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Psychopathology, Neuroscience, and Moral Theory
Abstract
Moral theorists often invoke sociopaths and psychopaths as the quintessential example of a morally impaired agent. In the current debate, both moral rationalists, who argue that moral competence consists in the ability to apply a set of moral rules, and moral sentimentalists, who define moral competence as appropriate emotional responding, refer to evidence regarding these pathologies to support their theory. Neither experimental data on antisocial pathologies nor neuroscientific data provide definitive support for either moral theory, but both of these empirical literatures suggest a deep complexity in the mechanisms supporting moral competence, and perhaps an inadequacy of our current conceptions of "emotional" versus "rational" or "cognitive" systems, and how these contribute to psychopathology and influence "moral" capacities.
... There are some individuals who are psychopaths who do not have any medical diagnosis (e.g., the so-called white collar psychopath). Psychopathy is not a subset of antisocial personality disorder (pace Tankersley 2011, andHerpertz andHabermeyer 2004). ...
Tankersley has provided an interesting collection of data about various groups of antisocial individuals. Is this a paper about the moral reasoning of psychopaths, or is it an attempt to address a philosophical question—whether moral behavior is primarily driven by emotions (moral sentimentalism) or by reasons (moral rationalism)—empirically? I think it attempts a little of both, although I concentrate on the latter.
The trouble with much of the literature on psychopathy is the terminological confusion, and Tankersley has not escaped this. Several disciplines, with their own languages, have an interest in antisocial individuals and use similar sounding words in different ways. It is easy to get confused. Doctors make diagnoses. Antisocial (or dissocial) personality disorder is a medical diagnosis, and has a clear, operationalized definition. By virtue of being a disorder, it must result in some impairment in the functioning of the individual. Psychopathy is a psychological construct, not a diagnosis, and attempts to measure (in a reliable and valid way, using the Psychopathy Checklist) aspects of a person's mind particularly relevant to antisocial behavior. Psychopathy and antisocial personality disorder are different approaches to the same natural phenomenon, but they are not coterminous. There are many individuals with antisocial personality disorder who are not psychopaths. There are some individuals who are psychopaths who do not have any medical diagnosis (e.g., the so-called white collar psychopath). Psychopathy is not a subset of antisocial personality disorder (paceTankersley 2011, and Herpertz and Habermeyer 2004).
Lawyers are also interested in such people, and the English Mental Health Act 1983 contains the term "psychopathic disorder." This is a legal concept with its own legal definition. Again, this clearly has some overlap with the above terms, but they are not the same.
Finally, Tankersley also uses the word "sociopath," sometimes with the rider "acquired." This seems to mean a group of individuals, previously thought to have normal brains, who have an acquired neurological lesion that seems to have led to antisocial behavior and/or to the cognitive/ affective deficits of the psychopath (it is not quite clear from the paper which). This seems to be a resurrection of and a new use for the term coined by Partridge in the 1930s. Its use adds further to the confusion, I fear.
We are told at the outset that "psychopath" in the paper actually refers to the primary psychopath—an individual scoring highly on the Psychopathy Checklist who also has low levels of anxiety and arousal, and is said to commit crimes largely of instrumental (i.e., cold-blooded, planned, and premeditated) violence. From my own clinical experience, these are a rare breed, but they may nonetheless offer interesting insights for the philosophical question posed at the outset.
Unfortunately, I think that the literature cited by Tankersley has not particularly been concerned with helping choose between moral sentimentalism and moral rationalism. And for the very good reason that it has been concerned with other questions. Scientists are interested in understanding the etiology of the condition, clinicians with helping make it better, and policy makers with reducing antisocial behavior [regardless of whether this also makes the perpetrator feel better (or even, worse, as the moral sentimentalists would have it)]. I wonder if there is a problem, too, with the philosophy—is it really morally superior, as Tankersley suggests, for me, a man with no pedophilic interests, not to sexually assault children than it is for Joe, a man with pedophilic desires, to resist them? I suspect I might think that Joe is doing more moral work than me in this instance. I certainly do not feel as though I am doing anything worthy of approbation by not assaulting children, whereas I think Joe might have a claim.
The scientific literature may not have approached the question Tankersley hopes to answer. It does not, however, follow that we might not be able to use empirical evidence to choose between moral rationalism and moral sentimentalism. Surely the appropriate tool would be to compare the psychopath who is also antisocial with the "white collar" psychopath who is not. They presumably have some cognitive and affective deficits in common (because of their psychopathy) but their behavior differs...
Moral philosophy and psychology have sought to define the nature of right and wrong, and good and evil. The industrial turn of the twentieth century fostered increasingly technological approaches that conjoined philosophy to psychology, and psychology to the natural sciences. Thus, moral philosophy and psychology became ever more vested to investigations of the anatomic structures and physiologic processes involved in cognition, emotion and behavior - ultimately falling under the rubric of the neurosciences. Since 2002, neuroscientific studies of moral thought, emotions and behaviors have become known as – and a part of – the relatively new discipline of neuroethics. Herein we present Part 2 of a bibliography of neuroethics from 2002–2013 addressing the “neuroscience of ethics” – studies of putative neural substrates and mechanisms involved in cognitive, emotional and behavioral processes of morality and ethics.
A systematic survey of the neuroethics literature was undertaken. Bibliographic searches were performed by accessing 11 databases, 8 literature depositories, and 4 individual journal searches, and employed indexing language for National Library of Medicine (NLM) Medical Subject Heading databases. All bibliographic searches were conducted using the RefWorks citation management program.
This bibliography lists 397 articles, 65 books, and 52 book chapters that present (1) empirical/experimental studies, overviews, and reviews of neural substrates and mechanisms involved in morality and ethics, and/or (2) reflections upon such studies and their implications. These works present resources offering iterative descriptions, definitions and criticisms of neural processes involved in moral cognition and behaviors, and also provide a historical view of this field, and insights to its developing canon.
I would like to thank Wilson and Spicer for their thought-provoking comments and respond to two of the issues they raise. The first issue I address is the distinction Wilson draws between behavior that conforms to moral norms, and the variegated mechanisms by which such behavior is produced. The distinction is hinted at firstly when Wilson asks "is it really morally superior, as Tankersley suggests, for me, a man with no pedophilic interests, not to sexually assault children than it is for Joe, a man with pedophilic desires, to resist them?" (2011, 366). Wilson here is pointing to an important distinction between moral norms with which group members must comply (do not attack children, do not covet thy neighbor's wife), and moral dispositions, desires or predilections, which are one type of mechanism that can lead an individual to comply with the social rules. Importantly, for many moral norms the majority of group members most likely do not need to engage in self-restraint to behave in ways that conform to the norms, and Wilson is certainly right to think that the minority of members who lack these normative dispositions are "doing more moral work" (2011, 366), insofar as it is effortful for them to override their statistically deviant predilections in order to conform. Both scenarios involve moral, normative behavior, but via different mechanisms; for the normally disposed, there is a naturally occurring match between what society demands of him behaviorally and his preferences; for the self-restraining, dispositionally deviant Joe, some other preference overrides his deviant preferences, enabling him to conform to society's norms. Although most people would commend Joe for his effort, however, my guess is that most people would prefer to be and be surrounded by members who arrive at their moral behavior through the moral dispositions, because this mechanism probably more reliably produces the norm-conforming behavior. Still, Wilson's point that the struggle against one's natural dispositions may constitute true moral superiority is well-taken.
The behavior versus mechanism distinction also arises in Wilson's discussion of the treatment of antisocial offenders. Wilson argues that "it ought to be possible, empirically, to compare programs based primarily on emotional change with those based primarily on rational change" (2011, 366) to arbitrate between the rationalist and sentimentalist views of morality. In other words, if we can teach offenders to behave less antisocially by teaching them to feel bad when they deviate from social norms, this provides support for the sentimentalist position, whereas teaching offenders to behave less antisocially by teaching them consequentialist rules provides support for the rationalist position. Here we must be wary of conflating the moral-conforming behavior and the mechanism by which one arrives at this behavior. The Blair study is a nice illustration of how antisocial offenders might use rule-based heuristics to mimic the moral behavior to which, in normal individuals, a moral disposition gives rise. Violent offenders correctly categorized behaviors as bad, presumably using consequentialist-based reasoning, but were unable to distinguish between what nonviolent offenders distinguished as moral transgressions (e.g., hitting someone) and conventional transgressions (e.g., speaking out of turn in class). If the psychopath were taught some heuristic that mapped onto this moral-conventional distinction, say, for example, transgressions that cause physical harm are worse than those that do not, then he could probably match the nonviolent offenders' discrimination performance. The fact that the nonviolent offenders do not consciously apply such heuristics, however, suggests that moral behavior is being affected in them by some other mechanism, some disposition toward violence or the observable effects it has on others. Rule-based learning is tedious and painstaking, with each new instance requiring a new rule. A significant advantage of a dispositional mechanism, such as an appropriate emotional response to the observable reactions of victims, is the generalizability of these dispositional responses to a range of situations. For example, the rule "Transgressions causing physical harm are worse than transgressions not causing physical harm" does not generalize to moral transgressions involving hurtful verbal abuse. Whereas a normally disposed individual would generalize appropriately by producing a similar response to the observable effects of verbal abuse, the psychopath would require...
Tankersley's paper is a very useful summary of where we stand on two topics: the nature of psychopathy and the nature of moral cognition. The two topics are of course linked: two of the symptoms that mark out psychopaths are poor moral behavior and moral judgment. A key question guiding the discussion is: can evidence from the nature of psychopathy tell us anything about nonpathological moral cognition? Tankersley's view is that currently it cannot—not because of any paucity in the evidence coming from experiments on psychopaths, but because of conceptual confusions in the current state of the debate about moral cognition. In this reply I am a little more upbeat.
Tankersley's discussion of psychopathy takes the form of a helpful summary of the current thinking on the etiology of psychopathy, with a review of some pertinent studies on these subjects' moral cognition. The second part of Tankersley's paper is a discussion of moral cognition; she describes the current division of the debate into the moral rationalists on one side and the sentimentalists on the other, and questions the assumptions underlying the drawing of this divide. Her conclusion is that there is little in current empirical work that can help to decide between the rival views, because of the crude way these views distinguish themselves. In this, comment I suggest that we ought to be a little more upbeat about the prospects for moving the debate between the rationalists and sentimentalists forward in the light of work in psychopathology. I do not find any reason for pessimism—either about the current state of the debate or the future prospects. Most of what I have to say focuses on the second part of the paper—the discussion of the debate between moral rationalists and sentimentalists. I say a little about psychopaths first.
Tankersley distinguishes psychopaths from Damasio's category of acquired sociopaths; the latter are patients who present with symptoms after a lesion to the prefrontal cortex (PFC), amygdala, and/or limbic system. She discusses symptomatic differences and etiological differences between the two, and draws some lessons about what these types of deficit might tell us about nonpathological moral cognition.
One such lesson researchers have drawn is that among acquired sociopaths, we find two distinct impairments that underlie their poor performance on a certain task—Damasio's gambling task. Damasio's gambling task is a task in prudential reasoning—a matter of working out and pursuing what is in one's own best interest. The relation between such reasoning and moral reasoning is an interesting question—and it is a question that divides the moral rationalists and the sentimentalists. Moral rationalists perhaps see prudential reasoning and moral reasoning as distinct competences—dissociable; sentimentalists most likely see them as interdependent. Things may not divide quite so neatly, however; therefore, it is difficult to draw conclusions about moral cognition from experiments on the gambling task.
An interesting conclusion about prudential reasoning can be drawn from the gambling task experiments. Both patients with lesions in the amygdala and the ventromedial (vm)PFC showed similarly impaired performance on the gambling task, but their performance should be explained differently for each subgroup. Both groups fail to settle on choosing cards from the better deck, but in the case of amygdala patients, this is because they do not feel the hits of the draws they make from the bad deck; in the case of vmPFC patients, they feel the hits, but fail to associate these negative emotions with their choice (or with the deck from which the poor choice was made). Explanations such as this of how different patient groups differ provide fuel for building more detailed hypotheses about how prudential reasoning proceeds in normal subjects. It proceeds in a way that involves two stages: feeling emotional hits when a choice turns out poorly and then associating that feeling with the prior choice in a way that modifies future preference away from that choice.
So experiments on psychopaths can tell us about the nature of nonpathological prudential reasoning. Is there any reason to think that there is a difference between moral reasoning and prudential reasoning such that we should not expect analogous...
This project advocates an urgent role for neurobiological evidence and models in the study of altruism. I argue for two claims: that neurobiological evidence should be used to constrain candidate scientific accounts of altruistic behavior, and that neurobiological techniques can be used to elucidate component mechanisms of altruistic behavior.
Chapter 1 reviews the historical progression of theories of altruism, and the empirical observations that motivated their development. A distinction is drawn between evolutionary altruism -- any self-sacrificial, fitness-reducing behavior, and psychological altruism -- self-sacrificial behaviors that are caused by psychological states like desire and motivation. Three theories of psychological altruism are described, and it is argued that the crucial difference between these theories is their conceptions of the role of affect in motivation, and how the processes of affect and motivation contribute to psychological altruism.
Chapter 2 describes dominant theories of motivation and the neurobiological and psychological mechanisms that support motivated behavior. Although the evidence is not conclusive, I argue that our best scientific models and neurobiological evidence support affective models of psychological altruism, and that other models are at best incomplete and possibly implausible in light of neurobiological considerations.
Chapter 3 introduces mind reading approaches to altruism, which argue that the capacity for altruistic motivations depends upon the capacity to represent the psychological states or circumstances of others. I conclude that altruism requires at a minimum the ability to attribute affective experiences to others. Further, I argue that the representations produced by mind reading processes provide a means for distinguishing between self-regarding and altruistic motivations. In contrast with the dominant philosophical theory of psychological altruism, the mind reading model I propose is compatible with the affective theory of motivation depicted in Chapter 2. My own empirical work is described as an example of how neurobiological techniques can reveal the differential role of neural systems in producing self-regarding and altruistic behavior.
Chapter 4 departs from the mechanistic approach to altruism discussed in the previous chapters, and presents an overview of how the fields of philosophy, psychology, psychobiology and genetics, have investigated altruism as a stable characteristic or personality trait. Recent technological advances make this a promising approach for investigating the psychological and neurobiological systems supporting altruistic behavior.
Dissertation
Socialization is the important process by which individuals learn and then effectively apply the rules of appropriate societal behavior. Response modulation is a psychobiological process theorized to aid in socialization by allowing individuals to utilize contextual information to modify ongoing behavior appropriately. Using Hare’s (1991) Psychopathy Checklist and the Welsh (1956) anxiety scale, researchers have identified a relatively specific form of a response modulation deficit in low-anxious, Caucasian psychopaths. Preliminary evidence suggests that the Antisocial Process Screening Device (APSD; Frick & Hare, 2001) may be used to identify children with a similar vulnerability. Using a representative community sample of 308
16-year-olds from the Child Development Project (Dodge, Bates, & Pettit, 1990), we tested and corroborated the hypotheses that participants with relatively low anxiety and high APSD scores would display poorer passive avoidance learning and less interference on a spatially separated, picture-word Stroop task than controls. Consistent with hypotheses, the expected group differences in picture-word Stroop interference were found with male and female participants, whereas predicted differences in passive avoidance were specific to male participants. To the extent that response modulation deficits contributing to poor socialization among psychopathic adult offenders also characterize a subgroup of adolescents with mild conduct problems, clarification of the developmental processes that moderate the expression of this vulnerability could inform early interventions.
Leading conceptions of psychopathy originated from a clinical perspective, which assumed abnormality and sought to explain it. This perspective has led to three related potential explanations of psychopathy: the sociological (i.e. the psychopath as nonconformist); the physiological (i.e. the psychopath as characterized by a deficiency in the behavioral inhibition system); and the developmental (i.e. the psychopath as a product of poor early socialization). These three models are examined in this paper, and all are found to be deficient in explanatory power, even when combined. An alternative approach to psychopathy is suggested, which begins with the assumption that psychopathy is not a mental disorder, but rather reflects a philosophy of life centering around the trivialization of others. It is further suggested that such a philosophy of life may be far more pervasive than is generally recognized.
The development of the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1994) included 12 field trials to assess proposed revisions. This article provides results from the antisocial personality disorder (APD) field trial that was conducted to obtain data of relevance to the proposals for simplification and for the inclusion of more traditional traits of psychopathy. Provided herein are the results from 4 sites that had sampled from populations of particular relevance to the diagnosis of APD (i.e., prison inmates, psychiatric inpatients, outpatients with substance use disorders, and homeless persons). The results indicated that some items from the 3rd revised Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1987) could be deleted without affecting the diagnosis. The field trial provided mixed support for the proposal to include more traditional traits of psychopathy.
The literature on autonomic responsivity in psychopaths is reviewed and critically evaluated with Fowles' (1980) psychophysiological adaptation of Gray's two-factor learning theory used as an organizing framework. It is concluded that, although much recent research has focused on assessing psychopaths' response to punishment in familiar paradigms, several intriguing new paradigms for assessing psychopaths' autonomic responsivity have been developed. A new conceptualization of the existing data is considered involving a motivational imbalance theory based on the Gray/Fowles model. This theory connects autonomic psychophysiological research on psychopaths to literatures on cognition, emotion, and behavior. Research directions for evaluating the validity of the theory are proposed.
In the Cambridge Study in Delinquent Development, 411 South London males have been followed up since age 8. This article investigates the ability of psychosocial risk factors measured at age 8 - 10 to predict antisocial personality measures at ages 18 and 32 and convictions between ages 21 and 40. The most important childhood predictors were a convicted parent, large family size, low intelligence or attainment, and child-rearing factors, including a young mother and a disrupted family. The accuracy of prediction of antisocial personality at age 32 on the basis of childhood risk factors measured more than 20 years before was surprising: nearly half of boys with a convicted parent at age 10 were antisocial at age 32, compared with one in six of the remainder. Over 60% of boys very high risk at age 8 - 10 became antisocial at age 32. While the present research shows how far adult antisocial and criminal behavior can be predicted in childhood, more research is needed to establish the precise causal mechanisms involved.
Psychopaths are not only antisocial, but also have a callous and unemotional personality profile. This article selectively reviews evidence that psychopathic personality traits are an important factor in understanding and predicting the development of persistent antisocial conduct. Cognitive neuroscience research and more tentative genetic work on psychopathy will be discussed, especially as they relate to possible developmental trajectories to psychopathy.
A personality-based approach has been successful in clarifying the conceptual boundaries of psychopathy and delineating a group of antisocial individuals with a distinct profile of offending and clear neurocognitive markers indicating problems in processing distress in others and punishment directed to oneself. These markers are also present in children with psychopathic tendencies, suggesting that psychopathy may be a developmental disorder. The neurocognitive profile relates to the callous and unemotional personality traits at the core of psychopathy and may index particular vulnerability to persistent antisocial conduct. Preliminary twin studies suggest that personality traits at the core of psychopathy are much more highly heritable than other personality traits. There are as yet no molecular genetic studies of psychopathy.
It is argued that an interdisciplinary approach that integrates cognitive neuroscience and genetics will enhance understanding of the development of psychopathy.
A great deal of human behavior and motivation is based on the intrinsic emotional significance of rewarding or aversive events, as well as on the associations formed between such emotional events and concurrent environmental stimuli. Recent functional neuroimaging studies have implicated the ventral striatum, orbitofrontal cortex (OFC), and amygdala in the representation of reward values and/or in the anticipation of rewarding events. Here, we use functional magnetic resonance imaging to compare brain activation during the presentation of reward with that during presentation of (conditioned) stimuli that have been paired previously with reward. Specifically, we aimed to investigate conditioned reward in the absence of explicit reward anticipation. Twenty-two healthy volunteers were scanned while monochrome visual patterns were incidentally associated with reward or negative feedback in the context of a simple card game. In the subsequent session, visual patterns, including the conditioned stimuli, were presented without reward or negative feedback, and the affective valence of these stimuli was assessed behaviorally. The presentation of reward compared with negative feedback activated the ventral striatum and OFC. Activation in the same OFC region was observed when, in the subsequent session, subjects passively viewed the stimuli that had been paired with reward, without the administration of reward and with subjects being essentially unaware of the conditioning manipulation. These findings suggest that the OFC in humans plays an important role in the representation of both rewarding stimuli and conditioned stimuli that have acquired reward value.