The Journal of Forensic Psychiatry & Psychology, 2014

Vol. 25, No. 6, 658672, http://dx.doi.org/10.1080/14789949.2014.943797

Antisocial personality disorder comorbid with borderline

pathology and psychopathy is associated with severe violence
in a forensic sample
Richard C. Howarda*, Najat Khalifaa,b and Conor Duggana,c
a
Institute of Mental Health, Nottingham, UK; bNottinghamshire Healthcare Trust, Wells
Road Centre, Nottingham, UK; cPartnerships in Care, Calverton Hill Hospital, Arnold,
UK

(Received 16 May 2014; accepted 8 July 2014)

Background: Evidence suggests the relationship between personality disorder (PD) and violence in offenders might be claried by considering subgroups of PD offenders dened by patterns of PD comorbidity. Aim: to
identify patterns of PD comorbidity associated with severe violence,
dened by its severity, quantity and age of onset (Violence Index: VI) in a
forensic sample of 100 PD offenders. Methods: Correlations were rst
computed between VI and a range of personality and criminological variables; next, patients with antisocial/borderline comorbidity were compared
with other PD patients; nally, regression analysis was conducted to identify unique predictors of VI. Results: The antisocial deviance factor of psychopathy and antisocial/borderline comorbidity were each signicantly and
independently associated with severe violence. Patients showing both a
high psychopathy score and antisocial/borderline comorbidity had a signicantly greater VI than those without these characteristics. Conclusion: PD
patients with high psychopathy co-occurring with borderline and antisocial
PDs show a criminal prole characterised by a high degree of serious violence.
Keywords: personality disorder; psychopathy; antisocial; borderline;
comorbidity; violence

Introduction
Personality disorder, comorbidity and violence
Despite a well-documented association between personality disorders (PDs)
and violence (Yu, Geddes, & Fazel, 2012), the nature of this link remains
obscure (Duggan & Howard, 2009). Yu et al. (2012) reported a threefold
increase in odds of violent outcomes in individuals with all PDs compared
with general population controls, increasing to an odds ratio of 12.8 for those
with antisocial PD (ASPD). Nonetheless, only 14% of those with ASPD were
*Corresponding author. Email: richard.howard@nottingham.ac.uk
2014 Taylor & Francis

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violent, and Yu et al.s results highlighted the importance of considering subgroups, particularly those dened by gender and PD comorbidity, in the nexus
between PD and violence. A recent study of American prisoners further underlines the importance of considering PD comorbidity when considering the relationship between psychopathology and violent crime (Baskin-Sommers,
Baskin, Sommers, & Newman, 2013). In this study, comorbidity between
ASPD and psychopathy, dened by a high score on the Psychopathy Checklist-Revised (PCL-R: Hare, 2003), was associated with signicant increases in
both the severity and versatility of violent offending.
Another comorbidity commonly reported in forensic samples, particularly
at the high severity end of the PD spectrum, is the co-occurrence of antisocial
with borderline PD (Becker, Grilo, Edell, & McGlashan, 2000; Coid et al.,
2009; Duggan & Howard, 2009). This co-occurrence likely reects risk factors
that these PDs share in common over and above those that convey risk for
cluster B PDs in general (Torgersen et al., 2008). Antisocial/borderline comorbidity has been found to be associated with a broad spectrum of antisocial outcomes, including violence, and with the presence of comorbid Axis I
disorders, particularly severe childhood conduct disorder and drug/alcohol
dependence, and with cognitive disturbance (Freestone, Howard, Coid, &
Ullrich, 2012).
A caveat regarding comorbidity
Use of the term comorbidity here should not be taken to imply that ASPD
and BPD represent true disorders, i.e. discrete clinical entities, nor that antisocial/borderline comorbidity represents a super-disorder. Rather, as suggested
by the networks perspective proposed by Borsboom and Cramer (2013), the
symptoms and traits of ASPD and BPD can be seen as representing a complex
network of causally interlinked thoughts, feelings and behaviours that are
linked not just with each other, but also with traits/symptoms of other disorders, including Axis I disorders. According to this network perspective, symptoms and traits that are shared by both ASPD and BPD, e.g. impulsivity,
hostility, are said to act as bridge symptoms that connect the two disorders
and enable causal relationships to be established between their symptoms and
traits. In this context it is important, when addressing the relationship between
PD and violence, to consider higher order dimensions of personality disorder
that cut across conventional PD categories and that may underlie PDs conceived more broadly, as coherent constellations of traits.
Blackburn, Logan, Renwick and Donnelly (2005) were able to identify two
high-order dimensions of personality disorder based on factor analysis of
responses made by mentally disordered offenders to items in the International
Personality Disorder Examination (IPDE: Loranger et al., 1994). One
dimension, labelled acting out by Blackburn et al. (2005) and considered as
equivalent to psychopathy, was construed as externalising. ASPD loaded

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strongly (.65) on this dimension, while borderline PD loaded strongly (.70) on

a second dimension, labelled anxious inhibited, construed as internalising.
Co-occurring ASPD/BPD can therefore be regarded as a particularly severe
form of PD characterised by high levels of both internalising and externalising
personality traits that manifest as disturbances in affect/emotion, cognition and
behaviour. These, in turn, would be expected to give rise to a propensity to
engage in seriously violent criminal conduct.
The present study
While longitudinal studies will ultimately be required to denitively answer the
question of whether, and how, PD is causally related to violence, nonetheless
cross-sectional studies offer two possible research strategies. The rst, in which
violence is treated as an independent variable, is illustrated by a recent study
by Schroeder, Ifand, Hill, Berner, and Briken (2013). Offenders were categorised by severity of violent offences in their history, ranging from low (no violent offences) to high (both sexual and violent [S + V] offending). Importantly,
in comparison with other groups of offenders, S + V offenders showed the
highest rates of PD overall (68.3%), with every second offender being diagnosed with ASPD and every third offender with BPD. Comorbidity between
ASPD and BPD was not considered in this study.
An alternative approach, adopted in the current study, is to treat violence
as a dependent variable and to attempt to identify those personality features
that, in a sample of male forensic PD patients, are uniquely associated with
violence, and could therefore be said to characterise individuals who suffer
from a particularly severe form of PD, and give rise to a propensity to engage
in severely violent conduct. Consistent with the suggestion that violence measurement should move from simply dening violence towards quantication
across different dimensions of violence (Harris, Oakley, & Picchioni, 2013),
violence as an outcome was operationalised using a Violence Index (VI) which
summed scores across three dimensions: rst, its severity, indexed by the
degree of harm inicted on the victim by the patient; second, the amount of
violence shown during the patients criminal career, indexed by the number of
convictions for violence; and third, the age at which the patients violence
started, younger age of onset indicating more serious and persistent violence
(Stattin & Magnusson, 1996; Tolan & Gorman-Smith, 1998).
We hypothesised, rst, that those patients showing antisocial/borderline PD
comorbidity would be identiable by a broad spectrum of PD comorbidity and
a history of severe childhood CD, as indicated by previous research (Freestone
et al., 2012). Since this comorbid group appears to show a blend of externalising and internalising psychopathology, we further hypothesised that they would
show high scores on both the acting out (externalising) and anxious inhibited (internalising) IPDE factors identied by Blackburn et al. (2005). IPDE
items (see Table 1) contributing to acting out include those related to early

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661

Table 1. IPDE items contributing to the acting out and anxious inhibited IPDE
factors described by Blackburn et al. (2005).
Factor 1 acting out

Factor 2 anxious inhibited

APD7: Lack of remorse (.62)

AVO5: Inhibited in new interpersonal

situations (.68)
AVO6: Views self as inept (.65)
TYP1: Ideas of reference (.58)
TYP9: Excessive social anxiety (.53)

CD2: Initiated ghts before age 15 (.62)

CD4: Cruel to people before age 15 (.60)
CD1: Often bullied others before age 15
(.60)
APD2: Repeated lying (.51)
APD4: Irritable and aggressive (.49)
NAR7: Lacks empathy (.48)
BOR4: Impulsivity (.45)
CD12: Stole without confronting victim
before age 15 (.45)
NAR6: Exploitative (.44)
BOR8: Inappropriate anger (.43)
HIS6: Exaggerated emotion (.42)
HIS8: Considers relationships intimate (.41)
CD5: Cruel to animals before age 15 (.41)
NAR5: Sense of entitlement (.39)
NAR1: Grandiose self-importance (.39)
HIS2: Sexually seductive (.36)
CD6: Stole while confronting victim before
15 (.36)
APD5: Reckless disregard for safety (.35)

BOR7: Chronic emptiness (.51)

BOR6: Affective instability (.50)
AVO1: Avoids contact at work (.47)
PAR2: Doubts loyalty or trustworthiness
(.46)
DEP4: Difculty doing things on his
own (.46)
AVO7: Avoids personal risks (.45)
TYP3: Unusual perceptual experiences
(.45)
BOR9: Paranoid ideation (.44)
BOR5: Recurrent suicidal gestures (.41)
PAR3: Reluctant to conde (.39)
DEP1: Needs reassurance (.38)
CD15: Often truant at school (.38)
TYP5: Suspiciousness (.36)
SCH5: Lacks close friends (.34)
PAR1: Suspects exploitation or harm
(.33)

CD13: Often stayed out at night before 15

(.33)
NAR4: Requires admiration (.32)
Notes: Factor loadings are in brackets. Abbreviations (with their corresponding IPDE dimensional
item numbers) refer to the following DSM-IV Axis I/Axis II disorders: APD: antisocial personality
disorder; BOR: borderline personality disorder; CD: childhood conduct disorder; HIS; histrionic
personality disorder; NAR: narcissistic personality disorder; AVO: avoidant personality disorder;
TYP: schizotypal personality disorder; PAR: paranoid personality disorder; and DEP: dependent
personality disorder.

antisocial deviance, grandiosity, impulsivity, lack of emotion, emotional dysregulation and traits of psychopathy commonly measured using the Psychopathy Checklist-Revised (PCL-R: Hare, 2003).
We further hypothesised that while there would be some overlap between
antisocial/borderline PD comorbidity and PCL-R psychopathy, each would, in
regression analysis, independently predict violence operationalised by VI, even
when other variables expected to correlate with violence, including impulsiveness and acting out, were accounted for. Since evidence suggests that it is the
antisocial deviance factor (Factor 2) of the PCL-R, rather than core personality

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R.C. Howard et al.

features (Factor 1) that is predictive of violence (Leistico, Salekin, DeCoster,

& Rogers, 2008; Yang, Wong, & Coid, 2010; Walters, 2003), we further
hypothesised that PCL-R Factor 2, but not PCL-R Factor 1, would signicantly
associate with violence.
As pointed out by several authors (e.g. Kennealy, Skeem, Walters, &
Camp, 2010; Patrick, Edens, Poythress, Lilienfeld, & Benning, 2006), all postdictive studies in which previous criminal behaviour is correlated with measures of psychopathy and antisocial personality raise the possibility of criterion
contamination. This was a particular concern in the present study with regard
both to PCL-R Factor 2 and childhood CD. Two PCL-R Factor 2 items, juvenile delinquency and early behaviour problems, might include early onset violence, while childhood CD might manifest as early onset violence. We
therefore rst carried out regression analyses with early onset violence included
in the outcome variable (VI), and then, in order to mitigate criterion contamination, we repeated the analyses with early onset violence omitted from VI.
Methods
The sample
The study was conducted as part of a wider study assessing the relationship
between personality development and alcohol abuse. Data across the sites were
collected by the second author who was not blind to the ndings of the assessments. One hundred male offenders detained under the 1983 UK Mental
Health Act were recruited from the personality disorder services at two English
high-secure hospitals (including a specialised unit for treating patients deemed
as suffering from dangerous and severe personality disorder (DSPD)) and
one medium-secure hospital. All patients gave their informed consent to participate in the study, which was approved by the local Research Ethics Committee. Criteria for inclusion were: (i) at least one denite DSM-IV personality
disorder (PD); (ii) a full-scale IQ of 70 or greater (on the basis of Wechsler
Adult Intelligence Scale: Wechsler, 1997); (iii) no identiable Axis I diagnoses
of psychosis or bipolar affective disorder on DSM-IV (American Psychiatric
Association [APA], 1994); and (iv) no history of head injury or neurological
disorder such as epilepsy. After excluding those who had incomplete data (n =
14), those with ASPD/BPD comorbidity comprised 44 patients and those without such comorbidity comprised 56 patients. Groups were well-matched for
full-scale IQ (means of 90.0 and 90.2 for those with and without ASPD/BPD
comorbidity, respectively) and age at assessment (means of 35.0 and 35.3
years, respectively).
Assessment of psychopathology
The computerised version of the National Institute of Mental Health Diagnostic
Interview Schedule (C-DIS: Robins, Helzer, Cottler, & Goldring, 1989) was

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663

used to make diagnostic assessments of the following DSM-IV Axis I disorders

(APA, 1994): childhood conduct disorder, attention decit hyperactivity disorder, schizophrenia, bipolar affective disorder and alcohol abuse/dependence.
C-DIS has been found to show adequate diagnostic reliability and validity (e.g.
Dascalu, Compton, Horton, & Cottler, 2001; Horton, Compton, & Cottler,
1998). DSM-IV PDs were assessed using the IDPE (Loranger et al., 1994),
interview version which has good inter-rater reliability ( of .70 and above:
Zimmerman, 1994) and temporal stability (Loranger et al., 1994). IPDE is
designed to assess the 10 DSM-IV Axis II personality disorders and personality
disorder not otherwise specied. It allows dimensional scores to be derived for
individual personality disorders as well as personality disorder clusters (cluster
A, cluster B and cluster C). Severity of personality disorder was measured on
a ve-point severity scale ranging from 0 (no personality disorder) to 4 (severe
personality disorder) (Tyrer & Johnson, 1996). An additional point (5) was
added to the scale to indicate very severe personality disorder, where, as well
as meeting the Tyrer and Johnson criteria for severe, the patient additionally
scored 25 or above on the PCL-R. In addition to DSM-IV PDs, assessed both
categorically and dimensionally, scores were obtained on two higher order factors, acting out and anxious inhibited, derived by Blackburn et al. (2005)
from a primary factor analysis of 93 IPDE items. Twenty-one items contributed
to the acting out factor, and 19 items to the anxious inhibited factor: see
Table 1 for items.
Assessment of psychopathy
Psychopathy was assessed using guidelines for the Hare Psychopathy Checklist-Revised (Hare, 2003). Total score out of 40 and scores on the two PCL-R
factors were obtained (F1, selsh, callous and remorseless use of others; and
F2, chronically unstable & antisocial lifestyle).
Assessment of impulsivity
Impulsivity was assessed using the UPPS, a 44-item self-report inventory
designed to measure four distinct personality pathways to impulsive behaviour:
Urgency, (lack of) Perseverance, (lack of) Premeditation, and Sensation Seeking (Whiteside & Lynam, 2001). Each UPPS item was rated on a four-point
scale with higher scores reecting greater impulsivity.
Assessment of drug and alcohol use
Details of the drug and alcohol assessment have been presented previously
(see Howard, Khalifa, Duggan, & Lumsden, 2012; Khalifa, Duggan, Lumsden,
& Howard, 2012). Detailed information was obtained about lifetime use of the
following classes of drugs: opiates, stimulants, cannabis and hallucinogens;
and in particular, about the age of onset of alcohol abuse.

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Assessment of violence
Severity of violence in patients criminal records was assessed using a modied version of the Gunn and Robertson (1976) scale, validated in hospitalised
offender patients by Wong, Lumsden, Fenton, and Fenwick (1993). A VI was
derived by summing across scores for severity, quantity and age of onset,
yielding a maximum score of 12. Severity was rated on a ve-point scale ranging from 0 (=no violence) to 4 (=severe violence, e.g. victim died or life and
health were seriously endangered). Quantity was operationalised as the number
of ofcially recorded convictions for violent offences committed by the patient
across his lifetime, as documented in his case le, coded as follows: >10 violent offences = 4; 59 violent offences = 3; 24 violent offences = 2; 1 violent
offence = 1; and 0 = no violent offences. Age of onset was taken as the age at
which the patient rst offended violently, coded as follows:<15 years = 4;
1518 years = 3; 1920 years = 2; 21 years or more = 1; and no violence = 0).

Analytic strategy
Data analysis proceeded in four stages. First, weighted sum scores on the two
higher order factors, acting out and anxious inhibited (Blackburn et al.,
2005), were computed by multiplying the loading of each item with the score
for each IPDE item before summing (DiStefano, Zhu, & MIndril, 2009).
Next, between-group (those with antisocial/borderline comorbidity v the rest)
comparisons on all variables were carried out using SPSS version 21. For continuous variables, MannWhitney U-tests were used to compare means on any
variable not found to be normally distributed, otherwise t-tests were used. The
2 statistic was used for all categorical variables. Thirdly, Pearsons correlations
were computed between the various measures and the VI. Fourthly, multiple
linear regression was used to test the hypothesis that both antisocial/borderline
personality disorder comorbidity and Factor 2 of the PCL-R, but not Factor 1,
would each be independently associated with the VI. Since early onset of violence is characterised by higher rates of offending and more serious offences
in adolescence (Stattin & Magnusson, 1996; Tolan & Gorman-Smith, 1998),
including early onset of violence in the outcome variable ran the risk of
criterion contamination, i.e. overlap between the outcome variable (VI) and the
predictor variables (ASPD/BPD comorbidity, which includes childhood conduct disorder, and PCL-R Factor 2, which includes early antisocial deviance).
The regression analysis was therefore run twice, rst with inclusion of early
age of violence onset in VI and subsequently, to mitigate criterion contamination, with its exclusion. Multicollinearity diagnostics, including tolerance tests
and the variance ination factor (VIF), were applied to assess the linearity of
any relationship between personality variables and VI. Finally, in order to see
whether a particular combination of psychopathy and ASPD/BPD comorbidity
might be applied as a rule of thumb in designating PD individuals as either

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665

high or low in terms of their risk for violence, various PCL-R cut scores were
assessed for their association, in combination with ASPD/BPD comorbidity,
with a high VI score.
Results
Sample characteristics
Patients mean age at the time of assessment was 35.2 years (SD = 9.2; range
2164). All patients had a history of mostly violent offending starting from a
young age: mean age of rst offence was 15 years (SD = 4.5), and of rst violent offence, 18 years (SD = 5.1). Patients had a history of chronic offending,
with a mean number of 33 lifetime offences (range 1154) and of 12.5 violent
offences (range 1135). Most (91%) had received a DSM-IV Cluster B PD
diagnosis: antisocial (72%), borderline (47%), histrionic (7%) or narcissistic
(13%) PD; fewer received Cluster A (45%) or Cluster C (42%) diagnoses.
Three-quarters of the sample (76%) had a history of childhood CD, and a quarter (25%) had a diagnosis of childhood ADHD. A large proportion received
comorbid lifetime diagnoses of major depression and alcohol dependence (56
and 54%, respectively).
Comparison between antisocial/borderline comorbid group and others
The 44 men in the comorbid personality disorder group had a mean total PCLR score of 25.7 (SD = 5.7) and the 56 men in the other personality disorder
group had a mean total score of 23 (SD = 7.5), this difference being non-significant (F[1, 98]=1.838, p = .058). There were no signicant between-group
differences for either PCL-R Factor 1 or Factor 2: F[1, 98]=1.096, p = .08 and
F[1, 98] = .368, p = .14, respectively. Patients in the comorbid group, however,
did obtain both a signicantly higher IPDE acting out factor score (M = .49,
SD = .14) than the others (M = .38, SD = .14; F[1, 98]=.503, p < .001) and a
signicantly higher IPDE anxious inhibited factor score (comorbid M = .40,
SD = .17; other PD M = .23, SD = .14; F[1, 98] = 1.802, p < .001). The comorbid group showed signicantly more severe personality pathology overall,
across each personality disorder cluster and in all personality disorder categories except schizoid, schizotypal and obsessive compulsive, as well as greater
PD severity according to the Tyrer and Johnson (1996) scale. They also
showed signicantly higher scores on all facets of impulsiveness as measured
by the UPPS, with the exception of sensation seeking. The comorbid group
showed signicantly (F[1, 98] = 1.16, p = .03) greater severity of violence in
their criminal record compared with the remainder, but the groups did not
differ signicantly on VI (F[1, 98] = .10, p = .2).
With respect to other comorbidities, the antisocial/borderline comorbid
group were signicantly more likely to have been alcohol dependent

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R.C. Howard et al.

(2 = 6.303, p = .01), to have used various illicit drugs regularly or daily,

including cannabis (2 = 5.593, p = .02), stimulants (2 = 4.127, p = .065), opioids (2 = 5.412, p = .027) and hallucinogens (2 = 8.764, p = .003), and to have
had more severe symptoms of conduct disorder in childhood (F[1, 98] = 4.894,
p = .002).
Correlates of VI
Correlates of VI are shown in Table 2, where it may be seen that the VI correlated with both F1 and F2 of the PCL-R, but more strongly with F2 than with
F1. VI also correlated signicantly with degree of ASPD/BPD comorbidity,
and with APD and BPD considered separately (but negatively with schizoid
traits). VI correlated very modestly with UPPS impulsiveness, and signicantly
only with UPPS Premeditation and Urgency. VI correlated signicantly with
regular recreational drug use (particularly stimulants), and with early onset alcohol abuse.
Regression analysis
Results of multiple linear regression (enter method) revealed that both PCL-R
F2( = .53, p < .0001) and antisocial/borderline comorbidity ( = .256, p = .003)
signicantly predicted VI as an outcome (R2 = .46; p < .0001). When age of
onset was omitted from VI as the outcome variable, both PCL-R F2( = .52,
p < .0001) and antisocial/borderline comorbidity ( = .18, p = .047) remained
signicant predictors of VI (R2 = .38; p < .0001). The covariates (PCL R Factor
1, UPPS total score, early EOAA total weighted score and cannabis use) were
initially entered into the regression model individually to assess their effects on
the parameters of the model. Additionally, patient location was treated as a
confounder and was entered into the model separately to assess its effect on
the model. Since none of the factors signicantly predicted VI, they were
excluded from the nal regression models. Multicollinearity was considered
acceptable given the tolerance and VIF values were .80 and 1.3, respectively.
Associations between VI and antisocial/borderline comorbidity using
different PCL-R cut scores
When a PCL-R cut score of 30 or greater combined with antisocial/borderline
comorbidity was applied to separate an a priori high risk group from remaining PD patients, the former were found to score signicantly higher on VI than
the latter (means of 9.2 and 7.9, respectively; p < .01). A PCL-R cut score of
25 also yielded a between-group difference for VI in the expected direction
(p = .05). Applying PCL-R cut scores of less than 25 failed to yield signicant
between group differences for VI. Applying the criterion of antisocial/borderline comorbidity combined with a PCL-R cut score of 30 identied 23.7% of

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Table 2.

667

Correlates of VI. EOAA: early onset alcohol abuse.

Violence
Index

Patients age at the time of assessment

Global IQ
Total PCL-R score
PCL Factor 1 score
PCL Factor 2 score
IPDE Cluster A dimensional score
IPDE Cluster B dimensional score
IPDE Cluster C dimensional score
PD Severity dimensional score (Tyrer & Johnson)
CD dimensional score
APD+BPD dimensional score
IPDE Paranoid PD dimensional score
IPDE Schizoid PD dimensional score
IPDE Schizotypal PD dimensional score
IPDE Antisocial PD dimensional score
IPDE Borderline PD dimensional score
IPDE Histrionic PD dimensional score
IPDE Narcissistic PD dimensional score
IPDE Avoidant PD dimensional score
IPDE Dependent PD dimensional score
IPDE Obsessive compulsive PD dimensional score
Age at index offence
Age at rst offence
Total number of non-violent offences across lifetime (including index
offence)
EOAA total weighted score
UPPS total score
UPPS premeditation score
UPPS urgency score
UPPS sensation seeking score
UPPS Perseverance score
Stimulants regular or daily use
Cannabis regular/daily use
Opioid regular/daily use
Hallucinogen regular/daily use

.14
.09
.57**
.42**
.65**
.18
.43**
.01
.08
.39**
.50**
.06
.32**
.16
.54**
.20*
.13
.09
.06
.07
.04
.04
.65**
.29**
.28**
.36**
.28**
.23*
.17
.11
.33**
.21*
.22*
.18

Signicant correlation coefcients are indicated in bold: *p < .05; **p < .01.

DSPD patients as high risk, compared with 3.2% of other high-secure

patients, and 9.7% of medium-secure patients.
Discussion
Results of this study suggest that both the antisocial deviance factor of PCL-R
psychopathy and ASPD/BPD comorbidity are independently associated with
early onset, severe violence in forensic psychiatric patients. Those patients who

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R.C. Howard et al.

show a pattern of disinhibited deviance from a young age, indicated by a high

PCL-R Factor 2 score and severe childhood CD, together with antisocial/borderline comorbidity in adulthood, arguably manifest a particularly severe form
of PD that has been previously described as secondary psychopathy
(Blackburn, 2009; Skeem, Johansson, Andershed, Kerr, & Louden, 2007;
Swogger & Kosson, 2007). Our data indicate that an appropriate criterion for
identifying this severe type among personality disordered offenders might be a
combination of ASPD/BPD comorbidity with a PCL-R score of 25 or greater,
since this resulted in a signicant group difference in the VI, while combining
ASPD/BPD comorbidity with PCL-R scores of less than 25 did not.
These results conrm and extend ndings by Baskin-Sommers et al. (2013)
indicating an important role for PD comorbidity in violence severity among
offenders. They further extend and conrm previous ndings from studies of
community-resident PD patients in showing that ASPD/BPD comorbidity is
associated with greater overall PD severity (greater comorbidity across all three
PD clusters), more severe childhood CD, and with impulsiveness and a history
of violence (Freestone et al., 2012; Howard, Huband, & Duggan, 2012; Howard, Huband, Mannion, & Duggan, 2008). However, correlates of VI other
than PCL-R Factor 2 and ASPD/BPD comorbidity, when entered into the
regression equation, did not show signicant independent associations with
severe early onset violence. In particular, no clear relationship between impulsiveness and violence could be demonstrated, which implies that impulsiveness, despite being a salient feature of both ASPD and BPD, is not critically
involved in linking ASPD/BPD comorbidity with violence.
A critical factor linking this comorbidity with violence is likely to be problems with emotion regulation that characterise BPD patients and which may
enhance their risk of violence (Newhill, Eack, & Mulvey, 2012; Scott, Stepp,
& Pilkonis, 2014). Newhill et al. (2012) found emotion dysregulation to be a
signicant longitudinal mediator of violent behaviour among individuals with
BPD. Scott et al. (2014) reported that while both ASPD and BPD were associated with aggressive behaviour, associations between BPD symptoms and
aggression were uniquely mediated by difculties with emotion regulation.
However, emotion dysregulation in BPD patients may in part reect a cognitive disturbance, namely delusional thinking, that may give rise to the decits
in social cognition noted by Lis and Bohus (2013) in borderline patients. These
decits would impact negatively on borderline patients social interactions,
where they appear particularly susceptible to affective instability (Reich,
Zanarini, Hopwood, Thomas, & Fitzmaurice, 2014). Therefore, the possibility
must be considered that the relationship between ASPD/BPD comorbidity and
violence may be mediated, at least in part, by delusional ideation, especially
considering that Freestone et al. (2012) reported a signicant association
between antisocial/borderline PD comorbidity and a high score on the
Psychosis Screening Questionnaire.

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669

Limitations of the study

Possible criterion contamination is a problem with this as with all postdictive
studies that examine the relationship between antisocial personality and violence (Kennealy et al., 2010; Patrick et al., 2006). However, exclusion of early
onset violence from VI to mitigate its overlap with PCL-R Factor 2 items that
focus on early deviance and with childhood CD did not substantially alter the
model derived from regression analysis.
While the VI used in the present study did encapsulate those dimensions of
violence quantity, severity of impact and age of onset that are key to a
description of its overall severity, we were unfortunately not able to characterise violence in terms of its motivation (see Howard, 2011). A ner differentiation of violence in terms of its motivation might have enabled more nuanced
relationships between personality disorder and violence to be discerned, and
future studies should include, as far as possible, a description of violent acts in
terms of their motivation.
Finally, the relatively small sample size used in this study means that it
was lacking in statistical power, which should caution against too strong conclusions being drawn. Nonetheless, the sample comprised patients with conrmed PD, and most had been convicted of violent crimes, making it, despite
its relatively small size, well-suited to studying relationships between PD and
violence.

Implications for treatment and intervention

Given their history of severe childhood CD and their early onset alcohol abuse,
individuals who, as adults, show antisocial personality comorbid with borderline personality disorder are in principle identiable in childhood or early adolescence. Interventions to prevent a progression from childhood and adolescent
antisocial behaviour to adult personality pathology should focus on preventing
early onset alcohol abuse, previously found to partially mediate the link
between childhood CD and adult antisociality (Howard, Finn, Gallagher, &
Jose, 2012; Khalifa et al., 2012).

Conclusion
This study indicates that a severe type of personality disorder, characterised
by a triple comorbidity ASPD, borderline PD and psychopathy is associated with severe violence. Adopting a criterion of antisocial/borderline
comorbidity combined with a PCL-R score of 25 or greater should successfully identify this severe type, but prospective studies will be required to
conrm this.

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