Dysphagia is common after stroke, with a reported incidence of 51% to 73%¹. Lesions in the cortex, subcortex, or brainstem related to strokes can result in swallowing difficulties. Dysphagia after stroke can lead to several complications such as malnutrition and aspiration pneumonia. Thus, assessing the swa-llowing function of patients with stroke is important.

The Killian-Jamieson diverticulum is an uncommon esophageal diverticulum that originates as an out-growth from the upper esophageal lateral wall. It arises from a region of anatomical weakness known as the Killian-Jamieson space, which is located infe-rior to the cricopharyngeus muscle and laterally to the longitudinal muscle of the cervical esophagus². Esophageal dysphagia and hoarseness may occur. In addition, remnant food boluses in the diverticulum may be aspirated, resulting in life-threatening com-plications such as aspiration pneumonia.

There are many reports of swallowing disorders after cerebral infarction. However, worldwide, few studies have reported Killian-Jamieson diverticulum as the cause of dysphagia after cerebral infarction; and to our knowledge, there have been no reported cases in Korea. Herein, we report the clinical features and findings based on our experience with an incidental finding of Killian-Jamieson diverticulum discovered during a videofluoroscopic swallowing study (VFSS) in a patient complaining of swallowing difficulties after cerebral infarction.

A 66-year-old female patient was brought to the emergency room with a three-day history of right hemiplegia. Past medical history revealed hypertension and type 2 diabetes diagnosed 10 years prior to ad-mission, for which she was being treated with angio-tensin II antagonists, glimepiride, metformin, and gemigliptin.

On admission, the muscle strength in the left upper and lower extremities was normal; however, the right upper and lower extremity strengths were grade 3/4 and 0/1, respectively. Diffusion-weighted brain mag-netic resonance imaging revealed a distinct signal from the left periventricular white matter (PVWM). (Fig. 1) Cerebral infarction was diagnosed, and anti-thrombic medication was initiated.

Figure 1. (A) Brain magnetic resonance imaging showing a distinct signal in the region of the left periventricular white matter in a diffusion-weighted image. (B) Apparent diffusion coefficient map.

Upon hospitalization, no specific findings were observed in the screening test for dysphagia. However, the patient complained of intermittent aspiration, chest discomfort, difficulty swallowing during meals with odynophagia, and halitosis after eating. The patient reported that she had not experienced any dysphagia symptoms prior to the onset of cerebral infarction.

An initial VFSS was performed six days after admission. No abnormalities were observed during the oral and pharyngeal phase of swallowing. There were no swallowing abnormalities with the consumption of liquids. However, during the esophageal phase, with viscous foods such as semisolids (food bolus mixed with thickener in water or yogurt), the food bolus remained in the esophageal area at the C5-6 level from the lateral view.(Fig. 2) A Killian-Jamieson diverticulum was suspected. No reflux or aspiration from residues in the suspected diverticulum was observed. Therefore, additional tests were not con-ducted as we judged that the Killian-Jamieson diver-ticulum found incidentally was not related to the patient’s symptoms.

Figure 2. Initial videofluorographic image, obtained six days after admission, showing contrast deposited in the esophageal area at the C5-6 level.

However, the patient complained of persistent dysphagia. The patient had esophagogastroduode-noscopy about 3 months ago, but there were no specific findings. Therefore, a computed tomography (CT) was performed focusing on the neck-to-chest region to detect any anatomical abnormalities that could be causing the swallowing difficulties. A Killian- Jamieson diverticulum of approximately 12 mm was noted on the left side of the esophagus at the C5-6 level.(Fig. 3) In addition, bronchial wall thickening and endobronchial secretions were observed in the posterior segment of the right upper lobe and in both lower lobes in CT, indicating bronchopneumonia or chronic aspiration pneumonia. This result may have been associated with intermittent aspiration.

Figure 3. A chest computed tomography showing the Killian- Jamieson diverticulum on the left side (arrow) of the upper esophagus.

Immediately after CT, a second VFSS was perfo-rmed because there was no other reason to account for the patient’s symptoms and chronic pneumonia besides Killian-Jamieson diverticulum. The Killian- Jamieson diverticulum was visible in the left side of the esophagus in the anteroposterior view.(Fig. 4) Multiple swallowing or the addition of liquids did not compensate for the stagnant food bolus in the diverticulum. Furthermore, with continued attempts to swallow, reversed flow and aspiration were confir-med by the VFSS. Any other abnormal findings were checked related to the patient’s symptoms.

Figure 4. Second videofluorographic image (anterioposterior view) showing that double swallowing did not compensate for the contrast deposited in the diverticulum (arrow).

Based on these findings, diverticulum was iden-tified as the cause of the dysphagia and chronic pneumonia. Consequently, we emphasized the impor-tance of treating the diverticulum to the patient and caregivers. However, the patient’s caregivers disagreed with the aggressive treatment options, which inclu-ded surgical procedures such as diverticulectomy and cricopharyngeal myotomy, because these procedures would necessitate the temporary discontinuation of antithrombotic medication. Furthermore, in addition to the dysphagia, the patient’s other functions were affected by the cerebral infarct. The patient scored 22 points on the Korean Mini-Mental State Examina-tion and 32 points (out of a possible 100) on the modified Barthel Index, indicating severe dependency for activities of daily living. These results also contri-buted to the caregivers’ decision regarding more aggressive treatment in the patient. Fortunately, as of two months from discharge to the date of this report, the patient has had no complications such as aspiration pneumonia. We will continue to closely monitor the diverticulum by performing follow-up VFSS every three months. If the follow-up VFSSs reveal significant changes, it may be necessary to persuade the patient/caregivers to consider appropriate treatment.

Killian-Jamieson diverticulum is associated predo-minantly with females, at a mean age of 58. Like in our patient, the majority of instances are unilateral and on the left side. Typically asymptomatic, Killian- Jamieson diverticulum is frequently discovered by chance during radiological imaging. The most preva-lent symptom in patients who are symptomatic is dysphagia³. Other signs and symptoms include halitosis, hoarseness, regurgitation, odynophagia, coughing, neck ache, and swelling. An esophageal diverticulum re-quires rapid diagnosis as it can lead to dangerous complications such as aspiration pneumonia and com-plicated diverticulitis.

The pathophysiology of the Killian-Jamieson diver-ticulum remains unknown; however, a Killian-Ja-mieson diverticulum develops because of functional outflow restriction in the proximal esophagus because of improper contraction of the circular muscle fibres⁴. And esophageal muscle atrophy may lead to swallo-wing difficulties⁵.

Asymptomatic diverticula or diverticula that are small do not require treatment. Patients can be ma-naged expectantly until symptoms occur. However, if symptoms occur and are severe, treatment is indi-cated. Surgery is the definitive treatment for sympto-matic Killian-Jamieson diverticula and involves diver-ticulectomy and cricopharyngeal myotomy. Recently, minimally invasive surgical approaches are preferred due to reduced morbidity, absence of surgical scars, and rapid postoperative recovery^6,7.

Cerebral infarction is major cause of swallowing disorders. The left hemispheric PVWM is a common site of acute brain injury associated with dysphagia. Lesions in the left PVWM may be more disruptive to swallowing behavior than lesions in the right⁸.

PVWM, the white matter adjacent to the body of the lateral ventricles, is involved in the neural control of swallowing. Somatosensory and descending motor fibers and intrahemispheric corticocortical pathways are segregated within the PVWM. PVWM lesions may disconnect the anterior and posterior cortical regions that are critical for swallowing coordination⁹. Thus, with dysphagia caused by PVWM infarction, the patient typically complains of difficultly with initiating swa-llowing or coordination during swallowing, which can be seen on the VFSS; however, that was not consistent with this case.

The patient had no dysphagia before cerebral infarction. In this regard, several possibilities could explain the relation between cerebral infarction and Killian-Jamieson diverticulum. In our opinion, the most likely possibility is that there was originally a Killian-Jamieson diverticulum and the food bolus was impacted there. But considering the size and location, it was not enough to elicit symptoms. However, it became severe enough to cause symptoms after the onset of cerebral infarction. It is believed that the cerebral infarction changes the coordination and esophageal pressure of the esophagus, and this leads the food impaction in the Killian-Jamieson diverticulum to reflux.

Another possibility is that considering the patho-physiology of Killian-Jamieson diverticulum, it was formed because of the cerebral infarction. Kim¹⁰ reported incomplete opening of the upper esopha-geal sphincter, and elevation of the oropharyngeal and hypopharyngeal pressures in patients after medullary cerebrovascular accidents. We do not think it is likely in this case because the diverticulum was observed in the VFSS conducted six days after the stroke, which is a very short time for the diverticulum to form because of the stroke. Although, there were no specific findings that were observed during an esophagogastroduodenoscopy performed approximately three months prior, esophagus, near UES, thinks that due to the pressure of UES, it is difficult to observe closely, so it may have missed the diverticulum.

This report presents the case of an esophageal diverticulum incidentally found during a VFSS in a patient with cerebral infarct and complaints of swallowing difficulties. In the present case, a diver-ticulum was not initially suspected as the cause of the dysphagia because we did not think that the location of the esophageal diverticulum and size were serious factors that could cause dysphagia. However, after checking more closely in the follow-up VFSS, we could observe aspiration and reflux, which are belie-ved to be the cause of dysphagia. This case underlies the importance that even if the size of the diverti-culum is small and located at the lower level, it could be exacerbated by cerebral infarction and should be considered as the cause of dysphagia.

This study was approved by the Dong-Eui Hospital Institutional Review Board (IRB No. DEMC-2023-02).

Woosup Song, Kihun Hwang, Kyungmin Kim, and Sanggyu Seo declare that they have no conflict of interest.

Woosup Song and Kihun Hwang: reviewed the topic and supervised all aspects of data collection, analysis, and report writing; Kyungmin Kim and Sanggyu Seo: conception and design. All authors contributed to data analysis and manuscript writing.