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 ones 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 persons ability to navigate stage
  salient developmental tasks, form appropriate
  interpersonal relationships, and develop healthy
  strategies for coping with distress.