An Equifinality Model of Borderline Personality Disorder
Joseph Santoro, Ph.D., Michael Tisbe, M.D., Michael Katsarakes
Supervised Lifestyles Behavioral Health Systems



Borderline 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 patients.

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 II).

Equifinality is 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.

The purpose 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, and/or trivialized."

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 trauma responses.

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.

The implication 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.

Perry identified five factors which determine a person's specific response to PTS:

  1. history of previous stressors
  2. age at onset of PTS
  3. specific cognitive meaning attached to the event
  4. the specific type of trauma
  5. 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.

Perry's analysis identifies the neurobiological processes that translate environmentally delivered psychotraumatic contingency effects into altered neuro-behavioral function.

Trauma histories in BPO

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

Berzirganian et 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.

Finally, Briere (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.

Neurotransmitter and EEG Findings in BPD

Other studies 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: Biological Vulnerability

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.

Torgerson (1994) 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.

Gasperini et. 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 behaviors.

Muller (1992) 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.

Childhood bipolar 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 exposure.

The Equifinality 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.

Stress hypersensitivity (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 reinforcement control.

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 self-inflicted psychotraumatization.

The childhood 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 psychotraumatization.

The Factor II Pathway

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 syndrome.

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.

Implications for 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).

Attention deficit 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.

Clinical and Research Implications of the Model

Open questions for Factor I BPD:

Does everyone 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?

Open questions 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?

Other research needs suggested by the model include the following:

  1. Studies that can define critical exposure parameters (the type, severity, duration, age at onset) of PTS that lead to enduring behavioral and neurological changes.
  2. 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 PTS-plus-BV-induced.
  3. Studies that assess whether the hippocampus of people with BPD are reduced in volume.
  4. 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.
  5. Primate studies to asses the effects of PTS exposure on their behavioral and neurological development.
  6. Development of definitions and reliable measures of dysfunctional family interaction patterns that produce psychotraumatic events.
  7. In-depth prospective studies of abused and neglected children to evaluate the behavioral, neurological, and learning effects of PTS.
  8. Development of a database register of psychotraumatic events complete with operational definitions, specific examples, relative severity, cultural modifiers, and measurement instruments.
  9. Studies that determine the effects of critical period exposure to PTS versus non-critical period exposure on the progression to BPD.
  10. 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 following:

  1. 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.
  2. 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.
  3. If the role of PTS, as suggested by this model, is confirmed, the diagnostic criteria for borderline personality disorder may require modification.

Summary

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.

References

Berzirganian,, S., Cohen, P., Brook, J. S. (1993) The impact of mother-child interaction on the development of borderline personality disorder. American Journal of Psychiatry. 150 (12) 1836-1842.

Biederman, J. (1997) Is there a childhood form of bi-polar disorder? Harvard Mental Health Letter, 13 (9), 8.

Bower, B. (1995). Child abuse leave mark in the brain. Science News. 147 (1), 395

Briere, J. Psychological Assessment of Adult Posttraumatic States. Washington, D.C.:

American Psychological Association, 1997

De Vegvar, M. L., Siever, L. J., and Trestman, R. L. (1994). Impulsivity and serotonin in borderline personality disorder. In Silk, K. R.(Ed). Biological and Neurobehavioral Studies of Borderline Personality Disorder. Washington, DC: American Psychiatric Press, 1994.

Erikson, E. Childhood and Society New York: Norton and Company, 1950.

Famularo, R., Kinscherff, R., and Fenton, T. (1991). Posttraumatic stress disorder among children clinically diagnosed as borderline personality disorder. Journal of Nervous and Mental Disease, 179(7), 428431.

Gasperini, M, Battaglia, M., Scherillo, P, Sciuto, G, Diaferia, G, Bellodi, L. (1991) Morbidity risk for mood disorders in the families of borderline patients. Journal of Affective Disorders. 21(4), 265-272.

Goldman, S.J., D'Angelo, E. J., DeMaso, D. R., Mezzacappa, E. (1992). Physical and sexual abuse histories among children with borderline personality disorder. American Journal of Psychiatry. 149 (12)1723-1726.

Goldman, S. J., DAngelo, E. J., DeMaso, D. R. (1993). Psychopathology in the families of children and adolescents with borderline personality disorder. American Journal of Psychiatry. 150 (12) 1832-1835.

Herman, J.L., Perry;J. C., van der Kolk, B. A. (1989). Childhood trauma in borderline personality disorder. American Journal of Psychiatry, 146, 490495.

Hollander, F., Stein, D. J., DeCaria, C. M., Cohen, L., Saoud, J. B., Skodol, A. E., Kellman, D., Rosnick, L., Oldham, J.M. (1994). Serotonergic sensitivity in borderline personality disorder preliminary findings. American Journal of Psychiatry. 151(2), 277-280.

Kernberg, 0. Borderline Conditions and Pathological Narcissism. New York: Jason Aronson, 1975.

Korzekwa, M., Links, P., Steiner, M (1993). Biological markers in borderline personality disorder New Perspectives. Canadian Journal of Psychiatry. 38 Supplement (1) 11-15.

Kroll, J. The Challenge of the Borderline Patient New York: Norton and Company,1988

Linehan, M. Cognitive-Behavioral Treatment of Borderline Personality Disorder New York:

Guilford Press, 1993.

Mackintosh, N.J. The Psychology of Animal Learning. New York: Academic Press, 1974.

Miller, F. T., Abrams, T., Dulit, R, and Fyer, M. (1993). Substance abuse in borderline personality disorder. American Journal of Drug and Alcohol Abuse, 19,491497

Miller, J. G. Living Systems. New York: McGraw-Hill, 1978

Muller, R. J. (1992). Is there a neural basis for borderline splitting? Comprehensive Psychiatry. 33(2), 92-104.

Nevin, J. A. The Study of Behavior Illinois: Scott, Foresman and Company, 1973.

Ogiso, Y., Moriya, N., Ikuta, N., Maher-Nishizono, A., Takase, M., Miyake, Y., Minakawa, K. (1993). Relationship between clinical symptoms and EEG findings in borderline personality disorder. Japanese Journal of Psychiatry and Neurology. 47(1), 3746.

Paris, J and Zweig-Frank, H. (1992). A critical review of the role of childhood sexual abuse in the etiology of borderline personality disorder. Canadian Journal of Psychiatry. 37(2), 125-128.

Paris, J., Zweig-Frank, H., Guzder, J. (1994). Risk factors for borderline personality disorder in male outpatients. Journal of Nervous and Mental Disease. 182(7), 375-380.

Perry, B., Pollard, R., Blakley, T., Baker, W., and Vigilante, 0. (1996). Childhood trauma, the neurobiology of adaptation and use-dependent development of the brain: How states become traits. In Press: Infant Mental Health Journal.

Reiger, D., Narrow, W., Rae, D., Manderscheid, R., Locke. B., and Goodwin, F. (1993). The de facto US mental and addictive disorders service system: epidemiologic catchment area prospective 1-year prevalence rates of disorders and services. Archives of General Psychiatry, 50, 85-93.

Runeson, B., Beskow, J. (1991). Borderline personality disorder in young Swedish suicides. Journal of Nervous and Mental Disease. 179(3), 152-156.

Salzman, J. P., Salzman, C., Wolfson, A. N., Albanese, M. Looper, J., Ostacher, M., Schwartz, J., Chinman, G., Land, W., Myawaki, E. (1993). Association between borderline personality structure and history of childhood abuse in adult volunteers. Comprehensive Psychiatry. 34(4), 254-257.

Silk, K. R. Biological and Neurobehavioral Studies of Borderline Personality Disorder Washington, DC: American Psychiatric Press, 1994.

Silk, K.R., Lee, S., Hill, E. M., and Lohr, N. E. (1995). Borderline personality disorder symptoms and severity of sexual abuse. American Journal of Psychiatry, 152(7), 1059-1064.

Silverman, J. M., Pinkham, L., Horvath, T. B., Coccaro, E. F., KIar, H., Schear, S., Apter, S., Davidson, M., Mohs, R. C., Siever, L. J. (1991). Affective and impulsive personality disorder traits in the relatives of patients with borderline personality disorder. American Journal of Psychiatry. 148 (10), 1378-1385.

Stone, J. The Fate of Borderline Patients. New York: Guilford, 1990.

Diagnostic and statistical Manual IV. Washington, DC: American Psychiatric Press, 1994.

Teicher, M. H., Ito, Y., Glad, C. A., Schiffer, F., and Gelbard, H. A. (1994). Early abuse limbic system dysfunction, and borderline personality disorder. In K. R. Silk (Ed). Biological and Neurobehavioral Studies of Borderline Personality Disorder Washington. DC: Amercian Psychiatric Press, 1994.

Torgersen, S. (1994) Genetics in Borderline Conditions. Acta Psychiatrica Scandinavian, supplementum. 379, 19-25.

Towbin, K. E., Dykens, E. M., Pearson, G.S., Cohen, D.J. (1993). Conceptualizing "Borderline Syndrome of Childhood" and "Childhood Schizophrenia" as a developmental disorder. Journal of the American Academy of Child and Adolescent Psychiatry. 32(4), 775-782.

Waller, G. (1924) Childhood sexual abuse and borderline personality disorder in the eating disorders. Child Abuse and Neglect 18 (1), 97-101.

Weaver, T. L., Clum, G. A. (1993). Early family environments and traumatic experiences associated with borderline personality disorder. Journal of Consulting and Clinical Psychology 61 (6) 1068-1075.

Yehuda, R., Southwick, S. M., Perry, B. D., Giller, E. L. Peripheral catecholamine alterations in borderline personality disorder. In K. R. Silk (Ed). Biological and Neurobehavioral Studies of Borderline Personality Disorder Washington, DC: American Psychiatric Press, 1994.

Zanarini, M. C., Kimble, C. R., Williams, A. A. (1994) Neurological dysfunction in borderline patients and Axis II Control Subjects. In K. R. Silk (Ed). Biological and Neurobehavioral Studies of Borderline Personality Disorder Washington, DC: American Psychiatric Press, 1994.

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