Abstract

Delusional Misidentification Syndrome with Response to Donepezil and Behavioral Intervention in a Patient with Dementia

Muhammad Ubaid Hafeez, Katherine T. Mun, Haris Kamal and Kinga Szigeti

Introduction: Delusional Misidentification Syndrome (DMS) encompasses a group of disorders in which a person persistently believes the identity of people, places, or objects are altered. Historically, described in psychotic disorders, DMS prevalence is 15.8% in Alzheimer's disease (AD) and 16.6% in dementia with Lewy bodies (DLB). We present a case of DMS in a patient with dementia that incorporates elements of mirrored self-misidentification and phantom boarder syndrome and therapeutic response to a combination of a behavioral intervention and donepezil.

Case: 75-year-old white female presented with a four months history of DMS and visual hallucinations. Patient perceived her own reflection in picture glass as an older lady who was trying to steal her "boyfriends." Her "boyfriends" were three pictures of soldiers in her apartment. MMSE was 27/30 (WORLD) and 23/30 (Serial 7s). MRI showed biparietal and right hippocampal atrophy. NPT showed impaired language, spatial abilities, memory, and executive control. She scored <1 percentile on category word fluency, judgement of line orientation, raw complex figures and Beery VMI. Patient was diagnosed with probable AD, using NINCDS-ADRDA and findings on neuropsychological testing (NPT) and MRI. DLB was excluded using McKeith's criteria. After a failed trial of risperidone, she received donepezil and family was instructed to remove photographs. MMSE stable with resolution of the mirrored selfmisidentification at 4 months follow up.

Conclusion: Patient's poor response to risperidone is consistent with previous studies suggesting limitations of antipsychotic treatment for psychotic symptoms in AD. Removal of potential symptom trigger along with an acetylcholinesterase inhibitor resulted in remission for up to 4 months. The potentiating effect of donepezil on the cholinergic component of the visuo-amygdaloid pathway/dorsal visual pathway may account for these changes.