The Changing Perspectives on Borderline Personality Disorder

By Garry Cooper, LCSW

 

It seems increasingly likely that when the new DSM is issued, the very conceptualization of borderline personality disorder (BPD) will change. Previously, BPD, as the name implies, has been considered as an intractable part of personality, and therefore predominantly fixed and static. The corollary to this view is that once a person has it, they’ll always have it, and treatment is likely to have minimal effect. Obviously, according to this view, untreated BPD will never go away.

Yet a growing body of research suggests that these views may not be true. The McLean Study of Adult Development, for example, finds that as many as 40 percent of patients with borderline personality disorder remit after 2 years, and after 10 years, 88 percent of the people no longer meet DSM criteria for BPD (Zanarini, 2006). “We have been studying the prospective course of BPD for the past 14 years,” Zanarini writes. “In terms of BPD as a disorder, we have found that remissions are common and recurrences are relatively rare.” Using six-year revalence data, Zanarini, et. al. (2003) found that all 24 symptoms of BPD significantly declined over the period of time. The Collaborative Longitudinal Personality Disorders Study suggests that about one-half of those who meet DSM BPD criteria for several types of BPD at intake no longer meet the criteria two years later (McGlashan, et. al. 2005).

A study of 160 people with BPD, led by Harvard University psychiatrist John Gunderson, sheds some light on how and why this remission occurs. The study was an offshoot of the McLean Study. Researchers had stumbled upon 18 people who, within the first six months of the study, quickly went from meeting at least five DSM criteria for BPD to meeting two or fewer criteria—insufficient for a diagnosis of BPD. They remained that way for at least a year, the length of the study. Gunderson then decided to look more closely at these anomalous cases. How could an intractable, lifelong condition like BPD melt away? The obvious answer is original misdiagnosis, but Gunderson’s team found that only one of the 18 had definitely been misdiagnosed, and that only one other had possibly been misdiagnosed. The study, in the June, 2003 Psychiatry Interpersonal and Biological Processes, finds that leaving stressful relationships, stopping substance abuse, or successfully addressing the symptoms of accompanying mood disorders like depression or anxiety–sometimes with medication and sometimes with old-fashioned therapeutic insight—seemed to cure BPD.

Because they tracked the 18 for only a year, and because BPD is conceptualized as a permanent part of the personality structure, Gunderson talks abut remission rather than cure. His study, and the accompanying commentaries (Allan, 2003; Fritsch, 2003; Waugaman, 2003) caution that a traumatic incident or a return to a stressful condition could trigger the return of BPD. But that still suggests that BPD may be less a personality structure than a way of responding to highly stressful events. And if that’s the case, it calls into question whether borderline personality disorders should even have their own axis in the DSM. The original justification and thinking about personality disorders is that the condition isn’t a reaction but an immutable part of personality structure, and that personality disorders are completely different in their origins and prognosis and possibly require different treatments than mood disorders do.

The commentaries in the journal say that Gunderson’s study suggests that the DSM distinctions between Axis I mood disorders and Axis II personality disorders are more artificial than usually supposed. This new perspective allows therapists to rethink treatment strategies and goals for some clients with BPD. Instead of a long-term strategy that trains clients to moderate such ingrained traits as idealizing or demonizing others, therapists might focus on addressing symptoms and changing current stressful situations in their client’s lives.

Of course, only 10 percent of the original, larger study sample were able to successfully leave their BPD behind. One commentary hypothesizes that Gunderson’s 10 percent were a subset whose BPD hadn’t developed out of the usual profound trauma or abuse. Gunderson and the accompanying commentaries call for more studies of this surprising phenomenon of vanishing BPD. Interventions that were “neither heroic nor extended,” he says, seemed to have a significant effect on lifting the burden of BPD.

The thinking that BPD is not any one thing is growing more prevalent among researchers like Gunderson who have been doing longitudinal research of people with BPD. It’s similar to the view of depression which has evolved: there is no one cause—despite the multimillion dollar pharmaceutical marketing blitz that’s tried to pin it on one or two neurotransmitters—and no one best treatment, and the diagnosis of BPD is coming more and more to seem like the family doctor’s diagnosis of virus—too general to be of much value, and more of a gateway to trying different kinds of treatments to see what works. Which antibiotic is most effective? In treating the virus, it’s also important to treat the damage caused by the virus.

Skodol. et. al (2002) point out several hypotheses to explain the high incidence of comorbidity between BPD and Axis I disorders. Some Axis I disorders may be primary and lead to the development of BPD traits and behaviors. (For example, depressed, anxious or traumatized children may suffer rejection or abuse by other people, which triggers the kinds of reactions and primitive defenses characteristic of BPD). BPD may be primary and lead to the development of Axis I traits and behaviors. (Someone with BPD, for example, is likely to experience repeated relationship failures, which can lead to depression, anxiety or other mood disorders). BPD and Axis I disorders may be unrelated, but because both are common among certain populations, they may influence the development of each other. Or they may share some common causes. The hypotheses are not mutually exclusive. Researchers are still trying to sort out the treatment implications of various combinations of comorbidities, but there’s widespread agreement on this: a thorough assessment of both BPD and co-morbid Axis I disorders is important. Merely labeling someone as BPD will compromise treatment.

Reinforcing the viewpoint of the Psychodynamic Diagnostic Manual (see Article #2) Skodol, et. al. point out an additional problem in the way the DSM, with its clear-cut symptom checklists, diagnoses BPD. There is no clear cut-off point between whether someone has or doesn’t have it. Instead, it makes more sense to think of BPD as existing on a continuum. Once you begin to conceptualize BPD on a continuum rather than as a discrete entity, it becomes possible, even necessary, to rethink its causes, course and treatment. Zanarini (2006) says, “We have come to the conclusion that the DSM system with its polythetic nature and short list of criteria may not represent the patients we have been studying for the last 20 years. It leaves out important areas of borderline psychopathology, such as intense subjective emotional pain (Zanarini, Frankenburg, DeLuca, Hennen, Khera, & Gunderson, 1998; Zittel Conklin & Westen, 2005) and allows patients who specialize in only a few sectors of psychopathology to receive the borderline diagnosis.” That polythetic classification of the DSM—the symptom checklists, which, people like Westen and Shedler (2004) have argued, create a “Chinese menu list” that artificially separates types of personality disorders and creates a kind of taxonomy that has little relation to clinical reality—has, by arbitrarily distinguishing between types of personality disorders, actually obscured real-world diagnosis. Clarkin et al (1983) found 93 different ways a client could meet the DSM-III (and DSM-III-R) polythetic diagnostic criteria for BPD (i.e., any combination of 5 of 8, 6 of 8, 7 of 8, or 8 of 8 diagnostic criteria). “DSM-IV, points out Zanarini, “added an additional diagnostic criterion without changing the threshold for the diagnosis, contributing to even further heterogeneity. There are now 151 different ways of meeting the DSM-IV criteria for BPD.” Small wonder that with such a cumbersome system, rooted more in artificial taxonomy than real-world clinical practice, BPD doesn’t always follow the predicted course.

Zanarini and associates have developed a complex model of BPD which casts a more realistic light on the etiology of BPD and may lead to a better conceptualization of treatment. In this model, people with BPD are born with a vulnerability or “hyperbolic temperament.” After some type of “kindling” event or experience, she writes, “BPD symptoms develop. Some of these symptoms are acute in nature and others are temperamental in nature. Acute symptoms, which are akin to the positive symptoms of schizophrenia, resolve relatively quickly, are the best markers for the disorder (Zanarini, Gunderson, Frankenburg, & Chauncey, 1990), and are often the immediate reason for needing costly forms of treatment, such as psychiatric hospitalizations.” The temperamental symptoms, on the other hand, take longer to resolve, may not be specific to the BPD but perhaps more related to Axis I disorders, and related to ongoing psychosocial impairment. Zanarini finds that half of the 24 BPD symptoms are acute and half temperamental in nature. A spread like this may explain why some symptoms remit, even without treatment, while others don’t, and it may go a long way to explain the “mysterious” vanishing BPD that Gunderson and others have found.

Which symptoms resolved more quickly? Zanarini identifies them as the symptoms indicative of core areas of impulsivity such as suicidal attempts and self-mutilation, and “active attempts to manage interpersonal difficulties (e.g., problems with demandingness/entitlement, serious treatment regressions.” On the other hand, she writes, symptoms reflecting areas of chronic dysphoria (e.g., anger, loneliness/emptiness) and interpersonal symptoms reflecting abandonment and dependency issues (e.g., intolerance of aloneness, counterdependency problems)” seemed more entrenched and long-lasting.

Zanarini suggests several changes in how the DSM should describe BPD. The next edition should include (as the Psychodynamic Diagnostic Manual does) subjective measures, such as the client’s level of emotional pain. Interestingly, Shedler and Westen (2004), after years of polling clinicians, find that therapists routinely give such measures more weight when diagnosing BPD than they do to the DSM checklists. Zanarini also recommends that the DSM, in order to make a valid diagnosis of BPD, requires the presence of symptoms from all four clusters of symptomology that her research finds is present in BPD: affect, cognition, impulsivity, and interpersonal relationships. Third, the DSM should recognize that different symptoms take different courses. This will encourage therapists to see BPD not as an ingrained and intractable kind of personality but as a complex disorder that is indeed amenable to therapy. “One could argue that if only the acute symptoms of BPD…define the disorder or at least that some of these symptoms were required to be diagnosed with BPD, it would be recognized that BPD is a relatively slow to resolve disorder and not a chronic one. Improvement and even resolution of symptoms would be expected for most patients. Alternatively, one could argue that if only or mostly temperamental symptoms came to define BPD, one would needlessly discourage patients, their families, and the mental health professionals treating them. In addition, focusing on these more stable symptoms would perhaps be to unnecessarily pathologize those with certain inborn temperamental traits that are not in themselves indicative of being psychiatrically ill or more accurately, suffering from BPD.”

 
References

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Clarkin JF, Widiger TA, Frances AJ, Hurt SW, Gilmore M (1983): Prototypic typology and the borderline personality disorder. Journal of Abnormal Psychology, 92:263-275.

Fritsch, RC and Ingraham, LJ (2003). “Remission of Personality or Remission of Symptoms?” Psychiatry Interpersonal and Biological Processes, 66 (2), 124-128

Gunderson, JG, Bender, D, Sanislow, C, Yen, S, Bame Rettew, J, Dolan-Sewell, R, Dyck, I, Morey, LC, McGlashan, TH, Shea, MT, and Skodol, AE (2003). “Plausibility and possible determinants of sudden ‘remissions’ in borderline patients,” Psychiatry Interpersonal and Biological Processes, 66 (2), 111-119

McGlashan TH, Grilo CM, Sanislow, CA, Ralevski E, Morey LC, Gunderson JG, Skodol AE, Shea MT, Zanarini MC, Bender DS, Stout RL, Yen S, Pagano ME (2005). Two-year prevalence and stability of individual criteria for schizotypal, borderline, avoidant, and obsessive-compulsive personality disorders, American Journal of Psychiatry, 162(5):883-889, 2005

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Skodol, AE, Gunderson, JG, Pfohl, B,Widiger, TA, Livesley, WJ, Siever, LJ (2002), The borderline diagnosis I: psychopathology, comorbidity, and personality structure, Biological Psychiatry, 51 (12), 936-950

Skodol, AE. Siever, LJ, Livesley, WJ, Gunderson, JG, Pfohl, B, Widiger, TA (2002). The borderline diagnosis II: biology, genetics and clinical course, Biological Psychiatry, 51 (12), 951-963.

Waugaman, RM and Goldstein. WN (2003) “The Pivotal Role of Interpersonal Relationships in the Outcome of Borderline Patients,” Psychiatry Interpersonal and Biological Processes, 66 (2), 129-131

Zanarini, M. C., Frankenburg, F. R., Hennen, J., Reich, D. B., & Silk, K. R. (2006). Prediction of the 10-year course of borderline personality disorder. American Journal of Psychiatry, 163, 827-832.

Zanarini, MC (2006). “The longitudinal course of the borderline phenotype,” presentation to the Borderline Personality Research Foundation.

Zanarini, M. C., Frankenburg, F. R., Hennen, J., & Silk, K. R. (2003). The longitudinal course of borderline psychopathology: 6-year prospective follow-up of the phenomenology of borderline personality disorder. American Journal of Psychiatry, 160, 274-283.

Zanarini, M. C., Frankenburg, F. R., DeLuca, C. J., Hennen, J., Khera, G. S., & Gunderson, J. G. (1998). The pain of being borderline: Dysphoric states specific to borderline personality disorder. Harvard Review of Psychiatry, 6, 201-207.

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Zittel Conklin C., Westen, D. (2005). Borderline personality disorder in clinical practice. American Journal of Psychiatry, 162, 867-75.

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