Gastrointestinale Störungen als frühes nicht-motorisches Symptom bei Patienten mit der REM- Schlaf- Verhaltensstörung und dem idiopathischen Parkinson Syndrom

Delayed gastric emptying is an early non-motor symptom of Parkinson’s disease and can preexist several years before the typical motor symptoms tremor, rigidity and hypokinesia occur. Nausea and vomitus have an affect on the health-related quality of life. Moreover the delayed gastric emptying can influence the L-dopa resorption and the resulting motor fluctuations. Braak et al described one of the earliest lesions-Lewy bodies- of the neurodegenerative process in the dorsal motor nucleus of the vagal nerve (DMNV) of the central nervous system. In further stages the Lewy bodies are seen in nuclei of the lower brainstem and the cerebral cortex. Moreover this degenerative process of DMNV could also be in patients with the idiopathic rapid-eye-movement sleep behavior disorder (RBD), a presumable pre-motor stage of Parkinson’s disease. The consequence is delayed gastric emptying because of the reduced parasympathetic activity of the vagal nerve. A hormonal cause of the delayed gastric emptying could be an orexigenic peptide namely Ghrelin, that promotes gastrointestinal motility. It has been shown that Ghrelin has also a neuroprotective potential in the MPTP-toxin mouse model of Parkinson disease. The aim of the study was to analyze the nerval und humoral changes of the delayed gastric emptying in different and early stages of Parkinson disease. We therefore investigated the delayed gastric emptying with the 13C-octonaote breath test and the postprandial Ghrelin response in healthy volunteers, in patients with RBD, and in patients with Parkinsons disease with medication and those without. 20 healthy controls, 13 patients with RBD, 21 drug-naïve patients with Parkinson’s disease (de novo PD) and 18 under treatment (PD) underwent standardized 13C-octonaote breath test to measure changes in gastric emptying. Furthermore the fasting and postprandial Ghrelin serum concentrations were measured using a commercial radioimmunassay in 20 healthy controls, 11 patients with RBD and 39 (including 19 drug-naïve) patients with Parkinson’s disease (all PD). The patients with de novo PD and PD showed significant delayed gastric emptying compare to the healthy controls (p< 0.001). The patients with RBD had normal gastric emptying as well. The serum concentration of Ghrelin on healthy controls was decreased in the early postprandial phase and increased after 60 minutes following the feeding and reached the maximum level on 300 minutes. In the late post prandial phase a significant change in Ghrelin concentration was seen between healthy controls and RBD (p=0.037) as well as between healthy controls and all PD patients (p=0.002) Our results pointed out the delayed gastric emptying of the patients in the early stage of drug-naïve PD in comparison to healthy controls and RBD. The RBD patients, presumable pre-motor stage of PD, had normal gastric emptying, however it doesnt exclude the pathoanatomic changes in RBD. Probably the neurodegenerative changes of RBD in DMNV and enteric nervous system could not detectable using 13C-octonaote breath test. The abnormal Ghrelin concentrations in RBD and PD could be a possible cause of delayed gastric emptying, leading to reduced vagal innervation due to neurodegenerartive changes. The potential of Ghrelin as a biomarker or as a neuro protective agent for therapeutical aspects should be investigated in further studies.