Summary
The Capgras syndrome is a delusional condition usually characterized by a belief that an impostor has replaced a closely related person.1 Although its etiology is not well understood, the development of Capgras syndrome is associated with either idiopathic psychiatric disorders (eg, schizophrenia) or organic conditions (eg, different types of dementia).2 To the best knowledge of the author, there is only 1 report on the Capgras syndrome resulting from the use of benzodiazepines.3
Original Article
Capgras Syndrome Associated With Bromazepam in a Patient With Vascular Dementia
Clinical Neuropharmacology
Margetić, Branimir MD, PhD
To the Editor:
The Capgras syndrome is a delusional condition usually characterized by a belief that an impostor has replaced a closely related person.1 Although its etiology is not well understood, the development of Capgras syndrome is associated with either idiopathic psychiatric disorders (eg, schizophrenia) or organic conditions (eg, different types of dementia).2 To the best knowledge of the author, there is only 1 report on the Capgras syndrome resulting from the use of benzodiazepines.3
This article describes the case of a patient with dementia whose psychotic symptoms of Capgras syndrome completely withdrew after discontinuation of bromazepam intake.
CASE
Mrs. A was an 88-year old woman when I first met her in March 2018. The appointment was initiated by the patient's son, who revealed that over the past 6 months, in addition to long lasting impaired recent memory, his mother has had transient, but more and more frequent, recurrent episodes during which she was saying that his brother and he were replaced by other persons and that her home was not hers. Her son also informed me that the patient had been taking bromazepam (3 mg before bedtime) because of anxiety and insomnia and antihypertensive drugs (lisinopril, 10 mg; hydrochlorothiazide, 12.5 mg). Doctors also prescribed warfarin (5 mg) after she survived pulmonary embolism in 2016. She never smoked or drank alcohol and had no previous psychiatric or neurologic history. She did not have any vision or hearing impairments that limited her activities.
Because she was a patient with psychomotor retardation, disoriented in time, and angry because “that person” presented himself as her son, she was diagnosed with dementia and organic psychosis with Capgras syndrome. A diagnostic workup was suggested, as well as quetiapine (25 mg) in the evening and bromazepam (1,5 mg to half of the previous dose).
The only diagnostic procedure she underwent was a brain computed tomography scan (in May 2018) that revealed several old bilateral periventricular infarctions in the white matter and an old lacunar vascular lesion in the head of the right nucleus caudate. The findings indicated vascular dementia.
However, although we scheduled the next appointment after 3 weeks (as suggested), the next time we met was in November 2019. In the meantime, she followed her “previously prescribed therapy” (bromazepam 3 mg/d) and refused to see a psychiatrist.
During the appointment, her son informed us that her memory loss was now pervasive and severe and that her delusional episodes during which she claimed that his brother and he had been replaced by imposters were now continuously present. He described the patient as mostly numb, but also with unpredictable outbursts of anger, crying, and verbally aggressive episodes directed at the “imposters.” The patient's son also said that the patient occasionally conversed with voices that only she could hear. The patient's thought processes and speech were slow and lacked ideas. The described symptoms of the Capgras syndrome were present, but the patient was not able to recall whether she had auditory hallucinations. Her score in the Mini-Mental State Examination was 16/30. I prescribed quetiapine (25 mg) in the evening and gradual discontinuation of bromazepam.
The last appointment was 3 weeks later, in December 2019. The patient's son said that the patient gradually completely stopped taking bromazepam during the course of 1 week after the last appointment, and also that immediately after that time delusional symptoms completely disappeared.
The patient was not showing symptoms of the Capgras syndrome and did not recall her previous delusional beliefs.
DISCUSSION
In this case, the gradual discontinuation of bromazepam intake that prompted the withdrawal of the Capgras delusional symptoms strongly indicates that although the syndrome developed years after the bromazepam had been first prescribed, its development was drug-induced.
On the other hand, she developed delusional symptoms at the same time the deterioration of the neurodegenerative processes impacted her cognitive abilities. Accordingly, the time needed for the Capgras syndrome symptom development or withdrawal reveals that cognitive changes take place when the 2 factors, benzodiazepine and dementia, are simultaneously present. It is also worth mentioning that approximately 15% of all reported cases of Capgras syndrome were associated with various types of dementia (more often with Parkinson disease, and only 1% of cases with the vascular type of dementia).2
In any case, we need to be cautious when prescribing benzodiazepines, especially in elderly patients, because they may produce psychotic features, including the syndrome of Capgras.
