1317 Treatment Emergent Central Sleep Apnea Following Hypoglossal Nerve Stimulator Placement for Obstructive Sleep Apnea

Abstract Introduction Treatment-emergent central sleep apnea (TECSA) is characterized by the presence of central events after resolution of obstructive sleep apnea (OSA) with therapy, typically positive airway pressure (PAP). TECSA with hypoglossal nerve stimulation (HGNS) is rare, with reported prevalence around 3.3% in cohort studies of non-PAP therapies such as surgery and dental mandibular advancements devices. Mechanisms may involve ventilatory instability, and it is often transient. Report of case(s) A 62-year-old male with a medical history of anxiety, depression, gastroesophageal reflux disease (GERD), obesity with BMI 27.3 and Severe OSA presented for management after CPAP intolerance. The patient reported no significant comorbidities like heart failure or opiate use that could explain alternative CSA etiologies, and physical exam was unremarkable. Baseline polysomnography (PSG) in 2019 showed an apnea-hypopnea index (AHI) of 31.3 events/h with no significant central sleep apnea. The patient underwent HGNS implantation combined with radiofrequency ablation (RFA) of lingual tonsils by otolaryngology in March 2025 followed by activation of device in April 2025 at an amplitude of 1.1 V. During the subsequent September 2025 HGNS titration PSG, the device was initiated at 1.6 V (0.2 V below the incoming amplitude of 1.8 V), revealing predominantly central events. The overall AHI was 53.9 events/h, with cAHI 30.52 events/h (suggestive of TECSA), and no REM sleep observed. Further titration up to 2.0V resulted in a residual AHI of 33 events/h. Conclusion This case highlights TECSA as a potential complication of HGNS for OSA, manifesting as a shift from obstructive to predominantly central events during titration, despite initial low central indices. TECSA's transient nature in many cases supports initial supportive management with close monitoring and setting adjustments to the lowest effective voltage for patient tolerance. For persistent or symptomatic TECSA, options include transitioning to bilevel PAP, acetazolamide to reduce loop gain, or arousal threshold-raising agents. Emerging approaches, such as concurrent phrenic nerve stimulation for dual neuromodulation, have shown promise in refractory cases. In-lab post-implantation titration is essential to detect TECSA, optimize therapy, and facilitate shared decision-making, balancing residual AHI with quality of life. Further studies are needed to establish HGNS-specific resolution rates and risk factors. Support (if any)