THE FIRST EDITION of this book was based primarily on experience with adult male psychopaths hospitalized in a closed institution. Though a great many other psychopaths had come to my attention, most of the patients who were observed over years and from whom emerged the basic concepts presented in 1941 were from this group. During the next decade a much more diverse group became available. Female patients, adolescents, people who had never been admitted to a psychiatric hospital, all in large (...) numbers, became available for study and afforded an opportunity to observe the disorder in a very wide range of variety and of degree. This additional clinical experience, helpful comment in the reviews of the first edition, enlightening discussion with colleagues, and an improved acquaintance with the literature all contributed to modify concepts formulated approximately ten years earlier. In attempting to revise the book for the second edition (1950), I found it was impossible to do justice to the subject by minor additions, deletions, and modifications. It was necessary to write a new and much larger book. (shrink)

Psychopathic behavior has long been attributed to a fundamental deficit in fear that arises from impaired amygdala function. Growing evidence has demonstrated that fear-potentiated startle (FPS) and other psychopathy-related deficits are moderated by focus of attention, but to date, no work on adult psychopathy has examined attentional modulation of the amygdala or concomitant recruitment of relevant attention- related circuitry. Consistent with previous FPS findings, here we report that psychopathy-related differences in amygdala activation appear and disappear as a function of goal-directed (...) attention. Specifically, decreased amygdala activity was observed in psychopathic offenders only when attention was engaged in an alternative goal-relevant task prior to presenting threat-relevant information. Under this condition, psychopaths also exhibited greater activation in selective-attention regions of the lateral prefrontal cortex (LPFC) than did nonpsychopaths, and this increased LPFC activation mediated psychopathy’s association with decreased amygdala activation. In contrast, when explicitly attending to threat, amygdala activation did not differ in psychopaths and nonpsychopaths. This pattern of amygdala activation highlights the potential role of LPFC in mediating the failure of psychopathic individuals to processfear and other important information when it is peripheral to the primary focus of goal-directed attention. (shrink)

Research on passive avoidance learning has demonstrated reliable differences between psychopaths and controls when avoidance errors result in electric shock but not in loss of money (Schmauk, 1970). Using monetary punishments, Newman, Widom, and Nathan (1985) found that psychopathic delinquents performed more poorly than controls in an experimental paradigm employing monetary reward as well as the avoidance contingency. The present study was conducted to replicate and extend these findings using adult psychopaths and a computer controlled task. Sixty white male prisoners (...) were assigned to groups using Hare's (1980) Psychopathy Checklist and administered a "go/no-go" discrimination task involving monetary incentives. One condition entailed competing reward and punishment contingencies; the other, two punishment contingencies. As predicted, psychopaths made significantly more passive avoidance errors than nonpsychopaths when the task contained competing goals (p < .05)but performed as well as controls when the subjects' only goal was avoiding punishment. Results corroborate earlier findings that psychopaths are relatively poor at learning to inhibit reward-seeking behavior that results in monetary punishment. (shrink)

This study investigates the ability of individuals with psychopathy to perform passive avoidance learning and whether this ability is modulated by level of reinforcement/punishment. Nineteen psychopathic and 21 comparison individuals, as defined by the Hare Psychopathy Checklist Revised (Hare, 1991), were given a passive avoidance task with a graded reinforcement schedule. Response to each rewarding number gained a point reward specific to that number (i.e., 1, 700, 1400 or 2000 points). Response to each punishing number lost a point punishment specific (...) to that number (i.e., the loss of 1, 700, 1400 or 2000 points). In line with predictions, individuals with psychopathy made more passive avoidance errors than the comparison individuals. In addition, while the performance of both groups was modulated by level of reward, only the performance of the comparison population was modulated by level of punishment. The results are interpreted with reference to a computational account of the emotional learning impairment in individuals with psychopathy. (shrink)

Linking psychopathy to a specific brain abnormality could have significant clinical, legal, and scientific implications. Theories on the neurobiological basis of the disorder typically propose dysfunction in a circuit involving ventromedial prefrontal cortex (vmPFC). However, to date there is limited brain imaging data to directly test whether psychopathy may indeed be associated with any structural or functional abnormality within this brain area. In this study, we employ two complementary imaging techniques to assess the structural and functional connectivity of vmPFC in (...) psychopathic and non-psychopathic criminals. Using diffusion tensor imaging, we show that psychopathy is associated with reduced structural integrity in the right uncinate fasciculus, the primary white matter connection between vmPFC and anterior temporal lobe. Using functional magnetic resonance imaging, we show that psychopathy is associated with reduced functional connectivity between vmPFC and amygdala as well as between vmPFC and medial parietal cortex. Together, these data converge to implicate diminished vmPFC connectivity as a characteristic neurobiological feature of psychopathy. (shrink)

A common feature of the antisocial, rule-breaking behavior that is central to criminal, violent and psychopathic individuals is the failure to follow moral guidelines. This review summarizes key findings from brain imaging research on both antisocial behavior and moral reasoning, and integrates these findings into a neural moral model of antisocial behavior. Key areas found to be functionally or structurally impaired in antisocial populations include dorsal and ventral regions of the prefrontal cortex (PFC), amygdala, hippocampus, angular gyrus, anterior cingulate and (...) temporal cortex. Regions most commonly activated in moral judgment tasks consist of the polar/medial and ventral PFC, amygdala, angular gyrus and posterior cingulate. It is hypothesized that the rule-breaking behavior common to antisocial, violent and psychopathic individuals is in part due to impairments in some of the structures (dorsal and ventral PFC, amygdala and angular gyrus) subserving moral cognition and emotion. Impairments to the emotional component that comprises the feeling of what is moral is viewed as the primary deficit in antisocials, although some disruption to the cognitive and cognitive-emotional components of morality (particularly self-referential thinking and emotion regulation) cannot be ruled out. While this neurobiological predisposition is likely only one of several biosocial processes involved in the etiology of antisocial behavior, it raises significant moral issues for the legal system and neuroethics. (shrink)