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A Mouse Model of Dysphagia After Facial Nerve Injury. | LitMetric

A Mouse Model of Dysphagia After Facial Nerve Injury.

Laryngoscope

Otolaryngology-Head and Neck Surgery, University of Missouri, Columbia, Missouri, U.S.A.

Published: January 2021

Objective: Dysphagia is common following facial nerve injury; however, research is sparse regarding swallowing-related outcomes and targeted treatments. Previous animal studies have used eye blink and vibrissae movement as measures of facial nerve impairment and recovery. The purpose of this study was to create a mouse model of facial nerve injury that results in dysphagia to enhance translational research outcomes.

Study Design: Prospective animal study.

Methods: Twenty C57BL/6J mice underwent surgical transection of the main trunk (MT) (n = 10) or marginal mandibular branch (MMB) (n = 10) of the left facial nerve. Videofluoroscopic swallow study (VFSS) assays for drinking and eating were performed at baseline and 14 days postsurgery to quantify several deglutition-related outcome measures.

Results: VFSS analysis revealed that MT transection resulted in significantly slower lick and swallow rates during drinking (P ≤ .05) and significantly slower swallow rates and longer inter-swallow intervals during eating (P ≤ .05), congruent with oral and pharyngeal dysphagia. After MMB transection, these same VFSS metrics were not statistically significant (P > .05).

Conclusion: The main finding of this study was that transection of the facial nerve MT leads to oral and pharyngeal stage dysphagia in mice; MMB transection does not. These results from mice provide novel insight into specific VFSS metrics that may be used to characterize dysphagia in humans following facial nerve injury. We are currently using this surgical mouse model to explore promising treatment modalities such as electrical stimulation to hasten recovery and improve outcomes following various iatrogenic and idiopathic conditions affecting the facial nerve.

Level Of Evidence: NA Laryngoscope, 131:17-24, 2021.

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Source
http://dx.doi.org/10.1002/lary.28560DOI Listing

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