Emergence of Psychopathy PDF

Cognition 101 (2006) 414442
www.elsevier.com/locate/COGNIT
The emergence of psychopathy: Implications

for the neuropsychological approach
to developmental disorders
R.J.R. Blair *
Mood and Anxiety Disorders Program, National Institute of Mental Health, USA
National Institutes of Health, Department of Health and Human Services, USA
Abstract
In this paper, I am going to examine the disorder of psychopathy and consider how genetic
anomalies could give rise to the relatively specic neuro-cognitive impairments seen in individ-
uals with this disorder. I will argue that genetic anomalies in psychopathy reduce the salience
of punishment information (perhaps as a function of noradrenergic disturbance). I will argue
that the ability of the amygdala to form the stimuluspunishment associations necessary for
successful socialization is disrupted and that because of this, individuals with psychopathy
do not learn to avoid actions that will harm others. It is noted that this model follows the neu-
ropsychological approach to the study of developmental disorders, an approach that has been
recently criticized. I will argue that these criticisms are less applicable to psychopathy. Indeed,
animal work on the development of the neural systems necessary for emotion, does not sup-
port a constructivist approach with respect to aect. Importantly, such work indicates that
while environmental eects can alter the responsiveness of the basic neural architecture medi-
ating emotion, environmental eects do not construct this architecture. However, caveats to
the neuropsychological approach with reference to this disorder are noted.
Published by Elsevier B.V.
Keywords: Psychopathy; Reward and punishment; Development; Amygdala
*
Tel.: +1 301 496 5198; fax: +1 301 594 9959.
E-mail address: blairj@intra.nimh.nih.gov.
0010-0277/$ - see front matter Published by Elsevier B.V.

doi:10.1016/j.cognition.2006.04.005
R.J.R. Blair / Cognition 101 (2006) 414442 415
1. Introduction
The intellectual roots of psychopathy can be traced to Pritchard (1835); see

(Pichot, 1978). Pritchard developed the concept of moral insanity to account
for socially damaging or irresponsible behavior that was not associated with known
forms of mental disorder. He attributed morally objectionable behavior to be a con-
sequence of a diseased moral faculty. Psychiatric and legal classications have fol-
lowed this tradition; Antisocial Personality Disorder is a classication within the
American Psychiatric Associations DSM-IV.
Unfortunately, the psychiatric diagnoses of Conduct Disorder (CD) and Antiso-
cial Personality Disorder (APD: American Psychiatric Association, 1994) are seri-
ously awed. These diagnoses of CD and APD focus on the presence of antisocial
behavior and tend to identify a highly heterogeneous sample. Indeed, DSM-IV
acknowledges this heterogeneity by specifying two forms of CD: childhood- and
adolescent- onset types. In childhood-onset type, onset of at least one criterion char-
acteristic of CD must have occurred prior to 10 years of age. In adolescent-onset
type there should be not be any criteria characteristic of CD prior to 10 years of
age. Because of their lack of precision, the diagnostic rate of CD can reach 16%
of boys in mainstream education (American Psychiatric Association, 1994) while
the diagnostic rate of APD can reach over 80% in adult forensic institutions (Hart
& Hare, 1996). Unsurprisingly, therefore, diagnoses of CD and APD are relatively
uninformative regarding an individuals prognosis.
In sharp contrast, the classication of psychopathy, introduced by Hare (1980,
1991), is highly informative. The classication is a very useful predictor of a patients
future behavior (Hare, 1991) and is at the basis of many recidivism risk assessments.
The classication of psychopathy involves aective-interpersonal (e.g., such as lack
of empathy and guilt) and behavioral components (e.g., criminal activity and poor
behavioral controls); (Frick, OBrien, Wootton, & McBurnett, 1994; Hare, 1980,
1991; Harpur, Hare, & Hakstian, 1989). It is a developmental disorder (Harpur &
Hare, 1994). In childhood and adolescence, psychopathic tendencies are identied
principally by either the use of the Antisocial Process Screening Device (Frick &
Hare, 2001) or by the Psychopathy Checklist: Youth Version (Forth, Kosson, &
Hare, 2003; Kosson, Cyterski, Steuerwald, Neumann, & Walker-Matthews, 2002).
In adulthood, psychopathy is identied though use of the Psychopathy Checklist
Revised (Hare, 1991).
A remarkable feature of the behavioral prole of individuals with psychopathy is
their excessive displays of instrumental aggression (Cornell et al., 1996; Williamson,
Hare, & Wong, 1987). The term instrumental aggression (also referred to as proac-
tive aggression) is used to distinguish aggression that is purposeful and goal directed.
The aggression is used instrumentally to achieve a specic desired goal such as
obtaining the victims possessions or to increase status within a group hierarchy
(Berkowitz, 1993). Bullying is an example of instrumental aggression and, unsurpris-
ingly, individuals who engage in bullying behaviors, frequently engage in other forms
of instrumental antisocial behavior in other contexts (Roland & Idsoe, 2001). In
contrast, reactive aggression (also referred to as aective aggression) occurs when
416 R.J.R. Blair / Cognition 101 (2006) 414442
a frustrating or threatening event triggers the aggressive act and frequently also
induces anger (Barratt, Stanford, Dowdy, Liebman, & Kent, 1999; Barratt, Stan-
ford, Kent, & Felthous, 1997; Berkowitz, 1993; Crick & Dodge, 1996; Linnoila
et al., 1983). Importantly, the aggression is initiated without regard for any potential
goal. Elevated levels of reactive aggression are found in many disorders; e.g., psy-
chopathy, depression, anxiety, bipolar disorder and post traumatic stress disorder
(see, for a review, Blair, 2003a). However, only individuals with psychopathy show
elevated levels of instrumental aggression. Instrumental aggression is, of course, a
form of instrumental behavior. Whether an individual displays a particular instru-
mental behavior is a product of their developmental learning experiences and deci-
sion-making regarding the current context. The suggestion that will be made here
is that the impairment seen in individuals with psychopathy disrupts their capacity
for normal socialization such that antisocial behavior is more likely to be displayed
(Blair, 1995; Lykken, 1957; Trasler, 1973).
The disorder of psychopathy should be of interest to developmental cognitive
neuroscientists for at least two main reasons. First, psychopathy allows us to under-
stand the cognitive mechanisms necessary for the development of morality, an issue
that is of clear intrinsic interest. Second, and more importantly, psychopathy repre-
sents a developmental disorder which aects a relatively specic set of neuro-cogni-
tive systems. The pathology seen in individuals with psychopathy does not lead to
global decits in the development of a variety of neuro-cognitive systems. Instead,
the eects of the pathology inuence a relatively specic series of systems. In this
paper, I will consider why this is. However, rst I will describe the functional impair-
ment seen in individuals with psychopathy.
1.1. What is the functional impairment shown by individuals with psychopathy?
Psychopathy is associated with a core set of empirically demonstrated behavioral

diculties. There are clear diculties with emotional processing (Blair, 1995;
Blair, Jones, Clark, & Smith, 1997; Cleckley, 1976; Eysenck, 1964; Fowles, 1988; Gray,
1987; Lykken, 1995; Mealey, 1995; Patrick, 1994; Pichot, 1978; Trasler, 1978, 1973)
and some indications of diculty with some forms of attentional processing (Jutai &
Hare, 1983; Raine & Venables, 1988). I will concentrate on the diculties with
emotional processing as these have the clearest developmental implications.
There is a considerable body of literature revealing that individuals with psychop-
athy are impaired in the processing of fear-related stimuli. Thus, individuals with
psychopathy show impairment in: (1) aversive conditioning (Flor, Birbaumer, Her-
mann, Ziegler, & Patrick, 2002; Lykken, 1957); (2) generating autonomic responses
to anticipated threat (Hare, 1982; Oglo & Wong, 1990); (3) the augmentation of the
startle reex to visual threat primes (Herpertz et al., 2001; Levenston, Patrick, Brad-
ley, & Lang, 2000); (4) passive avoidance learning (Lykken, 1957; Newman & Kos-
son, 1986); and (5) response reversal (Mitchell, Colledge, Leonard, & Blair, 2002;
Newman, Patterson, & Kosson, 1987). In addition, individuals with psychopathy
show clear diculties in empathic responding. Thus, individuals with psychopathy
show impaired processing of the sadness and fear of others (Aniskiewicz, 1979; Blair,
1999; Blair et al., 1997; House & Milligan, 1976). In addition, individuals with psy-
chopathy show impaired recognition of/autonomic responding to sad and fearful
facial and vocal expressions (Aniskiewicz, 1979; Blair et al., 2002; Blair, Colledge,
& Mitchell, 2001; Blair, Colledge, Murray, & Mitchell, 2001; Blair, Monson, & Fred-
erickson, 2001; Blair et al., 1997).
The fear-related data have led to repeated suggestions that individuals with psy-
chopathy show impairment in the neuro-physiological systems modulating fear
behavior (Cleckley, 1976; Eysenck, 1964; Fowles, 1988; Gray, 1987; Lykken, 1995;
Mealey, 1995; Patrick, 1994; Pichot, 1978; Trasler, 1978, 1973). Developmentally,
these positions all assume that moral socialization is achieved through the use of
punishment (Eysenck & Gudjonsson, 1989; Trasler, 1978). In essence, they assume
that the healthy individual is frightened by punishment and associates this fear with
the action that resulted in the punishment thus making the individual less likely to
engage in the action in the future. They suggest that individuals with psychopathy,
because they are less aversively aroused by punishment, make weaker associations
and thus are more likely to engage in the punished action in the future than healthy
individuals. However, several researchers have questioned the assumption that con-
ditioned fear responses play a crucial role in moral socialization (Blackburn, 1988;
Blair & Morton, 1995). Thus, the developmental literature indicates that moral
socialization is not achieved through the formation of conditioned fear responses
but rather through the induction and fostering of empathy (Homan, 1984). Studies
have shown, for example, that moral socialization is better achieved through the use
of induction (reasoning that draws childrens attention to the eects of their misde-
meanors on others and increases empathy) than through harsh authoritarian or
power assertive parenting practices which rely on the use of punishment (Baumrind,
1971; Baumrind, 1983; Homan & Saltzstein, 1967). Indeed, several researchers have
suggested that while empathy may facilitate moral socialization, fear may actually
obstruct it (Brody & Shaer, 1982; Homan, 1994).
On a related note, if healthy individuals learn to avoid antisocial behavior because
of fear of punishment, it must be assumed that the healthy child judge all rules/trans-
gressions in a similar way. In other words, if we learn to avoid talking in class and
hitting other individuals because we are punished when we commit these actions,
there is no reason for us to distinguish between these two transgressions. However,
healthy developing children make a distinction between moral (victim-based) and
conventional (social order based) transgressions from the age of 36 months (Sme-
tana, 1981, 1985, 1993). In other words, children do not judge all transgressions in
an identical fashion. Instead, they dierentiate between those transgressions that
result in harm to another from those that simply cause social disorder.
The importance of empathy for moral socialization was one of the reasons for the
development of the Violence Inhibition Mechanism model of psychopathy and mor-
al development (Blair, 1995; Blair et al., 1997). At its simplest, I argued that the Vio-
lence Inhibition Mechanism (VIM) was a system that when activated by distress cues
(the sad and fearful expressions of others) results in increased autonomic activity,
attention and activation of the brainstem threat response system (usually resulting
in freezing); (Blair, 1995); see Fig. 1. I considered the VIM to be activated whenever
Fig. 1. The Violence Inhibition Mechanism model. Key to Fig. 1: arrows indicate information ow. The
broken arrow represents that transgression stimuli will only come to activate the VIM after learning has
occurred; pairings of the transgression representations with distress cues. Boxes indicate putative
mechanisms.
distress cues are displayed rather than being reliant upon contextual information
about ongoing violence for activation. In line with the model, the display of distress
cues has been found to result in the inhibition of not only aggression (Perry & Perry,
1974) but also non-violent disputes over property ownership (Camras, 1977) and sex-
ual activity (Chaplin, Rice, & Harris, 1995).
The main focus of the model was to describe the cognitive prerequisites for moral
development. According to the model, moral socialization occurs through the
pairing of the activation of the mechanism by distress cues with representations of
the act that caused the distress cues (Blair, 1995). Through association these
representations of moral transgressions become triggers for the mechanism. The
appropriately developing child thus initially nds the pain of others aversive and
then, through socialization, the thoughts of acts that cause pain to others aversive.
I proposed that individuals with psychopathy have had disruption to this system
such that representations of acts that cause harm to others do not become triggers
for the VIM (Blair, 1995).
One early index of appropriate moral socialization, and thus the developmental
integrity of the VIM, is the demonstration by the child of the moral/conventional
distinction mentioned above. Children with psychopathic tendencies and adults with
psychopathy show impairment in distinguishing moral and conventional transgres-
sions (Blair, 1995, 1997; Blair, Jones, Clark, & Smith, 1995; Blair, Sellers, et al.,
1995; Blair, Colledge et al., 2001; Blair, Colledge, Murray et al., 2001; Blair, Monson
et al., 2001); see, for related work with children with Behavior Disorder and CD
(Arsenio & Fleiss, 1996; Nucci & Herman, 1982). In addition, and in line with the
VIM position, psychopathic adults show reduced comprehension of situations likely
to induce guilt although they show appropriate comprehension of happiness, sadness
and even complex social emotions such as embarrassment (Blair, Jones et al., 1995;
Blair, Sellers, et al., 1995). Moreover, and a direct prediction of the model, children
and adults with psychopathy show pronounced impairment in processing sad and
fearful facial and vocal expressions (Aniskiewicz, 1979; Blair et al., 2002; Blair,
1999; Blair, Colledge et al., 2001; Blair, Colledge, Murray et al., 2001; Blair, Monson
et al., 2001; Blair et al., 1997; House & Milligan, 1976).
However, while the original VIM model could provide an account of the emer-
gence of instrumental antisocial behavior in individuals with psychopathy and
while it did generate a variety of predictions that have been empirically con-
rmed, it faced a serious diculty; it could not account for the data associated
with the fear hypotheses. Moreover, it could not account for data on the interac-
tion of temperament and socialization practice on the development of moral
development/ conscience. Kochanska has stressed the role of fearfulness as the
important temperamental factor (Kochanska, 1993, 1997). Indeed, she and others
have found fearful children to show higher levels of moral development/con-
science using a variety of measures (Asendorpf & Nunner-Winkler, 1992;
Kochanska, 1997; Kochanska, De Vet, Goldman, Murray, & Putman, 1994;
Rothbart, Ahadi, & Hershey, 1994). In addition, Kochanska has stressed that dif-
ferent socialization practices may promote moral development in children with
dierent temperaments (Kochanska, 1993, 1997). In line with this, she found that
for fearful children, maternal gentle discipline promoted moral/conscience devel-
opment. In contrast, for fearless children, alternative socialization practices,
presumably capitalizing on mother-child positive orientation (secure attachment,
maternal responsiveness), promoted the development of conscience (Kochanska,
1997). Because of these diculties for the VIM model, I recently expanded it
at both the cognitive and neural levels (Blair, 2003a, 2003b, 2003c, 2004; Blair
& Charney, 2003); see below.
1.1.1. Summary
Individuals with psychopathy are profoundly impaired in the processing of fear-
related stimuli and in the processing of the fearful and sad expressions of others. The
Violence Inhibition Mechanism (VIM) model provided an account of the impair-
ment in the processing of sad and fearful expressions in individuals with psychopathy
and the implications of this impairment for moral development in these individuals.
However, the VIM model cannot be considered a complete model of psychopathy;
notably, it could not account for the impairments in the processing of fear-related
stimuli in individuals with psychopathy.
In the following sections of this paper, I will consider a series of issues. First, I will
consider whether there is a genetic basis to this disorder. Second, I will consider the
neural and neuro-chemical systems on which I believe this genetic contribution may
be operating (the systems which mediate the basic response to threat). Two options
will be considered: (a) the genetic anomalies disrupt the functioning of the amygdala;
and (b) the genetic anomalies disrupt the functioning of specic neurotransmitter(s)
which are involved in specic aspects of amygdala functioning, in particular coding
punishment information. Third, I will consider other neural systems that may be dys-
functional in psychopathy, in particular, the extent of orbital frontal cortex dysfunc-
tion in psychopathy. Within these second and third issues, I will develop a neuro-
cognitive account of psychopathy, the Integrated Emotion Systems model. Fourth,
I will consider the dissimilarities between psychopathy and another disorder linked
to impairment in social cognition, autism. Fifth, I will consider psychopathy with
respect to the neuropsychological approach to developmental disorders. I will point
out the considerable benet the study of psychopathy has gained from the neuro-
psychological approach. However, I will also point out the limits of the neuro-psy-
chological approach; specically, the pathology associated with psychopathy is not
equivalent to that seen subsequent to an amygdala lesion.
1.2. What is the ultimate cause of psychopathy?
Growing evidence suggests a genetic contribution to psychopathy. Early twin,

adoption, and family studies indicated that antisocial behavior was heritable (Rhee
& Waldman, 2002). However, such studies are dicult to interpret. Much antisocial
behavior is goal directed: the individual mugs the victim for their wallet, the individ-
ual steals the bag to obtain its contents, the individual engages in an elaborate sting
operation to gain another persons money. It is extremely unlikely that there is a
direct genetic contribution to these behaviors or at least it is as likely as there is a
direct genetic contribution to the use of a light switch to enable the navigation of
a dark room. An individual might learn to use a light switch and under particular
conditions, alternatively he/she might learn to mug people for their wallets. Howev-
er, where genetics are likely to play a role is in determining the probability that the
individual will learn an antisocial strategy to gain money (mugging other people) as
opposed to a strategy sanctioned by society (using an ATM machine at the end of
the workday). Many individuals have argued that the emotional dysfunction shown
by individuals with psychopathy makes them more likely to learn antisocial strate-
gies to reach goals (Blair, 1995; Eysenck, 1964; Lykken, 1995; Trasler, 1973). The
argument developed here is that there may be a genetic contribution to the emotional
dysfunction and that it is this which results in an apparent genetic contribution to
antisocial behavior. Recent data suggests that this is indeed the case.
Blonigen, Carlson, Krueger, and Patrick (2003) collected data from 353 adult
male twins using the self-report Psychopathic Personality Inventory [PPI] (Lilienfeld
& Andrews, 1996). The PPI includes 163 items and forms a global index of psychop-
athy with eight sub-scales. Most of these subscales showed moderate heritability
(h2 = 0.290.56) and negligible shared environmental inuence (Blonigen et al.,
2003). Moreover, in a considerably larger study, examining almost 3500 twin pairs
within the Twins Early Development Study (TEDS), the callous and unemotional
component of psychopathic tendencies was indexed at age 7 (Viding, Blair, Mott,
& Plomin, 2005). This study revealed a signicant group heritability of h2g :67 and
no shared environmental inuence on the callous-unemotional component; i.e.,
genetic factors account for two thirds of the dierence between the callous-unemo-
tional probands and the population.
As yet, the roles of environmental inuences on the emergence of psychopathy
remain unclear. The genetics studies above suggested relatively little inuence. How-
ever, there is a considerable literature indicating a relationship between socioeco-
nomic status (SES) and antisocial behavior (Raine, 1993). With respect to
psychopathy, it would be surprising if social variables did not impact on the proba-
bility of antisocial behavior; SES, for example, is likely to constrain the possibility of
alternative behavioral choices to antisocial behavior as well as increase the salience
of the money contained in a potential victims wallet. Indeed, in line with this, a rela-
tionship between SES and the antisocial behavior component of psychopathy has
been reported (Hare, 2003). Thus, genetics would determine the level of emotional
dysfunction while the environment would inuence how this genetically determined
emotion dysfunction was expressed.
1.2.1. Summary
It is likely that there is a genetic contribution to psychopathy. I argue that this
contributes to the emotional dysfunction that is the basis of the disorder. The emo-
tional dysfunction, in turn, puts the individuals for learning antisocial behaviors to
solve goals. Social environmental variables are likely to have an inuence, most
importantly constraining the possibility of alternative behavioral choices to antiso-
cial behavior as well as potentially increasing the salience of the rewards the might
accrue through antisocial behavior. In the following section, I will consider the neu-
ral and neuro-chemical architecture upon which this genetic contribution may be
operating.
1.3. The basic threat response
Three basic responses to threat are freezing, escape behaviors and reactive aggres-
sion (a rage attack at the threat); (Blanchard, Blanchard, & Takahashi, 1977). Which
behavioral response is initiated is determined by the threats intensity and proximity.
At low levels of intensity, from a distant threat, the animal will freeze. At higher lev-
els, from a closer threat, the animal will attempt to escape the environment. At high-
er levels still, when the threat is very close and escape is impossible, the animal will
display reactive aggression (Blanchard et al., 1977).
These responses to threat are mediated by a neural circuit that is common to
many mammalian species (Gregg & Siegel, 2001; Panksepp, 1998). It runs from
medial amygdaloidal areas downward, largely via the stria terminalis to the medial
hypothalamus, and from there to the dorsal half of the periaqueductal gray (PAG).
With respect to the basic response to threat, these systems function as a unitary
entity. Stimulation of any of these systems may induce the basic threat responses.
Which one is elicited is determined by the level of stimulation.
An important neuro-chemical response to threat involves the noradrenergic sys-
tem (Charney, 2003; Francis & Meaney, 1999). When specic neurons in the central
nucleus of the amygdala are activated by threat, they activate, in turn, the locus coe-
ruleus, leading to an increase in noradrenaline release. Rogers and others have
argued that noradrenaline inuences the salience of aversive cues (Rogers, Lancas-
ter, Wakeley, & Bhagwager, 2004); greater noradrenaline levels should allow faster
learning about information associated with the aversive cues.
With regards to psychopathy, I suggest that the genetic anomalies potentially
present in individuals with psychopathy (Blonigen et al., 2003; Viding et al., 2005),
aect particularly a component of this circuit; the amygdala. I argue that this leads
to an individual who is less responsive to aversive stimuli. I will consider here two
possibilities regarding how this might occur. First, the genetic anomalies disrupt
the functioning of the amygdala (Blair, 2001, 2002; Blair, Morris, Frith, Perrett, &
Dolan, 1999; Patrick, 1994). Second, the genetic anomalies disrupt the functioning
of specic neurotransmitter(s) which are involved in specic aspects of amygdala
functioning, in particular coding punishment information (Blair, Leonard, Morton,
& Blair, 2006a; Blair et al., 2006b).
1.3.1. Summary
The mammalian basic response to threat is mediated by a circuit that runs from
the amygdala to the hypothalamus and from there to the peri-aqueductal gray. An
important neuro-chemical response to threat involves the noradrenergic system. In
the following sections we will consider whether the genetic contribution to psychop-
athy disrupts the functioning of the amygdala or, perhaps, disrupts the functioning
of specic neurotransmitter(s) which are involved in specic aspects of amygdala
functioning.
1.4. Psychopathy and amygdala dysfunction
The suggestion that psychopathy might be due to early amygdala dysfunction has
generated considerable research. In line with the suggestion, individuals with psy-
chopathy show reduced amygdaloid volume relative to comparison individuals
(Tiihonen et al., 2000) and reduced amygdala activation during emotional memory
(Kiehl et al., 2001) and aversive conditioning tasks (Veit et al., 2002). Moreover,
the positions origins in the neuropsychological approach to developmental disorders
(Baron-Cohen, 1998; Frith, 2002; Leslie, 1992) has allowed the generation of a vari-
ety of predictions regarding the functional impairment. Thus, human and animal
neuropsychological work has informed us that the eects of amygdala lesions include
impairment in: (1) aversive conditioning (Bechara, Damasio, Damasio, & Lee, 1999;
Bechara et al., 1995; LaBar, Gatenby, Gore, LeDoux, & Phelps, 1998); (2) the
augmentation of the startle reex to visual threat primes (Angrilli et al., 1996;
Funayama, Grillon, Davis, & Phelps, 2001); (3) passive avoidance learning
(Ambrogi Lorenzini, Baldi, Bucherelli, Sacchetti, & Tassoni, 1999); and (4)
expression recognition that is particularly marked for fearful expressions (Adolphs,

2002; Blair, 2003a). If psychopathy is associated with amygdala dysfunction, the neu-
ropsychological approach would predict that individuals with psychopathy are
impaired in the above tasks. Considerable data shows that they are (Blair, Colledge
et al., 2001; Blair, Colledge, Murray et al., 2001; Blair, Monson et al., 2001; Flor
et al., 2002; Herpertz et al., 2001; Levenston et al., 2000; Lykken, 1957; Newman &
Kosson, 1986).
Not only has the amygdala dysfunction position generated a host of predictions it
has also allowed the reconciliation of fear (Lykken, 1995; Patrick, 1994) and empa-
thy (Blair, 1995) dysfunction positions. Many of the ndings associated with both
positions are direct results of amygdala dysfunction (see above). Moreover, it
becomes easier to understand ndings indicating the importance of fearfulness
as an important temperamental factor in socialization (Kochanska, 1993, 1997).
The temperamental variable fearfulness can be understood as an index of the
integrity of the amygdala (Blair, 2003a). While fear conditioning is not considered
to be important in socialization (Brody & Shaer, 1982; Homan, 1994), I argue that
the amygdalas response to the fear and sadness of victims, during empathy induc-
tion, is crucial for socialization. Murray and colleagues argue that the amygdala is
crucially involved in the formation of stimulusreward and stimuluspunishment
associations (Baxter & Murray, 2002). I argue that the associations required for
appropriate socialization are associations between moral transgressions and victims
distress. Empathy induction and other positive parenting techniques should aid the
formation of associations between the moral transgression and the victims distress
(empathy induction focuses the childs attention on the aversive stimulus that is the
victims distress). A considerable literature shows that these parenting techniques do
reduce antisocial behavior in children (Brody & Shaer, 1982). Individuals with psy-
chopathy are less likely to form these associations and so should be more likely to
engage in actions that will harm others. Indeed, interestingly, while positive parent-
ing techniques are associated with reduced antisocial behavior levels in healthy chil-
dren, they have no impact on the level of antisocial behavior expressed by children
who present with the emotional dysfunction associated with psychopathy (Wootton,
Frick, Shelton, & Silverthorn, 1997).
Despite the success of the amygdala dysfunction position, two caveats should be
considered here. First, very few patients with amygdala lesions acquired in adult-
hood present with instrumental aggression [though this may not be the case if the
lesion occurs early in life (Fine, Lumsden, & Blair, 2001)]. Of course, this should
be expected. My argument is that the amygdala is required for the formation of mor-
al transgressionvictims distress associations. However, typically, goal directed
behavior does not require the accessing of these associations. Instead, these moral
transgressionvictims distress associations resulted in the individual failing to learn
antisocial behaviors to achieve their goals. The behaviors the individual does use to
achieve their goals will be a function of their learning history. While the individual
with psychopathy might learn that a solution to a lack of money was to mug another
(rewarded by the money but not punished by the victims distress), the individual
with an acquired amygdala lesion would have learnt, before their lesion, that this
was not appropriate (such actions were punished by the victims distress). When con-
sidering how to rectify a lack of money, the individual with an acquired amygdala
lesion would activate previously successful motor programs for achieving this goal
(a visit to an ATM).
The second caveat is slightly more problematic. As noted above, the amygdala is
crucially involved in the formation of stimulusreward and stimuluspunishment
associations; animals with amygdala lesions show impairment in both reward and
punishment related behavior (Baxter & Murray, 2002). Yet, the impairment in indi-
viduals with psychopathy is far more marked for processing dependent on stimulus
punishment associations than for stimulusreward associations (Levenston et al.,
2000; Patrick, 1994; Blair et al., 2006a, 2006b). Thus, whereas individuals with psy-
chopathy do not show augmentation of the startle reex following a negative visual
prime relative to comparison individuals, they do show a comparable reduction in
startle reex following a positive visual prime relative to comparison individuals
(Levenston et al., 2000; Patrick, 1994). Moreover, in an aective priming study, Pesc-
hardt et al. found that whereas individuals with psychopathy showed no congruence
facilitation for negative target words, they did show congruence facilitation for posi-
tive target words (Blair et al., 2006a). In other words, while a positive prime primed
the output response associated with positive valence in individuals with psychopathy
(albeit less so than in comparison individuals), a negative prime did not prime the
output response associated with negative valence. Finally, in a decision making
study, individuals with psychopathy showed particular diculty, relative to controls,
when choosing between stimuli associated with dierent levels of punishment. Their
impairment in choosing between stimuli associated with dierent levels of reward
was far less marked (Blair et al., 2006a).
In addition to the above, the amygdala has also been considered to play a role in
certain aspects of social cognition, at least in humans and possibly primates; in par-
ticular, aect-related judgments based on facial stimuli (Adolphs, 2003; Baron-Co-
hen et al., 2000). Thus, in one paradigm, participants were shown pictures of
individuals in natural poses and asked to judge the trustworthiness of these individ-
uals. While healthy individuals typically judge some individuals faces less trustwor-
thy than others, patients with amygdala lesions present with atypical judgment
patterns (Adolphs, Tranel, & Damasio, 1998). Moreover, recent neuro-imaging work
has indicated that healthy individuals show greater amygdala activation to faces
judged to be untrustworthy relative to faces judged to be trustworthy (Winston,
Strange, ODoherty, & Dolan, 2002). In a second paradigm, participants must judge
the complex social emotion being displayed by an individual based on information
only from the eye region (Baron-Cohen, Wheelwright, & Jolie, 1997). Individuals
with amygdala lesions show impairment on this task (Adolphs, Baron-Cohen, &
Tranel, 2002; Stone, Baron-Cohen, Calder, Keane, & Young, 2003) while neuro-im-
aging work has indicated the involvement of the amygdala whilst performing this
task (Baron-Cohen et al., 1999). However, despite this apparent role of the amygdala
in these two aspects of social cognition, individuals with psychopathy are not
impaired either in making trustworthiness judgments (Richell et al., 2005) or in
judging complex social emotions from the eyes (Richell et al., 2003).
1.4.1. Summary
Individuals with psychopathy are impaired on many tasks that require the
functional integrity of the amygdala. Both the impairments in fear-related and
empathic responding found in individuals with psychopathy can be attributed
to amygdala dysfunction. In short, predictions developed from human and animal
neuropsychological work with respect to amygdala dysfunction in individuals with
psychopathy have been useful with respect to the impairment in emotional learning
and basic emotional responding seen in individuals with psychopathy. However,
individuals with psychopathy are not equivalent to patients with amygdala lesions;
functions that appear to require the amygdala such as the formation of stimulus
reward associations and certain aspects of social cognition are instead only mildly,
or not at all, impaired in individuals with psychopathy. This suggests that the genetic
anomalies present in individuals with psychopathy do not lead to the development of
the disorder through a global disruption of the functioning of the amygdala. Instead,
they may have a more selective eect, disrupting the functioning of specic
neurotransmitter(s) which are involved in specic aspects of amygdala functioning.
This will be considered in the following section.
1.5. Psychopathy, neurotransmitter dysfunction and developing the neuro-cognitive

model
Polymorphisms of particular genes can alter the functioning of specic neuro-

transmitter systems (Lichter et al., 1993; Shih, Chen, & Ridd, 1999; Vandenbergh
et al., 1992). Currently, it remains unclear which neurotransmitter systems might
be dysfunctional in individuals with psychopathy. However, one possibility is that
the noradrenergic response to stress/threat stimuli, described above, is disturbed in
individuals with psychopathy (Blair, 2003a; Blair et al., 2006b). Interestingly, there
have been recent suggestions that noradrenaline is involved in mediating the impact
of aversive cues in human choice (Rogers et al., 2004). Moreover, recent pharmaco-
logical data imply that noradrenergic manipulations selectively impact on the pro-
cessing of sad expressions (Harmer, Perrett, Cowen, & Goodwin, 2001; Sustrik,
Coupland, & Blair, in preparation). Further support for this suggestion comes from
studies linking NA abnormalities to antisocial behavior/Conduct Disorder (Raine,
1993; Rogeness, Cepeda, Macedo, Fischer, & Harris, 1990; Rogeness, Javors, Mass,
& Macedo, 1990). In this regard it is interesting to note that NA function appears to
be increased in a range of anxiety disorders (Charney, Heninger, & Breier, 1984); i.e.,
it is increased in populations that present with a heightened responsiveness to aver-
sive cues, the opposite of the emotional impairment seen in psychopathy. I therefore
argue that the genetic anomalies considered to be present in individuals with psy-
chopathy disrupt the functioning of the noradrenergic system such that the impact
of aversive stimuli is muted.
The integrated emotion systems (IES) model represents a neuro-cognitive model
of the interactions of the systems involved in emotional processing (Blair, 2004). Ini-
tial components of this model, those most related to the earlier VIM model, are
depicted in Fig. 2. Three systems are depicted. One allows sensory representations;
Fig. 2. The basics of the Integrated Emotion Systems model. Key to Fig. 2: the ovals indicate
representational systems. The lled in circles indicate representations within these systems. The lines
indicate connections between the systems while the arrows denote the direction of information ow.
CS = Conditioned stimulus; US = Unconditioned stimulus; S1 and S2 are competing sensory represen-
tations; R1 and R2 are alternative motor responses.
e.g., the representation of objects currently in the environment, including moral

transgressions. At the neural level, this system is primarily implemented by temporal
cortex. The second contains valence representations; i.e., representations that can
be activated by unconditioned stimuli (e.g., loud noises but also distress cues). At the
neural level, this system is implemented by the amygdala. The third will be discussed
below.
The valence representations can represent both appetitive and aversive stimuli
following claims that the amygdala is crucially involved in the formation of stimu-
lusreward and stimuluspunishment associations (Baxter & Murray, 2002). The
strength of the connections between representations in the dierent systems increase
through Hebbian learning (Hebb, 1949); if two representations in dierent systems
are simultaneously active the connection between these two representations will
strengthen. In short, activation of a valence representation by an observed distress
cue will increase the connection between this valence representation and currently
active sensory representations (perhaps a representation of the moral transgression
that has caused this distress cue). This computation was also the basis of the VIM
model (see above and Fig. 1). The connections between the representations in the dif-
ferent systems are reciprocal, reecting the interconnections of the amygdala with
cortical regions (Amaral, Price, Pitkanen, & Carmichael, 1992). These reciprocal
connections allow the valence representations to bias the processing of emotional
sensory representations (an emotional sensory representation will activate the
valence representations, leading to greater activation of the emotional sensory repre-
sentation). In short, activation of the valence representations can increase attention
to the sensory representation which activated them.
If we assume that the genetic anomalies considered to be present in individuals
with psychopathy disrupt the functioning of the noradrenergic system such that neg-
ative valence representations are less activated by aversive stimuli, we can predict
many of the behavioral phenomena associated with psychopathy. Aversive condi-
tioning will be impaired, and passive avoidance errors will be more common, because
sensory representations will be more weakly associated with negative valence (Flor
et al., 2002; Lykken, 1957; Newman & Kosson, 1986). Reduced activation of nega-
tive valence representations by sad and, particularly, fearful expressions will result in
reduced autonomic responses to these expressions and may impair the naming of
these expressions (Aniskiewicz, 1979; Blair, 1999; Blair et al., 1997; House & Milli-
gan, 1976; Stevens, Charman, & Blair, 2001).
The third system depicted in Fig. 2 mediates the production of motor responses
(and, at the neural level, is implemented by basal ganglia and motor cortex). The
valence representations are not involved in the formation of stimulusresponse asso-
ciations (the linking of sensory representations to motor responses). At the neural
level, it is known that the amygdala is not necessary for the formation of stimu-
lusresponse associations (Baxter & Murray, 2002). Instrumental learning tasks reli-
ant on stimulusresponse associations, such as object discrimination, are not
impaired by amygdala lesions while instrumental learning tasks that are reliant on
stimulusreinforcement associations (within the IES, the linking of sensory represen-
tations with valence representations), such as passive avoidance are (Baxter & Mur-
ray, 2002). Interestingly, and in line with the suggestion of disruption of the valence
representations, individuals with psychopathy are not impaired on object discrimina-
tion tasks (Mitchell et al., 2002) but are impaired on passive avoidance learning
(Newman & Kosson, 1986).
1.5.1. Summary
In this section, I have suggested that the genetic contribution to psychopathy may
inuence the functioning of the noradrenergic system such that the formation of
stimulusreinforcement, particularly stimuluspunishment, associations is impaired.
I have also begun to develop the neuro-cognitive Integrated Emotion Systems model.
1.6. Psychopathy and orbital frontal cortex
Orbital frontal cortex is considerably involved in the regulation and mediation of

emotional behavior. Patients with orbital frontal cortex lesions may present with
emotional dys-regulation and antisocial behavior (Anderson, Bechara, Damasio,
Tranel, & Damasio, 1999; Blair & Cipolotti, 2000; Blumer & Benson, 1975; Dama-
sio, 1994; Pennington & Bennetto, 1993). This has led to considerable claims that
psychopathy might be due to early orbital frontal cortex damage and that patients
with orbital frontal cortex damage and psychopathy present similarly (Damasio,
1994). Such claims have received questionable empirical support however.
Orbital frontal cortex does play a role in the regulation of the brainstem systems
involved that mediate the basic responses to threat (including reactive aggression);
(Gregg & Siegel, 2001; Panksepp, 1998). Damage to orbital frontal cortex should thus
lead to a dys-regulation of brainstem systems involved in mediating the basic respons-
es to threat and potentially increase the risk of threat/ frustration-based reactive
aggression. Patients with lesions of orbital frontal cortex do indeed display a height-
ened risk of reactive aggression (Anderson et al., 1999; Blair & Cipolotti, 2000; Pen-
nington & Bennetto, 1993). However, patients with lesions of orbital frontal cortex do
not display a heightened risk of goal-directed, instrumental aggression, even if their
lesions occur in early childhood (Anderson et al., 1999; Pennington & Bennetto,
1993). Yet, individuals with psychopathy are particularly notable for their use of
instrumental aggression (Cornell et al., 1996; Williamson et al., 1987). Moreover,
empirically, while patients with orbital frontal cortex lesions display generally
impaired expression recognition (Blair & Cipolotti, 2000; Hornak, Rolls, & Wade,
1996), individuals with psychopathy do not show such general impairment but rather
a relatively more selective impairment for fearful, and to a lesser extent, sad expres-
sions (Blair, Colledge et al., 2001; Blair, Colledge, Murray et al., 2001; Blair, Monson
et al., 2001). Additionally, ndings such as the impairment in aversive conditioning
shown by individuals with psychopathy (Flor et al., 2002; Lykken, 1957) are not
found in patients with orbital frontal cortex lesions (Bechara et al., 1999).
This is not to suggest that individuals with psychopathy are without impairment
for functions in which orbital frontal cortex is involved. There is a considerable neu-
ropsychological and neuro-imaging literature demonstrating that orbital frontal cor-
tex is crucially involved in response reversal and extinction (Cools, Clark, Owen, &
Robbins, 2002; Rahman, Sahakian, Hodges, Rogers, & Robbins, 1999; Rolls, Hor-
nak, Wade, & McGrath, 1994). Response reversal and extinction involve changing a
response to a stimulus as a function of a change in contingency; i.e., learning to with-
hold a response that is now punished though previously it had been rewarded (Rolls,
1997). The dierence between response reversal and extinction is that in response
reversal tasks, the participant learns to respond to a second stimulus rather than
the rst while in extinction tasks the participant learns to withhold responding all
together.
In Fig. 3, the depiction of the IES model is extended to include two systems inu-
enced by input from the valence representations and therefore likely to be disrupted
in individuals with psychopathy. The rst of these, the response selection system,
represents expected level of reinforcement associated with the stimulus (and, poten-
tially, the form of response to this stimulus), information that is provided by the
valence representations. If two or more stimuli are present in the environment, each
of which is associated with a dierent response, it is important that the system can
rapidly select the stimulus that will elicit the greatest level of reward. The response
selection system allows this to occur (the computational details of this process are
described elsewhere, Blair, 2004). At the neural level, this system is implemented
Fig. 3. An expansion of the Integrated Emotion Systems model. Key to Fig. 3: the ovals indicate
representational systems. The lled in circles indicate representations within these systems. The lines
indicate connections between the systems while the arrows denote the direction of information ow. The
lines from the response gating system to the connections between the sensory representation and motor
response systems, that terminating in small circles represent the gating by the response gating system of
responses activated by these connections. CS = Conditioned stimulus; US = Unconditioned stimulus; S1
and S2 are competing sensory representations; R1 and R2 are alternative motor responses. The
computational details of response selection are described elsewhere (Blair, 2004).
by medial regions of orbital frontal cortex. The second, the response gating system, is
particularly activated when expected reinforcement information, provided by the
response selection system, diers from actually received reinforcement. In Fig. 3, I
propose that this system alters stimulusresponse associations (the connections
between the sensory representations and the motor responses) to alter the probability
that that response to that stimulus will be made in the future (usually to reduce the
probability that that response will be made in the future). This system is crucial for
response reversal. At the neural level, this system is implemented by ventrolateral
frontal cortex.
Adults with psychopathy are notably impaired on response reversal and
extinction tasks (Mitchell et al., 2002; Newman et al., 1987). However, children
with psychopathic tendencies are only mildly impaired on these tasks. In
Newmans card playing task (Newman et al., 1987), the participant has to
decide whether to play a card. Initially, the participants choice to play is always
reinforcing; if the participant plays the card he/she will win points or money.
However, as the participant progresses through the pack of cards, their proba-
bility of reward decreases. The participant should terminate his/her responding
before he/she receives greater levels of punishment than reward. Children with
psychopathic tendencies, like adults with psychopathy, are impaired on this task
(Fisher & Blair, 1998; Newman et al., 1987; OBrien & Frick, 1996). In the
ID-ED task (Dias, Robbins, & Roberts, 1996), the participant learns that
responding to one of two stimuli gains reward while responding to the other
is punished. This contingency is then reversed; i.e., responding to the rst stim-
ulus is no longer rewarded but punished while responding to the second is now
rewarded. While adults with psychopathy are impaired on this task, children
with psychopathic tendencies are not (Blair, Colledge et al., 2001; Blair,
Colledge, Murray et al., 2001; Blair, Monson et al., 2001; Mitchell et al.,
2002). A major dierence between these two tasks is in the salience of the
contingency change. In the card-playing task, the probability of reinforcement
decreases by 10% over every ten trials. In the ID-ED task, the probability of
reinforcement changes from 100% to 0% once the initial learning criterion has
been achieved. This indicates that while both children with psychopathic tenden-
cies and adult individuals with psychopathy are impaired in the detection of
contingency change, this impairment is markedly greater in the adult individuals
with psychopathy. Moreover, this suggests that if we reduce the salience of the
contingency change, we should see impairment in the children with psychopathic
tendencies and that the degree of impairment will be a function of the salience
of the contingency change. This was tested using a probabilistic response rever-
sal paradigm. Participants were presented with pairs of stimuli. The probability
of reward was dierent across pairs (i.e., for pair 1, stimulus A was rewarded
100% of the time, for pair 2, stimulus C was rewarded 90% of the time etc).
Following a set number of trials the contingency was reversed (i.e., for pair
1, stimulus B was rewarded 100% of the time, for pair 2, stimulus D was
rewarded 90% of the time). While the children with psychopathic tendencies
showed no diculty reversing their responses for salient contingency changes
[pair 1], they did show signicant diculty as the salience of the contingency
change decreased [pair 2] (Budhani & Blair, 2005).
This dierence between children and adults with psychopathy is of interest.
Response reversal and extinction occur following the successful identication of vio-
lations between expected reward and received punishment (or absence of reward).
Failure to perform response reversal and extinction could be due to impairment in
systems necessary for: (1) detecting the violation; (2) changing the stimulusreward
associations; or (3) representing the punishment. We have argued that there is
reduced punishment sensitivity in individuals with psychopathy. Children with psy-
chopathic tendencies seem to be at least as insensitive to punishing stimuli as adults
with psychopathy. They are comparably impaired on tasks such as passive avoidance
learning (Newman & Kosson, 1986; Newman, Widom, & Nathan, 1985), the pro-
cessing of fearful expressions (Blair, Colledge et al., 2001; Blair, Colledge, Murray
et al., 2001; Blair, Monson et al., 2001) and aversive conditioning (Lykken, 1957;
Raine, Venables, & Williams, 1996). However, the impairment of children with psy-
chopathic tendencies for response reversal is far less marked. This suggests that
adults with psychopathy are impaired in systems necessary for detecting the viola-
tion/changing the stimulusreward associations; i.e., orbital/ventrolateral frontal
cortex dysfunction.
Given the evidence of selective amygdala dysfunction discussed above, there
are several possibilities regarding the origins of the orbital frontal cortex
pathology found in adults with psychopathy. First, the orbital frontal cortex
pathology could be developmentally independent of the amygdala pathology.
For example, the genetic anomalies associated with psychopathy might aect
the development of the amygdala and orbital frontal cortex independently of
one another. Second, there are considerable interconnections between the amyg-
dala and orbital frontal cortex (Amaral et al., 1992; Carmichael & Price, 1995).
It is possible that a lack of aerent input from the amygdala to orbital frontal
cortex could disrupt the development of orbital frontal cortex to an increasingly
greater degree as development progresses. Thirdly, individuals with psychopathy
present with higher levels of drug abuse, dependence, and poly-drug use than
comparison individuals (Hemphill, Hart, & Hare, 1994; Smith & Newman,
1990). Alcohol and drug dependent individuals are impaired on measures
assessing the functioning or orbital frontal cortex (Bechara et al., 2001; Grant,
Contoreggi, & London, 2000; Rogers & Robbins, 2001). It is thus also possible
that the apparent developmental eect seen here is simply a consequence of the
lifestyle chosen by psychopathic individuals.
1.6.1. Summary
Damasio and others have suggested that psychopathy might be due to orbital
frontal cortex damage. However, recent data suggest that the decits expected from
orbital frontal cortex damage do not mirror those seen in individuals with psychop-
athy. This is not to suggest that there is no orbital frontal cortex dysfunction in psy-
chopathy. Children and adults with psychopathic tendencies show impairment in
response reversal, a function known to recruit orbital frontal cortex. Interestingly,
while the children and adults with psychopathic tendencies perform similarly with
respect to their lack of guilt for their actions and on measures of, or based on, stim-
ulusreinforcement learning, the impairment in response reversal is far more marked
in adults with psychopathy than children with psychopathic tendencies. This sug-
gests a developmental progression to the orbital frontal cortex pathology found in
psychopathy. The reasons for this progression remain unclear.
1.7. Psychopathy and autism
Psychopathy is not the only disorder linked to impairments in social cognition.

Autism is a severe developmental disorder where there is marked neuro-cognitive
impairment. It is described by the American Psychiatric Associations Diagnostic
and Statistical Manual (DSM-IV, American Psychiatric Association, 1994) as the
presence of markedly abnormal or impaired development in social interaction and
communication and a markedly restricted repertoire of activities and interests (p.

66). Like psychopathy, autism has also been lined to impairments in amygdala func-
tioning (Baron-Cohen et al., 2000).
Individuals with autism may show structural amygdala abnormalities. However,
these have been reported as an increase in grey matter volume in the amygdala/peri-
amygdaloid cortex (Abell et al., 1999) rather than the decrease seen in individuals
with psychopathy (Tiihonen et al., 2000). Functionally, the situation is complex.
As discussed above, the amygdala is involved in the formation of stimuluspun-
ishment and stimulusreward associations as well as some aect laden components
of social cognition. My colleagues and I argue that the sensitivity of individuals with
psychopathy to punishment, and therefore the ability to form stimuluspunishment
associations, is disproportionately impaired (Blair et al., 2006a). However, there is
no reason to believe that this is the case in individuals with autism. Indeed, individ-
uals with autism are at increased risk of presenting with anxiety (Gillott, Furniss, &
Walter, 2001; Rumsey, Rapoport, & Sceery, 1985), rather than the decreased risk
seen in individuals with psychopathy (Frick, Lilienfeld, Ellis, Loney, & Silverthorn,
1999; Patrick, 1994; Verona, Patrick, & Joiner, 2001). In contrast, there may be
impairment in aspects of social cognition that involve the amygdale in individuals
with autism. Thus, patients with autism, unlike individuals with psychopathy, are
impaired on both the Eyes task and the face trustworthiness judgment tasks dis-
cussed earlier (Adolphs, Sears, & Piven, 2001; Baron-Cohen, Wheelwright, Hill, Ras-
te, & Plumb, 2001). Of course, these impairments may not reect amygdala
dysfunction per se. It is possible that they are developmental consequences of impov-
erished face representations due to dysfunction in regions such as fusiform gyrus and
superior temporal sulcus (Schultz et al., 2003).
1.7.1. Summary
Autism, like psychopathy, is associated with impairment in social cognition and,
at the anatomical level, amygdala dysfunction. However, while psychopathy is asso-
ciated with impairment in the formation of stimulusreinforcement associations, a
function that animal and human work, has clearly indicated amygdala involvement
in, there is little reason to suspect such impairment in autism. In contrast, several
aspects of social cognition that have been related to amygdala functioning, though
which may reect the functioning of nearby neural systems, are impaired in autism
but are not impaired in individuals with psychopathy.
1.8. Psychopathy and the neuropsychological approach to developmental disorders
The model that I have developed here follows a tradition of pre-supposing the
existence of relatively independent neuro-cognitive systems that may be selectively
impaired in developmental disorders (Baron-Cohen, 1998; Frith, 2002; Leslie,
1992). With respect to the predictions of the position, I have taken care taken to con-
sider neuropsychological ndings with adult lesions cases and, sometimes, to use
tasks that have been previously used with these patients (Blair et al., 2002; Blair,
Colledge et al., 2001; Blair, Colledge, Murray et al., 2001; Blair, Monson et al.,
2001; Mitchell et al., 2002). Indeed, it was this neuropsychological approach which
allowed the reconciliation of the fear-relevant and empathy-relevant data described
above; most could be accounted for by assuming dysfunction in systems involved in
emotional processing, in particular the amygdala. However, this approach
has been recently criticized and sometimes considered to be not developmental
(Karmilo-Smith, Brown, Grice, & Paterson, 2003; Paterson, Brown, Gsodl,
Johnson, & Karmilo-Smith, 1999). In short, Karmilo-Smith and colleagues argue
that the existence of separable neuro-cognitive systems in the adult does not imply
that these separable systems are present in the young child. They suggest that the
separable systems seen in the adult may be constructed through development and
may not be discrete systems at birth.
I do not propose to debate these issues fully here. The systems at which these
attacks are made (systems for number and language processing) are usually cortically
represented as opposed to the interaction of cortical and sub-cortical systems consid-
ered here. Whether or not this dichotomy is important, it is clear that such criticisms
must be tempered when considering psychopathy. Work with animals allows consid-
erable specication of the emotional systems that are dysfunctional in individuals
with psychopathy as well as their development. Thus, let us consider the basic neural
architecture for emotional processing; i.e., the amygdala, hypothalamus and peri-
acqueductal gray. This neural architecture is present from birth, primarily genetically
determined, and highly similar to that found in other mammalian species. In short, it
is not constructed from environmental experience. Of course, this does not mean that
this architecture functions equivalently in the child and adult or that environmental
eects do not eect its functioning. Interestingly, animals during infancy do not dem-
onstrate HPA axis responses to stress. However, infant animals exposed to stressors
demonstrate increases in the expression of immediate early genes (e.g., c-fos and
nerve growth factor inducible gene) in the paraventricular nucleus of the hypothal-
amus (Charney, 2003). In short, early postnatal adverse experiences increase the
responsiveness of these stress response systems, eects which last throughout the life-
time of the individual (Heim, Owens, Plotsky, & Nemero, 1997; Liu et al., 1997;
Plotsky & Meaney, 1993). Thus, the environment has an eect, by partially determin-
ing the responsiveness of these basic threat systems. However, it is important to
again note here that this neural architecture is not constructed out of environmental
experience [in contrast to processes proposed to underlie the development of some
cortical neuro-cognitive systems (Karmilo-Smith et al., 2003; Paterson et al.,
1999)], it is present from birth.
But more generally, how appropriate is a neuropsychological approach when con-
sidering psychopathy? In many respects, the empirical literature on psychopathy
demonstrates the clear advantages of the neuropsychological approach. However,
at the same time, it identies the need for caution. Following the neuropsychological
approach, and assuming amygdala dysfunction, has allowed the generation of an
array of predictions, many of which have been conrmed. The amygdala is involved
in the formation of stimuluspunishment associations (Baxter & Murray, 2002) and
individuals with psychopathy are impaired in a variety of tasks dependent on the for-
mation of stimuluspunishment associations. However, the amygdala is involved in
the formation of stimulusreward associations and certain aect-relevant aspects of

social cognition. Individuals with psychopathy show far less impairment in these
aspects of amygdala functioning. Thus, the impairment in psychopathy is not equiv-
alent in impact to the eects of an amygdala lesion to a healthy adult.
However, it should be noted that even results where data obtained from individ-
uals with psychopathy diers from that of patients with amygdala lesions are infor-
mative. Thus, the neuro-psychological and neuro-imaging literatures indicate a role
of the amygdala in specic aect-relevant aspects of social cognition. Faces judged to
be untrustworthy activate the amygdala (Winston et al., 2002) and patients with
amygdala lesions are poor at judging a faces trustworthiness (Adolphs et al.,
1998). The neuropsychological approach might therefore predict problems in
trustworthiness judgments in individuals with psychopathy but this prediction is
not supported (Richell et al., 2003). This suggests either that the ability to make
trustworthiness judgments involves neuro-cognitive systems independent of those
involved in stimuluspunishment association formation (taking a rened neuro-
psychological approach) or that individuals with psychopathy are making
trustworthiness judgments using a neuro-cognitive architecture that is very dierent
from that used by healthy individuals. The predictions of these contrasting positions
are clear. The rst suggests that individuals with psychopathy will show appropriate
amygdala responses to untrustworthy faces even if their amygdala responses during
aversive conditioning are reduced (Veit et al., 2002). The second suggests that the
neural responses of individuals with psychopathy to untrustworthy faces will be very
dierent from those of comparison individuals. The data to resolve these contrasting
predictions should soon be available.
1.8.1. Summary
The study of psychopathy has gained considerably from the neuro-psychological
approach. Predictions generated from following this approach have been systemati-
cally conrmed allowing a relatively tight specication of the impairment at the basis
of this disorder. However, the neuropsychological approach cannot be followed slav-
ishly. Psychopathy is not the equivalent to an amygdala lesion. The decits in psy-
chopathy are only a subset of those functions mediated by the amygdala.
1.9. Conclusions
The main goal of this paper was to consider how genetic anomalies could give
rise to the relatively specic neuro-cognitive impairments seen in individuals with
psychopathy. With respect to this goal, the suggestion is that genetic anomalies
reduce the salience of punishment information (perhaps as a function of noradren-
ergic disturbance). This impairs various aspects of amygdala function, most impor-
tantly the ability to form stimuluspunishment associations. In order to achieve
successful socialization, the child needs to form associations between representa-
tions of moral transgressions (acts which harm others) and the aversive punish-
ment caused by the victims distress. This allows the child to learn to avoid
actions that will harm others. As individuals with psychopathy nd the distress
of the victim signicantly less aversive, they are less likely to learn to avoid actions
that will harm others.
Why should the genetic eects operate so selectively, aecting primarily the sal-
ience of punishment information? It is likely that if a neurotransmitter such as nor-
adrenaline is implicated in psychopathy, it may serve more functions than simply
the coding of the salience of punishment information. This may mean that other
systems are aected in individuals with psychopathy. Dysfunction in these other
systems may have no causal role in the development of the core emotional aspects
of psychopathy but may contribute to the full behavioral prole of the disorder.
Certainly, by analogy, some individuals with autism show executive dysfunction
in addition to their diculties with Theory of Mind. While the executive dysfunc-
tion does not appear to be related to their social diculties, it does appear to be
related to other components of the behavioral prole such as their repetitive
behavior (Turner, 1997). Individuals with psychopathy may show certain attention-
al abnormalities (Jutai & Hare, 1983; Raine & Venables, 1988). The role of these
diculties in the development of the emotional component of psychopathy remains
unclear. However, it is possible that they reect the more general inuences of
genetically mediated neurotransmitter anomalies. Alternatively, of course, the
genetic anomalies may inuence the functioning of one particular neurotransmitter
receptor. Certain neurotransmitter receptors appear to be far more neural location
specic than others. If this possibility is the case, the relatively selective nature of
the decits seen in individuals with psychopathy may reect, for example, the
impact of genetic anomalies on the density of particular neurotransmitter receptors
in the amygdale crucial for punishment coding. At present, it is impossible to dis-
tinguish between these speculations. However, future work will allow the situation
to be resolved.
The model that has been developed here follows a tradition of pre-supposing the
existence of relatively independent neuro-cognitive systems that may be selectively
impaired in developmental disorders. This neuropsychological approach has been
recently criticized and sometimes considered to be not developmental. However, I
would argue, at least with respect to psychopathy, and particularly given animal data
on the development of the neural systems mediating emotion, that these criticisms
are unfounded. I suggest that the neuropsychological approach will continue to be
an invaluable tool with respect to the understanding, and ultimately the cure, of this
pernicious disorder.
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Cognition 101 (2006) 414442

The emergence of psychopathy: Implications

Keywords: Psychopathy; Reward and punishment; Development; Amygdala

0010-0277/$ - see front matter Published by Elsevier B.V.

The intellectual roots of psychopathy can be traced to Pritchard (1835); see

1.1. What is the functional impairment shown by individuals with psychopathy?

Psychopathy is associated with a core set of empirically demonstrated behavioral

1.2. What is the ultimate cause of psychopathy?

Growing evidence suggests a genetic contribution to psychopathy. Early twin,

1.3. The basic threat response

1.4. Psychopathy and amygdala dysfunction

expression recognition that is particularly marked for fearful expressions (Adolphs,

1.5. Psychopathy, neurotransmitter dysfunction and developing the neuro-cognitive

Polymorphisms of particular genes can alter the functioning of specic neuro-

e.g., the representation of objects currently in the environment, including moral

1.6. Psychopathy and orbital frontal cortex

Orbital frontal cortex is considerably involved in the regulation and mediation of

1.7. Psychopathy and autism

Psychopathy is not the only disorder linked to impairments in social cognition.

communication and a markedly restricted repertoire of activities and interests (p.

1.8. Psychopathy and the neuropsychological approach to developmental disorders

the formation of stimulusreward associations and certain aect-relevant aspects of

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