, the description of the functional contributions of the two core regions that are dysfunctional in psychopathy, and the data indicating dysfunction in the functioning of these regions in individuals with the disorder are presented. In this section, a brief consideration of why this dysfunction may lead to the development of the disorder is provided.
As noted above, the amygdala is crucial for stimulus–reinforcement learning and responding to emotional expressions, particularly fearful expressions that, as reinforcers, are important initiators of stimulus–reinforcement learning. Moreover, the amygdala is involved in the formation of both stimulus–punishment and stimulus–reward associations. Individuals with psychopathy show impairment in stimulus–reinforcement learning (whether punishment or reward based) and responding to fearful and sad expressions. It is argued that this impairment drives much of the syndrome of psychopathy. Stimulus–reinforcement learning is crucial for socialization, for learning that some things are bad to do, and individuals with psychopathy fail to take advantage of standard socialization techniques (Wootton et al. 1997
). As such, they are more likely to learn to use antisocial strategies to achieve their goals. The reduced amygdala responding also diminishes empathy-based learning following the witnessing of another's distress and leads to reduced empathy generally. Finally, the impairment in stimulus–reward learning may relate to the reduced attachment reported in this disorder (Hare 2003
); individuals with psychopathy may find their carers to be rewarding stimuli and consequently be less motivated to maintain contact with them.
VmPFC is considered critical for the representation of reinforcement information that can then be used by other structures, such as dorsomedial frontal cortex, to implement behaviour. Impairment in vmPFC functioning means that individuals with psychopathy will show impaired decision making. This will contribute to their disordered lifestyle and may increase the risk for drug abuse. Moreover, because vmPFC is very important for successful decision making, its dysfunction will increase the probability that individuals with the disorder will make less than optimal decisions when attempting to achieve their goals. As such this will increase the risk for frustration and potentially frustration-based reactive aggression.
Can the model described above explain all aspects of psychopathy? The answer is almost certainly not. There are aspects of psychopathy (e.g. the grandiose sense of self, superficial charm), which are not clear developmental consequences of the impairment described above. It will be interesting to determine whether these relate to additional impairments or they are consequences of how the dysfunction described interacts with the individual's social environment.
Importantly, the above suggests pharmacological treatment strategies. While some pharmacological compounds, such as propranolol, decrease amygdala activity, others, such as yohimbine, increase it. Theoretically, it might be possible to increase the responsiveness of the systems described above such that clinically based socialization strategies (e.g. empathy induction and victim awareness) might allow the individual to form more appropriate associations regarding the distress of others and actions that harm others. In short, it is to be hoped that the increased basic understanding of this disorder may soon be translated into therapeutic strategies that will help the individuals concerned.