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Background <p>Borderline Personality Disorder (BPD) is characterized by unstable relationships, affective dysregulation, and impulsivity. A growing body of evidence suggests that deficits in socio-cognitive domains (i.e., mentalization, empathy, and emotion recognition) contribute to the core psychopathology of BPD. However, the neural circuits underlying these deficits remain inconclusive.</p> Methods <p>We conducted a review of studies retrieved from PubMed, Scopus, and PsycINFO. We included structural MRI (sMRI) and functional MRI (fMRI) studies that compared individuals with BPD or borderline traits to healthy or clinical control groups. Eligible studies assessed social cognition using task-based paradigms (i.e., emotion recognition, empathy, Theory of Mind) or resting-state protocols focused on connectivity within social brain networks.</p> Results <p>Twenty-nine studies met the inclusion criteria. Most employed task-based fMRI (k = 24), with fewer using resting-state fMRI (k = 2) or structural MRI (k = 3). Common findings indicate hyperactivation of the amygdala under emotionally salient conditions, altered anterior cingulate cortex (ACC) responses (either hyper- or hypoactivation depending on stimulus valence), and insular hyperresponsivity to social threat contexts. Frontal hypoactivation (i.e., IFG) commonly co-occurred with limbic imbalance. Temporal and temporoparietal areas (STS, TPJ) showed variable patterns, with emotional empathy linked to increased activity and cognitive empathy to reduced activation.</p> Conclusions <p>Aberrant activation and connectivity in fronto-limbic and temporoparietal networks contribute to socio-cognitive dysfunction in BPD, underlying emotional dysregulation, impulsivity, interpersonal instability, and self-disturbance. Future standardized paradigms and longitudinal designs should clarify the progression of these neural disruptions and guide targeted psychotherapeutic and neuromodulatory interventions.</p>

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Neural correlates of social cognition in BPD: a review of MRI evidence

  • 期刊论文

  • 发表日期：

    2025年12月29日

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  • Francesca D’Adda,
  • Mauro Scala,
  • Margherita Magro,
  • Micaela Mitolo,
  • Giovanni Sighinolfi,
  • Caterina Tonon,
  • Raffaele Lodi,
  • Marco Menchetti

摘要

Background

Borderline Personality Disorder (BPD) is characterized by unstable relationships, affective dysregulation, and impulsivity. A growing body of evidence suggests that deficits in socio-cognitive domains (i.e., mentalization, empathy, and emotion recognition) contribute to the core psychopathology of BPD. However, the neural circuits underlying these deficits remain inconclusive.

Methods

We conducted a review of studies retrieved from PubMed, Scopus, and PsycINFO. We included structural MRI (sMRI) and functional MRI (fMRI) studies that compared individuals with BPD or borderline traits to healthy or clinical control groups. Eligible studies assessed social cognition using task-based paradigms (i.e., emotion recognition, empathy, Theory of Mind) or resting-state protocols focused on connectivity within social brain networks.

Results

Twenty-nine studies met the inclusion criteria. Most employed task-based fMRI (k = 24), with fewer using resting-state fMRI (k = 2) or structural MRI (k = 3). Common findings indicate hyperactivation of the amygdala under emotionally salient conditions, altered anterior cingulate cortex (ACC) responses (either hyper- or hypoactivation depending on stimulus valence), and insular hyperresponsivity to social threat contexts. Frontal hypoactivation (i.e., IFG) commonly co-occurred with limbic imbalance. Temporal and temporoparietal areas (STS, TPJ) showed variable patterns, with emotional empathy linked to increased activity and cognitive empathy to reduced activation.

Conclusions

Aberrant activation and connectivity in fronto-limbic and temporoparietal networks contribute to socio-cognitive dysfunction in BPD, underlying emotional dysregulation, impulsivity, interpersonal instability, and self-disturbance. Future standardized paradigms and longitudinal designs should clarify the progression of these neural disruptions and guide targeted psychotherapeutic and neuromodulatory interventions.