Implications for Treatment and Prognosis of Borderline and Substance Use Disorders

Borderline personality disorder (BPD) is a severe disorder characterized by a pervasive pattern of instability in the regulation of emotion, interpersonal relationships, self-image, and impulse control. Approximately 2% of the general population meet criteria for BPD.¹ In psychiatric treatment settings, prevalence rates for BPD are considerably higher, with rates of 8% for outpatients and 15% for inpatients.² An estimated 3% to 10% of persons with BPD commit suicide.³ The disorder constitutes a significant social and economic burden on family resources and health care systems since it is associated with severe functional impairment and high rates of treatment utilization.

BPD and substance use disorder (SUD) often co-occur. Comorbid BPD and SUD is related to a variety of severe adverse outcomes, including participation in the sex trade; a large number of sexual partners; needle sharing; polysubstance use; more frequent and more serious drug overdoses; increased risk of suicide attempts; and more severe psychiatric, family, and legal problems.^4-12 BPD has also been found to complicate the treatment of SUD.^13-15 This article provides an overview of the prevalence of co-occurring BPD and SUD, neurobiologic hypotheses for the link between BPD and SUD, and treatment options that have proved effective for persons with comorbid BPD and SUD.

BPD and SUD comorbidity
Apart from antisocial personality disorder, BPD is probably the most common personality disorder in persons with SUD. Nearly one third of those with a lifetime SUD diagnosis also have BPD (median, 27%; range, 5.2% to 74.0%).^16,20 BPD appears to be less prevalent in persons with alcohol use disorders (median, 16%; range, 3.2% to 27.4%) than in those with drug use disorders, especially cocaine and opioid abuse.^17,20 For example, Ross and colleagues¹⁷ found that almost half (47%) of individuals using heroin who entered treatment for SUD also had BPD. Note that the prevalence of BPD in this sample is far higher than that reported in other studies. Diagnostic discrepancies across studies examining the rates of comorbidity in persons with SUD are probably due to confounding methodologic factors, including the use of different assessment instruments, variable evaluator training, and differing sample characteristics (eg, treatment-seeking vs nontreatment-seeking). Women with SUD are more likely to have BPD than men.^17,20

Conversely, more than half of those who have BPD also have a lifetime SUD diagnosis (median, 56.5%; range, 22.7% to 86%).^20-22 Alcohol use disorders tend to be slightly more common in those with BPD (median, 48.9%; range, 21% to 100%) than in those with drug use disorders (median, 43.1%; range, 19% to 76%).^20,21,23 Comorbidity rates have not always been reported separately for men and women, but in a study by Zanarini and colleagues,²¹ the researchers found that male psychiatric patients with BPD were more likely to have SUD (81.9%) than their female counterparts (59.1%)

Explanations for the association
There are several explanations for the strong association between BPD and SUD. First, the core BPD traits (affect dysregulation, impulse dyscontrol) are known to predispose patients to SUD and to affect the severity of substance use. Second, BPD and SUD have common familial precursors, such as family history of SUD and antisocial personality disorder,²⁴ child abuse, and neglect. Finally, core dimensions of BPD appear to have a neurobiologic cause,^25-27 most saliently evidenced as prefrontal cortex (PFC) dysfunction, which is also implicated in the development of SUD.^28,29

Neurobiologic hypotheses
Imaging research, both MRI and positron emission tomography (PET), offers evidence that neurologic dysfunction is at the root of the affective and behavioral dysregulation intrinsic to BPD. Structural studies using MRI have demonstrated volume loss in the hippocampus and/or amygdala in women with BPD more than in healthy controls.^30-33 These findings have been related to histories of childhood abuse, with the volume loss related to severity of childhood trauma.³⁴

Additional evidence stems from investigations measuring the metabolic function of the brain using PET technologies. For example, prefrontal hypometabolism and diminished metabolic response to serotonergic activation in areas of the PFC have been found in PET studies of persons who have BPD (and other impulsive personality disorders).^35-39 The affected areas include the orbitofrontal and ventromedial regions that are important in the regulation of affect and impulse. Damage to this area of the brain results in a syndrome of disinhibited, socially inappropriate, impulsive, and aggressive behavior.

Functional MRI studies in BPD have demonstrated abnormal responses to social cues (such as face recognition) in the amygdala, which increases the likelihood of inappropriate emotional and behavioral responding.^40,41 Taken together, these findings suggest that some symptoms of BPD may be mediated in part by a disorder in serotonergic regulation and the prefrontal and limbic dysfunction that results in impaired inhibitory control.

A large body of evidence implicating PFC dysfunction is also seen in the literature on neuropsychology.^25-27 Using tests of cognitive capacity and efficiency that are sensitive to and validated for detecting lateralized and localized cortical dysfunction, many studies have observed a pattern of impairment in PFC function. Dysfunction in PFC is associated with a variety of cognitive impairments subsumed within the rubric of executive cognitive functioning capacity. These functions include, but are not limited to, strategic planning, flexible problem solving, attention control/ working memory, self-monitoring goal-directed behavior, and cognitive control over emotion and behavior. Low executive cognitive functioning capacity is commonly manifested by impulsivity, labile emotion, distractibility, and aggression following minimal provocation. These are core characteristics of BPD and play a significant role in SUD.

The treatment of BPD
It is generally recognized that psychotherapy is needed in order to achieve clinically significant and durable improvements in those who have BPD,^42,43 although psychopharmacologic treatments are considered to be helpful ancillary interventions.³Consequently, psychosocial intervention studies have typically allowed BPD patients to receive concurrent psychotropic medications. However, the benefits of pharmacologic agents in the treatment of BPD are relatively modest,⁴³ and controlled studies testing the augmenting effects of these agents on psychotherapy outcomes have not yet been conducted.

While early reports on the effectiveness of psychotherapy for BPD have been guarded in their conclusions, research conducted over the past 15 years has provided support for the efficacy of psychotherapy interventions. Six randomized controlled trials (RCTs)^44-49 and numerous other controlled clinical trials demonstrate the benefits of dialectic behavior therapy (DBT) over treatment as usual for patients with BPD. Several follow-up studies indicate that DBT had a sustained effect on some of the core BPD symptoms for up to 1 year after treatment completion.^50-52 Another cognitive-behavioral treatment, Systems Training for Emotional Predictability and Problem Solving, is currently being tested in an RCT.⁵³

Two RCTs have tested psychodynamic treatments for BPD. In the first study, mentalization-based therapy proved to be more effective than treatment as usual throughout the 18-month follow-up period.^54,55 In the second trial, both schema-focused therapy (an integrative cognitive therapy) and transference-focused therapy (a psychodynamic therapy) were efficacious in reducing BPD and related symptoms.⁵⁶ However, schema-focused therapy was more efficacious across all outcome measures. A third RCT comparing transference-focused therapy, DBT, and supportive therapy is currently under way.⁵⁷

Current data suggest that different types of psychotherapy are effective for BPD, but DBT has received the strongest empiric support so far. Additional research is needed to document the long-term benefits of psychotherapy interventions and the role of pharmacologic agents.

With respect to substance use behavior, 4 of the 10 studies reviewed excluded persons with any concurrent SUD^44,47,53,54 and 3 excluded patients with an SUD if it was deemed that the SUD was so debilitating that primary treatment was required.^49,56,57 None of these studies reported on the impact of treatment on substance use. Two studies used DBT adapted for the treatment of SUD and included those with BPD and SUD^45,48 and 1 study tested standard DBT without excluding persons with SUD, regardless of SUD severity.⁴⁶

The treatment of comorbid BPD and SUDDBT is the only intervention that has been adapted and tested specifically for the treatment of patients with BPD and SUD.^45,48,58,59 This is a cognitive-behavioral treatment that incorporates methods for learning adaptive coping skills, generalizing such skills into everyday contexts, enhancing patients' commitment to treatment, and preventing the demoralization of therapists. DBT for SUD also typically includes pharmacotherapy consisting of drug replacement medication and the pharmacologic treatment of other psychiatric symptoms. Patients receive a 1-hour individual therapy session and a 2-hour group-skills training session each week. In addition, they are encouraged to contact their therapist for brief telephone consultations between sessions. Therapists participate in weekly consultation team meetings.

Two small RCTs examined the effects of DBT for SUD.^45,48 In both studies, treatment lasted for 1 year and patients with stimulant or opiate dependence received replacement medication pharmacotherapy. Linehan and colleagues⁴⁵ compared DBT for SUD with treatment as usual in a sample of 28 women with comorbid BPD and SUD. Illicit stimulants were replaced with methylphenidate and opiates were replaced with methadone. Patients with SUD receiving DBT were more likely to complete treatment and evidenced greater reductions in drug use (ie, the proportion of days abstinent from alcohol and drugs) assessed both by structured interview and urine toxicology screen (ie, the ratio of negative urinalyses to total urinalyses) throughout the treatment year and at 4-month follow-up. Urinalyses were performed on urine samples collected at 4 assessment points and at random on 1 occasion between assessment periods. The patients in the DBT for SUD group also showed greater improvements in global and social functioning 4 months following treatment.

In their second study, Linehan and colleagues⁴⁸ compared DBT for SUD with treatment consisting of therapist validation combined with a 12-step program in 23 women with heroin dependence. Opiates were replaced with levomethadyl acetate hydrochloride oral solution or methadone. Both treatments reduced opiate use and psychopathology and led to improvements in global adjustment. These results were maintained 4 months after treatment. The principal drug outcome measure was the proportion of positive urinalysis tests for opiates based on 3-times-a-week urine samples throughout the 12 months of treatment and a single urine sample collected 4 months after completion of treatment. There were few between-condition differences. The combination of validation therapy and 12-step program was associated with better treatment retention. DBT for SUD led to better maintenance of treatment gains (ie, reduced opiate use based on urine toxicology tests) throughout the 12 months of treatment compared with validation therapy, which was associated with a significant increase in opiate use during the last 4 months of treatment. However, the single urinalysis at 4-month follow-up failed to show any between-treatment difference.

Verheul and colleagues⁴⁶ compared the efficacy of standard DBT with that of treatment as usual in 58 women with BPD, more than half of whom had clinically significant substance abuse problems. Patients were allowed to use psychotropic medications but did not receive drug replacement medications. Outcomes were assessed via patient self-report. No toxicology tests were conducted to validate patients' reports on substance use. DBT resulted in lower attrition rates and greater reductions in self-injurious and self-damaging impulsive behaviors (including alcohol use), and these gains were maintained 6 months following treatment.⁵² However, DBT was not associated with lower rates of drug use, highlighting the importance of augmenting standard DBT protocols for the treatment of those who have comorbid BPD and SUD.

Modifications of standard DBT for SUD
According to Linehan,⁶⁰ BPD is primarily a disorder of emotion regulation. Consequently, DBT aims to enhance a patient's ability to regulate emotions in order to prevent maladaptive behaviors such as suicide attempts, self-injury, or substance use. In DBT for SUD,⁵⁹ patients must agree to work toward abstinence from all substances.

Symptoms are targeted along a hierarchy of problems: (1) reducing life-threatening and self-injurious behaviors; (2) reducing therapy-interfering behaviors; and (3) reducing quality-of-life interfering behaviors, beginning with substance use. The first SUD-specific target is the reduction of substance abuse. However, in order to prevent dropout, the first sessions include more therapist validation and less emphasis on immediate change than is typical in standard DBT. Other "attachment strategies" include increasing contact with patients toward the beginning of treatment (via telephone or e-mail), reaching out to patients who miss appointments, adjusting the length of therapy sessions according to patients' needs, and meeting with the patient's friends or family.

Examples of skills specific to DBT-SUD include tolerating substance use cravings through "urge surfing" (ie, being aware of urges to use while imagining a wave as the urge is "surfed"), thinking of ways to cope with cravings, increasing activities associated with a decreased likelihood of using (eg, attending Narcotics Anonymous meetings), and burning bridges (ie, cutting previous links to substance use). Individual therapy is focused on developing and maintaining patients' motivation to overcome obstacles to change by validation and dialectic strategies. Another goal is to enhance skills learned during group therapy through the use of behavior chain analysis and diary cards. That is, patients complete daily diary cards to record a variety of treatment targets such as the intensity of urges to use and the frequency of substance use. Individual sessions address the most relevant targets revealed on these diary cards.

Several principles guide the management of psychopharmacologic agents that are particularly relevant to DBT for SUD, including the prescription of nonlethal medications, use of simple medication regimens in order to limit adverse effects that may interfere with treatment, and the rapid adjustment of medication dosages in order to hasten clinical improvement. Additional strategies may consist of choosing drug replacement medications that require fewer clinic visits, thereby reducing patient burden and increasing treatment adherence, and those that eliminate the need for take-homes to prevent misuse. For example, Linehan and colleagues⁴⁸ chose levomethadyl acetate hydrochloride oral solution over methadone as opiate-replacement medication because it only requires 3 weekly visits for dosing and there can be no replacements.

Conclusion
The severe risks associated with comorbid BPD and SUD highlight the need to screen for this comorbidity. This may be particularly relevant for persons presenting to SUD treatment programs in which personality disorders other than antisocial personality have traditionally received little attention. Knowing whether persons have BPD in addition to SUD would allow clinicians to augment standard SUD treatments with interventions that promise to be effective for BPD (eg, emotion regulation skills) or to refer comorbid patients to programs that specialize in the treatment of BPD (with or without SUD).

Unfortunately, there are few treatment programs for BPD and virtually none for comorbid BPD and SUD. As a result, individuals with BPD and SUD are likely to receive treatment for either SUD or BPD. This is problematic because treatments for SUD may not be effective in reducing the potentially life-threatening behaviors associated with BPD13 and standard treatments for BPD may not be effective in reducing substance abuse.^46,52 In addition, persons with comorbid BPD and SUD are at risk for being rejected by both programs-by SUD treatment programs for presenting with clinically significant suicidal behaviors and by BPD treatment programs for presenting with clinically significant substance abuse. Thus, there is a clear need for interventions that address both disorders.

Little is known about the most effective treatment for those with BPD and SUD. The only intervention that has been designed and tested specifically for use with this high-risk population is DBT for SUD. Initial results are promising, but further research is needed for more definitive conclusions. One National Institute of Drug Abuse–sponsored treatment trial testing the benefits of DBT for SUD plus buprenorphine/ naloxone for patients with BPD and opiate dependence is currently under way. It is hoped that this and similar research efforts will lead to the development of effective interventions for persons with comorbid BPD and SUD.

Dr Feske is assistant professor of pharmaceutical sciences and psychiatry at the University of Pittsburgh. She is coinvestigator of the NIDA-funded Center for Education and Drug Abuse Research (CEDAR; P50 DA05605; Tarter, PI) and principal investigator of the NIDA-funded R01 "Drug Abuse and Risky Sex in Borderline Personality Disorder" (DA020130).

Dr Soloff is professor of psychiatry at the Western Psychiatric Institute and Clinic at the University of Pittsburgh. His work focuses on the biology of suicidal behavior in borderline personality disorder.

Dr Tarter is professor of pharmaceutical sciences, psychiatry, and psychology at the University of Pittsburgh. He is principal investigator of CEDAR (P50 DA05605).

The authors report that they have no conflicts of interest concerning the subject matter of this article. This work was supported, in part, by grants P50 DA05605 and DA020130.

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