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Comprehensive Psychiatry 54 (2013) 321 325


www.elsevier.com/locate/comppsych

Antisocial and borderline personality disorders revisited


Joel Paris, Marie-Pierre Chenard-Poirier, Robert Biskin
Institute of Community and Family Psychiatry, Department of Psychiatry, McGill University, Montreal, Canada

Abstract
Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) have an overlap in both symptoms and risk factors,
suggesting that they might reflect the same form of psychopathology, shaped by gender. However other lines of evidence point to the
presence of partly unique, albeit overlapping, trait dimensions, specifically affective instability which differentiates BPD from ASPD. Our
conclusion is that ASPD and BPD are separate disorders.
2013 Elsevier Inc. All rights reserved.

1. Defining disorders
Fifteen years ago, our research group [1] suggested that
ASPD and BPD could have a common base in personality
traits, and that their behavioral differences could be largely
attributable to gender. This review aims to update research
on these relationships, and to reconsider earlier conclusions.
To examine this question, we conducted a literature search.
Using the keyword antisocial personality disorder and
borderline personality disorder, we found 331 articles published
since 1950, but of these, only 31 were relevant to the issue of
differential diagnosis. The selection was augmented by including
papers that examine theoretical issues related to our question.
ASPD has a very large empirical literature. First described
in the early nineteenth century, terms such as psychopathy,
sociopathy, or dyssocial personality have also been used to
describe this clinical picture [2]. While dissocial personality is
the preferred term in the International Classification of
Diseases [3], psychopathy describes a more specific syndrome
emphasizing abnormal personality traits rather than criminal
and irresponsible patterns of behavior [4], and some of these
traits can be identified early in development [5].
In DSM-5 [6], patients must meet overall criteria for a
personality disorder: impairments in self and interpersonal
relationships, associated with pathological personality traits.
DSM-5 requires general overall criteria for a personality
disorder, with a characteristic trait profile marked by
antagonism (manipulativeness, deceitfulness, callousness,
Corresponding author.
E-mail address: joel.paris@mcgill.ca (J. Paris).
0010-440X/$ see front matter 2013 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.comppsych.2012.10.006

and hostility) and disinhibition (irresponsibility, impulsivity,


and risk-taking). The requirement in DSM-IV [7] that
conduct disorder beginning before the age of 15 must be
present has been removed, but predisposing traits are
assumed to be stable from childhood to adulthood.
Callousness, the hallmark of psychopathy [5], defined as
the absence of concern or guilt over painful experiences felt
or induced in others, is listed as a modifier in children with
conduct disorder. As before, a diagnosis of ASPD can only
be made in patients aged 18 or over.
BPD, which also has a large empirical literature, is
defined in DSM-5 by a personality trait profile consisting of
negative affectivity (emotional lability, anxiousness, separation insecurity, depressiveness) disinhibition (impulsivity
and risk-taking), and antagonism (hostility). Thus the last
two domains overlap both disorders, while negative
affectivity, particularly affective instability (also called
emotional lability or emotional dyresgulation), is more
unique to BPD. One does not usually see this feature in
ASPD, in which comorbidity for anxiety and depression may
be present, but emotions tend to be shallow [2]. In research,
these symptoms are often understood as reflecting affective
instability [8], also called emotional dysregulation [9], and
have been considered to be a core feature of BPD. Moreover,
antagonism takes a different form in BPD: instead of the
manipulativeness, deceitfulness, and callousness that characterize ASPD, one sees persistent anger in response to
slights. Finally, while disinhibition is common to both
disorders, it also presents differently: ASPD patients take
advantage of others, and are irresponsible, impulsive, and
risk-taking, but BPD patients, due to their interpersonal

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J. Paris et al. / Comprehensive Psychiatry 54 (2013) 321325

difficulties, often find themselves in abusive or violent


relationships, leading to higher rates of victimization [10].
There is no age requirement for BPD, and the definition
gives little weight to cognitive symptoms, chronic depersonalization, subdelusional paranoid trends, and auditory
hallucinations that have been shown to differentiate patients
with BPD from those with other forms of personality
disorder [11]. However, similar phenomena, transient and
stress-related, can be seen in ASPD [2]. In summary, while
there remains an overlap, the trait profiles described in DSM5, particularly the predominance of affective instability in
BPD, point to major differences between these disorders.

2. Epidemiological and clinical surveys


ASPD was the first personality disorder for which
epidemiological surveys measured community prevalence
[12,13]. However, prevalence has ranged greatly in different
studies [1418]. If the higher numbers, approaching 4%, are
correct, then ASPD would be one of the more common
mental disorders. While it presents less often in clinical
settings [19], it may be present as a comorbid diagnosis when
other complaints are prominent. In all studies, ASPD is about
five times as common in men as in women. Most
epidemiological studies of BPD [1014] have found BPD
to be less common than ASPD, with a prevalence of less than
1%, or no higher than 2% [20]. While one study [21] found a
much higher prevalence for BPD (over 6%), this probably
reflects an error in methodology, and re-analysis of the data
using more stringent criteria [20] produced a rate consistent
with other research.
The effects of gender are crucial for whether or not ASPD
and BPD are separate or similar disorders. While clinical
populations of BPD are largely female [10], community
studies, with one exception [17], have found an equal
prevalence of men and women [14]. This surprising finding
could be explained if men with BPD are less help-seeking
than women, and/or if they tend to have more subsyndromal features of the disorder [22]. It is also possible that a
failure to observe gender differences reflects a loose
definition of BPD. There are problems with the polythetic
DSM-IV criteria, in that many different combinations of
symptoms can produce the same diagnosis [23]. For this
reason, some researchers have developed a semi-structured
interview to identify a narrower range of patients with more
severe symptoms and problems in multiple domains [24].
Finally, in clinical samples of men with BPD, comorbidity
between ASPD and BPD is rare [25].
Both ASPD and BPD seem to have increased in
prevalence since the Second World War. There is good
support for cohort effects in ASPD, but the evidence for
increases in BPD is indirect [26], based on increases in
accompanying symptoms (parasuicide, youth suicide, and
substance abuse). Research shows cross-cultural differences
in the prevalence of ASPD: for example, Taiwan [27] and

Japan [28] have low rates, while Korea has a higher


prevalence [29]. Unfortunately, there have been no
systematic cross-cultural studies of that kind on BPD. It
has been hypothesized that this disorder is uncommon in
traditional societies, but is increasing in urban areas around
the world [26,30].

3. Risk factors
Like other mental disorders, ASPD and BPD can be
understood in a biopsychosocial model [31]. Genetic
factors account for approximately 40% of the variance in
both personality dimensions [32] and disorders [33].
Although twin studies have not been conducted on
ASPD, heritability has been established for criminality
[34], and for behavioral patterns and traits related to the
disorder [35]. In BPD, twin studies find that genetic factors
account for nearly half the variance [33]. However, the
nature of the vulnerabilities to both disorders is unknown:
while a relationship between impulsive and affective trait
dimensions with central serotonergic activity has been
suggested in BPD [36], no specific genetic polymorphisms
or biomarkers have been identified.
The psychosocial risk factors for ASPD and BPD clearly
overlap. In ASPD, paternal antisocial features, associated
with family dysfunction and parental inconsistency, are long
established risks [37]. Studies of psychological factors in
BPD strongly implicate parental psychopathology family
dysfunction, and psychological trauma, with similar risks in
males and females [38]. However, since these risk factors are
not specific to any mental disorder, their presence in both
ASPD and BPD cannot determine whether they should be
considered separate.

4. Outcome and treatment


A comprehensive study of ASPD outcome [39] found that
by late middle age, most patients no longer meet criteria, but
that many continue to suffer from severe interpersonal
problems and poor work histories. In general, impulsivity is
a trait that tends to burn out as people grow older [40].
Studies of the long-term outcome of BPD, both retrospective
[41], and prospective [42,43], paint a similar picture. Most
patients are no longer diagnosable by middle age, largely due
to reduced impulsivity, while many achieve stable employment, and about half eventually find a stable partner. While
both disorders have suicide rates ranging from 5% to 10%
[44], the overall prognosis of BPD is somewhat more
favorable, while that of ASPD is largely unfavorable. There
is also evidence for increased mortality in ASPD, associated
with risk-taking behaviors and the possibility of becoming a
victim of homicide [2]. These findings point to an essential
distinction between the two disorders.

J. Paris et al. / Comprehensive Psychiatry 54 (2013) 321325

Treatment results reflect these differences in outcome.


ASPD is difficult to treat [45,46], and there is little evidence
that any existing intervention helps. In contrast, clinical trials
show that specialized forms of psychotherapy are often
effective in BPD [46,47]. These findings, which must reflect
the traits underlying these diagnoses, point to separation
between the disorders.

5. Gender, personality, and psychopathology


How gender shapes personality and psychopathology
helps to explain some of the differences between patients
with ASPD or BPD. The most consistent and pervasive
difference affecting interpersonal behavior is in aggressiveness, so that men tend to be more assertive and dominant,
while women tend to be more focused on attachment [48].
These effects of gender on personality are seen in cultures all
over the world: in the Five-Factor Model, neuroticism,
agreeableness, conscientiousness, and extraversion are all
higher in women, while openness to experience is greater in
men [49]. These differences are likely to be intrinsic, and
they are supported by the strong relationship between
testosterone and aggression [50].
Gender differences are also apparent in the most basic
distinction in psychopathology: the distinction between
externalizing and internalizing symptoms [51]. These broad
spectra are sensitive to gender. In children, boys have a much
higher prevalence of externalizing disorders, such as conduct
disorder and attention deficit disorder, while girls are more
likely to develop internalizing disorders, such as anxiety and
mood disorders [52]. In adults, men have a higher rate of
substance abuse, differences that are robust in societies around
the world [53], while women have a higher rate of depression,
a difference that is cross-culturally consistent [54].
It has been suggested that some gender differences could
be artefactual, related to diagnostic criteria that provide
different weightings for internalizing and externalizing
psychopathology [55,56], but that conclusion seems unlikely
[57]. If gender differences are real for the prevalence of
depression and substance abuse, there is no reason to doubt
that they can be just as real in personality disorders.
Finally, while ASPD (and psychopathy) is uncommon in
females, some researchers have found an overlap between
scales measuring psychopathic and borderline features in
female prisoners and students samples [58,59]. However
these findings are based on self-report data in non-clinical
settings, and may not be generalizable to clinical populations. In BPD, while gender clearly shapes clinical
presentation, antisocial features are uncommon [60,61].

6. Diagnostic boundaries
The ultimate source of confusion in separating BPD and
ASPD lies in the way that DSM-IV criteria, the basis for most

323

current epidemiological studies, were written. Surveys


showing that BPD is common in untreated men suggest
that the current definition is too broad, or that it is not picking
up the severe psychopathology that brings patients to clinical
attention. Moreover, as is the case for so many other
categories in the manual, a diagnosis of BPD that requires
only 5 out of 9 listed criteria inevitably leads to heterogeneity.
It is possible that if more criteria (say 7 out of 9) had been
required, researchers would have observed sharper gender
differences in prevalence. Also, if the most characteristic
symptoms of BPD are specific to gender, a semi-structured
interview requiring symptoms in all domains [24] could make
these differences clearer. Research in clinical samples has
found that comorbidity in men with BPD reflects genderspecific patterns, particularly substance abuse [61]. Future
studies will be based on DSM-5, a system that focuses on
characteristic trait profiles. But while the DSM-5 definition of
BPD does not use the same cutoff points for diagnosis, it does
not escape the problem of heterogeneity.
The deeper problem is that in the absence of biological
markers, it is very difficult to say whether patients, male or
female, suffer from one specific mental disorder, and not
from another. Some of these problems may eventually be
illuminated by research, but we still know too little. For
example, while ASPD has a few established biological
markers, such as reduced prefrontal gray matter and
reduced autonomic activity [62], these features are only
consistent when symptomatology is severe. Biological and
genetic markers are even more inconsistent for BPD, with
little specificity [63,64]. In short, while these disorders
share risk factors, clinical outcome reflects the principle of
multifinality [65].

7. Conclusions
The strength of the research literature on ASPD and BPD
supported the retention of these categories in DSM-5, and
both diagnoses will continue to have an impact on practice.
Applying the DSM-5 view of personality disorders, which
focuses on trait profiles, the differences between these
disorders are rooted in trait dimensions shaped by gender.
For this reason, the influence of gender on symptoms is not
an artefact, but a factor that partly determines specific
psychopathological constellations.
In summary, several lines of evidence suggest that BPD
and ASPD are different disorders associated with unique
trait profiles. We therefore reject our earlier conclusion [1],
that ASPD and BPD are different aspects of the same
underlying psychopathology.
References
[1] Paris J. Antisocial and borderline personality disorders: two separate
diagnoses or two aspects of the same psychopathology? Compr
Psychiatry 1997;38:237-42.

324

J. Paris et al. / Comprehensive Psychiatry 54 (2013) 321325

[2] Lykken DT. The antisocial personalities. Berkley, CA: Psychology


Press; 1995.
[3] World Health Organization. International classification of diseases,
10th edition: mental disorders. Geneva: WHO; 1993.
[4] Hare RD, Hart SD, Harpur TJ. Psychopathy and the DSM-IV criteria
for antisocial personality disorder. J Abnorm Psychol 1991;100:391-8.
[5] Rutter M. Psychopathy in childhood: is it a meaningful diagnosis? Br J
Psychiatry 2012;200:191-6.
[6] American Psychiatric Association. Diagnostic and statistical manual of
mental disorders, 5th ed, www.dsm-5.org. [in press].
[7] American Psychiatric Association. Diagnostic and statistical manual of
mental disorders, 3rd ed., text revision. Washington, DC: American
Psychiatric Publishing; 2000.
[8] Koenigsberg H. Affective instability: toward an integration of
neuroscience and psychological perspectives. J Personal Disord
2010;24:60-82.
[9] Gunderson JG, Linehan MM. Cognitive behavioral therapy for
borderline personality disorder. New York: Guilford; 1993.
[10] Gunderson JG, Links P. Borderline personality disorder: a clinical
guide2nd ed. . Washington, DC: American Psychiatric Press; 2007.
[11] Zanarini MC, Gunderson JG, Frankenburg FR. Cognitive features of
borderline personality disorder. Am J Psychiatry 1990;147:57-63.
[12] Robins LN, Regier DA, editors. Psychiatric disorders in America. New
York: Free Press; 1991.
[13] Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M,
Eshleman S. Lifetime and 12-month prevalence of DSM-III-R
psychiatric disorders in the United States. Results from the National
Comorbidity Survey. Arch Gen Psychiatry 1994;51:8-19.
[14] Paris J. Estimating the prevalence of personality disorders. J Pers
Disorders 2010;24:405-11.
[15] Coid J, Yang M, Tyrer P, Roberts A, Ullrich S. Prevalence and
correlates of personality disorder in Great Britain. Br J Psychiatry
2006;188:423-33.
[16] Lenzenweger MF, Lane MC, Loranger AW, Kessler RC. DSM-IV
personality disorders in the National Comorbidity Survey Replication.
Biol Psychiatry 2007;62:553-6.
[17] Torgersen S, Kringlen E, Cramer V. The prevalence of personality
disorders in a community sample. Arch Gen Psychiatry 2001;58:590-6.
[18] Samuels J, Eaton WW, Bienvenu OJ, Nestadt G, Brown CH, Costa PJ.
Prevalence and correlates of personality disorders in a community
sample. Br J Psychiatry 2002;180:536-42.
[19] Zimmerman M, Chelminkis I, Young D. The frequency of personality
disorders in clinical settings. Psychiatr Clin North Am
2008;31:405-20.
[20] Trull TJ, Jahng S, Tomko RL, Wood PK, Sher KJ. Revised NESARC
personality disorder diagnoses: gender, prevalence, and comorbidity
with substance dependence disorders. J Personal Disord 2010;
24:412-26.
[21] Grant BF, Chou SP, Goldstein RB, Huang B, Stinson FS, Saha TD, et
al. Prevalence, correlates, disability, and comorbidity of DSM-IV
borderline personality disorder. J Clin Psychiatry 2008;65:948-58.
[22] Zanarini MC, Frankenburg FR, Reich DB, Silk KR, Hudson JI,
McSweeney LB. The subsyndromal phenomenology of borderline
personality disorder: a 10-year follow-up study. Am J Psychiatry
2007;164:929-35.
[23] Skodol AE, Clark LA, Bender DS, Krueger RF, Morey LC, Verheul R,
et al. Proposed changes in personality and personality disorder
assessment and diagnosis for DSM-5 part I: description and rationale.
Personal Disord Theory Res Treat 2011;2:4-22.
[24] Zanarini MC, Gunderson JG, Frankenburg FR. The revised diagnostic
interview for borderlines: discriminating BPD from other axis II
disorders. J Personal Disord 1989;3:10-8.
[25] Paris J, Zweig-Frank H, Guzder J. Risk factors for borderline
personality in male outpatients. J Nerv Ment Dis 1994;182:375-80.
[26] Paris, J, Lis, E (in press): Can sociocultural and historical mechanisms
influence the development of borderline personality disorder?
Transcult Psychiatry.

[27] Hwu HG, Yeh EK, Change LY. Prevalence of psychiatric disorders in
Taiwan defined by the Chinese Diagnostic Interview Schedule. Acta
Psychiatr Scand 1989;79:136-47.
[28] Sato T, Takeichi M. Lifetime prevalence of specific psychiatric
disorders in a general medicine clinic. Gen Hosp Psychiatry
1993;15:224-33.
[29] Lee KC, Kovac YS, Rhee H. The national epidemiological study of
mental disorders in Korea. J Korean Med Sci 1987;2:19-34.
[30] Millon T. Borderline personality disorder: a psychosocial
epidemic. In: Paris J, editor. Borderline personality disorder: etiology
and treatment. Washington, DC: American Psychiatric Press; 1993.
p. 197-210.
[31] Engel GL. The clinical application of the biopsychosocial model. Am J
Psychiatry 1980;137:535-44.
[32] Jang KL, Livesley WJ, Vernon PA, Jackson DN. Heritability of
personality traits: a twin study. Acta Psychiatr Scand 1996;94:438-44.
[33] Torgersen S, Lygren S, Oien PA, Skre I, Onstad S, Edvardsen J. A twin
study of personality disorders. Compr Psychiatry 2000;41:416-25.
[34] Brennan PA, Mednick SA. Genetic perspectives on crime. Acta
Psychiatr Scand 1993;87:19-26.
[35] Rhee S, Waldman I. Genetic and environmental influences on
antisocial behavior: a meta-analysis of twin and adoption studies.
Psychol Bull 2002;128:490-529.
[36] Siever LJ, Davis KL. A psychobiological perspective on the
personality disorders. Am J Psychiatry 1991;148:1647-58.
[37] Robins L. Deviant children grown up. Baltimore: Williams and
Wilkins; 1966.
[38] Zanarini MC. Childhood experiences associated with the development
of borderline personality disorder. Psychiatr Clin North Am
2000;23:89-101.
[39] Black DW, Baumgard CH, Bell SE. A 1645 year follow-up of 71 men
with antisocial personality disorder. Compr Psychiatry 1995;
36:130-40.
[40] Moeller FG, Barratt ES, Dougherty DM, Schmitz JM, Swann AC.
Psychiatric aspects of impulsivity. Am J Psychiatry 2001;158:1783-93.
[41] Paris J, Zweig-Frank H. A 27-year follow-up of patients with
borderline personality disorder. Compr Psychiatry 2001;42:482-7.
[42] Gunderson JG, Stout RL, McGlashan TH, Shea T, Morey LC, Grilo
CM, et al. Ten-year course of borderline personality disorder:
psychopathology and function from the collaborative longitudinal
personality disorders study. Arch Gen Psychiatry 2011;68:827-37.
[43] Zanarini MC, Frankenburg FR, Reich DB, Fitzmaurice G. Time to
attainment of recovery from borderline personality disorder and
stability of recovery: a 10-year prospective follow-up study. Am J
Psychiatry 2010;167:663-7.
[44] Paris J. Personality disorders over time. Washington DC: American
Psychiatric Press; 2003.
[45] Gibbon S, Vollm BA, Duggan C, Khalifa N, Stoffers J, Huband N, et
al. Pharmacological and psychological interventions for antisocial
personality disorder results of two Cochrane reviews. Eur Psychiatr
Rev 2011;4(1):52-8.
[46] Kendall T, Pilling S, Tyrer P, Duggan C. Borderline and antisocial
personality disorders: summary of NICE guidance. BMJ 2009:338,
http://dx.doi.org/10.1136/bmj.b93.
[47] Paris J. Effectiveness of differing psychotherapy approaches in the
treatment of borderline personality disorder. Curr Psychiatry Rep
2010;12:56-60.
[48] Feingold A. Gender differences in personality: a meta-analysis.
Psychol Bull 1994;116:429-56.
[49] Costa PT, Terracciano A, McCrae RR. Gender differences in
personality traits across cultures: robust and surprising findings. J
Pers Soc Psychol 2001;81:322-31.
[50] Baghaei F, Rosmond R, Landen M, Westberg L, Hellstrand M, Holm
G, et al. Phenotypic and genotypic characteristics of women in relation
to personality traits. Int J Behav Med 2003;10:365-78.
[51] Krueger RF. The structure of common mental disorders. Arch Gen
Psychiatry 1999;56:921-6.

J. Paris et al. / Comprehensive Psychiatry 54 (2013) 321325


[52] Achenbach TM, McConaughy SH. Empirically based assessment of
child and adolescent psychopathology: practical applications. 2nd ed.
Thousand Oaks, CA: Sage; 1997.
[53] Helzer JE, Canino GJ, editors. Alcoholism in North America, Europe,
and Asia. New York: Oxford University Press; 1992.
[54] Weissman MM, Klerman GL. Gender and depression. Trends
Neurosci 1985;8:416-20.
[55] Anderson KG, Sankis LM, Widiger TA. Pathology versus statistical
infrequency: potential sources of gender bias in personality disorder
criteria. J Nerv Ment Dis 2001;189:661-8.
[56] Skodol AE, Bender DS. Why are women diagnosed borderline more
than men? Psychiatr Q 2003;74(4):349-60.
[57] Paris J. Gender differences in personality traits and disorders. Curr
Psychiatry Rep 2004;6(1):71-4.
[58] Hicks BM, Vaidyanathan U, Patrick CJ. Validating female psychopathy subtypes: differences in personality, antisocial and violent
behavior, substance abuse, trauma, and mental health. Personal Disord
Theory Res Treat 2010;1:38-57.
[59] Sprague J, Javdani S, Sadeh N, Newman JP, Verona E.
Borderline personality disorder as a female phenotypic expression

[60]

[61]

[62]

[63]

[64]
[65]

325

of psychopathy. Personal Disord Theory Res Treat 2012;3:


127-39.
Zlotnick C, Rothschild L, Zimmerman M. The role of gender in the
clinical presentation of patients with borderline personality disorder.
J Personal Disord 2002;16:277-82.
Johnson DM, Shea MT, Yen S. Gender differences in borderline
personality disorder: findings from the Collaborative Longitudinal
Personality Disorders Study. Compr Psychiatry 2003;44:284-92.
Raine A, Lencz T, Bihrle S, Lacasse L, Colleti P. Reduced prefrontal
gray matter volume and reduced autonomic activity in antisocial
personality disorder. Arch Gen Psychiatry 2000;57:119-27.
New AS, Goodman M, Triebwasser J, Siever LJ. Recent advances in
the biological study of personality disorders. Psychiatr Clin North Am
2008;31:441-61.
Livesley WJ, Jang K. Behavioral genetics of personality disorder.
Annu Rev Clin Psychol 2008;4:247-74.
Beauchaine TP, Klein DN, Crowell SE, Derbidge C, Gatzke-Kopp L.
Multifinality in the development of personality disorders: a biology
sex environment interaction model of antisocial and borderline traits.
Dev Psychopathol 2009;21(3):735-70.

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