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Key Points Youths with conduct disorder and psychopathic traits are particularly difficult to treat. Psychopathic traits are associated with two main impairments: a reduced empathic response to distress in others and impairment in reinforcement-based decision making. The reduced empathic response to distress principally reflects a reduced amygdala response to the distress of others (their fear, sadness or pain). The impairment in reinforcement-based decision making reflects dysfunction in the roles of the ventromedial prefrontal cortex (vmPFC) and caudate in representing expected reward and punishment and in detecting inconsistencies between obtained and expected rewards or punishments. These two main impairments interfere with socialization, leading to the development of an individual with reduced guilt and increased probability of using instrumental antisocial behaviour to achieve their goals. Heritability studies implicate a genetic contribution to these impairments; however, molecular genetic information on this disorder remains in its infancy. Environmental variables that affect the development of the amygdala, vmPFC and caudate have been identified, but their role in the development of psychopathic traits has not been clearly demonstrated. Not all youths with conduct disorder show psychopathic traits — there are individuals with a notably different pathophysiology marked by anxiety and increased responsiveness to threat. Effective treatment of conduct disorder may require differentiating patients into those with psychopathic traits versus those with anxiety and increased responsiveness to threat and developing distinct treatment approaches for each group. Children with conduct disorder show persistent aggressive or antisocial behaviour and, in some cases, psychopathic traits. In this Review, Blair describes the neural and cognitive mechanisms — and their interaction with environmental factors — that underlie psychopathic behaviour. Conduct disorder is a childhood behaviour disorder that is characterized by persistent aggressive or antisocial behaviour that disrupts the child's environment and impairs his or her functioning. A proportion of children with conduct disorder have psychopathic traits. Psychopathic traits consist of a callous–unemotional component and an impulsive–antisocial component, which are associated with two core impairments. The first is a reduced empathic response to the distress of other individuals, which primarily reflects reduced amygdala responsiveness to distress cues; the second is deficits in decision making and in reinforcement learning, which reflects dysfunction in the ventromedial prefrontal cortex and striatum. Genetic and prenatal factors contribute to the abnormal development of these neural systems, and social–environmental variables that affect motivation influence the probability that antisocial behaviour will be subsequently displayed.

Borderline personality disorder (BPD) is highly prevalent among incarcerated populations; however, research has yet to examine whether prisoners diagnosed with BPD experience greater interpersonal dysfunction and institutional misconduct while incarcerated. This study drew from a sample of 184 male and female prisoners diagnosed with major depressive disorder (MDD) in a randomized trial of depression treatment. The presence of a BPD diagnosis (n = 69) was analyzed as a predictor of disciplinary incidents/infractions (i.e., fights, arguments with staff, disciplinary infractions, isolation), time spent in isolation, and types of aggression and victimization experiences during incarceration. There was a trend suggesting prisoners with BPD were about twice as likely as those without BPD to report disciplinary incidents/infractions (OR = 1.76 [0.93, 3.32], p = 0.075). Having a BPD diagnosis was unrelated to time in isolation and overall aggression and victimization. However, prisoners with BPD were more likely than those without BPD to perpetrate and be victimized by psychological aggression. Due to high rates of antisocial personality disorder (ASPD) in the sample as a whole (72%), additional analyses compared outcomes across prisoners with no BPD or ASPD diagnosis, BPD diagnosis only, ASPD diagnosis only, and comorbid BPD and ASPD. Prisoners with comorbid BPD and ASPD were no more likely than prisoners with ASPD only to report disciplinary incidents/infractions, but were significantly more likely than those with ASPD only to report perpetrating and being victimized by psychological aggression. Among prisoners with MDD, those with a BPD diagnosis have increased risk of psychological aggression and disciplinary infractions during incarceration. •Examined institutional misconduct, aggression, & victimization in inmates with BPD•Compared outcomes in inmates with co-occurring BPD and ASPD to those with either disorder alone•Inmates with BPD had higher risk of disciplinary infractions & psychological aggression.•Co-occurring BPD and ASPD associated with more psychological aggression than ASPD only•Inmates with BPD at risk of verbal misconduct during incarceration

The impact of the Fast Track intervention on externalizing disorders across childhood was examined. Eight hundred-ninety-one early-starting children (69% male; 51% African American) were randomly assigned by matched sets of schools to intervention or control conditions. The 10-year intervention addressed parent behavior-management, child social cognitive skills, reading, home visiting, mentoring, and classroom curricula. Outcomes included psychiatric diagnoses after grades 3, 6, 9, and 12 for conduct disorder, oppositional defiant disorder, attention deficit hyperactivity disorder, and any externalizing disorder. Significant interaction effects between intervention and initial risk level indicated that intervention prevented the lifetime prevalence of all diagnoses, but only among those at highest initial risk, suggesting that targeted intervention can prevent externalizing disorders to promote the raising of healthy children.

How to mitigate the dramatic increase in the number of self-inflicted deaths from suicide, alcohol-related liver disease, and drug overdose among young adults has become a critical public health question. A promising area of study looks at interventions designed to address risk factors for the behaviors that precede these —often denoted—“deaths of despair.” This paper examines whether a childhood intervention can have persistent positive effects by reducing adolescent and young adulthood (age 25) behaviors that precede these deaths, including suicidal ideation, suicide attempts, hazardous drinking, and opioid use. These analyses test the impact and mechanisms of action of Fast Track (FT), a comprehensive childhood intervention designed to decrease aggression and delinquency in at-risk kindergarteners. We find that random assignment to FT significantly decreases the probability of exhibiting any behavior of despair in adolescence and young adulthood. In addition, the intervention decreases the probability of suicidal ideation and hazardous drinking in adolescence and young adulthood as well as opioid use in young adulthood. Additional analyses indicate that FT’s improvements to children’s interpersonal (e.g., prosocial behavior, authority acceptance), intrapersonal (e.g., emotional recognition and regulation, social problem solving), and academic skills in elementary and middle school partially mediate the intervention effect on adolescent and young adult behaviors of despair and self-destruction. FT’s improvements to interpersonal skills emerge as the strongest indirect pathway to reduce these harmful behaviors. This study provides evidence that childhood interventions designed to improve these skills can decrease the behaviors associated with premature mortality.

Background Antisocial personality disorder (ASPD) is an under-researched mental disorder. Systematic reviews and policy documents identify ASPD as a priority area for further treatment research because of the scarcity of available evidence to guide clinicians and policymakers; no intervention has been established as the treatment of choice for this disorder. Mentalization-based treatment (MBT) is a psychotherapeutic treatment which specifically targets the ability to recognise and understand the mental states of oneself and others, an ability shown to be compromised in people with ASPD. The aim of the study discussed in this paper is to investigate whether MBT can be an effective treatment for alleviating symptoms of ASPD. Methods This paper reports on a sub-sample of patients from a randomised controlled trial of individuals recruited for treatment of suicidality, self-harm, and borderline personality disorder. The study investigates whether outpatients with comorbid borderline personality disorder and ASPD receiving MBT were more likely to show improvements in symptoms related to aggression than those offered a structured protocol of similar intensity but excluding MBT components. Results The study found benefits from MBT for ASPD-associated behaviours in patients with comorbid BPD and ASPD, including the reduction of anger, hostility, paranoia, and frequency of self-harm and suicide attempts, as well as the improvement of negative mood, general psychiatric symptoms, interpersonal problems, and social adjustment. Conclusions MBT appears to be a potential treatment of consideration for ASPD in terms of relatively high level of acceptability and promising treatment effects. Trial registration ISRCTN ISRCTN27660668 , Retrospectively registered 21 October 2008

This study examined the impact of the Family Check-Up (FCU) and linked intervention services on reducing health-risk behaviors and promoting social adaptation among middle school youth. A total of 593 students and their families were randomly assigned to receive either the intervention or middle school services as usual. Forty-two percent of intervention families engaged in the service and received the FCU. Using complier average causal effect analyses, engagement in the intervention moderated intervention outcomes. Families who engaged in the intervention had youth who reported lower rates of antisocial behavior and substance use over time than did a matched control sample. Results extend previous research indicating that a family-centered approach to supporting youth in the public school setting reduced the growth of antisocial behavior, alcohol use, tobacco use, and marijuana use throughout the middle school years.

Antisocial personality disorder (ASPD) often presents with highly impulsive, violent behavior, and pathological changes in the orbitofrontal cortex (OFC) and ventral striatum (VS) are implicated. Several compelling reasons support a relationship between low monoamine oxidase-A (MAO-A), an enzyme that regulates neurotransmitters, and ASPD. These include MAO-A knockout models in rodents evidencing impulsive aggression and positron emission tomography (PET) studies of healthy subjects reporting associations between low brain MAO-A levels and greater impulsivity or aggression. However, a fundamental gap in the literature is that it is unknown whether brain MAO-A levels are low in more severe, clinical disorders of impulsivity, such as ASPD. To address this issue, we applied [(11)C] harmine PET to measure MAO-A total distribution volume (MAO-A VT), an index of MAO-A density, in 18 male ASPD participants and 18 age- and sex-matched controls. OFC and VS MAO-A VT were lower in ASPD compared with controls (multivariate analysis of variance (MANOVA): F2,33=6.8, P=0.003; OFC and VS MAO-A VT each lower by 19%). Similar effects were observed in other brain regions: prefrontal cortex, anterior cingulate cortex, dorsal putamen, thalamus, hippocampus, and midbrain (MANOVA: F7,28=2.7, P=0.029). In ASPD, VS MAO-A VT was consistently negatively correlated with self-report and behavioral measures of impulsivity (r=-0.50 to -0.52, all P-values<0.05). This study is the first to demonstrate lower brain MAO-A levels in ASPD. Our results support an important extension of preclinical models of impulsive aggression into a human disorder marked by pathological aggression and impulsivity.

The amygdala is a key region in current neurocircuitry models of reactive aggression as it is crucially involved in detecting social threat and provocation. An increased amygdala reactivity to angry faces has been reported in aggression-prone individuals and the neuropeptide oxytocin (OT) could dampen anger-related amygdala reactivity in a number of mental disorders. One example is the antisocial personality disorder (ASPD) which has so far only been studied in limited numbers. To address the question whether OT can normalize amygdala hyperreactivity to emotional faces, we conducted a functional magnetic resonance imaging experiment with 20 men and 18 women with ASPD and 20 male and 20 female healthy control (HC) participants in a double-blind, randomized, placebo (PLC)-controlled within-subject design. Participants were exposed to an emotion classification task (fearful, angry, and happy faces) after receiving an intranasal dose (24 IU) of synthetic OT or PLC. We found OT to attenuate right amygdala hyperactivity to angry faces in participants with ASPD to such an extent that the intensity of amygdala activity in the ASPD group in the OT condition decreased to the level of amygdala activity in the PLC condition in the HC group. There was also a trend that OT effects were generally larger in women than in men. These findings suggest that OT differentially modulates the amygdala following social threatening or provoking cues in dependence of psychopathology (ASPD vs. HC) and sex (male vs. female). Particularly female ASPD patients could benefit from OT in the treatment of reactive aggression.

Child conduct problems (CPs) are a robust predictor of adult mental health; the concurrence of callous–unemotional (CU) traits confers specific risk for psychopathy. Psychopathy may be related to disturbances in the oxytocin (OXT) system. Evidence suggests that epigenetic changes in the OXT receptor gene (OXTR) are associated with lower circulating OXT and social–cognitive difficulties. We tested methylation levels of OXTR in 4- to 16-year-old males who met DSM criteria for a diagnosis of oppositional–defiant or conduct disorder and were stratified by CU traits and age. Measures were DNA methylation levels of six CpG sites in the promoter region of the OXTR gene (where a CpG site is a cytosine nucleotide occurs next to a guanine nucleotide in the linear sequence of bases along its lenth, linked together by phosphate binding), and OXT blood levels. High CU traits were associated with greater methylation of the OXTR gene for two cytosine nucleotide and guanine nucleotide phosphate linked sites and lower circulating OXT in older males. Higher methylation correlated with lower OXT levels. We conclude that greater methylation of OXTR characterizes adolescent males with high levels of CU and CPs, and this methylation is associated with lower circulating OXT and functional impairment in interpersonal empathy. The results add genetic evidence that high CU traits specify a distinct subgroup within CP children, and they suggest models of psychopathy may be informed by further identification of these epigenetic processes and their functional significance.