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Tania Singer

Publications and source records attributed to Tania Singer.

11 recordsLinked to original sources

The neuronal basis of empathy and fairness.

The emerging fields of social neuroscience and neuroeconomics have started to investigate the neural foundations of empathy and fairness. Even though not frequently linked, both concepts point to humans as altruistic beings who care for others. Recently social neuroscientists have measured brain activity associated with different empathic processes and revealed common neural responses when feeling sensations such as disgust, touch or pain in ourselves, and when perceiving someone else being disgusted, touched or in pain. At the same time, research in neuroeconomics has used game theoretical paradigms to study our sense of fairness. Several functional magnetic resonance imaging (fMRI) studies show involvement of anterior insula and anterior cingulate cortex in response to unfair compared with fair offers during such monetary exchange games. Interestingly, the same brain regions are also involved in empathy for pain or disgust of others. More generally, anterior insula cortex is suggested to subserve neural representations of feeling and bodily states in the self and may play a crucial role for the emergence of social emotions related to others.

Brain↗

The empathic brain: how, when and why?

Recent imaging results suggest that individuals automatically share the emotions of others when exposed to their emotions. We question the assumption of the automaticity and propose a contextual approach, suggesting several modulatory factors that might influence empathic brain responses. Contextual appraisal could occur early in emotional cue evaluation, which then might or might not lead to an empathic brain response, or not until after an empathic brain response is automatically elicited. We propose two major roles for empathy; its epistemological role is to provide information about the future actions of other people, and important environmental properties. Its social role is to serve as the origin of the motivation for cooperative and prosocial behavior, as well as help for effective social communication.

Automatism↗

The neuronal basis and ontogeny of empathy and mind reading: review of literature and implications for future research.

Social neuro-science has recently started to investigate the neuronal mechanisms underlying our ability to understand the mental and emotional states of others. In this review, imaging research conducted on theory of mind (ToM or mentalizing) and empathy is selectively reviewed. It is proposed that even though these abilities are often used as synonyms in the literature these capacities represent different abilities that rely on different neuronal circuitry. ToM refers to our ability to understand mental states such as intentions, goals and beliefs, and relies on structures of the temporal lobe and the pre-frontal cortex. In contrast, empathy refers to our ability to share the feelings (emotions and sensations) of others and relies on sensorimotor cortices as well as limbic and para-limbic structures. It is further argued that the concept of empathy as used in lay terms refers to a multi-level construct extending from simple forms of emotion contagion to complex forms of cognitive perspective taking. Future research should investigate the relative contribution of empathizing and mentalizing abilities in the understanding of other people's states. Finally, it is suggested that the abilities to understand other people's thoughts and to share their affects display different ontogenetic trajectories reflecting the different developmental paths of their underlying neural structures. In particular, empathy develops much earlier than mentalizing abilities, because the former relys on limbic structures which develop early in ontogeny, whereas the latter rely on lateral temporal lobe and pre-frontal structures which are among the last to fully mature.

Brain↗

Empathic neural responses are modulated by the perceived fairness of others.

The neural processes underlying empathy are a subject of intense interest within the social neurosciences. However, very little is known about how brain empathic responses are modulated by the affective link between individuals. We show here that empathic responses are modulated by learned preferences, a result consistent with economic models of social preferences. We engaged male and female volunteers in an economic game, in which two confederates played fairly or unfairly, and then measured brain activity with functional magnetic resonance imaging while these same volunteers observed the confederates receiving pain. Both sexes exhibited empathy-related activation in pain-related brain areas (fronto-insular and anterior cingulate cortices) towards fair players. However, these empathy-related responses were significantly reduced in males when observing an unfair person receiving pain. This effect was accompanied by increased activation in reward-related areas, correlated with an expressed desire for revenge. We conclude that in men (at least) empathic responses are shaped by valuation of other people's social behaviour, such that they empathize with fair opponents while favouring the physical punishment of unfair opponents, a finding that echoes recent evidence for altruistic punishment.

Brain↗

Pupillary contagion: central mechanisms engaged in sadness processing.

Empathic responses underlie our ability to share emotions and sensations with others. We investigated whether observed pupil size modulates our perception of other's emotional expressions and examined the central mechanisms modulated by incidental perception of pupil size in emotional facial expressions. We show that diminishing pupil size enhances ratings of emotional intensity and valence for sad, but not happy, angry or neutral facial expressions. This effect was associated with modulation of neural activity within cortical and subcortical regions implicated in social cognition. In an identical context, we show that the observed pupil size was mirrored by the observers' own pupil size. This empathetic contagion engaged the brainstem pupillary control nuclei (Edinger-Westphal) in proportion to individual subject's sensitivity to this effect. These findings provide evidence that perception-action mechanisms extend to non-volitional operations of the autonomic nervous system.

Adult↗

Empathy for pain involves the affective but not sensory components of pain.

Our ability to have an experience of another's pain is characteristic of empathy. Using functional imaging, we assessed brain activity while volunteers experienced a painful stimulus and compared it to that elicited when they observed a signal indicating that their loved one--present in the same room--was receiving a similar pain stimulus. Bilateral anterior insula (AI), rostral anterior cingulate cortex (ACC), brainstem, and cerebellum were activated when subjects received pain and also by a signal that a loved one experienced pain. AI and ACC activation correlated with individual empathy scores. Activity in the posterior insula/secondary somatosensory cortex, the sensorimotor cortex (SI/MI), and the caudal ACC was specific to receiving pain. Thus, a neural response in AI and rostral ACC, activated in common for "self" and "other" conditions, suggests that the neural substrate for empathic experience does not involve the entire "pain matrix." We conclude that only that part of the pain network associated with its affective qualities, but not its sensory qualities, mediates empathy.

Adult↗

Brain responses to the acquired moral status of faces.

We examined whether neural responses associated with judgments of socially relevant aspects of the human face extend to stimuli that acquire their significance through learning in a meaningful interactive context, specifically reciprocal cooperation. During fMRI, subjects made gender judgments on faces of people who had been introduced as fair (cooperators) or unfair (defector) players through repeated play of a sequential Prisoner's Dilemma game. To manipulate moral responsibility, players were introduced as either intentional or nonintentional agents. Our behavioral (likebility ratings and memory performance) as well as our imaging data confirm the saliency of social fairness for human interactions. Relative to neutral faces, faces of intentional cooperators engendered increased activity in left amygdala, bilateral insula, fusiform gyrus, STS, and reward-related areas. Our data indicate that rapid learning regarding the moral status of others is expressed in altered neural activity within a system associated with social cognition.

Adult↗

Plasticity of memory for new learning in very old age: a story of major loss?

Longitudinal survivors of the Berlin Aging Study (N = 96, mean age = 84 years, range 75-101 years) were instructed and trained in a mnemonic skill to examine plasticity of episodic memory performance in very old age. Performance gains after mnemonic instruction were modest, and most individuals were unable to further enhance their performance during 4 sessions of mnemonic practice. Whereas the proportion of variance explained by measures from the broad fluid-ability domain (e.g., perceptual speed) increased with training, the proportion of variance explained by crystallized-ability domain (e.g., word knowledge) and sociobiographical variables decreased. Furthermore, prior 6-year longitudinal changes (loss) in perceptual speed predicted individual differences in plasticity. Results suggest that aging-induced biological factors are a prominent source of individual differences in cognitive plasticity in very old age.

Age Factors↗

The fate of cognition in very old age: six-year longitudinal findings in the Berlin Aging Study (BASE).

The authors report full-information longitudinal age gradients in 4 intellectual abilities on the basis of 6-year longitudinal changes in 132 individuals (mean age at T1 = 78.27, age range = 70-100) from the Berlin Aging Study. Relative to the cross-sectional parent sample (N = 516, mean age at T1 = 84.92 years), this sample was positively selected because of differential mortality and experimental attrition. Perceptual speed, memory, and fluency declined with age. In contrast, knowledge remained stable up to age 90, with evidence for decline thereafter. Age gradients were more negative in old old (n = 66, mean age at T1 = 83.04) than in old (n = 66, mean age at T1 = 73.77) participants. Rates of decline did not differ reliably between men and women or between participants with high versus low life-history status. They conclude that intellectual development after age 70 varies by distance to death, age, and intellectual ability domain.

Age Factors↗

Longitudinal selectivity in aging populations: separating mortality-associated versus experimental components in the Berlin Aging Study (BASE).

The authors examined 3.7-year selectivity in the Berlin Aging Study by comparing the T1 parent sample (N = 516) with the T3 sample (N = 206). Selectivity was partitioned into a mortality-associated component, reflecting the degree to which individuals still alive at T3 (T3 survivors, N = 313) differ from the T1 parent sample (N = 516) from which they originated, and an experimental component, reflecting the degree to which the T3 sample (N = 206) differed from T3 survivors (N = 313). Across 48 variables representing medical, sensorimotor, cognitive, personality-related, and socioeconomic domains, the mortality-associated component accounted for 64% of total selectivity, and the experimental component for 36% (0.18 vs 0.10 SD units; t = 7.20, p <.01). Except for age and intelligence, experimental selectivity effects regarding means and prevalence rates were generally small. Partitioning selectivity into mortality-associated and experimental components is a useful tool in the longitudinal study of aging populations.

Aged↗