Abstract
The enteric nervous system is involved in the pathology of Parkinson´s disease and patients frequently have symptoms related to delayed gastric emptying. However, the pathophysiology of gastric dysmotility is yet not well understood. The objective of this study was to assess interdigestive gastric motility in Parkinson´s disease. Using an electromagnetic capsule system, the dominant gastric contraction frequency (primary outcome measure) and the gastric transit time were assessed in 16 patients with Parkinson´s disease and 15 young healthy controls after a fasting period of 8 h. Motor and non-motor symptoms were assessed using the Movement Disorder Society Unified Parkinson´s Disease Rating Scale III (MDS-UPDRS III), the Non-Motor Symptoms Questionnaire (NMS-Quest), and Hoehn & Yahr staging. The Gastroparesis Cardinal Symptom Index was used to record symptoms related to delayed gastric emptying. In healthy controls and patients with Parkinson's disease, the dominant contraction frequency was 3.0 cpm indicating normal function of interstitial cells of Cajal. In patients with Parkinson's disease, the gastric transit time was longer than in younger controls (56 vs. 21 min). The dominant contraction frequency and gastric transit time did not correlate with age, disease duration, Hoehn & Yahr stage, levodopa equivalent daily dose, MDS-UPDRS III, NMS-Quest, and Gastroparesis Cardinal Symptom Index. Changes of gastric motility in Parkinson´s disease are not caused by functional deficits of the gastric pacemaker cells, the interstitial cells of Cajal. Therefore, gastroparesis in Parkinson's disease can be attributed to disturbances in neurohumoral signals via the vagus nerve and myenteric plexus.
Highlights
Parkinson's disease (PD) is a multisystem neurodegenerative disorder characterized by motor and non-motor symptoms.[1]
The frequency of movements per minute did not correlate with age, disease duration, Hoehn & Yahr stage, levodopa equivalent daily dose, motor (MDS-UPDRS III) or non-motor burden (NMS-Quest), and did not significantly differ between PD patients taking proton pump inhibitors and PD patients who did not take proton pump inhibitors
In our study we focused on the interdigestive motility period where the motility pattern can be described by the migrating motor complex (Fig. 1)
Summary
Parkinson's disease (PD) is a multisystem neurodegenerative disorder characterized by motor and non-motor symptoms.[1] The involvement of the entire gastrointestinal tract can cause a plethora of gastrointestinal symptoms.[2] These symptoms can originate from functional and structural changes in the gut and its associated neural structures.[3,4] It was hypothesized that pathological processes could be initiated in the enteric nervous system and spread to the central nervous system via the vagus nerve.[5] this gut-to-brain scenario is still widely debated,[6] and there is an urgent need to better characterize the enteric nervous system pathology in PD.[7] the assessment of gastric motility and gastric emptying is important for the diagnosis of gastroparesis, which contributes to motor fluctuations
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