Dysphagia Characteristics and Its Neuroanatomical Correlates in Korean Patients With Subcortical Vascular Cognitive...

Subcortical vascular cognitive impairment (SVCI) is frequently associated with dysphagia, but its specific characteristics and underlying neural mechanisms remain unclear. This study aims to investigate the swallowing characteristics in SVCI patients and examine their neuroanatomical correlates using diffusion tensor imaging-voxel-based morphometry (DTI-VBM).

Eighty-five SVCI patients and 20 normal controls underwent videofluoroscopic swallowing studies and 3.0-Tesla magnetic resonance imaging. Swallowing components were evaluated using Modified Barium Swallow Impairment Profile, Penetration-Aspiration Scale, and temporal measurements. Fractional anisotropy and mean diffusivity maps were analyzed to determine neuroanatomical correlates.

SVCI patients exhibited significant differences in tongue control during bolus hold, bolus preparation/mastication, bolus transport/lingual motion, oral residue in the oral stage and anterior hyoid excursion, epiglottic movement, laryngeal vestibular closure, tongue base retraction, vallecular residue, pyriform sinus residue, pharyngeal esophageal segment opening in the pharyngeal stage. Temporal measurements revealed significant delay in pharyngeal transit times (PTT). Time gap was shorter between initiation and maximal displacement of hyoid, hyoid maximal displacement and aryepiglottic closure, and longer between initiating movement of hyoid and bolus head reaching vallecula. DTI-VBM demonstrated that prolonged oral transit time correlated with the right corona radiata and anterior cingulate cortex. Prolonged PTT significantly correlated with microstructural alterations in the anterior insula, anterior cingulate cortex, corona radiata, internal capsule, corpus callosum, thalamus, brainstem, and cerebellar circuits.

SVCI patients manifest dysphagia in the oral and pharyngeal stage. Temporal measurements reveal delay in PTT which is correlated with widespread disruptions in the corticobulbar tract, frontal subcortical circuits, and cerebellar control circuits.