Although parasuicidal behavior in adolescence is poorly understood, evidence suggests that it may be a developmental precursor of borderline personality disorder (BPD). Current theories of both parasuicide and BPD suggest that emotion dysregulation is the primary precipitant of self-injury, which serves to dampen overwhelmingly negative affect. To date, however, no studies have assessed endophenotypic markers of emotional responding among parasuicidal adolescents. In the present study, we compare parasuicidal adolescent girls (n = 23) with age-matched controls (n = 23) on both psychological and physiological measures of emotion regulation and psychopathology. Adolescents, parents, and teachers completed questionnaires assessing internalizing and externalizing psychopathology, substance use, trait affectivity, and histories of parasuicide. Psychophysiological measures including electrodermal responding (EDR), respiratory sinus arrhythmia, and cardiac pre-ejection period (PEP) were collected at baseline, during negative mood induction, and during recovery. Compared with controls, parasuicidal adolescents exhibited reduced respiratory sinus arrhythmia (RSA) at baseline, greater RSA reactivity during negative mood induction, and attenuated peripheral serotonin levels. No between-group differences on measures of PEP or EDR were found. These results lend further support to theories of emotion dysregulation and impulsivity in parasuicidal teenage girls.This work was supported by grants from the Seattle Children's Hospital and Regional Medical Center, the Pediatric Clinical Research Center at Seattle Children's Hospital (M01-RR 00037), and the National Foundation for Suicide Prevention to Cindy J. Smith, and by a grant from the National Institute of Mental Health to Theodore P. Beauchaine (R01 MH63699). We express thanks to Trevor Aerts, Anna Amen, Tyson Bailey, Jordan Campbell, Breyen Engelhardt, Ashleigh Freize, Jennifer Gross, Barbara Kleine, Dana Kovalchick, Jenna Lee, Eileen Magill, Elise Mallman, Emily Miller, Andrea Moore, Seamus Morrone, Shelby Soike, and Aubriana Teeley.

Attention-deficit/hyperactivity disorder (ADHD) is a behavioral syndrome that arises in early childhood, often co-occurs with conduct disorder and leads, developmentally, to antisocial behavior and substance abuse. Models from cognitive and affective neuroscience have been invoked in an effort to understand the development of ADHD, leading to a broad array of interrelated theories and hypothesized mechanisms. In this paper, we highlight core mechanisms that may cut across several theories and constructs, and thus provide some leverage for further study and conceptualization from a neuroscience perspective. We emphasize the joint operations of frontostriatal and frontocerebellar neural loops in detecting and predicting what and when important events in the environment will occur and their interaction with frontoamygdala loops in assigning emotional significance to these events. We note that weaknesses in the development of these basic operations could lead to decrement in the development of cognitive and affective control and other mental operations mediated by prefrontal cortex during development. In turn, such decrement could lead to many of the phenotypic cognitive and neuropsychological features seen in children with ADHD.This work was supported by National Institute of Mental Health Grants R01-MH59105 and R01-MH63146 to J.T.N. and NIMH R01 MH63255 and NIDA R21 DA15882 to B.J.C.

This study examined whether attachment theory could be used to shed light on the often high degree of discordance between self- and observer ratings of behavioral functioning and symptomatology. Interview-based assessments of attachment organization, using the Adult Attachment Interview, were examined as predictors of the lack of agreement between self- and other reports of behavioral and emotional problems among 176 moderately at-risk adolescents. Lack of agreement was measured in terms of concordance of adolescent and parent or close friend report on equivalent measures of behavioral and emotional adjustment. Insecure–dismissing attachment was linked to less agreement in absolute terms between self- and mother reports of externalizing symptoms, and between adolescent and close friend reports of behavioral conduct. Insecure–preoccupied attachment was associated with higher levels of adolescent reporting of internalizing and externalizing symptoms relative to parent reports of adolescent symptomatology. The findings suggest that attachment organization may be one factor that accounts for individual differences in the degree of discordance between self- and other reports of symptoms in adolescence.

This study was focused on contextual variations in the parenting dimensions salient for preadolescent adjustment. The sample consisted of 614 sixth graders from two communities, one low and the other high income. Parenting dimensions included those known to be significant in each socioeconomic context: isolation from parents (emotional and physical), and parents' emphasis on achievements (overall expectations and emphasis on integrity over success). Adjustment outcomes included subjective well-being as well as school competence. Contradicting stereotypes, results showed that on average, very affluent children can perceive their parents as emotionally and physically unavailable to the same degree that youth in serious poverty do. The ramifications for adjustment also seem to be largely similar: Closeness to parents was beneficial for all, just as criticism was deleterious. Even after considering the quality of parent–child relationships, parents' physical absence (e.g., at dinner) connoted vulnerability for distress and for poor school performance in both groups. The connotations of a few parenting dimensions varied by context and gender; these variations are discussed as are overall implications for future research and practice.Preparation of the manuscript was funded in part by grants from the National Institutes of Health (RO1-DA10726, RO1-DA11498, R01-DA14385), the William T. Grant Foundation, and the Spencer Foundation.

We review different conceptions of inhibitory control that may be relevant to the regulatory problems featured in borderline personality disorder (BPD). These conceptions have often been framed with regard to personality traits of inhibitory control, but can also be related to cognitive measures of response suppression as well as affect regulation. Reactive behavioral inhibition is relatively unstudied in relation to BPD. A substantial amount of literature links executive function problems with BPD, but that literature has not isolated executive response inhibition nor been controlled for other personality disorder symptoms of antisociality, attention-deficit/hyperactivity disorder (ADHD), or depression, anxiety, or posttraumatic symptoms. We therefore conducted a study of this question looking at BPD symptoms in an adult sample with a small number of BPD subjects and other disorders. Results indicated that symptoms of BPD were correlated with response inhibition (measured by stop signal reaction time) even after controlling for the overlap of stop inhibition with ADHD, antisociality, and other Axis II disorder symptoms. We conclude by hypothesizing discrete developmental routes to BPD, based on different mechanism breakdowns, which would be amenable to empirical investigation at the cognitive or trait level of analysis.Portions of this work were supported by National Institute of Mental Health Grant R01-MH63146 (J.N., PI).

Most studies of attention-deficit/hyperactivity disorder (ADHD) have focused on the combined type and emphasized a core problem in response inhibition. It is proposed here that the core problem in the truly inattentive type of ADHD (not simply the subthreshold combined type) is in working memory. It is further proposed that laboratory measures, such as complex-span and dual-task dichotic listening tasks, can detect this. Children with the truly inattentive type of ADHD, rather than being distractible, may instead be easily bored, their problem being more in motivation (underarousal) than in inhibitory control. Much converging evidence points to a primary disturbance in the striatum (a frontal–striatal loop) in the combined type of ADHD. It is proposed here that the primary disturbance in truly inattentive-type ADHD (ADD) is in the cortex (a frontal–parietal loop). Finally, it is posited that these are not two different types of ADHD, but two different disorders with different cognitive and behavioral profiles, different patterns of comorbidities, different responses to medication, and different underlying neurobiologies.Preparation of this manuscript was supported by grants from NIDA (R01 DA19685-16A2) and the McDonnell Foundation (JSMF Grant 21002016). The author gratefully thanks Russ Barkley, Dante Cicchetti, Michael Posner, and Margaret Weiss for comments on an earlier draft of the manuscript. Of course, only the author bears responsibility for any errors in this paper.

The central question addressed in this study was whether upper class, suburban teenagers can engage in various problem behaviors and still maintain adequate academic grades, because of environmental safety nets, unlike their low-income, inner-city counterparts. Three problem behavior dimensions were assessed among tenth graders, that is, substance use, delinquency, and low school engagement. Academic achievement was assessed in terms of grades across four major subjects. Variable-based analyses indicated unique links with grades for self-reported delinquency and school disengagement in high- and low-income samples, but for substance use only among the former. Person-based analyses showed that in both schools, grades were clearly compromised among youth with disturbances in all three problem domains. In addition, in the suburban school only, grades were low in the cluster characterized chiefly by high substance use. Results are discussed in terms of stereotypes regarding risks (or lack thereof) stemming from families' socioeconomic status; implications for theory and interventions are also considered.Preparation of this manuscript was funded in part by grants from the National Institutes of Health (RO1-DA10726, RO1-DA11498, R01-DA14385), the William T. Grant Foundation, and the Spencer Foundation.

This study compared the structure and quality of emotion language in adolescents with externalizing disorders (N = 21), internalizing disorders (N = 18), and without a behavioral or emotional disorder (N = 16). Emotion language was elicited in response to vignette material prototypical for anger/sadness and fear, to autobiographical experiences, and to an actual emotional challenge. The findings reveal different emphases in the emotion language of internalizing and externalizing youth rather than a relative weakness for externalizing adolescents. Overall, clinical adolescents used fewer emotion terms that were semantically specific for anger, sad, or fear than typical adolescents. The results also show that emotion language is affected differentially for externalizing and internalizing adolescents depending on the emotion domain. Internalizing youth's emotion language to anger/sad events used inner-directed terms, situational references, and reduced intensity while their representation of emotions in response to salient threatening material was dominated by terms with a cognitive focus. Externalizing adolescents' emotion language responses to anger/sad events were more outer directed and intense, and their emotion language in a salient threat situation more orientated to direct affective terms. The results suggest that examining emotion language for specific emotion domains in adolescents with specific disorders will better clarify the role of emotion language in the regulation of emotions than approaches that globalize emotion language competencies or deficits.

From an affective neuroscience perspective, the goal of achieving a deeper, more mechanistic understanding of the development of depression will require rigorous models that address the core underlying affective changes. Such an understanding will necessitate developing and testing hypotheses focusing on specific components of the complex neural systems involved in the regulation of emotion and motivation. In this paper, we illustrate these principles by describing one example of this type of approach: examining the role of disruptions in neural systems of positive affect in major depressive disorder in school-age children and adolescents. We begin by defining positive affect, proposing that positive affect can be distinguished from negative affect by its neurobehavioral features. We provide an overview of neural systems related to reward and positive affect, with a discussion of their potential involvement in depression. We describe a developmental psychopathology framework, addressing developmental issues that could play a role in the etiology and maintenance of early-onset depression. We review the literature on altered positive affect in depression, suggesting directions for future research. Finally, we discuss the treatment implications of this framework.This research was supported by a Klingenstein Third Generation Foundation Postdoctoral Fellowship, NIMH Training Grant T32 MH018269, and NIMH Research Network R24 MH67346. We thank David J. Kupfer for his compelling suggestions about clinical course and development across the life span, and we thank Anna Lotze for help with references.

Cluster A odd or eccentric personality disorder (PD) symptoms may reflect a schizophrenia spectrum biological vulnerability in at least some persons. Consequently, this symptom pattern may have particularly negative effects on the transition from adolescent to adult roles. A general population sample of 200 young adults was assessed on Cluster A PD at mean ages 17 and 22, and subsequently provided detailed narratives about their monthly experiences and behaviors between these two ages. Adolescent Cluster A PD was related to the developmental trajectories of residential, career, financial, romantic, and family formation roles during this period, and trajectories were related to a change in symptoms over this period. Symptoms were associated with early parenthood and less advanced education, but for other developmental outcomes tended to differ for men and women. These gender differences were attributable, in part, to the differential meaning and consequences of early parenthood for men and women.This work was funded by NIMH Grant MH-54161 to Patricia Cohen, and by the New York State Office of Mental Health.

This longitudinal study extended previous work of Wiesner and Capaldi by examining the validity of differing offending pathways and the prediction from the pathways to substance use and depressive symptoms for 204 young men. Findings from this study indicated good external validity of the offending trajectories. Further, substance use and depressive symptoms in young adulthood (i.e., ages 23–24 through 25–26 years) varied depending on different trajectories of offending from early adolescence to young adulthood (i.e., ages 12–13 through 23–24 years), even after controlling for antisocial propensity, parental criminality, demographic factors, and prior levels of each outcome. Specifically, chronic high-level offenders had higher levels of depressive symptoms and engaged more often in drug use compared with very rare, decreasing low-level, and decreasing high-level offenders. Chronic low-level offenders, in contrast, displayed fewer systematic differences compared with the two decreasing offender groups and the chronic high-level offenders. The findings supported the contention that varying courses of offending may have plausible causal effects on young adult outcomes beyond the effects of an underlying propensity for crime.Support for the Oregon Youth Study was provided by a grant (R37 MH 37940) from the Prevention, Early Intervention, and Epidemiology Branch, National Institute of Mental Health (NIMH), US Public Health Service (PHS). Support for the Couples Study was provided by a grant (HD 46364) from the National Institute of Child Health and Human Development (NICHD) and National Institute on Drug Abuse (NIDA), US PHS. Support was also provided by a grant (MH 46690) from the Prevention, Early Intervention, and Epidemiology Branch, NIMH, Office of Research on Minority Health, US PHS. We thank Jane Wilson, Rhody Hinks, and the Oregon Youth Study team for high-quality data collection, and Lee Owen for assistance with data preparation.

The aim of this paper is to clarify how neural mechanisms at the molecular level, specifically the serotonergic (5-HT) system and the hypothalamic–pituitary–adrenal axis system (HPA) in conjunction with early life stress may contribute to the emergence of aggression, self-directed and otherwise, in borderline personality disorder (BPD). Chronic dysregulation of these biological systems, which function to regulate stress and emotion, may potentiate the development of impulsive aggression in borderline personality conditions. Our central premise in this paper is that brain development, stress regulation, and early pathonomic experience are interactive and cumulative in their mutual influence on the development of impulsive aggression in BPD. We review the parameters of impulsive aggression in BPD, followed by a discussion of the neurobiological and neuroendocrine correlates of impulsive aggression with and without BPD. We then focus on the developmental continuities in BPD with attention to brain maturation of 5-HT and HPA axis function during the life span and the influence of early adverse experiences on these systems. Finally, we comment on the data of the relative stability of aggression in BPD, adolescence as a developmental stage of potential vulnerability, and the course of aggressive behavior during the life span.The authors thank Caroline Cozza, Michael McCloskey, and Kurt Knoblett for their comments during the preparation of this manuscript. This research was supported by research funding from the American Foundation of Suicide Prevention (J.K.G.), Grant MH066888-01 (R.L.), and the Borderline Personality Disorder Research Foundation (E.F.C.).

Reflective thinking occurs when information stored in long-term memory (LTM) is not sufficient to allow one to respond “automatically” to an object or event. Instead, stored information must be entered into working memory and a novel response or solution produced. In this article I argue that mental imagery plays a central role in this process, and that over the course of normal cognitive development the process of reflective thinking “programs” LTM so that an increasingly large number of tasks can be performed without reflective thinking. Normal cognitive development thus results in a decreasing reliance on imagery. However, if highly emotional images are formed, additional retrieval cues can be entered into LTM, making such images more likely to occur in the future. Such images induce arousal, similar to that induced by the actual event. This line of thinking leads to a novel perspective on the neurocognitive deficits that underlie the development of posttraumatic stress disorder, and may also help to explain some symptoms seen in hyperactivity, impulsiveness, and difficulties in self-control.The work summarized in this paper was supported in part by NSF ROLE Grant REC-0106760 and NIH Grant 5 R01 MH60734. Portions of this article were adapted from a draft of Kosslyn (2005). I thank the Editors and Robin Rosenberg for helpful comments on earlier drafts.

Borderline personality disorder (BPD) is characterized by a pervasive instability of interpersonal relationships, affects, self-image, marked impulsivity, dissociation, and paranoia. The cognitive dimension of the disorder has received relatively little attention and is poorly understood. This paper proposes that neurocognitive impairment is a key moderator in the development of BPD and elaborates a possible pathway for the expression of the cognitive domain. Neurocognitive impairment is hypothesized to moderate the relationship between caretaking and insecure disorganized attachment and pathological dissociation in the formation of the disorder contributing to impaired metacognition and a range of cognitive difficulties. The empirical evidence from studies of cognitive processes, brain function, attachment, and dissociation that support this theory are reviewed and discussed. Areas for future research that might verify or refute this theory are suggested.The author thanks Geralyn Windt for assistance in manuscript preparation, Dr. Jack Maser for early review of the manuscript, and Dr. Elizabeth Twamley for her invaluable consultation and expert review of the manuscript.

Four models of psychopathy (frontal lobe dysfunction, response set modulation, fear dysfunction, and violence inhibition mechanism hypotheses) are reviewed from the perspective of cognitive neuroscience. Each model is considered both with respect to the psychopathy data and, more importantly, for the present purposes, with respect to the broader cognitive neuroscience fields to which the model refers (e.g., models of attention with respect to the response set modulation account and models of emotion with respect to the fear dysfunction and violence inhibition mechanism models). The paper concludes with an articulation of the more recent integrated emotion systems model, an account inspired both by recent findings in affective cognitive neuroscience as well as in the study of psychopathy. Some directions for future work are considered.

Functional neuroimaging recently has been used to localize brain dysfunction in borderline personality disorder (BPD). Initial studies have examined baseline activity or emotional reactivity, and our group has investigated what we consider to be a crucial interaction between negative emotion and behavioral (dys)control. This research is beginning to identify abnormal frontolimbic circuitry likely underlying core clinical features of this condition. We review the evidence for dysfunction in specific frontolimbic regions, leading to a mechanistic model of symptom formation in BPD. In addition, we offer an integration of these neuroimaging findings with developmental perspectives on the emergence of borderline psychopathology, focusing on the ways in which early psychosocial experience may interact with developing brain systems. We also consider possible mechanisms of psychotherapeutic change at the neural systems level in BPD. Finally, we propose that future neuroimaging studies of BPD should integrate multiple levels of observation (structural, functional, neurochemical, genetic, and clinical) in a model-driven fashion to further understand the dynamic relationship between biological and psychological factors in the development and treatment of this difficult condition.

The natural history and course of borderline personality disorder (BPD) has long been the focus of speculation, typically guided by impressions from clinical work with BPD-affected individuals. Not unlike the other personality disorders (PDs), it has long been assumed that BPD is relatively stable, traitlike, and enduring in nature. The extent to which BPD is or is not a plastic construct has implications not only for understanding its longitudinal course, but also for understanding its development and, ultimately, its treatment and/or prevention. This paper consists of two parts. The first part reviews the longitudinal research corpus that bears directly upon the issue of stability of BPD in both adolescents and adults. The consistent trend in very nearly all studies, whether using a categorical or dimensional approach to assessment, is one of considerable change over time. This literature presents complexities, however, because most of the extant studies examine BPD-affected individuals who have been exposed to treatment. However, at least two large-scale longitudinal studies, which include both treated and untreated persons, also provide support for viewing BPD as a malleable disorder that declines in severity over time. The second part presents original data from the Longitudinal Study of Personality Disorders that specifically examine the predictors of change in BPD using a neurobehavioral model of personality within an individual growth curve (IGC) analytical framework. This IGC analysis revealed important predictors of both overall level of BPD features as well as rate of change in BPD features, with particularly important roles played by the agentic positive emotion (i.e., incentive motivation) and anxiety (negative emotion) systems. The benefits of the IGC approach for understanding the developmental psychopathology of BPD is also stressed.This research was supported in part by NIMH Grant MH 45448 to Mark F. Lenzenweger for the Longitudinal Study of Personality Disorders.