In response to the resolution made in 2008 by the US Congress that proclaimed May to be borderline personality disorder (BPD) awareness month, the American Psychiatric Association (APA) decided to make BPD a key track of this year’s meeting. Among the several excellent presentations on BPD was Dr John G. Gunderson’s lecture on the ontogeny of the disorder. Having spent the past 30+ years studying BPD, both as a researcher and a clinician, Dr Gunderson of McLean Hospital of Harvard Medical School is an expert on the history of BPD.
Obviously, the disorder itself has remained the same, but its recognition and diagnosis have evolved considerably in the past several decades. Before 1970, BPD was a psychoanalytical colloquialism. Patients were thought to be difficult, untreatable, and neurotic. And the designation itself—borderline personality disorder—was rarely used within the psychotherapeutic community.
According to Dr Gunderson, identification of patients with BPD arose in the 1930s, in an era when the psychoanalytic paradigm predominated. At that time, classification was primitive and was based on analyzability—patients who were analyzable were neurotic; patients who were not analyzable were psychotic. Stern and Knight identified the tendency of certain groups of patients to regress in unstructured environments into what they called “borderline schizophrenic states.” In 1937, Adolf Stern wrote the first significant psychoanalytic work to use the term “borderline.” In 1953, Robert Knight dubbed it the “borderline state.”
By the 1970s, recognition of BPD was moving from personality organization to syndrome. In 1978, Dr Gunderson1 published a set of discriminating criteria for borderline disorder. These criteria were based on a structured interview, and they became the backbone of the DSM-III definition. In 1980, BPD became official with its inclusion in DSM-III, with symptoms that included:
• Impulsivity (substance abuse, promiscuity)
• Heightened affectivity
• Brief psychotic experience
• Intolerable aloneness (fears of abandoment)
• Close relationships marked by idealization/devaluation
Although there was now a set of identified symptoms and borderline syndrome was being recognized, it was still unclear exactly what it was. One thing that was clear was that it had no relationship to schizophrenia; but perhaps there was some correlation between BPD and depression. Finally, during this period, treatment for BPD was almost exclusively psychoanalytic psychotherapy. However, negative therapeutic reactions were common with the use of psychoanalytic psychotherapy for patients with BPD.2 At the time, these negative reactions were explained as the pernicious motives of the patient group.
In the 1980s, psychiatry moved toward biologic versus psychoanalytic paradigms. Biologic psychiatry was coming to the fore, and the topic of BPD was increasingly becoming interesting to academic psychiatrists, as illustrated by the influx of new psychiatric books. At the time, DSM-III encouraged a wave of research to see whether disorders were valid. Robbins and Gruze3 developed a standard for validation of disorders. They said to be valid, a disorder had to be descriptively distinct, had to run a course so that prediction could be made, had to run in families, had to have some type of specific response to treatment, and had to have biologic markers to separate it from other groups.
The new body of research taking place during this decade showed that BPD is not a variation of, nor closely related to, either schizophrenia or depression, but that there may be a connection with posttraumatic stress disorder. This belief was based on ideological considerations: study findings indicated that 70% of patients with BPD had a history of childhood physical abuse. However, feminist concerns that the theory was a result of negative gender biases created a largely pejorative meaning for BPD diagnosis.
By the end of the 1980s, sufficient clinical wisdom was starting to accumulate about treating patients with BPD, and clinicians who worked with hospitalized patients were beginning to revise their opinion of the disorder. They started to realize that treatment did help. The change in phenomenology could be made coherent if patients felt held (attached) by the clinician, rather than rejected. And it was becoming clear that nonpsychoanalytic modalities were often helpful (eg, group or family therapies). Multimodal treatment was beginning to replace psychoanalytic therapy.
The decade of the 1990s marked several advances in BPD treatment. In this decade, BPD went from being an unwanted personality disorder to having some treatment specificity. Larry Siever4 proposed 2 psychobiological dispositions for BPD: affective disregulation hyperesponsivity of the neuroadrenergic system and behavioral discontrol with reduced serotonergic modulation. This concept provided a scientific structure for understanding the origins of BPD as well as a way to explain its comorbidities and spectrum relationship with other disorders. Based on these criteria, BPD would be recognized as primarily an impulse spectrum disorder or affective disregulation disorder.
In 1993, Marsha Linehan developed dialectical behavior therapy (DBT) specifically to treat BPD. This was an innovative departure from earlier therapies in that the primary focus of this therapy is the patient-therapist interaction. With this treatment, self-harm, suicidality, hospitalizations, and need for medication are diminished. Because DBT was effective, it met all of the Robbins and Gruze validation criteria. It was a psychosocial intervention that had specificity and, thus, it had integrity and meaning.
Anthony Bateman developed the mentalization-based treatment (MBT), which was based on Peter Fonagy’s theory of development. MBT is a psychoanalytic derivative with an emphasis on early childhood development. It was designed to treat underlying handicaps in mentalizing by adopting an empirical developmental base and a “not-knowing” noninterpretive stance to help patients with BPD recognize and accept their own mental state as well as that of the therapist. The treatment had to be applicable within different institutions. This treatment linked problematic parent/child interactions into a prescription for what the patient-therapist diad should correct.
By the first decade of the new millennium, BPD was being recognized as a “good prognosis brain disease.” The decade is associated with an underlying etiological basis for psychiatric disorders, which reflects impatience with growing comorbidities that have existed in the diagnostic system and excitement about the newly available neuropsychological and genetic technology.
Based on advocacy of parents of children with BPD, the National Alliance on Mental Illness and the National Institute of Mental Health, as well as the US Congress, formally recognized BPD. This recognition legitimized BPD as a subject for scientific study and public awareness and resulted in 2 major research findings: that BPD is a disorder that is significantly heritable, and heritability helped establish BPD as a brain disease; and that BPD has an unexpectedly good prognosis.5
In 2001, despite the relative absence of an empirical basis, the APA published Practice Guidelines for the Treatment of BPD. Clinicians were finally beginning to understand what not to do and beginning to know what should be done:
• Need for patient-therapist collaboration
• Need for family involvement in psychoeducation
• Use of medication based on algorithm of Paul Soloff6
Clearly, great strides have been made in the recognition and treatment of BPD, but there are many remaining issues that need to be resolved. BPD remains stigmatized, and many mental health professionals want to avoid working with and actively dislike working with patients who have BPD. The disorder also remains far behind in awareness, research and, consequently, public funding. And unless there is a new cadre of young trained investigators, the future for BPD will be bleak. According to Dr Gunderson, many of the original researchers are getting older and are retiring, but there was never enough money or time to train new specialists.
1. Gunderson JG, Kolb JE. Discriminating features of borderline patients. Am J Psychiatry. 1978;135:792-796.
2. Kernberg OF. Structural change and its impediment. In: Hartocollis P, ed. Borderline Personality Disorders. New York: International Universities Press; 1977:275-306.
3. Robbins E, Gruze SB. Establishment of diagnostic validity in psychiatric illness: its application to schizophrenia. Am J Psychiatry. 1970;126:983-987.
4. Siever LJ, Davis KL. A psychobiological perspective on the personality disorders. Am J. Psychiatry. 1991;148:1647-1658.
5. Zanarini MC, Frankenburg FR, Hennen J, Silk KR. The longitudinal course of borderline psychopathology: 6-year prospective follow-up of the phenomenology of borderline personality disorder. Am J Psychiatry. 2003;160:274-283.
6. Soloff PH. Algorithms for pharmacological treatment of personality dimensions: symptom-specific treatments for cognitive-perceptual, affective, and impulsive-behavioral dysregulation. http://www.mhsanctuary.com/Borderline/soloff1.htm. Accessed June 9, 2009.