Central neuronal mechanisms of gastric electrical stimulation in diabetic gastroparesis

The mechanisms underlying symptom improvement in gastric electrical stimulation (GES) are not fully understood. Modulation of the central nervous system excitability may be involved. The objective of the study was to investigate the central effects of GES, including the possible modulation of the visceral sensory nervous system.

A gastric electrical stimulator was implanted in seven diabetic patients with medically refractory gastroparesis. A double-blinded protocol was used to investigate the patients at baseline and one month after recovery with the stimulator turned on and off (1-month periods). The following assessments were carried out: mechanical, thermal and electrical stimulations with sensory recordings in the esophagus and duodenum, and standardized, self-administered, daily symptom questionnaires.

No difference was found between baseline and the on- and off periods in overall gut pain thresholds across all stimulus modalities in the esophagus (p=0.63), duodenum (p=0.19) or esophagus and duodenum combined (p=0.76). No difference in the sensory response to mechanical stimulation was found in the esophagus before (all p>0.31) and after (all p>0.43) smooth muscle relaxation with butylscopolamine. Similar findings were observed in the duodenum. No differences were found in thermal sensitivity (esophagus (p=0.67) and duodenum (p=0.17)), sensory response to electrical stimulation (esophagus (p=0.57) and duodenum (p=0.52)) or induced somatic referred pain areas (esophagus (p=0.75) and duodenum (p=0.51)). No difference was seen in the induced somatic referred pain areas or self-reported symptoms.

No evidence was found for GES-induced modulation of the visceral sensory system and central excitability. However, GES has been proven to modulate the central nervous system in animal studies, necessitating further human experiments in order unambiguously to establish the possible central effects of GES.