Discussion
To our knowledge, this was the first report to biomechanically clarify the pathophysiology of severe dysphagia due to LMS using HRM. The primary finding of this study was that the UES closed strongly during swallowing in a bulbar dysphagic patient with LMS. During normal swallowing, UES pressure drops to zero or below, whereas UES pressure in our patient increased abnormally during swallowing.
Notably, we calculated the pharyngeal CI as a measure of contractility to evaluate the pressure gradient between pharyngeal contraction and an impaired UES function. The CI was calculated as amplitude × duration × length of muscular contraction ≥ 20 mmHg. It can act as a useful indicator of pharyngeal swallowing disorders.2 The CI is a measure of the “vigor” of contractility, and it has the potential to provide objective representations of pharyngeal and UES muscular functions. Compared with normal subjects, this patient’s VPCI and MHPCI values were low owing to pharyngeal contractile weakness, whereas his UESCI was dramatically high owing to abnormal UES closing. The weakened pharyngeal contraction and dramatically closed UES during swallowing significantly interfere with the pharyngeal passage of a bolus in this patient with severe bulbar dysphagia.
HRM provided a more accurate and quantitative assessment of swallowing function. The high-pressure zone of the UES is narrow and asymmetric, and it moves up and down with the elevation of the larynx during swallowing. Therefore, a catheter with circumferential sensors is necessary to evaluate the UES function precisely. Decreased pharyngeal contraction and elevation of UES pressure during swallowing was reported using conventional sensors in these studies.2,5 It is difficult to precisely measure the “vigor” of abnormal UES contractility with these conventional sensors.
The central pattern generator (CPG) for swallowing, located in the medulla, manipulates and controls the oropharyngeal phase of the swallowing sequence.1 Abnormalities in the UES function owing to dysphagia-causing LMS have been reported, but there have been few reports regarding the associated pathophysiology. The NA and NTS, located in the lateral medulla of the CPG, control the muscles of the pharynx and UES. Therefore, an LMS lesion that includes the NA and NTS can cause weak pharyngeal contraction and abnormal UES relaxation. This may lead to severe bolus residue in the pyriform sinuses after swallowing and, therefore, the possibility of subsequent aspiration. Patients with bulbar dysphagia due to lesions in LMS may experience deficits in pharyngeal and UES function, such as UES and pharyngeal incoordination, abnormal UES relaxation and forceful closure, and weak pharyngeal contraction.
Continuous swallowing rehabilitation (i.e., balloon catheter dilation and Shaker exercise), nutritional treatment, and respiratory muscle training would be beneficial for these patients with failed UES relaxation. If there is no sufficient improvement with these approaches, then clinicians could apply cricopharyngeal myotomy as an additional treatment. This is the only case report on this topic, which may be a limitation. Therefore, future studies should evaluate additional cases to verify our case findings.