Brain Structural Changes Underlying Dysphagia in Parkinson’s Disease: An Exploratory Multimodal Quantitative MRI Study
Brain Structural Changes Underlying Dysphagia in Parkinson’s Disease: An Exploratory Multimodal Quantitative MRI Study
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Original abstract
Abstract Dysphagia is a substantial and often underrecognized burden in Parkinson’s disease (PD), and its neural underpinnings remain poorly understood. In this retrospective study, we employed a multimodal neuroimaging approach to investigate structural brain changes associated with dysphagia in PD. We included 105 participants in the age range of 45 to 84 years: 35 PD with dysphagia (PDD), 35 PD without dysphagia (PDnD), and 35 age- and sex-matched healthy controls (HC). Oropharyngeal dysphagia was confirmed through clinical swallowing evaluation or video fluoroscopic swallow study. We obtained T1 and diffusion-weighted MRI from all our participants. We analyzed them using voxel-based morphometry, surface-based morphometry, tract-based spatial statistics, and graph-theoretical structural connectivity analysis. Relative to HC and PDnD groups, the PDD group showed widespread gray matter atrophy ( p < .05) in the cerebellum, temporal lobes, subcortical regions, and prefrontal cortices. Surface-based morphometry revealed significant cortical thinning ( p < .00001), reduced sulcal depth, altered fractal dimension, and increased gyrification (all p < .05) in motor, limbic, and orbitofrontal regions. The PDD group also showed significant white matter atrophy in brainstem, cerebral, and cerebellar areas, with reduced fractional anisotropy and increased mean diffusivity in key sensorimotor and autonomic pathways ( p < .05). No widespread differences were observed between the PDD and PDnD groups across structural modalities. Graph-theoretical analysis showed trends toward reduced global network integration and segregation in the PDD group, though these did not reach statistical significance. Together, these findings support a model in which dysphagia in PD reflects widespread, network-level structural degeneration across both gray and white matter, extending beyond classical brainstem swallowing centers.