Overlap Between Borderline and Schizotypal Disorders Richard
J. Kavoussi
Borderline personality was split into two diagnotic categories in DSM-III: borderline personality disorder (BPD) and schizotypal personality disorder (SPD). There remains a great deal of diagnostic overlap between these two categories despite modifications in DSMIII-R. This report discusses four possible hypotheses for this overlap: (1) an independent, random association; (2) a&factual overlap due to imperfections in the
S
INCE THE TIME of Bleuler, psychiatrists have identified patients with attenuated symptoms of schizophrenia-poverty of affect, impaired interpersonal relatedness, and magical thinking.‘” Danish adoption studies suggested that these “borderline schizophrenics” had personality features that might represent a phenotypic expression of a “schizophrenic genotype.“’ Simultaneously, other investigators identified a group of patients with unstable affective symptoms and impulsivity who appeared to lie “on the border” of classic affective disorder.‘.” The identification of these two groups of patients led to the development of diagnostic criteria for two separate personality disorders: schizotypal personality disorder (SPD) and borderline personality disorder (BPD).” Yet, although defined as separate diagnostic categories, these personality disorders frequently overlap. The degree of this overlap has ranged from 7% to 58% in samples of borderline and schizotypal patients previously reported in the literature (Table 1). The extent of overlap in these studies is, in part, a function of the particular sample studied. Studies with approximately equal numbers of SPD and BPD in the sample show more overlap, while studies with unequal samples have reported low overlap. Thus, it is imperative to take base rates into account when evaluating studies of diagnostic overlap.” Some changes were made in DSM-III-R in an attempt to reduce the degree of overlap. For example, depersonalization and derealization are no longer examples of unusual sensory experiences for SPD and a new criterion-odd behavior-was added to the criteria for SPD. Still, even with these changes, the degree of overlap is still significant’4-‘h and overlap beComprehens/vefsychiatry,
Vol. 33, No. 1 (January/February),
Personality
and Larry J. Siever criteria sets; (3) a synergistic association of the two personality disorders; and (4) a manifestation of dimensional psychopathology. Empirical evidence for each of the first three hypotheses is weak and contradictory. Recent biologic and treatment studies appear to most strongly support the use of dimensional models of “borderline” and “schizotypal” personality traits. Copyright 0 1992 by W.B. Saunders Company
tween these two disorders remains a concern for DSM-III-R and the development of DSM-IV. This substantial overlap has prompted questions regarding the validity of the current criteria sets for these two personality disorders.” It has also generated concern since accurate diagnosis of these disorders is important in determining response to treatment. There are four plausible hypotheses that might account for the overlap between schizotypal and borderline personality disorders. First, the overlap may simply be an independent, random association between the two personality disorders. Second, the overlap between BPD and SPD may be an artifact of the nature of the criteria sets used in DSM-III and DSM-III-R. Third, there may be an inherent association or “synergism” between these two disorders. Finally, these disorders may not exist as discrete categorical entities, but rather as dimensional manifestations of personality psychopathology. Various empirical methods can be used to test these hypotheses by studying differences between three groups: “pure” BPD, “pure” SPD, and “mixed” BPD-SPD. These methods include phenomenological studies, family history and genetic studies, biologic marker studies, treatment response studies, and outcome studies. In this report, we will present each hypothesis and evaluate the empirical evidence for each.
From the Department of PsychiatT, Medical College of Pennsylvania, Philadelphia, PA; and the Department of Psychiatty, Mount Sinai Medical Center, New York, NY. Address reprint requests to Richard J. Kavoussi, M.D., Department of Psychiatry, Medical College of Pennsylvania at EPPI, 3200 Henry Ave, Philadelphia, PA 19129. Copyright 0 I992 by WB. Saunders Company OOlO-44OXl9213301-0006$03.0010
1992: pp 7-12
7
8
KAVOUSSI
Table 1. Overlap of BPD and SPD Study
S
B
SB
%SB
Silk, 1990’6
0
31
8
20.5
Vaglum.
6
41
7
13.0
Morey, 1988 (DSM-III-R)‘4
27
97
9
6.8
Widiger, 1987”
19
24
29
40.3
McGlashan, 198724
10
81
18
16.5
4
24
18
39.1 39.0
1989 (DSM-III-R)15
George, 198625 Jacobsberg, 198627
19
6
16
F’fohl, 198640
6
23
6
17.1
Baron, 1985’*
16
17
20
37.7
Gunderson, 198321 Spitzer, 197912
8
6
13
48.1
145
170
436
58.0
Abbreviations: S, DSM-III schizotypal personality disorder; B, DSM-III borderline personality disorder; SB, both and borderline
personality
schizotypal
disorder.
RANDOM
OVERLAP
The overlap between BPD and SPD may simply be an independent, random association between the two personality disorders. Then it would be expected that the prevalence of overlap would be equal to the product of the prevalence of each personality disorder (% overlap = %SPD x %BPD). In most studies, the overlap between SPD and BPD has been higher than would be expected by chance association alone (see Table 1). The high degree of overlap in these samples also may reflect the possibility that the overlap group is more ill than those with either SPD or BPD alone and thus are more likely to seek treatment in a clinical setting. Yet, even in nonclinical samples, the degree of overlap is still higher than would be expected from random overlap.‘” Thus, it is unlikely that this hypothesis alone is correct. ARTIFACTUAL
OVERLAP
The overlap between BPD and SPD may be an artifact of the nature of the criteria sets used in DSM-III and DSM-III-R. First, because DSM-III uses a prototypic system of classification, there is much heterogeneity among members of each diagnostic category. For example, there are 93 combinations of criteria that will lead to a diagnosis of BPD. While the sensitivity of a particular diagnostic category is enhanced when there is a broad range of combinations of criteria sufficient to make a diagnosis, such a strategy reduces specificity, leading to increased overlap among diagnostic categories.”
AND
SIEVER
Artifactual overlap also may result from imprecise definitions of criteria. This may be especially true for BPD and SPD, since the criteria for these disorders had their origins in overlapping criteria sets.20For example, Gunderson’s criteria for BPD stress the importance of psychotic-like symptoms while DSM-III does not incorporate criteria for these symptoms. Those who work with clinical samples argue for the importance of including psychotic like experiences in the diagnostic criteria for SPD since this corresponds to current clinical diagnoses and is thus useful to practicing clinicians in their conceptualization of patients. On the other hand, those who study genetic and biological markers of SPD argue that schizotypal patients (as in the original conceptions of Rado and Meehl) should be defined less by psychotic experiences and more by social-interpersonal dysfunction, impoverished affect, asociality, and somatization.” Imprecise criteria for axis II disorders may hinder the differentiation of psychotic-like personality traits in BPD and SPD. Patients meeting criteria for both SPD and BPD may represent those borderlines with psychotic-like features as originally proposed by Gunderson. However, psychotic-like symptoms in the borderline patient may reflect different underlying psychopathology than psychotic-like symptoms in schizotypes, just as psychotic symptoms in bipolar patients do not necessarily reflect the same pathologic process as psychosis in schizophrenics. There are several ways in which psychotic symptoms in borderline patients can occur.2’,23 First, in some borderline patients, mood congruent psychotic symptoms may reflect a coexisting axis I affective disorder and not the underlying psychopathology of this personality disorder. Second, borderline patients may produce dramatic and bizarre psychotic symptoms to engage caregivers or when faced with disruptions in their chaotic interpersonal relations. Third, altered cognitive-perceptual symptoms and paranoia in the borderline may be closely associated with intolerable, intense, and rapidly changing affective states (guilt, anger, sadness, etc.). These types of psychotic symptoms are different from the persistent psychotic-like symptoms (ideas of reference, paranoia, magical thinking) found in
BORDERLINE
AND
SCHIZOTYPAL
OVERLAP
schizotypal patients. DSM-IV will need to address these issues by defining more precisely the nature of psychotic like experiences included in the criteria sets. There are other ways in which current criteria for BPD and SPD may not adequately differentiate affective-related traits from schizophreniarelated traits. For example, both borderline and schizotypal patients can exhibit social isolation and social anxiety, although these are criteria only for SPD. Yet, these symptoms may reflect different underlying psychophysiologic processes. The impairment in affective regulation seen in BPD may lead to intense, stormy relationships resulting in social isolation. Impaired cognitive-perceptual ability in the interpersonal sphere in the schizotypal patient would lead to chronic discomfort around others and a lack of interpersonal contact. Future criteria for these personality disorders must explicitly define these traits to improve their nosologic utility. If the overlap group in a particular study consists of borderline patients with hysterical or transient psychoses who are diagnosed as having both BPD and SPD, then the overlap group should resemble the pure BPD group on the validating measures noted above. There is some empirical support for this model. Several studies have found that patients in the mixed SPDBPD group have symptoms more like pure borderline patients than pure schizotypal patients.‘4.‘5 The overlap group appears to resemble the schizotypal group with respect to psychotic-like SPD criteria (suspiciousness, magical thinking), but is more like the borderline group with respect to the absence of “negative” schizotypal symptoms (social isolation, inadequate rapport).” These findings suggest that the diagnosis of SPD in the overlap group is in part based on the presence of psychotic-like symptoms and may represent an artifact of the criteria sets. Unfortunately, not all studies have replicated these findings.“,” Twin and family studies provide some support for the artifactual overlap hypothesis. In the only twin study conducted to date,2y 33% of monozygotic schizotypal probands and 4% of dizygotic probands were concordant for SPD. On the other hand, none of the monozygotic probands and 29% of dizygotic borderline probands were concordant for BPD. There
9
were no diagnoses of SPD or BPD in the twins of mixed borderline-schizotypal probands. One family study found an increased risk for SPD in the relatives of pure SPD probands and no increased risk of SPD in the relatives of the mixed SPD-BPD sample.‘* Thus, it would appear that pure SPD has a clearer genetic component than both BPD and the overlap group and that the overlap group is a subset of BPD with psychotic-like features. One study looking at discharge status, treatment variables, psychopathology, functional outcome, and global outcome found that the mixed group resembled the pure borderline group more than the pure schizotypal group on most indices of outcome.30 The only measures on which the overlap group resembled the pure SPD group were on lack of drug abuse and problems in heterosexual relationships. Another study also found that while the mixed group was as impaired as schizophrenics at admission (and significantly lower functioning than pure borderlines), at follow-up these patients were functioning as well as the pure borderlines.“’ While these studies would appear to support the artifactual hypothesis, another study found that the mixed diagnosis patients were more like the pure schizotypes in having a poorer outcome than the pure borderlines.” Biologic studies in these groups have not supported the artifactual hypothesis. Amphetamine challenge tests performed on a sample of borderline patients32 demonstrated that those patients with pure BPD showed global improvement in mood, while those patients with both SPD and BPD had an increase in psychotic symptoms and a decreased sense of well-being. Smooth pursuit eye movements were abnormal more often in patients with pure SPD, and the overlap group than in a control group of other personality disorders.33 These findings argue against the artifactual hypothesis as the sole or major cause of the overlap between these personality disorders. SYNERGISTIC
MODEL
A third explanation for the high degree of SPD-BPD overlap is that there is an inherent association or “synergism” between these two disorders. In this model, etiologic factors for each disorder are likely to act together to
10
KAVOUSSI
produce distress and dysfunction as in hypertension and adult onset diabetes. These disorders are associated with each other much more commonly than chance alone would dictate, sharing common etiologic factors (family history, diet, obesity) and outcome (increased risk of arterial disease). One method to investigate synergistic overlap of SPD and BPD is to study the correlation between the DSM-III item sets for each disorder independent of the degree of overlap. In the original study by Spitzer et al.” although there was 58% overlap between the two diagnoses, there was only a .06 correlation between criteria sets. More recent studies have found a somewhat higher correlation between SPD and BPD criteria, ranging from .19 to .62,34-36 suggesting an inherent correlation between the two disorders. If the overlap group represents a synergistic association between SPD and BPD, the mixed group would have characteristics and symptoms not observed in either diagnosis alone. Although, as noted above, several family studies favor the artifactual hypothesis, one study reported higher rates of schizophrenia in the relatives of patients with mixed BPD-SPD than in pure SPD or BPD probands. Unfortunately, there has been little other empirical evidence to support this hypothesis. DIMENSIONAL
MODEL
Since the inception of the DSM-III personality disorders section, many nosologists have argued that it is better to think of personality disorders along dimensions of psychopathology than as categorical entities.” In fact, in attempting to explain the overlap of BPD and SPD, Spitzer and Endicott3’ noted that these disorders may be better considered as independent dimensions of personality that may coexist in the same individual than as mutually exclusive diagnoses. Phenomenological studies have suggested that multidimensional scalings of personality traits have more validity than categorical diagnoses.3y-4’ There is increasing evidence that certain dimensions of psychopathology in personality disordered patients (e.g., affective instability, cognitive-perceptual impairment, impulsivity) may correspond more precisely than categorical
AND SIEVER
diagnoses to biological markers.42 Abnormalities in central serotonergic functioning as measured by the prolactin response to the serotonergic agonist fenfluramine have been associated with disordered impulse control, irritability, and aggressivity in patients with personality disorders, regardless of categorical diagnosis.43 Measures of plasma and cerebral spinal fluid homovanillic acid (HVA), which reflect central dopaminergic functioning, have been found to correlate with “positive” schizotypal symptoms (e.g., magical thinking, ideas of reference), but not with “negative” symptoms (e.g., social isolation, odd speech, inadequate rapport).44,45 Treatment studies also support a dimensional model. In a double-blind trial of haloperidol, amitriptyline, and placebo, haloperidol was significantly better than both amitriptyline and placebo in reducing phobic anxiety, hostility, paranoia, psychoticism, and obsessive symptoms.46No specific differences between diagnostic groups were reported. In another doubleblind study comparing thiothixene with placebo, drug effects were present, but were related more to specific symptoms (such as illusions, ideas of references, phobic anxiety, obsessions, and somatization) than to measures of global improvement across diagnoses.47 In a doubleblind, cross-over study comparing the effects of various medications on the symptoms of borderline personality, the monoamine oxidase inhibitor tranylcypromine was most effective in improving mood and impulse control, while carbamzepine was most effective in the treatment of behavioral dyscontro1.48 These results suggest that treatment response in a given patient depends more on specific dimensions of symptoms, rather than on the categorical personality diagnosis. CONCLUSIONS
None of the above hypotheses fully account for the overlap found between SPD and BPD as defined by DSM-III and DSM-III-R. However, the empirical evidence tends to support the dimensional model of overlap. This model is supported by biologic marker studies, treatment response studies, and conflicting results of empirical studies in categorical models. The association of specific personality traits with specific biological markers and specific treatment re-
BORDERLINE AND SCHIZOTYPAL
OVERLAP
11
sponse suggests that personality pathology may be best studied using dimensional models. Various traits such as impulsivity, avoidance, affective lability, avoidance, and perceptual deficits should be studied independently and correlated with genetic vulnerability, phenomenologic manifestations, biological features, and treatment response. This hypothesis of overlap does not necessarily exclude the previous hypotheses discussed since models of dimensional psychopathology may coexist with categorical models. It is possible for an individual to have traits that occur along a continuum with a syndromal disease state. For example, myocardial oxygen demands
vary across individuals depending on congenital factors, exercise, and life-style. When coronary artery disease occurs, manifestations of this disease will depend as much on preexisting myocardial functioning as on the degree of CAD and can range from no symptoms to angina to myocardial infarction. Similarly, categorical psychiatric disorder will be influenced in their expression by underlying traits that will vary across individuals. Until more empirical data are available, it would be prudent to use both categorical and dimensional models to improve our diagnostic ability with respect to BPD and SPD.
REFERENCES 1. Bleuler E. A Textbook of Psychiatry (1924). Brill A (tram). New York, NY: Macmillan, 1944. 2. Zilboorg G. Ambulatory schizophrenia. Psychiatry 1941;4:149-144. 3. Deutsh H. Some forms of emotional disturbance and their relationship to schizophrenia. Psychoanal Q 1942;ll: 301-321. 4. Hoch P, Polatin P. Pseudoneurotic forms of schizophrenia. Psychiatr Q 1949;23:248-276. 5. Rado S. Dynamics and classification of disordered behavior. Am J Psychiatry 1853;110:406-416. 6. Meehl P: Schizotaxia. schizotypy, and schizophrenia. Am Psycho1 1962;17:827-837. 7. Kendler KS, Gruenberg AM, Strauss JS: An independent analysis of the Copenhagen sample of the Danish adoption study of schizophrenia: II. the relationship between schizotypal personality disorder and schizophrenia. Arch Gen Psychiatry 1981;38:982-984. 8. Kernberg 0. Borderline Conditions and Pathological Narcissism. New York, NY: Aronson, 1975. 9. Gunderson JG. Singer MT. Defining borderline patients. An overview. Am J Psychiatry 1975;132:1-10. IO. Stone MH. The Borderline Syndrome: Constitution, Coping and Character. New York, NY: Aronson. 1978. 1I. Akiskal HS. Subaffective disorders: dysthymic, cyclothymic and bipolar II disorders in the “borderline” realm. Psychiatr Clin North Am 1981;4:25-46. 12. Spitzer RL, Endicott J, Gibbon M. Crossing the border into borderline personality and borderline schizophrenia. Arch Gen Psychiatry 1979;36:17-24. 13. Widiger TA, Frances A, Warner L, Bluhm C. Diagnostic criteria for the borderline and schizotypal personality disorders. J Abnorm Psycho1 1986:95:43-51. 14. Morey LC. Personality disorders in DSM-III and DSM-III-R: convergence, coverage, and internal consistency. Am J Psychiatry 1988;145:573-577. 15. Vaglum P, Friis S, Vaglum S. Larsen F. Comparison between personality disorder diagnoses in DSM-III and DSM-III-R: reliability, diagnostic overlap, predictive validity. Psychopathology 1989:22:309-314. 16. Silk KR, Westen D, Lohr NE, Benjamin J, Gold L.
DSM-III and DSM-III-R schizotypal symptoms in borderline personality disorder. Compr Psychiatry 1990:31:103110. 17. Widiger TA, Frances A, Spitzer RL, Williams JB. The DSM-III-R personality disorders, an overview. Am J Psychiatry 1988;145:786-795. 18. Baron M, Gruen R, Asnis L, Lord S. Familial transmission of schizotypal and borderline personality disorders. Am J Psychiatry 1985;142:927-934. 19. Clarkin JF, Widiger TA, Frances A, Hurt SW, Gilmore M. Prototypic typology and the borderline personality disorder. J Abnorm Psycho1 1983;92:263-275. 20. Perry JC, Klerman GL. The borderline patient: a comparative analysis of four sets of diagnostic criteria. Arch Gen Psychiatry 1978;35:141-152. 21. Gunderson JG. Siever LJ, Spaulding E. The search for a schizotype: crossing the border again. Arch Gen Psychiatry 1983;40:15-22. 22. Pope HG, Jonas JM, Hudson JI, Cohen BM. An empirical study of psychosis in borderline personality disorder. Am J Psychiatry 1985;142:1285-1290. 23. Links PS, Steiner M, Mitton J. Characteristics of psychosis in borderline personality disorder. Psychopathology 1989:22:188-193. 24. McGlashan TH. Testing DSM-III symptom criteria for schizotypal and borderline personality disorders. Arch Gen Psychiatry 1987;44:143-148. 25. George A, Sololf PH. Schizotypal symptoms in patients with borderline personality disorder. Am J Psychiatry 1986:143:212-215. 26. Siever LJ, Klar HM, Coccaro EF, Silverman J. Sween L, Davis KL. Schizotypal and borderline personality overlap. Presented at the American Psychiatric Association Annual Meeting, Chicago, IL, 1987. 27. Jacobsberg L, Hymowitz P, Barasch A, Frances AJ. Symptoms of schizotypal personality. Am J Psychiary 1986; 143:1222-1227. 28. Widiger TA, Frances A, Trull TJ. A psychometric analysis of the social-interpersonal and cognitive-perceptual items for the schizotypal personality disorder. Arch Gen Psychiatry 1987;44:741-746.
12
29. Torgessen S. Genetic and nosological aspects of schizotypal and borderline personality disorders: a twin study. Arch Gen Psychiatry 1984;41:555-564. 30. McGlashan TH: Schizotypal personality disorder: Chestnut Lodge follow-up study: Long-term follow-up perspectives. Arch Gen Psychiatry 1986;43:329-334. 31. Plakun EM, Burkhardt PE, Muller JP. 14-year follow up of borderline and schizotypal personality disorders. Compr Psychiatry 1985;24:119-212. 32. Schulz SC, Cornelius J, Schulz PM, Soloff PM. The amphetamine challenge test in patients with borderline disorder. Am J Psychiatry 1988;145:809-814. 33. Siever LJ, Keefe R, Bernstein DP, Coccaro EF, Klar HM, Zemishlary Z, et al. Eye tracking impairment in clinically identified patients with schizotypal personality disorder. Am J Psychiatry 1990;147:740-745 34. Kass F, Skodol AE, Charles E, Spitzer R, Williams JB. Scaled ratings of DMS-III personality disorders. Am J Psychiatry 1985;142:627-630. 35. Hyler S, Lyons M. Factor analysis of the DSM-III personality disorder clusters. Compr Psychiatry 1988;29:304308. 36. Livesley WJ, Jackson DN. The internal consistency and factorial structure of behaviors judged to be associated with DSM-III personality disorders. Am J Psychiatry 1986; 143:1473-1474. 37. Soloff PH, Millward JW. Psychiatric disorders in the families of borderline patients. Arch Gen Psychiatry 1983;40: 37-44. 38. Spitzer RL, Endicott J. Justification for separating schizotypal and borderline personality disorders. Schizophr Bull 1979;5:95-100. 39. Widiger TA, Trull TJ, Hurt SW, Clarkin J, Frances A. A multidimensional scaling of the DSM-III personality disorders. Arch Gen Psychiatry 1987;44:557-563. 40. Livesley WJ, Schroeder ML: Dimensions of personality disorder: the DSM-III-R cluster A diagnoses. J Nerv Ment Dis 1990;178:627-635.
KAVOUSSI
AND SIEVER
41. Zimmerman M, Coryell WI-I. DSM-III personality disorder dimensions. J Nerv Ment Dis 1990;178:686-692. 42. Siever LJ, Klar H, Coccaro E. Psychobiologic substrates of personality. In: Klar H, Siever LJ (ed): Biologic Response Styles: Clinical Implications. Washington, DC: American Psychiatric Press, 1985, pp 38-66. 43. Coccaro EF, Siever LJ, Klar HM, Maurer G, Cochrane K, Cooper TB, et al. Serotonergic studies in affective and personality disorder patients: correlations with behavioral aggression and impulsivity. Arch Gen Psychiatry 1989; 46:587-599. 44. Siever LJ, Amin F, Coccaro EF, Bernstein D, Kavoussi RJ, Kalus 0, et al. Plasma homovanillic acid in schizotypal personality disorder. Am J Psychiatry 1991;148: 1246-1248. 45. Amin F, Coccaro EF, Trestman RL, Knott P, Mahon T, Davidson M, et al. CSF HVA concentrations in schizotypal and other personality disorders. Presented at the Society of Biological Psychiatry Annual Meeting, New Orleans, LA, May 1991. 46. Soloff PH, George A, Nathan RS, Schulz PM, Ulrich RF, Perel JM. Progress in pharmacotherapy of borderline disorders: a double blind study of amitriptyline, haloperidol, and placebo. Arch Gen Psychiatry 1986;43:691-697. 47. Goldberg SC, Schulz SC, Schulz PM, Resnick RJ, Hamer RM, Friedel RO. Borderline and schizotypal patients treated with low dose thiothixene vs placebo. Arch Gen Psychiatry 1986;43:680-686. 48. Cowdry RW, Gardner DL. Pharmacotherapy of borderline personality disorder: alprazolam, carbamazepine, trifluoperazine, and tranylcypromine. Arch Gen Psychiatry 1988;45:111-119. 49. Pfohl B, Coryell W, Zimmerman M, Stangl D. DSMIII personality disorders: diagnostic overlap and internal consistency of individual DSM-III criteria. Compr Psychiatry 1986; 27121-34.
J. Kavoussi
Borderline personality was split into two diagnotic categories in DSM-III: borderline personality disorder (BPD) and schizotypal personality disorder (SPD). There remains a great deal of diagnostic overlap between these two categories despite modifications in DSMIII-R. This report discusses four possible hypotheses for this overlap: (1) an independent, random association; (2) a&factual overlap due to imperfections in the
S
INCE THE TIME of Bleuler, psychiatrists have identified patients with attenuated symptoms of schizophrenia-poverty of affect, impaired interpersonal relatedness, and magical thinking.‘” Danish adoption studies suggested that these “borderline schizophrenics” had personality features that might represent a phenotypic expression of a “schizophrenic genotype.“’ Simultaneously, other investigators identified a group of patients with unstable affective symptoms and impulsivity who appeared to lie “on the border” of classic affective disorder.‘.” The identification of these two groups of patients led to the development of diagnostic criteria for two separate personality disorders: schizotypal personality disorder (SPD) and borderline personality disorder (BPD).” Yet, although defined as separate diagnostic categories, these personality disorders frequently overlap. The degree of this overlap has ranged from 7% to 58% in samples of borderline and schizotypal patients previously reported in the literature (Table 1). The extent of overlap in these studies is, in part, a function of the particular sample studied. Studies with approximately equal numbers of SPD and BPD in the sample show more overlap, while studies with unequal samples have reported low overlap. Thus, it is imperative to take base rates into account when evaluating studies of diagnostic overlap.” Some changes were made in DSM-III-R in an attempt to reduce the degree of overlap. For example, depersonalization and derealization are no longer examples of unusual sensory experiences for SPD and a new criterion-odd behavior-was added to the criteria for SPD. Still, even with these changes, the degree of overlap is still significant’4-‘h and overlap beComprehens/vefsychiatry,
Vol. 33, No. 1 (January/February),
Personality
and Larry J. Siever criteria sets; (3) a synergistic association of the two personality disorders; and (4) a manifestation of dimensional psychopathology. Empirical evidence for each of the first three hypotheses is weak and contradictory. Recent biologic and treatment studies appear to most strongly support the use of dimensional models of “borderline” and “schizotypal” personality traits. Copyright 0 1992 by W.B. Saunders Company
tween these two disorders remains a concern for DSM-III-R and the development of DSM-IV. This substantial overlap has prompted questions regarding the validity of the current criteria sets for these two personality disorders.” It has also generated concern since accurate diagnosis of these disorders is important in determining response to treatment. There are four plausible hypotheses that might account for the overlap between schizotypal and borderline personality disorders. First, the overlap may simply be an independent, random association between the two personality disorders. Second, the overlap between BPD and SPD may be an artifact of the nature of the criteria sets used in DSM-III and DSM-III-R. Third, there may be an inherent association or “synergism” between these two disorders. Finally, these disorders may not exist as discrete categorical entities, but rather as dimensional manifestations of personality psychopathology. Various empirical methods can be used to test these hypotheses by studying differences between three groups: “pure” BPD, “pure” SPD, and “mixed” BPD-SPD. These methods include phenomenological studies, family history and genetic studies, biologic marker studies, treatment response studies, and outcome studies. In this report, we will present each hypothesis and evaluate the empirical evidence for each.
From the Department of PsychiatT, Medical College of Pennsylvania, Philadelphia, PA; and the Department of Psychiatty, Mount Sinai Medical Center, New York, NY. Address reprint requests to Richard J. Kavoussi, M.D., Department of Psychiatry, Medical College of Pennsylvania at EPPI, 3200 Henry Ave, Philadelphia, PA 19129. Copyright 0 I992 by WB. Saunders Company OOlO-44OXl9213301-0006$03.0010
1992: pp 7-12
7
8
KAVOUSSI
Table 1. Overlap of BPD and SPD Study
S
B
SB
%SB
Silk, 1990’6
0
31
8
20.5
Vaglum.
6
41
7
13.0
Morey, 1988 (DSM-III-R)‘4
27
97
9
6.8
Widiger, 1987”
19
24
29
40.3
McGlashan, 198724
10
81
18
16.5
4
24
18
39.1 39.0
1989 (DSM-III-R)15
George, 198625 Jacobsberg, 198627
19
6
16
F’fohl, 198640
6
23
6
17.1
Baron, 1985’*
16
17
20
37.7
Gunderson, 198321 Spitzer, 197912
8
6
13
48.1
145
170
436
58.0
Abbreviations: S, DSM-III schizotypal personality disorder; B, DSM-III borderline personality disorder; SB, both and borderline
personality
schizotypal
disorder.
RANDOM
OVERLAP
The overlap between BPD and SPD may simply be an independent, random association between the two personality disorders. Then it would be expected that the prevalence of overlap would be equal to the product of the prevalence of each personality disorder (% overlap = %SPD x %BPD). In most studies, the overlap between SPD and BPD has been higher than would be expected by chance association alone (see Table 1). The high degree of overlap in these samples also may reflect the possibility that the overlap group is more ill than those with either SPD or BPD alone and thus are more likely to seek treatment in a clinical setting. Yet, even in nonclinical samples, the degree of overlap is still higher than would be expected from random overlap.‘” Thus, it is unlikely that this hypothesis alone is correct. ARTIFACTUAL
OVERLAP
The overlap between BPD and SPD may be an artifact of the nature of the criteria sets used in DSM-III and DSM-III-R. First, because DSM-III uses a prototypic system of classification, there is much heterogeneity among members of each diagnostic category. For example, there are 93 combinations of criteria that will lead to a diagnosis of BPD. While the sensitivity of a particular diagnostic category is enhanced when there is a broad range of combinations of criteria sufficient to make a diagnosis, such a strategy reduces specificity, leading to increased overlap among diagnostic categories.”
AND
SIEVER
Artifactual overlap also may result from imprecise definitions of criteria. This may be especially true for BPD and SPD, since the criteria for these disorders had their origins in overlapping criteria sets.20For example, Gunderson’s criteria for BPD stress the importance of psychotic-like symptoms while DSM-III does not incorporate criteria for these symptoms. Those who work with clinical samples argue for the importance of including psychotic like experiences in the diagnostic criteria for SPD since this corresponds to current clinical diagnoses and is thus useful to practicing clinicians in their conceptualization of patients. On the other hand, those who study genetic and biological markers of SPD argue that schizotypal patients (as in the original conceptions of Rado and Meehl) should be defined less by psychotic experiences and more by social-interpersonal dysfunction, impoverished affect, asociality, and somatization.” Imprecise criteria for axis II disorders may hinder the differentiation of psychotic-like personality traits in BPD and SPD. Patients meeting criteria for both SPD and BPD may represent those borderlines with psychotic-like features as originally proposed by Gunderson. However, psychotic-like symptoms in the borderline patient may reflect different underlying psychopathology than psychotic-like symptoms in schizotypes, just as psychotic symptoms in bipolar patients do not necessarily reflect the same pathologic process as psychosis in schizophrenics. There are several ways in which psychotic symptoms in borderline patients can occur.2’,23 First, in some borderline patients, mood congruent psychotic symptoms may reflect a coexisting axis I affective disorder and not the underlying psychopathology of this personality disorder. Second, borderline patients may produce dramatic and bizarre psychotic symptoms to engage caregivers or when faced with disruptions in their chaotic interpersonal relations. Third, altered cognitive-perceptual symptoms and paranoia in the borderline may be closely associated with intolerable, intense, and rapidly changing affective states (guilt, anger, sadness, etc.). These types of psychotic symptoms are different from the persistent psychotic-like symptoms (ideas of reference, paranoia, magical thinking) found in
BORDERLINE
AND
SCHIZOTYPAL
OVERLAP
schizotypal patients. DSM-IV will need to address these issues by defining more precisely the nature of psychotic like experiences included in the criteria sets. There are other ways in which current criteria for BPD and SPD may not adequately differentiate affective-related traits from schizophreniarelated traits. For example, both borderline and schizotypal patients can exhibit social isolation and social anxiety, although these are criteria only for SPD. Yet, these symptoms may reflect different underlying psychophysiologic processes. The impairment in affective regulation seen in BPD may lead to intense, stormy relationships resulting in social isolation. Impaired cognitive-perceptual ability in the interpersonal sphere in the schizotypal patient would lead to chronic discomfort around others and a lack of interpersonal contact. Future criteria for these personality disorders must explicitly define these traits to improve their nosologic utility. If the overlap group in a particular study consists of borderline patients with hysterical or transient psychoses who are diagnosed as having both BPD and SPD, then the overlap group should resemble the pure BPD group on the validating measures noted above. There is some empirical support for this model. Several studies have found that patients in the mixed SPDBPD group have symptoms more like pure borderline patients than pure schizotypal patients.‘4.‘5 The overlap group appears to resemble the schizotypal group with respect to psychotic-like SPD criteria (suspiciousness, magical thinking), but is more like the borderline group with respect to the absence of “negative” schizotypal symptoms (social isolation, inadequate rapport).” These findings suggest that the diagnosis of SPD in the overlap group is in part based on the presence of psychotic-like symptoms and may represent an artifact of the criteria sets. Unfortunately, not all studies have replicated these findings.“,” Twin and family studies provide some support for the artifactual overlap hypothesis. In the only twin study conducted to date,2y 33% of monozygotic schizotypal probands and 4% of dizygotic probands were concordant for SPD. On the other hand, none of the monozygotic probands and 29% of dizygotic borderline probands were concordant for BPD. There
9
were no diagnoses of SPD or BPD in the twins of mixed borderline-schizotypal probands. One family study found an increased risk for SPD in the relatives of pure SPD probands and no increased risk of SPD in the relatives of the mixed SPD-BPD sample.‘* Thus, it would appear that pure SPD has a clearer genetic component than both BPD and the overlap group and that the overlap group is a subset of BPD with psychotic-like features. One study looking at discharge status, treatment variables, psychopathology, functional outcome, and global outcome found that the mixed group resembled the pure borderline group more than the pure schizotypal group on most indices of outcome.30 The only measures on which the overlap group resembled the pure SPD group were on lack of drug abuse and problems in heterosexual relationships. Another study also found that while the mixed group was as impaired as schizophrenics at admission (and significantly lower functioning than pure borderlines), at follow-up these patients were functioning as well as the pure borderlines.“’ While these studies would appear to support the artifactual hypothesis, another study found that the mixed diagnosis patients were more like the pure schizotypes in having a poorer outcome than the pure borderlines.” Biologic studies in these groups have not supported the artifactual hypothesis. Amphetamine challenge tests performed on a sample of borderline patients32 demonstrated that those patients with pure BPD showed global improvement in mood, while those patients with both SPD and BPD had an increase in psychotic symptoms and a decreased sense of well-being. Smooth pursuit eye movements were abnormal more often in patients with pure SPD, and the overlap group than in a control group of other personality disorders.33 These findings argue against the artifactual hypothesis as the sole or major cause of the overlap between these personality disorders. SYNERGISTIC
MODEL
A third explanation for the high degree of SPD-BPD overlap is that there is an inherent association or “synergism” between these two disorders. In this model, etiologic factors for each disorder are likely to act together to
10
KAVOUSSI
produce distress and dysfunction as in hypertension and adult onset diabetes. These disorders are associated with each other much more commonly than chance alone would dictate, sharing common etiologic factors (family history, diet, obesity) and outcome (increased risk of arterial disease). One method to investigate synergistic overlap of SPD and BPD is to study the correlation between the DSM-III item sets for each disorder independent of the degree of overlap. In the original study by Spitzer et al.” although there was 58% overlap between the two diagnoses, there was only a .06 correlation between criteria sets. More recent studies have found a somewhat higher correlation between SPD and BPD criteria, ranging from .19 to .62,34-36 suggesting an inherent correlation between the two disorders. If the overlap group represents a synergistic association between SPD and BPD, the mixed group would have characteristics and symptoms not observed in either diagnosis alone. Although, as noted above, several family studies favor the artifactual hypothesis, one study reported higher rates of schizophrenia in the relatives of patients with mixed BPD-SPD than in pure SPD or BPD probands. Unfortunately, there has been little other empirical evidence to support this hypothesis. DIMENSIONAL
MODEL
Since the inception of the DSM-III personality disorders section, many nosologists have argued that it is better to think of personality disorders along dimensions of psychopathology than as categorical entities.” In fact, in attempting to explain the overlap of BPD and SPD, Spitzer and Endicott3’ noted that these disorders may be better considered as independent dimensions of personality that may coexist in the same individual than as mutually exclusive diagnoses. Phenomenological studies have suggested that multidimensional scalings of personality traits have more validity than categorical diagnoses.3y-4’ There is increasing evidence that certain dimensions of psychopathology in personality disordered patients (e.g., affective instability, cognitive-perceptual impairment, impulsivity) may correspond more precisely than categorical
AND SIEVER
diagnoses to biological markers.42 Abnormalities in central serotonergic functioning as measured by the prolactin response to the serotonergic agonist fenfluramine have been associated with disordered impulse control, irritability, and aggressivity in patients with personality disorders, regardless of categorical diagnosis.43 Measures of plasma and cerebral spinal fluid homovanillic acid (HVA), which reflect central dopaminergic functioning, have been found to correlate with “positive” schizotypal symptoms (e.g., magical thinking, ideas of reference), but not with “negative” symptoms (e.g., social isolation, odd speech, inadequate rapport).44,45 Treatment studies also support a dimensional model. In a double-blind trial of haloperidol, amitriptyline, and placebo, haloperidol was significantly better than both amitriptyline and placebo in reducing phobic anxiety, hostility, paranoia, psychoticism, and obsessive symptoms.46No specific differences between diagnostic groups were reported. In another doubleblind study comparing thiothixene with placebo, drug effects were present, but were related more to specific symptoms (such as illusions, ideas of references, phobic anxiety, obsessions, and somatization) than to measures of global improvement across diagnoses.47 In a doubleblind, cross-over study comparing the effects of various medications on the symptoms of borderline personality, the monoamine oxidase inhibitor tranylcypromine was most effective in improving mood and impulse control, while carbamzepine was most effective in the treatment of behavioral dyscontro1.48 These results suggest that treatment response in a given patient depends more on specific dimensions of symptoms, rather than on the categorical personality diagnosis. CONCLUSIONS
None of the above hypotheses fully account for the overlap found between SPD and BPD as defined by DSM-III and DSM-III-R. However, the empirical evidence tends to support the dimensional model of overlap. This model is supported by biologic marker studies, treatment response studies, and conflicting results of empirical studies in categorical models. The association of specific personality traits with specific biological markers and specific treatment re-
BORDERLINE AND SCHIZOTYPAL
OVERLAP
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sponse suggests that personality pathology may be best studied using dimensional models. Various traits such as impulsivity, avoidance, affective lability, avoidance, and perceptual deficits should be studied independently and correlated with genetic vulnerability, phenomenologic manifestations, biological features, and treatment response. This hypothesis of overlap does not necessarily exclude the previous hypotheses discussed since models of dimensional psychopathology may coexist with categorical models. It is possible for an individual to have traits that occur along a continuum with a syndromal disease state. For example, myocardial oxygen demands
vary across individuals depending on congenital factors, exercise, and life-style. When coronary artery disease occurs, manifestations of this disease will depend as much on preexisting myocardial functioning as on the degree of CAD and can range from no symptoms to angina to myocardial infarction. Similarly, categorical psychiatric disorder will be influenced in their expression by underlying traits that will vary across individuals. Until more empirical data are available, it would be prudent to use both categorical and dimensional models to improve our diagnostic ability with respect to BPD and SPD.
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