Objective: To detect white matter abnormalities in PSP patients and their correlation with motor and cognitive impairment.

Background: Progressive Supranuclear Palsy (PSP) is a tauopathy characterized by a complex and heterogenic clinical presentation [1]. It has been hypothesized that clinical deficits in PSP could be associated with the degeneration of long-range white matter tracts.

Method: Twenty healthy controls (HC) and nineteen progressive supranuclear palsy (PSP) patients were evaluated using diffusion-weighted MRI on a 3T scanner. Voxelwise statistical analysis of the FA and MD data was carried out using Tract-Based Spatial Statistics [2] (TBSS) and FSL’s randomise [3]. PSPRS scale [4] and Frontal Assessment Battery (FAB) [5] were used to measure disease severity and executive dysfunction, respectively.

Results: Tract-based statistics (TBSS) showed global reductions of FA across most tracts of PSP patients compared with matched healthy controls. Specifically, reduced FA and increased MD was predominantly detected in the corpus callosum, bilateral superior longitudinal fasciculus, bilateral superior and anterior corona radiata, bilateral posterior thalamic radiation and cerebellar peduncles. FA in these tracts also positively correlated with FAB scores in PSP patients. Motor disease severity as measured by the PSPRS scale showed a significant negative correlation with TBSS FA tracts in the corpus callosum, the bilateral superior coronal radiata, the left anterior coronal radiata and left anterior thalamic radiation. No regions showed decreased FA or increased MD in HC compared with PSP patients. No correlation was detected between the MD tracts and FAB and PSPRS scale.

Conclusion: These findings confirm previous results of white matter abnormalities in long-range tracts in PSP patients. More importantly, reduced integrity in these tracts correlate with measures of executive dysfunction and motor disease severity, indicating the predominance of these long-range pathways in the evolution and symptomatology of the disease.

References: [1] Armstrong, M.J., 2018. Progressive Supranuclear Palsy: an Update. Curr. Neurol. Neurosci. Rep. 18, 12. [2] S.M. Smith, M. Jenkinson, H. Johansen-Berg, D. Rueckert, T.E. Nichols, C.E. Mackay, K.E. Watkins, O. Ciccarelli, M.Z. Cader, P.M. Matthews, and T.E.J. Behrens. Tract-based spatial statistics: Voxelwise analysis of multi-subject diffusion data. NeuroImage, 31:1487-1505, 2006. [3] Winkler AM, Ridgway GR, Webster MA, Smith SM, Nichols TE. Permutation inference for the general linear model. NeuroImage, 2014;92:381-397. [4] Golbe, L.I., Ohman-Strickland, P.A., 2007. A clinical rating scale for progressive supranuclear palsy. Brain 130, 1552–1565. [5] Dubois, B., Slachevsky, A., Litvan, I., Pillon, B., 2000. The FAB: a Frontal Assessment Battery at bedside. Neurology 55, 1621–6.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/white-matter-abnormalities-correlate-with-clinical-features-in-psp-patients/