Neuroethics (2008) 1:149157
DOI 10.1007/s12152-008-9016-6
REVIEW PAPER
The Cognitive Neuroscience of Psychopathy
and Implications for Judgments of Responsibility
R. J. R. Blair
Received: 11 April 2008 / Accepted: 16 April 2008 / Published online: 14 June 2008
# Springer Science + Business Media B.V. 2008
Abstract Psychopathy is a developmental disorder
associated with specific forms of emotional dysfunc-
tion and an increased risk for both frustration-based
reactive aggression and goal-directed instrumental
antisocial behavior. While the full behavioral mani-
festation of the disorder is under considerable social
influence, the basis of this disorder appears to be
genetic. At the neural level, individuals with
psychopathy show atypical responding within the
amygdala and ventromedial prefrontal cortex (vmPFC).
Moreover, the roles of the amygdala in stimulus-
reinforcement learning and responding to emotional
expressions and vmPFC in the representation of
reinforcement expectancies are compromised. The
implications of these functional impairments for
responsibility are discussed.
Keywords Psychopathy . Emotion . Amygdala .
Responsibility
R. J. R. Blair (*)
Mood & Anxiety Program, National Institute of Mental
Health, National Institutes of Health,
15k North Drive,
Bethesda, MD 20892, USA
e-mail: blairj@intra.nimh.nih.gov
Introduction
This paper is based on a talk delivered to the American
Philosophy Association in Baltimore 2007. The paper
was part of a special Session Arranged by the APA
Committee on Philosophy and Law entitled: Are
Psychopaths Responsible? The goal of this paper is to
briefly lay out the current understanding regarding the
cognitive neuroscience of psychopathy before using
these data to consider what can be said regarding issues
of responsibility.
The Disorder of Psychopathy
Psychopathy can be considered to involve two
components: emotional dysfunction and antisocial
behavior [36, 41, 44]. The emotional dysfunction
reflects reduced guilt, empathy and attachment to
significant others. The antisocial behavior component
reflects a predisposition to antisocial behavior from an
early age. Psychopathy is typically indexed in adults
with the revised psychopathy checklist [41, 42] and in
children and adolescents, through the antisocial process
screening device [37] or the Psychopathy Checklist-
Youth version [35]. The disorder is developmental in
that it emerges before the age of 10 years and persists
deep into adulthood [45, 58].
The disorder is not equivalent to the Diagnostic
and Statistical Manual of Mental Disorder (DSM)-IV
DO09016; No of Pages
150
diagnoses of conduct disorder or antisocial personality
disorder or their International Classification of
Diseases (ICD)-10 counterparts. These diagnoses con-
centrate on the antisocial behavior and do not include
any extensive investigation of the presence or absence
of the form of emotion dysfunction seen in psychopathy
[14]. Individuals with psychopathy appear to represent
only a fraction of those who would receive these
psychiatric diagnoses and thus it is important to note
that data obtained with populations defined by these
psychiatric criteria will not necessarily appear identical
to that obtained from a group of individuals with
psychopathy.
There are also notable differences between individuals
with acquired sociopathy following lesions of ventrome-
dial prefrontal cortex (vmPFC) despite earlier claims
based on the increased risk for aggressions shown by
some of these patients cf. [26]. Psychopathy is associated
with a series of core functional impairments. These are
not seen following lesions of orbitofrontal cortex (OFC).
For example, while individuals with psychopathy show
impairment in aversive conditioning [6], patients with
OFC lesions do not [4]. Similarly, while individuals
with psychopathy [12] show impaired fear recognition
in facial expressions, patients with vmPFC lesions show
a more generalized impairment for all negative
emotional expressions [47].
Instrumental and Reactive Aggression
Numerous investigators have previously made a
distinction between instrumental a.k.a. instrumental
or premeditated; cf. [78] aggression and reactive a.k.a.
affective, impulsive or defensive; cf. [78] aggression
[3, 5, 25, 56]. Instrumental aggression is purposeful
and goal directed (e.g., to obtain the victims
possessions). It need not be accompanied by an
emotional state, such as anger, and can be considered
cold [78]. In contrast, reactive aggression is
triggered by a frustrating or threatening event and
involves unplanned, enraged attacks on the object
perceived to be the source of the threat/frustration.
This aggression type is often accompanied by anger
and can be considered hot. Importantly, it is
initiated without regard for any potential goal.
Many psychiatric disorders are associated with an
increased risk for reactive aggression; e.g., post
R.J.R. Blair
traumatic stress disorder [76, 82] and childhood
bipolar disorder [54]. Psychopathy is a remarkable
condition in that it is associated with increased risk
for both instrumental and reactive aggression [24, 38].
This is important to note because when considering
responsibility it is necessary to make a distinction
between instrumental and reactive antisocial behavior.
The Basis of the Disorder
There have been suggestions that psychopathy might
be due to early physical/ sexual abuse or neglect [74].
These factors certainly do increase the risk of
antisocial behavior, particularly frustration and threat
based reactive aggression (see below) [29]. However,
importantly, the impact of extreme stressors and
neglect on the development of the mammalian brain
is now relatively clear. Work shows that these factors
increase emotional responsiveness to threatening
stimuli [18, 71]. Psychopathy, however, is a disorder
marked by reduced rather than increased emotional
responsiveness (see below).
Current data suggests that there is a genetic basis to
this disorder [16, 80]. In one of the largest of relevant
studies involving around 3,500 twin pairs, callous
unemotional traits were shown to be strongly heritable
(67% heritability) at 7 years [80]. However, currently we
have no understanding of psychopathy at the molecular
genetic level although it is important to note that recent
work has identified a variety genetic polymorphisms
that influence the responsiveness of those neural
systems, the amygdala and vmPFC, implicated in
psychopathy [43, 62, 70]. For example, several studies
have reported that individuals who are long/long
homozygotes for the serotonin transporter (5-HTTLPR)
gene show significantly reduced amygdala responding
to emotional expressions relative to those who have the
short form polymorphism of the gene [43]. It is possible
that there is an array of genes whose polymorphisms
affect the functional integrity of the amygdala and
medial frontal cortex. The basic genetic risk for
psychopathy may emerge if an individual possesses a
sufficient number of polymorphisms predisposing the
individual to reduced emotional and amygdala
responsiveness.
Importantly, while psychopathy may be under
considerable genetic influence, social factors do still
influence its development. For example, socioeco-
The cognitive neuroscience of psychopathy and implications
nomic status is associated with the emergence of the
full syndrome; it is significantly less likely to appear
in individuals of higher social status [77]. Social
disadvantage provides motive for goal directed
instrumental antisocial behavior and increases the risk
of frustration and consequent reactive aggression.
Dysfunctional Neural Systems in Psychopathy
On the basis of the neuropsychological literature, two
core neural regions appear dysfunctional in psychopathy:
the amygdala and vmPFC. The core functional
impairments seen in psychopathy (e.g., deficits in
aversive conditioning, the augmentation of the startle
reflex by visual threat primes and fearful expression
recognition) are all seen following lesions of the
amygdala (for a review of this literature, see [8].
Psychopathy is also associated with problems in reversal
learning and on tasks such as the Iowa gambling task
[20, 64]. These impairments are seen following lesions
of vmPFC [4, 49].
The neuroimaging literature on psychopathy has
proven highly consistent with the neuropsychological
data in that it too has suggested a pathophysiology that
includes the amygdala and vmPFC. Thus, functional
magnetic resonance imaging (fMRI) studies have
found that adults with psychopathy show reduced
activation of both the amygdala and rostral anterior
cingulate cortex/vmPFC in response to emotional
words in the context of emotional memory paradigms
[51] and during aversive conditioning [6]. Moreover,
work with sub-clinical populations has found that
individuals with psychopathic traits show reduced
amygdala and vmPFC responses to emotional expres-
sions [39] and less amygdala and vmPFC differentia-
tion in responding when making cooperation relative to
defection choices in a prisoners dilemma paradigm
[72]. Recent work with adolescents with psychopathic
tendencies has shown reduced amygdala responses to
fearful expressions and reduced connectivity between
the amygdala and vmPFC [61]. In addition, a study
examining reversal learning reported that adolescents
with psychopathic tendencies failed to show the
reduction in vmPFC activity that is associated with
an unexpected punished response [33].
The neuro-imaging literature on psychopathy has
also implicated other structures, specifically dorsal
151
anterior cingulate cortex [51], inferior frontal cortex
[39], parietal cortex [61], posterior cingulate cortex
[61], insula [6, 61], and caudate [33]. However, there
has been a lack of consistently with only one or two
studies reporting atypical activity in these regions. It
is likely that this thus either reflects stochastic
influences or reduced input from core regions in the
particular task studied. One additional region that
should be considered however is superior temporal
cortex (STC). Atypical activity in this region was seen
in most of the above studies [6, 33, 51, 61]. Of course,
STC has considerable reciprocal connections with the
amygdala [1] and thus the atypical activity in this region
in individuals with psychopathic tendencies may be a
consequence of the amygdala dysfunction. Importantly,
the suggestion of STC dysfunction in psychopathy cf.
[50], unlike the evidence for amygdala and vmPFC
dysfunction, remains currently unsubstantiated by
neuropsychological findings (and therefore we cannot
be sure that they do not simply reflect reduced input
from core regions).
The Functional Contributions of the Amygdala
and vmPFC
The amygdala is crucial for stimulus-reinforcement
learning [27, 31]. This learning allows representations
of conditioned stimuli within temporal cortex to be
linked to emotional responses mediated by the
amygdala and other structures. In humans and other
primates, fearfulness and potentially sadness serve as
reinforcers, stimuli associated with expression are
avoided, and this type of stimulus-reinforcement
learning relies on the amygdala too [46, 63]. In short,
the amygdala allows the individual to learn the
goodness and badness of objects and actions whether
the goodness and badness to be associated with these
objects involves non-social rewards and punishments
(e.g., desirable foods/money or pain/loud noises) or
social rewards and punishments (e.g., fearful or happy
facial expressions).
The amygdala sends outputs forward to vmPFC.
VmPFC has been implicated through both animal [75]
and human fMRI work [52] in stimulus-outcome
processing. Importantly, vmPFC can represent the
reinforcement outcomes associated with multiple
objects [68]. In line with this, recent fMRI work has
reported that activity in vmPFC is better predicted by
152
total available reinforcement (e.g., reinforcement
associated with two different objects) rather than only
reinforcement associated with the chosen object [15].
This is not to suggest that vmPFC codes total
available reinforcement. Instead, the suggestion is
that what is being seen is activity in separable
populations of neurons representing reinforcement
associated with the different objects [68]. This is seen
as a cumulative signal when indexed by the imprecise
signal that is the blood oxygenation level dependent
(BOLD) response.
VmPFC itself does not appear to choose between
the objects associated with different reinforcement
expectancies. Parameters that are associated with
decision difficulty (e.g., the number of objects to
choose between or the difference in the reinforcement
expectancies associated with the two objects) do not
influence activity in vmPFC [15, 60]. They do,
however, influence activity in other regions, in
particular dorsal anterior cingulate cortex [15, 60].
Dorsal anterior cingulate cortex has been implicated
in the resolution of response conflicts [17, 23]; i.e., it
allows the resolution of difficult decisions. In short,
vmPFC appears to be critical for the representation of
reinforcement outcome expectancies associated with
objects, information that is then used by other systems
to affect decision making.
The Functional Impairment In Psychopathy
As noted above, psychopathy is associated with
atypical responding within the amygdala, vmPFC
and, potentially, superior temporal gyrus (STG) (this
latter structure will not be discussed here as a
functional account concerning why dysfunction in
STG should relate to psychopathy has yet to be
provided). It appears clear that individuals with psy-
chopathy show impairment in stimulus-reinforcement
learning [34, 57); impairment that is reflected also in
reduced amygdala and vmPFC activity to conditioned
stimuli during aversive conditioning paradigms [6].
Individuals with psychopathy also show impairment in
the processing of the fearful and sad expressions of
others. This is seen in reduced arousal responses
(indexed by skin conductance) to distress cues
[2, 10], impaired recognition of fearful and, to a lesser
extent, sad expressions [11, 30, 59] and reduced BOLD
responses within the amygdala to fearful expressions
R.J.R. Blair
[61]. In short, individuals with psychopathy show
impairment in the form of emotional learning, stimu-
lus-reinforcement learning, that is necessary for learn-
ing the goodness and badness associated with
representations of objects and actions. Moreover, they
show impairment in responding to those social
reinforcers, fearful and sadness expressions, which
are so important for moral socialization. In short, it
would be expected that their ability to be socialized
would be compromised and the literature suggests that
this is indeed the case [67, 81]. Disrupted moral
socialization may lead to an increased probability that
the individual will use antisocial methods to achieve
their goals as they are less likely to represent the
aversive consequences of antisocial actions (the
distress to victims).
The amygdala is thought to output expectancies of
reinforcement outcomes to vmPFC which then repre-
sents this information to allow successful decision
making [75]. Due to the amygdala dysfunction, it is
likely that individuals receive impoverished reinforce-
ment expectancy information within vmPFC. Indeed,
the reduced amygdala and vmPFC differentiation in
individuals with psychopathy when making coopera-
tion relative to defection choices in a prisoners
dilemma paradigm [72] and the reduced connectivity
between the amygdala and vmPFC in adolescents
with psychopathic tendencies when responding to
facial expressions is strongly suggestive of this [61].
It is thought that the decision making impairment seen
in psychopathy [13, 64, 65] relates to this impairment
in the receipt and representation of reinforcement
expectancy information [9].
It is worth noting that there may also be structurally
reduced connectivity between the amygdala and
vmPFC in psychopathy. Investigations employing
Diffusion Tensor Imaging which attempts to index
the structural integrity of fiber bundles passing
through white matter are actively investigating this
issue. Moreover, either as an indirect result of this
reduced input from the amygdala or as a direct
consequence of the likely genetic contribution, it
appears that the functional integrity of vmPFC is
disrupted in psychopathy.
In reversal learning paradigms, the individual
initially learns to make a response to gain a reward
[20]. After a number of trials, the reinforcement
contingency changes such that the previously correct
response no longer results in reward, and a new
The cognitive neuroscience of psychopathy and implications
response must be learned to achieve the reward.
Reversal learning is reliant on the functional integrity
of vmPFC [28, 32, 48, 73]. However, the animal
literature, at least, strongly suggests that the amygdala
is not necessary for reversal learning. In other words,
the observation of impaired reversal learning in
individuals with psychopathy [19, 20, 64], suggests
the existence of vmPFC dysfunction independent of,
and additional to, the amygdala dysfunction.
The functional integrity of vmPFC may be critical
for reversal learning because vmPFC is necessary for
the detection of contingency change due to its role in
the responding to prediction errors [21]. On the basis
of this account, vmPFC dysfunction in psychopathy
would result in reduced detection of the contingency
change and thus a reduced probability of changing
behavior. Alternatively, or additionally, vmPFC may
be critical for reversal learning because of its role in the
representation of reinforcements associated with objects
[40]. If this is disrupted, there will be weaker tracking
of the changing reinforcement values associated with
the two objects (i.e., that the good object is now bad
while the bad object has become good) and thus
impaired decision making; there will be an increased
tendency to stay with the object that was originally
good.
Importantly, the impairment in reversal learning
and the related difficulties with operant extinction as
indexed by the one pack card playing task; [66] as
well as the more general impairment in decision
making impairment will all lead to an individual at
greater risk of frustration. Frustration occurs when an
action is taken to gain a particular outcome and that
outcome is not forthcoming [5]. It has been suggested
that the increased risk for reactive aggression seen in
psychopathy is due to this increased risk of experiencing
frustration [9].
Implications for Judgments of Responsibility
In this last section of the paper, I will briefly consider
potential implications of the above cognitive neuro-
science data for judgments of responsibility related to
psychopathy. It should be noted that the goal of my
work is to understand the nature of the emotional
deficit associated with this disorder so that it might
come to be effectively treated. Considerations of
153
responsibility are out of the scope of this work and,
as such, I offer up personal speculations in the hope
that they are of interest to those whose goal it is to
consider such issues.
One major factor when considering responsibility
is the individuals intention/ whether the action is
planned. The individual who purposely drives their
car at another individual is considered far more
responsible and blameworthy than the individual who
accidentally runs another over. As noted earlier,
psychopathy is associated with an increased risk for both
instrumental and reactive aggression. By definition,
instrumental aggression is intentional; the individual is
engaged in a planned actionusing the antisocial
behavior to achieve their goals. In contrast, reactive
aggression is not. Instead, it is triggered by a frustrating
event and involves unplanned, enraged attacks on the
object perceived to be the source of the threat/frustration.
In the previous section, the role of vmPFC dysfunction in
the increased risk for reactive aggression seen in
psychopathy was discussed. In short, part of the
syndrome of psychopathy does likely increase the risk
of behavior that could be considered to occur in a state of
diminished responsibility.
One of the problems with the instrumental-reactive
aggression dichotomy is the difficulty in characteriz-
ing individual antisocial acts [22]. For example, it
appears that an individual shooting a romantic partner
caught in the arms of a lover is regarded as less
responsible for their actions than if the antisocial act
but not the revelation had occurred. The action is
clearly instrumental in that the nature of the action,
the use of a gun, is not an automatic but rather a goal
directed action. However, the action is not cold but
rather charged with considerable affect. It is possible
that the knowledge of this affect leads to people
judging the individual as less responsible for their
actions.
Psychopathy is associated with reductions in some
forms of emotion; e.g., guilt, fearfulness and sadness
[69, 79]. However, it does not appear that all
emotional responding is diminished. Indeed, the
increased risk for reactive aggression [24, 38] would
suggest that the propensity to anger is not diminished
but rather may be increased. In short, the pathology
associated with psychopathy, in particular the vmPFC
dysfunction, may lead to an increase risk for anger
based antisocial behavior that could be considered to
occur in a state of diminished responsibility.
154
So far we have considered reactively aggressive
actions and instrumental antisocial behavior that is
reactively charged, but what about more general
instrumental antisocial actions? In recent work, Levy
has argued that by failing the moral/conventional
distinction task [7], individuals with psychopathy
show a fundamental inability to categorize moral
harms and as such their moral responsibility for their
actions is reduced [55]. Certainly, as argued above,
individuals with psychopathy are impaired in the
ability to learn the badness of actions and objects and
their subsequent decision making is consequently
dysfunctional. Whether an instrumental action occurs
is determined by decision making; the individual
weighs up the reward that may be accrued as a
consequence of the action against any potential costs
associated with the action [53]. The amygdala and
vmPFC dysfunction described above will seriously
impair the decision making in psychopathy and thus,
following Levys arguments, it can be considered that
the instrumental antisocial actions engaged in by
individuals with psychopathy occur in a state of
diminished responsibility.
Conclusions
Psychopathy is a developmental disorder associated
with specific forms of emotional dysfunction and an
increased risk for antisocial behavior. The increased
risk is for both frustration-based reactive aggression
and goal-directed instrumental antisocial behavior.
Psychopathy is not equivalent to the DSM diagnoses
of Conduct Disorder and Antisocial Personality
Disorder, nor is it similar in nature to acquired
sociopathy following lesions of vmPFC.
The full manifestation of psychopathy is likely to
be under considerable social influence. At the very
least, increased socioeconomic status (SES) and IQ
are likely to mitigate the increased risk for antisocial
behavior resulting from the disorder; the individual
with higher SES/IQ will have an increased range of
activities that may achieve their goals beyond
antisocial behavior. However, current data suggests
that the basis of this disorder is genetic although the
details of this contribution, which genes are involved,
remain unknown.
At the neural level, psychopathy appears to be
related to dysfunction within the amygdala, vmPFC
R.J.R. Blair
and perhaps also superior temporal cortex. In partic-
ular, it appears that the role of the amygdala in
stimulus-reinforcement learning and responding to
specific forms of facial expression, in particular the
fearful and sad expressions of other individuals, is
compromised. In addition, the role of vmPFC in the
representation of reinforcement expectancies is com-
promised. Together these functional impairments
disrupt appropriate moral socialization and impair
decision making. They also put the individual at
increased risk for frustration based reactive aggression.
As such, from some perspectives [55], it can be argued
that the functional impairments seen in psychopathy
diminish responsibility.
Acknowledgments This research was supported by the
Intramural Research Program of the NIH: NIMH.
References
1. Amaral, D.G., J.L. Price, A. Pitkanen, and S.T. Carmichael.
1992. Anatomical organization of the primate amygdaloid
complex. In The amygdala: neurobiological aspects of
emotion, memory, and mental dysfunction, ed. J.P. Aggleton,
166. New York: Wiley.
2. Aniskiewicz, A.S. 1979. Autonomic components of vicar-
ious conditioning and psychopathy. Journal of Clinical
Psychology 35: 6067.
3. Barratt, E.S., M.S. Stanford, L. Dowdy, M.J. Liebman, and
T.A. Kent. 1999. Impulsive and premeditated aggression: a
factor analysis of self-reported acts. Psychiatry Research
862: 163173.
4. Bechara, A., H. Damasio, A.R. Damasio, and G.P. Lee.
1999. Different contributions of the human amygdala and
ventromedial prefrontal cortex to decision-making. Journal
of Neuroscience 19: 54735481.
5. Berkowitz, L. 1993. Aggression: its causes, consequences,
and control. Philadelphia: Temple University Press.
6. Birbaumer, N., R. Veit, M. Lotze, M. Erb, C. Hermann, W.
Grodd, et al. 2005. Deficient fear conditioning in psychopathy:
a functional magnetic resonance imaging study. Archives of
General Psychiatry 627: 799805.
7. Blair, R.J.R. 1995. A cognitive developmental approach to
morality: investigating the psychopath. Cognition 57: 129.
8. Blair, R.J.R. 2006. The emergence of psychopathy: implica-
tions for the neuropsychological approach to developmental
disorders. Cognition 101: 414442.
9. Blair, J. 2007. Dysfunctions of medial and lateral orbito-
frontal cortex in psychopathy. Annals of the New York
Academy of Sciences 1121(1): 461479.
10. Blair, R.J.R., L. Jones, F. Clark, and M. Smith. 1997. The
psychopathic individual: a lack of responsiveness to
distress cues? Psychophysiology 34: 192198.
The cognitive neuroscience of psychopathy and implications
11. Blair, R.J.R., E. Colledge, L. Murray, and D.G. Mitchell.
2001. A selective impairment in the processing of sad
and fearful expressions in children with psychopathic
tendencies. Journal of Abnormal Child Psychology 29(6):
491498.
12. Blair, R.J.R., D.G.V. Mitchell, E. Colledge, R.A. Leonard,
J.H. Shine, L.K. Murray, et al. 2004a. Reduced sensitivity
to others fearful expressions in psychopathic individuals.
Personality & Individual Differences 37: 11111121.
13. Blair, R.J.R., D.G.V. Mitchell, A. Leonard, S. Budhani, K.
S. Peschardt, and C. Newman. 2004b. Passive avoidance
learning in individuals with psychopathy: modulation by
reward but not by punishment. Personality and Individual
Differences 37: 11791192.
14. Blair, R.J.R., D.G.V. Mitchell, and K.S. Blair. 2005. The
psychopath: emotion and the brain. Oxford: Blackwell.
15. Blair, K.S., A.A. Marsh, J. Morton, M. Vythilingham, M.
Jones, K. Mondillo, et al. 2006. Choosing the lesser of two
evils, the better of two goods: specifying the roles of
ventromedial prefrontal cortex and dorsal anterior cingulate
cortex in object choice. Journal of Neuroscience 26(44):
1137911386.
16. Blonigen, D.M., B.M. Hicks, R.F. Krueger, C.J. Patrick,
and W.G. Iacono. 2005. Psychopathic personality traits:
heritability and genetic overlap with internalizing and
externalizing psychopathology. Psychological Medicine
35: 637648.
17. Botvinick, M.M., J.D. Cohen, and C.S. Carter. 2004.
Conflict monitoring and anterior cingulate cortex: an
update. Trends in Cognitive Science 8(12): 539546.
18. Bremner, J.D., and E. Vermetten. 2001. Stress and
development: behavioral and biological consequences.
Development and Psychopathology 13: 473489.
19. Budhani, S., and R.J. Blair. 2005. Response reversal and
children with psychopathic tendencies: success is a func-
tion of salience of contingency change. Journal of Child
Psychology and Psychiatry 46(9): 972981.
20. Budhani, S., R.A. Richell, and R.J. Blair. 2006. Impaired
reversal but intact acquisition: probabilistic response
reversal deficits in adult individuals with psychopathy.
Journal of Abnormal Psychology 115(3): 552558.
21. Budhani, S., A.A. Marsh, D.S. Pine, and R.J. Blair. 2007.
Neural correlates of response reversal: considering acqui-
sition. Neuroimage 34(4): 17541765.
22. Bushman, B.J., and C.A. Anderson. 2001. Is it time to pull
the plug on the hostile versus instrumental aggression
dichotomy? Psychological Review 108(1): 273279.
23. Cohen, J.D., M. Botvinick, and C.S. Carter. 2000. Anterior
cingulate and prefrontal cortex: whos in control. Nature
Neuroscience 3(5): 421423.
24. Cornell, D.G., J. Warren, G. Hawk, E. Stafford, G. Oram,
and D. Pine. 1996. Psychopathy in instrumental and
reactive violent offenders. Journal of Consulting and
Clinical Psychology 64: 783790.
25. Crick, N.R., and K.A. Dodge. 1996. Social information-
processing mechanisms on reactive and proactive aggres-
sion. Child Development 67(3): 9931002.
26. Damasio, A.R. 1994. Descartes error: emotion, rationality
and the human brain. New York: Putnam (Grosset Books).
27. Davis, M., and P.J. Whalen. 2001. The amygdala: vigilance
and emotion. Molecular Psychiatry 6(1): 1334.
155
28. Dias, R., T.W. Robbins, and A.C. Roberts. 1996. Dissociation
in prefrontal cortex of affective and attentional shifts. Nature
380: 6972.
29. Dodge, K.A., G.S. Pettit, J.E. Bates, and E. Valente. 1995.
Social information-processing patterns partially mediate the
effect of early physical abuse on later conduct problems.
Journal of Abnormal Psychology 104: 632643.
30. Dolan, M., and R. Fullam. 2006. Face affect recognition
deficits in personality-disordered offenders: association
with psychopathy. Psychological Medicine 36(11): 1563
1569.
31. Everitt, B.J., R.N. Cardinal, J.A. Parkinson, and T.W.
Robbins. 2003. Appetitive behavior: impact of amygdala-
dependent mechanisms of emotional learning. Annual New
York Academy of Sciences 985: 233250.
32. Fellows, L.K., and M.J. Farah. 2003. Ventromedial frontal
cortex mediates affective shifting in humans: evidence from
a reversal learning paradigm. Brain 126: 18301837.
33. Finger, E.C., A.A. Marsh, D.G. Mitchell, M.E. Reid,
C. Sims, S. Budhani, D.S. Kosson, G. Chen, K.E. Towbin,
E. Leibenluft, D.S. Pine, and J.R. Blair. 2008. Abnormal
ventromedial prefrontal cortex function in children with
psychopathic traits during reversal learning. Archives of
General Psychiatry 65(5): 586594.
34. Flor, H., N. Birbaumer, C. Hermann, S. Ziegler, and C.J.
Patrick. 2002. Aversive Pavlovian conditioning in psycho-
paths: peripheral and central correlates. Psychophysiology
39: 505518.
35. Forth, A. E., D.S. Kosson, and R.D. Hare. 2003. The
psychopathy checklist: youth version. Toronto, Ontario,
Canada: Multi-Health Systems.
36. Frick, P.J. 1995. Callous-unemotional traits and conduct
problems: a two-factor model of psychopathy in children.
Issues in Criminological and Legal Psychology 24: 4751.
37. Frick, P.J., and R.D. Hare. 2001. The antisocial process
screening device. Toronto: Multi-Health Systems.
38. Frick, P.J., T.R. Stickle, D.M. Dandreaux, J.M. Farell, and
E.R. Kimonis. 2005. Callous-unemotional traits in predicting
the severity and stability of conduct problems and delinquen-
cy. Journal of Abnormal Child Psychology 33: 471487.
39. Gordon, H.L., A.A. Baird, and A. End. 2004. Functional
differences among those high and low on a trait measure of
psychopathy. Biological Psychiatry 567: 516521.
40. Hampton, A.N., P. Bossaerts, and J.P. ODoherty. 2006.
The role of the ventromedial prefrontal cortex in abstract
state-based inference during decision making in humans.
Journal of Neuroscience 2632: 83608367.
41. Hare, R.D. 1991. The hare psychopathy checklist-revised.
Toronto, Ontario: Multi-Health Systems.
42. Hare, R.D. 2003. Hare psychopathy checklist-revised PCL-
R, 2nd Edn. Toronto: Multi Health Systems.
43. Hariri, A.R., V.S. Mattay, A. Tessitore, B. Kolachana, F.
Fera, D. Goldman, et al. 2002. Serotonin transporter
genetic variation and the response of the human amygdala.
Science 297(5580): 400403.
44. Harpur, T.J., A.R. Hakstian, and R.D. Hare. 1988. The
factor structure of the psychopathy checklist. Journal of
Consulting and Clinical Psychology 56: 741747.
45. Harpur, T.J., and R.D. Hare. 1994. Assessment of psychopathy
as a function of age. Journal of Abnormal Psychology 103:
604609.
156
46. Hooker, C.I., L.T. Germine, R.T. Knight, and M. DEsposito.
2006. Amygdala response to facial expressions reflects
emotional learning. Journal of Neuroscience 26(35): 8915
8922.
47. Hornak, J., J. Bramham, E.T. Rolls, R.G.O. Morris, J.
Doherty, et al. 2003. Changes in emotion after circum-
scribed surgical lesions of the orbitofrontal and cingulate
cortices. Brain 126: 16911712.
48. Izquierdo, A., and E.A. Murray. 2005. Opposing effects of
amygdala and orbital prefrontal cortex lesions on the
extinction of instrumental responding in macaque monkeys.
European Journal of Neuroscience 22(9): 23412346.
49. Izquierdo, A., R.K. Suda, and E.A. Murray. 2004. Bilateral
orbital prefrontal cortex lesions in rhesus monkeys disrupt
choices guided by both reward value and reward contingency.
Journal of Neuroscience 24(34): 75407548.
50. Kiehl, K.A. 2006. A cognitive neuroscience perspective on
psychopathy: evidence for paralimbic system dysfunction.
Psychiatry Research 142: 107128.
51. Kiehl, K.A., A.M. Smith, R.D. Hare, A. Mendrek, B.B.
Forster, J. Brink, et al. 2001. Limbic abnormalities in
affective processing by criminal psychopaths as revealed by
functional magnetic resonance imaging. Biological Psychiatry
50: 677684.
52. Knutson, B., and J.C. Cooper. 2005. Functional magnetic
resonance imaging of reward prediction. Current Opinion
in Neurology 18(4): 411417.
53. Knutson, B., S. Rick, G.E. Wimmer, D. Prelec, and G.
Loewenstein. 2007. Neural predictors of purchases. Neuron
53: 147157.
54. Leibenluft, E., R.J. Blair, D.S. Charney, and D.S. Pine.
2003. Irritability in pediatric mania and other childhood
psychopathology. Annual New York Academy of Sciences
1008: 201218.
55. Levy, N. 2007. The responsibility of the psychopath
revisited. Philosophy, Psychiatry and Psychology 14(2):
129138.
56. Linnoila, M., M. Virkkunen, M. Scheinin, A. Nuutila, R.
Rimon, and F.K. Goodwin. 1983. Low cerebrospinal fluid
5-hydroxy indoleacetic acid concentration differentiates
impulsive from nonimpulsive violent behavior. Life Scien-
ces 33: 26092614.
57. Lykken, D.T. 1957. A study of anxiety in the sociopathic
personality. Journal of Abnormal and Social Psychology
55: 610.
58. Lynam, D.R., A. Caspi, T.E. Moffitt, R. Loeber, and M.
Stouthamer-Loeber. 2007. Longitudinal evidence that psy-
chopathy scores in early adolescence predict adult psychop-
athy. Journal of Abnormal Psychology 116(1): 155165.
59. Marsh, A.A., and R.J. Blair. 2007. Deficits in facial affect
recognition among antisocial populations: a meta-analysis.
Neuroscience and Biobehavioral Reviews 32(3): 454465.
60. Marsh, A.A., K.S. Blair, M. Vythilingam, S. Busis, and R.J.
Blair. 2007. Response options and expectations of reward in
decision-making: the differential roles of dorsal and rostral
anterior cingulate cortex. Neuroimage 35(2): 979988.
61. Marsh, A.A., E.C. Finger, D.G.V. Mitchell, M.E. Reid, C.
Sims, D.S. Kosson, et al. (2008). Reduced amygdala
R.J.R. Blair
response to fearful expressions in children and adolescents
with callous-unemotional traits and disruptive behavior
disorders. American Journal of Psychiatry 165(6): 712720.
62. Meyer-Lindenberg, A., J.W. Buckholtz, B.A.R.H. Kolachana,
L. Pezawas, G. Blasi, et al. 2006. Neural mechanisms of genetic
risk for impulsivity and violence in humans. Proceedings of the
National Academy of Sciences of the United States of America
103(16): 62696274.
63. Mineka, S., and R. Zinbarg. 2006. A contemporary learning
theory perspective on the etiology of anxiety disorders: its not
what you thought it was. American Psychologist 61(1): 1026.
64. Mitchell, D.G.V., E. Colledge, A. Leonard, and R.J.R.
Blair. 2002. Risky decisions and response reversal: Is there
evidence of orbitofrontal cortex dysfunction in psychopathic
individuals? Neuropsychologia 40: 20132022.
65. Newman, J.P., and D.S. Kosson. 1986. Passive avoidance
learning in psychopathic and nonpsychopathic offenders.
Journal of Abnormal Psychology 95: 252256.
66. Newman, J.P., C.M. Patterson, and D.S. Kosson. 1987.
Response perseveration in psychopaths. Journal of Abnormal
Psychology 96: 145148.
67. Oxford, M., T.A. Cavell, and J.N. Hughes. 2003.
Callous-unemotional traits moderate the relation between
ineffective parenting and child externalizing problems: a partial
replication and extension. Journal of Clinical Child and
Adolescent Psychology 32: 577585.
68. Padoa-Schioppa, C., and J.A. Assad. 2006. Neurons in the
orbitofrontal cortex encode economic value. Nature 441
(7090): 223226.
69. Patrick, C.J. 1994. Emotion and psychopathy: startling new
insights. Psychophysiology 31: 319330.
70. Pezawas, L., A. Meyer-Lindenberg, E.M. Drabant, B.A.
Verchinski, K.E. Munoz, B.S. Kolachana, et al. 2005. 5-
HTTLPR polymorphism impacts human cingulate-amygdala
interactions: a genetic susceptibility mechanism for depression.
Nature Neuroscience 8(6): 828834.
71. Rilling, J.K., J.T. Winslow, D. OBrien, D.A. Gutman, J.M.
Hoffman, and C.D. Kilts. 2001. Neural correlates of maternal
separation in rhesus monkeys. Biological Psychiatry 49(2):
146157.
72. Rilling, J.K., A.L. Glenn, M.R. Jairam, G. Pagnoni, D.R.
Goldsmith, H.A. Elfenbein, et al. 2007. Neural correlates of
social cooperation and non-cooperation as a function of
psychopathy. Biological Psychiatry 61(11): 12601271.
73. Rolls, E.T., J. Hornak, D. Wade, and J. McGrath. 1994.
Emotion-related learning in patients with social and emo-
tional changes associated with frontal lobe damage. Journal
of Neurology, Neurosurgery, and Psychiatry 57: 15181524.
74. Rutter, M. 2005. Commentary: what is the meaning and
utility of the psychopathy concept? Journal of Abnormal
Child Psychology 33(4): 499503.
75. Schoenbaum, G., and M. Roesch. 2005. Orbitofrontal
cortex, associative learning, and expectancies. Neuron 47
(5): 633636.
76. Silva, J.A., D.V. Derecho, G.B. Leong, R. Weinstock, and
M.M. Ferrari. 2001. A classification of psychological
factors leading to violent behavior in posttraumatic stress
disorder. Journal of Forensic Sciences 46(2): 309316.
The cognitive neuroscience of psychopathy and implications
77. Silverthorn, P., and P.J. Frick. 1999. Developmental path-
ways to antisocial behavior: the delayed-onset pathway in
girls. Development and Psychopathology 11(1): 101126.
78. Steiner, H., K. Saxena, and K. Chang. 2003. Psychophar-
macologic strategies for the treatment of aggression in
juveniles. CNS Spectrum 8: 298308.
79. Verona, E., C.J. Patrick, and T.E. Joiner. 2001. Psychopathy,
antisocial personality, and suicide risk. Journal of Abnormal
Psychology 110(3): 462470.
80. Viding, E., R.J.R. Blair, T.E. Moffitt, and R. Plomin. 2005.
Evidence for substantial genetic risk for psychopathy in
157
7-year-olds. Journal of Child Psychology and Psychiatry
46: 592597.
81. Wootton, J.M., P.J. Frick, K.K. Shelton, and P. Silverthorn.
1997. Ineffective parenting and childhood conduct
problems: the moderating role of callous-unemotional
traits. Journal of Consulting and Clinical Psychology 65:
292300.
82. Zoccolillo, M. 1992. Co-occurrence of conduct disorder
and its adult outcomes with depressive and anxiety
disorders: a review. Journal of the American Academy of
Child and Adolescent Psychiatry 31(3): 547556.