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SUBCLINICAL PSYCHOPATHYAND EMPATHY
Bachelor Degree Project in Cognitive NeuroscienceECTS 15Spring term 2013
Björn Persson
Supervisor: Stefan BerglundExaminer: Daniel Broman
SUBCLINICAL PSYCHOPATHY AND EMPATHY 2
Subclinical Psychopathy and Empathy
Submitted by Björn Persson to the University of Skövde as a final year project towards
the degree of B.Sc. in the School of Humanities and Informatics. The project has been
supervised by Stefan Berglund.
12 June, 2013
I hereby certify that all material in this final year project which is not my own work
has been identified and that no work is included for which a degree has already been
conferred on me.
Signature:
SUBCLINICAL PSYCHOPATHY AND EMPATHY 3
Abstract
Psychopathy is a severe personality disorder that results in antisocial, manipulative,
and callous behavior. The main diagnostic instrument for assessing psychopathy is the
Psychopathy Checklist-Revised. This thesis will introduce the psychopathy construct,
including what is known as subclinical psychopathy. Subclinical psychopathy refers to
individuals who exhibit many of the characteristics of psychopathy, except for some of
the more severe antisocial behaviors. This constellation of traits allows the subclinical
psychopath to avoid incarceration. The fundamental difference between clinical and
subclinical psychopaths is a major question in the field of psychopathy and is the main
theme of this thesis. Impaired empathy is one of the key aspects of psychopathy and it
may be a significant factor in both clinical and subclinical psychopaths. Subclinical
psychopathy may be related to a moderated or altered expression of empathy. Hence,
the empathy construct is a secondary concern in this thesis. This thesis has two aims:
(a) to argue that the conceptualization of subclinical psychopathy is flawed and needs
revision in accordance with less ambiguous criteria; and (b) to present data in support
of the hypothesis that subclinical psychopaths have intact, or even enhanced, cognitive
capacities in contrast to clinical psychopaths.
Keywords: psychopathy, clinical psychopathy, subclinical psychopathy, cognitive
empathy, affective empathy
SUBCLINICAL PSYCHOPATHY AND EMPATHY 4
Table of Contents
Abstract 3
Introduction 5
Clarifying the Psychopathy Construct 7
Antisocial Personality Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . 7
The Psychopathy Checklist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
Gender Differences in Psychopathy . . . . . . . . . . . . . . . . . . . . . . . . 11
Clinical and Subclinical Psychopathy 13
Subclinical Psychopathy as a Manifestation of the Disorder . . . . . . . . . . . 14
Subclinical Psychopathy as a Moderated Expression of the Full Disorder . . . . 15
Subclinical Psychopathy from a Dual-Process Perspective . . . . . . . . . . . . 15
Empathy 17
Cognitive and Affective Empathy . . . . . . . . . . . . . . . . . . . . . . . . . 18
Motor Empathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
Empathizing–Systemizing Theory . . . . . . . . . . . . . . . . . . . . . . . . . 22
The Neurophysiological Basis of Psychopathy 26
Structural Deficits and Abnormalities in Psychopaths . . . . . . . . . . . . . . 26
Amygdala . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
Prefrontal cortex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
Temporal lobe . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
Hippocampus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
Corpus callosum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Neuroimaging and Empathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Discussion 31
References 38
SUBCLINICAL PSYCHOPATHY AND EMPATHY 5
Subclinical Psychopathy and Empathy
Psychopathy is a severe personality disorder characterized by self-centeredness,
callousness, and a profound lack of empathy, which hinders the individual to form
warm emotional relationships with others (Hare, 1999b). The psychopathy construct
is a complex issue, and even amongst professionals there remains doubt as to what a
valid, working description of psychopathy really encompasses (Hare & Neumann,
2006; Skeem, Polaschek, Patrick, & Lilienfeld, 2011). In 1941, Hervey Cleckley
published the first edition of The Mask of Sanity, which became a milestone in the
field. Cleckley presented a description of the typical psychopath by the use of
countless clinical observations of adult male patients categorized as “psychopathic”.
Cleckley (1941/1988) introduced 16 characteristics distinguishing the psychopath:
superficial charm, absence of delusions, absence of nervousness or psychoneuroticism,
unreliability, insincerity, lack of remorse, antisocial behavior, poor judgment,
pathologic egocentricity and incapacity for love, lack of affect, specific loss of insight,
unresponsiveness in interpersonal relations, fantastic and uninviting behavior, suicides
rarely carried out, impersonal sex life, and failure to meet life plans.
These criteria were used as a starting point for Robert D. Hare during the
creation of the Psychopathy Checklist (PCL; Hare, 1985) and in the subsequent
development of the Psychopathy Checklist-Revised (PCL-R; Hare, 1991, 2003). The
PCL-R has since become the premier assessment instrument in the area of psychopathy
(Patrick, 2006). In contrast to the PCL-R, the current edition of the Diagnostic and
Statistical Manual of Mental Disorders (American Psychiatric Association [APA], 2000)
equates psychopathy with the term antisocial personality disorder (ASPD), which has
sparked controversy because such a distinction inevitably creates unnecessary
construct ambiguity (Hare, 1996; Hare & Neumann, 2006).
The public image of a psychopath is very broad, including conceptions such as
the corporate psychopath, the manipulative boss who achieves what he wants at any
cost. The con artist, the charismatic, and highly intelligent individual with
chameleon-like qualities. The chronic offender, who from an early age is burdensome
SUBCLINICAL PSYCHOPATHY AND EMPATHY 6
to society by causing all sorts of trouble, perpetually coming and going to and from
detention centers, and later in life, prisons; and the serial killer. These descriptions
overlap in part, but they are also very distinct (Skeem et al., 2011). Psychopathy is
dissociable from violence, but the key measure of psychopathy, namely the PCL-R
(Hare, 2003), contain items that predict violence.
The main focus of this thesis is subclinical psychopathy, or what is sometimes
referred to as successful psychopathy. The subclinical psychopath is described as an
individual that embody most of the psychopathic behaviors, but refrains from serious
antisocial traits, and is therefore rarely imprisoned or institutionalized (Hall &
Benning, 2006). The term has its root in Cleckley’s previously mentioned book, which
described individuals that had the essential characteristics of a clinical psychopath, but
without behaving in a way that led to frequent arrests or convictions (Cleckley, 1988).
Current research suggests that the subclinical psychopath, like the clinical psychopath,
is devoid of affective empathy (Gao & Raine, 2010), which is a related concern in this
thesis. Relatively little empirical research has been conducted on subclinical
psychopathy (Hall & Benning, 2006), but when the material permits, the two groups
will be contrasted.
This thesis first outlines psychopathy as a construct and its relation to ASPD.
Second, there is a brief overview of the conceptual frameworks regarding the
differences between the clinical and subclinical psychopath. Third, an outline of the
empathy construct and its relation to psychopathy is presented. Lack of affect is a
significant part of the psychopathy construct, and empathy is therefore a relevant and
related construct. Fourth, empirical evidence pertaining to both empathy and
psychopathy will be reviewed, which includes subsequent discussion regarding the
state of the psychopathy construct. The main argument presented in this thesis
concerns the conception of subclinical psychopathy, and it is argued that the current
conception is problematic in several different ways. The conclusion states that the
conception of subclinical psychopathy needs revision in terms of more objective
criteria.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 7
Clarifying the Psychopathy Construct
Antisocial Personality Disorder
ASPD was first introduced in the third edition of the DSM (DSM-III; APA, 1980),
and contrary to both Cleckley’s and Hare’s criteria of psychopathy, the DSM relied
solely on behavioral characteristics (e.g. aggressive outbursts and impulsivity) rather
than affective or interpersonal traits, such as: egocentricity, deceit, shallow affect,
manipulativeness, selfishness, and lack of empathy, guilt or remorse; which have been
key in the conceptualization and diagnosis of psychopathy (Hare, 1996).
The DSM-IV-TR (APA, 2000), describes an individual with ASPD as someone
with: “a pervasive pattern of disregard for, and violation of, the rights of others that
begins in childhood or early adolescence and continues into adulthood. This pattern
has also been referred to as psychopathy, sociopathy, or dyssocial personality disorder.”
(pp. 701-702). (Complete diagnostic criteria are available in Table 1.) It is important
to note that the quite rigid terminology of the DSM-IV-TR is not necessarily a rule of
law within contemporary psychiatry. For instance, DeWall and Anderson (2011)
defines antisocial behavior via reference to actions that violate personal or cultural
standards for appropriate behavior. Thus, antisocial behavior often encompasses
violence and aggression, but it also includes behavior such as cheating, stealing and
breaking other laws. This clarification does not make a very significant difference in
relation to subclinical psychopathy. The subclinical psychopath is not necessarily
devoid of antisocial behavior as such, but rather of the more severe antisocial traits
(LeBreton, Binning, & Adorno, 2006).
According to DSM-IV-TR (APA, 2000) psychopathy and ASPD can be considered
synonymous constructs, which has since been a point of controversy (Hare &
Neumann, 2006). Personality traits were deemed too difficult for clinicians to gauge,
and were therefore disqualified from the ASPD diagnosis (Hare, 1996; Hare &
Neumann, 2006). Hare has argued that the creation of ASPD resulted in an entirely
new construct which is related to – but not synonymous with – psychopathy, as
measured by the PCL-R (Hare & Neumann, 2006). The evidence to support this claim
SUBCLINICAL PSYCHOPATHY AND EMPATHY 8
Table 1
Diagnostic criteria for antisocial personality disorder (DSM-IV-TR)
A) There is a pervasive pattern of disregard for and violation of the rights of othersoccurring since age 15 years, as indicated by three or more of the following:
1. failure to conform to social norms with respect to lawful behaviors asindicated by repeatedly performing acts that are grounds for arrest;
2. deception, as indicated by repeatedly lying, use of aliases, or conningothers for personal profit or pleasure;
3. impulsiveness or failure to plan ahead;4. irritability and aggressiveness, as indicated by repeated physical fights or
assaults;5. reckless disregard for safety of self or others;6. consistent irresponsibility, as indicated by repeated failure to sustain
consistent work behavior or honor financial obligations;7. lack of remorse, as indicated by being indifferent to or rationalizing having
hurt, mistreated, or stolen from another;B) The individual is at least age 18 years.C) There is evidence of conduct disorder with onset before age 15 years.D) The occurrence of antisocial behavior is not exclusively during the course of
schizophrenia or a manic episode.
can be found in forensic populations, in which there is an asymmetric association
between ASPD and PCL-R, that is to say, most inmates that score high on the PCL-R
meet the criteria for ASPD, but most with high scores of ASPD do not meet the criteria
for PCL-R psychopathy (Hare, 1996; Hare & Neumann, 2006).
The prevalence of psychopathy in the general public is a much debated issue.
Hare (1999a) estimated that the prevalence rates are around 1%. Blair, Mitchell, and
Blair (2005) has estimated that the prevalence of psychopathy .75% in the general
population. The authors do not specify in which part of the world these measurements
were carried out. This is significant because there are cultural differences in the
prevalence of psychopathy traits (Cooke, 1998), however, details in regards to that
subject is beyond the scope of this thesis. Furthermore, Blair et al. (2005) inferred
their results from the prevalence rates of ASPD, which in turn has been estimated at a
rate of 3% in the general population (APA, 2000), and 50-80% in prison populations
(Ogloff, 2006). Coid and colleagues (2009) conducted a study which estimated that
the prevalence rate of psychopathy in Great Britain is 0.6% (95% CI: 0.2–1.6).
SUBCLINICAL PSYCHOPATHY AND EMPATHY 9
There are a number of difficulties with providing an exact prevalence rate. One
such difficulty is that psychopaths are almost exclusively studied inside prisons.
Psychopathy is also much more frequent in prison populations (about 25%) than in
the general population, thus making the numbers difficult to generalize from one
paradigm to another (Hare, 1996; Hare & Neumann, 2006). Furthermore, the
difficulties surrounding the construct have led to dubious data regarding prevalence
rates. The studies of psychopathy prevalence in prison populations have varied
depending on the cut-off score used on the PCL-R questionnaire. Thus, it has been
argued that the cut-off score has an element of arbitrariness, and is essentially as good
as the knowledge and ability of the researcher (Blackburn, 2009).
Rogers, Salekin, Sewell, and Cruise (2000) had the following comment on the
construct validity issue: “DSM-IV does considerable disservice to diagnostic clarity in
its equating of A[S]PD to psychopathy” (p. 237). Further, they argued that the
intermittent changes in ASPD shatter any illusion of a possibility of a unitary
diagnosis. The relationship between ASPD and PCL-R psychopathy is still under
dispute (Coid & Ullrich, 2010; Hare, 1996, 2003; Hare & Neumann, 2006, 2008).
Recently, Coid and Ullrich (2010) hypothesized that ASPD and psychopathy
belong on the same continuum because they may share etiology. The researchers were
unable to show that ASPD and psychopathy are distinct diagnostic entities, and
accordingly, they found no evidence to suggest that individuals with both ASPD and
psychopathy constitute a specific subcategory. Instead they suggested that psychopathy
is too complex to measure dichotomously, based on an arbitrary cut-off point.
The Psychopathy Checklist
Robert D. Hare created a diagnostic tool (the PCL) which corresponds more
closely to Cleckley’s original definition of psychopathy (Hare, 1996; Hare & Neumann,
2006). Originally, Hare and his colleagues rated prison inmates along a 7-point (low
to high) rating scale based on Cleckley’s criteria for psychopathy. This yielded over
100 items, some of which were deemed too vague or difficult to score. A series of
subsequent statistical analyses determined which items had the best psychometric
SUBCLINICAL PSYCHOPATHY AND EMPATHY 10
properties. These items were used in the original PCL questionnaire, which consisted
of 22 items. Each item was measured on a three point (0, 1, 2) ordinal scale, where 0
indicated that the characteristic was not present or did not apply, 1 indicated
uncertainty as to whether it applied or not, and 2 indicated that the characteristic was
definitely present. Each item is scored on the basis of an interview and file
information, which is the standard PCL procedure (Hare & Neumann, 2006).
Over the years, the PCL has been subject to minor revisions, including the
removal of two items due to scoring difficulties and reliability issues. The current (2nd)
edition of the PCL-R (Hare, 2003), contains 20 items (See Table 2), yielding a
maximum score of 40, with a cut-off score typically set to 30 (Hare & Neumann,
2005). The cut-off score is generally adjusted depending on the purposes of the
procedure (e.g., research, forensic, or risk assessment). Adjusting the cut-off scores
has been seen as problematic, because it potentially renders the PCL-R measurements
arbitrary (Leygraf & Elsner, 2008). In order to understand any psychological
construct, a clear underlying dimensionality needs to be developed.
In the case of psychopathy, recent exploratory factor analytic research has shown
that between two to five factors (Cooke & Michie, 2001; Hare, 2003; Hare et al.,
1990; Hare & Neumann, 2008; Widiger & Lynam, 1998) can be amassed from
psychopathy measurements (Hare & Neumann, 2006). There is an ensuing debate as
to whether or not psychopathy is a unitary or multifarious construct or in other words,
if there is a single underlying etiology or multiple etiologies (Lilienfeld & Fowler,
2006; Skeem et al., 2011).
Most researchers adhere to a two-factor model (viz. interpersonal-affective and
social deviance) which divides into four facets (viz. interpersonal, affective, lifestyle,
and antisocial), but whether or not the factors diverge in different directions has been
called into question (Skeem et al., 2011). There is some evidence that the two major
factors (i.e., interpersonal-affective, and social deviant) correlate to external variables
in different directions. An example of this is that the interpersonal factor is negatively
associated with emotional distress, and the social deviance factor is positively
SUBCLINICAL PSYCHOPATHY AND EMPATHY 11
Table 2
Psychopathy Checklist–Revised (PCL-R) Factors, Facets, and Items
Factor 1: Interpersonal-affective scale Factor 2: Social deviance scale
Facet 1Interpersonal
Facet 2Affective
Facet 3Lifestyle
Facet 4Antisocial
Glibness or super-ficial charm;Grandiose senseof self-worth;Pathological lying;Conning or ma-nipulative
Lack of remorseor guilt;Shallow affect;Callous or lack ofempathy;Failure to acceptresponsibility
Need for stimula-tion;Parasitic lifestyle;Lack of realisticlong-term goals;Impulsivity;Irresponsibility
Poor behavioral con-trols;Early behavioral prob-lems;Juvenile delinquency;Revocation of condi-tional release;Criminal versatility
From (Hare, 2003)Note. Two PCL-R items are not included in this factor structure: namely “promiscuoussexual behavior”, and “many short-term marital relationships”, because they do notload onto any specific factor (Hare & Neumann, 2006). Hare and Neumann (2008)refer to this model as a two factor higher-order representation of a four factorcorrelated model.
associated with emotional distress (Hicks & Patrick, 2006). This aspect of the
construct has not been conclusively proved either way, thus the field remains divided
(Skeem et al., 2011).
Gender Differences in Psychopathy
Gender differences in psychopathy will generally not be taken into account in
this thesis, in large part due to that the overwhelming majority of empirical research
has been on male offenders and psychiatric patients. However, there are a few
interesting differences that relate to subclinical psychopathy and problems with
assessment. One of these issues is the prevalence of psychopathy in women, which has
been estimated (in prisons and institutions) at 9% to 23% in women, compared to
15% to 30% in men (Nicholls, Ogloff, Brink, & Spidel, 2005; Vitale, Smith, Brinkley, &
Newman, 2002). The relatively high percentage span is because measurements were
made in different cultures, in which different cut-off scores are utilized for reasons
that are beyond the scope of this thesis (Logan & Weizmann-Henelius, 2012).
SUBCLINICAL PSYCHOPATHY AND EMPATHY 12
Another gender related issue regarding psychopathy is that women tend to
present with slightly different characteristics than men. The stereotypical gender roles
of men and women tend to be amplified in psychopaths. This means that psychopathic
men are more physically aggressive, dominant, are less anxious and emotional.
Psychopathic women are to a lesser extent physically violent, but instead rely more on
relational aggression (including child abuse and sexual coercion). Emotionally,
psychopathic men and women are believed to be very similar, with the difference
being that women are more emotionally unstable and anxious (Logan &
Weizmann-Henelius, 2012).
Hare (2003) argued that it is likely that the PCL-R score represents much the
same level of psychopathy in both male and female psychiatric patients and offenders.
This assumption may be erroneous, because the behavior related to the antisocial
items (Facet 4) may present more infrequently in women (Logan &
Weizmann-Henelius, 2012). Women also have a lower rate of criminal convictions and
reconvictions (Forouzan & Cooke, 2005; Gelsthorpe, 2004; Verona & Vitale, 2006),
which is interesting in relation to subclinical psychopathy, and especially in regards to
the criticism portrayed in this thesis.
Psychopathic women are also reported to be more flirtatious. More specifically, it
has been reported that they are charmed by the psychiatrist performing the PCL-R
interview, whereas psychopathic men tend to try to impress and charm the interviewer
(Forouzan & Cooke, 2005). Applying the PCL-R criteria to women may also have the
disadvantage of inferring behavior that has different social and psychological meaning
for men and women. One such example relates to sexual promiscuity, which in
psychopathic women may relate to manipulation and securing partners one can
exploit; the same criteria in psychopathic men on the other hand, may relate more to
sensation- or status-seeking efforts (Quinsey, 2002).
The PCL-R manual lack guidance when it comes to interpreting some of the items
in relation to women. For instance, the item parasitic lifestyle is ambiguous, because
women have a material and financial dependency on men to a larger extent than the
SUBCLINICAL PSYCHOPATHY AND EMPATHY 13
reverse scenario. In many societies, this is a social norm that is broadly accepted. The
opposite is not broadly accepted, and therefore, male financial dependency on women
is sometimes interpreted as parasitic behavior (Logan & Weizmann-Henelius, 2012).
The various facts mentioned here has led some researchers to conclude that gender
equivalence in the expression of psychopathy cannot be assumed (Forouzan & Cooke,
2005), which in turn may have a significant effect on prevalence scores, both in the
community and in forensic settings (Logan & Weizmann-Henelius, 2012).
Clinical and Subclinical Psychopathy
The subclinical psychopath is defined by the quite blunt criterion of whether or
not the individual has been imprisoned or institutionalized. Practically, the difference
between the clinical and subclinical psychopath is a behavioral one. The subclinical
psychopath is engaged in behaviors that breach social norms – but are not necessarily
illegal – such as achieving personal or professional success at the expense of others,
which is why the term successful psychopathy is often employed as a synonym (Hall &
Benning, 2006). There are two important caveats that need mentioning: first,
subclinical psychopaths are considerably less antisocial than the clinical psychopath,
but this does not mean that they are always non-violent. Second, the clinical or
unsuccessful psychopath is not defined simply by where the individual is currently
located, but rather by looking at criminal history etc. Thus, a psychopath that has
been convicted of several crimes, but is currently residing in the community is not
considered a successful psychopath (Gao & Raine, 2010).
There are several difficulties with studying subclinical psychopathy. First, it has
been argued that the focus on antisocial behavior in DSM-III, and DSM-IV have led to
an under-representation of other behaviors, and traits (Lilienfeld, 1998; Messick,
1995). Second, identifying subclinical psychopaths has proven a difficult task. Third,
the PCL-R was developed primarily based on data from incarcerated inmates (Hare,
Clark, Grann, & Thornton, 2000), and this data may not generalize onto psychopaths
(either clinical or subclinical) residing in the community (Hall & Benning, 2006).
SUBCLINICAL PSYCHOPATHY AND EMPATHY 14
Additionally, another difficulty relates to the screening of psychopaths in
subclinical environments, being that the PCL-R employs a semi-structured interview
and inmate conviction history etc. This level of rigor in screening procedure is not
possible in the general population (Hall & Benning, 2006). This led to the creation of
alternative instruments, such as the Psychopathic Personality Inventory (PPI; Lilienfeld
& Andrews, 1996). These are some of the reasons for the low output of studies
regarding subclinical psychopathy (Hall & Benning, 2006).
At least three important reasons have been proposed for studying the clinical and
subclinical psychopaths (Gao & Raine, 2010). First, the fact that an overwhelming
majority of the research on psychopathic individuals has been based on clinical
psychopaths means that the collected data may not generalize to subclinical
psychopaths. This is very important because, as stated previously, the prevalence of
psychopathy is estimated at around 0.6-1% in the general population (Coid, Yang,
Ullrich, Roberts, & Hare, 2009; Hare, 1999a) and 3.5% in the business world (Babiak
& Hare, 2009). Thus, subclinical psychopaths may outnumber clinical psychopaths.
Second, studying subclinical psychopaths may lead to etiological insights, and they
may function as a “control group”, in the sense of excluding, or diminish criminality as
a criterion. Third, the etiology of subclinical psychopathy may be different from
clinical psychopathy, and the factor, or factors that shield the subclinical psychopath
from incarceration may be relevant for rehabilitation and proactive purposes (Gao &
Raine, 2010). Researchers disagree about how the clinical and subclinical aspects of
psychopathy can converge. Hall and Benning (2006) have provided descriptions of the
three main conceptual perspectives.
Subclinical Psychopathy as a Manifestation of the Disorder
Subscribers of this perspective argue that the same etiological differences can be
found in the subclinical psychopath, but at reduced severity, in comparison to the
clinical psychopath (Hall & Benning, 2006). Gustafson and Ritzer (1995) argue that
clinical and subclinical psychopaths differ only in degree, not in type. Their research
rebranded the subclinical psychopath as an aberrant self-promoter which is
SUBCLINICAL PSYCHOPATHY AND EMPATHY 15
conceptualized as an individual that is exploitative, lack empathy, violate social norms,
and have highly narcissistic behavior, although the ASP’s behavior need not technically
be illegal. The purpose of this distinction is to find patterns between individuals who
are not necessarily psychopaths according to the PCL-R, and yet are socially
destructive in their everyday lives.
Subclinical Psychopathy as a Moderated Expression of the Full Disorder
This approach proposes that clinical and subclinical psychopaths share not only a
common etiology but also equivalent severity of the basic underlying pathology.
Lykken (1995) proposed that some of the heroes, leaders and adventurers of a society
have the same predisposition to fearlessness that can be found in psychopaths. Albeit,
with the difference of having an adequate level of socialization during their
upbringing, thus ridding them of antisocial behavior. The theory suggests that
expression of antisocial behavior may be reduced if an individual has compensatory
factors, such as a special talent, high intelligence, high socioeconomic status etc. (Hall
& Benning, 2006).
Subclinical Psychopathy from a Dual-Process Perspective
In this conceptualization, the interpersonal–affective features of psychopathy are
considered to be etiologically distinct from the antisocial behavior component, it has
been referred to as the dual-process, or dual-deficit model of psychopathy (Fowles &
Dindo, 2006). Being that these two trait dimensions are thought to reflect distinct
etiologies, certain individuals could exhibit an elevation in one dimension but not the
other (Hall & Benning, 2006). Thus, the subclinical psychopath would have elevated
levels of interpersonal-affective traits, but have about normal levels of traits related to
antisocial deviance. This model draws inspiration from the two factor model of
psychopathy, which in this framework allows for the possibility of diverging behavior,
which allows the possibility of scoring high on one factor, but low on the other.
Accordingly, if one scored high on the interpersonal-affective factor, but not the
antisocial factor, one would perhaps fit into this conception of subclinical psychopath
(Hall & Benning, 2006). It should be noted that the three distinctions presented here
SUBCLINICAL PSYCHOPATHY AND EMPATHY 16
are not necessarily mutually exclusive, but rather, different approaches to the same
problem (Hall & Benning, 2006). Furthermore, the first and second perspectives can
be interpreted as advocating that the psychopathy construct belongs on a spectrum,
whereas the third perspective argues that there is a difference in etiology between the
two groups.
These three conceptualizations are interesting in relation to current research. For
instance, Gao and Raine (2010) postulated that the subclinical psychopath is
successful because of a number of factors: “. . . intact or enhanced neurobiological
processes, including better executive functioning, increased autonomic reactivity,
normative volumes of prefrontal gray and amygdala, and normal frontal functioning”
(p. 194), which may serve as “. . . factors that protect successful psychopaths from
conviction and allow them to attain their life goals, using more covert and nonviolent
approaches” (p. 194). Surprisingly little has been said about these matters, that is,
what makes the successful psychopath successful. A skeptic could argue that
imprisonment is an arbitrary point of measure when it comes to such things as
behavior and personality, because imprisonment is in part dependent on culture,
socioeconomic status, skin color, age, etc. In other words, the skeptic would appeal to
a stronger conceptualization that utilizes something like biological or neuronal
empirical data.
Gao and Raine (2010) comment that serial killers who evade justice for a very
long time, but eventually get caught, could constitute a form of “semi-successful”
psychopathy. One could argue that such a conceptualization goes against all three
perspectives, because all three attempt to retain that subclinical psychopaths are not
as severely antisocial as clinical psychopaths. Serial killers constitute the very epitome
of severe antisocial behavior, and thus, calling them semi-successful yields serious
consequences for the traditional notions of a subclinical psychopath.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 17
Empathy
In Cleckley’s (1988) original description of the psychopath, a key characteristic
was lack of remorse, and a poverty of emotional reactions. This notion has since
become a major part in the psychopathy construct (Baron-Cohen, 2012; Blair, 2005;
Hare, 1999b, 2003). Empathy has been defined by Baron-Cohen (2012) in the
following way: “Empathy is our ability to identify what someone else is thinking or
feeling, and to respond to their thoughts and feelings with an appropriate emotion”
(p. 12), which suggests two stages of empathy: recognition and response. From a
conceptual perspective, empathy can be regarded a very broad term which is related
to a plethora of more finely defined terms used for a more comprehensive
categorization (e.g., mimicry, emotional contagion, sympathy, and compassion)
(Singer & Lamm, 2009).
Singer and Lamm (2009) stress the importance of the self-other distinction, in
other words, our ability to distinguish between whether or not the source of an
emotional response lies within ourselves or was triggered by the other. They further
distinguish between, on the one hand, empathy – and sympathy, empathic concern,
and compassion, on the other. Empathy allows one to “feel with” someone, whereas
the latter terms allow one to feel “for someone”. The practical difference between
these two is: feeling sadness for someone who is sad, rather than merely feeling pity,
or concern, for someone who is sad. Pity is not the appropriate empathic response, but
it may be a compassionate response. Also, if an observer notices that someone is
jealous of him, feeling jealousy towards that person is not an appropriate response,
feeling sorry for that person would be more appropriate (Singer & Lamm, 2009; for
similar arguments, cf. de Vignemont & Singer, 2006).
Singer and Lamm (2009) argue the self-other distinction is crucial, and that
many researchers have used these terms synonymously, thus creating both confusion,
and widely used psychometric measuring tools, which rely solely on self-report.
Ultimately, “empathy is conceived to be a first necessary step in a chain that begins
with affect sharing, followed by understanding the other person’s feelings, which then
SUBCLINICAL PSYCHOPATHY AND EMPATHY 18
motivates other-related concern and finally engagement in helping behavior” (Singer
& Lamm, 2009, p. 84). For a comprehensive list of distinctions currently used by
researchers in this field, see Batson (2009).
The terms empathy and sympathy have been used in various different ways in
scientific literature (cf. Dolan & Fullam, 2007), however, sympathy is not a concept
that this thesis will take into consideration. This thesis will treat empathy in
accordance with Blair’s (2007a) tripartite division into motor empathy, cognitive
empathy – also referred to as theory of mind (ToM; Premack & Woodruff, 1978), or
mentalizing (Frith, Morton, & Leslie, 1991) – and affective, or emotional empathy.
Motor empathy refers to where the individual mirrors the motor responses of the
observed actor; cognitive empathy refers to where the individual represents the
internal mental state of the other; and affective empathy refers to an individual’s
congruent emotional response to another individual’s emotional state (Blair, 2007a).
Cognitive and Affective Empathy
The scientific consensus is that the severe empathic dysfunction evident in
psychopaths is mainly due to lack of emotional (or what is also referred to as affective)
empathy, but with intact cognitive empathy (Blair, 2005, 2007a; Cox et al., 2012).
However, this is a complicated subject, partly due to the lack of scientific consensus
regarding the composition of the empathy construct (Blair, 2005; Mullins-Nelson,
Salekin, & Leistico, 2006). Happé and Frith (1996) found similarities between autistic
children and children with conduct disorder (CD) – which is a diagnosis similar to that
of adult ASPD – specifically, that both groups have difficulties with cognitive empathy
in comparison to control groups. Partly based on this finding, Söderström, Blennow,
Sjödin, and Forsman (2003) argue that psychopathic individuals are empathically
deficient in more aspects than the affective department. Blair (2007a) disagrees with
this conclusion. He argues that both ASPD and CD are flawed diagnoses, being that
the diagnostic rate of CD can reach more than 16% of boys in the general population
(DSM-IV; American Psychiatric Association, 1994). The same imprecision is found in
ASPD, which can reach a diagnostic rate of 50-80% in adult forensic institutions
SUBCLINICAL PSYCHOPATHY AND EMPATHY 19
(Ogloff, 2006). Blair (2007a) caveats that because of these imprecisions, researchers
need to be careful not to treat the constructs as more similar than they actually are.
Dolan and Fullam (2004) proposed that the deficits in cognitive empathy in
individuals with ASPD are subtle. They performed a variety of ToM tasks and found
significant differences during the so called faux pas task. The faux pas task is
described in the following way:
A faux pas occurs when someone says something that they should not have
said without realizing that they should not have said it. An understanding
of faux pas requires a person to represent the mental state of both the
speaker and hearer of the faux pas, i.e. it requires an understanding that
the speaker does not realize they should not have said it, and that the
person on the receiving end of the faux pas will feel hurt or insulted (Dolan
& Fullam, 2004, p. 1096).
The subjects were asked a series of questions pertaining to the mental state of
both the speaker and listener. An additional control question was asked in order to
make sure that the subjects were able to follow and understand the elements of the
story, and further, their ability to recognize how the people in the story might have
felt. Results showed significant differences between criminals (both psychopathic and
non-psychopathic) and controls, regarding the assessment of the mental state of both
the speaker and listener. There were no significant group differences in the control
question, indicating that the subjects were able to follow the story in a similar fashion.
Regarding the empathy related question, both psychopathic and non-psychopathic
criminals were impaired in comparison to controls. In conclusion, Dolan and Fullam
(2004) argue that the deficits found in psychopaths seem to relate to a general lack of
concern regarding the impact of their actions, rather than an inability to understand
that their actions impact others.
Very few studies have been conducted regarding empathy in subclinical
psychopaths – only one, according to Mullins-Nelson et al. (2006) – but at least one
more study has been conducted since then (viz. Gao & Raine, 2010). Mullins-Nelson
SUBCLINICAL PSYCHOPATHY AND EMPATHY 20
et al. (2006) studied psychopathy in a college population, and its relation to both
cognitive and affective empathy. The measuring instrument used was the Psychopathic
Personality Inventory–Short Form (PPI–SF; Lilienfeld & Andrews, 1996), an abridged
version of the PPI (Lilienfeld & Andrews, 1996), both of which are self-report
instruments. Both components of empathy were measured with the Interpersonal
Reactivity Index (IRI; Davis, 1983), which is also a self-measurement instrument. The
participant sample was composed of 44 males (25%) and 130 females (75%), which is
important to note due to the significant gender differences regarding subjective
reporting in both cognitive and emotional empathy (Baron-Cohen & Wheelwright,
2004; Schulte-Rüther, Markowitsch, Fink, & Piefke, 2007). As expected, the results
showed that the high scorers on the PPI–SF did not differ in their perspective-taking
ability (cognitive empathy), but they were also less likely to demonstrate affective
empathy, thus reinforcing the picture of the psychopath as someone who simply does
not care about negative consequences (Mullins-Nelson et al., 2006).
The original version of the PPI was based on eight subscales which, in the
PPI–SF, are condensed into two factors: stress immunity, social potency, fearlessness,
and coldheartedness (PPI–SF–I); and impulsive nonconformity, blame externalization,
Machiavellian egocentricity, and carefree non-planfulness (PPI–SF–II). Upon studying
the specific factors, the researchers found that high scorers on the psychopathy
measurement that also scored highly on the PPI–SF–II evidenced deficits in almost all
aspects of emotional functioning, including cognitive empathy. In accordance with
these findings, the researchers argue that the successful psychopath may be one that
scores high on the first factor but not on the second factor (Mullins-Nelson et al.,
2006).
Lilienfeld and Fowler (2006) have discussed several drawbacks with the PPI
instrument. Self-report instruments are always problematic, but especially when
dealing with psychopaths, who in their very nature are manipulative, and dishonest.
Psychopaths tend to lie either for some personal gain, or simply because they find it
entertaining, a phenomenon Ekman (1985) referred to as duping delight. A second
SUBCLINICAL PSYCHOPATHY AND EMPATHY 21
problem is the lack of insight any person may have into one’s personality, but with
psychopaths, who tend to have an unrealistic world view (e.g., lack of realistic long
term goals), the problem becomes even more significant. Third, asking individuals
who have an inherent lack of emotions (or at least an inability to utilize their emotions
in any meaningful way) what they feel is in and of itself problematic. For a lengthier
discussion of these matters, see Lilienfeld and Fowler (2006).
Motor Empathy
In relatively recent years, a further constructional division of empathy, known as
motor empathy, has been made (Carr, Iacoboni, Dubeau, Mazziotta, & Lenzi, 2003).
This account has its basis in the discovery of mirror neurons (Di Pellegrino, Fadiga,
Fogassi, Gallese, & Rizzolatti, 1992; Rizzolatti, Fadiga, Gallese, & Fogassi, 1996),
which are neurons that show activity during the execution of an action, and also
during the observation of the same or a similar action (Iacoboni, 2009). Evidence
suggests that motor empathy is when we understand what others feel, as relayed by a
mechanism of action representation. Our empathic emotions are therefore, at least
partially, moderated by the emotions associated with a specific movement (Carr et al.,
2003). The motor mirror neuron system is believed to be composed of regions in the
posterior inferior frontal gyrus (IFG) the ventral premotor cortex, and the rostral
inferior parietal lobule (IPL) (Shanton & Goldman, 2010). Whether or not
psychopathic individuals have deficient motor empathy is under debate. However,
Blair (2005) argues that this is unlikely, and that their empathic deficiencies are
limited to marked facial expressions and selective emotional empathy.
Avenanti, Bueti, Galati, and Aglioti (2005) studied what happens with motor
responses when a normal person (as opposed to a psychopath) observes a model hand
being pricked by a needle. They used transcranial magnetic stimulation (TMS)-induced
motor evoked potentials (MEP) to measure motor cortex excitability and the results
showed a reduction of MEP amplitude that was specific to the muscle that subjects
observed being pricked. The increase of reduction correlated with the observer’s
subjective empathic rating of the sensory, but not affective, qualities of the pain
SUBCLINICAL PSYCHOPATHY AND EMPATHY 22
ascribed to the model. Fecteau, Pascual-Leone, and Théoret (2008) used the PPI
(Lilienfeld & Andrews, 1996) in conjunction with the TMS-MEP methodology, in an
endeavor to find out whether or not psychopathic individuals would show the same
reduction. Their results showed that high scores on a PPI subscale called
coldheartedness correlated significantly with reduction in MEP amplitude, which
suggests that individuals with specific psychopathic characteristics (those related to
the coldheartedness subscale) are, at a sensorimotor level, more responsive than
individuals with a lower coldheartedness score. Lilienfeld and Andrews (1996) define
coldheartedness as “a propensity toward callousness, guiltlessness, and
unsentimentality” (p. 495). The coldheartedness factor correlates significantly to
Factor 1 of the PCL-R (Hare, 1991), but not to Factor 2 (Poythress, Edens, & Lilienfeld,
1998). The finding of Fecteau et al. (2008) gives credence to Blair’s (2005) conjecture
that psychopaths have intact motor empathy and that their lack of guilt or remorse
must be attributed to some other cognitive faculty.
Empathizing–Systemizing Theory
Simon Baron-Cohen has developed a theory known as the empathizing–
systemizing theory (E–S Theory; Baron-Cohen, Knickmeyer, & Belmonte, 2005). The
systemizing component of the theory incorporates the notion that the brain looks for
patterns in order to figure out how the world is connected, and how to predict the
future. The empathizing component is simply one’s ability and interest in empathizing
with someone else; both aspects conform to normal distribution. The theory states
that psychopathy is the polar opposite of autism. The hypothesis being that autistic
individuals have difficulties in understanding the emotional states of others, but if and
when they do understand them, they have the capacity to empathize. The psychopath
on the other hand, has the ability to understand that the observer feels, but not how or
what it feels (Baron-Cohen, 2012).
In 2006, Auyeung et al. examined fetal testosterone levels and its relation to
systemizing ability. The study found a significant difference in systemizing quotient
(SQ) between boys (mean = 27.79 ± 7.64) and girls (mean = 22.59 ± 7.53), thus
SUBCLINICAL PSYCHOPATHY AND EMPATHY 23
confirming the hypothesis that boys systemize to a larger extent than girls (Auyeung
et al., 2006), which connects to the fact that male fetuses are exposed to higher levels
of testosterone than are female fetuses (Knickmeyer & Baron-Cohen, 2006). Another
study found a significant negative correlation between fetal testosterone and measures
on an empathy task. The authors concede that levels of empathy are likely to be
influenced by post-natal experience that may override the pre-natal biological
environment (Chapman et al., 2006)
Testosterone has been proposed as an important part of psychopathy, due to its
relation to aggression – which is defined as behaviors that are intended to inflict harm
(Nelson & Trainor, 2007). However, very few studies have been published on the
subject to this date. Glenn, Raine, Schug, Gao, and Granger (2011) investigated the
ratio between cortisol and testosterone, because it had been suggested that the
cortisol-testosterone-ratio was associated with psychopathy (Terburg, Morgan, &
van Honk, 2009). The researchers were unable to find significant results when
manipulating the participants with stress, but they did observe a significant
relationship between baseline cortisol, and testosterone, which accounted for about
5% of the variance in psychopathic traits.
Söderström et al. (2001, 2003) conducted two consecutive studies
that showed a correlation between psychopathy and an increased ratio between
serotonin (5–HIAA), and dopamine (HVA) metabolites. This may have an effect on the
disinhibition of aggressive impulses that is typical of psychopaths. Thus, combining
dopamine and serotonin regulation may improve impulse control in psychopaths.
The neurotransmitter serotonin (5–HT) has been proposed to – in combination with a
high testosterone-cortisol ratio – facilitate between instrumental (i.e., associated with
premeditation, and not merely violence as a consequence of an affective reaction),
and impulsive aggression. Specifically, low cortisol, high testosterone and low levels
of 5–HT is believed to predispose impulsive aggression (Montoya, Terburg, Bos, &
van Honk, 2012; Terburg et al., 2009; van Honk, Harmon-Jones, Morgan, & Schutter,
2010). For a review of the neuroanatomy of aggression, see Nelson and Trainor (2007).
SUBCLINICAL PSYCHOPATHY AND EMPATHY 24
Furthermore, studies have shown that increased serotonin in the hypothalamus
may increase the production of cortisol (Glenn & Raine, 2008); thus, dysregulation of
serotonin may be connected to the low levels of cortisol observed in psychopaths. It is
also a possibility that serotonin interacts with testosterone levels and increase the
probability of aggression. One such study showed that high testosterone and low
serotonin may correlate to both intensity, and rates of aggression (Higley et al., 1996).
Glenn and Raine (2008) caution readers that the neuroendocrinology of psychopathy
is in its early stages: thorough understanding of the neurobiology of psychopathy
requires not only knowledge of brain region involvement, genetics, neurotransmitters,
and hormones, but rather, an assembly of all of these aspects. An important criticism
has been raised by Ellis, Beaver, and Wright (2009). In a discussion regarding
testosterone, they comment that most studies either use blood or saliva to measure
testosterone, neither of which are ideal measurements when it comes to behavior. The
brain causes behavior, blood and saliva do not. Therefore, they argue that it is
important to measure the levels of testosterone (and possibly many other hormones)
in the brain, which is most effectively carried out by performing a lumbar puncture,
which is a painful and invasive procedure that researchers often do not use.
At least 13 brain regions have been suggested to be part of the empathy network
(Baron-Cohen, 2012), which sheds some light on how complex the empathy construct
is. Empathy has been studied in a wide variety of ways, across several different
domains. Neuroimaging studies have been performed for a multitude of different
aspects of empathy, such as pain (Coll, Budell, Rainville, Decety, & Jackson, 2012;
Singer et al., 2004), disgust (Jabbi, Swart, & Keysers, 2007), touch (Keysers et al.,
2004), anxiety (Morelli, Rameson, & Lieberman, 2012), happiness, and anger
(Dimberg & Thunberg, 2012). In addition, empathy induction procedures are
traditionally either simple observation (Keysers et al., 2004), imagination (Jackson,
Brunet, Meltzoff, & Decety, 2006), or evaluation (Jackson, Meltzoff, & Decety, 2005).
The high variation in these studies do not make it clear, which, if any, underlying
neural regions that are consistently active in all, or most, scenarios. This was
SUBCLINICAL PSYCHOPATHY AND EMPATHY 25
subsequently investigated by Fan, Duncan, de Greck, and Northoff (2011), who
identified several clusters relevant for different empathy paradigms: the anterior
midcingulate cortex, dorsal anterior cingulate cortex (ACC), supplementary motor
area, and bilateral anterior insula (AI). The researchers confirmed their hypothesis
that these four areas are the core networks that lays the foundation for empathy.
However, the affective–perceptual and cognitive–evaluative forms of empathy are
believed to have different neural bases, but with extensive interconnections between
the two areas, which suggests a detailed division of specific functions. The affective
network has been suggested to be comprised of the right AI, thalamus, and
periaqueductal gray (PAG) (Kober et al., 2008). The cognitive-evaluative form of
empathy seems to be carried out by the left AI alone, but more thorough research is
yet to be carried out (Fan et al., 2011).
Additionally, based on the findings of the mirror neuron system (Di Pellegrino
et al., 1992; Rizzolatti et al., 1996), some researchers have proposed simulation as an
intimate component of empathy (Gallese, 2001, 2003; Schulte-Rüther et al., 2007).
Fan et al. (2011) did not find any evidence to suggest that the areas believed to be
involved in simulation (e.g., the left IFG and IPL) were consistently active during
empathizing. The researchers make caution that this discovery is by no means final,
and that simulation may be a core part of empathy, though not in terms of consistent
neural activity.
Shamay-Tsoory (2011) has hypothesized that the cognitive and affective
components of empathy are dissociable systems. Evidence is support of this claim
comes from ethological, psychiatric, and developmental studies. There is also evidence
that suggests that the neurotransmitter oxytocin plays a large role in emotional
empathy, but not in cognitive empathy (Hurlemann et al., 2010). Shamay-Tsoory
(2011) further suggests that the IFG and IPL are involved in simulation, which along
with the insular cortex and ACC makes up the emotional empathy network. The
cognitive network is believed to be comprised of the ventromedial prefrontal cortex
(VMPFC), dorsomedial prefrontal cortex (DMPFC), temporoparietal junction, and
SUBCLINICAL PSYCHOPATHY AND EMPATHY 26
medial temporal lobe (MTL). This network is believed to be involved with both
cognitive and affective mentalizing processes.
Thoma, Friedmann, and Suchan (2013) has commented that studies on
psychopathy has provided some support for the hypothesis that they are cognitively
impaired and that little has been done to investigate emotional empathy. Further, they
urge researchers to differentiate between subclinical and clinical psychopaths, because
of their importance in relation to cognitive and emotional empathy.
The Neurophysiological Basis of Psychopathy
Neuroscientists have looked for brain abnormalities in psychopaths since the
time of Phineas Gage. In 1848, Gage was severely injured by an iron rod which passed
through his skull, penetrating his prefrontal cortex (PFC) — mainly the orbitofrontal
cortex (OFC) — leaving Gage with profound personality changes (O’Driscoll & Leach,
1998). Gage, as well as other patients with similar damage, has been diagnosed as
having acquired sociopathy or pseudopsychopathy, which is categorized by impulsive
and antisocial behavior. Blair (2003) has commented that pseudopsychopaths do not
exhibit the instrumental violence typical of psychopaths, which is consistent with the
behavior of Gage, who became aggressive and exhibited reactive (impulsive) violence
Raine and Yang (2006b). Further evidence for this theory has been provided by
Broomhall’s (2005) finding that pseudopsychopaths tend to score highly only on
PCL-R factor 2, whereas clinical psychopaths score highly on both factors.
Structural Deficits and Abnormalities in Psychopaths
Amygdala. The amygdala has played a major role in hypotheses regarding the
psychopathy construct (Baron-Cohen, 2012; Blair, 2003, 2008; Kiehl, 2006; Raine &
Yang, 2006a; Yang, Glenn, & Raine, 2008). The amygdala is known to play a major
role in fear condition and emotion recognition (Adolphs, Tranel, Damasio, & Damasio,
1994; Adolphs & Tranel, 2003), as well as both increasing and decreasing aggressive
behavior (Blair, 2004). The decrease in aggression was seen in a patient after a
bilateral amygdalectomy (Ramamurthi, 1988), and increases in aggression have been
SUBCLINICAL PSYCHOPATHY AND EMPATHY 27
seen in patients with temporal lobe epilepsy (Van Elst, Woermann, Lemieux,
Thompson, & Trimble, 2000). Deficits in the amygdala have further been linked to
both social behavior and moral emotion (Adolphs, Tranel, & Damasio, 1998; Blair,
2007b). Specifically, studies have shown that psychopaths demonstrate a lower level
of amygdala activation when looking at fearful faces (Dolan & Fullam, 2009), or
moral violations (Harenski, Harenski, Shane, & Kiehl, 2010), in comparison to
controls. In terms of anatomical structure, Ermer, and colleagues (2012) conducted a
large-scale study involving 296 participants. The researchers found decreased regional
gray matter in several paralimbic and limbic areas, including bilateral
parahippocampal, amygdala, and hippocampal regions, bilateral temporal pole,
posterior cingulate cortex, and OFC. These findings were still relevant after controlling
for substance abuse, brain size, and age. Furthermore, they argue that these results
suggest that psychopathy may have its basis in a broader system of neural regions than
expected (Ermer, Cope, Nyalakanti, Calhoun, & Kiehl, 2012).
Thus, the amygdala may be intimately related to many aspects of psychopathic
behavior. Because both clinical and subclinical psychopaths have deficiencies in
affective empathy, it may be the case that damage to the amygdala will be
distinguishable only in comparison to controls, but not to subclinical psychopaths.
This question was investigated by Yang, Raine, Colletti, Toga, and Narr (2010). They
hypothesized that clinical psychopaths, but not subclinical psychopaths, would show
significant volume reductions in the OFC, dorsolateral prefrontal cortex (DLPFC), and
the amygdala, compared to controls. The group confirmed their hypothesis in finding
structural deficits in both prefrontal areas and the amygdala pertaining to clinical
psychopaths, but not subclinical psychopaths. Furthermore, clinical psychopaths
showed a 26% volume reduction in the left amygdala, and 20% reduction in the right
amygdala, compared to controls. In the subclinical psychopaths, the observed volume
reduction was smaller, notably 9.3% in the left, and 12.7% in the right amygdala.
Follow up analysis revealed that socioeconomic status or substance abuse was unlikely
to have an effect on the results.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 28
There is a related question regarding whether there are different brain deficits
associated with different types of psychopathic behavior, specifically, whether, and
how, variations in neurological disposition relate to instrumental versus affective
violence. Psychopathic offenders display a higher rate of both community, and
institutional violence than forensic patients, and the more general offender (Hart &
Hare, 1997; Hill, Rogers, & Bickford, 1996). A study by Woodworth and Porter (2002)
revealed that psychopaths show a much higher degree of instrumental violence than
nonpsychopaths. Their study showed that nearly all (93.3%) of the homicides
committed by psychopaths was primarily instrumental, compared to 48.4% in
nonpsychopaths. It should be noted that definitions and evaluations of instrumental
and affective violence are problematic, in the sense that they do not conform to a
scientific consensus.
Prefrontal cortex. Yang et al. (2005) found a negative correlation between
higher total PCL-R score and low gray matter volume in the PFC. Clinical psychopaths
had 22.3% reduction in prefrontal gray matter volume in comparison to controls.
Subclinical psychopaths, on the other hand, showed very little reduction
(non-significant) in prefrontal gray matter, which is evidence of an important
difference between the two. Increase in PCL-R score has also been found to be related
to reduction of cortical thickness in both temporal, and prefrontal gray matter (Yang,
Raine, Colletti, Toga, & Narr, 2009). A few studies found similar results in
psychopaths, and in alcoholics with antisocial personality disorder (Dolan, Deakin,
Roberts, & Anderson, 2002; Laakso et al., 2002). However, after controlling for
education and alcoholism, these significant differences in brain volume disappeared,
which has led to questions as to whether only clinical psychopaths are afflicted by
such structural impairments (Yang et al., 2009).
The OFC is the most common prefrontal region implicated neuroimaging
investigations of psychopathy (Anderson & Kiehl, 2012). Yang et al. (2010) published
the first study that found significant structural differences between clinical and
subclinical psychopaths in relation to the medial frontal cortex (MFC), and OFC. They
SUBCLINICAL PSYCHOPATHY AND EMPATHY 29
defined subclinical (they refer to it as successful) psychopaths as individuals with high
PCL-R scores that managed to escape detection for their crimes. A PCL-R cutoff score
of 23 and above was used. It should be noted that both groups reported that they had
committed the same number of crimes on average, 9.88 for the clinical group, and
9.37 for the subclinical group. In this case, the clinical psychopaths had higher
socioeconomic status than the subclinical group, although the difference was not
statistically significant (p = 0.06). The results showed structural deficits in MFC, OFC,
and amygdala in clinical psychopaths, but not in subclinical psychopaths. Interestingly,
the subclinical psychopaths had higher gray matter volume in the left middle frontal
cortex and superior frontal cortex than normal controls (Yang et al., 2010).
Though not directly related to psychopathy, Raine et al. (1998) observed that
impulsive murderers have lower prefrontal activity than predatory murderers.
Common to both groups were increased subcortical activity (midbrain, amygdala,
hippocampus, and thalamus) in comparison to controls. This supports the intuitive
hypothesis that the deficient prefrontal functioning prohibits the impulsive murderer
from regulating, and controlling aggressive impulses (Raine & Yang, 2006b).
Temporal lobe. Dolan et al. (2002) revealed a 20% volume reduction of the
temporal cortex in incarcerated personality-disordered offenders. These offenders
corresponded more closely to the ASPD criteria, which makes the finding difficult to
generalize, especially against the population of subclinical psychopaths. As noted
above, Yang et al. (2009) reported reductions in gray matter thickness in the anterior
and MTL, and also in the superior temporal regions and the insula. Müller et al.
(2008) found significant gray matter reductions in frontal and temporal brain regions
in psychopaths compared with controls. A specifically high volume loss was found in
the right superior temporal gyrus. In contrast to the prefrontal, and the left temporal
finding, right temporal volume loss was not because of other correlates, such as
education, alcohol, or drug consumption (Müller et al., 2008).
Hippocampus. Raine et al. (2004) reported an exaggerated anterior
hippocampal volume asymmetry (right > left) in clinical psychopaths, relative to both
SUBCLINICAL PSYCHOPATHY AND EMPATHY 30
control, and subclinical psychopaths. Neither environmental factors nor diagnostic
confounds could explain the phenomenon, which led the researchers to propose that
the asymmetry is probably a developmental problem.
Corpus callosum. Raine et al. (2003) investigated the potential differences in
the corpus callosum between 15 male subjects with high psychopathy scores, and
ASPD, as compared to controls. The ASPD subjects showed 22.6% increase in
estimated callosal white matter volume, 6.9% increase in callosal length, 15.3%
reduction in callosal thickness, and increased functional interhemispheric connectivity.
Larger callosal volumes were associated with affective and interpersonal deficits, low
autonomic stress reactivity, and low spatial ability.
Neuroimaging and Empathy
According to Decety, Skelly, and Kiehl (2013), the neural processes linked to
empathy have only been investigated with functional magnetic resonance imaging
(fMRI) once, in psychopaths. The group of researchers used a total of 80 men
incarcerated in a medium security correctional facility. The participants underwent a
full PCL-R investigation, including file reviews, and interviews. Those scoring 30 or
more on the PCL-R were assigned to a high-psychopathy group (n=27). Scores of
21-29 (n=28) were assigned to a medium-psychopathy group. The third group was
low-psychopathy scorers (n=25), with a score of 20 or less. Furthermore, second-level
analyses were conducted in order to compare PCL-R extremes. Participants with 30 or
more were selected for the psychopathy group, and 20 or less for the control group.
The subsequent testing involved two tasks for examining the neural processes linked
to empathy when observing others being harmed, or making pained facial expressions.
Participants in the psychopathy group showed less activation in the VMPFC, lateral
OFC, and PAG, in comparison to controls. Interestingly, the lateral, and medial parts of
the OFC are extensively interconnected with the amygdala, and hypothalamus, which
are involved in the mediation of emotional and affective behavior (Blair, 2003;
Decety, 2010a; Weber, Habel, Amunts, & Schneider, 2008). The psychopaths also
exhibited greater activation in the insula, which positively correlated with scores on
SUBCLINICAL PSYCHOPATHY AND EMPATHY 31
both PCL-R factors. The participants also showed greater activation in the anterior
insula (AI), dorsal striatum, dorsomedial prefrontal cortex, and posterior superior
temporal sulcus, where the latter three are involved in the cognitive aspect of
empathy, or ToM (Abu-Akel & Shamay-Tsoory, 2011; Carrington & Bailey, 2009;
Van Overwalle & Baetens, 2009). Decety et al. (2013) find the high activity in the AIC
surprising, due to it being the most consistently active brain region across all studies
concerning pain related empathy (Decety, 2010b; Lamm, Decety, & Singer, 2011).
Discussion
In the introduction, two hypotheses were stated which have by now been
discussed both theoretically and empirically. The first hypothesis regards the current
conceptualization of subclinical psychopathy, specifically, that the conceptualization of
subclinical psychopathy is flawed, because the criterion for being a subclinical
psychopath is arbitrary. The second hypothesis is that there is some difference
between clinical and subclinical psychopaths, and by this, I do not simply mean a
difference of location (institutionalized or not), but rather, that there is a substantial
difference in behavior.
The empirical evidence supporting the second thesis is, I think, convincing. The
structural deficits found in clinical but not subclinical psychopaths are a solid
foundation in support of the claim that there must be a significant difference. In a few
of the studies reviewed, the subclinical psychopath has been found to have more gray
matter than both clinical psychopaths and non-psychopathic controls. This suggests
that the subclinical psychopath may be anatomically different in a way that allows him
to, for one reason or another, behave in a significantly less antisocial manner.
However, the behavior of an individual is not possible to simply reduce to how much
white or gray matter there is in a given brain area. Due to factors such as neural
plasticity, the brain may utilize alternative pathways and thus the same function (i.e.,
behavior) may be retained. Ultimately, concluding that structural deficits of up to 26%
in the amygdala in clinical psychopaths (Yang et al., 2010) do not mean anything
SUBCLINICAL PSYCHOPATHY AND EMPATHY 32
whatsoever, is quite a stretch. Furthermore, at least one study has shown that
psychopaths may be different on a sensorimotor level, specifically in regards to motor
empathy (Fecteau et al., 2008). This study relied on self-measurement instruments in
order to assess psychopathy, which renders the study a bit more problematic. In any
case, studies such as these are important because they prod the important questions
and return valuable information; which brings me to the second hypothesis.
The first hypothesis is the chief concern of this thesis, and relates to the issue of
how subclinical psychopathy is currently discussed. The conceptualization of
subclinical psychopathy has, to my knowledge, not been established in any finer detail
than by how it has been presented in this thesis. Accordingly, subclinical psychopathy
refers to individuals that refrain from criminal activity for one reason or another. The
value of a distinction comes from what the distinction is supposed to be used for. Gao
and Raine (2010) proposed three reasons for studying subclinical psychopathy. The
first reason is to determine, with a greater degree of certainty, what the prevalence
rate of psychopathy is. Second, subclinical psychopaths may not be exactly like clinical
psychopaths, and hence, studying subclinical psychopaths may lead to etiological
insights. Third, understanding how subclinical psychopaths operate may help with
rehabilitation of all psychopaths. These three reasons are all good reasons for studying
subclinical psychopathy. The problem is that the current conceptualization is
ambiguous and depends on poorly chosen criteria.
To illuminate what I am referring to, one particular comment by Gao and Raine
(2010) can be analyzed. They proposed that serial killers who evade law enforcement
for long periods of time could constitute a form of semi-successful psychopathy. In my
opinion, this terminology speaks volumes about the intrinsic flaw in the
clinical-subclinical distinction, because subclinical psychopaths are supposedly not as
intensely antisocial as clinical psychopaths. It is difficult to imagine a group of people
that are more severely antisocial than serial killers, and thus, even amongst
researchers, there exists a conceptual inconsistency that needs resolution.
There is a long standing tradition amongst psychopathy researchers to regard the
SUBCLINICAL PSYCHOPATHY AND EMPATHY 33
entire construct as a subset of ASPD, as seen in Herpertz and Saß (2000). Coid and
Ullrich (2010) even goes so far as to suggest that ASPD and psychopathy belong on
the same spectrum. They argue that the cut-off point used when diagnosing
psychopaths with the PCL-R is arbitrary and that this has created a gap between the
constructs which is uncalled for. It should be noted that this is a controversial position
that does not conform to consensus. Other researchers have argued for the exact
opposite position, namely, that ASPD and psychopathy are two very different
constructs (Hare, 1996; Hare & Neumann, 2006; Perez, 2012). However, subclinical
psychopathy is very rarely mentioned in conceptual debates and it is not obvious that
subclinical psychopathy is simply a subset of psychopathy. The consequence of the
current conceptualization is that subclinical psychopaths are forced into the same
category as both clinical psychopaths, and in some conceptualizations, in the ASPD
category. This categorization must result in that subclinical psychopaths are
categorized as severely antisocial, which they, by definition, should not be.
The issue is that the behavior of subclinical psychopaths must be put into
question. Is there such a thing as a subclinical psychopath with a pervasive pattern of
antisocial behavior? The only criterion for determining whether or not an individual is
a clinical or subclinical psychopath depends on that individual’s location (i.e. mental
institution or prison), and this is problematic. As long as a psychopathic individual
behaves in a way that is tolerated (in the sense that he is able to get away with
whatever it is he is doing) within a given context and circumstance – the result must
be that the individual is classified as a subclinical psychopath. This is not a problem at
all if the point of the clinical-subclinical distinction is to determine where an
individual is located, but this hardly requires extra terminology. The conceptual
problem arises when one reflects about the reasons for studying subclinical
psychopaths. If these two groups are behaviorally different, which it stands to reason
that they are, then it may be possible to base the criteria on behavior.
In the subsequent discussion two things will be discussed: the problems of
psychopathy and empathy research, and a few areas where more research is needed.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 34
The empathy construct is an incredibly complex one, believed to involve at least 13
brain regions (Baron-Cohen, 2012). Apart from the terminology, which definitely
plays a role in the ambiguous nature of empathy, measuring empathy is very
problematic. Most research relies on self-measurement instruments, the problems of
which have been discussed previously. In relation to psychopathy, the main problem
with empathy is arguably that surprisingly few studies have been conducted,
especially concerning emotional empathy (Thoma et al., 2013). This is very peculiar,
because many theorize that lack of empathy is the key component of psychopathy.
Thus, breakthroughs in the field could lead to improvements in terms of rehabilitation.
Treatments need to distinguish between different empathic deficits, because antisocial
behavior has been linked to deficits in cognitive empathy to a larger extent than
affective empathy (Jolliffe & Farrington, 2004), and hence, interventions in antisocial
behaviors may need to focus on the former type.
The recently published fMRI-study by Decety et al. (2013) is an important one,
because it is a starting point when it comes to studying empathy with imaging
techniques in psychopaths. There remain many elusive facts regarding empathy that
are crucial in order to understand both psychopathy and empathy. Without a thorough
understanding of the relation between cognitive and affective empathy, drawing
conclusions regarding psychopathy will be problematic.
In order to improve insight into subclinical psychopathy, it may be beneficial to
control for PCL-R scores (on all four PCL-R facets) between groups. Other possible
confounding factors include intelligence, personality traits, socioeconomic status,
education, parenting (or other protective environmental factors), alcohol, and drug
abuse. Most of these factors have been studied regarding clinical psychopathy, but
remain unexplored concerning subclinical psychopathy. Furthermore, discussing all of
these topics is beyond the scope of this thesis, but a few words will be written about
gender, intelligence and personality.
Most psychopathy research is conducted with male participants, but studies on
female psychopaths have shown quite significant behavioral differences. These
SUBCLINICAL PSYCHOPATHY AND EMPATHY 35
differences may play a role in the difficulty of delineating the psychopathy construct,
as well as making it difficult to establish prevalence rates. Female psychopaths are
interesting in relation to subclinical psychopaths, because their behavior seems to be
less severely antisocial (in terms of violence and aggression); but they are also
interesting in relation to empathy and emotions in general. It may be the case that
female psychopaths are less callous than male psychopaths and thus, it is a possibility
that empathy is a moderating factor.
Intelligence and personality are interesting aspects of psychopathy that could
yield significant etiological insight. However, very few studies have been conducted
regarding both topics in relation to clinical psychopathy, and there is no study known
to the author regarding subclinical psychopaths in particular. Costa and MacCrae’s
(1992) five factor model of personality has been used to study psychopaths, but the
results of such studies are not of relevance to this topic, because no contrasting results
in subclinical psychopaths have been studied. Neuroscience has not yet reached a
stage at which it is possible to meaningfully infer behavior based on brain scans.
Hence, a social psychological perspective may be an efficient way of establishing
specific behavioral differences between the two psychopathy groups, which in turn
may lead to the possibility of clarifying the concepts involved.
Three frameworks for assessing the status of subclinical psychopathy have been
presented. Proponents of the first framework argue that the difference between
clinical and subclinical psychopaths is one of degree, not of type. Advocates of the
second suggest that both types share etiology and pathology, which means that the
essential difference is a matter of socialization. Good parenting, special talent, high
intelligence etc. is said to hinder the individual from fully developing into a clinical
psychopath. The third framework posits that there are two distinct etiologies, which
allow for the possibility of scoring high on one, and low on the other. This approach
converges well with the two factors of the PCL-R.
The second framework can be interpreted in a variety of ways, depending on
how strong of a claim one infers. The very strong claim would be to say that a good
SUBCLINICAL PSYCHOPATHY AND EMPATHY 36
upbringing will inevitably result in a well-functioning, pro-social individual. There is
quite a lot of anecdotal evidence to suggest that while a bad upbringing can have its
negative consequences, many also overcome such diversities. The same can be said
about a good upbringing, which in some cases ultimately results in antisocial behavior.
The weaker claim would be to say that the influence of socialization is significant, but
is not, in itself, enough to moderate the behavior of a significant neuroanatomical
deficit. Furthermore, these frameworks are not mutually exclusive. At the moment it is
very difficult to assess the epistemic status of the three frameworks, due to a lack of
research. The little evidence that do exist can be used in support of all three.
The frameworks spark the debate of difference as degree versus type. A
significant contribution to this debate can be foreseen in substantial advancements in
neuroscience, in terms of finding a double dissociation (e.g., Broca’s area and
Wernicke’s area). If one can demonstrate that damage to brain structure P impairs
affective empathy, but does not cause antisocial behavior, and that damage to brain
structure Q causes antisocial behavior, but spares affective empathy, one could infer
that the two areas are dissociable. With such evidence, the inference for a difference
in type would be very strong.
Studies pertaining to the neuroendocrinology of psychopathy may also prove
significant in the future. The field is currently in its infancy, but with continued
research and technical advancement, one can be hopeful about seeing significant
group differences in hormones and neurotransmitters. This includes Baron-Cohen’s
research regarding empathy and testosterone, which may one day prove to be
important aspects of psychopathy.
In conclusion: it has been argued that the conceptualization of subclinical
psychopathy is flawed and ultimately, my suggestion is that a better definition of
subclinical psychopathy would rely on both the available and the forthcoming
empirical data. Being that lack of empathy is a key aspect in both clinical and
subclinical psychopathy it needs to be studied extensively. Both the aspects of empathy
are relevant in order to understand psychopathic behavior, in both clinical and
SUBCLINICAL PSYCHOPATHY AND EMPATHY 37
subclinical psychopaths. With technical advancement and continued research, one can
be hopeful that more significant research will be carried out; the implications of which
may not only help in resolving etiological debates, but help in the treatment of
psychopathy.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 38
References
Abu-Akel, A. & Shamay-Tsoory, S. G. (2011). Neuroanatomical and neurochemical
bases of theory of mind. Neuropsychologia, 49(11), 2971–2984.
doi:10.1016/j.neuropsychologia.2011.07.012
Adolphs, R. & Tranel, D. (2003). Amygdala damage impairs emotion recognition from
scenes only when they contain facial expressions. Neuropsychologia, 41(10),
1281–1289. doi:10.1016/S0028-3932(03)00064-2
Adolphs, R., Tranel, D., & Damasio, A. R. (1998). The human amygdala in social
judgment. Nature, 393(6684), 470–474. doi:10.1038/30982
Adolphs, R., Tranel, D., Damasio, H., & Damasio, A. R. (1994). Impaired recognition
of emotion in facial expressions following bilateral damage to the human
amygdala. Nature, 372(6507), 669–672. doi:10.1038/372669a0
American Psychiatric Association. (1980). Diagnostic and Statistical Manual of Mental
Disorders. (3rd ed.). Washington, DC: Author.
American Psychiatric Association. (1994). Diagnostic and Statistical Manual of Mental
Disorders. (4th ed.). Washington, DC: Author.
American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental
Disorders. (4th ed., text rev.). Washington, DC: Author.
Anderson, N. E. & Kiehl, K. A. (2012). The psychopath magnetized: insights from
brain imaging. Trends in Cognitive Sciences, 16(1), 52–60.
doi:10.1016/j.tics.2011.11.008
Auyeung, B., Baron-Cohen, S., Chapman, E., Knickmeyer, R. C., Taylor, K., &
Hackett, G. (2006). Foetal testosterone and the child systemizing quotient.
European Journal of Endocrinology, 155(1), 123–130. doi:10.1530/eje.1.02260
Avenanti, A., Bueti, D., Galati, G., & Aglioti, S. M. (2005). Transcranial magnetic
stimulation highlights the sensorimotor side of empathy for pain. Nature
Neuroscience, 8(7), 955–960. doi:10.1038/nn1481
Babiak, P. & Hare, R. D. (2009). Snakes in suits: when psychopaths go to work. New
York: Regan.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 39
Baron-Cohen, S. (2012). Zero degrees of empathy: a new theory of human cruelty and
kindness. London: Penguin Books Ltd.
Baron-Cohen, S., Knickmeyer, R. C., & Belmonte, M. K. (2005). Sex differences in the
brain: implications for explaining autism. Science, 310(5749), 819–823.
doi:10.1126/science.1115455
Baron-Cohen, S. & Wheelwright, S. (2004). The empathy quotient: an investigation of
adults with asperger syndrome or high functioning autism, and normal sex
differences. Journal of Autism and Developmental Disorders, 34(2), 163–175.
Batson, C. D. (2009). These things called empathy: eight related but distinct
phenomena. In J. Decety & W. Ickes (Eds.), The social neuroscience of empathy
(pp. 14–34). Cambridge, MA: MIT Press.
Blackburn, R. (2009). Subtypes of psychopathy. In M. McMurran & R. C. Howard
(Eds.), Personality, personality disorder and violence: an evidence based approach
(pp. 113–132). United Kingdom: Wiley–Blackwell.
Blair, R. J. R. (2003). Neurobiological basis of psychopathy. The British Journal of
Psychiatry, 182(1), 5–7. doi:10.1192/bjp.182.1.5
Blair, R. J. R. (2004). The roles of orbital frontal cortex in the modulation of antisocial
behavior. Brain and Cognition, 55(1), 198–208.
doi:10.1016/S0278-2626(03)00276-8
Blair, R. J. R. (2005). Responding to the emotions of others: dissociating forms of
empathy through the study of typical and psychiatric populations. Consciousness
and Cognition, 14(4), 698–718. doi:10.1016/j.concog.2005.06.004
Blair, R. J. R. (2007a). Empathic dysfunction in psychopathic individuals. In T. F. D.
Farrow & P. W. R. Woodruff (Eds.), Empathy in mental illness (pp. 3–16). New
York: Cambridge University Press.
Blair, R. J. R. (2007b). The amygdala and ventromedial prefrontal cortex in morality
and psychopathy. Trends in Cognitive Sciences, 11(9), 387–392.
doi:10.1016/j.tics.2007.07.003
SUBCLINICAL PSYCHOPATHY AND EMPATHY 40
Blair, R. J. R. (2008). The amygdala and ventromedial prefrontal cortex: functional
contributions and dysfunction in psychopathy. Philosophical Transactions of the
Royal Society B: Biological Sciences, 363(1503), 2557–2565.
doi:10.1098/rstb.2008.0027
Blair, R. J. R., Mitchell, D., & Blair, K. (2005). The psychopath: emotion and the brain.
Malden, MA: Blackwell Publishing.
Broomhall, L. (2005). Acquired sociopathy: a neuropsychological study of executive
dysfunction in violent offenders. Psychiatry, Psychology and Law, 12(2), 367–387.
doi:10.1375/pplt.12.2.367
Carr, L., Iacoboni, M., Dubeau, M. C., Mazziotta, J. C., & Lenzi, G. L. (2003). Neural
mechanisms of empathy in humans: a relay from neural systems for imitation to
limbic areas. Proceedings of the National Academy of Sciences, 100(9),
5497–5502. doi:10.1073/pnas.0935845100
Carrington, S. J. & Bailey, A. J. (2009). Are there theory of mind regions in the brain?
a review of the neuroimaging literature. Human Brain Mapping, 30(8),
2313–2335. doi:10.1002/hbm.20671
Chapman, E., Baron-Cohen, S., Auyeung, B., Knickmeyer, R. C., Taylor, K., &
Hackett, G. (2006). Fetal testosterone and empathy: evidence from the empathy
quotient (eq) and the “reading the mind in the eyes” test. Social Neuroscience,
1(2), 135–148. doi:10.1080/17470910600992239
Cleckley, H. M. (1988). The mask of sanity. (Original work published 1941). New
American Library.
Coid, J. & Ullrich, S. (2010). Antisocial personality disorder is on a continuum with
psychopathy. Comprehensive Psychiatry, 51(4), 426–433.
doi:10.1016/j.comppsych.2009.09.006
Coid, J., Yang, M., Ullrich, S., Roberts, A., & Hare, R. D. (2009). Prevalence and
correlates of psychopathic traits in the household population of Great Britain.
International Journal of Law and Psychiatry, 32(2), 65–73.
doi:10.1016/j.ijlp.2009.01.002
SUBCLINICAL PSYCHOPATHY AND EMPATHY 41
Coll, M., Budell, L., Rainville, P., Decety, J., & Jackson, P. L. (2012). The role of gender
in the interaction between self-pain and the perception of pain in others. The
Journal of Pain, 13(7), 695–703. doi:10.1016/j.jpain.2012.04.009
Cooke, D. J. (1998). Cross-cultural aspects of psychopathy. In T. Millon, E. Simonsen,
M. Birket-Smith, & R. D. Davis (Eds.), Psychopathy: antisocial, criminal, and
violent behavior (pp. 260–276). New York: Guilford Press.
Cooke, D. J. & Michie, C. (2001). Refining the construct of psychopathy: towards a
hierarchical model. Psychological Assessment, 13(2), 171–188.
doi:10.1037111040-3590.13.2.171
Costa, P. T. & MacCrae, R. R. (1992). Revised NEO Personality Inventory (NEO PI-R)
and NEO Five-Factor Inventory (NEO FFI): professional manual. Odessa, FL:
Psychological Assessment Resources.
Cox, C. L., Uddin, L. Q., Di Martino, A., Castellanos, F. X., Milham, M. P., & Kelly, C.
(2012). The balance between feeling and knowing: affective and cognitive
empathy are reflected in the brain’s intrinsic functional dynamics. Social
Cognitive and Affective Neuroscience, 7(6), 727–737. doi:10.1093/scan/nsr051
Davis, M. H. (1983). The effects of dispositional empathy on emotional reactions and
helping: a multidimensional approach. Journal of Personality, 51(2), 167–184.
doi:10.1111/j.1467-6494.1983.tb00860
de Vignemont, F. & Singer, T. (2006). The empathic brain: how, when and why?
Trends in Cognitive Sciences, 10(10), 435–441. doi:10.1016/j.tics.2006.08.008
Decety, J. (2010a). The neurodevelopment of empathy in humans. Developmental
Neuroscience, 32(4), 257–267. doi:10.1159/000317771
Decety, J. (2010b). To what extent is the experience of empathy mediated by shared
neural circuits? Emotion Review, 2(3), 204–207.
doi:10.1177/1754073910361981
Decety, J., Skelly, L. R., & Kiehl, K. A. (2013). Brain response to empathy-eliciting
scenarios involving pain in incarcerated individuals with psychopathy. JAMA
Psychiatry, 70(6), 638–645. doi:10.1001/jamapsychiatry.2013.27
SUBCLINICAL PSYCHOPATHY AND EMPATHY 42
DeWall, C. N. & Anderson, C. A. (2011). The general aggression model. In P. R. Shaver
& M. Mikulincer (Eds.), Human aggression and violence: causes, manifestations,
and consequenses (pp. 15–33). Washington, DC: American Psychological
Association.
Di Pellegrino, G., Fadiga, L., Fogassi, L., Gallese, V., & Rizzolatti, G. (1992).
Understanding motor events: a neurophysiological study. Experimental Brain
Research, 91(1), 176–180.
Dimberg, U. & Thunberg, M. (2012). Empathy, emotional contagion, and rapid facial
reactions to angry and happy facial expressions. PsyCh Journal, 1(2), 118–127.
doi:10.1002/pchj.4
Dolan, M. C., Deakin, J. F. W., Roberts, N., & Anderson, I. M. (2002). Quantitative
frontal and temporal structural MRI studies in personality-disordered offenders
and control subjects. Psychiatry Research: Neuroimaging, 116(3), 133–149.
doi:10.1016/S0925-4927(02)00085-9
Dolan, M. C. & Fullam, R. S. (2004). Theory of mind and mentalizing ability in
antisocial personality disorders with and without psychopathy. Psychological
Medicine, 34(6), 1093–1102. doi:10.1017/S0033291704002028
Dolan, M. C. & Fullam, R. S. (2007). Empathy, antisocial behaviour and personality
pathology. In T. F. D. Farrow & P. W. R. Woodruff (Eds.), Empathy in mental
illness (pp. 33–48). New York: Cambridge University Press.
Dolan, M. C. & Fullam, R. S. (2009). Psychopathy and functional magnetic resonance
imaging blood oxygenation level-dependent responses to emotional faces in
violent patients with schizophrenia. Biological Psychiatry, 66(6), 570–577.
doi:10.1016/j.biopsych.2009.03.019
Ekman, P. (1985). Telling lies: clues to deceit in the marketplace, politics, and marriage.
New York: WW Norton & Company.
Ellis, L., Beaver, K. M., & Wright, J. (2009). Handbook of crime correlates. Oxford:
Academic Press.
SUBCLINICAL PSYCHOPATHY AND EMPATHY 43
Ermer, E., Cope, L. M., Nyalakanti, P. K., Calhoun, V. D., & Kiehl, K. A. (2012).
Aberrant paralimbic gray matter in criminal psychopathy. Journal of Abnormal
Psychology, 121(3), 649–658. doi:10.1037/a0026371
Fan, Y., Duncan, N. W., de Greck, M., & Northoff, G. (2011). Is there a core neural
network in empathy? an fMRI based quantitative meta-analysis. Neuroscience &
Biobehavioral Reviews, 35(3), 903–911. doi:10.1016/j.neubiorev.2010.10.009
Fecteau, S., Pascual-Leone, A., & Théoret, H. (2008). Psychopathy and the mirror
neuron system: preliminary findings from a non-psychiatric sample. Psychiatry
Research, 160(2), 137–144. doi:10.1016/j.psychres.2007.08.022
Forouzan, E. & Cooke, D. J. (2005). Figuring out la femme fatale: conceptual and
assessment issues concerning psychopathy in females. Behavioral Sciences & the
Law, 23(6), 765–778. doi:10.1002/bsl.669
Fowles, D. C. & Dindo, L. (2006). A dual-deficit model of psychopathy. In C. J. Patrick
(Ed.), The handbook of psychopathy (pp. 14–34). New York: Guilford Press.
Frith, U., Morton, J., & Leslie, A. M. (1991). The cognitive basis of a biological
disorder: autism. Trends in Neurosciences, 14(10), 433–438.
doi:10.1016/0166-2236(91)90041-R
Gallese, V. (2001). The shared manifold hypothesis. from mirror neurons to empathy.
Journal of Consciousness Studies, 8(5-7), 33–50.
Gallese, V. (2003). The roots of empathy: the shared manifold hypothesis and the
neural basis of intersubjectivity. Psychopathology, 36(4), 171–180.
doi:10.1159/000072786
Gao, Y. & Raine, A. (2010). Successful and unsuccessful psychopaths: a
neurobiological model. Behavioral Sciences & the Law, 28(2), 194–210.
doi:10.1002/bsl.924
Gelsthorpe, L. (2004). Female offending. In G. McIvor (Ed.), Women who offend
(pp. 13–37). London: Jessica Kingsley.
Glenn, A. L. & Raine, A. (2008). The neurobiology of psychopathy. Psychiatric Clinics
of North America, 31(3), 463–475. doi:10.1016/j.psc.2008.03.004
SUBCLINICAL PSYCHOPATHY AND EMPATHY 44
Glenn, A. L., Raine, A., Schug, R. A., Gao, Y., & Granger, D. A. (2011). Increased
testosterone-to-cortisol ratio in psychopathy. Journal of Abnormal Psychology,
120(2), 389–399. doi:10.1037/a0021407
Gustafson, S. B. & Ritzer, D. R. (1995). The dark side of normal: a psychopathy-linked
pattern called aberrant self-promotion. European Journal of Personality, 9(3),
147–183. doi:10.1002/per.2410090302
Hall, J. R. & Benning, S. D. (2006). The “successful” psychopath: adaptive and
subclinical manifestations of psychopathy in the general population. In C. J.
Patrick (Ed.), The handbook of psychopathy (pp. 459–478). New York: Guilford
Press.
Happé, F. & Frith, U. (1996). Theory of mind and social impairment in children with
conduct disorder. British Journal of Developmental Psychology, 14(4), 385–398.
doi:10.1111/j.2044-835X.1996.tb00713.x
Hare, R. D. (1985). The Psychopathy Checklist. Unpublished manuscript, University of
British Columbia, Vancouver, BC, Canada.
Hare, R. D. (1991). The Hare Psychopathy Checklist–Revised. Toronto, ON, Canada:
Multi-Health Systems.
Hare, R. D. (1996). Psychopathy and antisocial personality disorder: a case of
diagnostic confusion. Psychiatric Times, 13(2), 1–6.
Hare, R. D. (1999a). Psychopathy as a risk factor for violence. Psychiatric Quarterly,
70(3), 181–197. doi:10.1023/A:1022094925150
Hare, R. D. (1999b). Without conscience: the disturbing world of the psychopaths among
us. New York: Guilford Press.
Hare, R. D. (2003). The Hare Psychopathy Checklist–Revised, 2nd edition. Toronto, ON,
Canada: Multi-Health Systems.
Hare, R. D., Clark, D., Grann, M., & Thornton, D. (2000). Psychopathy and the
predictive validity of the PCL–R: an international perspective. Behavioral Sciences
& the Law, 18(5), 623–645.
doi:10.1002/1099-0798(200010)18:5<623::AID-BSL409>3.0.CO;2-W
SUBCLINICAL PSYCHOPATHY AND EMPATHY 45
Hare, R. D., Harpur, T. J., Hakstian, A. R., Forth, A. E., Hart, S. D., & Newman, J. P.
(1990). The revised Psychopathy Checklist: reliability and factor structure.
Journal of Consulting and Clinical Psychology, 2(3), 338–341.
doi:10.1037/1040-3590.2.3.338
Hare, R. D. & Neumann, C. S. (2005). Structural models of psychopathy. Current
Psychiatry Reports, 7(1), 57–64. doi:10.1007/s11920-005-0026-3
Hare, R. D. & Neumann, C. S. (2006). The PCL–R assessment of psychopathy. In C. J.
Patrick (Ed.), The handbook of psychopathy (pp. 58–88). New York: Guilford
Press.
Hare, R. D. & Neumann, C. S. (2008). Psychopathy as a clinical and empirical
construct. Annual Review of Clinical Psychology, 4, 217–246.
doi:10.1146/annurev.clinpsy.3.022806.091452
Harenski, C. L., Harenski, K. A., Shane, M. S., & Kiehl, K. A. (2010). Aberrant neural
processing of moral violations in criminal psychopaths. Journal of Abnormal
Psychology, 119(4), 863–874. doi:10.1037/a0020979
Hart, S. D. & Hare, R. D. (1997). Psychopathy: assessment and association with
criminal conduct. In D. M. Stoff, J. Breiling, & J. D. Maser (Eds.), The handbook
of psychopathy (pp. 22–35). John Wiley & Sons Inc.
Herpertz, S. C. & Saß, H. (2000). Emotional deficiency and psychopathy. Behavioral
Sciences & the Law, 18(5), 567–580.
doi:10.1002/1099-0798(200010)18:5<567::AID-BSL410>3.0.CO;2-8
Hicks, B. M. & Patrick, C. J. (2006). Psychopathy and negative emotionality: analyses
of suppressor effects reveal distinct relations with emotional distress, fearfulness,
and anger–hostility. Journal of Abnormal Psychology, 115(2), 276–287.
doi:10.1037/0021-843X.115.2.276
Higley, J. D., Mehlman, P. T., Poland, R. E., Taub, D. M., Vickers, J., Suomi, S. J., &
Linnoila, M. (1996). CSF testosterone and 5-HIAA correlate with different types
of aggressive behaviors. Biological Psychiatry, 40(11), 1067–1082.
doi:10.1016/S0006-3223(95)00675-3
SUBCLINICAL PSYCHOPATHY AND EMPATHY 46
Hill, C. D., Rogers, R., & Bickford, M. E. (1996). Predicting aggressive and socially
disruptive behavior in a maximum security forensic psychiatric hospital. Journal
of Forensic Sciences, (41), 56–59.
Hurlemann, R., Patin, A., Onur, O. A., Cohen, M. X., Baumgartner, T., Metzler, S., . . .
Kendrick, K. M. (2010). Oxytocin enhances amygdala-dependent, socially
reinforced learning and emotional empathy in humans. The Journal of
Neuroscience, 30(14), 4999–5007. doi:10.1523/JNEUROSCI.5538-09.2010
Iacoboni, M. (2009). Imitation, empathy, and mirror neurons. Annual Review of
Psychology, 60, 653–670. doi:10.1146/annurev.psych.60.110707.163604
Jabbi, M., Swart, M., & Keysers, C. (2007). Empathy for positive and negative
emotions in the gustatory cortex. Neuroimage, 34(4), 1744–1753.
doi:10.1016/j.neuroimage.2006.10.032
Jackson, P. L., Brunet, E., Meltzoff, A. N., & Decety, J. (2006). Empathy examined
through the neural mechanisms involved in imagining how i feel versus how you
feel pain. Neuropsychologia, 44(5), 752–761.
doi:10.1016/j.neuropsychologia.2005.07.015
Jackson, P. L., Meltzoff, A. N., & Decety, J. (2005). How do we perceive the pain of
others? a window into the neural processes involved in empathy. Neuroimage,
24(3), 771–779. doi:10.1016/j.neuroimage.2004.09.006
Jolliffe, D. & Farrington, D. P. (2004). Empathy and offending: a systematic review
and meta-analysis. Aggression and Violent Behavior, 9(5), 441–476.
doi:10.1016/j.avb.2003.03.001
Keysers, C., Wicker, B., Gazzola, V., Anton, J.-L., Fogassi, L., & Gallese, V. (2004). A
touching sight: SII/PV activation during the observation and experience of
touch. Neuron, 42(2), 335–346. doi:10.1016/S0896-6273(04)00156-4
Kiehl, K. A. (2006). A cognitive neuroscience perspective on psychopathy: evidence for
paralimbic system dysfunction. Psychiatry Research, 142(2), 107–128.
doi:10.1016/j.psychres.2005.09.013
SUBCLINICAL PSYCHOPATHY AND EMPATHY 47
Knickmeyer, R. C. & Baron-Cohen, S. (2006). Fetal testosterone and sex differences.
Early Human Development, 82(12), 755–760.
doi:10.1016/j.earlhumdev.2006.09.014
Kober, H., Barrett, L. F., Joseph, J., Bliss-Moreau, E., Lindquist, K., & Wager, T. D.
(2008). Functional grouping and cortical–subcortical interactions in emotion: a
meta-analysis of neuroimaging studies. Neuroimage, 42(2), 998–1031.
doi:10.1016/j.neuroimage.2008.03.059
Laakso, M. P., Gunning-Dixon, F., Vaurio, O., Repo-Tiihonen, E., Soininen, H., &
Tiihonen, J. (2002). Prefrontal volumes in habitually violent subjects with
Antisocial Personality Disorder and Type 2 alcoholism. Psychiatry Research:
Neuroimaging, 114(2), 95–102. doi:10.1016/S0925-4927(02)00005-7
Lamm, C., Decety, J., & Singer, T. (2011). Meta-analytic evidence for common and
distinct neural networks associated with directly experienced pain and empathy
for pain. Neuroimage, 54(3), 2492–2502.
doi:10.1016/j.neuroimage.2010.10.014
LeBreton, J. M., Binning, J. F., & Adorno, A. J. (2006). Subclinical psychopaths. In
J. C. Thomas & D. L. Segal (Eds.), Comprehensive handbook of personality and
psychopathology: volume 1 (pp. 388–411). Hoboken, NJ: John Wiley & Sons, Inc.
Leygraf, N. & Elsner, K. (2008). Risk of diagnosing psychopathic disorders. In A.
Felthous & H. Sass (Eds.), The international handbook of psychopathic disorders
and the law: volume I, diagnosis and treatment (pp. 135–146). West Sussex,
England: John Wiley & Sons Ltd.
Lilienfeld, S. O. (1998). Methodological advances and developments in the assessment
of psychopathy. Behaviour Research and Therapy, 36(1), 99–125.
doi:10.1016/S0005-7967(97)10021-3
Lilienfeld, S. O. & Andrews, B. P. (1996). Development and preliminary validation of a
self-report measure of psychopathic personality traits in noncriminal population.
Journal of Personality Assessment, 66(3), 488–524.
doi:10.1207/s15327752jpa6603_3
SUBCLINICAL PSYCHOPATHY AND EMPATHY 48
Lilienfeld, S. O. & Fowler, K. A. (2006). The self-report assessment of psychopathy. In
C. J. Patrick (Ed.), The handbook of psychopathy (pp. 107–132). New York:
Guilford Press.
Logan, C. & Weizmann-Henelius, G. (2012). Psychopathy in women: presentation,
assessment and management. In H. Häkkänen-Nyholm & J.-O. Nyholm (Eds.),
Psychopathy and law: a practitioner’s guide (pp. 99–125). United Kingdom:
Wiley-Blackwell.
Lykken, D. T. (1995). The antisocial personalities. New Jersey: Lawrence Erlbaum
Associates Inc.
Messick, S. (1995). Validity of psychological assessment: validation of inferences from
persons’ responses and performances as scientific inquiry into score meaning.
American Psychologist, 50(9), 741–749.
Montoya, E. R., Terburg, D., Bos, P. A., & van Honk, J. (2012). Testosterone, cortisol,
and serotonin as key regulators of social aggression: a review and theoretical
perspective. Motivation and Emotion, 36(1), 65–73.
doi:10.1007/s11031-011-9264-3
Morelli, S. A., Rameson, L. T., & Lieberman, M. D. (2012). The neural components of
empathy: predicting daily prosocial behavior. Social Cognitive and Affective
Neuroscience. doi:10.1093/scan/nss088
Müller, J. L., Gänßbauer, S., Sommer, M., Döhnel, K., Weber, T., Schmidt-Wilcke, T., &
Hajak, G. (2008). Gray matter changes in right superior temporal gyrus in
criminal psychopaths. evidence from voxel-based morphometry. Psychiatry
Research: Neuroimaging, 163(3), 213–222.
doi:10.1016/j.pscychresns.2007.08.010
Mullins-Nelson, J. L., Salekin, R. T., & Leistico, A. M. R. (2006). Psychopathy,
empathy, and perspective-taking ability in a community sample: implications for
the successful psychopathy concept. International Journal of Forensic Mental
Health, 5(2), 133–149. doi:10.1080/14999013.2006.10471238
SUBCLINICAL PSYCHOPATHY AND EMPATHY 49
Nelson, R. J. & Trainor, B. C. (2007). Neural mechanisms of aggression. Nature
Reviews Neuroscience, 8(7), 536–546. doi:10.1038/nrn2174
Nicholls, T. L., Ogloff, J. R. P., Brink, J., & Spidel, A. (2005). Psychopathy in women: a
review of its clinical usefulness for assessing risk for aggression and criminality.
Behavioral Sciences & the Law, 23(6), 779–802. doi:10.1002/bsl.678
O’Driscoll, K. & Leach, J. P. (1998). “no longer gage”: an iron bar through the head:
early observations of personality change after injury to the prefrontal cortex.
British Medical Journal, 317(7174), 1673–1674.
Ogloff, J. R. P. (2006). Psychopathy/antisocial personality disorder conundrum.
Australian and New Zealand Journal of Psychiatry, 40(6-7), 519–528.
doi:10.1080/j.1440-1614.2006.01834.x
Patrick, C. J. (2006). Handbook of psychopathy. Preface. New York: Guilford Press.
Perez, P. R. (2012). The etiology of psychopathy: a neuropsychological perspective.
Aggression and Violent Behavior, 17(6), 519–522. doi:10.1016/j.avb.2012.07.006
Poythress, N. G., Edens, J. F., & Lilienfeld, S. O. (1998). Criterion-related validity of
the Psychopathic Personality Inventory in a prison sample. Psychological
Assessment, 10(4), 426–430. doi:10.1037/1040-3590.10.4.426
Premack, D. & Woodruff, G. (1978). Does the chimpanzee have a theory of mind?
Behavioral and Brain Sciences, 1(4), 515–526.
doi:10.1017/S0140525X00076512
Quinsey, V. L. (2002). Evolutionary theory and criminal behaviour. Legal and
Criminological Psychology, 7(1), 1–13. doi:10.1348/135532502168324
Raine, A., Ishikawa, S. S., Arce, E., Lencz, T., Knuth, K. H., Bihrle, S., . . . Colletti, P.
(2004). Hippocampal structural asymmetry in unsuccessful psychopaths.
Biological Psychiatry, 55(2), 185–191. doi:10.1016/S0006-3223(03)00727-3
Raine, A., Lencz, T., Taylor, K., Hellige, J. B., Bihrle, S., Lacasse, L., . . . Colletti, P.
(2003). Corpus callosum abnormalities in psychopathic antisocial individuals.
Archives of General Psychiatry, 60(11), 1134–1142.
doi:10.1001/archpsyc.60.11.1134
SUBCLINICAL PSYCHOPATHY AND EMPATHY 50
Raine, A., Meloy, J. R., Bihrle, S., Stoddard, J., LaCasse, L., & Buchsbaum, M. S.
(1998). Reduced prefrontal and increased subcortical brain functioning assessed
using positron emission tomography in predatory and affective murderers.
Behavioral Sciences & the Law, 16(3), 319–332.
doi:10.1002/(SICI)1099-0798(199822)16:3<319::AID-BSL311>3.0.CO;2-G
Raine, A. & Yang, Y. (2006a). Neural foundations to moral reasoning and antisocial
behavior. Social Cognitive and Affective Neuroscience, 1(3), 203–213.
doi:10.1093/scan/nsl033
Raine, A. & Yang, Y. (2006b). The neuroanatomical bases of psychopathy. In C. J.
Patrick (Ed.), The handbook of psychopathy (pp. 278–295). New York: Guilford
Press.
Ramamurthi, B. (1988). Stereotactic operation in behaviour disorders. amygdalotomy
and hypothalamotomy. Acta Neurochirurgica, 44, 152–157.
doi:10.1007/978-3-7091-9005-0_29
Rizzolatti, G., Fadiga, L., Gallese, V., & Fogassi, L. (1996). Premotor cortex and the
recognition of motor actions. Cognitive Brain Research, 3(2), 131–141.
Rogers, R., Salekin, R. T., Sewell, K. W., & Cruise, K. R. (2000). Prototypical analysis
of antisocial personality disorder a study of inmate samples. Criminal Justice and
Behavior, 27(2), 234–255. doi:10.1177/0093854800027002006
Schulte-Rüther, M., Markowitsch, H. J., Fink, G. R., & Piefke, M. (2007). Mirror
neuron and theory of mind mechanisms involved in face-to-face interactions: a
functional magnetic resonance imaging approach to empathy. Journal of
Cognitive Neuroscience, 19(8), 1354–1372. doi:10.1162/jocn.2007.19.8.1354
Shamay-Tsoory, S. G. (2011). The neural bases for empathy. The Neuroscientist, 17(1),
18–24. doi:10.1177/1073858410379268
Shanton, K. & Goldman, A. (2010). Simulation theory. Wiley Interdisciplinary Reviews:
Cognitive Science, 1(4), 527–538. doi:10.1002/wcs.33
SUBCLINICAL PSYCHOPATHY AND EMPATHY 51
Singer, T. & Lamm, C. (2009). The social neuroscience of empathy. Annals of the New
York Academy of Sciences, 1156(1), 81–96.
doi:10.1111/j.1749-6632.2009.04418.x
Singer, T., Seymour, B., O’Doherty, J., Kaube, H., Dolan, R. J., & Frith, C. D. (2004).
Empathy for pain involves the affective but not sensory components of pain.
Science, 303(5661), 1157–1162. doi:10.1126/science.1093535
Skeem, J. L., Polaschek, D. L. L., Patrick, C. J., & Lilienfeld, S. O. (2011). Psychopathic
personality bridging the gap between scientific evidence and public policy.
Psychological Science in the Public Interest, 12(3), 95–162.
doi:10.1177/1529100611426706
Söderström, H., Blennow, K., Manhem, A., & Forsman, A. (2001). CSF studies in
violent offenders. i. 5-HIAA as a negative and HVA as a positive predictor of
psychopathy. Journal of Neural Transmission, 108(7), 869–878.
doi:10.1007/s007020170036
Söderström, H., Blennow, K., Sjödin, A. K., & Forsman, A. (2003). New evidence for an
association between the CSF HVA:5-HIAA ratio and psychopathic traits. Journal
of Neurology, Neurosurgery & Psychiatry, 74(7), 918–921.
doi:10.1136/jnnp.74.7.918
Terburg, D., Morgan, B., & van Honk, J. (2009). The testosterone–cortisol ratio: a
hormonal marker for proneness to social aggression. International Journal of Law
and Psychiatry, 32(4), 216–223. doi:10.1016/j.ijlp.2009.04.008
Thoma, P., Friedmann, C., & Suchan, B. (2013). Empathy and social problem solving
in alcohol dependence, mood disorders and selected personality disorders.
Neuroscience & Biobehavioral Reviews, 37(3).
doi:10.1016/j.neubiorev.2013.01.024
Van Elst, L. T., Woermann, F. G., Lemieux, L., Thompson, P. J., & Trimble, M. R.
(2000). Affective aggression in patients with temporal lobe epilepsy a
quantitative MRI study of the amygdala. Brain, 123(2), 234–243.
doi:10.1093/brain/123.2.234
SUBCLINICAL PSYCHOPATHY AND EMPATHY 52
Van Overwalle, F. & Baetens, K. (2009). Understanding others’ actions and goals by
mirror and mentalizing systems: a meta-analysis. Neuroimage, 48(3), 564–584.
doi:10.1016/j.neuroimage.2009.06.009
van Honk, J., Harmon-Jones, E., Morgan, B. E., & Schutter, D. J. L. G. (2010). Socially
explosive minds: the triple imbalance hypothesis of reactive aggression. Journal
of Personality, 78(1), 67–94. doi:10.1111/j.1467-6494.2009.00609.x
Verona, E. & Vitale, J. E. (2006). Psychopathy in women: assessment, manifestations,
and etiology. In C. J. Patrick (Ed.), The handbook of psychopathy (pp. 415–436).
New York: Guilford Press.
Vitale, J. E., Smith, S. S., Brinkley, C. A., & Newman, J. P. (2002). The reliability and
validity of the Psychopathy Checklist–Revised in a sample of female offenders.
Criminal Justice and Behavior, 29(2), 202–231.
doi:10.1177/0093854802029002005
Weber, S., Habel, U., Amunts, K., & Schneider, F. (2008). Structural brain
abnormalities in psychopaths—-a review. Behavioral Sciences & the Law, 26(1),
7–28. doi:10.1002/bsl.802
Widiger, T. A. & Lynam, D. R. (1998). Psychopathy as a variant of common personality
traits: implications for diagnosis, etiology, and pathology. In T. Millon, E.
Simonsen, M. Birket-Smith, & R. D. Davis (Eds.), Psychopathy: antisocial,
criminal, and violent behavior (pp. 171–187). New York: Guilford Press.
Woodworth, M. & Porter, S. (2002). In cold blood: characteristics of criminal
homicides as a function of psychopathy. Journal of Abnormal Psychology, 111(3),
436–445. doi:10.1037//0021-843X.111.3.436
Yang, Y., Glenn, A. L., & Raine, A. (2008). Brain abnormalities in antisocial
individuals: implications for the law. Behavioral Sciences & the Law, 26(1),
65–83. doi:10.1002/bsl.788
Yang, Y., Raine, A., Colletti, P., Toga, A. W., & Narr, K. L. (2009). Abnormal temporal
and prefrontal cortical gray matter thinning in psychopaths. Molecular
Psychiatry, 14(6), 561–562. doi:10.1038/mp.2009.12
SUBCLINICAL PSYCHOPATHY AND EMPATHY 53
Yang, Y., Raine, A., Colletti, P., Toga, A. W., & Narr, K. L. (2010). Morphological
alterations in the prefrontal cortex and the amygdala in unsuccessful
psychopaths. Journal of Abnormal Psychology, 119(3), 546–554.
doi:10.1037/a0019611
Yang, Y., Raine, A., Lencz, T., Bihrle, S., LaCasse, L., & Colletti, P. (2005). Volume
reduction in prefrontal gray matter in unsuccessful criminal psychopaths.
Biological Psychiatry, 57(10), 1103–1108. doi:10.1016/j.biopsych.2005.01.021