The Effect of Ansa Cervicalis Stimulation on Velopharyngeal Cross-sectional Area in Patients With Obstructive Sleep Apnea

Rationale: Obstructive sleep apnea (OSA) is characterized by recurrent pharyngeal obstruction during sleep. Ansa cervicalis stimulation (ACS) is proposed as an alternative therapeutic neurostimulation mechanism for maintaining airway patency, but it is currently unknown whether ACS dilates or stiffens the pharynx. Dilating forces reduce surrounding tissue pressure, increasing pharyngeal cross-sectional area (CSA) to the same degree across different intraluminal pressures, thereby generating a parallel shift in the slope of the pressure-area curve. Stiffening forces reduce pharyngeal compliance, which decreases the variation in CSA response at different intraluminal pressures and flattens the slope of the pressure-area curve. The effect of ACS was investigated in this study by plotting velopharyngeal CSA across a range of intraluminal pressures.Methods: Pharyngeal intraluminal pressure and cross-sectional area (CSA) were assessed in sixteen patients with moderate-to-severe OSA during drug-induced sleep endoscopy (DISE). Fine-wire percutaneous electrodes were placed bilaterally proximate to the branch of the ansa cervicalis innervating the sternothyroid muscle. Continuous positive airway pressure (CPAP) was applied by nasal mask. Changes in CSA were measured on and off ACS by endoscopy at end-expiration for intraluminal pressures ranging from non-flow-limited inspirations (POPEN) to atmospheric pressure or apneic inspirations (PCRIT). Pressure-area curves were plotted using a linear mixed effects model to investigate how ACS altered velopharyngeal CSA response across the investigated CPAP pressures. Results: ACS generally increased mean CSA (0.38±0.31 to 0.67±0.38 cm2; median Δ=156.6%; p<0.05). At PCRIT, CSA increased by 0.26±0.14 cm2(671%; p<0.05) and at POPEN, CSA increased by 0.28±0.25 cm2(141%; p<0.05). The absolute change in CSA did not differ significantly between PCRIT and POPEN with application of ACS (p=0.90). The slope of CSA response did not change significantly in a linear mixed effects model (see Figure 1; p=0.97). Conclusions: ACS increased velopharyngeal CSA over a range of airway pressures, but it did not alter the slope of CSA response to CPAP. The findings suggest that ACS primarily dilated the velopharyngeal lumen by reducing surrounding tissue pressures rather than stiffening the airway. ACS may have different local effects on other pharyngeal structures. Analyses are continuing across an expanded patient cohort. Figure 1. A linear mixed effects model plotting pharyngeal cross-sectional area (CSA) against nasal continuous positive airway pressure (CPAP). The slope of CSA response did not change significantly in a linear mixed effects model (p=0.97).

Duke Scholars

Author Christopher Lindsell Biostatistics & Bioinformatics, Division of Biostatistics