The Development of Borderline Personality and Self-Inflicted Injury Chapter 18 Sheila E. Crowell, Erin A. Kaufman, and Mark F. Lenzenweger

HISTORICAL CONTEXT Self-Inflicted Injury Most studies of SII have been conducted by suicide researchers, and important distinctions between suicidal and nonsuicidal self-injury have only been acknowledged recently (Linehan, 1997; Muehlenkamp & Gurierrez, 2004). Offer and Barglow (1960) identified a relatively large subgroup of hospitalized youth who harmed themselves without suicidal intent. Current research on adolescent suicide and nonsuicidal SII is focused on: Understanding the etiology of SII Placing adolescent SII within a theoretical context Determining how to represent SII within the DSM Developing a standard of care for adolescents who engage in SII

HISTORICAL CONTEXT Borderline Personality Disorder Historically, the term borderline resulted from difficulties diagnosing those who did not fit into the psychiatric nomenclature of the early to mid 20th century. Kernberg (1967) was among the first to identify borderline personality organization as a specific and stable personality pattern. DSM-III (APA, 1980) established diagnostic criteria for BPD. Current research focuses on the dysfunctional psychosocial and biological underpinnings of BPD.

HISTORICAL CONTEXT Borderline Pathology in Childhood Although research on childhood borderline pathology (BP) evolved in parallel with the adult literature, existing research with youth remains extremely limited in scope. Researchers studying the development of BPD generally describe a developmental pathway characterized by: Sequential comorbidity Heterotypic continuity

DIAGNOSTIC, TERMINOLOGICAL, AND CONCEPTUAL ISSUES DSM-IV-TR (2000) Self-inflicted injury is included in the criterion lists of major depression and BPD. Because BPD is a controversial diagnosis for adolescents many clinicians assign one or more Axis I disorders to self- injuring youth, especially major depression. Ongoing efforts to list SII within the DSM as a stand-alone diagnosis. Debate around BPD diagnosis, especially for adolescents. There is increasing evidence that precursors to BPD appear well before age 18 (Bradley, Zittel Conklin, & Westen, 2005).

ETIOLOGICAL FORMULATIONS Biosocial developmental model of borderline personality development (Crowell, et al., 2009) Trait impulsivity and emotional sensitivity are early-emerging biological vulnerabilities that confer risk for SII, BPD, and other disorders characterized by poor behavioral control. Extreme emotional lability is shaped and maintained within high-risk developmental contexts, which are characterized by intermittent reinforcement of aversive behaviors paired with chronic invalidation of intense expressions of emotion. Over time, biological vulnerabilities interact with environmental risks to potentiate more extreme behavioral and emotion dysregulation.

ETIOLOGICAL FORMULATIONS By adolescence, these Biology × Environment interactions promote a constellation of identifiable problems and maladaptive coping strategies such as SII, which indicates heightened risk for BPD. Early features of borderline pathology may further exacerbate risk for BPD by negatively affecting one’s abilities to navigate stage-salient developmental tasks, form appropriate interpersonal relationships, and develop healthy strategies for coping with distress.

FAMILIALITY AND HERITABILITY There are strong biological underpinnings for both BPD and SII. SII also aggregates in families and includes a clinical phenotype characterized by both suicide and suicide attempts (Brent & Mann, 2005). Family studies of those with BPD reveal significant familial aggregation of mood and impulse control disorders (White et al., 2003). BPD co-aggregates with mood and anxiety disorders, alcohol and drug abuse/dependence, pain disorder, and several personality disorders.

GENETICS AND NEUROTRANSMITTER DYSFUNCTION Dopamine There is consensus that DA dysfunction contributes to some of the behavioral traits seen in BPD, including SII (Osuch & Payne, 2009; Sher & Stanley, 2009). Serotonin Deficits in central 5HT have been associated consistently with mood disorders, suicidal behaviors, and aggression (Kamali, Oquendo, & Mann, 2002). Other Biological Vulnerabilities Chronic stress leads to elevated LHPA axis responses that are involved in suicidal behavior. Oxytocin dysregulation may contribute to the difficulty those with BPD experience in relationships (Stanley & Siever, 2010). Deficits within the prefrontal cortex may contribute to suicidal and other impulsive behaviors through a diminished capacity to inhibit strong impulses.

CONTEXTUAL AND FAMILY RISK FACTORS Family processes that shape emotion dysregulation have been well delineated in such samples and may translate well to youth at risk for BPD (Beauchaine et al., 2009). Invalidating caregiving environment. Emotional lability is shaped within families via operant conditioning. Mixed results on child abuse research highlights the importance of the interplay between biological and psychosocial risks.

THEORETICAL SYNTHESIS AND FUTURE DIRECTIONS BPD and SII likely emerge due to repeated, complex interactions between biological vulnerabilities and contextual stressors. By adolescence, there are a constellation of identifiable problems and maladaptive coping strategies, such as SII, that indicate heightened risk for BPD. BP features may further exacerbate risk for BPD by affecting a person’s ability to navigate stage salient developmental tasks, form appropriate interpersonal relationships, and develop healthy strategies for coping with distress.