Capgras syndrome secondary to frontal traumatic brain injury in a patient with bipolar Il disorder: a case report with neuropsychiatric correlation

Abstract

Introduction: Delusional misidentification syndromes are rare neuropsychiatric conditions characterized by the belief that emotionally significant individuals have been replaced by identical doubles. Although traditionally associated with primary psychotic disorders, increasing evidence supports their occurrence in the context of structural brain lesions, particularly involving frontal lobes and fronto-limbic circuits. Objective: To report a case of Capgras syndrome secondary to frontal traumatic brain injury (TBI) in a patient with bipolar II disorder, correlating clinical and neuroimaging findings. Method: Registered on the Brazil Platform, CAAE: 97486826.7.0000.0155, Opinion 8.448.140. The author of the case report submitted a document waiving the Informed Consent Form. The case was analyzed through detailed review of clinical history, hospital records, neuroimaging studies, and outpatient neuropsychiatric follow-up. Clinical and imaging criteria were used to identify frontal TBI, acquired neurocognitive disorder, and Capgras syndrome, correlating findings with pre-existing mood and personality traits. Follow-up included serial cognitive assessments, naturalistic observation of delusional behavior, and response to psychotherapeutic and pharmacological interventions. Case report: A 66-year-old male with prior bipolar II disorder experienced multiple TBIs between 2024 and 2025, evolving with a frontal-predominant neurocognitive disorder. He developed fluctuating Capgras delusions directed at his main caregiver, while semantic and professional memory remained preserved. After the second TBI, a qualitative personality change was observed, with reduced aggressiveness and increased affability. Brain computed tomography revealed frontal gliosis and encephalomalacia, enlargement of frontal peri-encephalic spaces, compensatory ventriculomegaly, and hypodense white matter lesions. Discussion: This case illustrates the perceptual-affective disconnection underlying Capgras syndrome associated with frontal damage. Pre-existing bipolar II disorder showed altered clinical expression following TBI, with reduced impulsivity. Delusional episodes emerged in contexts of affective distress and were partially modulated by non-confrontational psychotherapeutic strategies and atypical antipsychotics. Conclusion: The report highlights the complex interaction between acquired frontal brain injury, neurocognitive disorder, and secondary Capgras syndrome in a patient with bipolar II disorder, emphasizing the relevance of integrated clinical, neuroimaging, and psychodynamic assessment.