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.