Mechanisms of dysphagia in suprabulbar palsy with lacunar infarct

Background and Purpose-The objective of the present study was to investigat e the neural mechanisms of dysphagia in suprabulbar palsy (SBP) with multip le lacunar infarct. Methods-We evaluated the swallowing disorders of patients with SEP (n=34) a nd age-matched healthy control subjects (n=35) by means of an electrophysio logical method that recorded the oropharyngeal swallowing patterns. With th is method, dysphagia limit, the triggering of voluntarily initiated swallow s, duration of laryngeal relocation time, and total duration of oropharynge al swallowing were recorded and measured. In addition, the EMG behavior of the cricopharyngeal (CP) muscle of the upper esophageal sphincter was also assessed. Results-In patients with SEP, the dysphagia limit in all except 1 patient w as pathological with limits of <20-mL bolus volume, which is contrary to no rmal subjects, in whom the dysphagia limit exceeds the 20-mL bolus volume. Either triggering of swallowing reflex was delayed (P<0.04), or the swallow could hardly be triggered in 7 patients on the voluntary attempts for 3 mt water. Whenever the reflex swallowing could be triggered, it was slow and prolonged (P<0.01). The CP muscle of the upper esophageal sphincter appeare d to have become hyperreflexic and incoordinated with laryngeal movements d uring swallowing. Conclusions-It was proposed that the progressive involvement of the excitat ory and inhibitory corticobulbar fiber systems linked with the bulbar swall owing center is mainly responsible for the triggering difficulties of the s wallowing reflex and for the hyperreflexic/incoordinated nature of the CP s phincter. In addition, the dysfunction of the extrapyramidal system has a s pecific role in the slowing of oropharyngeal swallowing and the accumulatio n of saliva in the mouth.