Objective: To describe clinical and imaging differences in de novo PD with and without REM sleep Behaviour Disorder (dnPDRBD – de novo PD) and de novo DLB with RBD (dnDLBRBD) patients to gain insight on the neuronal α-synuclein diseases (NSDs) continuum.

Background: The new definition of NSDs suggests that a clear distinction between PD and DLB should be reconsidered.[1]

Method: 32 de novo PD (age 72.6±6; 23 males), 30 de novo DLB (age 78±5.4; 18 males) patients with evidence of RBD, and 31 de novo PD (age 71.8±6; 19 males), underwent clinical and neuropsychological evaluation, brain [¹⁸F]FDG PET and [¹²³I]FP-CIT SPECT. Between-group demographic, clinical, cognitive and imaging features were compared by performing an analysis of variance (ANOVA). [¹⁸F]FDG-PET and [¹²³I]FP-CIT SPECT images (48%) were flipped (More affected hemisphere-MAH= right; Less Affected Hemisphere-LAH= left).

Results: Compared with dnPDRBD and de novo PD, dnDLBRBD patients were older, with lower education and lower MMSE scores (p<0.001)[Table 1]. Differences in frequency of MCI, Parkinsonism, Visual Hallucinations and Fluctuations are summarized in Figure 1. We found a significant variance in [¹⁸F]FDG uptake in the temporal and occipital gyri, precuneus, and the right cuneus[Figure 2A]. At post-hoc, dnDLBRBD patients have a worst alteration of brain metabolism than de novo PD and dnPDRBD patients (p<0.0001)[Figure 2B]. De novo PD presents with a significantly lower [¹²³I]FP-CIT binding in the LAH Putamen (p=0.04), MAH Putamen (p=0.04), mean Putamen uptake (p=0.03) and LAH Caudate (p=0.02) compared to dnPDRBD. [¹²³I]FP-CIT binding profiles are shown in Figure 3. dnDLBRBD patients had a more severe global cognitive impairment than both de novo PD and dnPDRBD patients. de novo PD and dnPDRBD patients had a similar cognitive profile[Figure 4].

Conclusion: We confirmed that DLB and PD are placed on the same pathological NSDs continuum. In PD, presence of RBD helps determining in which end of the continuum patients fit better.

Table 1: Demographic and clinical features.

Figure 1: Frequency of core clinical features

Figure 2: FDG Analysis of variance (ANOVA) results

Figure 3: SPECT Analysis of variance (ANOVA)

Figure 4: NPS Analysis of variance (ANOVA) results

References: [1] Simuni, T., Chahine, L. M., Poston, K., Brumm, M., Buracchio, T., Campbell, M., … & Marek, K. (2024). A biological definition of neuronal α-synuclein disease: towards an integrated staging system for research. The Lancet Neurology, 23(2), 178-190.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/early-dementia-with-lewy-bodies-and-parkinsons-disease-with-rbd-two-faces-of-the-same-coin/