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Introduction: This study evaluates the modeling of gastric electrophysiology tracings during long-term gastric electrical stimulation for gastroparesis. We hypothesized that serosal electrogastrogram may change over time representing gastric remodeling from gastric stimulation. Patients: Sixty-five patients with gastroparesis underwent placement of gastric stimulator for refractory symptoms. Mean age at initial stimulator placement was 44 years (range, 8-76), current mean age was 49, and the majority of the subjects were female ( n = 51, 78 %). Only a minority had diabetes-induced gastroparesis ( n = 16, 25 %); the remainder were either idiopathic or postsurgical. Methods: At the time of stimulator placement, electrogastrogram was performed after the gastric leads were placed but before stimulation was begun. Patients underwent continuous stimulation until pacer batteries depleted. At the time of replacement, before the new pacemaker was attached, electrogastrogram was again performed. Results: After a mean of 3.9 years of stimulation therapy, the mean of baseline frequency before stimulation therapy was 5.06 cycles/min and declined to 3.66 after replacement ( p = 0.0000002). The mean amplitude was 0.33 mV before stimulation therapy and decreased to 0.31 mV ( p = 0.73). The frequency/amplitude ratio was 38.4 before stimulation therapy and decreased to 21.9 ( p = 0.001). Conclusion: Long-term gastric electrical stimulation causes improvement in basal unstimulated gastric frequency to near normal. [ABSTRACT FROM AUTHOR]

Abdominal pain physiology may be better understood studying electrophysiology, histology, and symptom scores in patients with the symptoms of gastroparesis (Gp) treated with gastric electrical stimulation (GES). Ninety-five Gp patients" symptoms were recorded at baseline and during temporary and permanent GES. Gastric-emptying times and cutaneous, mucosal, and serosal electrogastrograms were obtained. S100-stained, full-thickness gastric biopsies were compared with autopsy controls. Sixty-eight patients reported severe pain at baseline. Severe pain patients' mean pain scores decreased with temporary GES from 3.62 to 1.29 (P < 0.001) and nonsevere pain from 1.26 to 0.67 (P = 0.01). With permanent GES, severe mean pain scores fell to 2.30 (P < 0.001); nonsevere pain changed to 1.60 (P = 0.221). Mean follow-up was 275 days. Mean cutaneous, mucosal, and serosal frequencies and frequency-to-amplitude ratios were markedly higher than literature controls. For patients with Gp overall and subdivided by etiology and severity of pain, S-100 neuronal fibers were significantly reduced in both muscularis propria layers. GES improved severe pain associated with symptoms of Gp. This severe pain is associated with abnormal electrogastrographic activity and loss of $100 neuronal fibers in the stomach's inner and outer muscularis propria and, therefore, could be the result of gastric neuropathy. [ABSTRACT FROM AUTHOR]