James Blair’s research on the cognitive neuroscience of psychopathy is
widely regarded as having provided some of the most significant insights into
the condition; Karina Blair and Derek Mitchell both work in his laboratory and
have published many article with him. They are therefore extremely well
qualified to offer us an overview of the state of research into, not only
psychopathy, but also other causes of aggression. Their book is aimed primarily
at psychologists, neuroscientists, and workers in allied fields, but it is
accessible to the general reader. In it, they survey the recent experimental
work on psychopathy, as well as the rival explanations of the causes of the
disorder, and offer their own account of what it is, how it emerges and how it
ought to be distinguished from other disorders.

The authors argue that the existing DSM
categories into which people presenting with heightened aggression are sorted
are uninformative, bundling together too many disparate people suffering from
different problems. We need, first of all, to distinguish between instrumental and reactive aggression, they argue. Instrumental aggression is
aggression in pursuit of some goal: money, sex, respect, or what have you;
reactive aggression is aggression in response to frustration. Most of the
people diagnosed with either conduct disorder or antisocial personality
disorder present with heightened levels of reactive aggression: for whatever
reason (the authors will go on to argue that either because, for genetic or
environmental reasons, the baseline level of activation of their neural systems
mediating responses to threat is elevated, or the frontal systems involved in
regulating this system is dysfunctional) this population has a problem dealing
with frustration and is more likely to respond to it with violence. But
psychopaths present with heightened levels of instrumental, as well as reactive
aggression. It must therefore have a different etiology, and is likely to
respond to different treatments.

That said, psychopathy ought not to be characterized primarily as a
disorder leading to heightened aggression, Blair et al argue. Instead, it is
primarily characterized by an emotional impairment. Given the emotional
impairment, psychopaths will use violence to achieve their ends, if other, more
socially acceptable, means are not available to them. So their propensity to
instrumental violence is a function, not only of the emotional impairment, but
also their intelligence and socio-economic status: the factors directly
relevant to their possession of other means to achieve their goals. Psychopathy
is distributed across all social classes, but lower status psychopaths are more
likely to come to the attention of law enforcement, and thence of mental health
professionals.

Blair is best-known for his violence
inhibition mechanism (VIM) theory of psychopathy. That theory held that
psychopathy was caused by a dysfunction in an innate mechanism, shared by many
mammals, which causes us to experience distress in conspecifics as
adversive.  Building on the basis of
this feeling, normal people come to be socialized to think that moral
transgressions – which cause harm to others – are wrong in a distinctive
manner. However, Blair and his colleagues are now ready to abandon the VIM
model, because it cannot account for data associated with two rival hypotheses;
the fear hypothesis and the response modulation hypothesis. The fear hypothesis
suggests that psychopathy is caused by an abnormally weak fear of punishment,
which prevents normal moral socialization; the response modulation hypothesis
suggests that psychopathy is caused by dysfunctions in the ability to attend to
stimuli which are peripheral to the subject’s focal interest, leading to
perseveration in behavior when it is inappropriate. There is indeed evidence of
reduced response in anticipation of punishment in psychopaths, and evidence
that psychopaths persist in patterns of behavior after they are no longer
rewarded. However, there is also considerable evidence against each hypothesis.
Moral socialization occurs primarily through induction, and punishment is an
ineffective means of teaching moral rules. And the response modulation hypothesis,
which is an attention-based model, does not fit easily with the best validated
models of attention.

The account that Blair, et al, now prefer integrates the VIM model with
the fear hypothesis to yield what they call the integrated emotions systems (IES) model of psychopathy. The
neurological basis of the IES model lies in amygdala dysfunction. Crucially,
the amygdala is a central part of the emotional brain, and it is involved in
most of the impairments seen in psychopaths. The amygdala is involved in
attention, enhancing attention to emotionally laden information. In general,
people with amygdala dysfunction will perform worse at tasks requiring them to
form associations with conditioned stimuli, explaining both why psychopaths do
worse at certain tasks where performance is enhanced by such associations, and
why do they better than controls at tasks where the conditioned stimulus is a
distracter. But while the amygdala is crucial to the formation of conditioned
stimulus-affect associations, it is not involved in conditioned
stimulus-response associations. Hence, while psychopaths are impaired on
standard passive avoidance tasks (where the subject has to learn to avoid
choices associated with punishments, while selecting options associated with rewards),
they are not impaired on punishment-only passive-avoidance learning tasks.
Since the amygdala is involved in processing affect-laden representations, it
is crucial to moral socialization; its dysfunction in psychopaths is therefore
responsible for their failure to learn the difference between moral and merely
conventional wrongdoing.

But the picture is more complex than the forgoing suggests. Here Blair
and his colleagues get speculative. First, they need to explain the fact that
psychopaths are not impaired on some tasks mediated by the amygdala: for
example, judging the emotions of people from photographs showing the eye region
only. Accordingly, Blair et al. suggest that the genetic anomalies that cause
psychopathy do not globally damage the amygdala, but instead have a more
selective affect, probably on neurotransmitter action. Second, psychopaths give
evidence of neurological abnormalities beyond the amygdala, especially of
orbital/ventrolateral frontal cortex dysfunction. Some of their difficulties
show up in tasks requiring response modulation, where there is no emotional
component. Here Blair and colleagues suggest that the explanation might be
developmental. There are many connections between the amygdala and the orbital
frontal cortex; perhaps a lack of afferent input from the amygdala to the
orbital frontal cortex could disrupt its development to an increasingly greater
degree (explaining why psychopathic adults are more impaired on these measures
than children with psychopathic tendencies).

The picture that is presented is somewhat messy, and the authors frankly
admit that there are many loose ends. But there is little doubt that this book
represents the state of the art, not only on psychopathy, but also on the many
different causal factors involved in reactive aggression. It gives, not a full
and final picture, but an accurate representation of science as it is actually
practiced, in which puzzles proliferate faster than they can be solved. It is
marred, to my mind, only by an uncritical use of the distinction between
genetic and environmental causes. It is highly recommended.

© 2005 Neil Levy

Neil Levy is
a research fellow at the Centre for Applied Philosophy and Public Ethics,
University of Melbourne, Australia and is author of Being
Up-To-Date: Foucault, Sartre, and Postmodernity (Peter Lang, 2001), Moral
Relativism: A Short Introduction (Oneworld, 2002), Sartre
(Oneworld, 2002), and What
Makes Us Moral?: Crossing the Boundaries of Biology (Oneworld, 2004).