Case Report
A 41-year-old man presented with gait disorder, hoarseness, and
dysphagia. He was diagnosed with a left LMS due to infarction (Fig. 1),
and oral antiplatelet therapy was initiated. His neurological deficit
almost improved except for severe dysphagia. Eleven months after the
onset, he underwent a percutaneous endoscopic gastrostomy. Fourteen
months after the onset, he was transferred to the rehabilitation
department of our hospital for dysphagia treatment.
A videofluoroscopic examination of swallowing (VF) revealed weak
pharyngeal contractility and an impaired upper esophageal sphincter
(UES) function. The bolus remained in the pyriform sinus and did not
pass through the pharynx (Fig. 2). The swallowing pressure along the
pharynx and UES was measured using HRM. HRM revealed weak pharyngeal
constriction and strong constriction of the UES muscle zone (Fig. 3). We
used the pharyngeal contractile integral (CI; mmHg·cm·s) to evaluate the
pharyngeal swallowing pressure.3,4 The patient was
examined for five dry swallows. During swallowing, the velopharyngeal CI
(VPCI) and mesohypopharyngeal CI (MHPCI) values were 4.1 ± 2.9 and 72.0
± 16.2 respectively (As reference values for this patient data, the VPCI
and MHPCI values for 3 mL of thickened liquids in our previous report
were 124.3 ± 50.3 and 193.2 ± 34.1, respectively4).
Regarding the patient’s UES function, the UESCI was
713.7 ± 72.7, indicating strong
contraction during swallowing.
The patient received nutritional treatment, respiratory training, and
swallowing rehabilitation (i.e., balloon catheter dilation, Shaker
exercise, and vacuum swallowing therapies). He was discharged 16 months
after the initial onset. He is continuing his swallowing rehabilitation
at home and receiving treatment on an outpatient basis. This study was
approved by the Ethics Committee of our hospital.