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![]() The first paper ever published about BPD (1) described a group of patients with unusual resistance to standard forms of treatment. Although psychoanalysis was the standard therapy at the time, BPD patients still retain a reputation for being problematic. This perception is not imaginary: it is supported by the disorder’s chronicity as well as by inconsistent response to many forms of therapy that are effective for other disorders (2). Given these problems, clinicians are sometimes quite reluctant to make the diagnosis (3), focusing on comorbid Axis I conditions (particularly major depression) thought to be more readily treatable. However, when any Axis II disorder is present, the treatment of coexisting depression is much less likely to be successful (4). Avoiding the diagnosis of BPD has not made the clinical problem go away. We can call patients by a different name but still be in a quandary about what to do with them. BPD patients continue to present in emergency rooms and clinics suffering from overdoses and self-mutilation (5) and are frequently admitted to hospital (6). These are difficult cases for psychotherapy (7,8), and they are also a challenge for psychopharmacological treatment (9). Nevertheless, none of these observations need lead to undue pessimism. Psychiatrists treat many chronic patients with difficult clinical problems and do not expect quick and easy results. The prognosis for BPD is much better than that for most other personality disorders, including the antisocial type (10) and cluster A and cluster C disorders (11); it is also better than the prognosis for schizophrenia or BD (12). Treatment can be seen as speeding up a natural process of recovery. In long-term follow-up studies, about 90% of BPD patients diagnosed in their 20s no longer met criteria by middle age; they also showed notably improved functioning (2). Recent prospective studies (12,13) have documented even more rapid symptomatic improvement, although findings in these prospectively followed samples may not be generalizable to the wider range of patients. It should also be noted that the criteria for BPD reflect acute symptoms, so even when subjects no longer have the diagnosis, they retain low levels of functioning (14). This review examines some of the recent approaches to patients with BPD and considers evidence supporting their efficacy. It is divided into a consideration of psychotherapies and pharmacotherapy and examines how each treatment modality affects the disorder’s core symptoms. The setting in which treatment is carried out is also briefly examined. Table 1 summarizes the most recently published RCTs.
Psychotherapies for BPDDialectical Behaviour Therapy DBT is an adaptation of CBT that includes an eclectic mix of methods common to several other approaches (15). DBT is specifically designed to target the mood instability of BPD, but it also addresses impulsive behaviours. While applying behavioural analysis to incidents leading to self-injury and overdoses, DBT also emphasizes empathic responses to distress that provide validation for the patient’s inner experience. One of the first RCTs of psychotherapy designed for BPD showed DBT to be superior to treatment as usual (specifically, outpatient therapy in the community) (16). After a year, the subjects receiving DBT were less likely to make suicide gestures and spent less time in hospital. Although the 2 study samples had a narrower gap in results at 1-year follow-up, patients treated with DBT continued to show a higher functional level (17). In the original study (16), over 90% of patients treated with DBT stayed in therapy for the full year. This is a remarkable finding in a patient population known for its lack of treatment compliance (18). However, it should be noted that the patients in this study received free treatment (whereas the cohort receiving treatment as usual did not) and that replication studies in other centres have experienced higher rates of attrition. Nonetheless, replications have confirmed the efficacy of DBT (19–21), and the method also seems to be effective in BPD patients with substance abuse (22). Although the effectiveness of DBT is documented best, its specificity remains to be determined. Ordinary clinical management can be slipshod (23,24), particularly in comparison with a well-structured program like DBT. A second study (25) showed that DBT was still superior to a range of “treatment by experts” (mainly psychodynamic and client-centred therapies), although its advantage was somewhat narrower. In that study, the outcomes that differentiated the groups were again overdoses and subsequent hospitalizations within the first year of treatment; there were no differences in the frequency of self-mutilation. Although all the research studies on DBT have been small, they point in the same direction. However, selection biases affecting clinical research (24) might have led to some of the superiority in outcome shown by DBT. Not every BPD patient will follow through with DBT, and we do not know whether the treatment can be applied to the larger clinical population (25). We also do not know the long-term outcome of DBT. While the original cohort of one of the first RCTs received therapy 15 years ago (16), it has never been followed up. Linehan (15) has suggested that a full course of treatment could take several years, but only the first stage (in which parasuicidal behaviours are targeted and brought under control) has been tested. We not know whether treated patients maintain their gains and continue to improve or whether they relapse. The most difficult problem is that DBT is resource-intensive and expensive. For this reason, more than a decade after its introduction, its implementation has been spotty. Where it is available, there are usually long waiting lists—not surprising for a treatment whose initial phase lasts a full year. It would be important to determine whether DBT can be dismantled and streamlined for greater clinical impact. Other Forms of Cognitive Therapy Several other forms of CBT have been proposed for BPD, although they have only recently been subjected to clinical trials. In a large sample, Tyrer and others (26) found that manualized CBT was equivalent to treatment as usual for the treatment of recurrent deliberate self-harm and noted that this method was less effective for patients with a diagnosis of BPD. The concepts of CBT developed by Aaron Beck (that is, the correcting of maladaptive cognitions) have been applied to BPD, but the only clinical report thus far (27) was an open and uncontrolled trial. Schema therapy, developed by Young, is a hybrid of CBT and psychodynamic therapy in that it focuses on maladaptive schema deriving from adverse experiences in childhood (28). It has not yet been formally tested, although a clinical trial is being conducted in the Netherlands. The STEPPS program is yet another cognitive method that provides psychoeducation in a group format (29). It is also being subjected to clinical trials. Psychodynamic Therapies Despite Stern’s original observations (1), psychoanalysts are often interested in treating BPD and have frequently adapted classical methods to the needs of this patient population (7). Interestingly, many of the leading researchers on BPD have been either trained analysts or psychodynamically oriented therapists. Nevertheless, studies have shown that, when BPD patients are offered open-ended psychodynamic therapy, most drop out within a few months (30,31). In the first formal study of analytic therapy for BPD, Stevenson and Meares reported stable improvement in a group of patients who received 2 years of a therapy based on self-psychology (32). Unfortunately, there were no control subjects; outcome was only compared with outcome among untreated waiting list control subjects and with the overall course of the disorder. Moreover, the patients treated in this study stayed in treatment for 2 years with minimal attrition and may not be representative of clinical populations. The only RCT of psychodynamic therapy for BPD was conducted by Bateman and Fonagy (33,34). This approach yielded improvement in symptoms that remained stable after 18 months. The specific treatment method used, called “mentalization-based therapy” (35), is based on the theory that BPD patients need to be taught to “mentalize” (that is, to stand outside their feelings and accurately observe emotions in themselves and others). This concept is similar to one described many years ago by Adler, who suggested that developing a therapeutic alliance is the endpoint (not the beginning) of psychotherapy for patients with BPD (36). The ideas behind MBT also resemble the concept of decentering, long used in CBT (37). The study findings were, however, limited to a day-hospital setting; as has been shown in other studies (38), this milieu may account for some of the improvement. MBT is currently being tested in an outpatient setting, with encouraging preliminary results (39). “Transference-focused psychotherapy,” another psychodynamic method, is an adaptation of psychoanalysis that aims to correct distortions in the patient’s perception of significant others and of the therapist (40). It is currently being compared with DBT in RCTs, again, with encouraging preliminary findings (41). While some data remain unpublished, the findings concerning MBT and TFP suggest that psychodyamically oriented therapy can also be successful in treating BPD, provided that it is well structured. The most likely reason for the frequent failure of past therapies may be that they relied on unstructured techniques such as free association, which leave the BPD patient adrift. Group Therapy This modality can be used either as a primary method of treatment or as an adjunct to other treatments. In the case of BPD, there has only been one controlled trial, which examined long-term group therapy based on a model developed by Dawson and Macmillan (42). The outcome was only compared with individual therapy, and both methods achieved similar results (43). Family Psychoeducation Patients’ families were once blamed for BPD, but many therapists have come to realize that they are burdened by their children’s psychopathology and that they can be useful allies in treatment. Gunderson has developed a program for psychoeducation of family members (7) that parallels previous work on expressed emotion in schizophrenia but has not yet published systematic data on the effectiveness of his approach. Psychotherapy Efficacy in Relation to Long-Term Outcome Since BPD tends to improve with time, we need to know whether long-term treatments make this process occur more rapidly. A metaanalysis of treatment studies of patients with personality disorders compared results with rates of naturalistic recovery found in follow-up research (44). Although the authors concluded that psychotherapy is effective for Axis II pathology, the data in this metaanalysis were sparse, and most studies were uncontrolled. Moreover, the estimated yearly rate of recovery among patients with BPD might have been too low, when compared with recent studies (12,13). Pharmacotherapy in BPDNeuroleptics While low-dose neuroleptics have long been used to target impulsive symptoms in BPD (9), psychiatrists have been rightly cautious about prescribing agents with so many side effects. Studies of haldoperidol in this population have shown that patients tend to stop taking it and that short-term effects are not maintained on 6-month follow-up (45). However, atypical neuroleptics such as risperidal and olanzapine have milder side effect profiles, and 3 studies have supported the use of olanzapine in BPD (46–48), which seems to have a primary effect on impulsivity. Nevertheless, atypicals also have side effects, and there are data suggesting that these agents provoke obesity in this population (49). Selective Serotonin Reuptake Inhibitors SSRIs have been widely used to treat BPD, usually with the aim of targeting the prominent depressive symptoms seen in this population. While some research suggests that SSRIs do reduce mood disturbance (50–52), the results fail to match the dramatic effects of antidepressants in classical depression. Other studies suggest that SSRIs are most effective in reducing anger and impulsive symptoms (53,54). High dosages (for example, 60 to 80 mg of fluoxetine daily) may yield a specific effect on self-mutilation (54), but patients have difficulty tolerating these levels. There has also been research on MAOIs (45,55) and on tricylcic antidepressants (56) in BPD, but their side effects and potential lethality on overdose have not encouraged wide use. Although it is unusual today to see a patient with BPD who is not on an antidepressant, this practice rests more on clinical lore than on evidence from controlled trials. Antidepressants seem to “take the edge off” the symptoms of BPD, but one never sees remissions of the personality disorder itself. Mood Stabilizers The evidence for the use of mood stabilizers in BPD is equivocal. The only controlled study of lithium in BPD (57) failed to demonstrate efficacy, and few clinicians would wish to use a drug that is so dangerous on overdose. Carbamazepine may have some value in reducing impulsivity (55), but it is also dangerous on overdose. A controlled trial found that valproate had only marginal efficacy in BPD (58). A more extensive multicentre trial (59) and one other report (60) suggest that this agent has overall effectiveness for reducing impulsive aggression in personality disorders but is less useful for affective instability. Better results reported in another trial of valproate were limited to BPD patients with comorbid BD II (that is, those with clear-cut hypomanic episodes) (61). A recent RCT for lamotrigine in BPD found that its main effect was to reduce aggression (62). A recent controlled trial of topiramate showed that, like other mood stabilizers, its main effect on mood in BPD patients is anger reduction (63). More research on mood stabilizers is needed in large samples to determine whether they are consistently useful in this population. Present evidence suggests that they may be more useful for impulsivity and aggression than for mood stabilization itself. These conclusions may seem surprising, since these agents are often thought of as targeting affective instability. While this is a key feature of BPD that distinguishes it from other personality disorders (64), the mood stabilizers that are useful in BD do not seem to work in the same way in BPD. It is therefore possible that the emotional dysregulation seen in BPD patients is an entirely different phenomenon from that seen in bipolar spectrum disorders (65). As with antidepressants, the indications for mood stabilizers should not be limited by their name, since they show a broader spectrum of action. Other Pharmacologic Agents Zanarini and others reported that omega-3 fatty acids were an effective treatment for BPD symptoms in a small sample of patients obtained by advertisement (66). However, this single study does not provide sufficient evidence to recommend omega-3 fatty acids for a clinical population. Polypharmacy A wide variety of pharmacologic agents can be helpful in BPD. The most striking effect is reduced impulsivity; effects on mood instability are less consistent. While improvement of symptoms has been noted, none of the agents used for BPD produce clinical remission. Patients on medication frequently remain impulsive in actions and unstable in mood and relationships. Clinicians’ failure to recognize the limitations of pharmacologic intervention in BPD often leads to the prescription of additional agents, even if they are likely to have the same therapeutic effect (and limitations) as the first drug. This leads to polypharmacy, a practice that is not evidence-based and one that makes it more likely that patients will suffer from side effects. Patients with BPD are often taking 4 to 5 drugs, with at least one drug from each major group (18). Unfortunately, algorithims for drug treatment in BPD, now included in the APA guidelines for the treatment BPD (67), are not based on RCT evidence and lead directly to a practice of polypharmacy. The Setting of TreatmentBecause patients with BPD can be chronically suicidal, they are often hospitalized (6). However, the value of hospital admission for this population has never been demonstrated. While 1 in 10 of these patients will eventually complete suicide, mortality usually occurs late in the course of illness when patients are out of treatment (2). Thus the peak of perceived risk occurs in young patients who threaten suicide, whereas completions occur after age 30 years (68,69). It has never been shown that patients who are refused hospital admission are likely to respond by committing suicide. Moreover, hospitalization can sometimes produce negative effects associated with regression (70). Unfortunately, the APA guidelines (67) recommend routine hospitalization for suicidal threats and may thereby commit a disservice to clinicians. Day treatment is an evidence-based alternative to full admission. Controlled trials in a mixed population of patients with Axis II disorders (38) and in patients with BPD (34) show that severely ill patients can be managed effectively in this way. Day-treatment programs combine many types of intervention, including individual sessions, group therapy, family therapy, and psychopharmacology; improvement may occur through the therapeutic effects of a milieu focused on rehabilitation. Apart from these crisis periods, BPD can generally best be managed in an outpatient setting (8)—a setting in which therapists can better focus on dealing with real-life problems. Conclusions and Future DirectionsThe treatment of patients with BPD has followed developments in psychiatry as a whole. When psychoanalysis was a central model for the discipline, modified versions of analytic therapy were promulgated. As cognitive therapy became popular, a method was developed to specifically target the symptoms of BPD. As psychiatric treatments have been increasingly dominated by pharmacologic interventions, drugs from every existing group have been applied to the treatment of BPD. At our present state of knowledge, there is much stronger evidence for the effectiveness of psychotherapy in BPD than there is for any pharmacologic intervention. The main reason that psychological therapies are not more widely used is their cost. Also, according to a recent metaanalysis, there is reason to believe that several types of therapy, and not just one, can be effective (71). Further research on the treatment of BPD may need to take different directions. First, since BPD is a chronic disease, research on treatment has to move beyond short-term studies and examine long-term effects. Such studies are strikingly absent in both the psychotherapy and the psychopharmacology literature. At the same time, treatment effects in BPD need to be shown to be superior to naturalistic remission. Second, there may be factors common to all therapies that help patients with BPD. Much of the literature reviewed here suggests that improvement occurs with different methods rooted in different theories. As has been consistently shown in the psychotherapy research literature, common effects such as a strong alliance and a problem-solving orientation are more efficacious than any specific technique (72); this could well turn out to be the case for BPD. Finally, it remains possible that pharmacologic agents will play a large role in the treatment of BPD in the future. For this to happen, however, we may need to develop entirely new groups of drugs. The agents we use now (neuroleptics, SSRIs, and mood stabilizers) were developed for other purposes, and it is not surprising that they have limited value in treating BPD. We need to develop new classes of drugs that specifically target the traits that underlie BPD—most particularly, affective instability and impulsivity. References1. Stern A. 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J Personal Disord 2004;18:240–7. 71. Leichsenring F, Leibing E. The effectiveness or psychodynamic therapy and cognitive therapy in the treatment of personality disorders: a meta-analysis. Am J Psychiatry 2003:160:1223–32. 72. Wampold BE. The great psychotherapy debate: models, methods, and findings. Mahwah (NJ): Lawrence Erlbaum Associates; 2001. Author(s)Manuscript received and accepted April 2005. 1. Professor, Department of Psychiatry, McGill University, Montreal, Quebec; Research Associate, SMBD-Jewish General Hospital, Montreal, Quebec. Address for correspondence: Dr J Paris, Department of Psychiatry, McGill University, 1033 Pine Avenue West, Montreal, QC H3A 1A1 e-mail: joel.paris@mcgill.ca
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