Dysphagia in Lateral Medullary Infarction (Wallenberg’s Syndrome)

Abstract

Background and Purpose — We have investigated the pathophysiological mechanisms of dysphagia in Wallenberg’s syndrome (WS) that are due to lateral medullary infarction (LMI). Methods — Twenty patients with WS were evaluated by means of clinical and electrophysiological methods that measured the oropharyngeal phase of voluntarily initiated swallowing. For comparison, 22 patients with unilateral hemispheric infarction were investigated during the acute stage of stroke, and 4 patients with unilateral peripheral 9th and 10th cranial nerve palsies were studied. Age-matched 30 healthy control subjects were also included in the study. Results — It was found that dysphagia was clinically more severe in WS patients than in the patients in the other groups. The pharyngeal phase of swallowing was predominantly impaired, whereas in patients with hemispheric stroke, dysphagia was related only to the delay of triggering of the voluntarily induced swallowing. In WS patients, the swallowing reflex was extremely slow in spite of the unilateral involvement due to LMI, whereas the pharyngeal phase of reflex swallowing remained within normal limits in patients with unilateral hemispheric stroke and patients with unilateral peripheral 9th and 10th cranial nerve palsies. Conclusions — Although in WS the lesion due to LMI is unilateral, its effect on oropharyngeal swallowing is bilateral. In LMI, primarily the premotor neurons in the nucleus ambiguus and their connections seem to be affected. Consequently, a disruption and/or disconnection of their linkage to swallowing-related cranial motor neuron pools bilaterally and to the contralateral nucleus ambiguus could produce the swallowing disorders in WS. However, the remaining intact ipsilateral premotor neurons and the contralateral center in the medulla oblongata may eventually begin to operate and overcome the severity and long-term persistence of dysphagia.