Adaptation to violent environments across development involves a multitude of cascading effects spanning many levels of analysis from genes to behavior. In this review, we (a) examine the potentiating effects of violence on genetic vulnerabilities and the functioning of neurotransmitter systems in producing both internalizing and externalizing psychopathology, (b) consider the impact of violence on the developing human stress and startle responses, and (c) brain development including the hippocampus and prefrontal cortex. This review integrates literature on the developmental effects of violence on rodents, non-human primates, and humans. Many neurobiological changes that are adaptive for survival in violent contexts become maladaptive in other environments, conferring life-long risk for psychopathology.
abuse; adaptation; anxiety; depression; neurobiology
In this study, we evaluated predictors of resilience among 8- to 12-year-old children recruited from primarily low socioeconomic status neighborhoods, 117 of whom suffered from clinical levels of conduct problems and/or depression, and 63 of whom suffered from no significant symptoms. Tests of interactions were conducted between (a) paternal antisocial behavior and maternal depression and (b) several physiological indices of child temperament and emotionality in predicting (c) children’s conduct problems and depression. Both internalizing and externalizing outcomes among children were associated specifically with maternal melancholic depression, and not with nonmelancholic depression. In addition, low levels of respiratory sinus arrhythmia (RSA) among children conferred significant risk for depression, regardless of maternal melancholia, whereas high RSA offered partial protection. Furthermore, high levels of maternal melancholia conferred significant risk for child depression, regardless of paternal antisocial behavior, whereas low levels of maternal melancholia offered partial protection. Finally, low levels of electrodermal responding (EDR) conferred significant risk for conduct problems, regardless of paternal antisocial behavior, whereas high EDR offered partial protection. None of the identified protective factors offered complete immunity from psychopathology. These findings underscore the complexity of resilience and resilience-related processes, and suggest several potential avenues for future longitudinal research.
Although deficiencies in emotional responding have been linked to externalizing behaviors in children, little is known about how discrete response systems (e.g., expressive, physiological) are coordinated during emotional challenge among these youth. We examined time-linked correspondence of sad facial expressions and autonomic reactivity during an empathy-eliciting task among boys with disruptive behavior disorders (n = 31) and controls (n = 23). For controls, sad facial expressions were associated with reduced sympathetic (lower skin conductance level, lengthened cardiac preejection period [PEP]) and increased parasympathetic (higher respiratory sinus arrhythmia [RSA]) activity. In contrast, no correspondence between facial expressions and autonomic reactivity was observed among boys with conduct problems. Furthermore, low correspondence between facial expressions and PEP predicted externalizing symptom severity, whereas low correspondence between facial expressions and RSA predicted internalizing symptom severity.
Conduct problems; Disruptive behavior; Facial expression; Sadness; Autonomic reactivity
Taxometric procedures provide an empirical means of determining which psychiatric disorders are typologically distinct from normal behavioral functioning. Although most disorders reflect extremes along continuously distributed behavioral traits, identifying those that are discrete has important implications for accurate diagnosis, effective treatment, early identification of risk, and improved understanding of etiology. This article provides (a) brief descriptions of the conceptual bases of several taxometric procedures, (b) example analyses using simulated data, and (c) strategies for avoiding common pitfalls that are often observed in taxometrics research. To date, most taxometrics studies have appeared in the adult psychopathology literature. It is hoped that this primer will encourage interested readers to extend taxometrics research to child and adolescent populations.
Although antisocial personality disorder (ASPD) is more common among males and borderline personality disorder (BPD) is more common among females, some (e.g., Paris, 1997) have suggested that the two disorders reflect multifinal outcomes of a single etiology. This assertion is based on several overlapping symptoms and features, including trait impulsivity, emotional lability, high rates of depression and suicide, and a high likelihood of childhood abuse and/or neglect. Furthermore, rates of ASPD are elevated in the first degree relatives of those with BPD, and concurrent comorbidity rates for the two disorders are high. In this article, we present a common model of antisocial and borderline personality development. We begin by reviewing issues and problems with diagnosing and studying personality disorders in children and adolescents. Next, we discuss dopaminergic and serotonergic mechanisms of trait impulsivity as predisposing vulnerabilities to ASPD and BPD. Finally, we extend shared risk models for ASPD and BPD by specifying genetic loci that may confer differential vulnerability to impulsive aggression and mood dysregulation among males and impulsive self-injury and mood dysregulation among females. Although the precise mechanisms of these sex-moderated genetic vulnerabilities remain poorly understood, they appear to interact with environmental risk factors including adverse rearing environments to potentiate the development of ASPD and BPD.
antisocial; borderline; multifinality; genetics; environment
To examine sex differences in autonomic nervous system functioning in children and adolescents with conduct problems and to evaluate the role of aggression in predicting autonomic nervous system functioning, over and above the effects of disruptive behavior. Although deficiencies in autonomic responding among boys with oppositional defiant disorder and/or conduct disorder are well documented, it remains unclear whether such findings extend to girls or apply only to children with aggressive forms of conduct problems.
Electrodermal responding, cardiac pre-ejection period, and respiratory sinus arrhythmia were recorded while boys (n = 110; 53 with conduct problems, 57 controls) and girls (n = 65; 33 with conduct problems, 32 controls) between the ages of 8 and 12 sat for an extended baseline, then played a game with conditions of reward and frustrative nonreward.
Both sex effects and aggression effects were found. Aggressive boys with conduct problems demonstrated reduced autonomic functioning, consistent with previous research. In contrast, aggressive girls with conduct problems exhibited greater electrodermal responding than controls, with no differences in cardiovascular reactivity to incentives.
Observed sex differences in the autonomic correlates of conduct problems and aggression may suggest different etiological mechanisms of externalizing psychopathology for girls compared with boys.
conduct disorder; aggression; electrodermal responding; cardiac pre-ejection period; respiratory sinus arrhythmia
Most contemporary accounts of psychopathology acknowledge the importance of both biological and environmental influences on behavior. In developmental psychopathology, multiple etiological mechanisms for psychiatric disturbance are well recognized, including those operating at genetic, neurobiological, and environmental levels of analysis. However, neuroscientific principles are rarely considered in current approaches to prevention or intervention. In this article, we explain why a deeper understanding of the genetic and neural substrates of behavior is essential for the next generation of preventive interventions, and we outline 10 specific reasons why considering biological processes can improve treatment efficacy. Among these, we discuss (a) the role of biomarkers and endophenotypes in identifying those most in need of prevention; (b) implications for treatment of genetic and neural mechanisms of homotypic comorbidity, heterotypic comorbidity, and heterotypic continuity; (c) ways in which biological vulnerabilities moderate the effects of environmental experience; (d) situations in which Biology×Environment interactions account for more variance in key outcomes than main effects; and (e) sensitivity of neural systems, via epigenesis, programming, and neural plasticity, to environmental moderation across the life span. For each of the 10 reasons outlined we present an example from current literature and discuss critical implications for prevention.
In science, theories lend coherence to vast amounts of descriptive information. However, current diagnostic approaches in psychopathology are primarily atheoretical, emphasizing description over etiological mechanisms. We describe the importance of Polyvagal Theory toward understanding the etiology of emotion dysregulation, a hallmark of psychopathology. When combined with theories of social reinforcement and motivation, Polyvagal Theory specifies etiological mechanisms through which distinct patterns of psychopathology emerge. In this paper, we summarize three studies evaluating autonomic nervous system functioning in children with conduct problems, ages 4-18. At all age ranges, these children exhibit attenuated sympathetic nervous system responses to reward, suggesting deficiencies in approach motivation. By middle school, this reward insensitivity is met with inadequate vagal modulation of cardiac output, suggesting additional deficiencies in emotion regulation. We propose a biosocial developmental model of conduct problems in which inherited impulsivity is amplified through social reinforcement of emotional lability. Implications for early intervention are discussed.
Cardiac vagal control; Cardiac vagal tone; Respiratory sinus arrhythmia; Conduct disorder; Developmental psychopathology; Autonomic nervous system
Self-inflicted injury (SII) in adolescence marks heightened risk for suicide attempts, completed suicide, and adult psychopathology. Although several studies have revealed elevated rates of depression among adolescents who self injure, no one has compared adolescent self injury with adolescent depression on biological, self-, and informant-report markers of vulnerability and risk. Such a comparison may have important implications for treatment, prevention, and developmental models of self injury and borderline personality disorder. We used a multi-method, multi-informant approach to examine how adolescent SII differs from adolescent depression. Self-injuring, depressed, and typical adolescent females (n = 25 per group) and their mothers completed measures of psychopathology and emotion regulation, among others. In addition, we assessed electrodermal responding (EDR), a peripheral biomarker of trait impulsivity. Participants in the SII group (a) scored higher than depressed adolescents on measures of both externalizing psychopathology and emotion dysregulation, and (b) exhibited attenuated EDR, similar to patterns observed among impulsive, externalizing males. Self-injuring adolescents also scored higher on measures of borderline pathology. These findings reveal a coherent pattern of differences between self-injuring and depressed adolescent girls, consistent with theories that SII differs from depression in etiology and developmental course.
Self-inflicted injury in adolescence indicates significant emotional and psychological suffering. Although data on the etiology of self-injury are limited, current theories suggest that the emotional lability observed among self-injuring adolescents results from complex interactions between individual biological vulnerabilities and environmental risk. For example, deficiencies in serotonergic functioning, in conjunction with certain family interaction patterns, may contribute to the development of emotional lability and risk for self-injury. The authors explored the relation between peripheral serotonin levels and mother–child interaction patterns among typical (n = 21) and self-injuring (n = 20) adolescents. Findings revealed higher levels of negative affect and lower levels of both positive affect and cohesiveness among families of self-injuring participants. Peripheral serotonin was also correlated with the expression of positive affect within dyads. Furthermore, adolescents’ serotonin levels interacted with negativity and conflict within dyads to explain 64% of the variance in self-injury. These findings underscore the importance of considering both biological and environmental risk factors in understanding and treating self-injuring adolescents.
self-injury; adolescent; serotonin; family; discussion
The association between maternal smoking during pregnancy and childhood antisocial outcomes has been demonstrated repeatedly across a variety of outcomes. Yet debate continues as to whether this association reflects a direct programming effect of nicotine on fetal brain development, or a phenotypic indicator of heritable liability passed from mother to child. In the current study, we examine relations between maternal smoking and child behavior among 133 women and their 7–15-year-olds, who were recruited for clinical levels of psychopathology. In order to disentangle correlates of maternal smoking, women who smoked during pregnancy were compared with (a) those who did not smoke, and (b) those who did not smoke but experienced significant second-hand exposure. Second-hand exposure was associated with increased externalizing psychopathology in participant mothers’ offspring. Moreover, regression analyses indicated that smoke exposure during pregnancy predicted conduct disorder symptoms, over and above the effects of income, parental antisocial tendencies, prematurity, birth weight, and poor parenting practices. This is the first study to extend the findings of externalizing vulnerability to second hand smoke exposure.
Maternal smoking; Conduct disorder; Aggression; Second hand smoke; ADHD
Comorbid conduct problems (CPs) and depression are observed far more often than expected by chance, which is perplexing given minimal symptom overlap. In this study, relations between parental psychopathology and children’s diagnostic status were evaluated to test competing theories of comorbidity. Participants included 180 families with an 8–12-year-old child diagnosed with CPs, depression, both conditions, or neither condition. Although no single theory of comorbidity was supported fully, evidence suggested that CPs and depression may be inherited separately. Paternal antisocial characteristics and maternal depression provided independent prediction of both child depression and CPs. However, paternal antisocial behavior moderated the effect of maternal depression on CPs. For children with antisocial fathers, CPs were observed regardless of maternal depression levels. In contrast, a strong relation was observed between CPs and maternal depression for children without antisocial fathers.
Family history; Comorbidity; Antisocial personality disorder; Conduct disorder; Depression
Over the past several decades, research has focused increasingly on developmental precursors to psychological disorders that were previously assumed to emerge only in adulthood. This change in focus follows from the recognition that complex transactions between biological vulnerabilities and psychosocial risk factors shape emotional and behavioral development beginning at conception. To date, however, empirical research on the development of borderline personality is extremely limited. Indeed, in the decade since M. M. Linehan initially proposed a biosocial model of the development of borderline personality disorder, there have been few attempts to test the model among at-risk youth. In this review, diverse literatures are reviewed that can inform understanding of the ontogenesis of borderline pathology, and testable hypotheses are proposed to guide future research with at-risk children and adolescents. One probable pathway is identified that leads to borderline personality disorder; it begins with early vulnerability, expressed initially as impulsivity and followed by heightened emotional sensitivity. These vulnerabilities are potentiated across development by environmental risk factors that give rise to more extreme emotional, behavioral, and cognitive dysregulation.
borderline personality disorder (BPD); developmental psychopathology; child; adolescent; self-inflicted injury
Opposing theories of striatal hyper- and hypodopaminergic functioning have been suggested in the pathophysiology of externalizing behavior disorders. To test these competing theories, the authors used functional MRI to evaluate neural activity during a simple reward task in 12- to 16-year-old boys with attention-deficit/hyperactivity disorder and/or conduct disorder (n = 19) and in controls with no psychiatric condition (n = 11). The task proceeded in blocks during which participants received either (a) monetary incentives for correct responses or (b) no rewards for correct responses. Controls exhibited striatal activation only during reward, shifting to anterior cingulate activation during nonreward. In contrast, externalizing adolescents exhibited striatal activation during both reward and nonreward. Externalizing psychopathology appears to be characterized by deficits in processing the omission of predicted reward, which may render behaviors that are acquired through environmental contingencies difficult to extinguish when those contingencies change.
conduct disorder; ADHD; striatum; anterior cingulate cortex; fMRI