UCLA researchers have found that it is possible to assess a person’s ability to feel empathy by studying their brain activity while they are resting rather than while they are engaged in specific tasks.
Traditionally, empathy is assessed through the use of questionnaires and psychological assessments.
The findings of this study offer an alternative to people who may have difficulty filling out questionnaires, such as people with severe mental illness or autism, said senior author Dr. Marco Iacoboni, professor of psychiatry and biobehavioral sciences at the David Geffen School of Medicine at UCLA.
“Assessing empathy is often the hardest in the populations that need it most,” Iacoboni said.
“Empathy is a cornerstone of mental health and well-being. It promotes social and cooperative behavior through our concern for others. It also helps us to infer and predict the internal feelings, behavior and intentions of others.”
Iacoboni has long studied empathy in humans. His previous studies have involved testing empathy in people presented with moral dilemmas or watching someone in pain.
For the current study, published in Frontiers in Integrative Neuroscience, researchers recruited 58 male and female participants ages 18 to 35.
Resting brain activity data were collected using functional magnetic resonance imaging, or fMRI, a noninvasive technique for measuring and mapping brain activity through small changes in blood flow.
Participants were told to let their minds wander while keeping their eyes still, by looking at a fixation cross on a black screen.
Afterward, the participants completed questionnaires designed to measure empathy.
They rated how statements such as “I often have tender, concerned feelings for people less fortunate than me” and “I sometimes try to understand my friends better by imagining how things look from their perspective” described them on a five-point scale from “not well” to “very well.”
Researchers wanted to measure how accurately they could predict the participants’ empathic disposition, characterized as the willingness and ability to understand another’s situation, by analyzing the brain scans.
The predictions were made by looking into resting activity in specific brain networks that earlier studies demonstrated are important for empathy.
Researchers used a form of artificial intelligence called machine learning, which can pick up subtle patterns in data that more traditional data analyses might not.
The predictions were made by looking into resting activity in specific brain networks that earlier studies demonstrated are important for empathy.
“We found that even when not engaged directly in a task that involves empathy, brain activity within these networks can reveal people’s empathic disposition,” Iacoboni said.
“The beauty of the study is that the MRIs helped us predict the results of each participant’s questionnaire.”
The findings could help health care professionals better assess empathy in people with autism or schizophrenia, who may have difficulties filling out questionnaires or expressing emotion.
“People with these conditions are thought to lack empathy,” he said.
“But if we can demonstrate that their brains have the capability for empathy, we can work to improve it through training and the use of other therapies.”
Furthermore, said lead author Leonardo Christov-Moore, a postdoctoral fellow currently at USC’s Brain and Creativity Institute, this technique may be expanded to improve treatment as well as diagnosis.
“The predictive power of machine learning algorithms like this one, when applied to brain data, can also help us predict how well a given patient will respond to a given intervention, helping us tailor optimal therapeutic strategies from the get-go.”
The study adds to a growing body of research suggesting that brains at rest are as active as brains engaged in a task, and that brain networks in the resting brain may interact in a similar fashion as when they are engaged in a task.
Iacoboni said future, larger studies may help identify other regions of the brain associated with empathy.
Empathy, the capacity to resonate with and reflect upon the feelings and mental states of others1, is a core social ability sculpted by a long history of mammalian evolution to enhance species survival, afford group communication, and enable social life.
To tap the neural mechanisms and maturational process of empathy, research has employed a cross-species approach and demonstrated that both rodents and nonhuman primates exhibit rudimentary empathy expressed in contagion and mimicry2.
Complementing this effort, neuroimaging studies in humans, typically targeting the adult brain, show that while human empathy similarly implicates automatic resonance to others’ distress, it also integrates higher-order neural activations that afford mentalization of others’ feelings and generation of an empathic response that differentiates self from other3.
Yet, to understand the unfolding of human empathy from its origins, research must complement the phylogenetic approach with an ontogenetic one by utilizing prospective longitudinal studies that can pinpoint factors which over time facilitate or undermine maturation of the human empathic brain.
Developmental evidence indicates that the capacity for empathy emerges across the first years of life through complex interactions between the child’s biological dispositions and the quality of caregiving4,5.
In parallel, research in social neuroscience describes dramatic shifts in maturation of the neural systems that sustain empathy6,7; yet, the determinants that shape this neural development remain obscure.
To track how multiple factors integrate to support maturation of the neural empathic response, we utilized a longitudinal study of children followed from early childhood to preadolescence and focused on three factors known to impact children’s empathic abilities.
These include chronic early life stress (ELS), synchronous and attuned parent-child relationship, and temperamental reactivity implying heightened inborn responsivity to negative stimuli.
Since prolonged adversity, particularly exposure to ELS, negatively impacts various social functions8–10including empathy11–15, we followed a cohort living in a distinct ELS context, repeatedly observed mother–child interactions in the home environment, assessed temperamental reactivity in early childhood, and evaluated children’s anxiety disorders in late childhood to test their direct and indirect effects on the neural substrates of empathy at the transition to adolescence.
The daily experience of empathy involves both simulation of the bodily and affective states of others and drawing inferences about their mental states1,16,17.
Yet, the early studies on the neuroscience of empathy distinguished between these two processes and examined them separately under laboratory conditions. Subsequently, conceptual models differentiated two components of empathy; affective empathy/resonance and cognitive empathy/mentalization1,17, a dichotomy that was mapped into distinct brain structures and neural networks.
The first, affective empathy/resonance, was thought to involve automatic response to others’ pain and feelings and to rely on structures that support sensorimotor perception and their representation in one’s own brain, such as the primary somatosensory and motor cortices, anterior cingulate cortex, and sensorimotor area (SMA), implicating the embodied simulation network; the second, cognitive empathy/mentalization integrates higher-order cortical regions to understand others’ mental life and includes the prefrontal cortex (PFC), temporoparietal junction, superior temporal sulcus (STS), and temporal pole, which comprise the mentalizing network1,2,17.
Notwithstanding this distinct cerebral mapping (Fig. 1, right panel), such dual dissociation model is somewhat artificial. Drawing parallels between this and other dual models18, in real-life situations, one typically employs both processes, albeit to varying degrees pending on person and context.
Indeed, ecologically valid experiments that simulate real-life settings indicate that the two networks reflect two facets of social living and function in concert to support human empathy10,16,17,19.
One important observation from these studies was that under natural settings, the sensorimotor area and the middle cingulate cortex (SMA/MCC) underpin both embodied simulation and mentalizing processes, integrating the affective and cognitive components of empathy2,20,21 (Fig. 1, right panel in green).
For instance, an empathy paradigm that exposed participants to distressing stimuli of everyday life (triggering embodied simulation) while asking participants to take the target’s perspective (activating mentalizing) yielded activations containing the SMA/MCC node22. Here, we adopt the same paradigm to probe empathy (hereafter we use the term “empathy” for the two facets, unless otherwise specified) and test the developmental precursors of this shared empathy network.
Despite growing interest in the neuroscience of empathy, there are nearly no data on the developmental processes that tune the brain toward an empathic response. Several factors may contribute to neural empathy, the first is sensitive caregiving. In particular, the experience of parent-child synchrony, the parent’s ongoing resonance and online adaptation to the child’s nonverbal signals and verbal communications, is associated with children’s empathy across childhood and adolescence23.
The mother–child bond provides a setting where synchrony is first experienced and encoded in the brain24, creating a template for the child’s later resonance with the distress, feelings, and thoughts of others25.
When the mother’s capacity to provide synchronous parenting is compromised, for instance, in cases of postpartum depression, children show reduced empathic behavior26 and impaired neural empathic response to others’ pain in adolescence27.
Synchrony is the process by which mother’s brain impacts the child’s brain and wires it to social participation25; during moments of behavioral synchrony mother and child’s brains synchronize in the STS28, a social neural hub, and behavioral synchrony across the first 6 years predicts adolescents’ neural response to attachment cues in key nodes of the social brain, including the STS, STG, and Insula29.
Second, exposure to chronic adversity impairs social–emotional processing4,11–15 and the effect is most prominent when adversity begins early and persists throughout early childhood9,30,31.
Research utilizing fMRI13 and MEG11 show that trauma alters neural responses that underpin the affective and cognitive components of empathy. Adults exposed to early trauma exhibit abnormal neural response to negative emotional stimuli and impairments in the brain basis of social functions30,32, and children and adolescents exposed to ELS display impaired processing of affective facial expressions33,34, implying disruptions to emotional processing which sustains empathy.
Thus, while no direct evidence links ELS to children’s neural empathic response, these lines of research lend support to this hypothesis.
Although chronic ELS disrupts social functioning, substantial individual differences exist, which are shaped by biological dispositions as they interact with the specific adversity35.
Most studies on the long-term effects of ELS employed biology-by-context models that target variations in dispositional stress reactivity as they interact with stressful environments36.
Heightened stress reactivity reflects increased biological sensitivity to context, which augments the effects of stress on negative outcomes under conditions of ELS37,38.
One mechanism proposed to mediate the detrimental effects of ELS on social outcome is temperamental reactivity, the heightened dispositional response to negative stimuli. Early adversity augments attention to negative and frightening events31, and when combined with inborn reactivity to negative stimuli, it may lead to difficulties in disengaging from distressing cues39.
Such exaggerated response is often accompanied by repeated mentalization and ruminations over the distressful event40. Moreover, early temperamental reactivity increases the propensity to develop anxiety disorders in later childhood and adolescence41.
Anxiety disorders, in turn, impair the neural basis of multiple social–emotional functions42, are associated with increased ruminations over negative events, and link with inability to disengage from negative stimuli43.
The current decade-long prospective longitudinal study integrated repeated observations of parenting with lab-based assessment of negative reactivity and psychiatric evaluations to predict the neural basis of empathy among children exposed to ELS versus controls. We utilized a unique cohort of children exposed to war-related trauma since birth who experience frequent, unpredictable exacerbations of the traumatic situation.
Children and their families were followed from early childhood to early adolescence (Fig. 1) and thus, our study affords a rare “natural experiment” in ELS research that typically includes heterogeneous adversities.
In preadolescence (11–13 years), we used magnetoencephalography (MEG) to probe children’s oscillatory response to others’ distress and focused on alpha rhythms, which underpin empathic processes44,45 and express in children as late alpha-band enhancement in sensory cortex to others’ pain7.
Here, our paradigm additionally involved perspective-taking and was expected to activate substrates supporting both affective and cognitive empathy, such as the SMA and MCC2,20,21.
We formulated two hypotheses and one open research question. First, we expected that the neural empathic response in preadolescence will implicate structures that support the shared affective and cognitive empathy, namely the SMA and the MCC, and that these activations will be underpinned by late alpha-band enhancement.
Second, we hypothesized that activation of this neural network will be longitudinally predicted by mother–child synchrony across the first decade of life. Next, since no prior research linked ELS with the neural development of empathy, we explored direct and indirect ways by which ELS impacts the neural empathic response as an open research question. For this goal, we explored neural patterns that are specific to trauma-exposed youth and tested their associations with temperamental reactivity and anxiety disorders.
Consistent with the biological sensitivity to context model37, we expected that only among trauma-exposed youth, these putative neural patterns will be shaped by early reactivity. Additionally, we conjectured that these stress-specific activations would link with the consolidation of a distinct anxiety disorder in late childhood.
We find that at preadolescence, the neural empathic response implicates structures tapping the overlap of cognitive and affective empathy, such as SMA and MCC. In addition, adolescents’ neural empathic response is sensitive to caregiving across the first decade, particularly mother–child synchrony, and to chronic early trauma.
Finally, temperamentally reactive children reared in stressful contexts are more likely to develop anxiety disorders and show additional activation in nodes possibly reflecting hyper-mentalizing and difficulties in disengaging from negative cues.
Source:
UCLA
