Psychiatric Annals

CME Article 

Physical and Medical Dimensions of Borderline Personality Disorder and the Effect of Treatment

Glen O. Gabbard, MD; Valdesha L. Ball, MD

Abstract

For many years, psychiatrists tended to view personality disorders as “psychological disorders” that were fundamentally different from “biological disorders,” such as schizophrenia or bipolar illness.1 In an era in which genetic and neuroimaging studies have enhanced our knowledge of the etiology and pathogenesis of Axis II conditions, psychiatry has evolved to a point where we now know that there are complex interactions between genes and environment, biology and psychology, and “mind” and “brain” that must be taken into account if we are to fully understand these disorders.

Abstract

For many years, psychiatrists tended to view personality disorders as “psychological disorders” that were fundamentally different from “biological disorders,” such as schizophrenia or bipolar illness.1 In an era in which genetic and neuroimaging studies have enhanced our knowledge of the etiology and pathogenesis of Axis II conditions, psychiatry has evolved to a point where we now know that there are complex interactions between genes and environment, biology and psychology, and “mind” and “brain” that must be taken into account if we are to fully understand these disorders.

Glen O. Gabbard, MD, is Professor Psychiatry and Brown Foundation Chair of Pscyhoanalysis, Baylor College of Medicine. Dr. Valdesha Ball is an Instructor, Department of Psychiatry, Baylor College of Medicine and medical director of Returning OEF/OIF Veterans’ Environment of Recovery (ROVER) Inpatient Unit, Michael E. Debakey Veteran’s Hospital.

Dr. Gabbard and Dr. Ball have disclosed no relevant financial relationships.

Address correspondence to: Glen O. Gabbard, MD, 6655 Travis, Suite 500, Houston, TX 77030.

For many years, psychiatrists tended to view personality disorders as “psychological disorders” that were fundamentally different from “biological disorders,” such as schizophrenia or bipolar illness.1 In an era in which genetic and neuroimaging studies have enhanced our knowledge of the etiology and pathogenesis of Axis II conditions, psychiatry has evolved to a point where we now know that there are complex interactions between genes and environment, biology and psychology, and “mind” and “brain” that must be taken into account if we are to fully understand these disorders.

In borderline personality disorder (BPD), we see that early adverse experience leads to lasting neurobiological changes. Therefore, there are medical/physical consequences associated with BPD that must be considered in the comprehensive treatment of these patients. In this article, we summarize the medical and physical dimensions of BPD and outline how effective treatment strategies may influence those aspects of the disorder.

Sequelae of Trauma

BPD has a multifactorial etiology.2 However, probably 60% to 80% of such patients have experienced some form of childhood trauma. Prospective research3 has clearly linked borderline symptoms in adults to childhood sexual abuse and neglect.

One consequence of early interpersonal trauma is that borderline patients may have a hyperreactive hypothalamic-pituitary-adrenal (HPA) axis that secretes excessive amounts of cortisol. Neurobiological findings are confirming these sequelae of developmental trauma. Rinne et al4 studied 39 female BPD patients who were given combined dexamethasone/corticotropin releasing hormone (CRH) tests using 11 healthy subjects as controls. Twenty-four of these women had histories of sustained childhood abuse. Fifteen of them had no histories of sustained childhood abuse. When they examined the results, the chronically abused BPD patients had significantly enhanced adrenocorticotropic hormone (ACTH) and cortisol responses to the dexamethasone/CRH challenge, compared with nonabused subjects. In addition, there were no significant differences between nonabused BPD subjects and normal controls. They concluded that a history of sustained childhood abuse is associated with hyperresponsiveness of ACTH release. Their findings suggest that this hyperreactive physiological state is relevant to this subgroup of borderline patients but not necessarily to those who lack such histories.

Sustained childhood abuse and excessive secretion of cortisol have a number of negative effects on the developing child. The amygdala may be one area where the effect is substantial. A functional magnetic resonance imaging (fMRI) study5 comparing six female BPD patients with six female control subjects found that the amygdala on both sides of the borderline patients’ brains showed enhanced activation, compared with the control group. The investigators concluded that the perceptual cortex in a borderline patient may be modulated through the amygdala in such a way that attention to emotionally relevant environmental stimuli is increased.

Two different studies6,7 examined how borderline patients react to standard presentations of faces, compared with control subjects. In one study,5 borderline patients showed significantly greater left amygdalar activation to facial expressions of emotion compared with normal control subjects. A hyperactive amygdala may be involved in the predisposition to be hypervigilant and overreactive to relatively benign emotional expressions.

An overemphasis on the amygdala as an isolated structure may be misleading. Consideration of “top down” regulation by the prefrontal cortex is equally important in understanding the interpersonal difficulties and affective dysregulation seen in patients with borderline personality disorder.5 Both the medial prefrontal cortex and the orbital prefrontal cortex have direct, reciprocal connections with areas of the brain that are crucial to emotion. Both have an inhibiting effect on the amygdala.8–10 The dorsolateral prefrontal cortex also appears to exert a modulatory influence upon the amygdala indirectly via its direct connections with the medial and orbital prefrontal cortices.8,9

Investigators postulate that dualbrain pathology involving increased activity in the amygdala and decreased activity in the prefrontal regions may be central to understanding borderline phenomena. In two studies,11,12 reductions in medial and orbitofrontal volumes have been noted in the brains of borderline patients. Of particular interest in the fMRI study by Tebartz van Elst et al12 was that the left orbitofrontal volumes correlated significantly with amygdala volumes. Therefore, the weakening of prefrontal inhibitory controls may actually contribute to the hyperreactivity of the amygdala. This combination may be related to the common clinical situation in which a borderline patient cannot seem to “control” or “shut off” intense emotional responses.

Excessive cortisol release may have far-reaching effect on the brain of borderline patients. Among the multiple hormones and neurotransmitters involved in the formation of memories, glucocorticoids appear to play a preeminent role. Numerous studies suggest that increased levels of glucocorticoids can impair or enhance the formation of memories, depending on the content of the memory, the duration of exposure to elevated glucocorticoid levels, and the temporal relationship between exposure to elevated glucocorticoid levels and the item to be learned.13 Whereas acute increases in glucocorticoid exposure can enhance memory consolidation, they can also impair memory encoding and retrieval. This effect on memory occurs through direct impairment of a process called long-term potentiation.14

Patients with a history of BPD and early life trauma have smaller hippocampal and amygdalar volumes than those without a history of BPD.12,15,16 These decreased volumes could be due to multiple etiologies, such as neuronal cell death, neuronal atrophy, inhibited neurogenesis, or dendritic pruning.4 They are also possibly related to elevated glucocorticoid levels. Stress connected with childhood trauma and neglect may induce elevations of cortisol and decreased levels of brain-derived neurotrophic factor (BDNF).

Childhood sexual abuse is also associated with diminished central serotonergic regulation in adult women with BPD.17,18 Decreased serotonergic regulation is, in turn, linked to disinhibition, impulsive aggression to self and others, and suicidality. Therefore, patients with BPD often harm themselves intentionally through self-mutilation, inadvertently through impulsive behavior, or through suicide attempts. Traumatic brain injury, lacerations, fractures, or sequelae of overdoses all lead to increased utilization of the healthcare system, including emergency rooms, inpatient treatment, and outpatient visits to a variety of specialists.19 This is in large part secondary to the pervasive nature of their symptoms (ie, suicide attempts and parasuicidal behavior) and associated psychiatric and/or medical comorbidities. Patients who have been sexually abused have an increased prevalence of somatic disorders.20 Paras et al20 conducted a systematic review and meta-analysis of longitudinal case-control and cohort studies that investigated somatic outcomes of patients with and without a history of sexual abuse. Based on the review of the literature, they found a significant association between a history of sexual abuse and lifetime diagnosis of functional gastrointestinal disorders, nonspecific chronic pain, chronic pelvic pain, and psychogenic seizures.20 There was no significant association between a history of sexual abuse in general and a lifetime diagnosis of fibromyalgia. However, when analysis was restricted to sexual abuse classified as rape, they found that rape was specifically related to a lifetime diagnosis of fibromyalgia. Rape was also associated with chronic pelvic pain and functional gastrointestinal disorders. The overall results of this study suggest a strong association between a history of sexual abuse and lifetime diagnosis of multiple somatic disorders.

Treatment Effects

Medication Studies

Psychotherapy and medication are used in the treatment of BPD. Selective serotonin reuptake inhibitors (SSRIs) have been shown to be effective in improving anger dysregulation, dysphoria, and anxiety.1 SSRIs reduce the “affective noise” in BPD patients. As a result, patients are more stable emotionally and, therefore, are more apt to be better engaged in psychotherapy. They will then have an increased capacity to reflect on their internal world and to mentalize the experiences of others.

Recent evidence suggests that SS-RIs also have a significant effect on the hippocampus. They have been known to stimulate neurogenesis in the hippocampal regions, which subsequently results in improved verbal declarative memory.21 Additionally, SSRIs decrease the hypersecretion of corticotropin-releasing factor (CRF) hyperactivity of the HPA axis.22 Rinne et al23 evaluated the effects of fluvoxamine on the HPA axis in 30 women with BPD. They compared the effects of this medication to patients with and without a history of childhood abuse. Seventeen patients had a history of abuse, and 13 patients had no abuse history. Each patient was administered a combined dexamethasone and corticotropin-releasing hormone test (DEX/CRH) before and after treatment with fluvoxamine. The dose of fluvoxamine was 150 mg/d. There was a significant reduction of ACTH and cortisol response to the DEX/CRH test after both 6 and 12 weeks of fluvoxamine treatment. There was a greater magnitude of reduction in ACTH and cortisol response in patients who had a history of sustained experience with childhood abuse. Furthermore, the degree of the reduction was not correlated with the presence of comorbid posttraumatic stress disorder or major depression. These researchers concluded that fluvoxamine decreases HPA hyperresponsiveness in patients with BPD who have experienced sustained childhood abuse. This reduction in cortisol release may, in turn, mitigate against the brain and systemic changes related to excessive cortisol secretion.

Psychotherapy Studies

Because BPD patients have more frequent inpatient hospitalizations, increased emergency room visits, poorer adherence to hospital and clinic staff treatment plans, instability of consistent mental health providers, and are non-compliant with outpatient follow-up appointments, studies have proposed that integrated treatment with prolonged psychotherapy and medication management is highly cost-effective. The Table (see page 998) summarizes those studies. In 1992, Stevenson and Meares24 studied 30 patients with a diagnosis of BPD who received individual psychodynamic psychotherapy twice weekly. Each patient was evaluated before and after treatment a year later. Throughout the course of treatment, patients demonstrated marked improvement in various domains. Patients exhibited improvement in occupational functioning, self-injurious behavior, and utilization of medical resources. Before treatment, these patients spent an average of 4.47 months away from work each year. After completion of therapy, the time away from work diminished to an average of 1.37 months. The number of parasuicidal gestures decreased by 25% of the occurrences before initiation of treatment. Correspondingly, less parasuicidal behavior was one of the major contributors to the reduction in the necessity for medical care. The number of visits to medical providers declined to one-seventh of the pretreatment rates. Hospital admission decreased by 59%, and the course of hospital stays decreased by 50%. Thirty percent of the patients no longer met Diagnostic and Statistical Manual of Mental Disorders, third edition, (DSM-III) criteria for BPD after termination of treatment.

Effect of Psychotherapy on BPD

Table. Effect of Psychotherapy on BPD

These patients were followed up 5 years after the completion of treatment.25 Many of the treatment outcomes of year-long therapy remained. There continued to be a reduction in absences from work, medical visits, self-injurious behavior, hospital admissions, and hospital course. Additionally, there was less necessity for prescription drug use. These findings suggest that a specific modality of treatment for BPD has more continual efficacy. Meares et al26 compared these 30 patients with a group of 30 patients with BPD who received treatment as usual, which consisted of patients who were on a waiting list to receive psychotherapy at a clinic. Treatment as usual was characterized as crisis intervention, supportive therapy, and pharmacological management. At the completion of therapy, there was a significant reduction in DSM-IV symptoms scores for the patients receiving psychotherapy. However, scores for the treatment-as-usual control group were unchanged.

Hall et al27 conducted an economic analysis of the cost-effectiveness of psychotherapy for the same sample. They collected data on the use of inpatient hospitalizations, emergency room visits, ambulatory care, diagnostic tests, and medication 12 months before and after completion of psychotherapy. They also collaborated with two health economic researchers to assist with the analysis of economic data. Upon completion of therapy, there was a total of $670,000 in savings of health service use. The majority of these savings were secondary to decreased use of inpatient care. The cost of psychotherapy alone for these patients was $130,050. This resulted in a net savings of $546,509, or a net cost savings of approximately $18,000 per patient.

Linehan and colleagues28 evaluated 44 women with BPD in a randomized, controlled trial comparing dialectical behavioral therapy (DBT) to treatment as usual (TAU). DBT is a manualized treatment that combines strategies from behavioral, cognitive, and supportive therapies.29 Treatment entails weekly group psychotherapy and individual psychotherapy sessions. The treatment course is 1 year in duration. In this study, patients averaged 20 mental health visits per year in the TAU group. When compared with the TAU patients during this time frame, DBT patients had significantly fewer days in the psychiatric hospital (8.46 per year compared with 38.86 for TAU). There was also less parasuicidal behavior that necessitated treatment. The progress made by DBT patients were sustained at 6-month and 1-year follow-up.29 After 1 year of treatment, DBT patients continued to have better employment performance and fewer psychiatric hospitalizations compared with TAU patients. The cost savings averaged $10,000 per patient per year with the use of DBT compared with TAU in the community.30 Most of these savings are primarily attributed to the reduced use of inpatient beds.

Two-thirds of BPD patients meet criteria for a coexisting substance abuse diagnosis.31 Linehan and colleagues32 also conducted a randomized, controlled trial of women who had a dual diagnosis of BPD and substance abuse/dependence. In 1999, they studied 28 women with BPD using a modified version of DBT that focused on additional problems related to substance use. They compared this group with TAU. There was no difference between groups in severity of psychopathology. Urine drug screens were used to monitor substance use. Patients were evaluated at 4, 6, 8, and 12 months during the course of treatment. DBT patients demonstrated significant improvement in substance use compared with the TAU group. The medical consequences of substance abuse are well-known, so reduction in ingestion of alcohol and drugs can be expected to prevent those medical sequelae.

In 1999, Bateman and Fonagy33 conducted a randomized, controlled trial to compare the effectiveness of psychoanalytically oriented partial hospitalization with standard psychiatric care for patients with BPD. Thirty-eight patients were assigned to either a partially hospitalized group or general psychiatric services (control group) for 18 months. The partial hospitalization consisted of individual and group mentalization-based psychotherapy (MBT). The general psychiatric service entailed regular psychiatric review with a senior psychiatrist, averaging two times per month, inpatient admissions if necessary, and regular outpatient follow-up every 2 weeks. Members of this group did not receive formal psychotherapy. Results of this study showed that patients in the partial hospital group had a significant decrease in the frequency of suicide attempts and self-injurious behavior. There was also significant reduction in the number and duration of inpatient admissions, the use of psychotropic medications, symptoms of depression and anxiety, level of distress, interpersonal dysfunction, and social maladjustment. These changes were present after 6 months of treatment and were sustained until the discontinuation of treatment at 18 months.

In 2003, Bateman and Fonagy evaluated a cost analysis of the data from this previously mentioned trial.34 They collected information on the healthcare utilization of all BPD patients from case notes and service providers. Costs were compared for the 6 months before treatment, 18 months of treatment, and 18 months following the termination of treatment. The two groups had comparable health-related expenditures before the initiation of treatment. During treatment, the overall cost of the partial hospitalization group counterbalanced the lower costs of inpatient and outpatient care, medication, or emergency room treatment. However, for the 18-month treatment period, the annual costs were significantly lowered for the partial hospitalization and general psychiatric care groups, compared with the 6-month pretreatment rate. However, the cost of medication and emergency room care decreased significantly only in the partial hospitalization group. There was even more of a significant decrease in costs for the partial hospitalization group after discharge. The average annual cost for this group decreased by one-fifth of that for the general psychiatric care group. Moreover, only the partial hospitalization group demonstrated a significant reduction in emergency room costs.

An 8-year follow-up study of the same cohort35 showed continued superiority for those who had mentalization-based psychotherapy. Research psychologists conducted interviews of 41 patients from the original trial. They were blinded to which treatment group the patients belonged. Members of the mentalization-based treatment group continued to have less suicidality compared with the TAU group (23% vs. 74%). Only 13% of patients who had MBT met criteria for a diagnosis of BPD at the end of the follow-up period. Eight-seven percent of the TAU group maintained a diagnosis of BPD. Utilization of services was significantly decreased with MBT (2 versus 3.5 years of psychiatric outpatient treatment) along with the use of medication (0.02 versus 1.9 years taking three or more medications). Forty-five percent of MBT patients maintained a global functioning above 60, compared with 10% in TAU group. MBT patients also maintained better occupational functioning. They maintained employment for an average of 3.2 years, compared with 1.2 years in patients belonging to the TAU group.

The foregoing studies, summarized in the Table (see page 998), clearly indicate that there is a powerful effect on the utilization of medical services when psychotherapy is provided. In addition, there is a strong possibility that psychotherapy makes an effect on the brain abnormalities that are associated with BPD. Preliminary neuroimaging data suggest that the kind of conscious reflection required in psychotherapy may activate greater frontal cortical control over subcortical structures, such as the amygdala.36 A preliminary study involving five borderline patients and five controls used brain perfusion single-photon emission tomography (SPECT) to study these changes.37 All five BPD patients showed a lower level of activation in the frontal areas pre-treatment compared with controls. Each patient received 16 months of drug-free, mentalization-based psychotherapy, but only two of the five BPD patients who completed the treatment underwent the repeat SPET. The posttreatment neural patterns showed a strong frontal activation in these two subjects that was absent in pretreatment, suggesting more effective cortical modulation of subcortical areas. Although these data are by no means definitive, they suggest that psychotherapy may have far-ranging effects on the basic neurobiological phenomena associated with BPD.

Conclusions

BPD is a common condition that is accompanied by persisting neurobiological changes, hyperreactivity of the HPA axis, and a variety of medical and physical consequences that result in high utilization of healthcare services. Effective treatment of the condition with pharmacotherapy and psychotherapy results in beneficial changes in the brain and the body and dramatically decreases the utilization of healthcare services.

References

  1. Gabbard GO. Mind, brain, and personality disorders. Am J Psychiatry. 2005;162(4):648–655. doi:10.1176/appi.ajp.162.4.648 [CrossRef]
  2. Zanarini MC, Frankenburg FR. Pathways to the development of borderline personality disorder. J Pers Disord. 1997;11(1):93–104.
  3. Johnson JG, Cohen P, Brown J, Smailes EM, Bernstein DP. Childhood maltreatment increases risk for personality disorders during early adulthood. Arch Gen Psychiatry. 1999;56(7):600–606. doi:10.1001/archpsyc.56.7.600 [CrossRef]
  4. Rinne T, de Kloet ER, Wouters L, Goekoop JG, DeRijk RH, van den Brink W. Hyperre-sponsiveness of hypothalamic-pituitary-adrenal axis to combined dexamethasone/corticotropin-releasing hormone challenge in female borderline personality disorder subjects with a history of sustained childhood abuse. Biol Psychiatry. 2002;52(11):1102–1112. doi:10.1016/S0006-3223(02)01395-1 [CrossRef]
  5. Herpertz SC, Dietrich TM, Wenning B, et al. Evidence of abnormal amygdala functioning in borderline personality disorder: a functional MRI study. Biol Psychiatry. 2001;50(4):292–298. doi:10.1016/S0006-3223(01)01075-7 [CrossRef]
  6. Donegan NH, Sanislow CA, Blumberg HP, et al. Amygdala hyperreactivity in borderline personality disorder: implications for emotional dysregulation. Biol Psychiatry. 2003;54(11):1284–1293. doi:10.1016/S0006-3223(03)00636-X [CrossRef]
  7. Wagner AW, Linehan MM. Facial expression recognition ability among women with borderline personality disorder: implications for emotion regulation?J Pers Disord. 1999;13(4):329–344.
  8. Hariri AR, Mattay VS, Tessitore A, Fera F, Weinberger DR. Neocortical modulation of the amygdala response to fearful stimuli. Biol Psychiatry. 2003;53(6):494–501. doi:10.1016/S0006-3223(02)01786-9 [CrossRef]
  9. LeDoux J. Synaptic Self: How our Brains Become Who We Are. New York: Penguin Putnam; 2002.
  10. Rausch SL, Shin LM, Wright CI. Neuroimaging studies of amygdala function in anxiety disorders. Ann N Y Acad Sci. 2003;985:389–410.
  11. Lyoo IK, Han MH, Cho DY. A brain MRI study in subjects with borderline personality disorder. J Affect Disord. 1998;50(2–3):235–243. doi:10.1016/S0165-0327(98)00104-9 [CrossRef]
  12. Tebartz van Elst L, Hesslinger B, Thiel T, et al. Frontolimbic brain abnormalities in patients with borderline personality disorder: a volumetric magnetic resonance imaging study. Biol Psychiatry. 2003;54(2):163–171. doi:10.1016/S0006-3223(02)01743-2 [CrossRef]
  13. McGaugh JL, Roozendaal B. Role of adrenal hormones in forming lasting memories in the brain. Curr Opin Neurobiol. 2002;12(2):2005–2010. doi:10.1016/S0959-4388(02)00306-9 [CrossRef]
  14. Grossman R, Buschsbaum MS, Yehuda R. Neuroimaging studies in post-traumatic stress disorder. Psychiatr Clin North Am. 2002;25(2):317–340. doi:10.1016/S0193-953X(01)00011-9 [CrossRef]
  15. Driessen M, Herrmann J, Stahl K, et al. Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization. Arch Gen Psychiatry. 2000;57(12):1115–1122. doi:10.1001/archpsyc.57.12.1115 [CrossRef]
  16. Schmahl CG, Elzinga BM, Vermetten E, Sanislow C, McGlashan TH, Bremner JD. Neural correlates of memories of abandonment in women with and without borderline personality disorder. Biol Psychiatry. 2003;54(2):142–151. doi:10.1016/S0006-3223(02)01720-1 [CrossRef]
  17. Rinne T, Westenberg HG, den Boer JA, et al. Serotonergic blunting to meta-chlorophenyl-piperazine (m-CPP) highly correlates with sustained childhood abuse in impulsive and autoaggressive female borderline patients. Biol Psychiatry. 2000;47(6):548–556. doi:10.1016/S0006-3223(99)00181-X [CrossRef]
  18. Siever LJ, Davis KL. A psychobiological perspective on the personality disorders. Am J Psychiatry. 1991;148(12):1647–1658.
  19. Gabbard GO, Lazar SG, Hornberger J, Spiegel D. The economic impact of psychotherapy: a review. Am J Psychiatry. 1997:154(2):147–155.
  20. Paras ML, Murad MH, Chen LP, et al. Sexual abuse and lifetime diagnosis of somatic disorders: a systematic review and meta-analysis. JAMA. 2009;302(5):550–561. doi:10.1001/jama.2009.1091 [CrossRef]
  21. Vermetten E, Vythilingam M, Southwick SM, et al. Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder. Biol Psychiatry. 2003;54(7):693–702. doi:10.1016/S0006-3223(03)00634-6 [CrossRef]
  22. Nemeroff CB, Owens MJ. Pharmacologic differences among the SSRIs: focus on monoamine transporters and the HPA axis. CNS Spectr. 2004;9(6 Suppl 4):23–31.
  23. Rinne T, de Kloet ER, Wouters L, Goekoop JG, de Rijk RH, van den Brink W. Fluvoxamine reduces responsiveness of HPA axis in adult female BPD patients with a history of sustained childhood abuse. Neuropsychopharmacol. 2003;28(1):126:132.
  24. Stevenson J, Meares R. An outcome study of psychotherapy for patients with borderline personality disorder. Am J Psychiatry. 1992;149(3):358–362.
  25. Stevenson J, Meares R, D’Angelo R. Five-year outcome of outpatient psychotherapy with borderline patients. Psychol Med. 1995;35:79–87. doi:10.1017/S0033291704002788 [CrossRef]
  26. Meares R, Stevenson J, Comerford A. Psychotherapy with borderline patients: I. a comparison between treated and untreated cohorts. Aust N Z J Psychiatry. 1999;33(4):467–472.
  27. Hall J, Caleo S, Stevenson J, et al. An Economic Analysis of Psychotherapy for Borderline Personality Disorder Patients. J Ment Health Policy Eco. 2001;4:3–8.
  28. Linehan MM, Armstrong HE, Suarez A, et al. Cognitive-behavioral treatment of chronically parasuicidal borderline patients. Arch Gen Psychiatry. 1991;48(12):1060–1064.
  29. Linehan MM, Heard HL, Armstrong HE. Naturalistic follow-up of a behavioral treatment for chronically parasuicidal borderline patients. Arch Gen Psychiatry. 1993;50(12):971–974.
  30. Heard H. Behavior therapies for borderline patients. Presented at May meeting of the American Psychiatric Association. , Philadelphia, PA. ; 1994.
  31. Dulit RA, Fyer MR, Haas GL, et al. Substance use in borderline personality disorder. Am J Psychiatry. 1990;147(6):1002–1007.
  32. Linehan MM, Schmidt H, Dimeff LA, et al. Dialectical behavior therapy for patients with borderline personality disorder and drug-dependence. Am J Addict. 1999;8(4):279–292. doi:10.1080/105504999305686 [CrossRef]
  33. Bateman A, Fonagy P. Effectiveness of partial hospitalization in the treatment of borderline personality disorder: a randomized controlled trial. Am J Psychiatry. 1999;156(10):1563–1569.
  34. Bateman A, Fonagy P. Health service utilization costs for borderline personality disorder patients treated with psychoanalytically oriented partial hospitalization versus general psychiatric care. Am J Psychiatry. 2003;160(1):169–171. doi:10.1176/appi.ajp.160.1.169 [CrossRef]
  35. Bateman A, Fonagy P. Eight-year follow-up of patients treated for borderline personality disorder: mentalization-based treatment versus treatment as usual. Am J Psychiatry. 2008;165(5):631–638. doi:10.1176/appi.ajp.2007.07040636 [CrossRef]
  36. Ochsner KN, Bunge SA, Gross JJ, Gabrieli JD. Rethinking feelings: an fMRI study of the cognitive regulation of emotion. J Cogn Neurosci. 2002;14(8):1215–1229. doi:10.1162/089892902760807212 [CrossRef]
  37. Lai C, Daini S, Calcagni ML, Bruno I, De Risio S. Neural correlates of psychodynamic psychotherapy in borderline disorders--a pilot investigation. Psychother Psychosom. 2007;76(6):403–405. doi:10.1159/000107572 [CrossRef]

Effect of Psychotherapy on BPD

StudyNInterventionOutcome
Stevenson and Meares, 199225; Stevenson et al,199525; Meares et al, 199926; Hall et al, 200127302x/wk dynamic individual psychotherapy for 12 months (pre-post design)Medical visits reduced to 1/7 of pre-treatment rate; decreased hospital admissions; $670,000 in health service use savings
Linehan et al, 199128; Heard, 19943044; 22 DBT; 22 TAUDialectical behavior therapy for 12 months (RCT)Hospital duration 38.86 vs. 8.46 days/yr; parasuicidal gestures 1.76 vs. 0.64; Cost savings of $10,000 per pt per yr
Linehan et al, 19993228 BPD + substance use disorderDialectical behavior therapy (RCT)Significant reduction in substance abuse in DBT group vs. TAU group
Bateman and Fonagy, 199933; Bateman and Fonagy, 20033438; 19 MBT; 19 controlsMBT individual and group in partial hosp for 18 months (RCT)MBT group had significant reductions in suicide attempts, self-injury, ER care, and cost of medication; average annual cost of MBT group was 1/5 of controls
Bateman and Fonagy, 20083541MBT vs. TAU (RCT)Decreased use of medical services, less use of medications, better occupational functioning in MBT group

CME Educational Objectives

  1. Review the long-term physiological consequences of early interpersonal trauma.

  2. Identify the current neurobiological models of borderline personality disorder (BPD).

  3. List the current treatment strategies for BPD in terms of measurable effectiveness.

Authors

Glen O. Gabbard, MD, is Professor Psychiatry and Brown Foundation Chair of Pscyhoanalysis, Baylor College of Medicine. Dr. Valdesha Ball is an Instructor, Department of Psychiatry, Baylor College of Medicine and medical director of Returning OEF/OIF Veterans’ Environment of Recovery (ROVER) Inpatient Unit, Michael E. Debakey Veteran’s Hospital.

Dr. Gabbard and Dr. Ball have disclosed no relevant financial relationships.

Address correspondence to: Glen O. Gabbard, MD, 6655 Travis, Suite 500, Houston, TX 77030.

10.3928/00485718-20091123-01

Sign up to receive

Journal E-contents