorders scored higher on phonological test but lower on comprehension tests • Correlations between FA and phonological processing in the left Arcuate Fasciculus was strongest in behavioral disorders • Reduced capacity for engaging frontal regions for phonological processing in youth with mood disorders • The low passage-comprehension scores in mood disorder may result from engaging the left vs the right hemisphere.

The preschool age (3–6 years) is a unique period for development as both emotion regulation and foundational brain development are rapidly maturing. Emotions such as frustration are common during this age; however, there is extensive variability along the spectrum from typical to atypical. This juxtaposition of normative misbehaviors with stable irritable temperament presents unique challenges to the differentiation of normative variation from the onset of clinical problems. As such, recent research has focused efforts on improving methods for differentiating normative and clinically concerning behavior. Improved neuroimaging tools, in combination with behavioral and clinical assessment, have provided an additional tool for assessing pediatric irritability. The authors believe that joint consideration of brain–behavior atypicalities will enhance early identification of clinically concerning irritability. To this end, this chapter aims to summarize the rapid development occurring during the preschool years, describe advancements in developmentally appropriate irritability assessments, and integrate these measurements within a neurodevelopmental framework.

Parent-child synchrony-parent-child interaction patterns characterized by contingent social responding, mutual responsivity, and co-regulation-has been robustly associated with adaptive child outcomes. Synchrony has been investigated in both behavioral and biological frameworks. While it has been demonstrated that adversity can influence behavioral parent-child synchrony, the neural mechanisms by which this disruption occurs are understudied. The current study examined the association between adversity, parent-child behavioral synchrony, and parent-child neural synchrony across lateral prefrontal cortical regions using functional near-infrared spectroscopy hyperscanning during a parent-child interaction task that included a mild stress induction followed by a recovery period. Participants included 115 children (ages 4-5) and their primary caregivers. Parent-child behavioral synchrony was quantified as the amount time the dyad was synchronous (e.g., reciprocal communication, coordinated behaviors) during the interaction task. Parent-child neural synchrony was examined as the hemodynamic concordance between parent and child lateral PFC activation. Adversity was examined across two, empirically-derived domains: sociodemographic risk (e.g., family income) and familial risk (e.g., household chaos). Adversity, across domains, was associated with decreased parent-child behavioral synchrony across task conditions. Sociodemographic risk was associated with decreased parent-child neural synchrony in the context of experimentally-induced stress. These findings link adversity to decreased parent-child behavioral and neural synchrony.

Highlights • Negative Affectivity is associated with differences in bio-behavioral systems. • Attentional and regulatory systems in young children were multimodally assessed. • Decreased frustration PFC activation was associated with increased Negative Affectivity. • Decreased Happy face mouth fixation was associated with increased Negative Affectivity. • Preliminary evidence for coordinated development of Negative Affectivity systems., High Temperamental Negative Affectivity in early childhood has been found to predict later emotion dysregulation. While much work has been conducted to separately probe bio-behavioral systems associated with Negative Affectivity, very little work has examined the relations among multiple systems across age. In this study, we use multi-modal methods to index neurobiological systems associated with Negative Affectivity in 53 4-7-year-old children. Prefrontal activation during emotion regulation was measured using functional near-infrared spectroscopy over the lateral prefrontal cortex (PFC) while children played a game designed to elicit frustration in Social (Happy and Angry faces) and Nonsocial contexts. Gaze behaviors while free-viewing Happy and Angry faces were also measured. Finally, Negative Affectivity was indexed using a score composite based on factor analysis of parent-reported temperament. Using mixed-effects linear models, we found an age-dependent association between Negative Affectivity and both PFC activation during frustration and fixation duration on the mouth area of Happy faces, such that older children high in Negative Affectivity spent less time looking at the mouths of Happy faces and had lower PFC activation in response to frustration (ps

Behavioral and emotional dysregulation in childhood may be understood as prodromal to adult psychopathology. Additionally, there is a critical need to identify biomarkers reflecting underlying neuropathological processes that predict clinical/behavioral outcomes in youth. We aimed to identify such biomarkers in youth with behavioral and emotional dysregulation in the Longitudinal Assessment of Manic Symptoms (LAMS) study. We examined neuroimaging measures of function and white matter in the whole brain using 80 youth aged 14.0 (s.d.=2.0) from three clinical sites. Linear regression using the LASSO (Least Absolute Shrinkage and Selection Operator) method for variable selection was used to predict severity of future behavioral and emotional dysregulation measured by the Parent General Behavior Inventory-10 Item Mania Scale (PGBI-10M)) at a mean of 14.2 months follow-up after neuroimaging assessment. Neuroimaging measures, together with near-scan PGBI-10M, a score of manic behaviors, depressive behaviors and sex, explained 28% of the variance in follow-up PGBI-10M. Neuroimaging measures alone, after accounting for other identified predictors, explained ~1/3 of the explained variance, in follow-up PGBI-10M. Specifically, greater bilateral cingulum length predicted lower PGBI-10M at follow-up. Greater functional connectivity in parietal-subcortical reward circuitry predicted greater PGBI-10M at follow-up. For the first time, data suggest that multimodal neuroimaging measures of underlying neuropathologic processes account for over a third of the explained variance in clinical outcome in a large sample of behaviorally and emotionally dysregulated youth. This may be an important first step toward identifying neurobiological measures with the potential to act as novel targets for early detection and future therapeutic interventions.

Anger is among the earliest occurring symptoms of mental health, yet we know little about its developmental course. Further, no studies have examined whether youth with persistent anger are at an increased risk of exhibiting antisocial personality features in adulthood, or how cognitive control abilities may protect these individuals from developing such maladaptive outcomes. Trajectories of anger were delineated among 503 boys using annual assessments from childhood to middle adolescence (ages ∼7-14). Associations between these trajectories and features of antisocial personality in young adulthood (age ∼28) were examined, including whether cognitive control moderates this association. Five trajectories of anger were identified (i.e., childhood-onset, childhood-limited, adolescent-onset, moderate, and low). Boys in the childhood-onset group exhibited the highest adulthood antisocial personality features (e.g., psychopathy, aggression, criminal charges). However, boys in this group were buffered from these problems if they had higher levels of cognitive control during adolescence. Findings were consistent across measures from multiple informants, replicated across distinct time periods, and remained when controlling for general intelligence and prior antisocial behavior. This is the first study to document the considerable heterogeneity in the developmental course of anger from childhood to adolescence. As hypothesized, good cognitive control abilities protected youth with persistent anger problems from developing antisocial personality features in adulthood. Clinical implications and future directions are discussed.