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The PsychopathReview - The Psychopath
Emotion And The Brain
by James Blair
Blackwell, 2005
Review by Neil Levy, Ph.D.
Nov 1st 2005 (Volume 9, Issue 44)

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).


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