Abnormal gastric myoelectrical activity and delayed gastric emptying in patients with symptoms suggestive of gastroparesis

Gastric myoelectrical activity modulates gastric motor activity. Abnormalities in gastric myoelectrical activity may be associated with gastric motility disorders. The aim of this study was to investigate the correlation of gastric myoelectrical activity with gastric emptying in symptomatic patients with and without gastroparesis. Ninety-seven patients with symptoms suggestive of gastroparesis participated in the study. Gastric myoelectrical activity was recorded using surface electrogastrography. The electrogastrogram (EGG) was recorded for 30 min in the fasting state and for 120 min after a solid test meal. Gastric emptying of the solid meal was simultaneously monitored for 120 min. Patients with delayed gastric emptying showed a significantly lower percentage of normal gastric slow waves (P<0.03) and a significantly reduced increase of the dominant power in the postprandial EGG (P<0.02). Postprandial EGG parameters were found to be able to predict delayed emptying of the stomach. Postprandial gastric dysrhythmia predicts delayed gastric emptying with an accuracy of 78%, while the abnormality in postprandial EGG power predicts delayed gastric emptying with an accuracy of 75%. All patients with abnormalities in both the rhythmicity and the power had delayed gastric emptying. Patients with delayed gastric emptying have a lower percentage of normal gastric slow waves in the EGG and a lower postprandial increase in the dominant power. Abnormalities in the postprandial EGG seem to be able to predict delayed emptying of the stomach. However, a normal EGG does not seem to guarantee normal emptying of the stomach.     

Therapeutic potential of gastric electrical stimulation for obesity and its possible mechanisms: a preliminary canine study

Our aim was to investigate the effects of gastric electrical stimulation on food intake, weight, gastric myoelectrical, and parasympathetic activity. Dogs were implanted with serosal electrodes and a subcutaneous stimulator. The stimulator was turned on and off alternately every month for 4 months. Food intake, weight, gastric myoelectrical activity, and electrocardiograms were recorded. Daily food intake and weight were significantly decreased during the months with stimulation. Stimulation did not show any acute effect on gastric myoelectrical activity; however, it chronically and significantly impaired gastric myoelectrical activity in the fed state, but not in the fasting state. The parasympathetic activity in the fasting state assessed from the spectral analysis of heart rate variability was markedly decreased with stimulation both acutely and chronically. In conclusion, chronic gastric electrical stimulation results in a reduction in food intake, weight loss, a reduction in parasympathetic activity, and chronic inhibition of gastric myoelectrical activity. These data suggest that gastric electrical stimulation is a potential therapy for the treatment of obesity and its inhibitory effect on food intake and weight may involve both muscles and the vagal afferent pathway.     

Treatment of gastroparesis with electrical stimulation

Electrically stimulating the stomach to treat gastroparesis has been proposed by investigators for decades. With the development of techniques of implantable pacing devices and electrodes and promising preliminary results in chronic pacing studies, gastric electrical stimulation (GES) has received increasing attention recently among researchers and clinicians. A number of studies have been performed to investigate the effects of GES on gastric motility, gastric emptying, and gastrointestinal symptoms in both dogs and humans. Based on the frequency of the electrical stimulus used for chronic treatment of gastroparesis, gastric electrical stimulation can be classified into low-frequency stimulation (LFS) and high-frequency stimulation (HFS). Although some of the results are still controversial, the majority of these studies seem to indicate that LFS is able to normalize gastric dysrhythmias and entrain gastric slow waves and accelerate gastric emptying. On the other hand, HFS has no effect on gastric emptying but is able to significantly reduce symptoms of nausea and vomiting in gastroparetic patients. GES has provided an exciting new advance in the treatment of gastroparesis and management of upper gastrointestinal symptoms. This paper will review the available studies of GES in the treatment of gastroparesis and current status of this field.     

Gastric myoelectrical activity in patients with gastric outlet obstruction and idiopathic gastroparesis

Objective: The cause of gastroparesis may be uncertain in some patients. Mechanical obstruction of the stomach or duodenum should be excluded in patients with idiopathic gastroparesis. The objective of this study was to compare gastric myoelectrical activity in patients with idiopathic gastroparesis with that of patients with gastroparesis due to mechanical obstruction of the stomach or duodenum.
Methods: Electrogastrography techniques were used to record gastric myoelectrical activity in 20 patients with idiopathic gastroparesis and in nine patients with gastroparesis secondary to gastric outlet obstruction. Four of these nine patients initially were thought to have idiopathic gastroparesis. Electrogastrograms (EGGs) were recorded from 29 healthy subjects who served as controls. EGGs were recorded for 20–30 min 2 h after a standard 200-Kcal meal and were analyzed visually and by computer.
Results: Patients with gastroparesis due to outlet obstruction had high-amplitude and excessively regular 3–cycles-per-minute (cpm) EGG patterns, whereas patients with idiopathic gastroparesis had primarily 1- to 2-cpm patterns and little 3-cpm EGG activity. The percentage of total EGG power in the 3-cpm range was approximately 50% in patients with gastric outlet obstruction compared with 20% in patients with idiopathic gastroparesis (   p < 0.001  ). The percentage of EGG power in the normal 3-cpm range was greater in the obstructed patients (50%) than in the healthy controls (35%;   p < 0.052  ).
Conclusions: Gastric myoelectrical patterns recorded in the EGG distinguish mechanical and idiopathic causes of gastroparesis and may be useful in evaluating patients with nausea, vomiting, and gastroparesis of unknown cause.     

The "electrical way" to cure gastroparesis

The treatment of gastroparesis recently received a heavy blow from the restrictions on the use of the prokinetic drug cisapride, but, fortunately, at the same time, a nonpharmacological approach, such as gastric electrical stimulation, came up again with new techniques. After an ultra-decennial experimentation with a large variety of electrical stimuli delivered to the gastric wall of animals and patients with gastroparesis, three principal methods are available at the moment: gastric electrical pacing, high-frequency gastric electrical stimulation, and sequential neural electrical stimulation. The first method aims to reset a regular slow-wave rhythm, but is unable to re-establish efficient contractions and a normal gastric emptying. High-frequency gastric electrical stimulation, although inadequate to restore a normal gastric emptying, nevertheless strikingly improves the dyspeptic symptoms, such as nausea and vomiting, giving the patients a better quality of life and a more satisfactory nutritional status. The last method, neural electrical gastric stimulation, consists of a microprocessor-controlled sequential activation of a series of annular electrodes which encircle the distal two thirds of the stomach and induce propagated contractions causing a forceful emptying of the gastric content. The latter method is the most promising, but it has so far only been tested in animals and would need to be tested in patients with gastroparesis before it can be used as a solution for this disease. All the aforementioned clinical studies, however, are not controlled and nearly all were published in abstract form. Therefore, further controlled trials are needed to establish which of these techniques is more useful for the treatment of gastroparesis.     

Gastric Electrical Stimulation Does Not Significantly Affect Canine Gastric Acid Secretion and 24-Hour Gastric pH

Gastric electrical stimulation (GES) was shown to improve symptoms in patients with gastroparesis. However, the underlying mechanisms remain unclear. This study assessed the influence of various patterns of GES on fasting and postprandial gastric acid secretion and 24-hr gastric pH. Eight healthy dogs were studied and we found that in the fasting state, low-frequency, long-pulse (6/12-cpm, 375-msec, 4-mA) GES at the proximal stomach significantly inhibited the secretion of gastric juice (P < 0.05). No such effect was observed during GES (6/12 cpm) at the distal stomach. In the postprandial period, low-frequency, long-pulse GES at both proximal and distal sites and at both frequencies did not significantly affect gastric acid secretion. High-frequency, short-pulse GES, investigated for obesity (21 Hz, 8 mA, and 250 microsec, with 2 secs on, 3 sec off), at the proximal and distal stomach did not significantly affect the 24-hr gastric pH profile. In conclusion, GES with various stimulation parameters, and at various sites, has little effect on gastric acid secretion. The clinical effects induced by GES at these parameters may not be related to their effect on gastric acid homeostasis.     

Gastric electric stimulation for the treatment of gastroparesis

Gastric electric stimulation is an emerging therapy for refractory gastroparesis. Several methods have been used to electrically stimulate the stomach. Initial studies used gastric electrical pacing, which entrains and paces the gastric slow waves at a slightly higher rate than the patient’s normal myoelectric frequency of 3 cycles per minute (cpm). The technique currently practiced uses high-frequency, low-energy stimulation at four times the basal rate (12 cpm). Results from published studies with high-frequency stimulation reveal an improvement in symptoms, primarily of nausea and vomiting, and primarily in patients with diabetic gastroparesis, with only a modest change in gastric emptying. As treatment with gastric electric stimulation evolves, further delineation of its overall effectiveness, the type of patient that will likely respond, optimal electrode placement(s), and stimulus parameters should be explored.     

Calcitonin gene-related peptide released by capsaicin suppresses myoelectrical activity of gastric smooth muscle

BACKGROUND: It is widely accepted that the inhibition of gastric motor activity as well as the maintenance of gastric mucosal blood flow and mucous secretion are important for the homeostasis of the gastric mucosa. The present study was performed to ascertain whether or not capsaicin, which can protect the stomach from noxious stimuli, affects gastric motor activity. METHODS: Male Sprague-Dawley rats were anesthetized with urethane, and the stomach was cannulated by two catheters from esophageal and duodenal sides. A biopolar electrode was fixed to the serosal surface of the antrum and myoelectrical activity was recorded during the instillation of a small volume of solutions. RESULTS: The myoelectrical activity of rat gastric smooth muscle was increased at intragastric pressures of >2 cmH(2)O. Replacement of intragastric physiological saline with 1.6 mmol/L capsaicin solution significantly suppressed this myoelectrical activity by 50%. Intragastric capsaicin administration caused a significant release of substance P (SP) and calcitonin gene-related peptide (CGRP). The maximum released levels of CGRP in the gastric perfusates were 100-fold those of SP. The myoelectrical activity observed at an intragastric pressure of 2 cmH(2)O was avoided by continuous infusion of CGRP (0.1-3.0 nmol/kg per min) into the gastric artery in a dose-dependent manner, but not by that of SP (1.0 nmol/kg per min). Continuous CGRP-(8-37) infusion into the gastric artery completely blocked the reduction by intragastric capsaicin of myoelectrical activity. CONCLUSION: These results suggest that the suppression of the myoelectrical activity of gastric smooth muscle by capsaicin is attributable to the endogenous CGRP released.     

Gastric Electrical Stimulation With Parameters for Gastroparesis Enhances Gastric Accommodation and Alleviates Distention-Induced Symptoms in Dogs

Gastric electrical stimulation (GES) improves symptoms in patients with gastroparesis. We sought to determine if stimulation at fundus with parameters used for gastroparesis could affect gastric accommodation and distention-induced symptoms in dogs. Nine dogs were implanted with a gastric cannula at the anterior stomach and 1 pair of stimulation electrodes in the fundus. Assessment of gastric accommodation and a series of gastric distention were performed using a barostat. Stimulation parameters were of short pulse trains of 14 Hz, 5 mA, 0.3 ms, and 0.1 s on, 5 s off. GES at fundus significantly decreased fasting gastric tone. Fasting gastric volume was significantly increased from 56.3+/-10.4 mL at baseline to 102.4+/-23.1 mL with stimulation (P=.011). Postprandial gastric accommodation was significantly enhanced with stimulation. The extent of accommodation increased from 249.3+/-39.9 mL in the control session to 325.8+/-25.1 mL with stimulation (P=.011). Symptom scores induced by balloon distention of the stomach were significantly lower during stimulation in comparison with those of baseline (P=.016). In conclusion, GES with parameters for gastroparesis enhances postprandial gastric accommodation and reduces visceral perception in normal dogs. This effect, if seen also in humans, may explain in part the symptomatic improvement associated with GES therapy in patients with gastroparesis.     

Visceral response to acute retrograde gastric electrical stimulation in healthy human

AIM: To investigate the visceral response to acute retrograde gastric electrical stimulation (RGES) in healthy humans and to derive optimal parameters for treatment of patients with obesity. METHODS: RGES with a series of effective parameters were performed via a bipolar mucosal electrode implanted along the great curvature 5 cm above pylorus of stomach in 12 healthy human subjects. Symptoms associated with dyspepsia and other discomfort were observed and graded during RGES at different settings, including long pulse and pulse train. Gastric myoelectrical activity at baseline and during different settings of stimulation was recorded by a multi-channel electrogastrography. RESULTS: The gastric slow wave was entrained in all the subjects at the pacing parameter of 9 cpm in frequency, 500 ms in pulse width, and 5 mA in amplitude. The frequently appeared symptoms during stimulation were satiety, bloating, discomfort, pain, sting, and nausea. The total symptom score for each subject significantly increased as the amplitude or pulse width was adjusted to a higher scale in both long pulse and pulse train. There was a wide diversity of visceral responses to RGES among individuals. CONCLUSION: Acute RGES can result in a series of symptoms associated with dyspepsia, which is beneficial to the treatment of obesity. Optimal parameter should be determined according to the individual sensitivity to electrical stimulation.     

Clinical application prospects of gastric pacing for treating postoperative gastric motility disorders

Similar to the heartbeat, gastric peristalsis is regulated by an electrical rhythm generated by a pacemaker. Thus, electrical dysrhythmia of gastric slow waves will inevitably affect gastric peristalsis and emptying. The recurrence of postoperative gastroparesis is thereby closely related to the abnormalities of electrical dysrhythmia and ectopic pacemakers, resulting in postoperatively persistent gastric motility disorders in some severe cases, despite the use of prokinetic and antiemetic drugs. Recent studies have demonstrated that gastric pacing, analogous to pacing the human heart, is an attractive and promising therapy that is both feasible and safe. Gastric pacing has been shown to be strikingly effective in normalizing gastric dysrhythmia, increasing the activity of the gastric slow wave and thereby prompting gastric dynamia and emptying. Furthermore, the long-term utilization of gastric pacing can (i) relieve patients from clinical symptoms, such as nausea and vomiting; (ii) release patients with severe postoperative gastroparesis from relying on prokinetic drugs and the jejunal feeding tube; (iii) return patients to normal oral nutritional intake and provide a more satisfactory nutritional status and most importantly; and (iv) give patients a better quality of life. Overall, research focused on gastric pacing has demonstrated excellent prospects for clinical application in the treatment of postoperative gastroparesis disorders, especially for those unresponsive to prokinetic drugs.     

Management of Diabetic Gastroparesis

Symptoms suggestive of gastroparesis occur in 5% to 12% of patients with diabetes. Such a complication can affect both prognosis and management of the diabetes; therefore, practicing clinicians are challenged by the complex management of such cases. Gastroparesis is a disorder characterized by a delay in gastric emptying after a meal in the absence of a mechanical gastric outlet obstruction. This article is an evidence-based overview of current management strategies for diabetic gastroparesis. The cardinal symptoms of diabetic gastroparesis are nausea and vomiting. Gastroesophageal scintiscanning at 15-minute intervals for 4 hours after food intake is considered the gold standard for measuring gastric emptying. Retention of more than 10% of the meal after 4 hours is considered an abnormal result, for which a multidisciplinary management approach is required. Treatment should be tailored according to the severity of gastroparesis, and 25% to 68% of symptoms are controlled by prokinetic agents. Commonly prescribed prokinetics include metoclopramide, domperidone, and erythromycin. In addition, gastric electrical stimulation has been shown to improve symptoms, reduce hospitalizations, reduce the need for nutritional support, and improve quality of life in several open-label studies.     

Vomiting and gastric electrical dysrhythmia in dogs

Background: The correlation between gastric myoelectrical activity (GMA) and gastrointestinal symptoms such as nausea and vomiting is poorly understood. The aim of this study was to assess the association of GMA with vomiting induced by retrograde gastric electrical stimulation or duodenal balloon distention. Methods: Ten dogs were involved in this study. Vomiting was induced by retrograde gastric electrical stimulation in 6 dogs and by duodenal balloon distention in 4 dogs. Computerized spectral analysis and visual analysis were applied to detect the GMA change during various periods before and after vomiting. Results: Gastric dysrhythmia preceded vomiting but was of brief duration. The major pattern of dysrhythmia immediately before vomiting was tachyarrhythmia and gastric slow wave was completely uncoupled before vomiting. Gastric dysrhythmia and slow wave uncoupling were also noticed immediately after vomiting but the dogs recovered quickly. The major pattern of dysrhythmia after vomiting was arrhythmia. GMA was normal during the periods other than 5?min before and during vomiting and 5?min after vomiting. Conclusions: Gastric dysrhythmia seems to be the cause of vomiting induced by retrograde gastric electrical stimulation or duodenal balloon distention. It is brief and characterized with tachyarrhythmia and uncoupling.     

The use of SmartPill for gastric monitoring

Testing to define delayed gastric emptying is required to diagnose gastroparesis; rapid emptying is found in other patients. Commonly performed methods of gastric emptying testing include scintigraphy and breath testing. The SmartPill wireless motility capsule (WMC) system is US FDA-approved for evaluating suspected delayed emptying in gastroparesis and functional dyspepsia. The device measures transit in the stomach, small intestine, and colon by detecting characteristic pH transitions; and quantifies pressure waves in each gut region. WMC gastric emptying times correlate with scintigraphic measures. Incremental benefits of WMC testing in patients with suspected gastroparesis include delineation of pressure abnormalities and small intestinal and colonic transit delays. Acceptance of trial data confirming usefulness of WMC testing in suspected gastric motor disorders has been hampered by small sample sizes and design limitations. Ongoing multicenter studies will validate the utility of WMC methods in patients with suspected gastroparesis and other upper gastrointestinal motor disorders.     

Myoelectrical and mechanical activity of stomach and intestine in hypothyroid dogs

Myoelectrical activity was studied in normothyroid and hypothyroid Labrador dogs in the resting state, following injection of pentagastrin, bethanechol chloride, and after feeding. Hypothyroidism was produced by total thyroidectomy and chronic treatment with thiouracil. Electrodes were surgically implanted over the serosa of the stomach, duodenum, jejunum, and ileum and used for repeated recording of myoelectrical activity of gastrointestinal muscles. A strain gauge was implanted over the gastric antrum and served to record mechanical activity of the stomach. As compared with control dogs, hypothyroid animals showed (a) decreased frequency of electrical control activity of the stomach and jejunum, (b) decreased occurrence of electrical response activity (spike potentials) following stimulation, and (c) decreased mechanical response to the same stimulants, ie, pentagastrin, bethanechol chloride, and food.This work was supported by Medical Research Council of Canada grant No. MA 4837.     

Gastric electrical stimulation in intractable symptomatic gastroparesis

BACKGROUND: The treatment of gastroparesis remains unsatisfactory despite prokinetic and anti-emetic drugs. Gastric electrical stimulation has been proposed as a therapeutic option. We have assessed the effect of gastric electrical stimulation on symptoms, medical treatment, body weight and gastric emptying in patients with intractable symptomatic gastroparesis in a non-placebo-controlled study. METHODS: In this multicenter study, 38 highly symptomatic patients with drug-refractory gastroparesis were enrolled. Patients first received temporary electrical stimulation using percutaneous electrodes. The 33 responders to temporary stimulation then underwent surgical implantation of a permanent stimulator. Severity of vomiting and nausea was assessed before and after stimulation. Patients were reassessed 3, 6, and 12 months after permanent implantation. RESULTS: With stimulation, 35/38 patients (97%) experienced >80% reduction in vomiting and nausea. This effect persisted throughout the observation period (2.9-15.6 months, 341 patient-months). Gastric emptying did not initially change, but improved in most patients at 12 months. At 1 year, the average weight gain was 5.5% and 9/14 patients initially receiving enteral or parenteral nutrition were able to discontinue it. CONCLUSION: Electrical stimulation of the stomach has an immediate and potent anti-emetic effect. It offers a safe and effective alternative for patients with intractable symptomatic gastroparesis.     

Cutaneous gastric electrical stimulation alters gastric motility in dogs: New option for gastric electrical stimulation?

Background and Aim:  We investigated the effects of cutaneous gastric electrical stimulation (CGES) on gastric myoelectrical activity, postprandial antral contractions and gastric tone in dogs.
Methods:  CGES was carried out via abdominal surface electrodes over the stomach. After an overnight fast, gastric slow waves were recorded from the serosal electrodes in six dogs at a frequency of 4.4 cycles/min (c.p.m.) or 10 c.p.m. Nine dogs were used for the measurement of postprandial antral contractions. Gastric tone at baseline and during CGES was measured in six of the dogs.
Results:  We found that: (i) CGES at 4.4 c.p.m. decreased slow wave frequency (5.1 vs 4.6 c.p.m., P  < 0.05) and increased slow wave power (−6.2 vs 2.7 c.p.m., P  < 0.05); CGES at 10 c.p.m. increased slow wave frequency (5.1 vs 9.2 dB, P  < 0.05) and decreased normal slow waves (85.4% vs 60.0%, P  < 0.05); (ii) CGES at 10 c.p.m. significantly suppressed postprandial antral contractions ( P  < 0.01); (iii) CGES had no effects on gastric tone.
Conclusions:  CGES is capable of altering gastric slow waves and inhibiting gastric motility. It may have therapeutic potential for treating eating disorders, such as obesity. However, clinical studies are needed to explore the potential of CGES.     

Effects of proximal gastric vagotomy (PGV) followed by total vagotomy (TV) on postprandial and fasting myoelectrical activity of the canine stomach and duodenum.

Experiments were designed to study the effect of proximal gastric vagotomy (PGV) followed by total vagotomy (TV) on the myoelectrical activity of the canine stomach and duodenum after a meat meal and during fasting. Dogs were prepared with chronically implanted Ag-AgCl-electrodes on the stomach and duodenum. Recordings of electrical activity were made for one hour after the ingestion of a meat meal and records of four to six hours were taken on the fasting animals. In the postprandial records no effect on co-ordination of antral and duodenal myoelectrical activity was found after either PGV or TV. These results suggest that the co-ordinating mechanism is not dependent on vagal innervation. Impairment of gastric emptying after TV does not appear to be due to disturbance of antral-duodenal conduction. Normal patterns of fasting activity were found in control and after PGV. They were grossly disturbed after TV, probably because of delayed gastric emptying. These findings suggest that PGV does not delay gastric emptying as does TV, and that the proximal vagal supply to the stomach is unimportant in the control of fasting activity.     

Pathophysiology of idiopathic gastroparesis and implications for therapy

Objectives: Idiopathic gastroparesis is a gastric motility disorder characterized by chronic upper gastrointestinal symptoms and delayed gastric emptying without an identifiable underlying condition. This review summarizes recent understanding of the pathophysiology and treatment of idiopathic gastroparesis.

Materials and methods: Structured literature search in the PubMed, Embase and ClinicalTrials.gov databases.

Results: Idiopathic gastroparesis involves several alterations in gastric motility and sensation, including delayed gastric emptying, altered myoelectrical activity, impaired fundic accommodation, visceral hypersensitivity and disturbances in antropyloroduodenal motility and coordination. Multiple cellular changes have been identified, including depletion of interstitial cells of Cajal (ICC) and enteric nerves, as well as stromal fibrosis. The underlying cause of these changes is not fully understood but may be an immune imbalance, including loss of anti-inflammatory heme-oxygenase-1 positive (HO-1) macrophages. There is currently no causal therapy for idiopathic gastroparesis. The treatment ladder consists of dietary measures, prokinetic and antiemetic medications, and varying surgical or endoscopic interventions, including promising pyloric therapies. There are ongoing trials with several novel medications, raising hopes for future treatment.

Conclusions: Patients with idiopathic gastroparesis present several pathophysiological alterations in the stomach, where depletion of ICC is of special importance. Treatment is currently focused on alleviating symptoms through dietary adjustments, medication or surgical or endoscopic interventions.     

Advances in the management of gastroparesis

Opinion statement The treatment goals for patients with gastroparesis are to control symptoms; to correct fluid, electrolyte, and nutritional deficiencies; and to identify and treat the underlying cause of gastroparesis. For mild symptoms, dietary modifications and a low-dose antiemetic and/or prokinetic agent might provide satisfactory control of symptoms. Dietary treatments include decreasing the solid food component while increasing the liquid nutrient component of meals. Fat and fiber intake should be minimized. Metoclopramide, despite its potential for neurological side effects, remains a prokinetic treatment for symptomatic patients. In patients with diabetic gastroparesis, careful regulation of glycemic control may help to reduce symptoms. Medical management of patients with gastroparesis who do not respond to initial antiemetic or prokinetic therapy or who develop medication-related side effects involves the use of other prokinetic and antiemetic agents with different mechanisms of action. Combinations of prokinetic and antiemetic agents often are tried in patients with persistent symptoms. In some patients with persistent refractory symptoms and failure to maintain adequate fluid and/or nutritional intake, bypassing the stomach with jejunostomy feedings may be necessary. Gastric electrical stimulation is a treatment for refractory gastroparesis. Based on initial studies showing symptom benefit, especially in patients with diabetic gastroparesis, gastric electrical stimulation was granted humanitarian US Food and Drug Administration approval for the treatment of chronic, refractory nausea and vomiting secondary to idiopathic or diabetic gastroparesis. However, which patients are likely to respond, the optimal electrode position, and the optimal stimulation parameters remain areas that need to be addressed.