Cortical Activation and Functional Connectivity Changes during Swallowing in Patients with Dysphagia in Lateral...

Swallowing function is affected in patients with lateral medullary syndrome (LMS) due to impaired swallowing central pattern generator, but it remains unclear whether their cortical function is affected. To determine the level of cortical involvement during swallowing in LMS dysphagia patients. This is a cross-sectional study carried out from May 2023 and January 2024 in China. 21 patients with LMS dysphagia and 20 age-matched healthy controls were recruited. Functional near-infrared spectroscopy with 39 channels was utilized to detect the cortical hemodynamic changes when repeated salivary swallowing. Cortical activation and functional connectivity during swallowing were analyzed. Compared with healthy subjects, patients with LMS demonstrated reduced activation in bilateral dorsolateral prefrontal cortex(DLPFC), left temporopolar area, frontopolar area(PFA), and right pre-motor and supplementary motor cortex(pSMC) (channel 11, P = 0.031; channel 12, P = 0.042; channel 15, P = 0.042; channel 19, P = 0.031; channel 24, P = 0.031; channel 25, P = 0.031). The activation of patients with LMS in right primary somatosensory cortex (PSC), supramarginal gyrus (SMG), FPA and left pars triangularis (PTG) was negatively correlated with the PAS score (channel1, P = 0.019; channel 2, P = 0.005; channel 23, P = 0.017; channel 27, P = 0.047). The activation in right PSC and SMG was negatively correlated with the stroke duration (channel 2, P = 0.026; channel 16, P = 0.018). There is no difference in the mean functional connectivity strength between the channels of patients with LMS and healthy subjects (P = 0.565). The functional connectivity strength between the bilateral temporopolar areas was reduced in patients with LMS compared with healthy subjects(P = 0.015). Although the lesion site of patients with LMS dysphagia is in the medulla oblongata, cortical activation and functional connectivity during swallowing differ from those of healthy subjects, which may be related to damage of the ascending sensory pathways and cortical-medullary diaschisis.