• K Del Tredici and W H Jost.
• AG Klinische Neuroanatomie (Abteilung Neurologie), Zentrum Klinischer Forschung, Universität Ulm, Ulm, Deutschland.
• Nervenarzt. 2012 Oct 1;83(10):1282-91.

AbstractGastrointestinal dysfunction is frequent during all stages of Parkinson's disease. The entire gastrointestinal tract becomes involved and symptoms include sialorrhea, dysphagia (difficulties swallowing), delayed gastric emptying, absorption problems and constipation. These non-motor symptoms can be manifested even prior to the initial Parkinson diagnosis, i.e. during the so-called premotor phase of the disorder and may serve as prodromal markers of the early non-motor disease phase. In addition to causing patients major discomfort and a reduced quality of life, such gastrointestinal complaints can also negatively influence the therapy with antiparkinsonian medications. Thus, delayed gastric emptying is an important cause of unforeseen motor fluctuations.Gastrointestinal dysfunction is attributable in part to the presence of synucleinopathy (Lewy pathology) both in the dorsal motor nucleus of the vagus nerve, which supplies the parasympathetic innervation of the gut from the distal esophagus to the left colonic flexure, as well as in the intramural Meissner and Auerbach plexuses of the enteric nervous system (ENS). In all probability the development of the lesions in the lower brainstem and in the ENS precedes neurodegeneration of the dopaminergic nigrostriatal system. From a diagnostic standpoint, neurologists need not only a carefully taken patient history and the clinical findings but also esophagography (barium study), gastric scintigraphy and assessment of the colonic transit time. The therapeutic options for impaired upper gastrointestinal tract motility are still limited. Sialorrhea can be reduced by prescribing anticholinergics or injections of botulinum toxin and the peristalsis can be modulated by domperidone. In the lower gastrointestinal tract, constipation can be conservatively treated by using macrogol (polyethylene glycol) and, in the future, perhaps by serotonine (5-HT4) agonists.

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