personality disorder (BPD) affects as many as
six million Americans. It accounts for about 25%
of all psychiatric hospitalizations. As many as
thirteen percent of males and seven percent of
females commit suicide (Stone, 1990). Approximately,
69% of people with BPD are also substance abusers
(Miller et al., 1993). The causes of BPD are not
well understood. Therapist folklore often labels
people with BPD as difficult and treatment-resistant
This article outlines
a clinical model of BPD. The model is based upon
the clinical practice of the authors and the research
literature concerning the correlates of BPD. The
model identifies the roles played by traumatic
environmental conditioning, its effect on neurobiological
processes, and biological vulnerabilities in the
development of BPD. In this regard, the model
postulates two factors which can lead, singly
or in combination with equifinality, to BPD: early
childhood Psychotraumatic Stress (PTS) exposure
(Factor I) and Biologic Vulnerability (BV) (Factor
a systems theory concept (Miller, 1978) which
means "that a final state of any living system
[borderline personality disorder] may be reached
from different initial conditions [Factor I, Factor
II or both] and in different ways [antecedent
or consequent biological and family system dysfunction]."
The bracketed illustrations were added by us.
of this model is to serve as a heuristic
guide to clinical intervention, treatment, and
research as well as to stimulate creative thinking
about borderline personality disorders.
We first review
the evidence that supports Factor I initiation
of BPD followed by a review of Factor II evidence.
These two sections are followed by a description
of the Equifinality Model of BPD. The article
closes with a brief discussion of research questions
generated by the model and clinical implications
of the model.
FACTOR I SPD:
Psychotraumatic Stress (PTS) Exposure in Childhood
A number of authors
have suggested a role for environmentally mediated
aversive events in the development of BPD. Kroll
(1988) suggested that BPD symptoms rather than
being psychotic come closer in appearance to those
of post-traumatic stress disorder. He wrote, "I
am suggesting that many borderline symptoms, especially
the ones that have the appearances of ‘brief psychotic
episodes’ and which I have included under the
heading of cognitive disturbances, are no different
from the symptoms seen in post-traumatic stress
disorder." Kernberg (1975) observed that
"A frequent finding in patients with borderline
personality organization is the history of extreme
frustrations and intense aggression (secondary
or primary) during the first few years of life."
Linehan (1993) postulated that in addition to
being biologically vulnerable people with BPD
are exposed to invalidating environments "in
which communication of private experiences is
met by erratic, inappropriate. and extreme responses
In other words, the expression of private experiences
is not validated; instead, it is often punished,
Perry et. al's
Neurobiological Analysis of Early Trauma
Perry et al. (1996)
have presented a neurobiological analysis of childhood
trauma exposure. In it they outline the effect
trauma has on the human "fight or flight"
and "freeze or surrender" systems, and
the implications that repeated psychotraumatization
has for a developing child's brain systems. Perry
et. al describes the effects psychotrauma can
have on a child's brain as follows:
- The brain regions involved
in the threat-induced hyper-arousal response
play a critical role in regulating arousal,
vigilance, affect, behavioral irritability,
locomotion, attention, the response to stress,
sleep, and the startle response . . . Initially
following the acute fear response, these systems
in the brain will be reactivated when the
child is exposed to a specific reminder of
the traumatic event (e.g., gunshots, the presence
of a past perpetrator). Furthermore, these
parts of the brain my be reactivated when
the child simply thinks about or dreams about
the event. Over time, these specific reminders
may generalize (e.g., gunshots to loud noises,
a specific perpetrator to any strange male).
In other words, despite being distanced from
threat and the original trauma, the stress-response
apparatus of the child's brain is activated
again and again.
The pattern described
above reflects both stimulus and response generalization
processes which have been exhaustively studied
by behavioral researchers for some time (Mackintosh,
1974; Nevin, 1973). This body of research has
established that a primary generalization effect
is an increasing function of the number of shared
elements between the original stimulus and the
test stimulus (Nevin, 1973). This research provides
support for Perry et al.'s analysis of childhood
trauma by identifying the empirically validated
operant and respondent processes that are responsible
for conditioning all types of behavior including
Perry goes on
to explain that the neurobiological effect of
traumatic experiences delivered by environmental
contingencies is governed by two principles of
neurodevelopment: the use-dependent development/organization
of the brain and critical and sensitive periods.
They point out that during the early childhood
years the brain requires (critical periods) or
is more sensitive (sensitive periods) to certain
types of organizing experiences. These experiences
literally format some of the child's developing
brain structures and functions: "Experience
can change the mature brain-but experience during
the critical periods of early childhood organizes
brain systems . . . [it] can result in mal-organization
and compromised function in brain mediated functions
such as humor, empathy, attachment and affect
regulation." Trauma, occurring during critical/sensitive
periods, is an experience that is capable of affecting
the organizational development of the brain.
for the traumatized child is that the more frequent,
intense and persistent the traumatization, the
more the brain systems associated with fear are
activated. Such-frequent activation "builds
in" a chronic state of fear in the child.
This state of fear can trigger hyperarousal (fight
or flight) and/or dissociative (freeze or surrender)
behavior in the child With repeated exposure,
elicitation, and generalization this behavior
pattern takes on "trait" characteristics.
five factors which determine a person's specific
response to PTS:
- history of previous stressors
- age at onset of PTS
- specific cognitive meaning
attached to the event
- the specific type of trauma
- presence of exacerbating
and/or mitigating factors
To this list we
would add (6) intensity of the PTS and (7) the
duration of the PTS exposure.
identifies the neurobiological processes that
translate environmentally delivered psychotraumatic
contingency effects into altered neuro-behavioral
A number of researchers
have found an association between the diagnosis
of BPD and psychotraumatization during childhood.
Herman et al. (1989) found the following rates
of psychotraumatization for BPD patients: 71%
had been physically abused, 67% sexually abused,
and 62% had witnessed domestic violence. Histories
of early childhood psychotrauma (under age six)
were almost always only found in BPD patients
versus other personality disorder patients. Famularo
et. al. (1991) reported that 79% of nineteen children
ages seven to fourteen who had been recently diagnosed
as having BPD by DSM III-R criteria reported significant
traumatic experiences. Goldman et al. (1992) found
in a sample of 44 children diagnosed with BPD
versus 100 comparison children that BPD children
had significantly higher rates of physical and
physical/sexual abuse rates than the comparison
group. They concluded that the hypothesis that
a history of trauma is associated with the disorder
is supported. Goldman et al. (1993) found higher
rates of psychopathology among family members
of people with BPD. Weaver et al. (1993) found
that rate of childhood trauma (sexual abuse, physical
abuse, witnessing violence) was significantly
higher in 17 BPD females versus 19 non-BPD females.
Salzman et al. (1993), however, found lower than
expected rates of physical, sexual, or combined
trauma in a sample of 31 patients. They found
that only 19% reported such a history.
Stone (1990) in
his landmark outcomes study of BPD found that
the factor (in a factor analysis of 14 outcome
moderating factors) which accounted for the largest
amount of variance in outcomes for his combined
sample of male and female BPD patients was what
he termed parental brutality (physical abuse).
This factor accounted for 7% of the variance with
six additional factors accounting for an additional
5% of the variance. For females this factor accounted
for 6% of the variance and for males it accounted
for 15% of the variance. He also found the following
percentages of psychotraumatization in his sample
(broad definition of borderline): 38% had early
loss; 19% of females had parental incest; 8% of
males had parental incest; 13% of all borderlines
had experienced or witnessed parental brutality.
In a study of
61 male subjects with BPD versus 60 non-BPD subjects,
Paris et al. (1994) found that the BPD group had
significantly higher rate of childhood sexual
abuse, more severe sexual abuse, a longer duration
of physical abuse, increased rates of early separation
or loss, and higher paternal control score on
the Parental Bonding Index. Childhood sexual abuse
and loss/separation were significant in the muitivariate
analysis. They concluded that trauma and problems
with fathers are important factors in the development
of BPD in males. Waller (1994) found that childhood
sexual abuse prior to age fourteen rather than
later in life was associated with a diagnosis
of BPD in 115 eating-disordered females. Silk
et al. (1995) reported a 76% rate of sexual abuse
in a sample of 37 BPD inpatients
Runeson et al.
(1991) reported that BPD patients who committed
suicide showed more early parental absence, substance
abuse in the home, and lack of permanent residence
than other patient groups who committed suicide
in a sample of 58 consecutive suicides of people
ages 15 to 29 in an urban community
al. (1993) found in a prospective study of 776
adolescents that maternal inconsistency coupled
with maternal over-involvement predicted the emergence
of BPD. Weaver and Clum (1993) reported that significantly
more BPD patients reported sexual abuse than did
non-BPD patients in a sample of 17 and 19 patients
respectively. They also found that BPD families
were significantly more controlling than were
non-BPD families and that this factor significantly
predicted dimensional borderline score even after
controlling for sexual abuse.
(1997) reported that the Trauma Symptom Inventory,
a 100-item test designed to measure both acute
and chronic PTSD symptoms, correctly identified,
in a psychiatric inpatient sample. 89% of those
patients independently diagnosed with BPD.
and EEG Findings in BPD
have reported neurological and neurotransmitter
differences in people with BPD and people with
psychotraumatic exposures. Bower (1995) reported
that researchers found in MRI scans of 20 females
with histories of prolonged sexual abuse before
age 15 that, in comparison to 18 non-abused woman,
the abused woman had markedly smaller hippocampal
volume (the hippocampus is implicated in short
term memory). A second study by Yale researchers
confirmed this result in seventeen women who suffered
severe childhood sexual abuse. Yale researchers
also found that these abused woman scored significantly
lower on a test of verbal short-term memory. Bower
reports that similar MRI results (decreased hippocampal
volume) have been obtained with male Vietnam veterans
suffering from PTSD.
Hollander et al.
(1994) reported results which suggest that males
with BPD have serotonergic dysfunction as compared
to non-BPD males based upon a challenge with a
single dose of m-chlorophenylpiperazine (5-HT
serotonin postsynaptic agonist). De Vegvar et
al. (1994) summarized a series of studies linking
serotonin functioning and impulsive aggression.
In general the findings support a hypothesis linking
serotonergic dysfunction to impulsive aggression
toward others or self. Yehuda et al. (1994) reported
a series of studies on peripheral catecholamine
(epinephrine, norepinephrine, and dopamine) functioning.
They concluded, "The fact that catecholamine
metabolism in BPD is similar to that in PTSD in
preliminary studies may reflect the role that
chronic stress and trauma appear to play in the
etiology of many symptoms found in these disorders."
Perry et al.'s (1996) analysis implicates the
catecholamine system as one of the systems effected
by traumatic exposure
In a very interesting
study, Teicher et al. (1994) argued that the limbic
system, in particular the hippocampus and amygdala,
may be affected by experiences which create posttraumatic
stress disorder. They reported on the results
of a study which compared a history of early abuse
to symptoms of limbic system dysfunction. They
devised a 33 item Limbic System Checklist (LSC-33)
questionnaire to assess this latter effect. They
evaluated 253 outpatients with the Life Experiences
Questionnaire to assess abuse history. Their results
showed that as compared to patients who reported
no history of abuse, patients with physical but
not sexual abuse scored 38% higher on the LSC-33;
patients who were sexually but not physically
abused scored 49% higher, and patients who were
both sexually and physically abused scored 113%
higher. The effect was the same regardless of
sex. All differences between the abused patients
and non-abused patients were significant. Abuse
prior to age 18 had greater impact than abuse
after age 18. Patients who were physically or
sexually abused after the age of 18 had LSC-33
scores that were not significantly different from
those of the non-abused patients. They concluded,
"Our specific hypothesis is that early abuse
can lead to a variety of neurodevelopmentai abnormalities
with different behavioral sequelae."
Based on the findings
reviewed above and our clinical experience we
offer the following Factor I BPD postulate:
Factor I BPD
reflects the neuro-behavioral effects of psychotraumatic
stress (PTS) exposures mediated by dysfunctional
family interactions (DFI). The PTS exposures occur
prior to the age of 18 and have the following
characteristics: (1) they are of sufficient aversive
intensity, duration, and frequency to provoke
fear (2) they occur during critical or sensitive
developmental periods, and (3) they are psychologically
salient, personal and meaningful. Consequent to
these exposures, the child experiences neurological,
cognitive, and behavioral dysfunctions which,
if unmitigated or untreated (or inadequately
treated), progress to borderline personality disorder
The presence of a pre-existing biological
vulnerability is not required for the occurrence
of these effects.
FACTOR II BPD:
The other factor
which may initiate the development of BPD
is a pre-existing biological vulnerability (BV).
To qualify, a BV must biographically pre-date
the occurrence of any psychotraumatic stress and
may be expected to affect limbic system functioning
and/or attention control. A BV that is caused
by the effect psychotraumatic stress has on the
developing brain would not qualify in our model
as an independent biological cause of BPD. Potential
independent BV's might include a genetic defect,
an intrauterine neuro-toxin, or another psychiatric
disorder of early childhood.
reviewed published and unpublished studies of
the genetic transmission of BPO. Torgerson
concluded that there is little current evidence
to support a genetic transmission model of BPD.
at. (1991) concluded that a diagnosis of BPD predicts
a higher rate of mood disorders in family members
of people with BPD even in the absence of a mood
disorder in the BPD person. Silverman et al. (1991)
found greater independent risk of affective and
impulsive personality disorder traits in 129 relatives
of people with BPD than in people with other personality
disorders or with schizophrenia. Korzekwa et al.
(1993) concluded that dexamethasone suppression
test, thyrotropin-releasing hormone test, and
sleep studies indicate that BPD is not related
to depression but that serotonin studies point
to links with suicidal, aggressive and impulsive
suggested that a disruption of interhemispheric
communication within the brain from 18 to 36
months of age may create a neural template for
the borderline symptom of splitting. Towbin et
al. (1993) defined a complex developmental syndrome
which they hypothesize may be involved in the
development of BPD and childhood schizophrenia.
The criteria of this syndrome include disturbance
of affect modulation, social relatedness, and
thinking. Ogiso et al. (1993) compared EEG findings
of 19 females diagnosed with BPD to 21 females
without a BPD diagnosis. They failed to find EEG
results that were characteristic of the BPD group.
However, they did find that patients who scored
high on the Impulsive Action Pattern of the DIB
(Diagnostic Interview for Borderlines) did show
EEG abnormalities. This effect cut across the
two groups and was not solely characteristic of
the BPD group. Zanarini et al. (1994) found that
EEG abnormalities, while nonspecific to people
with BPD, did affect 46% of the BPD subjects in
the sample. They reported that these findings
were not correlated with a childhood history of
abuse. However, 40% of their BPD subjects had
a confounding history of head trauma (62%
of subjects who were physically abused also reported
head trauma) and 12% had a confirmed history of
grand mal seizures.
In our clinical
practice we have seen a high rate of comorbid
ADHD in males with BPD. In a sample of 26 males
diagnosed as having BPD according to DSM-IIIR
or DSM-IV criteria and treated by us from 1994
to 1996, 54% of them had a childhood diagnosis
of ADHD in their records. Many ADHD symptoms such
as impulsivity, affective lability, and anger
outbursts are similar to BPD symptoms.
disorder (Biederman, 1997) is an under
recognized disorder whose symptoms include unstable
moods, distractibility, impulsiveness, severe
aggressiveness, and hyperactivity. Unlike adult
bipolar disorder, childhood bipolar disorder symptoms
are chronic and continuous, This disorder is also
correlated with ADHD. The two disorders may be
genetically linked. All of its symptoms, especially
impulsiveness and aggression, overlap with those
of BPD. It is possible that untreated or ineffectively
treated childhood bipolar disorder and/or ADHD
could predispose the child to later develop BPD.
Based on the results
reported above our Factor II BPD postulate states:
Factor II BPD
is a set of biological vulnerabilities (BV) which
either alone or in combination can cause early
childhood neurobehavioral dysfunction. This results
in hyperreactivity to stressors which conditions
affective instability, impulsive actions,
aggressive tantrums, and impaired interpersonal
relationships. If unmitigated and untreated, the
S V induced neuro-behavioral dysfunctions progress
to BPD. This result does not require the prior
occurrence of DFI mediated psychotraumatic
Model of Borderline Behavior
The diagram on
page ten models the flow of events hypothesized
to initiate and condition borderline behavior.
The two factors are depicted along with their
influence pathways. The model's equifinality assumption
states that either factor can produce BPD despite
starting at different points and following different
paths to that end. The model has organized borderline
symptoms into five groups: relationship control
phobia (DSM-IV BPD criteria 1 and 2 are included
here), self-image dysfunction (criteria 3 and
7), stress hypersensitivity (criteria 6, 5, 9),
dependency on immediate gratification (criteria
4 and 5), and lifestyle mismanagement.
The Factor I Pathway
The Factor I pathway
maps the effects of multiple stress/alarm reactions
elicited by DFI mediated psychotraumatic stress
exposures. The model defines DFI (dysfunctional
family interaction) as the exchange of aversive
communication behaviors and consequences (often
unpredictable) among members of a family at a
rate that is in excess of norms for that family's
society and culture. PTS is defined
as an aversive event which triggers a fear response
capable of causing a person to become concerned
about his or her psychological or physical safety
while effectively inhibiting the person's ability
to protect him or herself by terminating or escaping
the aversive event.
As PTS exposure
is repeated and generalized, neurobiological changes
(as specified in Perry's 1996 analysis) begin
to take place. According to some of the findings
reviewed earlier, changes in catelcolamine functioning
and serotonin functioning may occur. At the same
time a relationship control phobia develops in
response to the PTS emitted by members of the
child's family. Basic trust, thought to form within
the first years of life (Erikson, 1950), is compromised.
As relationships, through generalization (the
generalization dimensions appear to be intimacy
and authority), become viewed as threatening,
the child also develops a negative image of him
or herself. Chronic aversive treatment, especially
at the hands of loved ones, condition a negative
self-image that leaves the child feeling that
he or she is "bad." The core self-image
of "badness" progresses to one of self-hatred.
These core beliefs condition the development of
other distorted cognitive beliefs and errors in
thinking (e.g., black and white thinking).
The emergent neurobiological
dysfunction further sensitizes the child to similar,
stressful experiences (stress hypersensitivity)
which trigger hyperarousal and/or dissociative
behavior. Withdrawal, aggressiveness, and mood
instability are postulated to be a product of
this sensitization process.
(and dysfunctional neurotransmitter mediation),
relationship problems, and a negative self-image
combine to create dysphoric and labile emotional
states which arrange negative reinforcement contingencies
that shape and reinforce a variety of impulsive
gratification (or escape) seeking behaviors. Addictive
activities (such as drug and alcohol abuse, eating
problems, or self-injury) develop that reduce
the dysphoric states and negatively reinforce
their continuing--and often escalating--use. Suicidal
behaviors emerge as an albeit extreme form of
negatively reinforced escape behavior. The repetitive
and manipulative nature of BPD suicidal actions
take on an addictive quality because of this negative
As the child grows
through adolescence into adulthood, lifestyle
functioning is impaired in work, relationships,
play, and education. Lifestyle failures further
intensify the person's self-hatred and add to
his or her dysphoria, which motivates further
escape and avoidance behaviors of the impulsive
and addictive type. This process creates the hallmarks
of borderline living: self-inflicted crisis and
and later-life effects of PTS can be mitigated
by several factors: strong, positive social support,
personal skills and attractiveness (Stone 1990),
low levels of ambient psychosocial stress, and
reinforcement contingencies (structure) for healthy
behavior. For example, if a child is exposed to
PTS by one caregiver but another is able to maintain
a warm and loving relationship with the child,
the effect of the PTS will be reduced. A borderline
adult living in a very supportive setting will
function better than one living without any close
support or structure.
The Factor I pathway
of the model postulates that any child exposed
to sufficient and critically timed PTS will develop
chronically dysfunctional behavior patterns and
will, in the absence of timely and sufficient
treatment and/or mitigation, develop borderline
behavior patterns and/or BPD. A second postulate
states that the stress hypersensitivity a person
experiences will be under discrete stimulus control
defined by the stimulus parameters of their early
The Factor II
The Factor II
pathway to BPD involves the presence of a BV that
at the neurobiological level impairs the child's
ability to develop age appropriate behavioral
self-control in the areas of impulse control,
mood stability, and aggression modulation. At
present there does not appear to be a consensus
BV candidate, The possibilities we reviewed included
untreated attention deficit disorder, untreated
childhood bipolar disorder, EEG abnormalities,
genetic transmission, familial affective/impulse
control dysfunction, or a complex developmental
The BV is hypothesized
to work by impairing the child's neurobiological
functioning by presumably disrupting limbic system
development and/or functioning. This then predisposes
the child to becoming hypersensitive to his environment
and its stressors. The child's moody, impulsive,
aggressive. irritable, distractible, oppositional,
and/or withdrawn behaviors initiate the model's
stress hypersensitivity pathway. The model postulates
that this behavior becomes aversive to the caregivers
and other members of the child's family and creates
dysfunctional interaction patterns within a previously
functional family. In the absence of timely and
sufficient mitigating or treatment factors, the
DFI worsens the child's behavior and creates significant
distress for caregivers and other family members.
The child's self-image is impaired by the conflict
their behavior causes at home and/or in school.
Impulsive gratification emerges for the same reasons
as it does in Factor I BPD.
The model postulates
DFI as a consequence of BV in Factor II BPD. It
also postulates the existence of a historical
period, framed by a functional family environment,
during which the child's behavior was observably
and significantly dysfunctional.
Mixed Factor BPD
In mixed factor
BPD both BV and PTS are independently present.
The model postulates that for a given degree of
PTS a more severe form of BPD develops when BV
is also present. We speculate that Factor I type
of BPD is the most common form, followed by mixed
type BPD, and then Factor II BPD. Based on the
childhood trauma prevalence studies reviewed earlier,
about 70 to 75% of BPD is either Factor I or Mixed
type BPD and about 25 to 30% is Factor II BPD.
Making a Diagnosis of BPD
As discussed earlier
the symptomatic behavior of BPD overlaps with
other disorders. In particular it is important
to rule out adult bipolar disorder. In addition
to bipolar disorder, attention deficit disorder
and atypical depression should also be assessed.
A rule of thumb that we have found helpful given
the apparently high incidence of psychotraumatic
childhood events in the histories of people with
BPD is to tentatively assume that, in the absence
of a credible history of childhood psychotrauma,
the patient is not borderline and then to assess
him or her for the above-mentioned disorders.
When bipolar disorder has been ruled out, and
if ADHD and atypical depression cannot completely
account for the presenting symptoms, then a diagnosis
of BPD can be applied.
A bipolar disorder
differential should consider the following: (1)
A history of bipolar disorder in the family; (2)
It may begin in childhood as major depression;
(3) In early adolescence look for irritability,
explosive anger, sustained hating, hostility and
hypersexuality; and (4) BPD patient usually does
not have family history of bipolar disorder; decreased
need for sleep is not seen in BPD; flight of ideas
is not seen, borderline does not follow the four
phases of bipolar disorder (depressed, manic-irritability,
mixed depression and mania; hypomania).
hyperactivity disorder (ADHD) can be distinguished
from BPD by taking a careful developmental history.
Of particular interest is early hyperactivity
especially at birth and even prenatally. Such
infants are often hard to satisfy despite consistent
effort to do so. Such children often have difficulty
playing with other children and making friends.
Often they will change the rules so they can win.
In school they cannot achieve because they cannot
sit and attend. They may have poor fine motor
coordination. They can be very bright and hyper-curious
but often have poor immediate recall. In BPD symptoms
become apparent in late teen years, not at birth.
BPD relationships are unstable. BPD has poor self-image
due to rejection, but ADHD has poor self-image
due to failure to achieve. BPD people hate themselves;
this is not the case in uncomplicated ADHD. In
BPD neurological soft signs are not necessarily
present but are often seen in ADHD.
Research Implications of the Model
for Factor I BPD:
exposed1 during critical sensitive periods, to
a certain intensity, duration and repetition of
psychotrauma develop BPD? If not, then do they
develop some borderline behaviors? If not, then
what inoculates them from doing so? Could the
inoculation come from a biological advantage of
some kind? Would early intervention and treatment
of DFI prevent the development of BPD?
for Factor II BPD:
What is the biological
vulnerability? Is it a single condition or many
conditions? If it is ADHD or child bipolar, then
does it progress to BPD because of a failure to
effectively treat these disorders? Does the BV
progress to BPD in the absence of DFI or is DFI
crucial to the development of BV initiated BPD?
If it is crucial, must DFI be effectively treated
to prevent progression to BPD?
needs suggested by the model include the following:
- Studies that can define critical
exposure parameters (the type, severity, duration,
age at onset) of PTS that lead to enduring
behavioral and neurological changes.
- A comprehensive assessment
protocol needs to be developed and studies
conducted of people with BPD to confirm or
disconfirm the model's classification of BPD
into PTS-only induced, BV-only induced, and
- Studies that assess whether
the hippocampus of people with BPD are reduced
- Studies which measure neurotransmitter
(serotonin and NE) levels of people with BPD
prior to and after imaginary and role play
exposure to their childhood PTS events to
determine whether neurotransmitter levels
are response to simulated exposure.
- Primate studies to asses
the effects of PTS exposure on their behavioral
and neurological development.
- Development of definitions
and reliable measures of dysfunctional family
interaction patterns that produce psychotraumatic
- In-depth prospective studies
of abused and neglected children to evaluate
the behavioral, neurological, and learning
effects of PTS.
- Development of a database
register of psychotraumatic events complete
with operational definitions, specific examples,
relative severity, cultural modifiers, and
- Studies that determine the
effects of critical period exposure to PTS
versus non-critical period exposure on the
progression to BPD.
- DFI is a potential common
link between the two types of BPD: in Factor
I it is the antecedent of psychotrauma and
in Factor II it is a familial behavioral consequence
of biological vulnerability. Studies to confirm
this are needed.
The model's implications
for the clinical treatment of BPD include the
- Reliable and valid clinical
measures of psychotraumatic events and the
symptomatic impact of those events are needed.
There are many psychometric instruments for
the measurement of trauma symptoms and events
(Briere 1997). A consensus diagnostic battery
that meets the needs of clinical settings
is needed to measure the PTS exposure of patients.
- Treatment of BPD depends
upon the accurate assessment of PTS exposure.
The presence of significant PTS history has
major implications for the treatment protocol
in theses areas:
- trust issues, need for
desensitization/exposure therapy of PTS
effects, PTS motivators of
- addictive activities,
the use of medications, and the role of
the family in treatment.
- If the role of PTS, as suggested
by this model, is confirmed, the diagnostic
criteria for borderline personality disorder
may require modification.
The paper presented
a heuristic model of the etiology of borderline
personality disorder. Borrowing the concept of
equifinality from systems theory, it postulated
that BPD can develop if one of two factors is
present during childhood. The data upon which
the model is based were reviewed and the research
and clinical implications of the model were discussed.
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