Reduplicative paramnesia as an early neuropsychiatric manifestation of posterior cortical atrophy

Background

Reduplicative paramnesia (RP) is a delusional misidentification syndrome in which a familiar place is believed to exist in duplicate. Although usually considered to have a neurological aetiology, RP lies firmly within neuropsychiatry, as it combines altered perception, disturbed familiarity attribution and delusional belief formation. It has been described due to tumours, strokes, traumatic brain injury and degenerative disorders, most often involving right hemisphere and/or frontal networks. These regions support visuospatial processing, spatial organisation, facial and place recognition.

Aims

To describe RP as the presenting neuropsychiatric feature of a progressive posterior visual syndrome and to discuss how focal right occipital pathology, Alzheimer’s disease biomarkers and later posterior cortical atrophy may have contributed to delusional misidentification.

Methods

We report a longitudinal single-case study of a 79-year-old man with no previous psychiatric history, followed between 2021 and 2025. Data were obtained from serial clinical interviews, collateral history from his wife and daughter, neurological and neuropsychiatric examinations, Mini-Mental State Examination (MMSE), structural magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) biomarkers, and amyloid positron emission tomography (PET). Cognitive scores, biomarker values and imaging findings are presented descriptively.

Results

The patient initially developed a highly structured belief that a second version of his street had been created parallel to the real one, containing identical shops and a house identical to his own, distinguished only by a different number. He repeatedly checked the exterior of the house to determine whether he was in the “correct” one. This was accompanied by misidentification of his wife and intermittent disorientation inside his home, but without hallucinations, formal thought disorder or previous psychotic symptoms. Initial MMSE was 26/30, with disproportionate visuoconstructive impairment. Examination suggested higher-order visual dysfunction.

MRI showed extensive periventricular ischaemic leukoencephalopathy and a right occipital cortico-subcortical lesion with microhaemorrhagic features, raising the possibility of cerebral amyloid angiopathy-related or ARIA-like pathology, although later multidisciplinary review considered an ischaemic lesion with haemorrhagic component as an alternative. CSF biomarkers supported Alzheimer’s disease pathology: Aβ42 781 pg/mL, Aβ42/Aβ40 ratio 0.067, total tau 540 pg/mL and phosphorylated tau 89.4 pg/mL. Amyloid PET later confirmed increased cortical beta-amyloid deposition. After starting donepezil, the RP resolved and MMSE improved to 29/30. Over time, however, the patient developed progressive visuoperceptive impairment, including simultanagnosia, apperceptive agnosia, alexia and inability to identify visually presented objects despite tactile recognition. MMSE later ranged from 19/30 to 24/30. Follow-up MRI demonstrated bilateral parieto-occipital atrophy, posterior cortical atrophy grade 2. Memantine was subsequently introduced.

Conclusions

This case adds to the observational literature on reduplicative paramnesia, particularly by illustrating its clinical phenomenology alongside detailed neuroimaging and biomarker characterisation. It highlights that the presence of delusions does not necessarily indicate a primary psychiatric disorder, especially in older individuals without prior psychiatric history. Instead, delusional misidentification may represent an early neuropsychiatric manifestation of underlying brain pathology, in this case associated with posterior cortical dysfunction and biomarker-supported Alzheimer’s disease. Early recognition of this presentation may improve diagnostic accuracy and guide appropriate management in atypical dementia.

References

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