Abstract
This dissertation focuses on empathy and disturbed empathy processing in psychopathy and, by extension, various computational tasks that may point to possible proxies for the empathy construct. Furthermore, the central question was whether the neuropeptide oxytocin can ameliorate psychopathic symptoms in psychopathic patients. We developed the Zipper Model of Empathy,
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a dynamic model in which bidirectional changes in empathy processing are induced by "zipping" forces, namely contextual factors and psychological (i.e., attentional and motivational) factors. Consequently, "zipping up" represents approaching mature empathy while "unzipping" symbolizes either a reduction of empathy or its loss altogether. In our first sub-study of oxytocin effects, we examined short-latency facial mimicry of both the corrugator supercilii and the zygomaticus major within 600 ms after stimulus as this may have diagnostic value for psychopathy. Oxytocin did not enhance short-latency mimicry responses of both facial muscles. However, psychopathic patients showed significantly weaker short-latency zygomaticus responses to happy faces, while there was a trend toward significantly weaker short-latency corrugator responses to angry faces. We therefore posit a lifetime developmental deficit in psychopathy pertaining short-latency mimicry of emotional facial expressions. Another sub-study focussed on reactive social dominance. Psychopathic patients were not more dominant compared to normal controls. However, contrary to normal controls, in the patients the severity of psychopathy was positively correlated with reactive dominance. Although oxytocin yielded no effect on reactive dominance in general, oxytocin was found to abolish the relationship between psychopathy severity and reactive dominance. We also explored moral decision-making. No differences in the percentage of utilitarian choices between the two groups were found. Contrary to our hypothesis, oxytocin did not reduce utilitarian choices in favor of deontological choices. Psychopathy severity in the normal controls was positively related to the percentage of utilitarian choices, but not in the psychopathic patients. On the contrary, psychopathy severity was negatively related to the percentage of utilitarian choices, meaning that the higher the PCL-R total score, the more deontological choices the psychopathic patients made. Finally, in the psychopathic patients, we examined cortisol and testosterone saliva levels (i.e., baseline levels and their change over time) and their relation to the psychopathy severity. Oxytocin did not affect steroid levels. We further concluded that the dual-hormone hypothesis appears to be incorrect in relation to psychopathy severity. Both steroid levels, particularly cortisol, decreased across the test procedure, which was compatible with the circadian rhythm of both. Only in those who scored high on the PCL-R facet 1 did steroid levels remain stable, while baseline testosterone levels were higher in psychopathic patients with high scores on the PCL-R facet 4. Together, these results confirm that basal steroid levels, as well as their fluctuation over time, can partially predict psychopathy severity. Combined with our finding that inflexibility of testosterone is positively linked to psychopathic patients who scored high in PCL-R facet 1, we therefore suggested that high testosterone levels might facilitate the actual expression of antisocial, mostly reactive aggressive, behavior and that inflexibility over time of testosterone (and cortisol) could pave the way to instrumental aggression.
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