Bioelectrical 'slow waves' regulate gastrointestinal contractions. We aimed to confirm whether the pyloric sphincter demarcates slow waves in the intact stomach and duodenum.

We developed and validated novel anatomically-specific electrode cradles and analysis techniques which enable high-resolution slow wave mapping across the in vivo gastroduodenal junction. Cradles housed flexible-printed-circuit and custom cradle-specific electrode arrays during acute porcine experiments (N = 9; 44.92 kg ± 8.49 kg) and maintained electrode contact with the gastroduodenal serosa. Simultaneous gastric and duodenal slow waves were filtered independently after determining suitable organ-specific filters. Validated algorithms calculated slow wave propagation patterns and quantitative descriptions.

Butterworth filters, with cut-off frequencies (0.0167 - 2) Hz and (0.167 - 3.33) Hz, were optimal filters for gastric and intestinal slow wave signals, respectively. Antral slow waves had a frequency of (2.76 ± 0.37) cpm, velocity of (4.83 ± 0.21) mm·s-1, and amplitude of (1.13 ± 0.24) mV, before terminating at the quiescent pylorus that was (46.54 ± 5.73) mm wide. Duodenal slow waves had a frequency of (18.13 ± 0.56) cpm, velocity of (11.66 ± 1.36) mm·s-1, amplitude of (0.32 ± 0.03) mV, and originated from a pacemaker region (7.24 ± 4.70) mm distal to the quiescent zone.

Novel engineering methods enable measurement of in vivo electrical activity across the gastroduodenal junction and provide qualitative and quantitative definitions of slow wave activity.

The pylorus is a clinical target for a range of gastrointestinal motility disorders and this work may inform diagnostic and treatment practices.

Sham feeding, reproducing the cephalic phase of digestion, and involving combined visual, olfactory, and taste stimulation affects gastrointestinal motility and secretory functions of the digestive system, as well as the sympathetic/parasympathetic balance (SPB). In this study, we aimed to check if taste stimulation with a single flavor affects the gastric myoelectrical activity (GMA) and/or SPB.

Eighteen healthy volunteers underwent, on four separate days, 30-min electrogastrographic and electrocardiographic recordings: basal, with stimulation - while keeping in the mouth an agar cube with taste-delivering substance, and postexposure. Concentrations of saccharose, NaCl, citric acid, and quinine hydrochloride within the cubes were adjusted to 100-fold the individual taste recognition thresholds. SPB was determined from the heart rate variability (HRV) analysis of the recorded electrocardiograms.

A moderate but statistically significant increase in tachygastria and bradygastria percentage time share was observed, regardless of the type of taste applied. Bitter taste elicited a considerable decrease in the normogastria time share (from 82.8 ± 2.5% to 73.5 ± 3.5%, P = 0.00076) and a diminution of the dominant frequency (from 3.07 ± 0.08 to 2.90 ± 0.10 cycles per minute (cpm) postexposure, P = 0.01). Sour taste brought about a drop of the dominant power (from 42.5 ± 1.1 to 40.1 ± 1.4 dB, P = 0.0015). Two tastes hindered propagation of the gastric slow waves - the average percentage of slow wave coupling decreased from 77.9 ± 3.1% to 69.5 ± 3.1% (P = 0.0078) and from 74.6 ± 2.5% to 68.2 ± 2.8% (P = 0.0054) with the bitter and the salty taste, respectively. Stimulation with sweet, salty, or sour taste evoked a significant decrease in the high frequency component of the HRV, whereas bitter taste did not affect the SPB.

Oral stimulation with tastes subjectively perceived as unpleasant brings about disturbances of the interdigestive GMA. This, however, does not coincide with its effect upon SPB.

Inflammatory bowel disease is characterized by the presence of gastrointestinal motility disturbances; however alterations in the gastric myoelectrical activity have not been characterized. In this study we have recorded the gastric myoelectrical activity in patients with ulcerative colitis (UC) and Crohn's disease (CD) during their clinical remission.

Gastric activity was assessed using electrogastrography (EGG) in patients with UC (n = 60), CD (n = 40) and healthy controls (n = 40). In each case, their response to water load test, as well as the dominant frequency (DF), dominant power (DP) and the power ratio (PR) of the electrical activity were recorded.

In healthy controls, the resting DF was 2.57 ± 1.05 cycles per minute (cpm), which decreased after water ingestion (2.34 ± 0.99 cpm; P = 0.001). Compared to healthy controls, patients with UC had low resting DF (bradygastria) (2.57 ± 1.05 vs. 1.86 ± 1.28 cpm; P = 0.01). The change in DF after water ingestion was insignificant in patients with UC and CD. Post-water ingestion, healthy controls exhibited an increase in the DP as compared to the resting state, (7.1 [2.93, 102.56] vs. 15.94 [3.92, 133.41] μV (2); P = 0.02). Patients with UC (1.26 [0.14, 9.83] vs. 3.27 [0.61, 42.12] μV(2)) and CD (2.54 [0.44, 47.06] vs. 15.8 [0.1, 126.68] μV(2)) also showed a significant increase in the DP post-water ingestion.

Patients with ulcerative colitis have altered resting gastric myoelectrical activity during the remission phase of the disease.

Multichannel electrogastrography (M-EGG) can be used to evaluate gastrointestinal motility. The myoelectric activity of the remnant stomach after surgery has not been measured by M-EGG. This study examined whether myoelectric activity varied with surgical technique and compared vagus nerve-preserving distal gastrectomy (VP-DG) with standard distal gastrectomy without vagus nerve preservation (DG). Furthermore, we examined the relationship between the M-EGG findings and patients' postoperative symptoms.

Twenty-six patients who underwent VP-DG, 20 who underwent DG, and 12 healthy volunteers as controls were examined with M-EGG. The Gastrointestinal Symptom Rating Scale (GSRS) was used to assess postoperative symptoms.

Longer periods of normal gastric function (normogastria, 2.0-4.0 cycle min(-1)) were detected in channel 1 in the VP-DG group than in the DG group in either the fasted or fed state (P<0.05). The percentage of slow wave coupling (%SWC) in the fed state correlated negatively with GSRS scores (reflux, r=-0.59, P=0.02; abdominal pain, r=-0.51, P=0.04, indigestion, r=-0.59, P=0.02 and total score, r=-0.75, P=0.02).

Slow waves can be recorded non-invasively using M-EGG in the remnant stomach following gastrectomy. The VP-DG group showed better preserved gastric myoelectric activity than the DG group, and the %SWC showed a significant negative correlation with scores of GSRS (reflux, abdominal pain, indigestion and total score) in the VP-DG group.

In humans, motion sickness is associated with disruption of normal gastric myoelectric activity, and it has been proposed that this results from an imbalance of autonomic nervous system activity. We used the established Suncus murinus (house musk shrew) model of motion-induced emesis to investigate the effect of horizontal motion on gastric myoelectric activity (recorded using telemetry) and the involvement of the abdominal vagi. Surgical vagotomy increased baseline dysrhythmia and reduced the dominant power of the gastric myoelectric signals. In response to motion, normal gastric myoelectric activity was reduced in sham-operated animals but not in vagotomized animals. Vagotomy, however, failed to affect motion-induced emesis. In conclusion, motion had a differential effect in sham-operated and vagotomized animals, which is consistent with the hypothesis that motion-induced dysrhythmia arises from an autonomic nervous system imbalance.

The electrogastrogram (EGG) was recorded for 24 hours in 17 Parkinson's disease (PD) patients, 17 multiple system atrophy (MSA) patients, and 8 healthy control subjects to elucidate the differences in the EGG findings between the two diseases. Eight EGG segments (3 preprandial, 3 postprandial, and 2 sleep segments) were selected from the total recording for spectral analysis, from which we obtained the dominant frequency (DF), instability coefficient of DF (ICDF), and low (LFR%), normal (NFR%), and high (HFR%) range power percentages of the total power. PD patients showed irregular slow waves, high HFR%, and high ICDF, whereas MSA patients showed regular slow waves and low ICDF. Although DF and NFR% increased after meal in controls, postprandial increases in DF and NFR% were less significant in both patient groups compared to the controls. The PD patients presented gastric dysrhythmias indicating gastric pacemaker disturbances. The MSA patients showed regular slow waves with low variability of the slow wave rhythm (low ICDF), which might have resulted from the involvement of gastric autonomic nerve function.

The aim of this article is to provide a better understanding of the roles of interstitial cells of Cajal (ICC) in regulating gastrointestinal motility by reviewing in vitro and in vivo physiological motility studies. Based on the in vitro studies, ICC are proposed to have the following functions: to generate slow waves, to mediate neurotransmission between the enteric nerves and the gastrointestinal muscles and to act as mechanoreceptors. However, there is limited evidence available for these hypotheses from the in vivo motility studies. In this review, we first introduce the major subtypes of ICC and their established functions. Three Kit mutant mouse and rodent models are presented and the loss of ICC subtypes in these mutants is reviewed. The physiological motility findings from various in vitro and in vivo experiments are discussed to give a critical review on the roles of ICC in generating slow waves, regulating gastrointestinal motility, mediating neural transmission and serving as mechanoreceptors. It is concluded that the role of ICC as pacemakers may be well established, but other cells may also be involved in the generation of slow waves; the theory that ICC are mediators of neurotransmission is challenged by the majority of the in vivo motility studies; the hypothesis that ICC are mechanoreceptors has not found supportive evidence from the in vivo studies yet. More studies are needed to explain discrepancies in motility findings between the in vitro and in vivo experiments.

Gastrointestinal (GI) motility dysfunction is a common complication of any abdominal surgical procedure. During fasting, the upper GI tract undergoes a cyclic change in motor activity, called the interdigestive migrating motor contraction (IMC). The IMC is divided into four phases, with phase III having the most characteristic activity. After digestive surgery, GI motility dysfunction shows a lack of a fed response, less phase II activity, more frequent phase III activity of the IMC, and some phase III activity migrating orally. Postoperative symptoms have been related to motor disturbances, such as interrupted or retrograde phase III or low postprandial activity. The causes of GI disorder are autonomic nervous dysfunction and GI hormone disruptions. The administration of a motilin agonist can induce earlier phase III contractions in the stomach after pancreatoduodenectomy. For nervous dysfunction, an inhibitory sympathetic reflux is likely to be important in postoperative motility disorders. Until recently, treatment for gut dysmotility has consisted of nasogastric suction, intravenous fluids, and observation; however, more effective treatment methods are being reported. Recent discoveries have the potential to decrease postoperative gut dysmotility remarkably after surgery.

Slow waves play an important role in controlling the frequency and propagation of gastrointestinal contractions. However, mechanisms involved in the modulation of slow wave activity in vivo are still unclear. In this study, the roles of different neurotransmitters in the regulation of gastrointestinal slow waves were investigated in conscious dogs.

Female dogs implanted with electrodes in the stomach and the small bowel were used in a seven-session study. Gastrointestinal myoelectrical activity was recorded at baseline and after i.v. saline, atropine, atropine methyl nitrate, guanethidine, Nomega-nitro-L-arginine (L-NNA), ondansetron or naloxone.

Both atropine and atropine methyl nitrate induced tachygastria, bradygastria and arrhythmia. No difference was noted in the effects between atropine and atropine methyl nitrate. L-NNA increased the dominant frequency of small-intestinal slow waves but had no effect on gastric slow waves. Guanethidine, ondansetron and naloxone did not affect the dominant frequency, power or percentage of normal gastrointestinal slow waves.

Acetylcholine acting at muscarinic receptors seems to play an important role in the regulation of gastric slow waves. Nitric oxide may play a role in modulating intestinal slow waves but not gastric slow waves. Sympathetic pathways, 5-HT(3) receptors and opioid receptors (especially micro-opioid receptors) do not play a role in the regulation of gastric or intestinal slow waves under normal physiological conditions.

Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease (GERD). The aim of this study was to determine whether laparoscopic fundoplication alters gastric myoelectric activity. Change of digestive symptoms was also assessed.

Sixteen patients with GERD (2 males, 14 females, mean age: 53 years) undergoing a laparoscopic fundoplication participated. Electrogastrography (EGG) was assessed before and after the subject ingested water until full (water load). Symptoms of upper abdominal discomfort, early satiety, postprandial abdominal distension, nausea, vomiting, and anorexia were recorded. At a 2-month postoperative follow-up, preoperative tests were repeated.

The EGG was abnormal in 11 of 16 patients (69%) preoperatively and 6 of 16 patients (38%) postoperatively. The EGG changed from abnormal to normal in 5 of 16 patients (31%). The percentage of power at 3 cpm increased significantly during the fasting state postoperatively (29.9% vs. 21.2%, P < 0.05). There was a significant improvement in epigastric pain (P < 0.001), early satiety (P < 0.01), and postprandial fullness (P < 0.001).

Increased presence of normal 3 cpm activity is the predominant effect of fundoplication on gastric myoelectric activity. Dyspeptic symptoms are also significantly improved postoperatively.

The aims of this study were to investigate the effects and mechanisms of a novel method of gastric electrical stimulation on the prevention of vasopressin-induced emetic response and gastric dysrhythmias.

Fifteen dogs (10 normal, 5 vagotomized) chronically implanted with gastric serosal electrodes were used in a 3-session study (vasopressin, vasopressin plus 2-channel stimulation [DCS], and vasopressin plus dual-pulse stimulation [DPS]).

Vasopressin induced gastric dysrhythmias and motion sickness-like symptoms (P < .05) and these effects were blocked partially with vagotomy. Both methods of DCS and DPS were capable of preventing vasopressin-induced gastric dysrhythmias (P < .05) and motion sickness-like symptoms (P < .05). The antiemetic effects of the proposed methods of DCS and DPS were abolished by vagotomy but their antidysrhythmic effects were not blocked by vagotomy.

DCS and DPS are able to reduce vasopressin-induced gastric dysrhythmia and symptoms of nausea and vomiting. The vagal pathway is involved in the antiemetic effect but not the antidysrhythmic effect of the proposed methods of stimulation.

The relationship between the motility and the size of the residual stomach after proximal gastrectomy was evaluated using electrogastrography (EGG). Based on fast Fourier transformation, recorded slow waves could be analyzed to obtain the following parameters: dominant frequency (DF), percentage normal frequency (% 3 cycles per minute [cpm]), and power ratio (PR). EGG parameters, the length of the greater curvature of the residual stomach (LGC), were recorded in 18 gastrectomized patients. Compared to 12 healthy controls, the gastrectomized patients had abdominal EGG parameters including lower %3cpm (43 +/- 21% vs 83 +/- 7%; P < 0.05), DF (2.2 +/- 0.4 vs 3.0 +/- 0.2 cpm; P < 0.05), and PR (1.5 +/- 0.8 vs 2.5+/- 0.8; P < 0.05). In relation to LGC and parameters, there was no difference between the patients whose LGC was > 20 cm and controls in PR (2.3+/- 0.9 vs 2.5+/- 0.8; n.s.). In conclusion, the motility of the residual stomach would be equal to that of the nonresected stomach as if the volume of the residual stomach was more than half.

Electrogastrograghy (EGG) was performed in 33 patients with Chagas' disease and in 15 healthy volunteers-control group. The EGG was performed in two different periods: in fasting and postprandial. The EGG was submitted to a continuous spectral analysis. The following parameters were evaluated: % dominant frequency in spectral bands: normogastria (2-4 cpm), bradygastria (1-2 cpm), tachygastria (4-10 cpm) and duod/resp (10-15 cpm). EGG was considered normal if normogastria > 65% in both EGG periods. The chagasic group showed % normogastria significantly lower (basal, P < 0.01), % bradygastria (basal, P = 0.01) and % tachygastria (basal and postprandial, P =.001) significantly higher than the control group. EGG was normal in 14/15 (93%) in control group x 16/33 (53%) in chagasic group (P < 0.05). It was concluded that: 1) the prevalence of gastric dysrhythmias was higher in chagasic patients than in comparison to a control group 2) gastric dysrhythmias may be considered one of the abnormalities presented in the chagasic gastropathy.

The aim of this study was to investigate the effects of two-channel gastric electrical stimulation (GES) on delayed gastric emptying, gastric dysrhythmias, and motion sickness-like symptoms induced by vasopressin. Seven dogs implanted with four pairs of gastric electrodes and a duodenal cannula were studied in four randomized sessions (saline, vasopressin, single-channel GES, and two-channel GES). The experiment in each session was conducted sequentially as follows: 30-min baseline, ingestion of a liquid meal, 30-min iv infusion of vasopressin or saline, and two 30-min postprandial recordings. In the GES sessions, GES was applied via the first pair of electrodes for single-channel GES or the first and third pairs of electrodes for two-channel GES. Gastric emptying was collected every 15 min via the cannula for a period of 90 min. Results were as follows. (1) Vasopressin induced gastric dysrhythmias, motion sickness-like symptoms, and delayed gastric emptying (P < 0.01, ANOVA). (2) GES normalized gastric dysrhythmias (P < 0.01) but showed no effects on vasopressin-induced emetic response. (3) Two-channel GES improved delayed gastric emptying induced by vasopressin. In comparison with the vasopressin session, two-channel GES, but not single-channel GES, significantly increased gastric emptying at 30 min (43.9+/-12.6 vs. 27.5+/-7.7%; P < 0.03), 60 min (75.3+/-15.1 vs. 54.0+/-17.8%; P < 0.05), and 90 min (91.6+/-9.8 vs. 80.3+/-9.0%; P < 0.05). GES with long pulses is able to normalize gastric dysrhythmias. Two-channel GES improves delayed gastric emptying induced by vasopressin.

The aim of this study was to investigate the effect of vasopressin and long pulse-low frequency gastric electrical stimulation (GES) on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs. The study was performed in eight healthy female dogs implanted with four pairs of gastric serosal electrodes and two pairs of small bowel serosal electrodes, and a duodenal fistula for the assessment of gastric emptying. Each dog was studied in three sessions on three separate days in a randomized order with recordings of gastric and small bowel slow waves. Each study session consisted of 30-min baseline, 30-min stimulation and 30-min recovery period. In sessions 1 and 2, infusion of either saline or vasopressin (0.75 U kg(-1) in 30 mL saline instilled in 30 min) was given during the second 30-min period. The protocol of session 3 was the same as session 2 except long pulse-low frequency GES was performed during the second 30-min period. It was found that: (i) Vasopressin significantly delayed gastric emptying 30 and 45 min after meal and GES did not improve the vasopressin induced delayed gastric emptying; (ii) Vasopressin induced gastric dysrhythmias and GES significantly improved vasopressin induced gastric dysrhythmia; (iii) Vasopressin also induced intestinal slow wave abnormalities but GES had no effect on vasopressin induced small bowel dysrhythmia; (iv) Vasopressin induced symptoms and behaviours suggestive of nausea that were not improved by GES. We conclude that: (i) Vasopressin delays gastric emptying and induces gastric and small bowel dysrhythmias and symptoms in the fed state, and (ii) long pulse-low frequency GES normalizes vasopressin induced gastric dysrhythmia with no improvement in gastric emptying or symptoms.

To investigate the electric and contractile mechanisms involved in the deranged function of the transposed stomach in relation to the course of the symptoms and the changes in contractile and electrical parameters over time.

Twenty-one patients after subtotal esophagectomy and 18 healthy volunteers were studied. Complaints were compiled by using a questionnaire, and a symptom score was formed. Synchronous electrogastrography and gastric manometry were performed in the fasting state and postprandially.

Eight of the operated patients were symptom-free and 13 had symptoms. The durations of the postoperative periods for the symptomatic (9.1+/-6.5 mo) and the asymptomatic (28.3+/-8.8 mo) patients were significantly different. The symptom score correlated negatively with the time that had elapsed since the operation. The percentages of the dominant frequency in the normogastric, bradygastric and tachygastric ranges differed significantly between the controls and the patients. A significant difference was detected between the power ratio of the controls and that of the patients. The occurrence of tachygastria in the symptomatic and the symptom-free patients correlated negatively both with the time that had elapsed and with the symptom score. There was a significant increase in motility index after feeding in the controls, but not in the patients. The contractile activity of the stomach increased both in the controls and in the symptom-free patients. In contrast, in the group of symptomatic patients, the contractile activity decreased postprandially as compared with the fasting state.

The patients' post-operative complaints and symptoms change during the post-operative period and correlate with the parameters of the myoelectric and contractile activities of the stomach. Tachygastria seems to be the major pathogenetic factor involved in the contractile dysfunction.

The aims of this study were to prospectively evaluate gastric function in esophageal cancer patients after chemoradiotherapy and following surgery, using cutaneous electrogastrography (EGG). Twenty-three patients with esophageal adenocarcinoma were recruited to the study. A subset of patients (n = 11) underwent neoadjuvant chemoradiotherapy and were also studied at 14 days after treatment. All patients underwent EGG studies prior to and following surgery, at 3 months postoperatively. Ten of these patients were also studied at medians of 6 months and 12 months after surgery. Twenty normal volunteers were used as controls. Post-operative EGG studies were monitored with a modified technique; the electrodes being placed in the subscapular region in the area of the transposed stomach. Following neoadjuvant treatment there was a significant increase in abnormal gastric myoelectrical activity involving changes in tachygastrias and decreased motility as measured by power ratio. Post-operatively there was a significant increase in bradygastria which persisted at 6 months but not at 12 months. There was a corresponding decrease in normogastria which persisted at 6 months and to a lesser extent at 12 months. Dominant frequency remained significantly depressed at 3, 6 and 12 months. Gastric myoelectrical activity is normal in untreated esophageal cancer. Neoadjuvant chemoradiotherapy causes a disruption to normal myoelectrical activity involving reduced motility and tachygastrias. Surgery causes a depression in dominant frequency with a reduced incidence of normogastria at 3 months and 6 months but with a tendency towards normality at 12 months.

We utilized transfer function analysis of heart rate variability (HRV) and respiration to investigate the effect of water intake on gastric myoelectrical activity and its relationship to vagal activity. The electrogastrography (EGG) and HRV were recorded simultaneously before and after drinking 500 ml of water in 10 healthy subjects. We observed good linearity between lung volumes and HRV signals at a ventilatory rate between 0.2 and 0.4 Hz before and after water intake. The EGG power of 3 cycles/min increased remarkably after the water intake. We found that there was a significant increase in the magnitude of the respiration-HRV transfer function after water intake (P < 0.05). The EGG 3 cycles/min power was positively correlated with the transfer magnitude throughout the study (r = 0.54, P = 0.01). These results confirm that transfer function analysis of HRV sensitively identifies subtle changes in the respiratory sinus arrhythmia that occurs with water intake. The present findings suggest that transfer function analysis of HRV and respiration after water intake can be used to evaluate vagal nervous activity in the human gut.

Patients undergoing pylorus-preserving pancreatoduodenenectomy (PPPD) have a risk of up to 50% for developing delayed gastric emptying (DGE) in the early postoperative course. From 1994 to August 2002, a total of 204 patients underwent PPPD for pancreatic or periampullary cancer (50%), chronic pancreatitis (42%), and other indications (8%). Retrocolic end-to-side duodenojejunostomy was performed below the mesocolon. DGE was defined by the inability to tolerate a regular diet after day 10 (DGE10) or day 14 (DGE14) postoperatively, as well as the need for a nasogastric tube at or beyond day 10 (DGE10GT). Postoperative morbidity was 38%, 30-day mortality was 2.9%, and median postoperative length of stay was 15 days. DGE occurred in 14.7% (DGE10), 5.9% (DGE14), and 6.4% (DGE10GT), respectively. After further exclusion of 21 patients (10.3%) with major complications and no possible oral intake (because of death, reoperation, or mechanical ventilation), the frequencies of DGE10, DGE14, and DGE10GT in the remaining group of 183 patients were 9%, 2%, and 2%, respectively. Multivariate analysis revealed postoperative complications (P<0.001), the presence of portalvenous hypertension (P<0.01), and tumors as indications for surgery (P<0.01) as independent risk factors for DGE10. The overall incidence of DGE was low after PPPD. In those patients experiencing DGE, however, other postoperative complications were the most important factor associated with its occurrence.

To analyze factors affecting the recovery course of phase 3 activity of the gastric migrating motor complex after pylorus-preserving pancreatoduodenectomy (PPPD) and investigate effects of the recovery of gastric phase 3 on gastric emptying after feeding.

Whether early recovery of gastric phase 3 during fasting would predict early recovery of the fed-state gastric emptying function after PPPD has not been well documented.

Manometric recording from the gastric antrum was repeated at a weekly interval until the first appearance of gastric phase 3 in 57 patients after PPPD. Twenty-three clinical parameters were assessed as possible factors affecting the recovery course of gastric phase 3 by simple and multiple regression analyses. A gastric emptying study after feeding of a test meal was performed by the acetaminophen method and the values were compared between patients with and without gastric phase 3 after PPPD.

The mean period before the first appearance of gastric phase 3 was 38 days. Among 23 parameters, only lymph node dissection along the hepatoduodenal ligament significantly delayed recovery of gastric phase 3 after PPPD by univariate and multivariate analyses. The presence or absence of gastric phase 3 in the early postoperative period did not influence gastric emptying after feeding in the intermediate period after PPPD.

Avoiding lymph node dissection along the hepatoduodenal ligament, if applicable, may contribute to early recovery of gastric phase 3 after PPPD. The recovery state of gastric phase 3 during fasting, however, is not necessarily consistent with the degree of improvement of gastric emptying after feeding.

Electrogastrography (EGG) is the non-invasive measurement of gastric electrical activity. With the development of modern technology, improved recording and automated analysis, it is a reliable and accurate technique for the measurement of gastric myoelectrical activity providing information about the frequency and regularity of the gastric slow wave.

The aim of this report is to evaluate its role in clinical practice.

The literature is reviewed and its role investigated.

EGG has been successfully used in the investigation of gastroparesis, non-ulcer dyspepsia (NUD), gastric emptying (GE) disorders and diabetes mellitus (DM). EGG also provides an insight into the effect of medications on gastric function, e.g. edrophonium, cisapride, erythromycin and proton-pump inhibitors (PPI).

EGG has a developing role in the assessment of gastric dysfunction and on the effect of medical treatment. The effect of surgery and anaesthesia on gastric myoelectric activity is less clear.

Electrogastrography (EGG) is a noninvasive method to study gastric myoelectrical activity in humans. Because frequency characteristics are the most reliable parameters and visual analysis of the EGG recordings is notoriously difficult, automated frequency analysis, especially running spectrum analysis, is often used. However, EGG frequency spectra can be misinterpreted easily. Movement artifacts and noise from various sources can result in abnormal frequency spectra with significant power in the low-frequency and high-frequency range, or even make the EGG completely uninterpretable. Signals that differ from a sinusoid waveform have harmonics in the high-frequency range of the spectrum and may be interpreted as abnormal. Visual inspection of raw signals and frequency spectra remains essential in the analysis of EGG signals. The value of computerized analysis should not be overrated. EGG is an important research tool, but a clinical role still needs to be established.

Parkinson's disease patients may experience various gastrointestinal symptoms; however, the exact pathophysiology of these symptoms is not fully understood. Therefore, the aim of this study was to investigate the pattern of gastric myoelectrical activity in patients with Parkinson's disease. Eleven patients with Parkinson's disease and 10 healthy subjects participated in the study. Patients were stratified as "receiving dopaminergic therapy" (N = 5) and "off therapy" (N = 6). Gastric myoelectrical activity was measured by means of surface electrogastrography (EGG) for 30 min before and for 90 min after a standardized meal. The dominant frequency, postprandial EGG power change, and the percentage of normal 2-4 cycles/min (cpm) slow-wave activity in the three groups were calculated and compared. The mean postprandial EGG power increase in the untreated patients was smaller than in the treated patients (-3.11 +/- 1.01 and 1.17 +/- 1.96 dB; P = 0.072). Moreover, both of these values were significantly decreased when compared to the control group (untreated vs control: -3.11 +/- 1.01 vs 8.01 +/- 1.86 dB; P = 0.04 and treated vs control: 1.17 +/- 1.96 vs 8.01 +/- 1.86 dB; P = 0.02). The percentage of normal 2-4 cpm slow waves in untreated patients was not different from the treated patients (82.6 +/- 6.6% vs 75.8 +/- 13.6%, P = NS) or from the control group (88.2 +/- 5.4%, P = NS). The dominant frequency after the meal was similar to that in the fasting state both in the untreated (3.3 +/- 0.1 vs 3.2 +/- 0.2 cpm; P = NS) and treated patients (3.2 +/- 0.1 vs 3.1 +/- 0.1 cpm, P = NS), whereas the dominant frequency significantly increased postprandially in the control group (2.88 +/- 0.12 vs 3.05 +/- 0.16; P < 0.05). Abnormalities in gastric myoelectrical activity in untreated Parkinson's disease patients reflect direct involvement of the gastrointestinal tract by the primary disease process. EGG can be regarded as a useful diagnostic tool in evaluating gastrointestinal involvement in neurodegenerative diseases.

Gastric pacing has received increasing attention recently. However, few studies have systematically assessed the effect of pacing on gastric dysrhythmias. The aims of this study were to investigate the effect of gastric pacing on gastric dysrhythmia and to explore whether the effect of gastric pacing was mediated via cholinergic nerves. Eight hound dogs implanted with three pairs of serosal electrodes were studied. Three study sessions were performed on each dog. The experiment was conducted sequentially as follows: a 30-min myoelectrical recording immediately after a meal, intravenous injection of atropine or saline, and three sequential 20-min myoelectrical recordings with or without gastric pacing during the second 20-min recording. The percentage of regular slow waves (3.5-7. 0 cycles/min) was calculated using spectral analysis. The percentage of the regular slow waves was progressively reduced from 96.7 +/- 1. 7% at baseline to 29.6 +/- 9.0 (P < 0.001), 23.1 +/- 7.1 (P < 0.001), and 27.3 +/- 4.3% (P < 0.001), respectively, during the first, second, and third 20 min after atropine injection. Normalization of the gastric slow wave was achieved with gastric pacing 2.3 +/- 1.0 min after the initiation of pacing. The percentage of regular slow waves was significantly increased both during pacing (93.6 +/- 2.4 vs. 23.1 +/- 7.1%, P < 0.002) and after pacing (70.9 +/- 6.8 vs. 27. 3 +/- 4.3%, P < 0.003) in comparison with the session without pacing. We conclude that 1) atropine induces gastric myoelectric dysrhythmia in the fed state, 2) gastric pacing is able to normalize gastric postprandial dysrhythmia induced by atropine, and 3) the effect of gastric pacing is not mediated by vagal cholinergic mechanism.

To study the recovery course of gastric emptying after Billroth I pylorus-preserving pancreatoduodenectomy (PPPD) and therapeutic effects of cisapride.

To examine gastric emptying, acetaminophen was given, admixed in a pasty liquid meal, to 16 patients undergoing PPPD before surgery and at 1, 3, 6, 9, and 12 months after surgery. Cisapride was given orally to 10 patients before they received the acetaminophen regimen. Electrogastrography was performed at 2 weeks to 1 month after surgery in eight patients and at 6 to 12 months after surgery in seven patients.

Gastric emptying was delayed but returned to the preoperative level by 6 months after surgery. Pretreatment with cisapride accelerated gastric emptying during months 1 to 6 but not during months 6 to 12 after surgery. Electrogastrography frequently showed tachygastria 2 weeks to 1 month after surgery, but seldom 6 to 12 months after surgery.

After Billroth I PPPD, gastric emptying is delayed but recovers by 6 months after surgery. Tachygastria may play a part in the pathogenesis of delayed gastric emptying, but it can be treated with cisapride.

Dyspeptic symptoms are common in patients with cervical spinal cord injury (SCI). The supraspinal control of sympathetic innervation to the stomach is interrupted in these patients. Gastric emptying has been reported to be delayed in some patients with cervical SCI. Gastric myoelectrical activity is known to regulate gastric motility and is correlated with gastric emptying. The change in gastric myoelectrical activity after cervical SCI is unknown; our aim was to investigate it.

The study was performed in 12 cervical SCI patients and 14 healthy controls. Gastric myoelectrical activity was recorded using surface electrogastrography for 30 min in the fasting state and 1 h after a standard test meal. Spectral analysis was performed to compute the following parameters from the electrogastrogram; investigated were the percentage of 2-4 cycles/min (cpm) slow waves, the instability coefficient (IC) of the dominant frequency, the postprandial increment of dominant frequency (deltaF), and its power (deltaP).

In both fasting and fed states, regular and stable gastric slow waves were observed in both the control group and patients with cervical SCI. The percentage of normal 2-4 cpm slow waves (preprandial, 80.7+/-3.6% vs 91.5+/-3.7%, p > 0.05; postprandial, 82.0+/-4.4% vs 87.2+/-4.2%, p > 0.05) and IC (preprandial, 0.19+/-0.04% vs 0.28+/-0.05%; postprandial, 0.24+/-0.04% vs 0.27+/-0.02%, p > 0.05) were not significantly different between the two groups. The dominant frequency and its power were also similar between the two groups, no matter whether in the fast (frequency, 2.92+/-0.3 vs 2.93+/-0.06 cpm; power, 30.05+/-1.29 vs 29.08+/-1.23 dB, p > 0.05) or fed (frequency, 3.17+/-0.07 vs 3.02+/-0.06 cpm; power, 32.55+/-0.90 vs 32.07+/-1.18 dB,p > 0.05) state. The postprandial response measured by deltaF (0.25+/-0.09 vs 0.09+/-0.07 cpm, p > 0.05) and deltaP (2.52+/-1.10 vs 2.24+/-1.20 dB, p > 0.05) were also similar between the two groups.

Gastric myoelectrical activity was not altered after cervical SCI.

Electrogastrography (EGG), in which the electrical activity of the smooth muscular layer of the stomach is recorded percutaneously through the abdominal wall, has been applied in recent years to humans as a non-invasive method. In acute abdominal disease in horses, it is considered diagnostically useful to analyze digestive activity using EGG. Electrocecography (ECG) was examined to determine its effectiveness in evaluating equine digestive motility through comparison, after xylazine administration, between the results of the percutaneous ECG method and the results obtained using a strain-gauge force transducer (Force Transducer) chronically attached to the serous membrane of the cecum. As subjects, the test used six male thoroughbreds (average weight: 457.5 +/- 9.2 kg). The test showed a reduction in both the percutaneous electrical potential of the cecum in ECG and in cecal contractions measured with the Force Transducer. After xylazine administration, an average rates of decrease of the amplitude from the control period were 17.8 +/- 3.4% and 20.0 +/- 4.6% respectively, demonstrating a significant correlation (r = 0.90) between the two methods. On the other hand, power distribution centered around 6 cycles per minute in a Fourier transform (FFT) analysis of ECG, thought similar to the contraction frequency of 5.4 +/- 3.0 per minute observed with the Force Transducer. After xylazine administration, the total frequency band (1.8-12 cycle per min) in the running spectrum total power in ECG decreased to 37.0 +/- 5.1% of the pre-xylazine value. Based on these findings, it appears that the ECG potential reflected electrical activity of cecal origin, suggesting high clinical applicability of ECG to the percutaneous evaluation of equine cecal motility.

This study assessed the reliability of an improved electrogastrographic (EGG) system in recording stomach myoelectrical parameters and tried to establish the normal ranges of myoelectricity using this system. The analytical software of the current system mainly included an autoregressive modelling program to compute myoelectrical frequency and power. Forty healthy subjects were enrolled to receive myoelectrical measurement in two consecutively fasting and one postprandial 30 min sessions. The myoelectrical frequencies in both fasting and postprandial sessions were almost three cycles per min (c.p.m.) and showed little variation. The percentage of dominant frequencies (2.5-3.5 c.p.m.) in three sessions was approximately 80% while the computed myoelectrical powers in the first and second fasting sessions exhibited a significant correlation (r=0.84, P<0.001). Meal ingestion increased the myoelectrical powers by 6.8dB compared with the second fasting recording (P< 0.001). The mean variation in myoelectrical amplitude for the ratio of second: first fasting session was 110.3+/-88.8% (16-478%, median 88%). This new EGG system is, indeed, reliable for measuring myoelectrical frequency and power, whereas the interassay of recorded amplitudes appears markedly variable.

Achalasia is a primary motor disorder of the oesophagus, in which the myenteric plexus is involved. However, abnormalities in other parts of the digestive tract have also been described in achalasia. Whether gastric myoelectrical and duodenal motor activity in these patients is also affected is unknown. Therefore, interdigestive and postprandial gastric myoelectrical and antroduodenal motor activity were studied in 11 patients with achalasia, using electrogastrography (EGG) and stationary antroduodenal manometry. Electrogastrographically, no differences were found in the gastric frequency, incidence of dysrhythmias and postprandial/fasting power ratio. In the interdigestive state a lower propagation velocity of phase III episodes was found in the achalasia patients, but other parameters were unaltered. Postprandially, no differences were found in the number of pressure waves, in the amplitude of pressure waves or in antroduodenal coordination. We conclude that gastric myoelectrical activity and antral motor activity in patients with achalasia is normal, suggesting an intact extrinsic and intrinsic neural innervation of the distal stomach. Although postprandial duodenal motility is normal, a lower propagation velocity of phase III suggests involvement of the small intestine in achalasia.

It was hypothesized that the transient post-prandial decrease of the dominant frequency in the electrogastrogram (EGG) is related to the temperature of the meal. In a randomized three-period cross-over design. EGG recordings were made in 10 healthy volunteers. A liquid meal (36 kcal, 300 mL) was ingested at either 4, 37 or 55 degrees C. The changes in the dominant EGG frequency that occurred in the first 25 min postprandial were calculated using running spectrum analysis. After the meal a transient shift in frequency was seen, which was significantly greater after the cold meal than after the other meals (P < 0.001), with a greater decrease in the dominant frequency (4 degrees C: -0.75 [-0.92(-)-0.68], 37 degrees C: -0.34 [-0.51(-)-0.18], 55 degrees C: -0.30 [-0.45(-)-0.12] cpm; P = 0.020) and a longer duration (4 degrees C: 16 [13-19], 37 degrees C: 12 [6-14], 55 degrees C: 5 [3-8] min; P = 0.014). No differences were found between the 37 degrees C and 55 degrees C meals, the power ratios or the number of dysrhythmias. The magnitude of the postprandial shift in frequency of gastric myoelectrical activity depends on the temperature of the meal. Meal temperature should be taken into account in studies on postprandial gastric motility.

The aim of this study was to compare quantitatively the variability of gastric electrical activity (GEA) recorded from asymptomatic patients with implanted serosal electrodes and patients with implanted and cutaneous electrodes. Three pairs of electrodes were inserted into the gastric wall in six patients undergoing laparotomy for other reasons. Normal GEA was assessed visually once patients were tolerating a normal diet. Mean frequency (MF) values of the GEA signal in successive 256 s intervals were obtained. Standard deviations of the MF values for each separate channel of each patient were calculated. Probability density functions (pdfs) of these values were also obtained and compared. 36 1 h simultaneous recordings were made for three patients with implanted and cutaneous electrodes. The recordings were assessed both visually and with computer. A fast Hartley transform was used to obtain the dominant MF values in 256 s time intervals. These values were statistically evaluated for each channel. Normal internal GEA had a mean frequency of 2.5-3.75 cycles min-1 (cpm) and a standard deviation range of 0-0.45 cpm. Bell-shaped pdfs with coinciding maxima were observed in all these recordings, indicating normal electrical coupling. In the comparative 36 h study, using the above definitions of normality, different cutaneous recordings were found to reflect GEA with a sensitivity of 94% and a specificity of 79%.

Vomiting is common in children with disorders of the central nervous system (CNS) and is usually ascribed to gastroesophageal reflux (GER). However, recent acquisitions on the pathophysiology of vomiting suggest that the dysmotility of the foregut may be more widespread.

Fifty-five children with CNS disorders, 50 of whom suffered from retching and/or vomiting (18 following fundoplication) were studied. We assessed GER by 24 hour pH monitoring and endoscopy, gastric electrical activity by electrogastrography, and gastric half-emptying time (T1/2) of a milk meal be electrical impedance tomography.

Of the 50 vomiting patients, 29 had GER (reflux index of 5.7%-87.4%; controls: < 5%), and 31 had gastric dysrhythmias (12 tachyarrhythmia at 5.5-11.2 cpm, 4 bradyarrhythmia at 1.7-1.9 cpm, 15 unstable electrical activity; controls; 2.2-4.0 cpm). Sixteen patients had GER and gastric dysrhythmias. Eleven of 18 patients with fundoplication had gastric dysrhythmias. Gastric T1/2 was delayed in 12 of 13 patients with gastric dysrhythmia (6 with GER), versus 2 of 5 with GER alone. No abnormalities were detected in the 5 patients who did not suffer from vomiting.

Children with CNS disorders who vomit have abnormal gastric motility as often as GER. Following fundoplication, many patients continue to have symptoms possibly related to gastric dysrhythmias, the effects of which may be unmasked by fundoplication. Foregut dysmotility may be related to abnormal modulation of the enteric nervous system by the CNS or to involvement of the enteric nervous system by the same process affecting the brain.

This study aimed to characterize the disturbance of gastric electrical control activity in chronic intestinal pseudoobstruction (CIP) and to determine whether surface electrogastrography (EGG) could be used to diagnose the presence and type of CIP. Gastric electrical control activity was recorded for 30 min in each of the fasting and fed states by EGG in 14 adults with CIP proven on clinical, radiological, and histological grounds, and in 14 age- and sex-matched controls. Electrical activity was recorded from four pairs of Ag-AgCl bipolar skin electrodes, the captured signal amplified and digitalized, and running spectral analysis performed. The dominant frequency and power of spectrum were calculated using a sequence of computerized algorithms. Results were correlated with the known pathological diagnoses [visceral myopathy (M), N = 7; visceral neuropathy (N), N = 4; undifferentiated (U), N = 3]. Dysrhythmias were present in 13 of 14 patients. Tachygastria (electrical control activity frequency >5 cycles/minute) and a normal amplitude response to food, was seen in five patients (N = 4, U = 1). Irregular continuous activity without a dominant frequency or bradyarrhythmia, together with a diminished electrical response activity (ERA) to food, were found in six patients (M = 5, U = 1). Mixed abnormalities were seen in two patients (M = 1, U = 1), and normal activity with a clear dominant frequency of 3 cycles/minute was present in only one patient (M = 1). This noninvasive technique is both sensitive and specific in providing evidence of a dysrhythmia in patients with CIP and discriminates between primary pathologies. EGG may prove diagnostically useful in these disorders and may provide insight into the disturbance of electrical control activity.

We have assembled an electrogastrographic device based on the main components of amplifiers, a band-pass filter, an analogue/digital converter, low band-pass digital filters and a personal computer. The analysis software uses autoregressive moving average modelling to compute the frequency of slow waves and uses fast Fourier transformation for power spectral computation. Twenty healthy young male volunteers were enrolled in the study to test meal-elicited responses of the slow wave. Subjects underwent a 15 min recording while fasting and then a standard breakfast, which included 250 mL milk and a cake with a total of 1.45 kj, was ingested within 5 min. The post-prandial 15 min recording was immediately resumed after the meal. A slight but significant increase in the frequency of slow waves was seen in post-prandial measurement (mean +/- s.d., 0.0506 +/- 0.0005 vs 0.0497 +/- 0.0005 Hz; P < 0.0001). Moreover, a significant enhancement of the power of slow waves was elicited following the meal (36.0 +/- 3.1 vs 27.6 +/- 3.1 dB; P < 0.0001). We conclude that this assembled electrogastrographic device is a reliable means of monitoring gastric myoelectrical activity because the phenomenon of post-prandial responses of slow waves in either frequency or power is well demonstrated.

Electrogastrography (EGG) is a method to record electrical activity of the stomach using cutaneous electrodes. Power ratio (PR) is one of the parameters and means the relative change of EGG power of gastric activity from before to after certain stimulations (e.g., meals, water or drugs). Autonomic nervous function is an important modulator of gastric activity, but its relation with the EGG parameters has not been well clarified. We recorded EGG and the R-R interval simultaneously both before and after drinking 150 ml water for 400 s, and spectrally analyzed them using the maximum entropy method in 12 healthy volunteers. We calculated PR from before to after water ingestion, and the power of the high-frequency component of R-R interval variability before (pre-HF) and after water ingestion (post-HF), and their ratio (rHF = post-HF/pre-HF). PR was positively correlated with rHR (r = 0.727; P < 0.05) and negatively correlated with pre-HF (r = 0.706; P < 0.05), and rHF was negatively correlated with pre-HF (r = 0.776; P < 0.05). These results suggest that simultaneous recording of EGG and ECG for frequency domain analysis is necessary to estimate the vagal nervous activity.

Electrogastrography (EGG) enables the cutaneous measurement of gastric electric activity. An association between electric abnormalities and gastrointestinal motility disorders has been shown. The primary objective of this study was to investigate whether diabetic gastroparesis could be predicted by EGG.

EGG was performed in 18 insulin-treated type-II diabetics (9 female, 9 male; median age, 64 years; range, 45-76 years) with chronic dyspepsia. After an overnight fast, during 1 h in the fasting and 1 h in the fed state after ingestion of a liquid-solid test meal (370 kcal; liquid phase labeled with 0.5 mCi 99mTc-colloid) antral electric activity was captured by one pair of electrodes sonographically placed on the skin overlying the gastric antrum. Several EGG variables including dominant frequency (DF), percentages of DF in the normal range (2-4 cycles per minute (cpm)), bradygastria (< 2 cpm), and tachygastria (4-10 cpm), dominant frequency instability coefficient (DFIC), and postprandial to preprandial power ratio (PR) were calculated by fast Fourier transform. The data were correlated to results obtained in 20 age- and gender-matched healthy subjects (10 female, 10 male; median age, 68 years; range, 53-90 years). In addition, the data were compared with the percentages of retention of the radionuclide in the stomach at 60 min, and lag times measured by simultaneous scintigraphy.

The EGG values obtained in diabetics did not differ significantly from those in healthy subjects and did not correlate with radioscintigraphy (p > 0.05). Moreover, the EGG values in diabetics with delayed gastric emptying (about 40%) did not differ from data in diabetics without gastroparesis. Furthermore, whereas dyspepsia correlated significantly with radioscintigraphy, no correlation with EGG could be found.

Electrogastrography seems to be unsuitable for assessment of motility disorders in type-II diabetics.

Electrogastrography (EGG) permits measurements of the gastric electrical activity. However, normal values of electrical activity are poorly defined. In addition, limited data are available on the effect of age and gender. Therefore, in 40 healthy subjects (age range: 19-90 years) normal values for several EGG parameters were assessed after an overnight fast for 1 hr in the fasting and fed state after ingestion of a standardized solid-liquid meal. The electrical signals were captured by a pair of surface electrodes sonographically placed on the skin overlying the gastric antrum. The dominant electrical frequency was predominantly in the defined normal frequency range between 2 and 4 cycles per minute (cpm) (P < 0.001) and was higher in the postprandial than in the preprandial period (3.1 cpm vs 2.8 cpm, P = 0.02). The instability of the electrical rhythm calculated by a dominant frequency instability coefficient (DFIC) was postprandially lower than in the fasting state (P = 0.04). The electrical power (amplitude) increased postprandially (postprandial to fasting power ratio = 2.4). To evaluate the influence of age and gender on normal values the subjects were divided into four groups (median age: male, 28 and 69 years; female, 25 and 67 years). The most parameters did not differ significantly between the groups. However, DFIC was different between the groups (P < 0.05), with elderly women revealing lowest DFIC. In conclusion, normal values for several EGG parameters evaluated in this study should be included in the analysis of gastric electrical activity. The magnitude of electrical frequency and power are not influenced by age and gender, whereas the instability of the electrical frequency is influenced by these factors.

Electrogastroenterography (EGEG) is a method to record electrical activities of the stomach and the intestine using skin electrodes. We investigated whether this method could be used to detect gastrointestinal dysfunction in patients with idiopathic Parkinson's disease. EGEG recordings were done with ten patients with idiopathic Parkinson's disease and ten control subjects before and after a meal. The patients showed changes in EGEG that were markedly similar to those of acute stage of vagotomized patients reported previously. Patients' increase rate in amplitude of gastric activity after the meal (median: 1.19) was significantly (P < 0.05, Mann-Whitney test) smaller than that of the controls (median: 2.84), and normal temporal frequency decrease of gastric activity after the meal was not seen in the patient group. These results suggest vagal nerve dysfunction of patients with Parkinson's disease, though other possibilities could not be denied. EGEG may be useful to assess patients' gastrointestinal dysfunction though we need further study to elucidate the relation between pathophysiology of their symptoms and EGEG findings.

Blood glucose concentration has been shown to be an important factor in gastric motility. However, the effect of hyperglycemia on gastric myoelectrical activity has not yet been studied in patients with diabetes.

Surface electrogastrography was performed in eight patients with type I diabetes mellitus under normoglycemic and hyperglycemic conditions (glucose clamp technique) and in eight normoglycemic control subjects.

In the early postprandial state, the frequency of the normal pacemaker rhythm tended to be higher during hyperglycemia than during normoglycemia (3.10 +/- 0.27 vs. 2.92 +/- 0.19 cycle/min; P = 0.061). The frequency decrease that occurs immediately after a meal was found less frequently during hyperglycemia (in 25% vs. 75% of the patients; P = 0.046). Higher harmonics of the 3-cycle/min component, indicating an electrogastrographic waveform change, were found less often during hyperglycemia (in 13% vs. 63% of the patients; P = 0.039). Dysrhythmias (in particular, tachygastrias) were more prevalent during hyperglycemia (40.6% vs. 6.5% of the time; P = 0.028). No differences were found between normoglycemic patients and control subjects.

This study has shown that hyperglycemia is an important factor in the generation of gastric myoelectrical disturbances and tachygastrias in particular.

The electrogastrograms of a cohort of normal controls and a group of functional and postvagotomy dyspeptic patients, recorded under conditions of varying gastric distension applied via a gastric barostat, have been captured and stored on a portable PC. Retrospective quantitative and qualitative analysis of the waveforms have been carried out in the frequency domain. Gastric distension induced a reduction in gastric baseline frequency levels, which recovered after removal of the bolus. Controlled distension at a moderate level (240-480 ml) caused more symptoms in patients than in controls, but did not seem to affect the electrogastrograms. However, under conditions of high gastric distension (> 480 ml), there was a significant difference between the controls and patients predominant electrogastrographic frequencies (mean difference = 0.013 Hz; 95% CL = 0.001 Hz to 0.025 Hz; p = 0.014). We conclude that functional and postvagotomy dyspeptic patients have greater gastric electrical instability than controls, which seems to be more apparent under conditions of high gastric distension. The use of the Fourier transform and running spectral analysis method of analysis allowed this difference to be detected and measured.