Blurred Boundaries: New Framework Links Self-Other Confusion to Empathy Problems in Schizophrenia

Empathy has long been treated as a single faculty that either works or fails. In schizophrenia research, that assumption has shaped decades of studies reporting that patients struggle to read other people’s minds, decode emotions, or take another person’s perspective. Yet a puzzle has stubbornly persisted in the clinical literature: many people with schizophrenia are not simply cold or detached. Alongside poor perspective-taking and reduced empathic accuracy, a substantial subset reports overwhelming personal distress, emotional contagion, and over-involvement in other people’s feelings. A purely deficit-based account cannot explain why the same person might fail to understand what someone else feels while simultaneously being flooded by that feeling. A new review published in Translational Psychiatry argues that the missing piece is not empathy itself but the boundary that empathy depends on: the distinction between self and other.

The review, led by ChaoZheng Huang and AiBao Zhou of Northwest Normal University in Lanzhou, together with YuHui Yang of Hunan Police Academy and Pei Xie of Sichuan Normal University, proposes a three-factor neurobehavioral framework that reframes empathy difficulties in schizophrenia as failures of self–other distinction regulation. Rather than asking whether empathic capacity is reduced, the authors ask where in the chain of empathic processing the sense of who is feeling what becomes unstable. The framework is a narrative synthesis rather than a single experiment, but it draws together behavioral findings, neuroimaging evidence, and theoretical models into a coherent architecture that makes testable predictions for future research.

The first factor in the model is spontaneous empathic access. This concerns whether cognitive and affective cues from another person—facial expressions, tone of voice, posture, words—actually enter the observer’s processing system when task demands are low. Empathy cannot begin unless social signals are registered, and this registration often happens automatically, before any deliberate effort. In schizophrenia, the authors argue, bottom-up access to social cues may be compromised by attentional abnormalities, sensory processing disturbances, or motivational deficits. A patient who never fully registers a companion’s subtle expression of worry cannot be expected to respond to it, regardless of how intact the rest of the empathic machinery might be. This stage explains some cases of apparent emotional coldness that are, at root, failures of signal capture rather than failures of feeling.

The second factor, inferential empathy, refers to the representation of another person’s beliefs, intentions, perspectives, and emotional states as mental content that belongs to someone else. This is the territory traditionally covered by theory of mind and mentalizing research, and it maps onto a well-characterized set of brain circuits, including the mentalizing network of the medial prefrontal cortex, temporoparietal junction, and posterior cingulate cortex, together with frontotemporal social-inference systems. Decades of work have documented theory-of-mind impairments in schizophrenia, and the framework does not dispute them. Instead, it situates them: inferential empathy is one stage among several, and impairments here cannot by themselves account for the full profile of empathic disturbance seen across patients.

The third and most novel factor is attributional empathy. Once emotions, thoughts, or perspectives have been activated in the observer’s mind, they must be assigned to their correct owner. Is this sadness mine, or does it belong to the person sitting across from me? Is this interpretation of the situation my own judgment, or am I borrowing someone else’s? In healthy cognition, this assignment happens largely outside awareness, supported by neural systems for self–other distinction and source attribution. The review proposes that in schizophrenia this labeling process becomes unstable. Emotions generated by another person’s distress may be experienced as one’s own, producing the elevated personal distress and emotional over-involvement frequently reported by patients. Conversely, one’s own internally generated thoughts and feelings may be attributed to external sources—a misattribution that resonates strikingly with core symptoms of the disorder, such as thought insertion and delusions of influence.

At the neural level, the framework distributes these three processes across interacting large-scale networks. Spontaneous empathic access is linked to the salience network, which detects behaviorally relevant signals, and to affective-sharing and mirror networks that allow another person’s state to resonate in the observer’s own affective circuitry. Inferential empathy recruits the mentalizing and frontotemporal social-inference circuits described above. Attributional empathy depends on self–other distinction and source-attribution systems, including regions such as the temporoparietal junction and prefrontal areas that have been implicated in distinguishing self-generated from externally generated mental content. Crucially, the authors emphasize that these networks do not operate in isolation; empathic success depends on their dynamic coordination, and empathic failure can arise from discoordination as readily as from damage to any single node.

A further layer of the model concerns interpersonal synchrony, the real-time coordination of self- and other-related signals during social interaction. Conversations involve continuous mutual adjustment of gaze, timing, rhythm, and affect. The review suggests that synchrony acts as a modulator across all three stages of empathic processing, helping to keep self- and other-related signals properly segregated and aligned as interaction unfolds. If synchrony mechanisms are disrupted in schizophrenia—as some evidence on sensorimotor coordination and social timing suggests—the stability of self–other distinction may degrade precisely in the live, fast-moving situations where empathy matters most. This may help explain why social difficulties in the disorder often appear more severe in dynamic interaction than in structured laboratory tasks.

The framework’s explanatory power lies in what it clarifies about existing accounts. Theory-of-mind models capture inferential failures but say little about emotional over-involvement. Empathic-disequilibrium models, which describe imbalances between cognitive and affective empathy, describe the pattern but do not fully explain its mechanism. By locating both under-response and over-response in the regulation of self–other distinction, the new framework unifies them: a person can show poor empathic accuracy because other-related representations are never clearly formed or are contaminated by self-related content, and simultaneously show heightened personal distress because other-related emotions are misattributed to the self. The apparent contradiction dissolves once empathy is understood as a multi-stage process whose stages can fail in different combinations in different patients.

This heterogeneity is perhaps the framework’s most clinically important implication. If empathy deficits in schizophrenia reflect less stable self–other distinction regulation across multiple stages, then patients may differ systematically in which stage is most affected. One patient’s primary problem might be spontaneous access to social cues, pointing toward interventions that enhance attention to and encoding of social signals. Another’s might be inferential representation, consistent with existing social-cognitive training programs targeting theory of mind. A third’s might be attributional, calling for approaches that strengthen the sense of mental ownership—helping patients learn to tag activated emotions and thoughts as self-generated or other-generated. The framework thus provides a mechanistic basis for profiling individual patients and matching them to targeted treatments, a step beyond one-size-fits-all social skills training.

Because the review is a theoretical synthesis, its claims now face the test of data. The authors frame their model explicitly in terms of testable predictions for behavioral studies, neuroimaging experiments, and intervention trials. Behavioral work could measure access, inference, and attribution as separable components within the same participants, testing whether they dissociate across patients. Neuroimaging studies could examine whether instability in self–other distinction networks predicts the specific pattern of empathic disturbance a patient shows. Intervention research could evaluate whether training that targets attributional processes reduces personal distress and emotional over-involvement in ways that theory-of-mind training alone does not. If those predictions hold, the humble question of where I end and you begin may turn out to be one of the most consequential frontiers in understanding the social brain—and in helping people with schizophrenia reclaim their place within it.

Subject of Research: Self–other distinction regulation and empathy processing in schizophrenia

Article Title: When “I” and “You” blur: self–other distinction failure and empathy dysregulation in schizophrenia

Article References: Huang, C., Yang, Y., Xie, P., & Zhou, A. (2026). When “I” and “You” blur: self–other distinction failure and empathy dysregulation in schizophrenia. Translational Psychiatry. https://doi.org/10.1038/s41398-026-04514-4

Image Credits: AI Generated

DOI: 10.1038/s41398-026-04514-4

Keywords: schizophrenia, empathy, self–other distinction, theory of mind, mentalizing, social neuroscience, personal distress, interpersonal synchrony, source attribution, Translational Psychiatry, social cognition, neurobehavioral framework