Conduct disorder and childhood head injuries frequently co-occur and are linked to a higher risk of later delinquency. While both are known to disrupt reward-related neural circuits, this study investigated whether their combined presence leads to a unique disruption in these pathways, potentially accounting for the increased risk of delinquency.

Using neuroimaging data from the baseline (age 9–10) assessment from the Adolescent Brain and Cognitive Development (ABCD) study, four groups were compared: children with conduct disorder (CD, n = 588), a mild traumatic brain injury (mTBI, n = 1,216), both (mTBI+CD, n = 252), and typically developing controls (TD, n = 705). Neural activation in eight regions of interest (amygdala, hippocampus, nucleus accumbens, caudal anterior cingulate cortex, rostral anterior cingulate cortex, medial orbitofrontal cortex, thalamus, and insula) during reward anticipation and receipt were assessed during the monetary incentive delay task.

After controlling for several covariates, including sex, ADHD, and internalizing problems, the mTBI+CD group displayed greater left amygdala and hippocampal activation during reward receipt compared to all other groups. While they displayed increased activation in the right hippocampus and thalamus compared to TD controls and the right hippocampus compared to the mTBI group, they did not differ from the CD group. No group differences emerged during reward anticipation.

Increased left amygdala and hippocampus activation in children with conduct disorder and a history of mild traumatic brain injury may reflect robust encoding of emotionally charged reward experiences, potentially reinforcing memory-guided, reward-seeking behaviors.

Machine learning (ML) has developed classifiers differentiating patient groups despite concerns regarding diagnostic reliability. An alternative strategy, used here, is to develop a functional classifier (hyperplane) (e.g. distinguishing the neural responses to received reward v. received punishment in typically developing (TD) adolescents) and then determine the functional integrity of the response (reward response distance from the hyperplane) in adolescents with externalizing and internalizing conditions and its associations with symptom clusters.

Two hundred and ninety nine adolescents (mean age = 15.07 ± 2.30 years, 117 females) were divided into three groups: a training sample of TD adolescents where the Support Vector Machine (SVM) algorithm was applied (N = 65; 32 females), and two test groups– an independent sample of TD adolescents (N = 39; 14 females) and adolescents with a psychiatric diagnosis (major depressive disorder (MDD), generalized anxiety disorder (GAD), attention deficit hyperactivity disorder (ADHD) & conduct disorder (CD); N = 195, 71 females).

SVM ML analysis identified a hyperplane with accuracy = 80.77%, sensitivity = 78.38% and specificity = 88.99% that implicated feature neural regions associated with reward v. punishment (e.g. nucleus accumbens v. anterior insula cortices). Adolescents with externalizing diagnoses were significantly less likely to show a normative and significantly more likely to show a deficient reward response than the TD samples. Deficient reward response was associated with elevated CD, MDD, and ADHD symptoms.

Distinguishing the response to reward relative to punishment in TD adolescents via ML indicated notable disruptions in this response in patients with CD and ADHD and associations between reward responsiveness and CD, MDD, and ADHD symptom severity.

Although the link between alcohol involvement and behavioral phenotypes (e.g. impulsivity, negative affect, executive function [EF]) is well-established, the directionality of these associations, specificity to stages of alcohol involvement, and extent of shared genetic liability remain unclear. We estimate longitudinal associations between transitions among alcohol milestones, behavioral phenotypes, and indices of genetic risk.

Data came from the Collaborative Study on the Genetics of Alcoholism (n = 3681; ages 11–36). Alcohol transitions (first: drink, intoxication, alcohol use disorder [AUD] symptom, AUD diagnosis), internalizing, and externalizing phenotypes came from the Semi-Structured Assessment for the Genetics of Alcoholism. EF was measured with the Tower of London and Visual Span Tasks. Polygenic scores (PGS) were computed for alcohol-related and behavioral phenotypes. Cox models estimated associations among PGS, behavior, and alcohol milestones.

Externalizing phenotypes (e.g. conduct disorder symptoms) were associated with future initiation and drinking problems (hazard ratio (HR)⩾1.16). Internalizing (e.g. social anxiety) was associated with hazards for progression from first drink to severe AUD (HR⩾1.55). Initiation and AUD were associated with increased hazards for later depressive symptoms and suicidal ideation (HR⩾1.38), and initiation was associated with increased hazards for future conduct symptoms (HR = 1.60). EF was not associated with alcohol transitions. Drinks per week PGS was linked with increased hazards for alcohol transitions (HR⩾1.06). Problematic alcohol use PGS increased hazards for suicidal ideation (HR = 1.20).

Behavioral markers of addiction vulnerability precede and follow alcohol transitions, highlighting dynamic, bidirectional relationships between behavior and emerging addiction.

The nature of the pathway from conduct disorder (CD) in adolescence to antisocial behavior in adulthood has been debated and the role of certain mediators remains unclear. One perspective is that CD forms part of a general psychopathology dimension, playing a central role in the developmental trajectory. Impairment in reflective functioning (RF), i.e., the capacity to understand one's own and others' mental states, may relate to CD, psychopathology, and aggression. Here, we characterized the structure of psychopathology in adult male-offenders and its role, along with RF, in mediating the relationship between CD in their adolescence and current aggression.

A secondary analysis of pre-treatment data from 313 probation-supervised offenders was conducted, and measures of CD symptoms, general and specific psychopathology factors, RF, and aggression were evaluated through clinical interviews and questionnaires.

Confirmatory factor analyses indicated that a bifactor model best fitted the sample's psychopathology structure, including a general psychopathology factor (p factor) and five specific factors: internalizing, disinhibition, detachment, antagonism, and psychoticism. The structure of RF was fitted to the data using a one-factor model. According to our mediation model, CD significantly predicted the p factor, which was positively linked to RF impairments, resulting in increased aggression.

These findings highlight the critical role of a transdiagnostic approach provided by RF and general psychopathology in explaining the link between CD and aggression. Furthermore, they underscore the potential utility of treatments focusing on RF, such as mentalization-based treatment, in mitigating aggression in offenders with diverse psychopathologies.

Youth with conduct problems (CP) may be more likely to exhibit aggression in the context of peer relations. Indices of dorsolateral prefrontal cortical functioning (DPCF), such as inhibitory control and planning, may be implicated in the behavioral presentation of CP. Further, youth living in violent communities may be more likely to use aggression as a means for problem-solving. However, little is known about how CP interact with DPCF indices to predict aggressive behaviors specifically in the context of environments with high levels of community violence. As such, the present study sought to use a multi-informant approach to examine relations between CP, DCPF, and different types of aggression among youth living in neighborhoods affected by community violence.

Participants were 104 children (M=9.93±1.22 years; 50% male; 96% African American, 4% Latinx) who resided in neighborhoods with elevated rates of poverty and crime. DPCF was indexed by Stockings of Cambridge planning task and caregiver-reported inhibitory control from the Behavior Rating Inventory of Executive Function. Teachers completed the Child and Adolescent Symptom Inventory-4R to assess youth conduct disorder (CD) symptoms and the Teacher Checklist to assess proactive (bullying, planful aggression) and reactive (angry, emotionally labile aggression) aggression.

Multiple regression analyses were conducted with aggressive behaviors as the dependent variable, and child sex, age, CD symptoms, and the CD × DPCF (i.e., CD × inhibitory control; CD × planning) interaction terms as predictors. Inhibitory control moderated the relation between CD symptoms and reactive (CD × inhibitory control, B = -1.39, p = .004) but not proactive (CD × inhibitory control, B = -.64, p = .063) aggression. Post-hoc probing of the CD symptoms × inhibitory control interaction term predicting reactive aggression revealed a significant slope for youth with both high (B = 1.65, p < .001) and low (B = 4.48, p < .001) levels of inhibitory control. Planning does not significantly moderate the relation between CD symptoms and proactive or reactive aggression, though there is a positive main effect of teacher reported CD symptoms on both proactive (B = 2.44, p < .001) and reactive (B = 2.36, p < .001) aggression.

This study is the first to consider the relations of CP, DPCF processes, and subtypes of aggression among youth living in environments with high rates of community violence. Among youth with CP, high levels of inhibitory control may be associated with lower rates of reactive aggression in the context of peer relations. As such, problem-solving interventions targeting processes related to DPCF, such as inhibitory control, may be useful among youth living in neighborhoods high in community violence who exhibit CP. Strengthening these cognitive processes may result in better behavioral outcomes and peer relations.

Affiliating with delinquent peers may stimulate the development of antisocial behavior, especially for adolescents who are sensitive to social rewards. The current study examines whether the association between delinquent peer affiliation (DPA) and disruptive behavior interacts with functional brain correlates of reward sensitivity in early onset male adolescents delinquents.

Childhood arrestees (n = 126, mean age = 17.7 [s.d. 1.6]) completed a DPA questionnaire, and participated in an fMRI study in which reward sensitivity was operationalized through responsiveness of the ventral striatum (VS), amygdala, and medial prefrontal cortex (mPFC) during the monetary incentive delay paradigm (reward anticipation and outcome). Symptoms of disruptive behavior disorders (DBD) were assessed through structured psychiatric interviews (Diagnostic Interview Schedule for Children) with adolescents.

DPA had a main effect on DBD symptoms. Adolescents with high VS reward responses showed a stronger significant positive association between DPA and DBD symptoms compared to low VS responders. No evidence for an interaction effect was found for the amygdala and mPFC. Post-hoc analyses revealed the positive association between DPA and DBD was only present in males, with a diminishing effect as age increased.

We found evidence for a biosocial interaction between DPA and reward sensitivity of the VS in relation to DBD symptom severity. This study provides the first evidence of an interaction effect between a brain mechanism and an environmental factor in relation to DBD symptoms, implying that susceptibility to influences of delinquent peers may intertwine with individual biological differences.

The quality of the relationship between mother and infant may have profound implications for the development of a child. Early indicators of psychological vulnerability may allow targeting of support for the child's cognitive, emotional and social development. A challenging mother–infant relationship could be one indicator of risk.

This study examined variations in psychological well-being and psychopathology among boys and girls according to early maternal perception of the mother–infant relationship.

This study is based on 64 663 mother–infant pairs from the Danish National Birth Cohort, for which data on the mother–infant relationship were collected at 6 months postpartum. Behavioural problems were assessed with the Danish version of the Strengths and Difficulties Questionnaire (SDQ) at child ages 7, 11 and 18 years, and we retrieved information on diagnosed childhood and adolescent psychiatric disorders and prescriptions of psychotropic drugs from Danish registries.

Children in the challenging mother–infant relationship group had higher odds of behavioural problems at age 7 among both boys and girls. The same pattern of elevated estimates was identified for boys across all SDQ domains and for girls in three of five SDQ domains. All associations were attenuated at age 18, but increased odds of behavioural problems still existed. A challenging early mother–infant relationship increased the offspring's risk of being diagnosed with a psychiatric disorder or being prescribed a psychotropic drug before the age of 18.

A challenging self-reported mother–infant relationship was associated with later psychopathological difficulties. Routine clinical enquiry may be useful in identification of future vulnerability.

The Covid-19 pandemic has significantly changed family dynamics and parents experience greater psychological distress. Conduct problems in young people have increased by 35%. However, it is not known how Covid-19 associated stresses have affected parenting practice, conduct problems, and comorbidities and what additional support is needed for families at risk.

This study uses self-report measures and semi-structured interviews to examine and explore the impact of Covid-19 on the families of young people with conduct problems and comorbid mental health conditions.

This is a sequential mixed-methods study. Eligible families with children aged between 11-18 years have participated. One-hundred-and-eighty-two families have completed eight online questionnaires and 12 have participated in semi-structured follow-up interviews.

Analyses indicate that parental harshness, warmth, educational background, and employment have a significant impact on Covid-19 exposure and worries, as well as significantly higher scores of conduct disorder symptoms. Interview codes reveal that young peoples’ behaviour became more severe during the pandemic, and this was associated with reduced in-person support services, reduced personal space at home, and parents taking on the additional role of educator.

The findings suggest that Covid-19 is a significant risk factor to young people with conduct problems and their families. For example, reduced parental warmth and increased parental harshness increased conduct problems for young people during the lockdown. This study highlights that policies and services should work to better support such families. Future online psychosocial interventions are needed to empower families and improve parenting practice at home during the lockdown period and in general.

No significant relationships.

Previous studies have reported brain structure abnormalities in conduct disorder (CD), but it is unclear whether these neuroanatomical alterations mediate the effects of familial (genetic and environmental) risk for CD. We investigated brain structure in adolescents with CD and their unaffected relatives (URs) to identify neuroanatomical markers of familial risk for CD.

Forty-one adolescents with CD, 24 URs of CD probands, and 38 healthy controls (aged 12–18), underwent structural magnetic resonance imaging. We performed surface-based morphometry analyses, testing for group differences in cortical volume, thickness, surface area, and folding. We also assessed the volume of key subcortical structures.

The CD and UR groups both displayed structural alterations (lower surface area and folding) in left inferior parietal cortex compared with controls. In contrast, CD participants showed lower insula and pars opercularis volume than controls, and lower surface area and folding in these regions than controls and URs. The URs showed greater folding in rostral anterior cingulate and inferior temporal cortex than controls and greater medial orbitofrontal folding than CD participants. The surface area and volume differences were not significant when controlling for attention-deficit/hyperactivity disorder comorbidity. There were no group differences in subcortical volumes.

These findings suggest that alterations in inferior parietal cortical structure partly mediate the effects of familial risk for CD. These structural changes merit investigation as candidate endophenotypes for CD. Neuroanatomical changes in medial orbitofrontal and anterior cingulate cortex differentiated between URs and the other groups, potentially reflecting neural mechanisms of resilience to CD.