Gastrointestinal dysfunction in parkinson’s disease: Frequency and pathophysiology
Although more extensive research is required to fully characterize the pathophysiology of the gastrointestinal symptoms in PD, much of the presently available data suggest that the primary PD process is the major factor in the etiology of gut dysfunction in this patient population. This may be mediated by both central and peripheral mechanisms. Involvement of the dorsal motor nucleus of the vagus might produce dysfunction of muscles controlling deglutition and esophageal motility, thereby leading to drooling, dysphagia, and gastroesophageal reflux. The presence of Lewy bodies, the primary neuropathologic finding in the CNS in PD, in the myenteric plexus of both the esophagus and colon suggests that the PD process may also affect the enteric nervous system and contribute to the development of esophageal dysmotility and constipation through this peripheral mechanism. Dopamine receptors have been identified in the lower esophageal sphincter and the esophageal body of animals. If similarly present in humans, involvement of this dopaminergic system could contribute to the development of dysphagia and nausea of PD. Constipation may reflect both peripheral involvement, indicated by Lewy bodies in the colonic myenteric plexus, leading to colonic inertia, and central mechanisms, leading to pelvic floor dysfunction.