Reduplicative Paramnesia: Not Only One

To the Editor: Reduplicative paramnesia (RP) is characterized by a subjective certainty that a place has been duplicated;¹ it is considered a type of delusional misidentification having a clear parallel with Capgras’ delusion, which involves reduplication of people.² Reduplicative paramnesia most often occurs in patients with neurodegenerative disorders, stroke, head trauma, or psychiatric disorders.^3–5 We describe four patients with RP and try to explain how RP helps us analyze the underlying causes of this delusional syndrome, related to implicit and explicit memory circuits.

Four Case Notes

• Patient #1: A 70-year-old-woman observed in the emergency room for ataxic syndrome and neuroimaging finding of right temporal meningioma. In the few days before surgical treatment, she was alert and oriented, and was able to describe “her two houses;” she was aware of having an apartment in Rome, but in the previous month, the apartment had “become” two, two identical houses, with identical furniture, on the same floor, and at the same address. She had been questioning herself about this strange condition, and she could explain it, she said, “because the government didn’t have money to give us, so they gave us some houses.” One month after the meningioma was removed, the patient was still oriented and did not have neurologic signs: she could talk about “her two-houses story,” and she was aware that there were not two houses. Neuropsychological examination (see Tab.) did not reveal memory impairment, and her neurological condition was unchanged on subsequent visits in the 18 months of follow-up.

• Patient #2: The patient was a 63-year-old man admitted to the neurology department because of the sudden onset of left hemiparesis. Brain CT and MRI disclosed an ischemic cortical lesion in the right frontal and temporal lobe. Three days after admission, the patient’s movements improved, but he was disoriented in time and place. On the 4th day after admission, he tried repeatedly to leave his room and the department because he “wanted to find his room.” When questioned, he descrbed “his room,” which was identical to his current one, but was in front of the department. The next day, the patient was again disoriented for a while and was convinced about “his room:” He said, “There are the same doctors, same beds, but this is not my room; I need to leave this room to find my clothes and belongings.” After being discharged, the patient was not always disoriented. He could walk, did not manifest reduplicative symptoms, and did not remember them. MMSE was 26/30. He did not attend the second visit because of a brain injury from a traffic accident, and the neuropsychological assessment was not completed.

• Patient #3: This was an 80-year-old man, with a high level of education, who presented with RP after years of treatment with venlafaxine and pregabalin prescribed for depressive and anxious syndromes. Six months earlier, he had manifested recurrent, episodic, brief language disturbance; epilepsy (aphasic seizures) was the most likely diagnosis, and sodium valproate was prescribed. At that time, symptoms of RP manifested rarely; if questioned about it, the patient unwillingly described “ his other house,” because he recognized it as a strange point of his life, but sometimes he had the feeling that he was in another house, identical to his, but, at same time, different. When his wife reminded him of the stories about their objects and furniture in the home, he admitted that really it “could” be his house. An MRI of the brain was performed twice and showed temporal and frontal lobe atrophy, more evident on the right side. A neuropsychological examination showed cognitive deterioration, with amnesic and attentive deficit. Frontal dysfunction might have been related to pronounced depression. After some months, the mental status of the patient worsened, with confusion, psychomotor agitation, and incoherent persecutory delusions. After neuroleptic treatment with haloperidol for 20 days, he remained confused.

• Patient #4: The patient was an 80-year-old woman with memory and behavior disorder due to frontotemporal dementia. The symptoms started 1 year before our clinical assessment, when she said to her daughter that her house was not hers, even if it was identical. When asked about this, she said that her husband had changed their house while she was outside. She was not able to critique this idea, and she repetitively kept saying to her daughter, “You haven’t ever seen my house. It’s no longer the house you knew; it’s another one, even if it seems the same house.” The CT of her brain showed brain atrophy in the frontal lobe. During a neuropsychological examination, she was alert and oriented, but with executive and amnesic dysfunction.

Discussion

In 1905, Pick⁶ described a hospitalized woman in Prague who was convinced of another identical hospital existing in the neighboring city, with identical rooms and doctors. Pick named the disorder RP because he saw the disorder as a reduplication of memory, and, since this first case, even if several patients have been reported, RP is considered an infrequent disorder that allows neurologists to explore the fascinating mechanism of memory circuits.

The description of these four cases gave us the opportunity to underline the heterogeneity of this disorder with regard to possible causes and type of manifestations.

Patient #1 had a temporal lobe lesion (meningioma); was never confused; and she could analyze her symptoms. Her neuropsychological examination and her daily autonomy did not reveal any memory damage.

Patient #2, with a frontotemporal stroke, was temporarily confused; he reduplicated his room in the hospital and was unaware of his disorder.

Patient #3 had been treated for depression for many years and manifested signs of RP some months before symptoms related to late-onset psychosis. He reduplicated his home, was not confused, and was initially aware of his unusual situation.

Patient #4 had chronic frontotemporal dysfunction from dementia. She reduplicated her home, initially sometimes and with partial awareness, then more constantly when the degenerative process was worsening.

Why does a patient reduplicate only temporarily their unfamiliar room in the hospital and others reduplicate a familiar place (their home)? Is there the same mechanism at work for these different cases? A confusional state is not always associated with RP, but, when patients with RP are confused, they reduplicate any place, even if is not a familiar place. As for other reduplicative syndromes, a theoretical dysfunction of implicit/emotional memory circuits is considered to be the underlying cause of RP, and many authors have underlined the importance of frontal or temporal lobe damage.⁷ Not all of these patients had abnormal functioning of episodic memory (see Patient #1), and this suggests that only an implicit memory disorder is necessary to RP manifestations.^8,9

Recent tractography evidence confirms that visually specialized cortical areas are connected by two parallel pathways: 1) the ventrolateral parieto-frontal U-shaped fibers; and 2) the direct occipito-temporal pathway or inferior longitudinal fasciculus (ILF), connecting pre-striate cortex to medial temporal structures (the hippocampus, parahippocampal gyrus, and amygdala). It is possible that the direct occipito-temporal pathway relates to emotional visual memory.¹⁰ Furthermore, the superior longitudinal fasciculus (SLF; connecting the visual parietal lobe and frontal cortex) and the inferior fronto-occipital fasciculus (IFOF; connecting areas in the occipital lobe and ventral frontal lobe) are likely to relate to functions such as visual working memory and visual attention. “Hodological” disorders relates higher function and dysfunction to connections between different locations, and RP can be considered a type of hodological disorder for a disconnection of visual and affective or memory regions.^11–13

Furthermore, implicit storage of information does not require attention,¹² so a confused patient can encode implicit information about a place, but when he sees that place again, with his fluctuating mental state, he does not recollect that place (SLF or IFOF dysfunction?); it is an old place, unconsciously, and a new place, consciously, so there are two identical places. Patients with no confusional state associated, as Patient #1, who present with temporary visuolimbic damage or, maybe, occipito-temporal fasciculus, can show symptoms of reduplication, but they are able to stigmatize their symptoms and try to find a logical explanation.

In conclusion, RP can occur transiently or chronically in relation to different causes; specific visual memory circuits (maybe including ILF or SLF and IFOF) can be damaged, producing different forms of reduplication related to familiar or unfamiliar places; amnesic syndrome is not necessary to produce RP (see Table 1).

In the future, it would be very interesting to study those cases with Diffusion Tensor Imaging (DTI) to demonstrate whether damage exists to specific tracts carrying reciprocal connections between the occipital lobe, the hippocampus, the amygdala, and the frontal lobe.