APA Citation
Bernhardt, B., & Singer, T. (2012). The Neural Basis of Empathy. *Annual Review of Neuroscience*, 35, 1--23. https://doi.org/10.1146/annurev-neuro-062111-150536
Core Concept: The Neural Architecture of Empathy
Bernhardt and Singer's comprehensive review establishes that empathy is not a single capacity but a constellation of distinct yet interacting neural processes. Their framework has become the standard model for understanding how the brain generates empathic responses, with profound implications for understanding empathy deficits in clinical populations including those with narcissistic personality disorder.
Affective Empathy: Feeling What Others Feel. The capacity to share another person's emotional state relies primarily on the anterior insula and anterior cingulate cortex. When you see someone in pain, these regions activate as if you yourself were experiencing pain. This 'shared affect' system creates the visceral experience of feeling moved by another's suffering---the gut response that motivates compassionate action. The anterior insula integrates bodily sensations with emotional experience, translating the observation of another's distress into your own felt sense of that distress. This is automatic and largely unconscious: you don't decide to feel bad when you see someone hurt; your brain generates that response before conscious deliberation.
Cognitive Empathy: Understanding Others' Minds. Distinct from actually feeling others' emotions is the capacity to understand what they think and feel. This mentalising or perspective-taking ability engages different brain regions: the medial prefrontal cortex, the temporoparietal junction, and portions of the superior temporal sulcus. These regions support 'theory of mind'---the understanding that others have mental states different from your own. Cognitive empathy allows you to grasp that someone is sad, predict what they might do next, and tailor your behaviour accordingly. Critically, this understanding can occur without any emotional response: you can know someone is suffering without feeling distressed yourself.
The Independence and Interaction of Empathy Systems. Bernhardt and Singer's central insight is that these systems, while they interact, can function independently. Lesion studies demonstrate that damage to affective empathy regions can leave cognitive empathy intact, and vice versa. This neurological independence explains one of the most bewildering phenomena in human psychology: how someone can clearly understand another's pain while remaining emotionally unmoved. In healthy empathy, cognitive understanding typically amplifies affective response, and emotional reactions sharpen cognitive attention. But when these systems are dissociated---as appears to occur in narcissistic personality disorder---understanding becomes disconnected from caring.
Empathy Modulation: Context, Motivation, and Individual Differences. The review documents extensive evidence that empathic responses are not fixed but are modulated by numerous factors. We empathise more with in-group members than out-groups, with those we perceive as 'deserving' versus 'undeserving' of suffering, and with those similar to ourselves. Emotional state affects empathy: stress, anxiety, and negative mood can dampen empathic responses. Critically, motivation matters: studies show that instructing participants to try to empathise increases activation in empathy-related brain regions. This modulation has important implications for understanding narcissism, where empathy appears to be deployed strategically rather than automatically.
Original Context: The State of Empathy Neuroscience in 2012
The Neuroimaging Revolution. By 2012, functional neuroimaging had transformed the study of empathy from philosophical speculation to empirical science. Dozens of studies had mapped brain responses to others' pain, emotions, and mental states. However, this wealth of data had not been systematically integrated. Different laboratories used different paradigms, stimuli, and analysis methods, making it difficult to synthesise findings into a coherent model. Bernhardt and Singer's review brought order to this complexity, identifying consistent patterns across studies and establishing the definitive account of empathy's neural basis.
Tania Singer's Foundational Discoveries. Singer's earlier neuroimaging studies had provided some of the most compelling evidence for 'shared affect' in empathy. Her 2004 study showing that watching a loved one receive painful shocks activated the same anterior insula and anterior cingulate regions as receiving shocks oneself was a landmark finding, demonstrating that the brain partially simulates observed experiences. This work established Singer as a leading figure in empathy neuroscience and positioned her to lead this comprehensive synthesis. The review integrated her laboratory's findings with the broader literature.
Clinical Implications Emerging. By 2012, researchers had begun applying empathy neuroscience to clinical populations, with preliminary findings on empathy abnormalities in autism, psychopathy, and other conditions. Bernhardt and Singer's framework provided the theoretical foundation for this clinical translation, explaining how different conditions might involve impairments in distinct empathy components. The distinction between affective and cognitive empathy would prove particularly important for understanding personality disorders, where cognitive empathy often remains intact while affective empathy is impaired.
Beyond Mirror Neurons. The mirror neuron system had dominated popular and scientific discussions of empathy in the preceding decade, sometimes to the point of oversimplification. Bernhardt and Singer situated mirror neurons within a more nuanced framework, acknowledging their likely contribution to action understanding and emotional contagion while emphasising that empathy involves multiple systems beyond motor resonance. This more complex account better explained clinical findings and provided a richer model for understanding empathy's full architecture.
For Survivors: Understanding the Narcissistic Empathy Deficit
Why They Understand But Don't Care. Perhaps no aspect of narcissistic abuse is more psychologically destabilising than the experience of being hurt by someone who clearly understands your pain. The narcissist can articulate exactly what you're feeling, can predict your reactions, can even appear to offer comfort with the 'right' words---yet their behaviour demonstrates no actual regard for your wellbeing. Bernhardt and Singer's research explains this phenomenon: cognitive and affective empathy rely on different neural systems that can be dissociated. The narcissist's mentalising network---the regions that support understanding others' minds---may function well, allowing them to read you accurately. But their affective empathy system---the anterior insula and anterior cingulate that would generate a visceral response to your distress---appears to be impaired or not engaged. They understand; they simply don't feel.
The Failure of Explanation. Survivors often exhaust themselves trying to explain their pain more clearly, believing that if only the narcissist truly understood, they would change. This research reveals why such efforts are futile. The problem was never understanding. The narcissist's cognitive empathy likely grasped your suffering from the beginning. What's missing is the affective response---the felt sense of your pain that would motivate them to stop causing it. No amount of articulation can generate a neural response that their brain is not producing. Your communication was never the problem; their neurobiology was.
Validation of Your Experience. The gaslighting and reality distortion characteristic of narcissistic abuse often leads survivors to doubt their own perceptions. Did they really lack empathy, or was I not explaining myself well enough? Were they really unmoved by my suffering, or was I too sensitive? Bernhardt and Singer's research provides external validation: the dissociation between cognitive and affective empathy is a documented neurobiological phenomenon. What you experienced was real. The disconnect between their apparent understanding and their actual emotional response has a neurological basis. You were not failing to communicate; you were interacting with someone whose brain did not generate normal affective responses to your distress.
Strategic Versus Automatic Empathy. The research on empathy modulation helps explain why narcissists can seem empathic in some contexts but utterly cold in others. Studies show that motivation and attention significantly affect empathic responses. Narcissists may be capable of accessing empathy when it serves their purposes---during love-bombing to secure your attachment, when trying to hoover you back after discard, or when performing for an audience. But this empathy is strategic, deployed when beneficial and withheld when not. It was never the automatic, consistent responsiveness that characterises healthy empathic functioning. Understanding this helps survivors stop waiting for the 'real' empathic person they glimpsed occasionally to return; that version was the performance, not the baseline.
For Clinicians: Neurobiological Assessment of Empathy
Differentiating Empathy Components. Bernhardt and Singer's framework provides clinicians with a more nuanced approach to assessing empathy in patients with suspected personality disorders. Rather than asking whether a patient 'has empathy,' clinicians should assess cognitive and affective components separately. Can the patient accurately identify others' emotions and mental states? (Cognitive empathy.) Does the patient show visceral, emotional responses to others' distress? (Affective empathy.) Do these capacities translate into prosocial behaviour? The pattern of intact cognitive empathy with impaired affective empathy and motivation to act prosocially is characteristic of narcissism and has different treatment implications than global empathy impairment.
The Limits of Cognitive-Behavioural Approaches. If a patient's empathy deficit primarily involves affective rather than cognitive systems, treatments focused on perspective-taking and understanding others' points of view may be insufficient. The patient may already understand others well enough; what's missing is the emotional response that would motivate different behaviour. Treatment approaches may need to target affective systems more directly, though this remains challenging. Singer's subsequent research on compassion meditation has shown some promise in increasing affective empathy-related brain activity, suggesting that repeated practices focusing on generating caring feelings toward others might have neurobiological effects. However, such approaches require patient motivation and engagement that may be lacking in NPD.
Assessing Motivation and Modulation. The research on empathy modulation has clinical implications. If a narcissistic patient can show empathic responses under certain conditions (when motivated, when rewards are present, when instructed to try), this suggests the underlying capacity exists but is not being automatically deployed. This differs from conditions involving more fundamental damage to empathy systems. For treatment, it may be more productive to focus on motivation and value systems than on building capacity that already exists. Why doesn't the patient choose to engage empathy more consistently? What would need to change for empathic responding to become more automatic?
Neuroimaging as Assessment Tool. While not yet standard clinical practice, neuroimaging protocols based on Bernhardt and Singer's framework could provide objective data on empathy functioning. Measuring anterior insula activation in response to others' distress, or default mode network activity during mentalising tasks, could help differentiate empathy profiles across patients. Such data might inform treatment planning and provide a baseline against which to measure treatment effects. As neuroimaging becomes more accessible, these research paradigms may increasingly translate into clinical tools.
Broader Implications: From Individual Brains to Social Systems
Empathy Deficits and Relationship Damage
The neurobiological dissociation between understanding and caring has profound implications for intimate relationships with narcissists. Partners often report feeling simultaneously understood and utterly unseen---understood because the narcissist accurately reads their emotions and can articulate their experiences, unseen because this understanding never translates into genuine consideration. Bernhardt and Singer's research validates this paradox: cognitive empathy without affective empathy produces precisely this experience. The narcissist may indeed understand you, may even be fascinated by understanding you (as a form of narcissistic supply through intellectual mastery), while remaining emotionally unmoved by your suffering. This is not contradiction or confusion; it's the predictable result of dissociated empathy systems.
Manipulation and Cold Empathy
Intact cognitive empathy in the absence of affective empathy creates the conditions for sophisticated manipulation. The narcissist can read others accurately, predict their responses, and tailor their behaviour accordingly---all without the emotional constraints that would normally limit exploitation. Some researchers have termed this 'cold empathy': understanding without caring, often weaponised. The narcissist's ability to know exactly what to say to win you back, to identify your vulnerabilities and exploit them, to present themselves as deeply understanding while orchestrating harm---these capacities all rely on cognitive empathy untempered by affective concern for your wellbeing. Bernhardt and Singer's framework explains how such apparently contradictory capacities can coexist.
Developmental Origins of Empathy Dissociation
While Bernhardt and Singer focus on adult neuroscience, their framework has implications for understanding developmental psychopathology. Affective empathy develops earlier than cognitive empathy and relies more heavily on early attachment experiences. Infants learn to share affect through co-regulation with caregivers; without attuned caregiving, the anterior insula may not develop normally. Cognitive empathy, developing later and relying on different substrates, might develop more normally even when affective empathy is impaired. This suggests that narcissistic empathy profiles might originate in early attachment failures that specifically disrupted affective empathy development while leaving cognitive development relatively intact. Understanding these developmental origins could inform prevention efforts.
Implications for Therapeutic Relationship
For clinicians treating survivors of narcissistic abuse, this research has implications for the therapeutic relationship itself. Survivors may be exquisitely attuned to any sign that the therapist understands them cognitively without caring affectively---having been burned by exactly this pattern. The therapeutic relationship may need to emphasise consistent affective attunement, not just accurate interpretation. Survivors may test whether the therapist's apparent understanding is backed by genuine emotional engagement. Therapist warmth, emotional responsiveness, and authentic care become not just pleasant additions but potentially essential demonstrations that understanding can indeed be coupled with caring.
Cross-Cultural Considerations
Empathy expression and experience vary across cultures, and Bernhardt and Singer's framework is based primarily on Western research populations. Different cultures may emphasise cognitive versus affective empathy differently, may have different norms for expressing emotional resonance, and may define prosocial behaviour differently. Clinical application of this framework requires cultural adaptation. What looks like affective empathy impairment in one cultural context might be normative emotional regulation in another. Similarly, treatment approaches developed in Western contexts may need modification for clients from different cultural backgrounds.
The Limits of Neuroscience for Moral Evaluation
While this research explains mechanisms, it does not determine moral evaluation. Understanding that narcissists may have neurobiological empathy impairments does not excuse their behaviour. Many people with atypical empathy neurobiology do not become abusive. Neurobiological differences may explain tendencies without determining choices. Adults have access to insight, treatment, and behavioural regulation that can compensate for empathy limitations. The research helps survivors understand what they experienced and stop blaming themselves; it does not provide exoneration for perpetrators.
Limitations and Considerations
Neuroimaging Constraints. Functional neuroimaging provides correlational rather than causal data. Observing that certain brain regions are active during empathy tasks does not prove they are necessary or sufficient for empathy. Lesion studies provide stronger causal evidence but are limited by the specificity of naturally occurring damage. The framework Bernhardt and Singer propose is well-supported but remains a model that future research may refine.
Individual Variation. The neurobiological patterns described are group-level findings. Individual variation is substantial. Not all narcissists will show identical empathy profiles; some may have more affective capacity than others. Clinical assessment must remain individualised rather than assuming neurotypical patterns apply uniformly.
Treatment Responsiveness Unknown. While this research identifies the neural systems involved in empathy, it does not establish whether those systems can be modified in adults with established personality disorders. The brain shows plasticity, but the extent to which narcissistic empathy deficits can be remediated through treatment remains unclear. Singer's subsequent research on compassion training shows promise for general populations but has not been extensively tested with NPD populations.
Complexity of Clinical Presentation. Narcissistic personality disorder involves far more than empathy deficits: grandiosity, entitlement, exploitativeness, and other features cannot be reduced to empathy impairment. This research illuminates one aspect of the disorder but does not explain it fully. Empathy deficits may be consequence as well as cause of narcissistic development.
Historical Context
Bernhardt and Singer's review appeared in 2012 in the Annual Review of Neuroscience, a prestigious invitation-only journal that publishes comprehensive reviews of major research areas. The article represented the culmination of nearly two decades of neuroimaging research on empathy, synthesising findings from dozens of laboratories into a coherent framework.
Tania Singer's earlier work had been instrumental in establishing the field. Her 2004 Science paper demonstrating shared neural responses to own and observed pain was a landmark finding that launched hundreds of subsequent studies. By 2012, enough data had accumulated to warrant systematic synthesis, and Singer was ideally positioned to lead this effort.
The review appeared at a moment when clinical applications of empathy neuroscience were emerging. Researchers were beginning to examine empathy abnormalities in autism, psychopathy, and personality disorders. Bernhardt and Singer's framework provided the theoretical foundation for this clinical translation, distinguishing empathy components whose differential impairment might characterise different conditions.
The distinction between affective and cognitive empathy, while suggested by earlier researchers, received its most rigorous neurobiological grounding in this review. This distinction would prove particularly important for understanding narcissism and psychopathy, conditions where cognitive empathy often remains intact while affective empathy is impaired.
The review has been cited over 3,500 times and remains the standard reference for understanding empathy's neural basis. Its influence extends beyond neuroscience into clinical psychology, psychiatry, and even philosophy of mind. For research on narcissistic empathy deficits specifically, this work provides the essential neurobiological framework within which clinical findings are interpreted.
Further Reading
- Singer, T., Seymour, B., O'Doherty, J., Kaube, H., Dolan, R.J., & Frith, C.D. (2004). Empathy for pain involves the affective but not sensory components of pain. Science, 303(5661), 1157-1162.
- Decety, J., & Ickes, W. (Eds.). (2009). The Social Neuroscience of Empathy. MIT Press.
- Klimecki, O.M., Leiberg, S., Ricard, M., & Singer, T. (2014). Differential pattern of functional brain plasticity after compassion and empathy training. Social Cognitive and Affective Neuroscience, 9(6), 873-879.
- Shamay-Tsoory, S.G., Aharon-Peretz, J., & Perry, D. (2009). Two systems for empathy: A double dissociation between emotional and cognitive empathy in inferior frontal gyrus versus ventromedial prefrontal lesions. Brain, 132(3), 617-627.
- Baron-Cohen, S. (2011). Zero Degrees of Empathy: A New Theory of Human Cruelty. Penguin UK.
- Lamm, C., Decety, J., & Singer, T. (2011). Meta-analytic evidence for common and distinct neural networks associated with directly experienced pain and empathy for pain. NeuroImage, 54(3), 2492-2502.