• G N Ali, K L Wallace, R Schwartz, D J DeCarle, A S Zagami, and I J Cook.
• Department of Gastroenterology, St. George Hospital, University of New South Wales, Sydney, Australia.
• Gastroenterology. 1996 Feb 1;110(2):383-92.

Background & AimsOral-pharyngeal dysphagia in Parkinson's disease is well recognized. The aim of this study was to establish the mechanisms of oral-pharyngeal dysphagia in these patients.MethodsUsing simultaneous videoradiography and pharyngeal manometry, we studied 19 patients with Parkinson's disease (12 with oral-pharyngeal dysphagia and 7 without oral-pharyngeal dysphagia) and compared them with 23 healthy controls.Resultsthe clinical severity of Parkinson's disease predicted neither the presence nor the severity of dysphagia. Minor alterations in oral function were common in controls and patients, but pharyngeal dysfunction was significantly more prevalent in patients. Incomplete upper esophageal sphincter (UES) relaxation was present in 4 patients (21%), all of whom showed increased hypopharyngeal intrabolus pressure, 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 compared with the controls (P = 0.007). Pharyngeal contraction pressures were lower in patients, but 6 patients with dysphagia and an abnormal pharyngeal wall motion had normal peak pressures.ConclusionsAn incomplete UES relaxation and a reduced UES opening, both associated with high intrabolus pressure, are prevalent in Parkinson's disease. Oral-pharyngeal dysphagia in Parkinson's disease is multifactorial, with the 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.

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