Transcript Child and Adolescent Psychopathology

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:
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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 selfinjuring 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.