Gastric dysmotility in Parkinson's disease is not caused by alterations of the gastric pacemaker cells

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.

Keywords: Parkinson's disease; Physiology.

Fig. 1

Physiology of gastric motility and the gastric migrating motor complex. Motilin and increased luminal pressure stimulate the release of 5-HT from duodenal enterochromaffin cells. The released 5-HT activates 5-HT3 receptors, and the signal is transduced via the vagus nerve afferents to the nucleus tractus solitarius. The vagus nerve stimulates gastric smooth muscle cells via myenteric neurons and interstitial cells of Cajal. Thus, motilin and 5-HT induce phase II and III of the migrating motor complex via the vago-vagal reflex. Figure adapted from Takahashi and Itoh.^,

Fig. 2

Phases of the migrating motor complex. a Fast Fourier transformation into a pseudo-three-dimensional running spectrum graph over a period of 10 min in a representative example of 3D-MAGMA recordings. The period in which the frequency is 3 cpm corresponds to phase I of the migrating motor complex. Then, a phase of intermittent contractions of varying strength and duration occur (phase II). In phase III, the motor activity is strongest and the capsule is leaving the stomach. Finally, the capsule reaches the duodenum with a frequency of approx. 15 cpm. b Distribution of gastric transit time and the dominant frequency in patients with Parkinson´s disease and young healthy controls

Fig. 3

3D-MAGMA system. a 3D-MAGMA sensor arrangement. b 3D-MAGMA capsule