Objective: To assess if there are differential metabolic brain patterns among Progressive Supranuclear Palsy(PSP) clinical variants and between them and Parkinson’s disease patients (PD).

Background: Current PSP-MDS criteria provides a guideline to establish the diagnose of the different PSP variants[1]. They were based on clinicopathological multicentre studies of patients with defined PSP[2–5]. An accurate clinical diagnosis is both challenging and worthy. They are frequently misdiagnosed with PD or other atypical parkinsonism, but also, they differ significantly with regard to survival time and frequency of cognitive deficits. Regarding  18F-FDG-PET/CT metabolism has been correlated to tau neuropathology and neuronal degeneration[6,7] it could be a useful diagnostic tool.

Method: It is an observational, retrospective cohort study. We recruited patients with the diagnosis of a clinical variant of PSP based on PSP-MDS criteria who were evaluated by 18F-FDG-PET/CT according to clinical practice between November 1997 and December 2018. Social, demographic and clinical data were collected from medical records. Preprocessing and statistical analyses were performed with SPM12 (p<0.05, corrected by multiple comparisons by FWE). They were not only compared between PSP variants but also with the healthy subject (n=20) and PD patient cohorts (n=21).

Results: We recruited 38 patients (17 women) with final diagnosis of PSP: 18 PSP with Richardson’s Syndrome (PSP-RS), 14 PSP with predominant parkinsonism (PSP-P), 5 PSP with progressive gait freezing (PSP-PGF) and 1 PSP with predominant speech/language disorder (PSP-SL). Both, PSP-RS and PSP-P variants showed a significative hypometabolism in mesencephalon, caudate nuclei and medial thalamus. Additionally, PSP-RS patients showed a significative hypometabolism in anterior-medium cingulate cortex, supplementary motor area and orbitofrontal cortex, and PSP-P showed a significant hypometabolism in the putamen contralateral to themore affected side. PSP-PGF showed a significant hypometabolism in the caudate nuclei and insula cortex contralateral to the more affected side, and an hypermetabolism in bilateral precentral cortex, motor supplementary area and vermis. Finally, PSP-SL showed an hypometabolism in mesencephalon, medial thalamus and Broca’s area.

Conclusion: Different PSP variants show differences in relation to metabolic brain pattern measured by 18F-FDG-PET/CT.

References: 1] G.U. Höglinger, G. Respondek, M. Stamelou, C. Kurz, K.A. Josephs, A.E. Lang, B. Mollenhauer, U. Müller, C. Nilsson, J.L. Whitwell, T. Arzberger, E. Englund, E. Gelpi, A. Giese, D.J. Irwin, W.G. Meissner, A. Pantelyat, A. Rajput, J.C. van Swieten, C. Troakes, A. Antonini, K.P. Bhatia, Y. Bordelon, Y. Compta, J.C. Corvol, C. Colosimo, D.W. Dickson, R. Dodel, L. Ferguson, M. Grossman, J. Kassubek, F. Krismer, J. Levin, S. Lorenzl, H.R. Morris, P. Nestor, W.H. Oertel, W. Poewe, G. Rabinovici, J.B. Rowe, G.D. Schellenberg, K. Seppi, T. van Eimeren, G.K. Wenning, A.L. Boxer, L.I. Golbe, I. Litvan, A.L. Boxer, A. Rajput, A. Pantelyat, A. Antonini, A.E. Lang, A. Giese, B. Mollenhauer, C. Colosimo, C. Kurz, C. Nilsson, C. Troakes, D.J. Irwin, D.W. Dickson, E. Gelpi, F. Krismer, G.D. Schellenberg, G. Respondek, G. Rabinovici, G.K. Wenning, G.U. Höglinger, H.R. Morris, I. Litvan, J.B. Rowe, J. Kassubek, J.C. Corvol, J.L. Whitwell, J. Levin, J. van Swieten, K.P. Bhatia, K.A. Josephs, K. Seppi, L.I. Golbe, M. Stamelou, M. Grossman, P. Nestor, R. Dodel, S. Lorenzl, T. van Eimeren, T. Arzberger, U. Müller, W.G. Meissner, W. Poewe, W.H. Oertel, Y. Compta, Y. Bordelon, Clinical diagnosis of progressive supranuclear palsy: The movement disorder society criteria, Mov. Disord. (2017). doi:10.1002/mds.26987. [2] D.W. Dickson, Z. Ahmed, A.A. Algom, Y. Tsuboi, K.A. Josephs, Neuropathology of variants of progressive supranuclear palsy, Curr. Opin. Neurol. 23 (2010) 394–400. doi:10.1097/WCO.0b013e32833be924. [3] D.R. Williams, R. De Silva, D.C. Paviour, A. Pittman, H.C. Watt, L. Kilford, J.L. Holton, T. Revesz, A.J. Lees, Characteristics of two distinct clinical phenotypes in pathologically proven progressive supranuclear palsy: Richardson’s syndrome and PSP-parkinsonism, Brain. 128 (2005) 1247–1258. doi:10.1093/brain/awh488. [4] G. Respondek, C. Kurz, T. Arzberger, Y. Compta, E. Englund, L.W. Ferguson, E. Gelpi, A. Giese, D.J. Irwin, W.G. Meissner, C. Nilsson, A. Pantelyat, A. Rajput, J.C. van Swieten, C. Troakes, K.A. Josephs, A.E. Lang, B. Mollenhauer, U. Müller, J.L. Whitwell, A. Antonini, K.P. Bhatia, Y. Bordelon, J.C. Corvol, C. Colosimo, R. Dodel, M. Grossman, J. Kassubek, F. Krismer, J. Levin, S. Lorenzl, H. Morris, P. Nestor, W.H. Oertel, G.D. Rabinovici, J.B. Rowe, T. van Eimeren, G.K. Wenning, A. Boxer, L.I. Golbe, I. Litvan, M. Stamelou, G.U. Höglinger, Which ante mortem clinical features predict progressive supranuclear palsy pathology?, Mov. Disord. (2017). doi:10.1002/mds.27034. [5] G. Respondek, G.U. Hoglinger, The phenotypic spectrum of progressive supranuclear palsy, Park. Relat. Disord. (2016). doi:10.1016/j.parkreldis.2015.09.041. [6] N. Zalewski, H. Botha, J.L. Whitwell, V. Lowe, D.W. Dickson, K.A. Josephs, FDG-PET in pathologically confirmed spontaneous 4R-tauopathy variants, J. Neurol. 261 (2014) 710–716. doi:10.1007/s00415-014-7256-4. [7] R. Smith, M. Schöll, M. Honer, C.F. Nilsson, E. Englund, O. Hansson, Tau neuropathology correlates with FDG-PET, but not AV-1451-PET, in progressive supranuclear palsy, Acta Neuropathol. (2017). doi:10.1007/s00401-016-1650-1. [8] T. Müller, Emerging approaches in Parkinson’s disease – Adjunctive role of safinamide, Ther. Clin. Risk Manag. (2016). doi:10.2147/TCRM.S86393.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/is-18f-fdg-pet-ct-a-helpful-tool-to-diagnose-psp-clinical-variants/