Friday, May 9, 2025
5/9/2025
Brain Networks Supporting Oral and Pharyngeal Swallow Function after Stroke - PROJECT SUMMARY Swallowing impairment, dysphagia, is common after stroke and can have serious consequences, leading to morbidity and reduced quality of life. Despite the significance of dysphagia, we lack fundamental knowledge regarding the neuroanatomical mechanisms underlying oral and pharyngeal dysphagia to allow us to accurately predict which patients will 1) spontaneously recover swallow function, 2) need treatment to recover function, or 3) have limited potential for recovery leaving clinicians making “best guesses” for prognosis guided decisions such as feeding tube placement and treatment. Such knowledge is critical to improving patient care and outcomes. It will ultimately lead to being able to prescribe swallowing treatment targeting precise brain network elements for optimal recovery. Current reasons for our limited understanding of the neural control of swallowing are three-fold. Most prior research has 1) used approaches to measure dysphagia that cannot quantify oral and pharyngeal swallow physiology, 2) neglected the simultaneous and concerted contribution of connected brain areas to swallowing, and 3) drawn inferences from small patient samples recruited from a single institution. Thus, we propose a mechanistic study to identify and assess the importance and generalizability of brain networks in oral and pharyngeal swallow impairments in a large cohort of patients. To overcome limitations from prior studies, we propose to use validated and standardized measures derived from the Modified Barium Swallow Study, use modern lesion-based symptom mapping analyses to identify a network of regions and connections (the circuitry) that collectively contribute to swallowing physiology, and recruit from two major stroke centers in the southern U.S. with a recruitment goal of N=400 individuals. Further, we will assess the impact of stroke damage on brain circuitries and the impact of age-related neuroanatomical changes, i.e., white matter hyperintensities. We hypothesize that both stroke lesions and white matter hyperintensities damage brain networks and contribute to the severity of oral and pharyngeal dysphagia after stroke. Our study has three aims: 1) to determine the neuronal circuitry supporting the oral phase of swallowing after stroke, 2) to determine the neuronal circuitry supporting the pharyngeal phase of swallowing after stroke, and 3) to determine the additional impact of disconnections caused by white matter hyperintensities on the neuronal circuitry supporting oral and pharyngeal swallowing after stroke. From our study, we expect to identify a set of brain regions and connections that form a brain network supporting oral swallowing and to identify an overlapping, albeit different, network supporting pharyngeal swallowing. Our findings will provide a theoretical foundation of swallowing control and contribute to a comprehensive explanatory neuroanatomical model of dysphagia. In the short term, our findings can improve estimations of dysphagia risks and patient counseling in the early stroke stages. In the long term, our findings will aid in identifying neuroanatomical targets for interventions and potentially prevent life-threatening complications associated with dysphagia.
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