Comparison
group
Gain
Loss
Value
Figure 7.1.: The predicted data pattern for healthy individuals as well as one of the predicted data patterns for individuals with psychopathy on the Subjective Value Task.
Preliminary work with healthy individuals is providing some support for these predictions. The predictions for individuals with psychopathy on this task are more complicated. Thus, assuming that they functionally simply operate at a lower level of sensitivity to reward, and even lower level of sensitivity to punishment, they should show the same S-shaped function as healthy individuals, only at a lower level (see Figure 7.1.). However, if they have a differential way of processing reward (and possibly punishment) they might not only take longer to learn the task overall, but also will not show the concave shape. Upcoming studies will test these predictions.
The affective priming data presented in Chapter Five indicated that individuals with psychopathy also operated on the basis of semantic information that was more weakly associated with affective information than comparison individuals, A second way that I would like to investigate this issue is by assessing the degree to which such individuals might show Optimistic Bias. Optimist Bias (OB) is the tendency to consider oneself invulnerable (or less likely compared to other individuals) to experience negative life events. It is found across cultures and age groups and is believed to exist in about 90% of the general population. OB is typically measured by questionnaires where people are asked to consider what the likelihood is of experiencing a negative life event (e.g., diabetes) compared to other individuals o f their age. There are two main accounts of OB. First, that OB is the product o f a cognitive defense mechanism to high levels of anxiety (Baker and Chapman 1962). If this position is correct, and given the reduced levels o f anxiety in individuals with psychopathy (Patrick 1994; Frick, Lilienfeld et al. 1999; Verona, Patrick et al. 2001) we must predict that individuals with psychopathy will not show OB. Secondly, OB is the product of ‘cognitive errors’; an individual’s lack of experience with the problem makes it difficult to imagine how it might affect themselves (Weinstein 1980; Weinstein 1982; Weinstein 1987). If OB simply reflects poor risk assessment then individuals with psychopathy may show appropriate levels of OB.
I have developed an assessment of OB based on the work of Weinstein (Weinstein 1980; Weinstein 1982; Weinstein 1987). In this paradigm, participants are presented with a questionnaire consisting of 20 negative life events (e.g., tooth decay, diabetes, becoming a murder victim) and asked to consider their likelihood o f experiencing each of these negative life events. In addition, the participants are presented with a questionnaire consisting o f 20 positive life events (e.g., winning the lottery). Finally, because OB is considered by some to be the product of a lack o f experience with a given event, I have administrated a questionnaire concerning their experience o f life events included in the first two questionnaires.
Finally, in Chapter Six, positive and negative picture content was found to interfere with the incongruent condition in a Number Stroop paradigm. The suggestion was made that the emotional material interfered with the numerical processing. This, of course, allows the prediction regarding individuals with psychopathy, that they will show superior performance (i.e., experience no interference and so respond faster), relative to comparison individuals, on these incongruent trials when they are presented together with emotional material.
7.3.2.: Examination of Reward/ Punishment Processing in Other Psychiatric Disorders In Chapter One I described how many other mood and anxiety disorders, in addition to psychopathy, have been linked to reward/ punishment processing abnormalities. Thus, Major Depressive Disorder (MDD) has been linked to a heightened sensitivity to negative information (Murphy, Sahakian et al. 1999), or alternatively attenuated sensitivity to positive information (Henriques, Glowacki et al. 1994). Generalized Anxiety Disorder (GAD) has also been linked to over-sensitivity to threat-related negative stimuli (Kagan and Snidman 1999). In contrast. Mania has been linked to an affective bias to positive stimuli (Murphy, Sahakian et al. 1999). However, although there have been speculations that these populations have such imbalance, relatively little empirical work has been conducted with these populations regarding reward and punishment processing. The tasks developed in this thesis, the Differential Reward/ Punishment Learning Task, the Affective Priming task, and the Affective Stroop task are all currently being applied to children and adults with GAD, adults with PTSD and children with Bipolar Disorder. Recent results with respect to the Affective Stroop paradigm and PTSD suggests increased interference on the incongruent conditions when these are presented together with negative, threat related material but not when presented together with positive material. In other words, as would be expected clinically, individuals with PTSD may indeed show a heightened sensitivity to threat. Other preliminary results with children with Bipolar Disorder and the Differential Reward/ Punishment Learning Task suggest generalized impairment relative to comparison individuals. In short, these children show no specific impairments for reward or punishment related processing but rather a generalized impairment in evaluating objects associated with different levels of reward/ punishment. On the basis of the IBS model, described in Chapter One, I have suggested that this is most likely to be due to dysfunction in the hypothesized medial orbital frontal cortical units allowing response selection.
I myself will be applying these tasks to patients with Major Depressive Disorder (MDD), which is probably the most exciting population for investigation as they might present the inverse of psychopaths. Thus, MDD has been linked to both a heightened sensitivity to negative information (Murphy, Sahakian et al. 1999) as well as attenuated sensitivity to positive information (Henriques, Glowacki et al. 1994). The predictions o f both these positions with respect to the tasks described in this thesis (as well as those briefly outlined above) are clear. For example, if patients with MDD have a heightened sensitivity to negative information they should show superior performance for discriminating objects associated with different levels of punishment on the Differential Reward/ Punishment Learning Task as well as superior facilitation by negative, relative to neutral, primes for negative targets in the Affective Priming
task. If patients with MDD have a attenuated sensitivity to positive information, their performance should be impaired on tasks involving the discrimination of objects associated with different levels o f reward. In addition, they should show reduced facilitation by positive primes, relative to neutral primes, for negative targets in the affective priming task.
7.3.3.: Specification of the Neuro-Chemical Basis of Reward/ Punishment Processing On the basis of the work presented in this thesis, I would argue that positions suggesting global dysfunction in specific neural systems in individuals with psychopathy need to be reconsidered. Positions suggesting amygdala dysfunction (Patrick 1994; Blair, Morris et al. 1999; Blair 2001), orbital fi-ontal cortex dysfunction (Damasio 1994; LaPierre, Braun et al. 1995) or even anterior cingulate dysfunction (Kiehl, Smith et al. 2001) all face the difficulty that these systems process both reward and punishment related information. None o f them provide a convincing explanation for why the impairment seen in individuals with psychopathy should be more marked for the processing o f stimuli associated with punishment rather than stimuli associated with reward. I have argued that the data I have collected in this thesis suggests that a neuro-chemical account o f psychopathy may be more appropriate. This is not to deny that individuals with psychopathy suffer from amygdala dysfunction. It is however to suggest that this position must be constrained; i.e., individuals with psychopathy may have particular problems with those functions of the amygdala that require neurotransmitter X.
If the above argument is correct it suggests that it would be useful to determine which neurotransmitters may be involved in the mediation o f the paradigms developed in the current thesis. In particular, it would be useful to know which neurotransmitter systems, when modulated, give rise to effects that are more pronounced for the processing of punishment- related material.
Recent data by Rogers et al. suggests that the non-specific beta-adrenoceptor blocker, propranolol, attenuated discrimination between the magnitude o f possible losses in situations where the probability o f winning was relatively low and the probability of suffering losses was relatively high (Rogers, Lancaster et al. submitted). That is, their data suggested that noradrenaline (NA) is involved in mediating the impact of aversive cues in human choice (Rogers, Lancaster et al. submitted). One exciting possibility is therefore that NA function is compromised in individuals with psychopathy, leading to impaired processing of aversive cues. Further support for this suggestion comes from studies linking NA abnormalities to antisocial behaviour/ Conduct Disorder (Rogeness, Cepeda et al. 1990; Rogeness, Javors et al. 1990; Raine 1993). In this regard it is interesting to note that NA function appears to be increased in
a range of anxiety disorders (Chamey, Heninger et al. 1984); i.e., in populations that are hypothesized to show a very different pattern of result to that o f individuals with psychopathy on reward/ punishment processing paradigms. Studies have shown that the a-2A adrenoceptor, which functions primarily as an autoreceptor, is abundant in the amygdala and orbitoffontal cortex (MacDonald and Scheinin 1995). In rodents, dense labelling of Oü-IA and IB adrenoceptor mRNA in nuclei of the amygdala and throughout the cerebral cortex has also been demonstrated (Pieribone, Nicholas et al. 1994). There is evidence that this is the case in humans also (Zilles, Qu et al. 1993; Ferry, Roozendaal et al. 1999).
A further future direction for my work therefore is to explore the impact of manipulations o f NA functioning on performance o f the tasks presented in this thesis.
7.4.: Summary
This thesis started off considering Garry who plunged to his death demonstrating the strength of the windows on the 24^ floor of his building. I suggested that most people are not nominated for Darwin awards, as they have two types of systems to regulate and help guide their behaviour: One system which regulates behaviour according to task demands or goals, and a second system which regulates behaviour according to reinforcement history. Now, these two systems can be difficult to disentangle. Executive function (EF) and emotion interact in guiding our behaviour. Thus, Garry probably carried out his actions not due to a faulty EF or stimulus-reinforcement mechanism, but due to the (faulty) overriding of a sense of danger in lieu of wanting to impress the visiting law students. The difficulty of teasing apart these two systems is reflected in the fact that just about all major disorders have been proposed to be the consequence of EF or alternatively a punishment insensitivity - or both. The first challenge then of affective neuroscience is to tease out the constituent parts of these two systems, hi this thesis I have developed a series of new measures for the indexing o f these two systems, and applied them to a disorder which has been associated with a dichotomous EF or fear/ punishment problem.
The second challenge o f affective neuroscience is to understand the modulatory effects o f emotion on EF. This second challenge is of less importance in psychopathy where there is a hypo-active amygdala or emotional input, but it is o f immense importance in relation to disorders such as MDD and Posttraumatic Stress Disorder where the strong suggestion is that there is a hyper-active amygdala or emotional input (Drevets 2001; Blair and Chamey 2003). In this thesis I have developed an instrument that will allow for an increased understanding of the emotional effects of emotion on EF. It may be too late for Garry, but others can be helped.
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