Current Psychiatry Reports (2018) 20:53

https://doi.org/10.1007/s11920-018-0929-4

PERSONALITY DISORDERS (K BERTSCH, SECTION EDITOR)

Correlates of Aggression in Personality Disorders: an Update

Falk Mancke 1 & Sabine C. Herpertz 1 & Katja Bertsch 1

# Springer Science+Business Media, LLC, part of Springer Nature 2018

Abstract
Purpose of Review This review article aims at giving an update on studies investigating correlates of aggression in personality
disorders during the last 5 years.
Recent Findings Most data refer to borderline personality disorder (BPD) and antisocial personality disorder (ASPD). In BPD,
emotion dysregulation, hypersensitivity to interpersonal rejection/threat, increased rumination, increased negative urgency,
aggression-related knowledge structures, and invalidation were either corroborated or emerged as psychological correlates of
aggression, while reduced ambiguity sensitivity, hyposensitivity to interpersonal threat, and reduced mindfulness were associated
with aggression in ASPD. Neurobiologically, alterations of the monoaminooxidase-A-, the oxytocinergic-, and the prefrontal-
limbic-system as well as increases of the thyroid hormone T3, γ-aminobutyric acid and several inflammatory markers were
associated with increased aggression across various personality disorders.
Summary Our understanding of correlates of aggression in personality disorders has increased over the last 5 years. More
efforts in improving the conceptualization of personality disorders and aggression are needed to develop innovative
treatments for those affected.

Keywords Borderline personality disorder . Antisocial personality disorder . Emotion dysregulation . Threat hypersensitivity .
Monoaminooxidase-A . Conceptualization of personality disorders and aggression

Introduction injuries due to aggression, and aggression costs society up to

Aggression can be defined as any behavior that is carried out
with the proximate intent to harm another individual who is
motivated to avoid such treatment [1] and is mostly classified
into reactive and premediated subtypes [2]. Reactive aggres-
sion is usually triggered by threats, frustration, or provocation
and is strongly associated with negative emotions, particularly
anger, whereas premediated aggression refers to planned,
goal-directed behavior. Aggression has detrimental individual
and societal consequences: In the USA, each year more than
501,000 people are treated in emergency departments for
This article is part of the Topical Collection on Personality Disorders
The editor and the authors would like to thank Dr. Robert Friedel for
taking the time to review this manuscript.
* Falk Mancke
Falk.Mancke@med.uni-heidelberg.de
1 in individuals with ASPD compared with the general popula-
Department of General Psychiatry, Center for Psychosocial
Medicine, University of Heidelberg, Voßstraße 2,
69115 Heidelberg, Germany
426 billion US dollars [3, 4].
A diagnosis of personality disorder may be regarded as a
risk factor for enhanced aggression since the odds for aggres-
sive behaviors are three times increased in individuals with
personality disorders compared with the general population
[5]. More specifically, within the ten personality disorders
described in the Diagnostic and Statistical Manual of Mental
Disorders-5 (DSM-5) [6], aggression has been typically asso-
ciated with the cluster B personality disorders (antisocial, bor-
derline, histrionic, and narcissistic personality disorder) [7]
and paranoid personality disorder [8•]. Most research has been
conducted in individuals with cluster B personality disorders,
showing that they were ten times more likely to have had a
criminal conviction and almost eight times more likely to have
spent time in prison compared to those with other personality
disorders [9]. Within the cluster B personality disorders, indi-
viduals with antisocial (ASPD) or borderline personality dis-
order (BPD) carry the highest risk of behaving aggressively.
There was a 12.8 increase in the odds of aggressive outcomes
tion [5] and up to 73% of individuals with BPD have engaged
in aggressive behaviors over the course of a year [10].
53 Page 2 of 14
Accordingly, most of the data presented in this review article
refers to these two disorders.
This review article aims at providing an update on studies
investigating correlates of aggression in personality disorders1
conducted within the last 5 years (starting from mid-2012 to
date, see Table 1 for details on the cited studies, including
sample characteristics, methodology, and key findings). We
will first give an overview of self-report, interview, and be-
havioral data and then present studies using neurobiological
methods. Finally, we will highlight questions that are currently
addressed in the field of aggression in personality disorders
and that may facilitate the development of innovative treat-
ment interventions.
Self-report, Interview, and Behavioral Data
Most studies using self-reports or interviews aimed at reveal-
ing mediators of aggressiveness (i.e., the enduring tendency to
behave aggressively [13]) in individuals with personality dis-
orders. Mediation addresses the question of “how” [14], e.g.,
which kinds of mechanisms underlie elevated aggressiveness
in individuals with personality disorders.
Emotion dysregulation (i.e., “deficits in the ability to mod-
ulate the experience and expression of emotions and to main-
tain goal directed behavior in the presence of intense negative
affect”, [15], p. 657) has been identified as a central mecha-
nism of aggressiveness particularly in individuals with BPD.
Newhill and colleagues used a longitudinal design in patients
with BPD (N = 220) and revealed that both elevated initial
status and less longitudinal improvement in emotion dysreg-
ulation fully mediated the effects of BPD on aggressiveness
over a 30-week periods [16]. Along with this, emotion dys-
regulation fully mediated the association between BPD symp-
toms and aggressiveness in a mixed clinical and community
sample of adults (N = 150) over the course of a year [17••].
These results are further corroborated by cross-sectional stud-
ies: emotion dysregulation predicted aggressiveness in BPD
outpatients (N = 79) [18] and maladaptive emotional coping, a
construct highly similar to emotion dysregulation, mediated
the association between aggressiveness and symptoms of
BPD in students (N = 226) [19].
Studies have been conducted to provide a more fine-
grained understanding of the role of emotion dysregulation
in aggression in BPD. Moor and colleagues investigated pa-
tients in residential substance abuse treatment (N = 118) and
reported that only the impulsive aspects of emotion dysregu-
lation mediated the association between BPD symptoms and
1
Psychopathy is another mental condition that is strongly associated with
aggression and shares aspects with personality disorders, especially ASPD.
This article focuses on personality disorders as defined in the current diagnos-
tic systems (DSM-5 and ICD-10), which do not include psychopathy (see [11,
12] for reviews on psychopathy and aggression).
Curr Psychiatry Rep (2018) 20:53
criminal justice involvement including aggression [20].
Additionally, emotion dysregulation mediated the association
between BPD symptoms and aggressiveness in BPD patients
(N = 95) via a sequential mediation with trait anger [21].
Emotion dysregulation may thus constitute an underlying fac-
tor that gives rise to other aspects of BPD symptomatology,
e.g., maladaptive anger regulation, and in turn to aggression.
Personality disorders are critically characterized by inter-
personal dysfunction [22]. In BPD, one specific aspect of the
interpersonal dysfunction is a hypersensitivity to interpersonal
rejection [23], which has also been related to aggression. In a
combined self-report and ecological momentary assessment
study, Scott and colleagues [24] investigated the within-
person processes leading to aggression in emerging adult
women (ages 18–24, N = 117) with recent histories of aggres-
sive behavior who were recruited from the community over a
period of 3 weeks. Results revealed that only in case of
existing BPD, but not ASPD symptoms, experiences of inter-
personal rejection were linked to aggression via increases in
negative affect (particularly anger). The authors concluded
that anger reactivity to perceived rejection is one unique path-
way, distinct from ASPD, by which BPD symptoms increase
the risk for aggression. In line with this, studies revealed that
negative interpersonal events [25] and interpersonal problems
[26] predicted subsequent aggressive behavior in subjects
scoring high on BPD symptoms. In addition, BPD symptoms
were related to especially relational aggression (i.e., forms of
aggression that aim at damaging and manipulating relation-
ships as a means to harm others, e.g., threats to withdraw
friendship, gossip, or exclusion) in a longitudinal study inves-
tigating children from the general population (N = 196) [27].
Closely related to hypersensitivity to interpersonal rejec-
tion is that individuals with personality disorders show also
an altered perception of interpersonal threat cues, such as an-
gry faces. This finding has mainly been studied by facial rec-
ognition tasks in patients with BPD and results suggest, de-
spite some inconsistencies [28], a hypersensitivity to cues of
interpersonal threat [29]. Recently, the knowledge on facial
emotion recognition in BPD has been expanded by an eye-
tracking study showing that BPD patients made more and
faster initial reflexive eye movements toward the eyes of very
briefly presented angry faces and thus the most threatening
and arousing facial region [30••]. In addition, the latency of
initial saccades and fixation duration for angry eyes correlated
negatively with BPD patients’ aggressiveness [31].
Interestingly, results in individuals with ASPD are more di-
verse: They showed a tendency to interpret ambiguous facial
stimuli as more angry compared with healthy controls (N = 55
for each group) [32], but required significantly higher levels of
emotional intensity to correctly identify the onset of an angry
facial expression [33•] rather suggesting a hypo- than hyper-
sensitivity for cues of interpersonal threat. One reason for this
discrepancy could be a moderating effect of psychopathy, a
Curr Psychiatry Rep (2018) 20:53
Table 1 Studies investigating correlates of aggression in personality disorders. The studies are listed in alphabetical order based on the author’s first
name
First author Year Sample Methodology
Alcorn 2015 6 male APD APD: SCID-II, aggression: point
subtraction aggression paradigm,
neurochemistry: application of
nasal oxytocin
Anderson 2017 738 forensic patients BPD/APD: DSM-5, dimensional
(27% female) of them psychopathology: Minnesota
23 BPD and 112 APD Multiphasic Personality Inventory-2
Restructured Form, aggression:
hospital-wide electronic database
using Special Incident Reports,
statistics: hierarchical Poisson
regression analyses
Banny 2014 196 children (62% female) BPD: Borderline Personality Features
Scale for Children, aggressiveness:
Children’s Social Behavior
Scale—Teacher Report II
Beier 2014 48 patients with major PD: SCID-II, aggressiveness:
depressive episode, of Brown–Goodwin Aggression
those 6 with BPD Inventory, neurochemical:
(24% female) eicosapentaenoic levels in CSF
Bertsch 2013 34 female BPD, 40 healthy BPD: IPDE, aggressiveness: Assessment
women of Factors of Aggression,
neurochemistry: plasma levels of
oxytocin
Bertsch 2017 20 female medication free BPD: International Personality Disorder
BPD, 24 healthy women Examination, aggressiveness: BPAQ,
behavioral: eye-tracking, emotion
classification paradigm
Bertsch 2013 13 male BPD-APD, 12 male BPD: International Personality Disorder
APD, 14 healthy men Examination, aggressiveness:
Questionnaire for Factors of
Aggressiveness, neuroimaging: sMRI,
voxel-based morphometry
Buckholtz 2017 77 individuals (20% female) BPD: SCID-II, aggression: Subtypes of
from a high-crime Antisocial Behavior Questionnaire,
community, of them 22 behavioral task: computerized
with APD decision-making paradigm
Checknita 2016 86 male APD, 73 male HV APD: Structured Clinical Interview,
DNA: peripheral leukocytes,
epigenetic: MAO-A promoter
methylation
Coccaro 2012 40 PDs (23% female), of PD: SCID-II, aggressiveness: Life
those 7 with BPD and History of Aggression assessment
5 with APD 3, 20 healthy and the aggression factor score from
volunteers (20% female) the Buss–Durkee Hostility Inventory,
neurochemical: neuropeptide-Y levels
in CSF
Coccaro 2013 28 PDs (32% female, 5 BPD, PD: according to DSM-IV criteria,
APD 3), 10 healthy aggressiveness: Life History of
volunteers (10% female) Aggression assessment, neurochemical:
glutamate levels in CSF
Coccaro 2015 17 PD (4 cluster B, PD: Structured Interview for the
18% female) Diagnosis of DSM-IV Personality
Disorder, aggressiveness: Life History
of Aggression assessment and the
Page 3 of 14 53
Key findings
Reactive aggression was partly increased
after oxytocin administration in APD
Dimensional psychopathology predicted
aggression beyond categorical diagnoses
in forensic patients
BPD symptoms promote engagement in
relationally aggressive behaviors among
girls, particularly in the context of emotional
dysregulation
Low plasma eicosapentaenoic acid levels
were associated with elevated aggressiveness
Plasma concentrations of oxytocin were
negatively associated with aggressiveness
in female BPD patients
Latency of initial saccades and fixation duration
correlated negatively with aggressiveness in
BPD patients
Patients with APD and comorbid BPD showed
smaller gray matter volume in orbitofrontal
and ventromedial prefrontal cortex compared
to controls, whereas patients with APD and
comorbid psychopathy showed less
volume in cortical midline areas
(dorsomedial prefrontal cortex and
precuneus)
APD show reduced ambiguity sensitivity
compared with individuals from a
high-crime community without APD.
Lower ambiguity sensitivity was
associated with higher aggression (but
not psychopathy)
APD show MAO-A promoter
hypermethylation, which leads to reduced
transcriptional activity
Increased CSF levels of neuropeptide-Y
correlated with increased
aggressiveness in PD.
Increased CSF levels of glutamate correlated
with increased aggressiveness in PD
Increased CSF levels of c-reactive protein
correlated with increased aggressiveness
in PD
53 Page 4 of 14
Table 1 (continued)
First author Year Sample Methodology
aggression factor score from the
Buss–Durkee Hostility Inventor,
neurochemical: C-reactive protein
levels in CSF
Coccaro 2015 38 PD (13 cluster B, PD: SIDP-IV, interleukin-1 receptor II:
24% female) CSF, aggressiveness: Life History of
Aggression assessment and the
aggression factor score from the
Buss–Durkee Hostility Inventor,
neurochemical: interleukin-1 receptor
II levels in CSF
Coid 2006 8397 individuals from the PD: SCID-II, aggressive: self-reported
general population. criminal convictions/period in prison,
statistics: hierarchical logistic
regression analyses
Ende 2016 26 female BPD, 22 female BPD: IPDE, aggressiveness: BPAQ,
attention-deficit-hyperactivity Anger: State-Trait Anger Expression
disorder, 30 female HV Inventory, neuroimaging: anterior
cingulate cortex MR-spectroscopy
for γ-aminobutyric acid and
glutamate
Evrensel 2016 96 male APD, 97 healthy PD: SCID-II; aggressiveness: BPAQ,
men neurochemistry: T3 serum levels
Gardner 2012 226 young adolescents BPD: Personality Diagnostic
(62% female) Questionnaire 4th Edition BPD scale,
aggressiveness: Reactive–Proactive
Aggression Questionnaire, statistics:
ordinary least squares path analytical
framework
Gilbert 2015 87 aggressive offenders PD: SCID-II, aggressiveness: The Life
(10% female) History of Aggression/Schedule of
Imagined Violence, Normative belief
about aggressions: Attitudes to
Violence, anger: State-Trait Anger
Expression Inventory-2
Herpertz 2017 56 BPD (59% female), BPD: International Personality Disorder
56 HV (56% female) Examination, aggressiveness: BPAQ,
Anger: State-Trait Anger Expression
Inventory, neuroimaging: fMRI during
script-driven imagery task of
aggression
Herr 2013 98 female undergraduates BPD: The Personality Assessment
Inventory Borderline Features
subscale, negative interpersonal
events: The Inventory of Small Life
Events, aggressiveness: six-item
behavior checklist from the aggression
questionnaire and Werner and Crick’s
the relational aggression
Curr Psychiatry Rep (2018) 20:53
Key findings
Increased CSF levels of interleukin-1
receptor II correlated with increased
aggressiveness in PD
Individuals with cluster B personality
disorders were 10 times more likely to
have had a criminal conviction and almost
8 times more likely to have spent time in
prison compared to those with other
personality disorders
Increased γ-aminobutyric acid in the ACC
was associated with increased
aggressiveness in a mixed sample of
patients with BPD and attention deficit
hyperactivity disorder
Increased serum T3 levels were associated
with increased aggressiveness in APD
Maladaptive emotional coping mediated
the relationship between BPD symptoms
and reactive aggressiveness
Aggression-related knowledge structures, i.e.,
internal representations of past experiences,
such as attitudes, goals, behavioral scripts,
and beliefs about appropriate behavior,
were stronger associated with aggressiveness
in individuals with BPD then in those
with APD
Male BPD patients revealed higher activity
in the left amygdala than female patients
while reacting aggressively. During the
aggression phase, male BPD patients
exhibited higher activity in the lateral
orbitofrontal and dorsolateral prefrontal
cortices compared with healthy men and
female patients. Male BPD patients
showed negative connectivity between
amygdala and posterior middle cingulate
cortex, while female BPD patients showed
a positive connectivity. Aggressiveness
modulated connectivity of the left
amygdala to the posterior thalamus in
male but not female patients
Negative interpersonal events mediated
the relation between BPD symptoms
and aggressiveness
Curr Psychiatry Rep (2018) 20:53
Table 1 (continued)
First author Year Sample Methodology
Herr 2015 69 undergraduates BPD Personality Assessment Inventory,
(61% females) aggressiveness: BPAQ, invalidation:
experimentally manipulated after a sad
mood induction
Kolla 2015 18 male APD, 18 male APD: SCID-II, neuroimaging: [11C]
volunteers harmine positron emission tomography
Kolla 2016 14 severe BPD, 14 moderate BPD: SCID-II, [11C] harmine positron
BPD, 14 MDE, emission tomography
14 healthy women
Kolla 2017 20 BPD,18 APD, 23 HV BPD: SCID-II, early adversity: childhood
trauma questionnaire, impulsivity:
Barratt Impulsiveness Scale-11, DNA:
peripheral leukocytes
Kolla 2017 18 APD, 20 healthy men APD: SCID-II, DNA: peripheral
leukocytes, neuroimaging: Multiple
Automatically Generated Templates
Brain pipeline
Lobbestael 2013 66 male individuals, of PD: Structured Clinical Interview for
those 24 with APD, DSM-IV Axis II disorders,
10 with BPD aggressiveness: Reactive and Proactive
Aggression Questionnaire, Hostile
interpretation bias: Thematic
Apperception Test
Mancke 2017 95 BPD patients BPD: International Personality Disorder
(78% female) Examination, aggressiveness: BPAQ,
Anger: State-Trait Anger Expression
Inventory, Statistics: ordinary least
squares path analytical framework
Mancke 2016 58 BPD patients BPD: International Personality Disorder
(64% female), 51 Examination, aggressiveness: BPAQ,
healthy volunteers Anger: State-Trait Anger Expression
Inventory, Neuroimaging: alterations
of amygdala volume and localized
amygdala shape using Oxfords Centre
for Functional Magnetic Resonance
Imaging of the Brain (FMRIB)
Integrated Registration & Segmentation
Tool (FIRST) as implemented in
FMRIB’s software library
Martino 2015 151 PD, of those 93 with BPD: SCID-II, rumination: Anger
BPD (60% female) Rumination Scale, aggressiveness:
BPAQ, emotion dysregulation: DERS,
statistics: hierarchical linear regression
analyses
Martino 2017 91 BPD (77% female) BPD: SCID-II, aggressiveness: BPAQ,
rumination: Anger Rumination Scale/
Ruminative Responses Scale, statistics:
hierarchical linear regression analyses
Moore 2017 118 patients in residential BPD: Borderline Evaluation of Severity
substance abuse treatment Over Time, impulsivity: impulse control
(24% female) difficulties subscale of the Difficulties in
Emotion Regulation Scale, criminal
justice charges: Legal status section of
the Addiction Severity Index, statistics:
structural equation modeling
Morandotti 2013 18 BPD (72% female), BPD: SCID-II, aggressiveness:
13 healthy women Buss–Durkee Hostility Scale,
(68% female)
Page 5 of 14 53
Key findings
Invalidation led to aggressiveness in those with
dysregulated emotions
Lower MAO-a density in OFC/ventral
striatum of APD compared to volunteers
Higher MAO-A density in ACC/PFC of
severe BPD compared with moderate
BPD patients, depressive patients, and
healthy volunteers
Interaction of MAOA-L and childhood abuse
predicted greater BIS-11 motor
impulsiveness in BPD
APD subjects with MAOA-L exhibited
decreased surface area in the right
basolateral amygdala nucleus and increased
surface area in the right anterior cortical
amygdaloid nucleus compared with healthy
MAOA-L carriers
Hostile interpretation bias predicted
reactive aggressiveness in a mixed
APD/BPD sample
Emotion dysregulation and trait anger
sequentially mediated the association
between BPD and aggressiveness
Outward deformations of the left superficial
and laterobasal amygdala of male BPD
patients were positively associated with
increased aggressiveness
Anger rumination was found to significantly
predict aggressiveness, over and above
emotion dysregulation in PD
Anger and depressive rumination were
related to aggressiveness
BPD symptoms were related to criminal
justice contact and criminal justice charges
through emotion-driven difficulties
controlling impulsive behavior
Gray matter volume loss in the right
ventrolateral prefrontal cortex was
53 Page 6 of 14
Table 1 (continued)
First author Year Sample Methodology
neuroimaging: sMRI with voxel-based
morphometry
Newhill 2009 220 BPD patients BPD: Structured Interview for DSM-III-R
(53% female) Personality aggression: arrest records,
collateral reports, patients report using
behaviors adapted from the conflict
tactics scale
Newhill 2012 801 psychiatric patients BPD: Structured Interview for DSM-III-R
Personality, Emotion Dysregulation:
scale derived from items contained in
an instrument, the Novaco Anger
Scale, aggression: arrest records,
collateral informants, and patient
self-report, statistics: Latent growth
curve modeling
Peters 2016 916 undergraduates BPD: Personality Assessment
(70.4% female) Inventory—Borderline Features Scale,
aggressiveness: BPAQ, rumination:
Anger Rumination Scale, shame/guilt:
Positive and Negative Affect Scale –
Expanded Form and The Test of
Self-Conscious Affect
Peters 2017 193 male undergraduates BPD: Borderline Personality Disorder
Profile, aggressiveness: Crime and
Analogous Behaviors Scale, negative
urgency: Urgency, Premeditation,
Perseverance, Sensation Seeking,
Positive Urgency, Impulsive Behavior
Scale, statistics: hierarchical linear
regression analyses
Rausch 2016 55 BPD (64% female), BPD: International Personality Disorder
47 healthy women Examination, aggressiveness: BPAQ,
(55% female) Anger: State-Trait Anger Expression
Inventory, neurochemistry: cortisol
awaking response
Schönenberg 2013 32 male APD, BPD: Mini International
32 healthy men Neuropsychiatric Interview,
aggressiveness, BPAQ, behavioral
task: emotion recognition task
Schönenberg 2014 55 APD, 55 healthy APD: Mini International
volunteers Neuropsychiatric Interview,
aggressiveness: BPAQ, behavioral
task: ambiguous facial affect task
Scott 2017 117 emerging adult women, of BPD: Structured Interview for DSM-IV
those 51 with clinical sign. Personality, rejection/aggression:
BPD symptoms (i.e., 3 or ecological momentary assessment,
more DSM-IV criterions) statistics: multilevel path analysis
Scott 2014 75 psychiatric outpatients BPD: SCID-II, aggression: revised
and 75 community residents Conflict Tactics Scale, emotional
(65% female) dysregulation: DERS, statistics:
multivariate regression
Selby 2013 47 behaviorally dysregulated BPD: SCID-II,
(66% female) patients, of rumination/emotions/dysregulated
those 16 with BPD behavior: ecological momentary
assessment, statistics: generalized
hierarchical linear modeling
Curr Psychiatry Rep (2018) 20:53
Key findings
associated with aggressiveness in those
BPD patients with a history of traumatization
73% of BPD subjects engaged in aggression
during the 1-year study period
Emotion dysregulation mediated the
association between BPD and
aggression
Shame mediated the association between
BPD features and anger rumination,
and only decreased guilt significantly
mediated the relationship between
BPD features and aggressiveness
Negative urgency mediated the association
between BPD and aggressiveness. Other
factors of impulsivity showed no mediation
Cortisol awakening responses were positively
related to anger and aggressiveness in
female patients with BPD
APD subjects required significantly higher
levels of emotional intensity to correctly
identify the onset of an angry facial
expression as compared to control
participants
APD subjects show bias toward anger in
ambiguous facial tasks
Increases in perceived rejection predicted
increases in neg. Affect. Increases in neg.
Affect predicted aggressive urges/behavior.
BPD symptoms exacerbated the link between
rejection and aggression via increases in neg.
Affect (particularly anger), this process was
attenuated in women with greater APD
symptoms
Emotion dysregulation mediated the
association between BPD symptoms at
baseline and later psychological and
physical aggression
Increased rumination interacted with increased
negative emotions and increased BPD
symptoms in the prediction of dysregulated
behaviors, including aggression
Curr Psychiatry Rep (2018) 20:53
Table 1 (continued)
First author Year Sample Methodology
Sinai 2016 92 female BPD, 57 healthy BPD: The DSM-IV and ICD-10
women Personality Interview, aggressiveness:
Karolinska Interpersonal Violence
Scale, neurochemistry: T3 serum levels
Smeijers 2017 40 forensic APD (0% female), BPD: Structured Clinical Interview for
30 forensic BPD (4.2% DSM-IV axis II personality disorders,
female), 23 non-forensic aggressiveness: The reactive–proactive
BPD (35% female), 47 questionnaire, behavioral task: Hostile
healthy volunteers Interpretation Bias Task
(43% female)
Soloff 2014 51 BPD (80% female) BPD: IPDE, Diagnostic Interview for
Borderline Patients-Revised,
aggressiveness: Brown–Goodwin
Lifetime History of Aggression,
neuroimaging: sMRI using
voxel-based morphometry
Soloff 2017 31 female BPD, 25 healthy BPD: IPDE, Diagnostic Interview for
women Borderline Patients-Revised,
aggressiveness: Brown–Goodwin
Lifetime History of Aggression,
neuroimaging: fMRI during
go/no-go task
Stepp 2012 138 psychiatric outpatients PD: SCID-II, aggression: Inventory of
(75% female) of them Interpersonal problems, third scale,
54 BPD, 55 with another PD interpersonal problems: Inventory of
Interpersonal Problems
Terzi 2017 79 BPD (80% female) BPD: SCID-II, impulsivity: Barratt
Impulsivity Scale, aggressiveness:
BPAQ, emotion dysregulation:
Difficulties in Emotion Regulation
Scale, statistics: hierarchical linear
regression analyses
Timmermann 2017 22 APD (36% female), BPD: IPDE, neuroimaging: functional
29 HV (38% female) MRI combined with emotion
classification paradigm with
oxytocin/placebo in a double-blind,
randomized, placebo-controlled
crossover trial
Velotti 2017 83 male violent offenders APD: Millon Clinical Multiaxial
(22 APD) Inventory-II, aggressiveness: BPAQ,
mindfulness: Five Facet Mindfulness
Questionnaire
Wegrzyn 2017 30 male aggressive inmates, PD: SCID-II questionnaire, behavioral
15 male child sex offender, task: recognition of ambiguous facial
17 volunteers, self-reported expressions
dimensions of personality
pathology was assessed for
each group
Yu 2012 10,007 PD, 12,742,916 PD: clinical and/or semistructured
individuals from the interviews using explicit criteria (e.g.,
general population DSM, ICD), aggression: various
methods (i.e., file-records, self-reports,
interviews), statistics: meta-regression
BPAQ Buss Perry Aggression Questionnaire, CSF cerebrospinal fluid, DSM Diagnostic and Statistical Manual of Mental Disorders, ICD International
Classification of Disease, IPDE International Personality Disorders Examination, SCID-II Structured Clinical Interview for DSM-IVAxis II Personality
Disorders
Page 7 of 14 53
Key findings
Increased serum T3 levels were associated
with increased aggressiveness in BPD
Forensic APD and forensic BPD patients
show a hostile interpretation bias across four
(anger, fear, happy, disgust) emotional
expressions compared with healthy
volunteers and for anger and fear compared
with non-forensic BPD. An increased
hostile interpretation bias in response to
angry, fearful, and disgusted faces was
associated with increased aggressiveness
Increased aggressiveness was associated
with increase in gray matter volume in
prefrontal and limbic structures in BPD
Increased aggressiveness was associated with
reduced brain activity in the orbital frontal
cortex, hippocampus, and basal ganglia in
response to negative emotional context
during a go/no-go task in BPD
Interpersonal problems predicted subsequent
aggressive behavior in subjects scoring high
on BPD traits
Emotion dysregulation predicted
aggressiveness in BPD, in addition to the
variance explained by impulsivity
APD showed deficits in recognizing fearful
and happy faces, which normalized under
oxytocin
Mindfulness deficits were associated with
APD traits. Mindfulness interacted
with aggressiveness in predicting APD
Aggressive inmates rated ambiguous
fear-anger expressions as more angry,
compared with child sex offenders
and volunteers
Threefold increased risk of aggressive
outcomes in PD (random-effects
pooled odds ratio [OR] = 3.0, 95%
CI = 2.6 to 3.5) compared with the
general population
53 Page 8 of 14
condition that is related to threat hyposensitivity [34]. Yet,
Schönenberg and colleagues [33•] did not assess psychopathy
and were therefore not able to test this notion.
Hypersensitivity to interpersonal threat may be the conse-
quence of a hostile interpretation bias. The hostile interpreta-
tion bias stems from Dodge’s and Crick’s Social Information
Processing model and refers to a tendency to interpret others’
ambiguous intentions as hostile, which, in turn, predisposes
toward aggression [35]. One study showed that forensic
ASPD (N = 40) and BPD (N = 30) patients rated facial expres-
sions as more hostile than non-forensic BPD (N = 23) patients
and healthy controls. Additionally, an increased hostile inter-
pretation bias was associated with increased aggressiveness
[36]. Furthermore, using verbal stimuli, i.e., short one or two
sentences vignettes depicting ambiguous provocative situa-
tions, Lobbestael et al. [37] found that a hostile interpretation
bias predicted reactive aggression in a mixed ASPD/BPD
sample (N = 57).
Recently, rumination (i.e., repetitive thinking focused
on upsetting emotions and their causes and consequences)
has attracted increased scientific interest. Specifically, in
BPD patients, anger rumination was found to predict ag-
gressiveness (N = 93) [38] and mediated the association
between emotion dysregulation and aggressiveness (N =
91) [39]. Corroborating a role of rumination in the emer-
gence of aggression in personality disorders, an ecological
momentary assessment study showed that increased rumi-
nation interacted with increased negative emotions and in-
creased BPD symptoms in the prediction of dysregulated
behaviors, including aggression in a sample of dysregulat-
ed individuals including BPD patients (N = 42) [40].
Within this framework, it is of interest that shame was
found to mediate the association between BPD symptoms
and anger rumination in undergraduate students (N = 916)
[41]. The same study also demonstrated that reduced guilt,
but not increased shame, mediated the association between
BPD symptoms and aggressiveness.
Aggression has often been related to aberrant risk process-
ing. Yet, many aggressive acts might reflect the outcomes of
decisions made under conditions of ambiguity rather than risk.
In line with this, individuals with ASPD showed a deficit in
ambiguity sensitivity when compared to individuals from the
community with considerable antisocial behaviors [42].
Finally, lower ambiguity sensitivity was also associated with
higher levels of aggressiveness (but not rule-breaking).
Furthermore negative urgency (i.e., impulsive behavior in
response to intense, negative emotions) mediated the associa-
tion between BPD symptoms and intimate partner violence in
a sample of 193 male undergraduates [43]. Interestingly,
aggressiveness-related knowledge structures, i.e., internal rep-
resentations of past experiences, such as attitudes, goals, be-
havioral scripts, and beliefs about appropriate behavior, were
stronger associated with aggressiveness in individuals with
Curr Psychiatry Rep (2018) 20:53
BPD than in those with ASPD, suggesting the existence of
an aggressive BPD-subtype characterized by aggressive
scripts and beliefs [44]. Moreover, aggressiveness increased
after an experience of invalidation (i.e., rejection of one’s
emotional experience) in a sample of undergraduate students
with difficulties in emotion in a similar range as BPD patients
[45]. Finally, deficits in mindfulness (i.e., the proneness to be
attentive to and aware of what is taking place in one’s inner
world in the present) were associated with ASPD symptoms
and interacted with aggressiveness in predicting ASPD [46].
Neurobiological Data
Theories on the biological underpinnings of aggression, and in
particular of reactive aggression, propose a model implicating
predominantly prefrontal and limbic structures. More precise-
ly, a brain-circuit comprising the amygdala, hypothalamus,
and periaqueductal gray has been identified, which, when ac-
tivated to a sufficient degree, initiates reactive aggression.
Whether the recruitment of these structures results in reactive
aggression or not depends on regulatory prefrontal systems
including the ventromedial prefrontal cortex, dorsomedial pre-
frontal cortex and the inferior frontal gyrus (see, e.g., [47•] for
a review). From a neurochemical perspective, the insufficien-
cy of prefrontal regions in regulating limbic hyperactivity has
been related to deficiency of the prefrontal serotonergic sys-
tem [48]. In the following, we will first present studies that
investigated neurochemical methods followed by those stud-
ies using neuroimaging methods to study correlates of aggres-
sion in personality disorders.
Several lines of evidence suggest an involvement of low or
absent monoamine oxidase-A (MAO-A)—an enzyme of crit-
ical importance for the serotonergic system—activity in ag-
gression. More specifically, individuals with a point mutation
of the MAO-A gene, which leads to complete and selective
deficiency of enzymatic activity of MAO-A, exhibited highly
enhanced levels of aggressive behavior [49]. Further,
knocking out MAO-A led to reactive aggressive adult mice
[50]. Prominently, MAO-A genetic polymorphisms that are
associated with lower MAO-A transcription have been shown
to interact with childhood adversity to increase the risk of
adult aggressive behavior [51].
Recently, Kolla and colleagues expanded these findings to
the issue of aggressiveness in personality disorders. First, in-
dividuals with ASPD showed reduced density of MAO-A in
comparison to healthy volunteers (N = 18 per group) in brain
regions including the prefrontal cortex, anterior cingulate cor-
tex, dorsal putamen, thalamus, hippocampus, and the mid-
brain [52••]. Second, severe BPD patients exhibited elevated
MAO-A density in the prefrontal and anterior cingulate cortex
compared to moderate BPD patients, depressive patients, and
healthy volunteers (N = 14 per group) [53]. Third, ASPD
Curr Psychiatry Rep (2018) 20:53
patients with the low-activity variant of MAO-A (MAOA-L)
had decreased surface area in the right basolateral amygdala
nucleus and increased surface area in the right anterior cortical
amygdaloid nucleus compared to healthy MAOA-L carriers
(N = 20) [54]. Finally, greater impulsiveness was predicted by
an interaction between MAOA-L carrier status and childhood
abuse in patients with BPD (N = 20), but not in patients with
ASPD (N = 18) or healthy volunteers (N = 20) [55].
Interestingly, alterations of the MAO-A system in personality
disorders have been extended to epigenetic processes as
shown by MAO-A promoter hypermethylation, which leads
to reduced transcriptional activity, in ASPD (N = 86) as com-
pared to healthy volunteers (N = 73) [56].
The role of the neuropeptide oxytocin in processes of social
cognition (i.e., the multiple integrative mental processes that
underlie social interactions, [57]) has attracted considerable
interest over the last years [58]. With regard to aggression in
personality disorders, one study demonstrated that plasma
concentrations of oxytocin were negatively associated with
aggressiveness in female BPD patients (N = 34) [59].
Additionally, results suggest a beneficial effect of oxytocin
on BPD patients’ threat hypersensitivity, as its intranasal ad-
ministration reduced the speed and number of reflexive eye
movements toward the eyes of angry faces and normalized the
hyperactivity of the amygdala for angry compared with happy
faces in female BPD patients (N = 40) [30]. Aligning this,
oxytocin normalized the deficits in recognizing fearful and
happy faces of ASPD patients (N = 22) [60]. Moreover, it also
modulated neuronal activity in brain areas involved in em-
pathic functioning [61]—although this has not yet been shown
in individuals with personality disorders. On the genetic level,
results showed that polymorphisms of the oxytocin receptor
were associated with aggressiveness in a nationwide twin
sample (N = 2372) [62]. In a preliminary report of six individ-
uals with ASPD, reactive aggression was partly increased after
oxytocin administration [63]. Of note, this study shows sever-
al limitations, such as a small number of participants and nei-
ther a placebo nor a comparison to a control group. Other
negative effects reported after oxytocin administration include
the increase of aggressive behavior and out-group aggression
in samples of healthy volunteers [64, 65]. These at first coun-
terintuitive results emphasize the need to consider contextual
aspects and interindividual differences influencing the effects
of oxytocin [66].
In addition to oxytocin, several other neurochemical com-
pounds have recently been associated with aggressiveness in
personality disorders. Specifically, increased aggressiveness
was found to be related to increased serum levels of the thy-
roid hormone T3 in BPD (N = 93) [67] as well as in ASPD
patients (N = 96) [68]. Cortisol awakening responses were
positively related to anger and aggressiveness in a mixed gen-
der sample patients with BPD (N = 55) [69]. Low plasma
eicosapentaenoic acid levels were associated with elevated
Page 9 of 14 53
aggressiveness and impulsivity in patients with major depres-
sive disorder and partly comorbid BPD (N = 48, of those N = 6
with comorbid BPD) [70]. In addition, Coccaro et al. investi-
gated the cerebrospinal fluid of individuals with a variety of
personality disorders and found an association between in-
creased aggressiveness and increased levels of neuropeptide-
Y (N = 40) [71], glutamate (N = 28) [72], C-reactive protein
(N = 17) [73], and interleukin-1 receptor (N = 38) [74•]. An
extensive discussion of these results is beyond the scope of
this review article, yet it stands out that many of these sub-
stances (cortisol, eicosapentaenoic acid, neuropeptide-Y, C-
reactive protein, and interleukin-1) are central to the regulation
of inflammatory processes. A scent that has also been picked
up in the fields of other major mental disorders, such as
schizophrenia [75] and depression [76] suggesting than in-
flammatory processes may be of transdiagnostic relevance in
the genesis of mental disorders.
Increased levels of the sex hormone testosterone have been
found to be weakly associated with aggression in the general
population (r = 0.08, see [77] for a meta-analysis). In BPD, a
recent study showed increased saliva testosterone levels in
female and male BPD patients (N = 55, 35 women) compared
to healthy volunteers (N = 47, 26 women) [69]. Notably, tes-
tosterone levels were the highest in those BPD patients with
low cortisol awakening responses. However, testosterone
levels were not associated with aggressiveness. This finding
corroborates the assumption of a more complex role of testos-
terone in aggression of personality disorders that needs to
consider potential interactions with factors, such as cortisol
levels or the social context of the aggressive behavior, e.g.,
whether it emerges within a competitive or provocative con-
text [78•].
Additionally, Bandelow and colleagues raised the question
of whether the opioid system may be implicated in behavioral
dyscontrol including aggression in patients with BPD [79] and
ASPD [80]. For BPD, this assertion has received empirical
support by the finding of reduced opioid receptor concentra-
tion and opioid system response to a negative emotional chal-
lenge in BPD patients (N = 18) compared to healthy volun-
teers (N = 14). Finally, γ-aminobutyric acid in the ACC was
associated with increased aggressiveness in a mixed sample of
patients with BPD (N = 26) and attention deficit hyperactivity
disorder (N = 22) [81].
Neuroimaging studies revealed new insights into the pro-
cesses underlying aggression in individuals with personality
disorders. Increased aggressiveness was associated with re-
duced brain activity in the orbital frontal cortex, hippocampus,
and basal ganglia in response to negative emotional context
during a go/no-go task in female BPD patients (N = 31) [82].
One study investigated a sample of female (N = 33) and male
(N = 23) patients with BPD and healthy women (N = 30) and
healthy men (N = 26) using a script-driven imagery task
consisting of narratives of both interpersonal rejection and
53 Page 10 of 14
directing physical aggression toward others [83••]. Results
revealed a sex by group interaction while imagining both in-
terpersonal rejection and acting out aggressively, in which
male BPD patients showed higher activity in the left amygdala
than female patients. Interestingly, during the aggression
phase, men with BPD exhibited higher activity in the lateral
orbitofrontal and dorsolateral prefrontal cortices compared
with healthy men and female patients. Further analyses re-
vealed a negative connectivity between amygdala and poste-
rior middle cingulate cortex in male BPD patients contrasted
by positive connectivity in female patients with BPD. Finally,
increased aggressiveness correlated with increased connectiv-
ity between the amygdala and the thalamus. As a whole, these
results suggest that female BPD patients are able to success-
fully dampen their inner tension during the imagination of
aggressive behavior, while male BPD patients appear to fail
in conducting top-down regulation despite their efforts.
Four structural neuroimaging studies provided more in-
sights into aggression of individuals with personality
MAO-A3 Oxytocin3
Thyriod
hormone T33, γ-
aminobutyric
acid3
Hyper- Hypersensivity
Emoon 1/hyposensivity to interpersonal
dysregulaon1 2 to interpersonal rejecon1
threat
Negave Aggression-related
urgency1 knowledge
structures1
Fig. 1 Correlates of aggression in personality disorders over the last
5 years. Lower half: emotion dysregulation, a hypersensitivity to
interpersonal rejection/threat, increased rumination, increased negative
urgency, aggression-related knowledge structures, and invalidation were
either corroborated or emerged as psychological correlates of aggression
in borderline personality disorder and reduced ambiguity sensitivity,
hyposensitivity to interpersonal threat, and reduced mindfulness were
associated with aggression in antisocial personality disorder. Upper
half: neurobiological correlates of aggression in various personality
Curr Psychiatry Rep (2018) 20:53
disorders. Soloff and colleagues showed that increased ag-
gressiveness was associated with gray matter volume increase
in prefrontal and limbic structures (N = 51) [84]. When com-
pared to controls, patients with ASPD and comorbid BPD
(N = 13) showed smaller gray matter volume in orbitofrontal
and ventromedial prefrontal cortex, whereas patients with
APD and comorbid psychopathy (N = 12) showed less vol-
ume in cortical midline areas (dorsomedial prefrontal cortex
and precuneus) that are involved in self-referential emotion
processing and self-reflection [85]. Moreover, gray matter
volume loss in the right ventrolateral prefrontal cortex
was specifically associated with aggressiveness in those
BPD patients (N = 18) with a history of traumatization,
indicating a particular impact of traumatization on prefron-
tal regions and in turn aggression [86]. Finally, aggressive-
ness was associated with an outward deformation in re-
gions of the left superficial and laterobasal amygdala of
male BPD patients (N = 21) and thus regions that are crit-
ically implicated in social information processing [87].
Prefrontal-
limbic3
Inflammatory
markers3
Aggression
in personality
disorders
Reduced
Increased
ambiguity
ruminaon1
sensivity2
Invalidaon1 Reduced
mindfulness2
disorders were alterations of the monoaminooxidase-A-, the
oxytocinergic-, and the prefrontal-limbic-system as well as
cerebrospinal fluid levels of the thyroid hormone T3, γ-aminobutyric,
and several inflammatory markers (cortisol, eicosapentaenoic acid,
neuropeptide-Y, C-reactive protein, and interleukin-1). 1This finding has
been observed in borderline personality disorder. 2This finding has been
observed in antisocial personality disorder. 3This finding has been
observed in various personality disorders. MAO-A monoaminooxidase-A
Curr Psychiatry Rep (2018) 20:53
Conclusion
This review article aimed at providing an update on studies
conducted within the last 5 years that investigated correlates of
aggression in personality disorders. It considered studies that
used self-reports, interviews, behavioral, and neurobiological
data. Within the personality disorders, aggression has been
typically related to BPD and ASPD. Accordingly, most of
the presented data refers to these two disorders. Results (see
also Fig. 1) showed that emotion dysregulation, an increased
sensitivity to interpersonal rejection/threat, increased rumina-
tion, increased negative urgency, aggression-related knowl-
edge structures, and invalidation were either corroborated or
emerged as psychological correlates of aggression in border-
line personality disorder, while reduced ambiguity sensitivity,
decreased sensitivity to interpersonal threat, and reduced
mindfulness were associated with aggression in antisocial per-
sonality disorder. On the neurobiological level alterations of
the monoaminooxidase-A-, the oxytocinergic-, and the
prefrontal-limbic-system as well as increases of the thyroid
hormone T3, γ-aminobutyric acid and several inflammatory
markers were associated with increased aggression across var-
ious personality disorders.
Last but not the least, the effectiveness of current
psychotherapeutical [88, 89] as well as psychopharmacologi-
cal [90, 91] treatment strategies of aggressive individuals with
personality disorders is limited. In this closing section, we will
therefore highlight questions that are currently addressed in
the field of aggression in personality disorders and that may
facilitate the development of innovative treatment
interventions.
First, the question of how to best conceptualize person-
ality disorders is subject of current debate. The discussion
fluctuates between using a categorical and dimensional or a
mixture between the two, a hybrid approach [92•].
Currently, the available diagnostic systems, the DSM-5
and the International Classification of diseases (ICD)-10,
use a solely categorical approach, which has its foundation
in the 1980s [93]. Yet, both systems have paved the way
toward a more dimensional approach by either suggesting
a hybrid model in section III of the DSM-5 or by proposing
a dimensional model with the possibility to add a categor-
ical specifier for BPD in its revised version (ICD-11). This
is in line with contemporary advances in psychopathology,
such as the Research Domain Criteria Project that classify
mental disorders on the basis of biobehavioral mechanisms
(i.e., basic dimensions of mental functioning, e.g., the re-
sponse to fear, that are grounded on neurobiological and
behavioral measures) [94]. It is additionally supported by
recent research showing the usefulness of a dimensional
approach to predict aggressive incidents in individuals
with personality disorders [95]. In sum, acknowledging
dimensional aspects of personality pathology may provide
Page 11 of 14 53
a basis to ground interventions on neurobiological process-
es and to more precisely tailor the interventions to the
specific symptomatology of the aggressive individual.
Second, controversy exists over how to best classify ag-
gression. Aggression is a complex social behavior [1] and
classical typologies, e.g., reactive aggression and impulsive
represent overlapping constructs [96] and fail in accommodat-
ing certain forms of aggression, such as appetitive aggression
(i.e., aggression that is not a response to threat or a mean to
obtain a certain goal, but just an end in itself) [97]. It may
therefore be beneficial to use a more differentiated classifica-
tion of aggression, such as the quadripartite violence typology
[98•]. According to this model, violence (as an extreme form
of aggression) may be either impulsive or controlled/and with-
in each of these categories, aggression is either appetitively or
aversively motivated. Usage of this framework could aid in
meeting the individual needs of aggressive individuals with
personality disorders, especially with regard to the different
motives driving the aggressive behavior.
Related to this, third, the construct validity of the existing
paradigms for the study of aggression in personality disorders
has been questioned [99]. The restriction to stimulus–response
sequences as conducted in most of the paradigms leaves out
underlying motives and intentions of aggressive behavior
[100] and the relationship between provocateur and aggressor
that seems to be of particular importance in BPD. Thus, in-
struments that mimic aggression in an ecologically valid man-
ner are needed.
Fourth, instead of being the consequence of a single per-
sonality disorder, it may rather be the combination of specific
aspects of personality pathology that are decisive for the emer-
gence of aggression. For instance, the combination of narcis-
sism, machiavellianism, and psychopathy has received nu-
merous empirical support for its role in aggression [101, 102].
Fifth, treatment response may differ depending on interin-
dividual aspects, such as sex, early adversity, or developmen-
tal aspects. While first studies have started to address this
matter [103], more work is needed to precisely disentangle
their effects.
As a whole, our understanding of the processes underlying
aggression in personality disorders has significantly increased
over the last 5 years. More efforts in improving the conceptu-
alization of personality disorders and aggression are needed to
develop innovative treatments for those affected.
Compliance with Ethical Standards
Conflict of Interest The authors declare that they have no conflict of
interest.
Human and Animal Rights and Informed Consent This article does not
contain any studies with human or animal subjects performed by any of
the authors.
53 Page 12 of 14
References
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
•• Of major Importance
1. Anderson CA, Bushman BJ. Human aggression. Annu Rev
Psychol. 2002;53:27–51.
2. Berkowitz L. Aggression: its causes, consequences, and control.
New York: McGraw-Hill; 1993.
3. Centers for Disease Control and Prevention. Youth Risk
Behavioral Surveillance—United States, 2013. Druid Hills, GA;
2014.
4. Miller T, Cohen M, Wiersma B. Victim costs and consequences: a
new look. National Institute of Justice - Research Report. 1996.
5. Yu R, Geddes JR, Fazel S. Personality disorders, violence, and
antisocial behavior: a systematic review and meta-regression anal-
ysis. J Personal Disord. 2012;26(5):775–92.
6. American Psychiatric Association. Diagnostic and statistical man-
ual of mental disorders. 5th ed. Arlington: American Psychiatric
Publishing; 2013.
7. Genovese T, Dalrymple K, Chelminski I, Zimmerman M.
Subjective anger and overt aggression in psychiatric outpatients.
Compr Psychiatry. Elsevier Inc. 2017;73:23–30.
8.• Lobbestael J, Cima M, Lemmens A. The relationship between
personality disorder traits and reactive versus proactive motivation
for aggression. Psychiatry Res. Elsevier; 2015;229(1–2):155–160.
This study investigated the relationship between reactive and
proactive aggression and traits of all DSM-5 PD and shows
that paranoid traits were positively related to reactive aggres-
sion, whereas proactive aggression was uniquely related to
antisocial PD traits.
9. Coid J, Yang M, Tyrer P, Roberts A, Ullrich S. Prevalence and
correlates of personality disorder in Great Britain. Br J Psychiatry.
2006;188:423–31.
10. Newhill CE, Eack SM, Mulvey EP. Violent behavior in borderline
personality. J Personal Disord. 2009;23(6):541–54.
11. Blair RJR. Psychopathy, frustration, and reactive aggression: the
role of ventromedial prefrontal cortex. Br J Psychol. 2010;101(Pt
3):383–99.
12. Anderson NE, Kiehl KA. Psychopathy and aggression: when
paralimbic dysfunction leads to violence. Curr Top Behav
Neurosci NIH Public Access. 2014;17:369–93.
13. Buss A. The psychology of aggression. Hoboken: John Wiley &
Sons Inc; 1961. 307 p
14. Hayes A. Introduction to mediation, moderation, and conditional
process analysis: a regression-based approach. 1st ed. New York:
Guilford Publications Inc.; 2012. 507 p
15. Stepp SD, Scott LN, Morse JQ, Nolf KA, Hallquist MN, Pilkonis
PA. Emotion dysregulation as a maintenance factor of borderline
personality disorder features. Compr Psychiatry. Elsevier Inc.
2014;55(3):657–66.
16. Newhill CE, Eack SM, Mulvey EP. A growth curve analysis of
emotion dysregulation as a mediator for violence in individuals
with and without borderline personality disorder. J Pers Disord
Guilford Publications Inc. 2012;26(3):452–67.
17.•• Scott LN, Stepp SD, Pilkonis PA. Prospective associations be-
tween features of borderline personality disorder, emotion dysreg-
ulation, and aggression. Personal Disord. 2014;5(3):278–88. This
longitudinal study shows that BPD symptoms at baseline and
later psychological and physical aggression were fully mediat-
ed by difficulties with emotion regulation.
Curr Psychiatry Rep (2018) 20:53
18. Terzi L, Martino F, Berardi D, Bortolotti B, Sasdelli A, Menchetti
M. Aggressive behavior and self-harm in borderline personality
disorder: the role of impulsivity and emotion dysregulation in a
s a m p l e o f o u t p a t i e n t s . P s y c h i a t r y R e s . E l s e v i e r.
2017;249(November 2016):321–6.
19. Gardner K, Archer J, Jackson S. Does maladaptive coping mediate
the relationship between borderline personality traits and reactive
and proactive aggression? Aggress Behav. 2012;38(5):403–13.
20. Moore KE, Tull MT, Gratz KL. Borderline personality disorder
symptoms and criminal justice system involvement: the roles of
emotion-driven difficulties controlling impulsive behaviors and
physical aggression. Compr Psychiatry. Elsevier Inc. 2017;76:
26–35.
21. Mancke F, Herpertz SC, Kleindienst N, Bertsch K. Emotion dys-
regulation and trait anger sequentially mediate the association be-
tween borderline personality disorder and aggression. J Personal
Disord. 2017;31(2):256–72.
22. Herpertz SC, Bertsch K. The social-cognitive basis of personality
disorders. Curr Opin Psychiatry. 2014;27(1):73–7.
23. Gunderson JG, Lyons-Ruth K. BPD’s interpersonal hypersensitiv-
ity phenotype: a gene-environment-developmental model. J
Personal Disord. 2008;22(1):22–41.
24. Scott LN, Wright AGC, Beeney JE, Lazarus SA, Pilkonis PA,
Stepp SD. Borderline personality disorder symptoms and aggres-
sion: a within-person process model. J Abnorm Psychol.
2017;126(4):429–40.
25. Herr NR, Keenan-Miller D, Rosenthal MZ, Feldblum J. Negative
interpersonal events mediate the relation between borderline fea-
tures and aggressive behavior: findings from a nonclinical sample
of undergraduate women. Personal Disord. 2013;4(3):254–60.
26. Stepp SD, Smith TD, Morse JQ, Hallquist MN, Pilkonis PA.
Prospective associations among borderline personality disorder
symptoms, interpersonal problems, and aggressive behaviors. J
Interpers Violence. 2012;27(1):103–24.
27. Banny AM, Tseng W, Murray-Close D, Pitula CE, Crick NR.
Borderline personality features as a predictor of forms and func-
tions of aggression during middle childhood: examining the roles
of gender and physiological reactivity. Dev Psychopathol.
2014;26(3):789–804.
28. Hagenhoff M, Franzen N, Gerstner L, Koppe G, Sammer G,
Netter P, et al. Reduced sensitivity to emotional facial expressions
in borderline personality disorder: effects of emotional valence
and intensity. J Personal Disord. 2013;27(1):19–35.
29. Izurieta Hidalgo NA, Oelkers-Ax R, Nagy K, Mancke F, Bohus
M, Herpertz SC, et al. Time course of facial emotion processing in
women with borderline personality disorder: an ERP study. J
Psychiatry Neurosci. 2016;41(1):16–26.
30.•• Bertsch K, Gamer M, Schmidt B, Schmidinger I, Walther S,
Kästel T, et al. Oxytocin and reduction of social threat hypersen-
sitivity in women with borderline personality disorder. Am J
Psychiatry. 2013;170(10):1169–77. In this pharmaco-challenge
study, oxytocin normalized behavioral and neural patterns of
threat hypersensitvity in female BPD patients.
31. Bertsch K, Krauch M, Stopfer K, Haeussler K, Herpertz C, Gamer
M. Interpersonal threat sensitivity in borderline personality disor-
der: an eye-tracking study. J Pers Disord. 2017;31(5):1–24.
32. Schönenberg M, Jusyte A. Investigation of the hostile attribution
bias toward ambiguous facial cues in antisocial violent offenders.
Eur Arch Psychiatry Clin Neurosci. 2014;264(1):61–9.
33.• Schönenberg M, Louis K, Mayer S, Jusyte A. Impaired identifi-
cation of threat-related social information in male delinquents with
antisocial personality disorder. J Personal Disord. 2013;27(4):
496–505. In this facial emotion recognition task, ASPD pa-
tients showed a hyposensitivity to cues of interpersonal threat.
34. Reidy DE, Shelley-Tremblay JF, Lilienfeld SO. Psychopathy, re-
active aggression, and precarious proclamations: a review of
Curr Psychiatry Rep (2018) 20:53
behavioral, cognitive, and biological research. Aggress Violent
Behav. Elsevier B.V. 2011;16(6):512–24.
35. Crick N, Dodge K. Social information-processing mechanisms in
reactive and proactive aggression. Child Dev. 1996;67(3):993–
1002.
36. Smeijers D, Rinck M, Bulten E, van den Heuvel T, Verkes RJ.
Generalized hostile interpretation bias regarding facial expres-
sions: characteristic of pathological aggressive behavior. Aggress
Behav. 2017;43(4):386–97.
37. Lobbestael J, Cima M, Arntz A. The relationship between adult
reactive and proactive aggression, hostile interpretation bias, and
antisocial personality disorder. Guilford Publications Inc.; 2013.
38. Martino F, Caselli G, Berardi D, Fiore F, Marino E, Menchetti M,
et al. Anger rumination and aggressive behaviour in borderline
personality disorder. Personal Ment Health. 2015;9:277–87.
39. Martino F, Caselli G, Di Tommaso J, Sassaroli S, Spada MM,
Valenti B, et al. Anger and depressive ruminations as predictors
of dysregulated behaviours in borderline personality disorder. Clin
Psychol Psychother 2017;(February):1–7.
40. Selby EA, Joiner TE. Emotional cascades as prospective predic-
tors of dysregulated behaviors in borderline personality disorder.
Personal Disord. 2013;4(2):168–74.
41. Peters JR, Geiger PJ. Borderline Personality Disorder and Self-
Conscious Affect: Too much shame but not enough guilt?
Personal Disord. 2016;7(Advanced online publication):303–8.
42. Buckholtz JW, Karmarkar U, Ye S, Brennan GM, Baskin-
Sommers A. Blunted ambiguity aversion during cost-benefit de-
cisions in antisocial individuals. Sci Rep Springer US. 2017;7(1):
2030.
43. Peters JR, Derefinko KJ, Lynam DR. Negative urgency accounts
for the association between borderline personality features and
intimate partner violence in young men. J Personal Disord.
2017;31(1):16–25.
44. Gilbert F, Daffern M, Talevski D, Ogloff JRP. Understanding the
personality disorder and aggression relationship: an investigation
using contemporary aggression theory. J Personal Disord.
2015;29(1):100–14.
45. Herr NR, Jones AC, Cohn DM, Weber DM. The impact of vali-
dation and invalidation on aggression in individuals with emotion
regulation difficulties. Personal Disord. 2015;6(4):310–4.
46. Velotti P, Garofalo C, D’Aguanno M, Petrocchi C, Popolo R,
Salvatore G, et al. Mindfulness moderates the relationship be-
tween aggression and antisocial personality disorder traits: prelim-
inary investigation with an offender sample. Compr Psychiatry.
Elsevier Inc. 2016;64:38–45.
47.• Blair RJR. The neurobiology of impulsive aggression. J Child
Adolesc Psychopharmacol. 2016;26(1):4–9. This study provides
a comprehensive overview on the neurobiology of reactive
(also known as impulsive) aggression.
48. Krakowski M. Violence and serotonin: influence of impulse con-
trol, affect regulation, and social functioning. J Neuropsychiatry
Clin Neurosci. 2003;15(3):294–305.
49. Brunner HG, Nelen M, Breakefield XO, Ropers HH, B a v O.
Abnormal behavior associated with a point mutation in the struc-
tural gene for monoamine oxidase A. Science. 1993;262(5133):
578–80.
50. Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, et al.
Aggressive behavior and altered amounts of brain serotonin and
norepinephrine in mice lacking MAOA. Science.
1995;268(5218):1763–6.
51. Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, et al.
Role of genotype in the cycle of violence in maltreated children.
Science. 2002;297(5582):851–4.
52.•• Kolla NJ, Matthews B, Wilson AA, Houle S, Michael Bagby R,
Links P, et al. Lower monoamine oxidase-A total distribution vol-
ume in impulsive and violent male offenders with antisocial
Page 13 of 14 53
personality disorder and high psychopathic traits: an [11C]
H a r m i n e p o s i t r o n e m i s s i o n t o m o g r a p h y s t u d y.
Neuropsychopharmacology Nature Publishing Group.
2015;40(11):2596–603. This positron emission tomography
study showed lower brain MAO-A levels in ASPD patients,
extending preclinical models of aggression into the area of
aggression in PD.
53. Kolla NJ, Chiuccariello L, Wilson AA, Houle S, Links P, Bagby
RM, et al. Elevated monoamine oxidase-A distribution volume in
borderline personality disorder is associated with severity across
mood symptoms, suicidality, and cognition. Biol Psychiatry.
2016;79(2):117–26.
54. Kolla NJ, Patel R, Meyer JH, Chakravarty MM. Association of
monoamine oxidase-A genetic variants and amygdala morpholo-
gy in violent offenders with antisocial personality disorder and
high psychopathic traits. Sci Rep. Springer US; 2017;(July):1–13.
55. Kolla NJ, Meyer J, Sanches M, Charbonneau J. Monoamine
oxidase-A genetic variants and childhood abuse predict impul-
s i v e n e s s i n b o r d e r l i n e p e r s o n a l i t y d i s o r d e r. C l i n
Psychopharmacol Neurosci. 2017;15(4):343–51.
56. Checknita D, Maussion G, Labonté B, Comai S, Tremblay RE,
Vitaro F, et al. Monoamine oxidase A gene promoter methylation
and transcriptional downregulation in an offender population with
antisocial personality disorder. Br J Psychiatry. 2015;206(3):216–
22.
57. Keech B, Crowe S, Hocking DR. Intranasal oxytocin, social cog-
nition and neurodevelopmental disorders: a meta-analysis.
Psychoneuroendocrinology. Elsevier. 2018;87(September 2017):
9–19.
58. Kirsch P. Oxytocin in the socioemotional brain: implications for
psychiatric disorders. Dialogues Clin Neurosci Clin Neurosc.
2015;17:463–76.
59. Bertsch K, Schmidinger I, Neumann ID, Herpertz SC. Reduced
plasma oxytocin levels in female patients with borderline person-
ality disorder. Horm Behav. 2013;63(3):424–9.
60. Timmermann M, Jeung H, Schmitt R, Boll S, Freitag CM,
Bertsch K, et al. Oxytocin improves facial emotion recogni-
tion in young adults with antisocial personality disorder.
Psychoneuroendocrinology. Elsevier. 2017;85(June):158–64.
61. Domes G, Kumbier E, Heinrichs M, Herpertz SC. Oxytocin pro-
motes facial emotion recognition and amygdala reactivity in adults
with Asperger syndrome. Neuropsychopharmacology. American
College of Neuropsychopharmacology. 2014;39(3):698–706.
62. Hovey D, Lindstedt M, Zettergren A, Jonsson L, Johansson A,
Melke J, et al. Antisocial behavior and polymorphisms in the
oxytocin receptor gene: findings in two independent samples.
Mol Psychiatry. 2016;21(7):983–8.
63. Alcorn JL, Rathnayaka N, Swann AC, Moeller FG, Lane SD.
Effects of intranasal oxytocin on aggressive responding in antiso-
cial personality disorder. Psychol Rec. 2015;65(4):691–703.
64. Alcorn JL, Green CE, Schmitz J, Lane SD. Effects of oxytocin on
aggressive responding in healthy adult men. Behav Pharmacol.
2015;26:798–804.
65. De Dreu CKW, Kret ME. Oxytocin conditions intergroup relations
through upregulated in-group empathy, cooperation, conformity,
and defense. Biol Psychiatry. Elsevier. 2016;79(3):165–73.
66. Bartz JA, Zaki J, Bolger N, Ochsner KN. Social effects of oxyto-
cin in humans: context and person matter. Trends Cogn Sci.
2011;15(7):301–9.
67. Sinai C, Hirvikoski T, Nordström A-L, Nordström P, Nilsonne Å,
Wilczek A, et al. Thyroid hormones and adult interpersonal vio-
lence among women with borderline personality disorder.
Psychiatry Res. Elsevier. 2015;227(2–3):253–7.
68. Evrensel A, Unsalver BO, Ozsahin A. The relationship between
aggression and serum thyroid hormone level in individuals
53 Page 14 of 14
diagnosed with antisocial personality disorder. Noro Psikiyatr Ars.
2016;53(2):120–5.
69. Rausch J, Gäbel A, Nagy K, Kleindienst N, Herpertz SC, Bertsch
K. Increased testosterone levels and cortisol awakening responses
in patients with borderline personality disorder: gender and trait
aggressiveness matter. Psychoneuroendocrinology. Elsevier Ltd.
2015;55:116–27.
70. Beier A, Lauritzen L, Galfalvy H, Cooper T, Oquendo M,
Grunebaum M, et al. Low plasma eicosapentaenoic acid levels
are associated with elevated trait aggression and impulsivity in
major depressive disorder with a history of comorbid substance
use disorder. J Psychiatr Res. 2014;57:133–40.
71. Coccaro EF, Lee R, Liu T, Mathé AA. Cerebrospinal fluid neuro-
peptide Y-like immunoreactivity correlates with impulsive aggres-
sion in human subjects. Biol Psychiatry. 2012;72(12):997–1003.
72. Coccaro EF, Lee R, Vezina P. Cerebrospinal fluid glutamate con-
centration correlates with impulsive aggression in human subjects.
J Psychiatr Res. 2013;47:1247–53.
73. Coccaro EF, Lee R, Coussons-Read M. Cerebrospinal fluid and
plasma C-reactive protein and aggression in personality-
disordered subjects: a pilot study. J Neural Transm. 2015;122(2):
321–6.
74.• Coccaro EF, Lee R, Coussons-Read M. Cerebrospinal fluid inflam-
matory cytokines and aggression in personality disordered sub-
jects. Int J Neuropsychopharmacol. 2015;18(7):1–7. This study
shows the association between increased inflammatory
markers in cerebrospinal fluid and increased aggression in PD.
75. Müller N, Weidinger E, Leitner B, Schwarz MJ. The role of in-
flammation in schizophrenia. Front Neurosci. 2015;9(OCT).
76. Miller AH, Raison CL. The role of inflammation in depression:
from evolutionary imperative to modern treatment target. Nat Rev
Immunol. 2016;16(1):22–34.
77. Archer J, Graham-Kevan N, Davies M. Testosterone and aggres-
sion: a reanalysis of book, Starzyk, and Quinsey’s (2001) study.
Aggress Violent Behav. 2005;10(2):241–61.
78.• Carre JM, Olmstead NA. Social neuroendocrinology of human
aggression: examining the role of competition-induced testoster-
one dynamics. Neuroscience. 2015;286:171–86. This article pro-
vides an overview on the interaction of testosterone and com-
petition in the modulation of human aggression.
79. Bandelow B, Schmahl C, Falkai P, Wedekind D. Borderline per-
sonality disorder: a dysregulation of the endogenous opioid sys-
tem? Psychol Rev. 2010;117(2):623–36.
80. Bandelow B, Wedekind D. Possible role of a dysregulation of the
endogenous opioid system in antisocial personality disorder. Hum
Psychopharmacol. 2015;30(9):391–3.
81. Ende G, Cackowski S, Van Eijk J, Sack M, Demirakca T,
Kleindienst N, et al. Impulsivity and aggression in female BPD
and ADHD patients: association with ACC glutamate and GABA
concentrations. Neuropsychopharmacology. Nature Publishing
Group. 2016;41(2):410–8.
82. Soloff PH, Abraham K, Burgess A, Ramaseshan K, Chowdury A,
Diwadkar VA. Impulsivity and aggression mediate regional brain
responses in borderline personality disorder: an fMRI study.
Psychiatry Res - Neuroimaging. 2017;260(June 2016):76–85.
83.•• Herpertz SC, Nagy K, Ueltzhöffer K, Schmitt R, Mancke F,
Schmahl C, et al. Brain mechanisms underlying reactive aggres-
sion in borderline personality disorder—sex matters. Biol
Psychiatry. 2017;82(4):257–66. This functional neuroimaging
study provided insights into sex differences in aggression of
patients with BPD. Male patients with BPD showed poor top-
down adjustment of aggressive behavior despite their efforts
at control. Female patients appeared to be less aroused
through rejection and to successfully dampen aggressive ten-
sion during the imagination of aggressive behavior.
Curr Psychiatry Rep (2018) 20:53
84. Soloff PH, White R, Diwadkar VA. Impulsivity , aggression and
brain structure in high and low lethality suicide attempters with
borderline personality disorder. Psychiatry Res Neuroimaging.
Elsevier. 2014;222(3):131–9.
85. Bertsch K, Grothe M, Prehn K, Vohs K, Berger C, Hauenstein K,
et al. Brain volumes differ between diagnostic groups of violent
criminal offenders. Eur Arch Psychiatry Clin Neurosci.
2013;263(7):593–606.
86. Morandotti N, Dima D, Jogia J, Frangou S, Sala M, De Vidovich
GZ, et al. Childhood abuse is associated with structural impair-
ment in the ventrolateral prefrontal cortex and aggressiveness in
patients with borderline personality disorder. Psychiatry Res
Neuroimaging. 2013;213(1):18–23.
87. Mancke F, Herpertz SC, Hirjak D, Knies R, Bertsch K. Amygdala
structure and aggressiveness in borderline personality disorder.
Eur Arch Psychiatry Clin Neurosci. 2016 Nov 22.
88. Gibbon S, Duggan C, Stoffers J, et al. Psychological interventions
for antisocial personality disorder. Cochrane Database Syst Rev.
2010; Issue 6. Art.No.:CD007668.
89. Stoffers JM, Völlm BA, Rücker G, et al. Psychological therapies
for people with borderline personality disorder. Cochrane
Database Syst Rev. 2012; Issue 8.Art.No.:CD005652.
90. Khalifa N, Duggan C, Stoffers J, et al. Pharmacological interven-
tions for antisocial personality disorder. Cochrane Database Syst
Rev. 2010; Issue 8. Art. No.: CD007667.
91. Lieb K, Völlm B, Rücker G, Timmer A, Stoffers JM.
Pharmacotherapy for borderline personality disorder: Cochrane
systematic review of randomised trials. Br J Psychiatry.
2010;196:4–12.
92.• Herpertz SC, Huprich SK, Bohus M, Chanen A, Goodman M,
Mehlum L, et al. The challenge of transforming the diagnostic
system of personality disorders. J Pers Disord. 2017;31(5):577–
89. This article provides an overview on the currrent discus-
sion on the conceptualiziation of personality disorders.
93. Gunderson JG. Borderline personality disorder: ontogeny of a
diagnosis. Am J Psychiatry. 2009;166(May):530–9.
94. Kozak MJ, Cuthbert BN. The NIMH research domain criteria
initiative: background, issues, and pragmatics.
Psychophysiology. 2016;53(3):286–97.
95. Anderson JL, Wood ME, Tarescavage AM, Burchett D, Glassmire
DM. The role of dimensional personality psychopathology in a
forensic inpatient psychiatric setting. J Personal Disord. 2017:1–18.
96. Babcock JC, Tharp ALT, Sharp C, Heppner W, Stanford MS.
Similarities and differences in impulsive/premeditated and
reactive/proactive bimodal classifications of aggression. Aggress
Violent Behav. Elsevier Ltd. 2014;19(3):251–62.
97. Elbert T, Moran JK, Schauer M. Lust for violence: appetitive
aggression as a fundamental part of human nature. e-
Neuroforum. 2017;23(2):77–84.
98.• Howard R. Personality disorders and violence: what is the link?
Borderline Personal Disord Emot Dysregulation. 2015;2(1):12.
This article introduces a new conceptualization of aggression,
the quadripartite violence typology.
99. Giancola PR, Chermack ST. Construct validity of laboratory ag-
gression paradigms: a response to Tedeschi and Quigly (1996).
Aggress Violent Behav. 1998;3(3):237–53.
100. Tedeschi JT, Quigley BM. A further comment on the construct
validity for laboratory aggression paradigms: a response to giancola
and chermack. Aggress Violent Behav. 2000;5(2):127–36.
101. Furnham A, Richards SC, Paulhus DL. The dark triad of personality: a
10 year review. Soc Personal Psychol Compass. 2013;7(3):199–216.
102. Jones DN, Neria AL. The dark triad and dispositional aggression.
Pers Individ Dif. Elsevier B.V. 2015;86:360–4.
103. Bertsch K, Hillmann K, Herpertz SC. Behavioral and neurobio-
logical correlates of disturbed emotion processing in borderline
personality disorder. Psychopathol. 2017.