Gastric myoelectrical and antroduodenal motor activity in patients with achalasia

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 antro-duodenal 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.     

Bitter taster status predicts susceptibility to vection-induced motion sickness and nausea

Background Sensitivity to bitter taste and susceptibility to nausea are both protective mechanisms that guard against toxin ingestion, and both these traits vary within and between populations. Thus, we postulated that they may have co‐evolved, such that they are associated. Methods Bitter taster status was determined in 40 subjects (13 men, 27 women) by measuring the differential perceived taste intensity between salt and n‐propylthiouracil using a labeled magnitude scale; susceptibility to vection‐induced motion sickness and nausea was assessed using an optokinetic drum, a validated multi‐symptom scoring scale, and electrogastrography. Key Results Taster status distribution was 25% non‐tasters (NT), 40% tasters (T), and 35% supertasters (ST). Gender had no impact on this distribution, but females had a higher mean maximum symptom score than males (12.4 ± 1.4 vs 7.3 ± 2.0). Non‐tasters displayed a faster and larger increase in mean symptom scores, had a higher percentage of subjects with high maximum symptom scores, and had a higher mean maximum score than T or ST, (14.8 ± 2.6 vs 7.1 ± 1.8, vs 9.8 ± 2.0). Taster status did not affect the gastric myoelectric frequency response to vection. Conclusions & Inferences Non‐tasters are more susceptible to vection‐induced motion sickness and nausea than T or ST, suggesting these two traits may have co‐evolved in a reciprocal manner: in environments where the NT trait conferred an evolutionary advantage by enabling intake of fruits and vegetables containing bitter, yet beneficial, phytonutrients, increased nausea susceptibility may have arisen to maintain protection against ingested toxins.     

Effects of fentanyl on gastric myoelectrical activity: a possible association with polymorphisms of the μ‐opioid receptor gene?

Background: Opioids have inhibitory effects on gastric motility, but the mechanism is far from clear. Electrical slow waves in the stomach determine the frequency and the peristaltic nature of gastric contractions. The primary aim of this study was to investigate the effects of the opioid fentanyl on gastric myoelectric activity. As there were large variations between the subjects, we investigated whether the variation was correlated to single nucleotide polymorphisms (SNP) of the μ-opioid receptor (MOR) gene.
Methods: We used cutaneous multichannel electrogastrography (EGG) to study myoelectrical activity in 20 patients scheduled for elective surgery. Fasting EGG was recorded for 30 min, followed by intravenous administration of fentanyl 1 μg/kg and subsequent EGG recording for 30 min. Spectral analysis of the two recording periods was performed and the variables assessed were dominant frequency (DF) of the EGG and its power (DP). Genetic analysis of the SNP A118G and G691C of the MOR gene was performed with the polymerase chain reaction technique.
Results: There was a significant reduction in DF and DP after intravenous fentanyl. However, there was a large variation between the patients. In eight subjects EGG was unaffected, five subjects had a slower DF (bradygastria) and in six subjects the slow waves disappeared. We found no correlation between the EGG outcome and the presence of A118G or G691C in the MOR gene.
Conclusions: Fentanyl inhibited gastric myoelectrical activity in about half of the subjects. The variation could not be explained by SNP in the MOR gene. Because of small sample size, the results must be regarded as preliminary observations.     

单纯性肥胖者胃肌电活动特征

目的探讨进餐前、后单纯性肥胖者的胃肌电活动特征。方法采用Digitrapper双电极EGG记录仪记录41例单纯性肥胖者餐前和餐后胃肌电活动,以32例正常体重健康志愿者为对照。结果①空腹状态下,肥胖组正常慢波节律百分比显著低于正常体重组(55.52±15.7比较70.83±14.31)(P<0.05);胃动过缓百分比显著高于正常体重组(17.07±10.88比较11.46±8.86)(P<0.05);无节律百分比显著高于正常体重组(9.70±5.70比较5.75±4.14)(P<0.01)。②进餐后,单纯性肥胖者正常慢波节律百分比仍显著低于正常体重组(53.19±17.77比较64.34±22.63)(P<0.05);主功率和胃动过速百分比显著高于正常体重组(36.50±4.86比较32.24±6.25,19.93±11.62比较12.94±11.72)(P<0.01和P<0.05)。③肥胖组餐后功率及振幅增加值显著高于正常体重组(P<0.01);餐后、餐前功率比显著高于正常体重组(P<0.05)。结论单纯性肥胖者空腹及餐后存在胃电节律异常,且餐后胃电主功率异常升高,可能是肥胖者胃动力亢进发生的电生理基础。     

Electrogastrography abnormality in eating disorders

Eating disorders are common psychiatric disorders in young women. The aim of the present study was to evaluate the gastric electrical activity of patients with eating disorders and its relation to their symptoms. The electrogastrography (EGG) was performed before and after a water load test for outpatients with eating disorders (n = 36; 14 anorexia nervosa, 14 bulimia nervosa, eight eating disorder not otherwise specified) and healthy women (n = 19). A structured interview (Eating Disorder Examination) was used to assess clinical symptoms. The percentage of normal gastric myoelectrical power was significantly smaller in the eating disorder patients (44.5% vs 74.2%; P < 0.05), while the percentage of bradygastric power was significantly greater, both before and after the water load test compared with the control subjects (30.4% vs 10.4%; P < 0.05). In addition, moderate correlation was found between the duration of illness and the percentage of bradygastria (P < 0.05). In conclusion, it is suggested that longstanding abnormal eating in patients with eating disorders may induce disturbances to gastric motor function, resulting in their abnormal, eating-related behavior, and form a symptomatic vicious circle. The EGG may be a promising method for determining the pathophysiology of eating disorders and for developing effective therapeutic approaches.