Background & Aims: Oral-pharyngeal dysphagia in Parkinson's disease is
well recognized. The aim of this study was to establish the mechanism
s of oral-pharyngeal dysphagia in these patients. Methods: Using simul
taneous videoradiography and pharyngeal manometry, we studied 19 patie
nts with Parkinson's disease (12 with oral-pharyngeal dysphagia and 7
without oral-pharyngeal dysphagia) and compared them with 23 healthy c
ontrols. Results: The clinical severity of Parkinson's disease predict
ed neither the presence nor the severity of dysphagia. Minor alteratio
ns in oral function were common in controls and patients, but pharynge
al dysfunction was significantly more prevalent in patients. Incomplet
e upper esophageal sphincter (UES) relaxation was present in 4 patient
s (21%), all of whom showed increased hypopharyngeal intrabolus pressu
re, but not all of whom had a diminished UES opening, The patients had
a reduced UES diameter (P = 0.004) and a higher intrabolus pressure c
ompared with the controls (P = 0.007). Pharyngeal contraction pressure
s were lower in patients, but 6 patients with dysphagia and an abnorma
l pharyngeal wall motion had normal peak pressures. Conclusions: An in
complete UES relaxation and a reduced UES opening, both associated wit
h high intrabolus pressure, are prevalent in Parkinson's disease. Oral
-pharyngeal dysphagia in Parkinson's disease is multifactorial, with t
he majority of patients showing oral and pharyngeal dysfunction, even
before the clinical expression of dysphagia. Impaired pharyngeal bolus
transport is the major determinant of dysphagia.