The Development of Borderline Personality and Self-Inflicted Injury

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

2. 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

3. 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.

4. 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

5. 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).

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.