Objectives/hypothesis: Given the complex pathology underlying unilateral vocal fold paralysis (UVFP), there has been limited systematic exploration of curative treatments in humans. Central to the investigation of experimental therapies includes establishing a reliable and analogous large animal model. The study goal was to create a standardized porcine model of UVFP by establishing characteristic pathophysiology and functional outcomes.
Methods: Four female Yucatan minipigs underwent transection of the right recurrent laryngeal nerve (R-RLN). Measurements of acoustic vocalization data, bilateral nerve conduction studies, and laryngeal adductor pressure (LAP) were obtained prior to transection (baseline) and 7weeks after transection. Laryngeal adductor muscle complex volume was analyzed via 3D ultrasound. Histological analysis with myofiber diameter measurement of bilateral thyroarytenoid muscles was conducted at study conclusion.
Results: Stimulation of the R-RLN 7weeks after transection demonstrated reduction of motor unit action potentials. In addition, there was a statistically significant reduction in LAP compared to preinjury when stimulating the R-RLN. Voice analysis notably revealed decreased intensity and frequency ranges at 7weeks postinjury, and statistically lower average intensity and frequency of glottic phonations. Denervated right-sided laryngeal muscle volume was statistically lower compared to noninjured side. Morphological changes consistent with denervation, including smaller myofibril diameters and decreased nerve-to-muscle contact, were observed in right thyroarytenoid muscle and associated neuromuscular junctions.
Conclusions: Given that our porcine model yielded histopathological and functional changes consistent with human UVFP, it has potential to serve as a viable model for systematic and controlled studies of potential treatments for UVFP.
Level of evidence: NA.
Keywords: Recurrent laryngeal nerve; Translational model; Unilateral vocal fold paralysis.
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