Striatal Dopaminergic Loss and Dysphagia in Parkinson Disease

Abstract

Purpose To better understand the development of dysphagia in patients with Parkinson disease (PD) and to identify possible neuromodulatory target regions of dysphagia, we studied the striatal dopamine transporter (DAT) availability distribution by subtype of dysphagia. Methods In this retrospective cross-sectional study, patients with PD who underwent videofluoroscopic swallowing study and N-(3-[18F]fluoropropyl)-2β-carbon ethoxy-3β-(4-iodophenyl) nortropane (18F-FP-CIT) PET at intervals of less than 1 month were analyzed. The 14 binarized subitem scores of the Videofluoroscopic Dysphagia Scale were analyzed using a voxel-wise Firth's penalized binary logistic regression model, adjusting for age and disease duration at videofluoroscopic swallowing study. Results Sixty-five patients with PD were finally included. Striatal mapping showed association of decreased DAT availability with 5 subitems with 1 or more clusters surviving the statistical threshold: 1 oral phase and 4 pharyngeal phase subitems. The overlap maps created by superimposing clusters for all 5 statistically significant subitems revealed associations of dysphagia in PD with decreased DAT availability in the bilateral ventral striatum. Of these, 4 subitems belonging to the pharyngeal phase-specific dysphagia were additionally found to be related to dopaminergic degeneration of the bilateral anterior-to-posterior caudate and ventral striatum. Conclusions These findings suggest that subitem/phase-specific striatal subregional dopaminergic depletion may explain the dysphagia of PD. This dopaminergic degeneration of striatal subregions specific to the phases of dysphagia may serve as a potential target for neuromodulatory brain stimulation through stimulation of cortices functionally connected.