A Simple and Reproducible In-Vivo Rabbit Phonation Model for Glottic Insufficiency
W. M. Swift, I. T. Churnin, O. A. Hamdi, A. M. Strumpf, H. A. Koehn, P. S. Cottler, J. J. Daniero
Abstract
IntroductionGlottic insufficiency can result from neurologic injury, surgery, radiation, and the aging larynx. Treatment includes voice therapy, vocal fold injection augmentation, surgical medialization, or laryngeal reinnervation procedures. The objective of this study is to describe an in-vivo rabbit phonation model for glottic insufficiency that is simple and reproducible by means of unilateral cricothyroid muscle stimulation and high-speed video recordings of evoked phonation. MethodsA non-randomized controlled trial utilizing seven New Zealand white rabbits was performed via a single operation including evoked phonation with bilateral and unilateral cricothyroid muscle stimulation conditions. The effect of stimulation method on glottic cycle, pitch and loudness was compared. Endoscopic recordings using 5,000 frames-per-second image capture technology and audiologic recordings were obtained for all phonation conditions. Primary outcome measures included means of maximum glottal area (MGA)/length pixel ratio, right and left amplitude/length pixel ratios, calculated cycle frequency, auditory recorded frequency, and maximum auditory intensity. Measurements were obtained via pixel counts using imageJ. Paired t-tests compared the average values obtained over five consecutive glottic cycles for each unilateral and bilateral stimulation during evoked phonation. ResultsMean (median, IQR) MGA/length was significantly greater with unilateral, 20.30 (19.13, 10.97), vs bilateral, 9.62 (8.33, 2.58), stimulation (p=0.043). Mean frequency (median, IQR), 683.46 Hz (658.5, 197.1) vs 479.92 Hz (458.1, 112); (p=0.027) and mean maximum intensity, 83.5 dB (83.5, 1) vs 76.3 dB (74.5, 4); (p=0.013) were significantly reduced from bilateral to unilateral stimulation. There was no significant difference of mean right amplitude/length between bilateral and unilateral. ConclusionThe described model demonstrates a simple and reproducible means of producing glottic insufficiency and represents a pathway for better understanding the biomechanics and pathophysiology of glottic insufficiency and offers the potential to compare treatment modalities through in-vivo study.
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