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Summary PERSONALITY DISORDERS NOTES
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Summary of 54 pages for the course Personality Disorders at UVT (Summary of the PDs)
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PERSONALITY DISORDERSChapter 20: Borderline Personality Disorder
CLINICAL ASPECTS
Historical Origins
Term “border line” first used by Adolf Stern, over 70 years ago, to describe atypical and
clinically troubling groups of patients
Term described patients who were inordinately hypersensitive, had problems with
reality testing, and who experienced negative reactions in therapy
Stern regarded them as being between the psychoses and the neuroses
“Borderline” reappeared two decades later when Knight (1953) used it to describe a
diagnostically uninformative state in which psychotic and neurotic features were present
in the same individual
Others previously described such as having “pseudo-neurotic schizophrenia”
Patients had severe impairments in their ego functions and manifested primitive
thought processes
In the late 1960s three developments set the stage for change:
1. The psychoanalyst Otto Kernberg began to offer new clinical and theoretical insights
into “borderline personality organization”
2. Grinker and his colleagues conducted the first study of the borderline syndrome and
offered a preliminary and empirically based criterion set for the disorder
3. They identified six features for typical borderline people, including: intense affect,
impulsivity, relationship problems, brief psychotic experiences
In the 1980s it was included in the DSM-III; however, the label “borderline” has
limitations: the name provides no descriptive information about the disorder, it is not clear
what “border” is referring to, is strongly associated with the psychoanalytic traditions
WHO’s International Classification of Diseases terms it “emotionally unstable disorder”
Clinical Description
DSM-IV-TR criteria for BPD (any 5 out of 9 for diagnosis):
1. Frantic efforts to avoid abandonment
2. Unstable and intense relationships
3. Identity disturbance
4. Impulsivity
5. Recurrent suicidal behavior
6. Affective instability
7. Chronic feelings of emptiness
8. Inappropriate or intense anger
9. Transient paranoid ideation or dissociation
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, Construct is polythetic in nature and no one specific symptoms is regarded as necessary;
hence, there are 126 different ways to find 5 out of 9 criteria (heterogeneous disorder from
a clinical perspective)
The hallmark of BPD is instability; people with BPD are “stably unstable”; mostly
manifested in: instability in emotion, interpersonal relationship, self-concept, behavior
Around 75% of BPD patients also have paranoid ideas and/or episodes of dissociation
BPD patients also experience higher levels of stress and stress-related psychosis
COMORBIDITY
Axis I comorbidity is the rule rather than the exception for people with BPD
In a study almost 70% had three or more current Axis I disorders
Most common comorbid disorders: concurrent major depression (61%), PTSD (36%),
bipolar disorder (20%), eating disorders (17%)
In a community sample 40% had “high-functioning BPD” (have not been hospitalized and
had no contact with a physician/mental health professional in previous year) – they were
much less likely to be suffering from comorbid Axis I conditions
Is Borderline Personality Disorder a Distinct Diagnosis?
Large overlap between BPD and mood disorder; idea: BPD as a variant of depression –
but recent neuroimaging study has shown that BPD people show different neural activity
to certain types of emotional stimuli
Also some overlap with PTSD; however, there is no evidence this is the case – traumatic
event is not necessary for BPD
EPIDEMIOLOGY
Prevalence
In outpatient samples, prevalence rates of BPD are around 10%-15%; however, data from
clinical settings cannot be used to estimate the prevalence
In community samples the lifetime prevalence ranges from 0.7% to 5.9%
Different factors make it difficult to estimate the prevalence, but it is reasonable to assume
that in the general population, the prevalence is in the range of 1%-2%
Sex Differences
Until recently it was commonly held that BPD was much more common in women, with
the female to male around 3:1 in psychiatric samples; but researchers now believe that this
may have been an artifact caused by sampling in clinical settings – recent studies of the
prevalence of BPD in community samples report no sex differences
Observed prevalence seems to decrease with age – some of this decreased prevalence may
be explained by the high rate of completed suicide in BPD or the results of treatments
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,Suicide
Having BPD is a major risk factor for suicide – 1/3 attempt suicide
Around 10% of patients with BPD die from suicide, mostly before becoming 40 years old
Studies attempting to identify who is most at risk for a suicide attempt have had smixed
results, but identified some factors:
Affective instability
Intensity of self-reported negative mood
Baseline major depressive disorder and poor social adjustment
However, it is difficult to predict suicidality in BPD patients
Course and Prognosis
People with BPD tend to be high consumers of psychiatric services, but maintaining a
clinical relationship can be challenging, because the instability of BPD patients also shows
itself in therapeutic relationships; it is not uncommon for BPD patients to terminate
treatment prematurely
10 years follow-up study by Zanarini et al., (2010) found:
93% showed significant reductions in symptoms and experienced a clinical remission
(they no longer meet criteria for diagnosis), lasted 2 years
86% experienced clinical remission that lasted for 4 years or more
Many patients clinically improved quickly with 39.3% showing clinical remission as
early as the 2-year follow-up
4.4% died of suicide
Recurrence of symptoms were not uncommon; around 1/3 patients who recovered lost
their recovery at some time in the 10 years
Important to note: although they achieved a clinical remission of their symptoms,
many still had problems in psychosocial functioning; only around 50% of recovered
from BPD when recovery was defined as not meeting diagnostic criteria for BPD and
having good social and vocational functioning
Predictors of more rapid time to clinical remission: young age, absence of history of
childhood sexual abuse, no family history of substance abuse, good recent work history,
agreeable temperament, low in neuroticism, not an anxious personality
Expressed emotion (EE) is a measure of the family environment that has been reliably
linked to relapse and poor clinical outcome in a wide range of disorders
In BPD patients, EE was not predictive of a more unfavorable course of illness
BPD patients did better if their family members showed high emotional
overinvolvement (EOI) (as opposed to depression and anxiety, for example)
Compared with dysthymic and healthy control participants, people with BPD showed
increased activation in left prefrontal cortex during EOI comments (left prefrontal
activation → positive experiences & approach motivation)
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, ETIOLOGY AND RISK FACTORS
Still no answer to what causes BPD; genetic and environmental factors are implicated
Genetic and environmental factors work together, can only be separated in the abstract
Genetic Aspects
BPD runs in families; difficult to find out how much higher the rates are, but it is
reasonable to believe that relatives have a 4-20 times higher prevalence; however, this
does not necessarily mean that it has a genetic basis, can also be environmental
Twin studies: strong support for BPD heritable component – concordance rate in
monozygotic twins: 35%; in dizygotic twins: 7%
Study of Distel et al. (2009) found:
Cultural transmission does not play a significant role in development of BPD, but the
pattern of findings provided strong evidence for genetic effects in BPD
Effects of the combined genes that are inherited are simply added together and the
sum of their effects in unison is the same as the sum of their effects when added
together (21% of variance)
However, it also seems to be the case that nonadditive genetic effects play a role in
BPD; this is when alleles within a given locus or across different loci interact in a way
that gives rise to different effects than those that might occur simply from the presence
of the genes themselves (24% of variance)
55% of the variance in BPD thought to be explained by unique environmental
influence
Complex syndromes such as BPD are almost certainly polygenetic and result from
multiple genes in combination
Different genotypes are associated with differential sensitivities to environmental stressors
Serotonin
Serotonin (5-HT), monoamine neurotransmitter, derived from L-tryptophan, degraded by
MAO, involved in mood and appetitive behavior
5-HT inhibits other neurotransmitter systems; low 5-HT → greater impulsivity
Negative affect and impulsivity are central to BPD, hence serotonin is interesting
Polymorphism = variation in the nucleotide sequence of the DNA that affects the
regulation of the gene or the functioning of its protein product
Dopamine
Dopamine is a neurotransmitter involved in reward pathways of the brain
Consistent with the hypothesized link between dopamine and BPD are the high rates
of substance abuse disorders in those with BPD
Dopamine is also implicated in psychosis
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