Psychopathy can be considered one of the prototypical disorders associated with empathic dysfunction. Reference to empathic dysfunction is part of the diagnostic criteria of psychopathy (Hare, 1991). The very ability to inflict serious harm to others repeatedly can be, and is (Hare, 1991), an indicator of a profound disturbance in an appropriate ‘empathic’ response to the suffering of another. The goal of this chapter will be to consider the nature of the empathic impairment in psychopathy. First, I will consider the (...) disorder of psychopathy and the definition of empathy. Second, I will consider whether individuals with psychopathy are impaired in ‘cognitive empathy’ or Theory of Mind. Third, I will consider the cognitive and neural architecture mediating ‘emotional empathy’. Fourth, I will consider whether individuals with psychopathy are impaired in ‘emotional empathy’. (shrink)

Davey reviews evidence purporting to distinguish between two accounts of selective associations – expectancy bias and evolved predispositions, although these hypotheses largely apply to different levels of causal analysis. Criticisms of primate studies in which subjects lack prior exposure to stimuli seem uncompelling. Expectancies may sometimes serve as proximal mediators in selective associations, but other factors, both proximate and ultimate, are clearly also involved.

Most phobias are focussed on a small number of fear-inducing stimuli (e.g., snakes, spiders). A review of the evidence supporting biological and cognitive explanations of this uneven distribution of phobias suggests that the readiness with which such stimuli become associated with aversive outcomes arises from biases in the processing of information about threatening stimuli rather than from phylogenetically based associative predispositions or “biological preparedness.” This cognitive bias, consisting of a heightened expectation of aversive outcomes following fear-relevant stimuli, generates and maintains (...) robust learned associations between them. Some of the features of such stimuli which determine this expectancy bias are estimates of how dangerous they are, the semiotic similarity between them and their aversive outcomes, and the degree of prior fear they elicit. Ontogenetic and cultural factors influence these features of fear-relevant stimuli and are hence important in determining expectancy bias. The available evidence does not exclude the possibility that both expectancy biases and specific evolved predispositions coexist, but the former can explain a number of important findings that the latter cannot. (shrink)

A review of data concerning the uneven distribution of phobias suggests that nonassociative, ethological models can account for most of tile important findings that cannot be attributed to expectancy biases. The origin of a variety of fears that appear in fixed developmental patterns across divergent cultures and species can best be explained by biological models.

In this paper we integrate claims and findings concerning the social functions of emotions at the individual, dyadic, group, and cultural levels of analysis. Across levels of analysis theorists assume that emotions solve problems important to social relationships in the context of ongoing interactions. Theorists diverge, however, in their assumptions about the origins, defining characteristics, and consequences of emotions, and in their preferred forms of data. We illustrate the differences and compatibilities among these levels of analysis for the specific case (...) of embarrassment. We close by suggesting research strategies that incorporate a social-functional perspective. (shrink)

Dans ce texte, nous proposons un cadre, qui vise à intégrer les contributions des approches constructionnistes et biologiques dans un domaine précis, celui des maladies mentales. Pour ce faire, nous utiliserons quelques propositions récentes faites par des philosophes de la biologie — plus spécifiquement les idées avancées par les tenants de la « théorie des systèmes développementaux » ainsi que la notion d’« enracinement génératif » .In this paper, we are proposing a framework to integrate the core insights of the (...) constructivist and biological approaches of mental illness. In order to do so, we will use some recent propositions by philosophers of biology, specifically ideas put forth by «developmental system theory» and the notion of «generative entrenchment». (shrink)

There is disagreement in the literature about the exact nature of the phenomenon of empathy. There are emotional, cognitive, and conditioning views, applying in varying degrees across species. An adequate description of the ultimate and proximate mechanism can integrate these views. Proximately, the perception of an object's state activates the subject's corresponding representations, which in turn activate somatic and autonomic responses. This mechanism supports basic behaviors that are crucial for the reproductive success of animals living in groups. The Perception-Action Model, (...) together with an understanding of how representations change with experience, can explain the major empirical effects in the literature. It can also predict a variety of empathy disorders. The interaction between the PAM and prefrontal functioning can also explain different levels of empathy across species and age groups. This view can advance our evolutionary understanding of empathy beyond inclusive fitness and reciprocal altruism and can explain different levels of empathy across individuals, species, stages of development, and situations. Key Words: altruism; cognitive empathy ; comparative; emotion; emotional contagion; empathy ; evolution; human; perception-action; perspective taking. (shrink)

Emotional disturbances are central to diverse psychopathologies. In this article, we argue that the functions of emotion are comparable for persons with and without psychopathology. However, impairment in one or more components of emotional processing disrupts the achievement of adaptive emotion functions. Adopting a theoretical conceptualisation of emotional processes that stresses activity in centrally mediated approach and withdrawal systems, we discuss the role of emotion in several forms of psychopathology, including major depression, some of the anxiety disorders, psychopathy, and schizophrenia. (...) In doing so, we highlight the nature of emotion disturbance and attendant behavioural and cognitive deficits. Finally, we discuss the merits of this approach for conceptualising emotional disturbance in psychopathology. (shrink)

Empathy is a lay term that is becoming increasingly viewed as a unitary function within the field of cognitive neuroscience. In this paper, a selective review of the empathy literature is provided. It is argued from this literature that empathy is not a unitary system but rather a loose collection of partially dissociable neurocognitive systems. In particular, three main divisions can be made: cognitive empathy , motor empathy, and emotional empathy. The two main psychiatric disorders associated with empathic dysfunction are (...) considered: autism and psychopathy. It is argued that individuals with autism show difficulties with cognitive and motor empathy but less clear difficulties with respect to emotional empathy. In contrast, individuals with psychopathy show clear difficulties with a specific form of emotional empathy but no indications of impairment with cognitive and motor empathy. (shrink)

This commentary acknowledges the importance of Davey's biocognitive approach to the uneven distribution of fears on the basis of its contribution to a human model for understanding fear. An integrated heredity-environment and developmental transactional approach based on field/system theory is recommended in place of the mechanistic heredity × environment interactionism that Davey uses to explain behavioral ontogeny.

In his critique of preparedness theory, Davey does not address the limitations of adaptationism. The purpose of this commentary is to outline problems that arise when one assumes that mental illness (e.g., phobic disorder)musthave had adaptive significance for it to have survived the vicissitudes of natural selection.

Failure to find an obvious or linear relationship between a developmental experiential factor and a developmental outcome often leads investigators to posit concepts such as “biological preparedness” and “evolved predispositions” that allude to hypothetical geneticmechanisms that may not exist. However, experiential nonlinearities alone may explain the development of certain instinctive behaviors, as shown by studies on alarm call responsivity in mallard ducklings.

This paper proposes that human expression of pain in the presence or absence of caregivers, and the detection of pain by observers, arises from evolved propensities. The function of pain is to demand attention and prioritise escape, recovery, and healing; where others can help achieve these goals, effective communication of pain is required. Evidence is reviewed of a distinct and specific facial expression of pain from infancy to old age, consistent across stimuli, and recognizable as pain by observers. Voluntary control (...) over amplitude is incomplete, and observers can better detect pain that the individual attempts to suppress rather than amplify or simulate. In many clinical and experimental settings, the facial expression of pain is incorporated with verbal and nonverbal vocal activity, posture, and movement in an overall category of pain behaviour. This is assumed by clinicians to be under operant control of social contingencies such as sympathy, caregiving, and practical help; thus, strong facial expression is presumed to constitute an attempt to manipulate these contingencies by amplification of the normal expression. Operant formulations support skepticism about the presence or extent of pain, judgments of malingering, and sometimes the withholding of caregiving and help. To the extent that pain expression is influenced by environmental contingencies, however, could equally plausibly constitute the release of suppression according to evolved contingent propensities that guide behaviour. Pain has been largely neglected in the evolutionary literature and the literature on expression of emotion, but an evolutionary account can generate improved assessment of pain and reactions to it. (shrink)

Imitation and mirroring processes are necessary but not sufficient conditions for children to develop human sociality. Human sociality entails more than the equivalence and connectedness of perceptual experiences. It corresponds to the sense of a shared world made of shared values. It originates from complex ‘open’ systems of reciprocation and negotiation, not just imitation and mirroring processes that are by definition ‘closed’ systems. From this premise, we argue that if imitation and mirror processes are important foundations for sociality, human inter-subjectivity (...) develops primarily in reciprocation, not just imitation. Imitation provides a basic sense of social connectedness and mutual acknowledgment of existing with others that are ‘like me.’ However, it does not allow for the co-construction of meanings with others. For human sociality to develop, imitation and mirroring processes need to be supplemented by an open system of reciprocation. Developmental research shows that from the second month, mirroring, imitative, and other contagious emotional responses are by-passed. Imitation gives way to first signs of reciprocation (primary intersubjectivity), joint attention to objects (secondary intersubjectivity), the emergence of values that are jointly represented and negotiated with others (tertiary intersubjectivity), and eventually the development of an ethical stance accompanying theories of mind by 4 years of age. We review this development and propose that if mirroring processes enable individuals to bridge their subjective experiences, human inter-subjectivity proper develops from reciprocal social exchanges that lead to value negotiation and mutual recognition, both cardinal trademarks of human sociality. (shrink)

Davey's discussion of phobias is criticized because of the lack of distinctions between the various classes of phobias. Psychopharmacological evidence indicates differing pathophysiologies. Clinical psychopharmacological distinctions are not congruent with either a strict phylogenetic preparedness model or with cognitive biases. Davey's critique of the laboratory bred animal studies seems far fetched. His hypothesis concerning the importance of historical significance is clearly ad hoc rather than based on comparative data.

Behavioral research suggests that rule-governed behavior should be less sensitive to environmental changes and thus more resistant to extinction (disconfirmation) than contingency-governed behavior. The opposite is implied in Davey's discussion of ontogenetic and phylogenetic contributions to fear development. The generality of the behavioral findings and their apparent inconsistency with the present article should be further explored with more sensitive research paradigms.

Davey suggests that increased resistance to extinction of CRs conditioned to fear-relevant stimuli may be due to more persistent expectancies of the UCS following these stimuli. However, this viewpoint is contradicted by existing empirical evidence that fear-relevant CRs survive an extinction trials series producing extinction of expectancies whereas CRs conditioned to non-fear-relevant CSs do not.

Studies on associative learning in normals and patients need appropriate dependent measures which are sensitive enough to reflect stimulus-specific responses and also consider the context in which the conditioning takes place. Patient's fear responses, once acquired, seem to be maintained by specific cognitive biases such as individual belief systems and a tendency to stay consistent with their previous judgments.

We endorse Davey's view that expectancy processes are intimately involved in fear reactions, but question his model on three grounds. First, the mechanism for generating expectancy bias to both ontogenetic and phylogenetic stimuli is not spelled out. Second, the selective association component is unnecessary. Third, the model fails to provide a clear explanation for the irrationality of phobic reactions.

This commentary focuses upon two issues raised by Davey's target article: (1) whether there are certain core features of stimuli we learn to fear, rather than specific types of objects or situations, which implies some element of innateness; and (2) whether expectancy biases serve to maintain rather than generate anxiety.

Davey has failed to clarify the critical evidence that could corroborate the expectancy bias hypothesis and refute preparedness theory. Such a clarification is necessary because each theory could potentially allow for multiple distal and proximal influences on selective associations. Expectancies are not the only proximal mediators. Our recent findings indicate that affective response matching may be an additional factor promoting such associations.

The present commentary emphasizes that the acquisition of fear always involves complex changes in several quasi-independent response systems. Stimulus-specific electrodermal response differentiation as well as the bias to overestimate the belongingness of certain stimulus pairs mainly indicates cognitive processes of selective orienting and attention. Emotion, however, also involves the activation of subcortical motivational circuits. Why certain stimuli acquire rapid access to these basic motivational systems is not explained by the expectancy bias model.

According to Davey, generalized expectancy biases cause fearrelevant behavior and may complement Seligman's biological preparedness model. Expectancy biases do not explain the preparedness phenomenon, because such cognitive (or covert behavioral) processes are themselves controlled by social and other environmentally based contingencies. Davey's own examination of the importance of cross-cultural factors can show the relationship between FR stimuli and behavior without needing cognitive agency to explain the behavioral phenomenon.

Expectations can facilitate rapid fear conditioning and this may explain some phenomena that have been attributed to preparedness. However, preparedness remains the best explanation for some aspects of clinical phobias and the difficulty of creating fears of modern dangers. Rapid fear conditioning based on expectancy is not an alternative to an evolutionary explanation, but has, like preparedness, been shaped by natural selection.

Because of their evolutionary importance, threat-detection mechanisms are likely to exist at a variety of levels. A recent study of face recognition suggests that novel stimuli receive enhanced processing when presented as fear-related. This suggests the existence of a complex, context-dependent threat-detection mechanism that can adaptively respond to spatiotemporally varying and unique environmental features.

The evolutionary origin of phobias is strongly supported by behavioral genetics and monkey vicarious conditioning data. Prepared Pavlovian conditioning may be only one of the mechanisms mediating the evolutionarily determined outcome in phobias, avoidance. Davey's alternative biased expectancy hypothesis has merit in accounting for some aspects of laboratory data, but it is insufficient to explain the unconscious origin of phobic fear.

We raise two objections to Slote’s article. First, empathy cannot provide information about the world in the direct way Slote proposes. Emotional contagion might be able to do so, but this type of process is different from the empathic one. Second, even if we accept his view of empathy, his claim that we make moral judgments via empathizing with the ‘warmth’ or ‘coldness’ of the actor seems misguided because, we usually empathize with the patient, and we empathize with emotions, not (...) “temperatures”. (shrink)

Many now consider “instinct” and “learning” opposite poles of a unidimensional continuum. An alternative model with two independently varying parameters predicts different selective pressures. Behavioral adaptation matches the organism's utilizations of stimuli and responses to their ecological validities: the mean validity over evolutionary time specifies the optimal initial potency of the prepared association; the variance specifies the optimal prepared plasticity.