Abstract

Introduction: Human disease models can help to better understand the pathophysiology and systematically characterize its consequences. Upper esophageal sphincter (UES) dysphagia is a common sequela of a number of disorders including CVA, reflux disease and aging. Intrinsic disorders of the UES such as fibrosis and inflammation can result in its diminished distensibility and restrict its opening causing dysphagia. Aim: To characterize the pharyngeal and UES deglutitive pressure phenomena in an experimentally induced restricted UES model in humans. Methods: We studied 15 patients (8 male, age 65±11 years) with various supraesophageal reflux symptoms. To induce UES restriction, we used a handmade simple device comprised of two components that could be comfortably worn around the neck: an elastic band and a cushion (5 X 3 X 2.5 CM). The cushion was placed horizontally at the center of the cricoid cartilage. By adjusting the elastic band, we selectively applied 0, 20, 30, 40 mmHg pressure perpendicular to the cricoid laryngeal structure inducing equivalent resistance against UES opening. In this model, the UES, in addition to relaxation, has to overcome the externally imparted pressure to open. Deglutitive pharyngeal and UES pressure phenomena were determined using high-resolution manometry, which recorded from entire pharynx, UES and proximal esophagus. We tested dry, 5 and 10ml swallows x 3. Results: Application of the external pressure band increased the length of the UES high pressure zone from 2.5 cm without the band to 3.1, 3.5 and 3.7 cm for 20, 30, 40mmHg cricoid restrictive pressure, respectively (p<0.05). Increased restrictive pressure against UES resulted in a significant increase in hypopharyngeal intra-bolus pressure (IBP) during all swallowed volumes (figure). Similarly, increased UES restrictive pressure resulted in increased UES nadir deglutitive relaxation pressure for all swallowed volumes (table, p<0.05). Swallowed volume had no effect on pharyngeal peak pressure, duration or velocity. None of these were affected by restrictive external UES pressures. Deglutitive velopharygeal pressure progressively increased with increased swallowed volume (p<0.05). These pressures were also not affected by UES restrictive external pressure. Conclusions: Acute experimental restriction of UES opening by external cricoid pressure in humans manifests the pressure characteristics of increased resistance to UES trans-sphincteric flow observed in disorders that are accompanied by reduced UES opening. These pressure characteristics include increased hypopharyngeal intra-bolus as well as nadir deglutitive UES relaxation pressures. This model can potentially be helpful in better understanding of UES pathophysiology. The effect of external cricoid (UES restrictive) pressure on UES nadir pressure

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