Finite Element Analysis of Upper Airway in Ansa Cervicalis Stimulation for Obstructive Sleep Apnea.

Gupta, Mukund; Li, Songrui; Luo, Haoxiang; Kent, David T; Li, Yike · Laryngoscope · 2026

biomechanical · Level V

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Abstract

To develop a subject-specific, three-dimensional finite element (FE) model of the human upper airway and evaluate how ansa cervicalis stimulation (ACS), a novel neurostimulation for obstructive sleep apnea (OSA), alters upper airway anatomy under physiologic loading. Upper airway anatomy was reconstructed from a head-and-neck CT of an adult female using a semi-automated pipeline, including segmentation, smoothing, tetrahedral meshing, and registration. Linear elastic material properties were assigned from the literature. ACS was simulated as a caudal load on the anterior thyroid cartilage, and inspiratory collapse tendency was mimicked with a -70 Pa luminal negative pressure. Structural displacement and cross-sectional area (CSA) changes were quantified at the soft palate, lateral pharyngeal wall, tongue base, and epiglottis. ACS produced caudal displacement of the thyroid cartilage by approximately 10 mm with coordinated motion of the hyolaryngeal complex and longitudinal pharyngeal wall strain. It also tilted the epiglottis antero-inferiorly and increased its curvature, reducing posterior-inferior motion under negative pressure by more than 50% (5.0 to 2.2 mm). Retro-epiglottic CSA increased by 68.8% without negative pressure (42.43 to 71.63 mm<sup>2</sup>) and by 2980.3% with negative pressure (0.79 to 24.19 mm<sup>2</sup>). Retropalatal CSA improved by 34.4% without negative pressure (65.04 to 87.42 mm<sup>2</sup>) and by 20.3% with negative pressure (16.98 to 20.43 mm<sup>2</sup>). This proof-of-concept, subject-specific FE model shows that ACS imparts caudal traction through the hyolaryngeal complex, producing multilevel anatomic stabilization under physiologic loading. The findings establish a quantitative, hypothesis-generating framework for interrogating ACS-mediated airway stabilization mechanisms and support further investigation across broader OSA populations and collapse phenotypes. N/A.