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. Keywordsborderline personality disorder (BPD); developmental psychopathology; child; adolescent; selfinflicted injury Borderline personality disorder (BPD), which is characterized by persistent and pervasive cognitive, emotional, and behavioral dysregulation, is among the most severe and perplexing behavioral disorders. BPD is a heterogeneous phenotype and results from a polythetic criterion set of which only five of nine behavioral features are required for a diagnosis. Thus, two individuals receiving a diagnosis of BPD could potentially overlap on only one diagnostic criterion. The BPD phenotype is broadly defined by features of emotion dysregulation, impulsivity, identity disturbance, problematic interpersonal relationships, and suicidal/selfinjurious behaviors, among others (American Psychiatric Association, 2000). Currently, the developmental trajectory or trajectories that lead to BPD in adulthood remain unclear. Despite steady progress toward outlining the etiology of BPD (see Lenzenweger & Cicchetti, 2005), longitudinal research is still needed to identify biological vulnerabilities, environmental risk and protective factors, and patterns of homotypic and/or heterotypic continuity that lead to the diagnosis.When compared with research on other psychological disorders, such as depression and antisocial personality disorder (ASPD), research on the development of BPD has been

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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. Keywordsantisocial; borderline; multifinality; genetics; environment Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) are among the most costly public health concerns confronting the US criminal justice and healthcare systems. Although ASPD affects only 3-6% of adult males and 1% of adult females (American

Numerous studies have revealed autonomic underarousal in conduct-disordered adolescents and antisocial adults. It is unknown, however, whether similar autonomic markers are present in at-risk preschoolers. In this study, the authors compared autonomic profiles of 4- to 6-year-old children with attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD; n = 18) with those of age-matched controls (n = 20). Children with ADHD and ODD exhibited fewer electrodermal responses and lengthened cardiac preejection periods at baseline and during reward. Although group differences were not found in baseline respiratory sinus arrhythmia, heart rate changes among ADHD and ODD participants were mediated exclusively by parasympathetic withdrawal, with no independent sympathetic contribution. Heart rate changes among controls were mediated by both autonomic branches. These results suggest that at-risk preschoolers are autonomically similar to older externalizing children.

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 ϭ 23! with age-matched controls~n ϭ 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.

Multilevel modeling analyses indicated that slopes in RSA collected across the three assessments were associated with later self-reported ER abilities at the transition into adolescence. These findings were replicated across contexts (baseline and emotional challenge), suggesting that adolescents whose physiological responding to emotional challenge improves also experience fewer difficulties with emotion regulation as they mature.

Low resting respiratory sinus arrhythmia (RSA), and to a lesser extent excessive RSA reactivity to emotion evocation, are observed in many psychiatric disorders characterized by emotion dysregulation, including syndromes spanning the internalizing and externalizing spectra, and other conditions such as nonsuicidal self-injury. Nevertheless, some inconsistencies exist. For example, null outcomes in studies of RSA-emotion dysregulation relations are sometimes observed among younger participants. Such findings may derive from use of age inappropriate frequency bands in calculating RSA. We combine data from five published samples (N = 559) spanning ages 4 to 17 years, and reanalyze RSA data using age-appropriate respiratory frequencies. Misspecifying respiratory frequencies results in overestimates of resting RSA and underestimates of RSA reactivity, particularly among young children. Underestimates of developmental shifts in RSA and RSA reactivity from preschool to adolescence were also observed. Although correlational analyses revealed weak negative associations between resting RSA and aggression, those with clinical levels of externalizing exhibited lower resting RSA than their peers. No associations between RSA reactivity and externalizing were observed. Results confirm that age-corrected frequency bands should be used when estimating RSA, and that literature-wide overestimates of resting RSA, underestimates of RSA reactivity, and underestimates of developmental shifts in RSA and RSA reactivity may exist.

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