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.