To the Editor: Capgras delusion, the delusional conviction that one's intimate person has been replaced by a persecutory imposter, is separately associated with schizophrenia and several neurodegenerative conditions, in particular, vascular dementia.^1,2 However, no reports are still available on the de-novo emergence of Capgras delusion in the late course of chronic schizophrenia as a concomitant symptom of its complication by vascular dementia.

A 67-year-old woman with a 45-year history of paranoid schizophrenia was admitted in our Department, by reason of an exacerbation of her chronic psychotic symptoms since last year, especially the de-novo emergence of Capgras delusions on the identities of her husband and son. More precisely, she was convinced that both had been assassinated by the person claiming to be her husband and replaced by physical doubles who, moreover, intended to harm her fatally also. Accordingly, she lived withdrawn in her room and behaved aggressively whenever her husband tried to bring her food. Her husband reported also patient’s concomitant forgetting of recent events, as well as several episodes of losing her way back home after going out for buying food, with progressive aggravation, especially during the last 6 months. Of note, for years, the patient was taking her prescribed antipsychotic and antihypertensive medications only irregularly, refusing to attend her outpatient hospital appointments. She consented to the proposed hospitalization only to protect herself from the malevolent “imposters.” On admission, the patient was irritable, aggressive, and emotionally labile, experienced hallucinations of verbal communication with the divine, and expressed grandiose and persecutory delusions. She scored 15/30 on the MMSE, and an MRI scan disclosed multiple focal lesions in frontal, subcortical, and periventricular areas, indicative of vascular dementia. On four additional neuropsychological tests assessing visuospatial memory (Paired Associates Learning, Spatial Recognition Memory) and executive functioning (Intra/Extradimensional Shift, Stockings of Cambridge), her performance ranged within the lowest 5%–10% of normative scores. The patient was started on olanzapine titrated up to 20 mg/day and donepezil 10 mg/day. Her behavioral disturbances subsided progressively, and she was discharged 2 months later, much improved. On her last follow-up, 5 months later, her Capgras delusion had subsided as well, along with her remaining psychotic symptoms, despite the persistence of her cognitive deterioration.

The well-attested separate association of Capgras syndrome with chronic schizophrenia and vascular dementia implies its increased risk in patients affected by both. However, as the temporal pattern of their association in our case suggests, Capgras delusion might also be a clinical concomitant of the complication of chronic schizophrenia by vascular dementia, moreover, amenable to adequate antipsychotic treatment. The patient’s diffuse brain lesions included those incriminated in Cotard’s delusion, namely frontal and temporo-parietal systems.¹ Three other cases of Capgras delusion in the early stage of vascular dementia, however, in patients with otherwise unremarkable psychiatric history, have already been reported in the literature.^3–5 Although anecdotal, our case suggests that clinicians should be alert to concomitant cognitive status changes in patients with chronic schizophrenia and de-novo Capgras delusion.