State-Dependent Biomechanical Behavior of Oropharyngeal Structures in Apneic and Control Subjects: A Proof-of-Concept Study

Rationale: Apneics have reduced airway caliber during sleep. The biomechanical changes in upper airway anatomy contributing to this airway narrowing are largely unknown. Objectives: To investigate the state-dependent (wake vs. sleep) biomechanical behavior of the upper airway soft-tissue and craniofacial structures. Methods: Upper airway magnetic resonance imaging was performed in 15 sleep-deprived controls (AHI<5; 0.3±0.5 events/hour) and 12 sleep-deprived apneics (AHI≥5; 35.2±18.1 events/hour) during wake and sleep and analyzed for airway measures and soft-tissue/mandibular movement. Results: In the retropalatal region, controls showed sleep-dependent reductions (p≤0.037) in average cross-sectional airway area (CSA), minimum CSA, anteroposterior, and lateral dimensions. Apneics showed sleep-dependent reductions (p≤0.002) in average CSA, minimum CSA, anteroposterior and lateral dimensions. In the retroglossal region, controls had no sleep-dependent airway reductions. However, apneics had sleep-dependent reductions in minimal CSA (p=0.001) and lateral dimensions (p=0.014). Controls only showed sleep-dependent posterior movement of the anterior-inferior tongue octant (p=0.039), while apneics showed posterior movement of the soft palate (p=0.006) and all tongue octants (p≤0.012). Sleep-dependent medial movement of the lateral walls was seen at the retropalatal minimum level (p=0.013) in controls and the retropalatal and retroglossal minimum levels (p≤0.017) in apneics. There was posterior movement of the mandible in apneics (p≤0.017). Conclusion: During sleep, controls and apneics showed reductions in retropalatal airway caliber; only apneics showed retroglossal airway narrowing. Reductions in anteroposterior and lateral airway dimensions were primarily due to posterior soft palate, tongue and mandibular movement and medial lateral walls movement. These data provide important initial insights into obstructive sleep apnea pathogenesis.