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Externalizing behavioral problems in young children are associated with later delinquency and crime,1 which can cause burdens at both personal and socialeconomic levels. The heterogeneity of externalizing problems emphasizes the importance of examining the etiological mechanisms that underlie externalizing problems and related behaviors. The present study focuses on 2 risk factors for externalizing behavioral problems in early childhood: callous-unemotional traits (CU), characterized as a lack of guilt and empathy,2 and irritability, a tendency to show anger and frustration.3 Behavioral genetic studies find that externalizing problems, CU, and irritability are heritable,4,5 raising the possibility of common genetic effects linking the 3 behaviors, but this has not been previously explored. Neurological evidence suggests distinct pathways from CU and irritability to externalizing problems,6 implying that the genetic and environmental factors linking externalizing problems and CU may differ from those linking externalizing problems and irritability. We predict that there will be common genetic influences operating across externalizing problems, CU, and irritability; but we also predict unique genetic and environmental influences representing distinctive risks shared between externalizing problems and CU, and between externalizing problems and irritability, respectively. [ABSTRACT FROM AUTHOR]

Objective: To test the developmental continuity, interrelationships, and predictive associations of the oppositional defiant disorder (ODD) subdimensions of irritable, headstrong, and hurtful. Method: Data were collected from 6,328 mother-child pairs participating in the Avon Longitudinal Study of Parents and Children (United Kingdom). Results: Developmental continuity for each subdimension was strong and interrelationships indicated that headstrong was associated mainly with irritable, whereas irritable did not cross associate with other ODD subdimensions; and hurtful was associated with lower levels of headstrong. With regard to associations at age 16 years, irritable at age 13 years was associated with depression, whereas headstrong at 13 was associated with delinquency and callous attitude; at age 13, hurtful failed to associate with any of the 3 age 16 outcomes. Conclusions: The results suggest that the ODD headstrong and irritable subdimensions are developmentally distinct, with small cross-over (i.e., headstrong to irritable), and are associated with unique outcomes. Hurtful does not appear to be associated with future maladjustment in children. [ABSTRACT FROM AUTHOR]

Objective: DSM-IV grants episodic irritability an equal status to low mood as a cardinal criterion for the diagnosis of depression in youth, yet not in adults; however, evidence for irritability as a major criterion of depression in youth is lacking. This article examines the prevalence, developmental characteristics, associations with psychopathology, and longitudinal stability of irritable mood in childhood and adolescent depression. Method: Data from the prospective population-based Great Smoky Mountains Study (N = 1,420) were used. We divided observations on 9- to 16-year-olds who met criteria for a diagnosis of depression into 3 groups: those with depressed mood and no irritability, those with irritability and no depressed mood, and those with both depressed and irritable mood. We compared these groups using robust regression models on adolescent characteristics and early adult (ages 19-21 years) depression outcomes. Results: Depressed mood was the most common cardinal mood in youth meeting criteria for depression (58.7%), followed by the co-occurrence of depressed and irritable mood (35.6%); irritable mood alone was rare (5.7%). Youth with depressed and irritable mood were similar in age and developmental stage to those with depression, but had significantly higher rates of disruptive disorders. The co-occurrence of depressed and irritable mood was associated with higher risk for comorbid conduct disorder in girls (gender-by-group interaction, F1,132 = 4.66, p = .03). Conclusions: Our study findings do not support the use of irritability as a cardinal mood criterion for depression. However, the occurrence of irritability in youth depression is associated with increased risk of disruptive behaviors, especially in girls. [ABSTRACT FROM AUTHOR]

The article presents a study on temperamental precursors such as emotionality and activity of a disruptive disorder oppositional defiant disorder (ODD). It uses Avon Longitudinal Study of Parents and Children (ALSPAC) community-based representative wherein analysis from Emotional Activity Sociability (EAS) scale determined the temperamental dimensions and predicts the psychiatric diagnoses. It concludes that ODD is prognosticated by early emotion irregularity and high temperamental activity.

The article presents a study which examines the hypothesis that youth with severe mood dysregulation (SMD) will less likely develop (hypo-)manic or mixed episodes rather than youth with bipolar disorder (BD). The study found that only one of the 84 SMD subjects experienced (hypo-)manic or mixed episodes. The study concludes that youth with SMD will unlikely develop (hypo-)manic or mixed episodes.

The article examines the longitudinal outcome of youth's oppositional behavior. Oppositionality encompasses an Irritable, a Headstrong, and a Hurtful dimension with distinct predictions. The Irritable dimension is associated with distress disorders both before and after adjustment for baseline psychopathology. Both Headstrong and Hurtful dimensions predict conduct disorder. The Headstrong dimension is the only predictor of attention-deficit/hyperactivity disorder while the Hurtful dimension serves as the strongest predictor of aggressive conduct disorder symptoms.

The article comments on the paper "A comparison of American and English hospital discharge rates for pediatric bipolar disorder" by A. James and colleagues. Topics discussed include more common diagnosis of early-onset bipolar disorder in the U.S. as compared to Great Britain, administrative and epidemiologic prevalence rates, and reasons for the differing diagnostic practice between the U.S. and Great Britain.

Suicide is a major public health concern.1 Although still rare in absolute numbers, suicide is the second cause of death in adolescents and seems to be on the rise.2 One of the strongest risk factors for suicide is suicidality (ie, suicide ideation and attempts) alongside depression, substance abuse and, of course, access to lethal means.3-5 Identifying modifiable early predictors of suicidality and suicide should therefore be a priority for mental health researchers. In this issue of the Journal, Orri et al. examine whether distinct childhood trajectories of irritability, one of the most common symptoms across psychiatric disorders in youth, are associated with suicidality in adolescence.6. [ABSTRACT FROM AUTHOR]

The author discusses the findings of the Treatment of Early Age Mania (Team) trial, particularly noting his belief in the need for an increase in the number of treatment trials in child and adolescent psychiatry. He addresses the improvements in second-generation antipsychotic medications, mitigating factors on the treatment outcomes, and the effects of comorbid psychiatric conditions including attention-deficit hyperactivity disorder (ADHD). Implications of the research are considered.

Reward processing has been implicated in adolescent depression, yet little is known about how it relates to fluctuations in mood over time and how it changes after treatment. Cross-sectional findings are consistent with previous findings demonstrating a statistically significant decreased activity in striatal areas during reward feedback in those with depression. [Extracted from the article]

Depression is one of the leading causes in the global burden of disease, yet its treatment remains unsatisfactory and its underlying mechanisms remain largely unknown. Parent-child psychotherapy versus waitlist and family versus individual treatment of depression both showed substantial improvements in children with depression. Moreover, sleep regulation and reward processing appear promising pathophysiological targets with implications for how to extend current treatments or develop novel interventions for child and adolescent depression. [Extracted from the article]

The associations of anxiety and depression with metabolic syndrome (MetS) are not consistent across studies. Anxiety and depression are highly correlated and traditional methods don't take the structure of this correlation into account. Our aim is to disentangle the relationship of these emotional conditions with MetS, using bifactor models, modelling both general and specific aspects between anxiety and depression. Bifactor models were tested using the baseline data from the Brazilian Longitudinal Study of Adult Health (n = 13,584). Anxiety and depression were accessed with the Clinical Interview Schedule - Revised. MetS was measured through assessment of its continuous components. A bifactor S-1 model better represent the 14 CIS-R indicators, composed by an internalizing factor corresponding to depressive symptoms, anxiety, worry and the shared variance of all remaining CIS-R indicators, and also by residual variance explained by a somatic (e.g., fatigue and pain) and fear (e.g., panic and phobias) specific factors. Internalizing spectrum (β = 0.116; p < 0.001) and the fear specific factor (β = 0.060; p = 0.008) were associated with MetS after adjusting for confounders, whereas somatic specific factor was unlikely to be associated with MetS (β = 0.002; p = 0.934). Anxiety and depression indicators were associated with MetS via a shared internalizing factor and also by a residual fear factor, but not by somatic residual factor. This finding has potential implications about shared biological and behavioral mechanisms that may link emotional conditions with MetS in adults. • Associations of anxiety and depression with metabolic syndrome (MetS) are inconsistent possibly due to high correlation. • Bifactor models can disentangle communalities and specificities from depression and anxiety. • Anxiety and depression can be modelled by an internalizing spectrum and residual fear and somatic specific factors. • Internalizing spectrum and fear are associated with MetS in an adjusted structural equation model. • Symptoms of anxiety and depression may share biological and behavioral mechanisms that are linked with MetS. [ABSTRACT FROM AUTHOR]

This study aimed to investigate longitudinal associations between changes in early childhood irritability, and depressive symptoms and self-harm at 14 years. We used data from 7,225 children in a UK-based general population birth cohort. Childhood irritability was measured at 3, 5, and 7 years using 4 items from 2 questionnaires (the Children's Social Behaviour Questionnaire [CSBQ] and the Strengths and Difficulties Questionnaire [SDQ]). Participants reported depressive symptoms via the short Mood and Feelings Questionnaire (sMFQ) and self-harm via a single-item question, at 14 years. We used multilevel models to calculate within-child change in irritability between 3 and 7 years and examined associations between irritability, and depressive symptoms and self-harm at 14 years using linear and logistic regression models, respectively. We adjusted for child and family sociodemographic/economic characteristics, mental health difficulties, and child cognitive development. Irritability at ages 5 and 7 years was positively associated with depressive symptoms and self-harm at age 14 years. Irritability that remained high between 3 and 7 years was associated with depressive symptoms and self-harm at 14 years in unadjusted (depressive symptoms: β coefficient = 0.22, 95 % CI = 0.08-0.37, p =.003; self-harm: odds ratio = 1.09, 95 % CI = 1.01-1.16, p =.019) and adjusted models (depressive symptoms: β coefficient = 0.31, 95 % CI = 0.17-0.45, p <.001; self-harm: odds ratio = 1.12, 95 % CI = 1.0.4-1.19, p =.004). Results were similar in imputed samples. Children with irritability that remains high between 3 and 7 years are more likely to report higher depressive symptoms and self-harm during adolescence. These findings support early intervention for children with high irritability and universal interventions in managing irritability for parents of preschool-aged children. [ABSTRACT FROM AUTHOR]

A response from the authors of the article "Unpacking the Differences in US/UK Rates of Clinical Diagnoses of Early-Onset Bipolar Disorder" published in the journal in 2014 is presented.

Irritability is impairing in youth and is the core feature of disruptive mood dysregulation disorder (DMDD). Currently, there are no established clinician-rated instruments to assess irritability in pediatric research and clinical settings. Clinician-rated measures ensure consistency of assessment across patients and are important specifically for treatment research. Here, we present data on the psychometric properties of the Clinician Affective Reactivity Index (CL-ARI), the first semistructured interview focused on pediatric irritability. The CL-ARI was administered to a transdiagnostic sample of 98 youth (M age = 12.66, SD = 2.47; 41% female). With respect to convergent validity, CL-ARI scores were (a) significantly higher for youth with DMDD than for any other diagnostic group, and (b) showed uniquely strong associations with other clinician-, parent-, and youth-report measures of irritability compared to measures of related constructs, such as anxiety. The three subscales of the CL-ARI (temper outbursts, irritable mood, impairment) showed excellent internal consistency. Test-retest reliability of the CL-ARI was adequate. These data support that irritability can be feasibly, validly, and reliably assessed by clinicians using the CL-ARI. A validated, gold-standard assessment of pediatric irritability is critical in advancing research and treatment efforts. [ABSTRACT FROM AUTHOR]

An abstract of the article "Acute effects of lurasidone on neural responses to reward: A double-blind, randomized, placebo-controlled study cross-over design in young adults" by Selina Wolke and Argyris Stringaris is presented.

An abstract of the article "Children With Oppositional Defiant Disorder in the Danish National Birth Cohort" by Rune V. Kristensen and colleagues is presented.

Abstract Background Studies of white matter connectivity in children with disruptive behavior have yielded inconsistent results, possibly owing to the trait's heterogeneity, which comprises diverse symptoms like physical aggression, irritability, and delinquency. This study examined associations of global and specific white matter connectivity with childhood disruptive behavior problems, while accounting for their complex multidimensionality. Methods In a large cross-sectional population-based study of 10-year-old preadolescents (n = 2567), we assessed four previously described empirically derived dimensions of disruptive behavior problems using the Child Behavior Checklist: physical aggression, irritability, disobedient behavior, and delinquent behavior. Global and specific white matter microstructure was assessed by diffusion tensor imaging. Results Global fractional anisotropy and mean diffusivity were not associated with broad measures of disruptive behavior, e.g., Child Behavior Checklist externalizing problems scale. Global fractional anisotropy was negatively associated with delinquent behavior (β = −.123, p false discovery rate adjusted =.028) and global mean diffusivity was positively associated with delinquent behavior (β =.205, p false discovery rate adjusted < 0.001), suggesting reduced white matter microstructure in preadolescents with higher levels of delinquent behavior. Lower white matter microstructure in the inferior longitudinal fasciculus, superior longitudinal fasciculus, cingulum, and uncinate underlie these associations. Global white matter microstructure was not associated with physical aggression, irritability, or disobedient behavior. Conclusions Delinquent behavior, a severe manifestation of childhood disruptive behavior, was associated with lower white matter microstructure in tracts connecting frontal and temporal lobes. These brain regions are involved in decision making, reward processing, and emotion regulation. This study demonstrated that incorporating the multidimensional nature of childhood disruptive behavior traits shows promise in advancing the search for elucidating neurobiological correlates of disruptive behavior. [ABSTRACT FROM AUTHOR]

The article discusses various reports published within the issue, including one by B. J. Casey and Rebecca M. Jones on adolescent brain and behavior, one by Dinesh K. Shukla and colleagues on the physiology of white matter in autistic children, and one by Michael T. Lynskey on substance use in adolescence.

The article discusses research in psychiatric genetics that examines the relationship between human genome and psychiatric disorders such as autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder, and bipolar disorder. According to the author, the study indicates that the genetic structure of psychiatric illness does not follow previous guidelines of psychiatric nosology.

The article discusses the use of positron emission tomography (PET) scans and functional magnetic resonance imaging (fMRI) to study the the mechanisms of drug actions in human patients. It addresses changes in brain activity as the result of pharmacological interventions and behavioral therapies, as well as comments on the identification of mental illnesses at a cerebral level.

Impairing emotional outbursts, defined by extreme anger or distress in response to relatively ordinary frustrations and disappointments, impact all mental health care systems, emergency departments, schools, and juvenile justice programs. However, the prevalence, outcome, and impact of outbursts are difficult to quantify because they are transdiagnostic and not explicitly defined by current diagnostic nosology. Research variably addresses outbursts under the rubrics of tantrums, anger, irritability, aggression, rage attacks, or emotional and behavioral dysregulation. Consistent methods for identifying and assessing impairing emotional outbursts across development or systems of care are lacking. The American Academy of Child and Adolescent Psychiatry Presidential Task Force (2019-2021) conducted a narrative review addressing impairing emotional outbursts within the limitations of the existing literature and independent of diagnosis. Extrapolating from the existing literature, best estimates suggest that outbursts occur in 4%-10% of community children (preschoolers through adolescents). Impairing emotional outbursts may respond to successful treatment of the primary disorder, especially for some children with attention-deficit/hyperactivity disorder whose medications have been optimized. However, outbursts are generally multi-determined and often represent maladaptive or deficient coping strategies and responses. Evidence-based strategies are necessary to address factors that trigger, reinforce, or excuse the behaviors and to enhance problem-solving skills. Currently available interventions yield only modest effect sizes for treatment effect. More specific definitions and measures are needed to track and quantify outbursts and to design and assess the effectiveness of interventions. Better treatments are clearly needed. [ABSTRACT FROM AUTHOR]

Adolescence is a critical period for circadian rhythm, with a strong shift toward eveningness around age 14. Also, eveningness in adolescence has been found to predict later onset of depressive symptoms. However, no previous study has investigated structural variations associated with chronotype in early adolescence and how this adds to the development of depressive symptoms. Assessment of 128 community-based adolescents (51% girls) at age 14 and 19 years was performed. Using whole-brain voxel-based morphometry, baseline (at age 14) regional gray matter volumes (GMVs), follow-up (at age 19) regional GMVs, and longitudinal changes (between 14 and 19) associated with Morningness/Eveningness Scale in Children score and sleep habits at baseline were measured. The association of GMV with depressive symptoms at 19 years was studied, and the role of potential clinical and genetic factors as mediators and moderators was assessed. Higher eveningness was associated with larger GMV in the right medial prefrontal cortex at ages 14 and 19 in the whole sample. GMV in this region related to depressive symptoms at age 19 in catechol-O-methyltransferase (COMT) Val/Val, but not in Met COMT , carriers. Larger GMV also was observed in the right fusiform gyrus at age 14, which was explained by later wake-up time during weekends. In adolescence, eveningness and its related sleep habits correlated with distinct developmental patterns. Eveningness was specifically associated with GMV changes in the medial prefrontal cortex; this could serve as a brain vulnerability factor for later self-reported depressive symptoms in COMT Val/Val carriers. [ABSTRACT FROM AUTHOR]

The article discusses the use of biomarkers in clinical diagnoses in psychiatry and pathophysiology. The author examines the use of such markers in the study of illnesses such as schizophrenia, autism, and other neuropsychiatric disorders. The article discusses a theory regarding the ratio of excitation to inhibition (E/I) in causing autism.

Objective: To investigate whether, compared to pre-pandemic levels, depressive and anxiety symptoms in adolescents with depression increased during the pandemic.Method: We used data from National Institute of Mental Health Characterization and Treatment of Depression (NIMH CAT-D) cohort, a longitudinal case-control study that started pre-pandemic. Most of the participants are from the states of Maryland and Virginia in the United States. We compared depressive symptoms (1,820 measurements; 519 measurements pre-pandemic and 1,302 during the pandemic) and anxiety symptoms (1,800 measurements; 508 measurements pre-pandemic and 1,292 ratings during the pandemic) of 166 adolescents (109 girls, 96 adolescents with depression) before and during the pandemic. Data were collected during yearly clinical visits, interim 4-month follow-up visits, inpatient stays, and weekly outpatient sessions, with additional data collection during the pandemic. Pre-pandemic, healthy volunteers (HVs) had a median of 1 depressive and anxiety rating (range, 1-3), and adolescents with depression had a median of 2 ratings (anxiety rating range, 1-25; depressive rating range, 1-26). During the pandemic, HVs had a median of 8 anxiety ratings and 9 depressive ratings (range, 1-13), and adolescents with depression had a median of 7 anxiety and depressive ratings (range, 1-29). We also analyzed adolescent- and parent-reported behaviors in the CoRonavIruS Health Impact Survey (CRISIS), totaling 920 self-reported measures for 164 adolescents (112 girls, 92 adolescents with depression). HVs had a median of 7 surveys (range, 1-8), and adolescents with depression had a median of 5 surveys (range, 1-8).Results: Pre-pandemic, adolescents with depression had a mean depressive score of 11.16 (95% CI = 10.10, 12.22) and HVs had a mean depressive score of 1.76 (95% CI = 0.40, 3.13), a difference of 9.40 points (95% CI = 7.78, 11.01). During the pandemic, this difference decreased by 22.6% (2.05 points, 95% CI = 0.71, 3.40, p = .003) due to 0.89 points decrease in severity of scores in adolescents with depression (95% CI = 0.08, 1.70, p = .032) and 1.16 points increase in HVs' depressive symptoms (95% CI = 0.10, 2.23, p = .032). Compared to their pre-pandemic levels, adolescents with depression reported overall lower anxiety symptoms during the pandemic. Parent-on-child reports also were consistent with these results.Conclusion: Contrary to our hypothesis, we found that both depressive and anxiety symptoms were lower for adolescents with depression during the pandemic compared to before. In contrast, the depression scores for the HVs were higher during the pandemic relative to their pre-pandemic ratings; these scores remained much lower than those of adolescents with depression.Clinical Trial Registration Information: Characterization and Treatment of Adolescent Depression; https://clinicaltrials.gov/; NCT03388606. [ABSTRACT FROM AUTHOR]

Objective: This study examines the extent to which children's positive attributes are distinct from psychopathology. We also investigate whether positive attributes change or "buffer" the impact of low intelligence and high psychopathology on negative educational outcomes.Method: In a community sample of 2,240 children (6-14 years of age), we investigated associations among positive attributes, psychopathology, intelligence, and negative educational outcomes. Negative educational outcomes were operationalized as learning problems and poor academic performance. We tested the discriminant validity of psychopathology versus positive attributes using confirmatory factor analysis (CFA) and propensity score matching analysis (PSM), and used generalized estimating equations (GEE) models to test main effects and interactions among predictors of educational outcomes.Results: According to both CFA and PSM, positive attributes and psychiatric symptoms were distinct constructs. Positive attributes were associated with lower levels of negative educational outcomes, independent of intelligence and psychopathology. Positive attributes buffer the negative effects of lower intelligence on learning problems, and higher psychopathology on poor academic performance.Conclusion: Children's positive attributes are associated with lower levels of negative school outcomes. Positive attributes act both independently and by modifying the negative effects of low intelligence and high psychiatric symptoms on educational outcomes. Subsequent research should test interventions designed to foster the development of positive attributes in children at high risk for educational problems. [ABSTRACT FROM AUTHOR]

Objective: Irritability is a dimensional trait in typical development and a common presenting symptom in many psychiatric disorders, including depression. However, little is known about the developmental trajectory of irritability or how child irritability interacts with maternal depression. The present study identifies classes of irritability trajectories from toddlerhood to middle childhood; characterizes maternal depression and other family, social environment, and child variables within each irritability trajectory class; and, as a more exploratory analysis, examines bidirectional associations between maternal depression and child irritability. Method: A total of 4,898 families from the Fragile Families and Child Wellbeing Study reported on irritability symptoms at ages 3, 5, and 9 years, assessed with items from the Child Behavior Checklist. Parental major depressive episode was assessed using the Composite International Diagnostic Interview-Short Form at child ages 1, 3, 5, and 9 years. Results: A latent class growth analysis identified 5 irritability classes: low decreasing; moderate decreasing; high steady; initially very high, then decreasing; and high increasing. Children with more severe irritability trajectories are more likely to have mothers with recurrent depression, and, with the exception of the most severe (high increasing irritability) class, were more likely to have mothers who were exposed to violence. Moreover, paternal depression and alcohol abuse, as well as maternal drug and alcohol abuse, were also risk factors for membership in the more severe irritability classes. A latent auto-regressive cross-lag model showed that child irritability at ages 3 and 5 years is associated with increased mother depression at ages 5 and 9, respectively. Conversely, mother depression at child ages 1 and 3 years is associated with increased child irritability at 3 and 5. Conclusion: Irritability development across toddlerhood and middle childhood has 5 main trajectory types, which differ on maternal depression recurrence and exposure to violence. Maternal depression and child irritability influence each other bidirectionally, particularly early in development. Understanding irritability development and its bidirectional relationship with maternal depression and association with violence exposure may help identify intervention targets. [ABSTRACT FROM AUTHOR]

Eating disorders are common in adolescence and are devastating and strongly comorbid with other psychiatric disorders. Yet little is known about their etiology, knowing which would aid in developing effective preventive measures. Longitudinal assessments of disordered eating behaviors (DEBs)—binge-eating, purging, and dieting—and comorbid psychopathology were measured in 1386 adolescents from the IMAGEN study. Development of DEBs and associated mental health problems was investigated by comparing participants who reported symptoms at ages 16 or 19 years, but not at age 14 years, with asymptomatic control participants. Voxel-based morphometry and psychopathological differences at age 14 were investigated to identify risk factors for the development of DEBs and associated mental health problems. DEBs and depressive symptoms developed together. Emotional and behavioral problems, including symptoms of attention-deficit/hyperactivity disorder and conduct disorder, predated their development. Alterations in frontostriatal brain areas also predated the development of DEBs and depressive symptoms. Specifically, development of binge-eating was predicted by higher gray matter volumes in the right putamen/globus pallidus at age 14. Conversely, development of purging and depressive symptoms was predicted by lower volumes in the medial orbitofrontal, dorsomedial, and dorsolateral prefrontal cortices. Lower gray matter volumes in the orbitofrontal and anterior cingulate cortices mediated the relationship between attention-deficit/hyperactivity disorder and conduct disorder symptoms and future purging and depressive symptoms. These findings suggest that alterations in frontal brain circuits are part of the shared etiology among eating disorders, attention-deficit/hyperactivity disorder, conduct disorder, and depression and highlight the importance of a transdiagnostic approach to treating these conditions. [ABSTRACT FROM AUTHOR]

Background: This report evaluated whether irritability in adults with stimulant use disorder is associated with suicidal ideation (SI) at the same visit (i.e., concurrently) and whether early changes in irritability predict subsequent levels of SI.Methods: Adults with stimulant use disorder (n=302) from nine residential addiction treatment programs were included. Participants were randomized to augmentation of usual care with dosed exercise or health education intervention. Irritability, SI, and depression were measured every week with 5-item irritability domain of Concise Associated Symptom Tracking scale, 3-item suicidal thoughts factor of Concise Health Risk Tracking scale, and 16-item Quick Inventory of Depressive Symptomatology Clinician-Rated version (excluding the suicide-related item) respectively during acute-(baseline-to-week-12) and continuation-(week-12-to-week-36) phase. Covariates included age, sex, race, ethnicity, treatment arm, type of substance(s) used, and comorbid psychiatric and medical disorders.Results: Higher irritability was associated with higher SI concurrently both in the acute-phase: r=0.28 (p<0.0001) and in the continuation-phase: r=0.33 (p<0.0001). Irritability was associated with concurrent SI after controlling for depression [acute-phase: β=0.17 (p<0.0001); continuation-phase: β=0.18 (p<0.0001)]. Greater baseline-to-week-2 reductions in irritability predicted lower levels of SI from week-2-to-week-12 (β=-0.11, p=0.003) and from week-12-to-week-36 (β=-0.22, p<0.0001) after controlling for baseline levels of depression and SI and baseline-to-week-2 changes in depression and SI.Limitations: Secondary analyses, self-report measures of irritability and SI, limited generalizability.Conclusions: Irritability is associated with SI concurrently, and greater reductions in irritability earlier in treatment are associated with lower levels of subsequent SI. Therefore, targeting irritability may reduce suicidality in adults with stimulant use disorder. [ABSTRACT FROM AUTHOR]

Both human and animal studies support the relationship between depression and reward processing abnormalities, giving rise to the expectation that neural signals of these processes may serve as biomarkers or mechanistic treatment targets. Given the great promise of this research line, we scrutinized those findings and the theoretical claims that underlie them. To achieve this, we applied the framework provided by classical work on causality as well as contemporary approaches to prediction. We identified a number of conceptual, practical, and analytical challenges to this line of research and used a preregistered meta-analysis to quantify the longitudinal associations between reward processing abnormalities and depression. We also investigated the impact of measurement error on reported data. We found that reward processing abnormalities do not reach levels that would be useful for clinical prediction, yet the available evidence does not preclude a possible causal role in depression. [ABSTRACT FROM AUTHOR]

An abstract of the article "Disruptive Mood Dysregulation Disorder in Children With Autism Spectrum Disorder" by William E. Copeland and colleagues is presented.

Objective: Research and clinical interest in irritability have been on the rise in recent years. Yet several questions remain about the status of irritability in psychiatry, including whether irritability can be differentiated from other symptoms, whether it forms a distinct disorder, and whether it is a meaningful predictor of clinical outcomes. In this article, we try to answer these questions by reviewing the evidence on how reliably irritability can be measured and its validity.Method: We combine a narrative and systematic review and meta-analysis of studies. For the systematic review and meta-analysis, we searched studies in PubMed and Web of Science based on preselected criteria. A total of 163 articles were reviewed, and 24 were included.Results: We found that irritability forms a distinct dimension with substantial stability across time, and that it is specifically associated with depression and anxiety in longitudinal studies. Evidence from genetic studies reveals that irritability is moderately heritable, and its overlap with depression is explained mainly by genetic factors. Behavioral and neuroimaging studies show that youth with persistent irritability exhibit altered activations in the amygdala, striatum, and frontal regions compared with age-matched healthy volunteers. Most knowledge about the treatment of irritability is based on effects of treatment on related conditions or post hoc analyses of trial data.Conclusion: We identify a number of research priorities including innovative experimental designs and priorities for treatment studies, and conclude with recommendations for the assessment of irritability for researchers and clinicians. [ABSTRACT FROM AUTHOR]

Objective: We performed meta-analyses of randomized controlled trials to examine the effects of neurofeedback on attention-deficit/hyperactivity disorder (ADHD) symptoms and neuropsychological deficits in children and adolescents with ADHD.Method: We searched PubMed, Ovid, Web of Science, ERIC, and CINAHAL through August 30, 2015. Random-effects models were employed. Studies were evaluated with the Cochrane Risk of Bias tool.Results: We included 13 trials (520 participants with ADHD). Significant effects were found on ADHD symptoms rated by assessors most proximal to the treatment setting, that is, the least blinded outcome measure (standardized mean difference [SMD]: ADHD total symptoms = 0.35, 95% CI = 0.11-0.59; inattention = 0.36, 95% CI = 0.09-0.63; hyperactivity/impulsivity = 0.26, 95% CI = 0.08-0.43). Effects were not significant when probably blinded ratings were the outcome or in trials with active/sham controls. Results were similar when only frequency band training trials, the most common neurofeedback approach, were analyzed separately. Effects on laboratory measures of inhibition (SMD = 0.30, 95% CI = -0.10 to 0.70) and attention (SMD = 0.13, 95% CI = -0.09 to 0.36) were not significant. Only 4 studies directly assessed whether learning occurred after neurofeedback training. The risk of bias was unclear for many Cochrane Risk of Bias domains in most studies.Conclusion: Evidence from well-controlled trials with probably blinded outcomes currently fails to support neurofeedback as an effective treatment for ADHD. Future efforts should focus on implementing standard neurofeedback protocols, ensuring learning, and optimizing clinically relevant transfer. [ABSTRACT FROM AUTHOR]

Objective: Neuroimaging findings have been reported in regions of the brain associated with emotion in both adults and adolescents with depression, but few studies have investigated whether such brain alterations can be detected in adolescents with subthreshold depression, a condition at risk for major depressive disorder. In this study, we searched for differences in brain structure at age 14 years in adolescents with subthreshold depression and their relation to depression at age 16 years.Method: High-resolution structural magnetic resonance imaging was used to assess adolescents with self-reported subthreshold depression (n = 119) and healthy control adolescents (n = 461), all recruited from a community-based sample. Regional gray and white matter volumes were compared across groups using whole-brain voxel-based morphometry. The relationship between subthreshold depression at baseline and depression outcome was explored using causal mediation analyses to search for mediating effects of regional brain volumes.Results: Adolescents with subthreshold depression had smaller gray matter volume in the ventromedial prefrontal and rostral anterior cingulate cortices and caudates, and smaller white matter volumes in the anterior limb of internal capsules, left forceps minor, and right cingulum. In girls, but not in boys, the relation between subthreshold depression at baseline and high depression score at follow-up was mediated by medial-prefrontal gray matter volume.Conclusion: Subthreshold depression in early adolescence might be associated with smaller gray and white matter volumes in regions of the frontal-striatal-limbic affective circuit, and the occurrence of depression in girls with subthreshold depression might be influenced by medial-prefrontal gray matter volume. However, these findings should be interpreted with caution because of the limitations of the clinical assessment methods. [ABSTRACT FROM AUTHOR]

Objective The authors performed meta-analyses of randomized controlled trials to examine the effects of cognitive training on attention-deficit/hyperactivity disorder (ADHD) symptoms, neuropsychological deficits, and academic skills in children/adolescents with ADHD. Method The authors searched Pubmed, Ovid, Web of Science, ERIC, and CINAHAL databases through May 18, 2014. Data were aggregated using random-effects models. Studies were evaluated with the Cochrane risk of bias tool. Results Sixteen of 695 nonduplicate records were analyzed (759 children with ADHD). When all types of training were considered together, there were significant effects on total ADHD (standardized mean difference [SMD] = 0.37, 95% CI = 0.09-0.66) and inattentive symptoms (SMD = 0.47, 95% CI = 0.14-0.80) for reports by raters most proximal to the treatment setting (i.e., typically unblinded). These figures decreased substantially when the outcomes were provided by probably blinded raters (ADHD total: SMD = 0.20, 95% CI = 0.01-0.40; inattention: SMD = 0.32, 95% CI = -0.01 to 0.66). Effects on hyperactivity/impulsivity symptoms were not significant. There were significant effects on laboratory tests of working memory (verbal: SMD = 0.52, 95% CI = 0.24-0.80; visual: SMD = 0.47, 95% CI = 0.23-0.70) and parent ratings of executive function (SMD = 0.35, 95% CI = 0.08-0.61). Effects on academic performance were not statistically significant. There were no effects of working memory training, specifically on ADHD symptoms. Interventions targeting multiple neuropsychological deficits had large effects on ADHD symptoms rated by most proximal assessors (SMD = 0.79, 95% CI = 0.46-1.12). Conclusion Despite improving working memory performance, cognitive training had limited effects on ADHD symptoms according to assessments based on blinded measures. Approaches targeting multiple neuropsychological processes may optimize the transfer of effects from cognitive deficits to clinical symptoms. [ABSTRACT FROM AUTHOR]

Objective: Clinically impairing irritability affects 25% to 45% of children with attention-deficit/hyperactivity disorder (ADHD); yet, we know little about what interventions are effective in treating children with ADHD and co-occurring irritability. We used data from the Multimodal Treatment Study of Children With ADHD (MTA) to address 3 aims: to establish whether irritability in children with ADHD can be distinguished from other symptoms of oppositional defiant disorder (ODD); to examine whether ADHD treatment is effective in treating irritability; and to examine how irritability influences ADHD treatment outcomes. Method: Secondary analyses of data from the MTA included multivariate analyses, and intent-to-treat random-effects regression models were used. Results: Irritability was separable from other ODD symptoms. For treating irritability, systematic stimulant treatment was superior to behavioral management but not to routine community care; a combination of stimulants and behavioral treatment was superior to community care and to behavioral treatment alone, but not to medication alone. Irritability did not moderate the impact of treatment on parent- and teacher-reported ADHD symptoms in any of the 4 treatment groups. Conclusion: Treatments targeting ADHD symptoms are helpful for improving irritability in children with ADHD. Moreover, irritability does not appear to influence the response to treatment of ADHD. [ABSTRACT FROM AUTHOR]

Objective: Fundamental questions in biological psychiatry concern the mechanisms that mediate between genetic liability and psychiatric symptoms. Genetic liability for many common psychiatric disorders often confers transdiagnostic risk to develop a wide variety of psychopathological symptoms through yet unknown pathways. This study examined the psychological and cognitive pathways that might mediate the relationship between genetic liability (indexed by polygenic scores; PS) and broad psychopathology (indexed by p factor and its underlying dimensions).Method: First, which of the common psychiatric PSs (major depressive disorder [MDD], attention-deficit/hyperactivity disorder [ADHD], anxiety, bipolar disorder, schizophrenia, autism) that were associated with p factor were identified. Then focused was shifted to 3 pathways: punishment sensitivity (reflected by behavioral inhibition system), reward sensitivity (reflected by behavioral activation system), and cognitive abilities (reflected by g factor based on 10 neurocognitive tasks). We applied structural equation modeling on the Adolescent Brain Cognitive Development (ABCD) Study dataset (n = 4,814; 2,263 girls; 9-10 years old).Results: MDD and ADHD PSs were associated with p factor. The association between MDD PS and psychopathology was partially mediated by punishment sensitivity and cognitive abilities (proportion mediated = 22.35%). Conversely, the influence of ADHD PS on psychopathology was partially mediated by reward sensitivity and cognitive abilities (proportion mediated = 30.04%). The mediating role of punishment sensitivity was specific to emotional/internalizing. The mediating role of both reward sensitivity and cognitive abilities was specific to behavioral/externalizing and neurodevelopmental dimensions of psychopathology.Conclusion: This study provides a better understanding of how genetic risks for MDD and ADHD confer risks for psychopathology and suggests potential prevention/intervention targets for children at risk. [ABSTRACT FROM AUTHOR]