A Longitudinal Perspective on Personality Disorder

| January 8, 2008 | 0 Comments

by Randy A. Sansone, MD, and Lori A. Sansone, MD

This ongoing column is dedicated to the challenging clinical interface between psychiatry and primary care—two fields that are inexorably linked. In this edition of The Interface, we discuss the symptom fluctuation observed in personality disorder symtomatology.

Dr. R. Sansone is a professor in the Departments of Psychiatry and Internal Medicine at Wright State University School of Medicine in Dayton, Ohio, and Director of Psychiatry Education at Kettering Medical Center in Kettering, Ohio; Dr. L. Sansone is a family medicine physician in practice (government service) at Wright-Patterson Air Force Base.

The views and opinions expressed in this column are those of the authors and do not reflect the official policy or the position of the United States Air Force, Department of Defense, or US government.


Personality disorder symptomatology can appear to exhibit an ethereal quality—the symptoms may be evident at one point in time (i.e., meet diagnostic criteria) but not at other times (i.e., fall below diagnostic threshold). This seeming lack of temporal stability in Axis II disorders may complicate diagnosis and therefore treatment. In this installment of The Interface, we discuss this Axis II clinical phenomenon, which is common in both mental health and primary care settings, and offer a model for conceptualizing personality disorder symptomatology from a longitudinal perspective.

Personality Disorders as “Enduring”

In the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), personality disorders are described as “enduring pattern(s) of inner experience and behavior” that are “inflexible and pervasive.”[1] These DSM descriptors indicate that personality disorder symptomatology is ongoing and ever-present over time (i.e., if an individual has a personality disorder now, he or she will have one in the future).

However, several empirical studies clearly challenge the enduring nature of personality disorders.[2–4] In these studies, participants who were diagnosed with a personality disorder at one point in time seemed to no longer manifest sufficient criteria at a subsequent follow-up point; in other words, they seemed to no longer evidence a personality disorder. Therefore, personality disorders have been described as having only moderate temporal stability in adults. Is there an explanation for this clinical paradox—one that addresses both the enduring yet temporally unstable nature of Axis II symptoms?

A Dynamic View of Personality Disorder Symptomatology

We believe that this confusion can be adequately addressed through a model that we have named the Dynamic Model of Longitudinal Personality Disorder Symptomatology. In this proposed dynamic model, core personality disorder symptoms are ever-present and enduring, but they are in constant dynamic flux, undergoing exacerbation and remission in response to a number of internal and external factors. In other words, from a longitudinal perspective, personality disorder symptomatology exhibits ever-changing amplitudes.

These fluctuations in personality disorder symptomatology are likely to be precipitated by a variety of factors. Examples of factors that may exacerbate symptoms include comorbid Axis I and II disorders, psychosocial stressors, biological stressors, and intoxication/abuse of alcohol/illicit drugs. Examples of factors that may decrease symptoms include psychotherapy, psychotropic medications, and maturation. While not an exclusive list of all of the factors that may temper the amplitude of personality disorder symptoms, there is clinical and empirical data to support each of the preceding contributors.

To illustrate the Dynamic Model of Longitudinal Personality Disorder Symptomatology, we will focus on one specific Axis II disorder as a working example: borderline personality disorder (BPD) (Figure 1).[5] We have elected BPD because it is a relatively common disorder (i.e., according to the DSM,[1] the prevalence in the general population is 2%). In addition, BPD is the personality disorder that has undergone the most empirical investigation. Like the other personality disorders, the symptoms of BPD appear to lack temporal stability. For example, in a study of 290 patients, Zanarini and colleagues found that 73.5 percent of participants no longer evidenced a formal BPD diagnosis at the end of a six-year follow-up period.[6]

Modifiers of BPD Symptomatology

Axis I and II disorders. There is strong empirical evidence that comorbid Axis I and II disorders may intensify the symptoms of BPD.[7,8] For example, Bellino and colleagues found in patients with BPD significant correlations between increasing depression scores and the severity of Axis II symptoms.[9] In turn, the alleviation of Axis I and II disorders appears to decrease the symptoms of BPD. In this regard, Gunderson and colleagues found that the treatment of Axis I disorders was an important determinant of BPD symptom remission.[10]

Psychosocial stressors. Patients with BPD appear to be exquisitely sensitive to a variety of interpersonal and environmental stressors. This hypersensitivity to the external environment has been confirmed under experimental conditions11–16 as well as in clinical studies.[17,18]

r would result in meaningful symptomatic improvement. As expected, Gunderson and colleagues found that the alleviation of situational stressors was one of the major determinants of symptom remission in BPD.[10]

Biological stressors. Biological stressors may also intensify BPD symptoms. As an example, Hull and colleagues reported that physical illness in patients with BPD was synchronized with Axis II acting out.[19]In addition, Frankenburg and Zanarini found that, compared with symptomatically active patients, BPD patients in remission were less likely to have a medical “syndrome-like condition,” such as chronic fatigue syndrome, fibromyalgia, or temporomandibular joint syndrome.[20]

Pain may also be a biological stressor and appears to be very poorly tolerated by patients with BPD.[6] Indeed, Harper stated that, “it [is] particularly difficult for…[the borderline patient]…to endure prolonged acute pain,” and “the borderline patient’s tolerance of discomfort will typically be of shorter duration than other individuals.”[21] While pain intolerance, itself, is not an Axis II symptom, such intolerance is likely to culminate in impulsivity with substances that alleviate pain (i.e., analgesic misuse). In support of this concern, Frankenburg and Zanarini found that remitted BPD patients were less likely to use pain medications than non-remitted patients.[20]

Alcohol/illicit substances. Links and Heslegrave describe impulsivity as a core symptom in individuals with BPD.[7] Alcohol and drugs tend to reduce inhibitions and self-restraint and amplify impulsivity; i.e., in this case, to exacerbate BPD symptoms, especially self-harm and aggressive behaviors. In support of this, Pihl confirmed a relationship between alcohol and substance disinhibition and an increase in BPD symptoms.[22] Likewise, the treatment of alcohol/substance abuse/dependence appears to result in an overall improvement in BPD symptoms. In this regard, Nace, Saxon, and Shore found that recovering alcoholics with BPD evidenced a decrease in hospitalizations as well as improved relationships with offspring.[23] In addition, Schaar and Ojehagen found that a reduction in alcohol and substance use was associated with a reduction in overall BPD symptoms.[24] Finally, Nace affirmed the beneficial effects of alcoholism treatment in individuals with BPD.[25]

Psychotherapy. A number of investigators have described and/or documented the effectiveness of various types of psychotherapy with regard to symptom reductions in BPD. These psychotherapies include dialectical behavior therapy (DBT),[26] systems training for emotional predictability and problem solving (STEPPS),[27] psychodynamically oriented trauma-focused therapy,[28] transference-focused therapy,[29] a conversational therapy model,[30] and intermittent-continuous eclectic therapy.[31] There cognitive-behavioral therapies that appear to be helpful in the treatment of BPD. Regardless of psychotherapy approach, each claims meaningful reductions in BPD symptoms.

Medications. Nearly every type of psychotropic medication has been explored in the treatment of BPD including antidepressants, anticonvulsants, anxiolytics, lithium, and antipsychotics, both typical and atypical. While the overall treatment effects have been modest,[6,32,33] most have resulted in varying degrees of symptom alleviation in patients with BPD.[6,33–35]

Maturity. Because a number of longitudinal follow-up studies indicate symptom remission with time in patients with BPD, one gets the global impression that time alone confers improvement for a substantial percentage of individuals. Therefore, the process of maturation itself may alleviate the symptoms of BPD.


According to the DSM-IV-TR,[1] personality disorders are enduring psychological disorders that are persistent throughout the individual’s lifetime. However, empirical studies indicate that personality disorder symptomatology can undergo unexpected remission, i.e., Axis II symptoms may acutely recede. We believe that viewing personality disorder symptomatology as enduring but ever-fluctuating is a more realistic approach to symptom conceptualization. Further, Axis II symptomatology appears to undergo ongoing exacerbations and remissions as a function of various internal and external influences. To conceptually illustrate this, we offer a longitudinal model of Axis II symptomatology: the Dynamic Model of Longitudinal Personality Disorder Symptomatology. We believe that being aware of this Axis II characteristic may not only improve diagnosis, but also facilitate treatment, both in psychiatric and primary care settings.


1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Press, Inc., 2000.
2. Grilo CM, McGlashan TH. Stability and course of personality disorders. Curr Opin Psychiatry 1999;12:157–62.
3. Grilo CM, McGlashan TH, Skodol AE. Stability and course of personality disorders: The need to consider comorbidities and continuities between Axis I psychiatric disorders and Axis II personality disorders. Psychiatr Q 2000;71:291–307.
4. Johnson JR, Williams JBW, Goetz RR, et al. Stability and change in personality disorder symptomatology: Findings from a longitudinal study of HIV+ and HIV- men. J Abnorm Psychol 1997;106:154–8.
5. Sansone RA, Sansone LA. Pharmacological approaches to borderline personality disorder. In: Sansone RA, Sansone LA (eds). Borderline Personality in the Medical Setting: Unmasking and Managing the Difficult Patient. Hauppauge, NY: Nova Publications, 2007:115–44.
6. Zanarini MC, Frankenburg FR, Hennen J, Silk KR. The longitudinal course of borderline psychopathology: Six-year prospective follow-up of the phenomenology of borderline personality disorder. Am J Psychiatry 2003;160:274–83.
7. Links PS, Heslegrave RJ. Prospective studies of outcome. Understanding mechanisms of change in patients with borderline personality disorder. Psychiatr Clin North Am 2000;23:137–50.
8. Links PS, Heslegrave R, van Reekum R. Prospective follow-up study of borderline personality disorder: Prognosis, prediction of outcome, and Axis II comorbidity. Can J Psychiatry 1998;43:265–70.
9. Bellino S, Patria L, Paradiso E, et al. Major depression in patients with borderline personality disorder: A clinical investigation. Can J Psychiatry 2005;50:234–8.
10. Gunderson JG, Bender D, Sanislow C, et al. Plausibility and possible determinants of sudden “remissions” in borderline patients. Psychiatry (Washington, DC) 2003;66:111–9.
11. Herpertz S, Gretzer A, Steinmeyer EM, et al. Affective instability and impulsivity in personality disorder. Results of an experimental study. J Affect Disord 1997;44:31–7.
12. Conrad SD, Morrow RS. Borderline personality organization, dissociation, and willingness to use force in intimate relationships. Psychology of Men and Masculinity 2000;1:37–48.
13. Domes G, Winter B, Schnell K, et al. The influence of emotions on inhibitory functioning in borderline personality disorder. Psychol Med 2006;36:1163–72.
14. Herpertz S, Gretzer A, Muehlbauer V, et al. Experimental detection of inadequate affect regulation in patients with self-mutilating behavior. Der Nervenarzt 1998;69:410–8.
15. Jennings ME. Emotion regulation in borderline personality disorder: A psychophysiological examination of emotional responding and recovery. Dissert Abstr Int 2004;64:5219B.
16. Korfine L, Hooley JM. Directed forgetting of emotional stimuli in borderline personality disorder. J Abnorm Psychol 2000;109:214–21.
17. Brodsky BS, Groves SA, Oquendo MA, et al. Interpersonal precipitants and suicide attempts in borderline personality disorder. Suicide Life Threat Beh 2006;36:313–22.
18. Daley SE, Burge D, Hammen C. Borderline personality disorder symptoms as predictors of 4-year romantic relationship dysfunction in young women: Addressing issues of specificity. J Abnorm Psychol 2000;109:451–60.
19. Hull JW, Okie J, Gibbons B, Carpenter D. Acting up and physical illness: Temporal patterns and emerging structure. J Am Psychoanal Assoc 1992;40:1161–83.
20. Frankenburg FR, Zanarini MC. The association between borderline personality disorder and chronic medical illnesses, poor health-related lifestyle choices, and costly forms of health care utilization. J Clin Psychiatry 2004;65:1660–5.
21. Harper RG. Borderline personality. In Harper RG (ed). Personality-Guided Therapy in Behavioral Medicine. Washington, DC: American Psychological Association, 2004:179–205.
22. Pihl RO. Personality disorders, behavioral disinhibition, and addition: A commentary. Biol Psychiatry 2007;62:551–2.
23. Nace EP, Saxon JJ, Shore N. Borderline personality disorder and alcoholism treatment: A one-year follow-up study. J Stud Alcohol 1986;47:196–200.
24. Schaar I, Ojehagen A. Severely mentally ill substance abusers: An 18-month follow-up study. Soc Psychiatry Psychiatr Epidemiol 2001;36:70–8.
25. Nace EP. Alcoholism and the borderline patient. In: Silver D, Rosenbluth M (eds). Handbook of Borderline Disorders. Madison, CT: International Universities Press, 1992:599–610.
26. Linehan MM. Cognitive-Behavioral Treatment of Borderline Personality Disorder. New York, NY: Guilford, 1993.
27. Blum N, Pfohl B, St. John DS, et al. STEPPS: A cognitive-behavioral systems-based group treatment for outpatients with borderline personality disorder: A preliminary report. Compr Psychiatry 2002;43:301–10.
28. Sachsse U, Vogel C, Leichsenring F. Results of psychodynamically oriented trauma-focused inpatient treatment for women with complex posttraumatic stress disorder (PTSD) and borderline personality disorder (BPD). Bull Menninger Clin 2006;70:125–44.
29. Clarkin JF, Yeomans FE, Kernberg OF. Psychotherapy for Borderline Personality: Focusing on Object Relations. Washington, DC: American Psychiatric Press, Inc., 2006.
30. Korner A, Gerull F, Meares R, Stevenson J. Borderline personality disorder treated with a conversational model: A replication study. Compr Psychiatry 2006;47:406–11.
31. Menchaca A, Perez O, Peralta A. Intermittent-continuous eclectic therapy: A group approach for borderline personality disorder. J Psychiatr Pract 2007;13:281–4.
32. Soloff PH. Psychopharmacology of borderline personality disorder. Psychiatr Clin North Am 2000;23:169–92.
33. Triebwasser J, Siever LJ. Pharmacotherapy of personality disorders. J Ment Health 2007;16:5–50.
34. Brinkley JR. Pharmacotherapy of borderline states. Psychiatr Clin North Am 1993;16:853–84.
35. Zanarini MC. Update on pharmacotherapy of borderline personality disorder. Curr Psychiatry Rep 2004;6:66–70.

Category: Past Articles, Personality Disorders, Primary Care, Psychiatry, The Interface

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.