B C Sonies1, M C Dalakas. 1. Department of Rehabilitation Medicine, Warren G. Magnuson Clinical Center, Bethesda, Md.
Abstract
BACKGROUND AND METHODS: Dysphagia may develop in some patients many years after an attack of acute paralytic poliomyelitis. To identify clinical or subclinical signs of oropharyngeal dysfunction, we examined 32 patients (mean age, 48.9 years) with the post-polio syndrome (defined by new weakness in the limbs). Of the 32 patients, 14 had symptoms of new swallowing difficulties, and 18 were asymptomatic in this respect; 12 had a history of bulbar involvement during acute poliomyelitis. Swallowing function was assessed objectively by ultrasonography, videofluoroscopy, and an oral motor index score for 10 components of oral function. RESULTS: All but 1 of the 32 patients, regardless of whether they had new symptoms or previous bulbar involvement, had some abnormality on detailed testing of oropharyngeal function; only 2 patients had any signs of aspiration. The mean oral motor index score (a quantitative measure of oral sensorimotor function) in the patients was higher than that in age-matched normal subjects (P less than 0.001). Videofluoroscopy showed abnormalities of varying severity, including unilateral bolus transport through the pharynx, pooling in the valleculae or pyriform sinuses, delayed pharyngeal constriction, and impaired tongue movements. On ultrasonography, the mean (+/- SD) duration of wet swallows was significantly longer in the symptomatic patients than in the asymptomatic patients (2.67 +/- 0.70 vs. 1.65 +/- 0.42 seconds). The four patients who were reexamined two years later had objective signs of worsening oropharyngeal function and corresponding new symptoms. CONCLUSIONS: In patients with the post-polio syndrome, the bulbar muscles often have clinical or subclinical signs of dysfunction. These abnormalities suggest that in bulbar neurons there is a slowly progressive deterioration similar to that in the muscles of the limbs.
BACKGROUND AND METHODS: Dysphagia may develop in some patients many years after an attack of acute paralytic poliomyelitis. To identify clinical or subclinical signs of oropharyngeal dysfunction, we examined 32 patients (mean age, 48.9 years) with the post-polio syndrome (defined by new weakness in the limbs). Of the 32 patients, 14 had symptoms of new swallowing difficulties, and 18 were asymptomatic in this respect; 12 had a history of bulbar involvement during acute poliomyelitis. Swallowing function was assessed objectively by ultrasonography, videofluoroscopy, and an oral motor index score for 10 components of oral function. RESULTS: All but 1 of the 32 patients, regardless of whether they had new symptoms or previous bulbar involvement, had some abnormality on detailed testing of oropharyngeal function; only 2 patients had any signs of aspiration. The mean oral motor index score (a quantitative measure of oral sensorimotor function) in the patients was higher than that in age-matched normal subjects (P less than 0.001). Videofluoroscopy showed abnormalities of varying severity, including unilateral bolus transport through the pharynx, pooling in the valleculae or pyriform sinuses, delayed pharyngeal constriction, and impaired tongue movements. On ultrasonography, the mean (+/- SD) duration of wet swallows was significantly longer in the symptomatic patients than in the asymptomatic patients (2.67 +/- 0.70 vs. 1.65 +/- 0.42 seconds). The four patients who were reexamined two years later had objective signs of worsening oropharyngeal function and corresponding new symptoms. CONCLUSIONS: In patients with the post-polio syndrome, the bulbar muscles often have clinical or subclinical signs of dysfunction. These abnormalities suggest that in bulbar neurons there is a slowly progressive deterioration similar to that in the muscles of the limbs.