Relating gastric scintigraphy and symptoms to motility capsule transit and pressure findings in suspected gastroparesis.

BACKGROUND: Wireless motility capsule (WMC) findings are incompletely defined in suspected gastroparesis. We aimed to characterize regional WMC transit and contractility in relation to scintigraphy, etiology, and symptoms in patients undergoing gastric emptying testing. METHODS: A total of 209 patients with gastroparesis symptoms at NIDDK Gastroparesis Consortium centers underwent gastric scintigraphy and WMCs on separate days to measure regional transit and contractility. Validated questionnaires quantified symptoms. KEY RESULTS: Solid scintigraphy and liquid scintigraphy were delayed in 68.8% and 34.8% of patients; WMC gastric emptying times (GET) were delayed in 40.3% and showed 52.8% agreement with scintigraphy; 15.5% and 33.5% had delayed small bowel (SBTT) and colon transit (CTT) times. Transit was delayed in ≥2 regions in 23.3%. Rapid transit was rarely observed. Diabetics had slower GET but more rapid SBTT versus idiopathics (P ≤ .02). GET delays related to greater scintigraphic retention, slower SBTT, and fewer gastric contractions (P ≤ .04). Overall gastroparesis symptoms and nausea/vomiting, early satiety/fullness, bloating/distention, and upper abdominal pain subscores showed no relation to WMC transit. Upper and lower abdominal pain scores (P ≤ .03) were greater with increased colon contractions. Constipation correlated with slower CTT and higher colon contractions (P = .03). Diarrhea scores were higher with delayed SBTT and CTT (P ≤ .04). CONCLUSIONS & INFERENCES: Wireless motility capsules define gastric emptying delays similar but not identical to scintigraphy that are more severe in diabetics and relate to reduced gastric contractility. Extragastric transit delays occur in >40% with suspected gastroparesis. Gastroparesis symptoms show little association with WMC profiles, although lower symptoms relate to small bowel or colon abnormalities.

Early satiety and postprandial fullness in gastroparesis correlate with gastroparesis severity, gastric emptying, and water load testing.

BACKGROUND: Early satiety (ES) and postprandial fullness (PPF) are often present in gastroparesis, but the importance of these symptoms in gastroparesis has not been well-described. The aims were: (i) Characterize ES and PPF in patients with gastroparesis. (ii) Assess relationships of ES and PPF with etiology of gastroparesis, quality of life, body weight, gastric emptying, and water load testing. METHODS: Gastroparetic patients filled out questionnaires assessing symptoms (PAGI-SYM) and quality of life (PAGI-QOL, SF-36v2). Patients underwent gastric emptying scintigraphy and water load testing. KEY RESULTS: 198 patients with gastroparesis (134 IG, 64 DG) were evaluated. Early satiety was severe or very severe in 50% of patients. Postprandial fullness was severe or very severe in 60% of patients. Severity scores for ES and PPF were similar between idiopathic and diabetic gastroparesis. Increasing severity of ES and PPF were associated with other gastroparesis symptoms including nausea/vomiting, satiety/early fullness, bloating, and upper abdominal pain and GERD subscores. Increasing severity of ES and PPF were associated with increasing gastroparesis severity, decreased BMI, decreased quality of life from PAGI-QOL and SF-36 physical health. Increasing severity of ES and PPF were associated with increasing gastric retention of a solid meal and decreased volume during water load test. CONCLUSIONS & INFERENCES: Early satiety and PPF are commonly severe symptoms in both diabetic and idiopathic gastroparesis. Early satiety and PPF severity are associated with other gastroparesis symptom severities, body weight, quality of life, gastric emptying, and water load testing. Thus, ES and PPF are important symptoms characterizing gastroparesis. ClinicalTrials.gov number: NCT NCT01696747.

Diabetic and idiopathic gastroparesis is associated with loss of CD206-positive macrophages in the gastric antrum.

BACKGROUND: Animal studies have increasingly highlighted the role of macrophages in the development of delayed gastric emptying. However, their role in the pathophysiology of human gastroparesis is unclear. Our aim was to determine changes in macrophages and other cell types in the gastric antrum muscularis propria of patients with diabetic and idiopathic gastroparesis. METHODS: Full thickness gastric antrum biopsies were obtained from patients enrolled in the Gastroparesis Clinical Research Consortium (11 diabetic, 6 idiopathic) and 5 controls. Immunolabeling and quantitative assessment was done for interstitial cells of Cajal (ICC) (Kit), enteric nerves protein gene product 9.5, neuronal nitric oxide synthase, vasoactive intestinal peptide, substance P, tyrosine hydroxylase), overall immune cells (CD45) and anti-inflammatory macrophages (CD206). Gastric emptying was assessed using nuclear medicine scintigraphy and symptom severity using the Gastroparesis Cardinal Symptom Index. RESULTS: Both diabetic and idiopathic gastroparesis patients showed loss of ICC as compared to controls (Mean [standard error of mean]/hpf: diabetic, 2.28 [0.16]; idiopathic, 2.53 [0.47]; controls, 6.05 [0.62]; P=.004). Overall immune cell population (CD45) was unchanged but there was a loss of anti-inflammatory macrophages (CD206) in circular muscle (diabetic, 3.87 [0.32]; idiopathic, 4.16 [0.52]; controls, 6.59 [1.09]; P=.04) and myenteric plexus (diabetic, 3.83 [0.27]; idiopathic, 3.59 [0.68]; controls, 7.46 [0.51]; P=.004). There was correlation between the number of ICC and CD206-positive cells (r=.55, P=.008). Enteric nerves (PGP9.5) were unchanged: diabetic, 33.64 (3.45); idiopathic, 41.26 (6.40); controls, 46.80 (6.04). CONCLUSION: Loss of antral CD206-positive anti-inflammatory macrophages is a key feature in human gastroparesis and it is associates with ICC loss.

Nausea and vomiting in gastroparesis: similarities and differences in idiopathic and diabetic gastroparesis.

BACKGROUND: Nausea and vomiting are classic symptoms of gastroparesis. It remains unclear if characteristics of nausea and vomiting are similar in different etiologies of gastroparesis. The aims of this article were as follows: to describe characteristics of nausea and vomiting in patients with gastroparesis and to determine if there are differences in nausea and vomiting in diabetic (DG) and idiopathic gastroparesis (IG). METHODS: Gastroparetic patients enrolling in the NIDDK Gastroparesis Registry underwent assessment with history and questionnaires assessing symptoms, quality of life, and a questionnaire characterizing nausea and vomiting. KEY RESULTS: Of 159 gastroparesis patients (107 IG, 52 DG), 96% experienced nausea, whereas 65% experienced vomiting. Nausea was predominant symptom in 28% and vomiting was predominant in 4%. Nausea was severe or very severe in 41%. PAGI-SYM nausea/vomiting subscore was greater with increased vomiting severity, but not nausea severity in DG than IG. Nausea was related to meals in 71%; lasting most of the day in 41%. Increasing nausea severity was related to decreased quality of life. Nausea often preceded vomiting in 82% of patients and vomiting often relieved nausea in 30%. Vomiting was more common in DG (81%) compared to IG (57%; p = 0.004). Diabetic patients more often had vomiting in the morning before eating, during the night, and when not eating. CONCLUSIONS & INFERENCES: Nausea is present in essentially all patients with gastroparesis irrespective of cause and associated with decreased quality of life. In contrast, vomiting was more prevalent, more severe, and occurred more often in DG than IG. Thus, characteristics of vomiting differ in IG vs DG.

Baseline features and differences in 48 week clinical outcomes in patients with gastroparesis and type 1 vs type 2 diabetes.

BACKGROUND: In studies of diabetic gastroparesis, patients with type 1 and type 2 diabetes mellitus (T1DM, T2DM) are often combined for analyses. We compared gastroparesis severity, healthcare utilization, psychological function, and quality of life in T1DM vs T2DM gastroparesis patients. METHODS: Questionnaire, laboratory, and scintigraphy data from patients with gastroparesis and T1DM and T2DM from seven centers of the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry were compared at enrollment and after 48 weeks. Multiple regression models assessed baseline and follow-up differences between diabetes subtypes. KEY RESULTS: At baseline, T1DM patients (N = 78) had slower gastric emptying, more hospitalizations, more gastric stimulator implantations, higher hemoglobin A1c (HbA1c), and more anxiety vs T2DM patients (N = 59). Independent discriminators of patients with T1DM vs T2DM included worse gastroesophageal reflux disease, less bloating, more peripheral neuropathy, and fewer comorbidities (p ≤ 0.05). On follow-up, gastrointestinal (GI) symptom scores decreased only in T2DM (p < 0.05), but not in T1DM patients who reported greater prokinetic, proton pump inhibitor, anxiolytic, and gastric stimulator usage over 48 weeks (p ≤ 0.03). Gastrointestinal symptoms at baseline and 48 weeks with both subtypes were not associated with HbA1c, peripheral neuropathy, psychological factors, or quality of life. CONCLUSIONS & INFERENCES: Baseline symptoms were similar in T1DM and T2DM patients, even though T1DM patients had worse gastric emptying delays and higher HbA1c suggesting other factors mediate symptom severity. Symptom scores at 48 weeks decreased in T2DM, but not T1DM patients, despite increased medical and surgical treatment utilization by T1DM patients. Defining causes of different outcomes in diabetic gastroparesis warrants further investigation.

Chest pain associated with mitral valve prolapse. Evidence for esophageal origin.

The cause of chest pain associated with mitral valve prolapse remains unclear. A young woman with chest pain ascribed to mitral valve prolapse is described. Response of chest discomfort to atenolol therapy had been poor. The patient's chest discomfort and concomitant esophageal spasm were provoked by intravenous infusion of edrophonium chloride during esophageal manometry. A Bernstein acid infusion test also induced her chest pain. Review of systems revealed intermittent dysphagia and postprandial heartburn. In certain patients with mitral valve prolapse, esophageal motility disorders may be the cause of chest discomfort.

Antibodies to herpes simplex type 1 in patients with active duodenal ulcer.

One hundred seventy-two patients requiring upper gastrointestinal tract endoscopy were examined prospectively for evidence of herpes simplex virus type 1 (HSV-1) infection. No viruses were recovered from active ulcers (11 with duodenal and eight with gastric ulcers). Using both enzyme-linked immunosorbent assay (ELISA) and standard complement fixation methods, patients with endoscopically proved active duodenal ulcer had significantly higher mean serum antibody levels to HSV-1 (but not to cytomegalovirus) than those without evidence of peptic ulcer. Neither patients with a history of or evidence of past peptic ulcer nor those with active gastric ulcer had higher serum antibody levels to HSV-1 compared with subjects without ulcers. These data provide support for an association between active duodenal ulcer and HSV-1 infection, the nature of which is not defined by these studies.

Vasopressin and oxytocin responses to illusory self-motion and nausea in man.

Vasopressin and oxytocin are nonapeptides secreted from the neurohypophysis; increases in vasopressin are associated with nausea and vomiting in some, but not all, species. Our aim was to determine whether plasma vasopressin and oxytocin levels were altered in healthy volunteers who did or did not develop nausea during vection, an optokinetic stimulus which produces the illusion of self-motion. Vection was produced by rotating a drum with an inner surface of black and white vertical stripes around the seated stationary subject. Gastric myoelectrical activity was recorded continuously throughout the experiment with electrodes positioned on the abdominal surface. Plasma samples were obtained before vection and after drum rotation stopped when nausea and tachygastria were present. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. During vection six subjects reported nausea and developed gastric dysrhythmias; six other subjects had no nausea and remained in normal 3-cpm myoelectrical rhythms. Vasopressin and oxytocin values before vection were similar in each group of subjects. One minute after vection stopped, plasma vasopressin levels were significantly greater (P less than 0.05) in subjects experiencing nausea and tachygastrias (35.4 +/- 26.7 pmol/L) than in those without symptoms (2.7 +/- 0.47 pmol/L). Oxytocin levels were unchanged by either vection or nausea. It is concluded that 1) vasopressin, not oxytocin, neurons in the magnocellular-neurohypophyseal system are activated during vection-induced nausea and gastric dysrhythmias; and 2) illusory self-motion may be used safely to study the neuroendocrine responses to brain-gut interactions and nausea in man.

Esophageal dysfunction and chest pain in patients with mitral valve prolapse: a prospective study utilizing provocative testing during esophageal manometry.

PURPOSE: The cause of chest discomfort in patients with mitral valve prolapse (MVP) remains unknown. Our aim was to determine prospectively the incidence of esophageal disorders and abnormal responses to edrophonium chloride and esophageal acid infusions in patients with MVP and troublesome non-ischemic chest pain. PATIENTS AND METHODS: After coronary artery disease was excluded, 20 patients with MVP and chest pain underwent esophageal manometry and provocative testing with edrophonium chloride and acid infusion. Seven patients with MVP but without chest pain served as control subjects; they also underwent esophageal manometry with provocative testing. RESULTS: Esophageal manometry revealed esophageal disorders in 16 patients: diffuse esophageal spasm in 14 patients, nutcracker esophagus in one, and hypotensive lower esophageal sphincter in one. Esophageal motility was normal in four patients. Injection of edrophonium and acid infusion tests evoked typical chest discomfort in three of 18 and five of 19 patients, respectively. In six of seven control subjects with MVP but with no chest discomfort, esophageal motility was normal and provocative testing did not produce chest discomfort (p less than 0.05 versus results in patients). CONCLUSION: Esophageal disorders were common and may account for chest discomfort in certain patients with MVP and persistent chest pain syndromes.

Afferent loop obstruction presenting as acute pancreatitis and pseudocyst: case reports and review of the literature.

Afferent loop obstruction after gastrectomy and Billroth II reconstruction is an uncommon problem. Complete acute obstruction requires emergent laparotomy. However, chronic obstruction may begin insidiously and its symptoms may reflect other gastrointestinal diseases. Two patients are described who developed acute abdominal pain, marked hyperamylasemia, and palpable abdominal masses 5 and 15 years after Billroth II gastrectomy. The masses were initially interpreted as pancreatic pseudocysts. Both patients were found to have chronically obstructed afferent limbs, and in one the obstruction was associated with hundreds of stasis stones within the afferent limb. Surgical decompression was accomplished in each patient. Patients who have undergone Billroth II reconstruction have signs, symptoms, and laboratory findings consistent with acute pancreatitis. A history of previous gastrectomy, recurrent or severe abdominal pain, hyperamylasemia with characteristic tomography, and endoscopic findings will establish the diagnosis and necessitate surgical evaluation and intervention.

Visceral perceptions and gastric myoelectrical activity in healthy women and in patients with bulimia nervosa.

UNLABELLED: Bulimia nervosa remains a common eating disorder in young women. Little is known about upper gastrointestinal symptoms or gastric motility in patients with bulimia nervosa. The aim of this study was to measure gastric myoelectrical activity and hunger/satiety and stomach emptiness/fullness before and after a non-nutrient water load and solid-phase gastric emptying in hospitalized patients with bulimia nervosa (n = 12) and in healthy women (n = 13). Gastric myoelectrical activity was measured by means of cutaneous electrodes; visual analogue scales were used to measure perceptions of hunger/satiety and stomach emptiness/fullness. Before and after a standard water load the bulimia patients reported significantly greater stomach fullness and satiety compared with control subjects (P < 0.01). The percentage of gastric myoelectrical power in the normal 3 cpm range was significantly less in bulimics compared with controls. Power in the 1-2 cpm bradygastria range was significantly greater in bulimia patients before and after the water load compared with the control subjects (P < 0.05). Solid-phase gastric emptying studies using radio-isotope-labelled scrambled eggs showed the lag phase was shortened in the bulimic patients (16 +/- 4 min vs 31 +/- 4 min in controls, P < 0.01), but the percentage of meal emptied at 2 h was similar to control values. IN CONCLUSION: bulimia patients had exaggerated perceptions of stomach fullness and satiety in response to water; and abnormal gastric myoelectrical activity and accelerated lag phase of gastric emptying were objective stomach abnormalities detected in hospitalized patients with bulimia nervosa.

Electrogastrographic biofeedback: a technique for enhancing normal gastric activity.

Biofeedback has been used effectively for approximately 40 years as a technique to help individuals learn to control muscle activity, brain waves, certain autonomic nervous system responses such as heart rate and blood pressure, and, more recently, constipation and fecal and urinary incontinence. In the present study, biofeedback of electrogastrographic (EGG) activity was used to determine the extent to which healthy subjects could increase normal 3 cpm gastric myoelectric activity. Thirteen experimental participants were provided with biofeedback of their EGG activity on a computer screen, and instructed to try to make their own EGG signal match a simulated 3 cpm signal that was also present on the screen. Subjects were told to relax using various forms of imagery, and to heighten their awareness of their stomach activity. Thirteen control participants did not receive any biofeedback but were otherwise given the same instructions. Both groups showed an increase in 3 cpm activity while relaxing. However, over four trials separated by 2-7 days, experimental participants showed an increased percentage of 3 cpm activity during biofeedback sessions, while control participants showed a decrease in 3 cpm activity during the corresponding sessions. In conclusion, we have demonstrated that healthy subjects can increase their normal gastric 3 cpm activity with the use of EGG biofeedback.

The stomach's response to unappetizing food: cephalic-vagal effects on gastric myoelectric activity.

The aim of this investigation was to determine the effects of sham feeding food that was perceived as unappetizing on the cephalic-vagal reflex as measured by changes in gastric myoelectric activity. Thirty-eight healthy human participants experienced one of two conditions: (i) an appetizing sham feeding condition in which participants chewed and expectorated two cooked frankfurters, and (ii) an unappetizing sham-feeding condition in which participants chewed and expectorated two cold tofu frankfurters. All participants were asked to chew each mouth-full of food 6-7 times and to be very careful not to swallow any of the food. Electrogastrograms (EGGs) were recorded for 10 min prior to, during, and for 15 min after sham feeding. A questionnaire was given to each participant after the procedure as a manipulation check and to assess food palatability. Results from the questionnaire showed, as expected, that the cooked frankfurters were significantly more appetizing than the cold tofu frankfurters (P < 0.01). In the group sham fed appetizing food, 3 cycles per minute (cpm) power increased during sham feeding, but the change was not significant; however, 3 cpm power decreased in the group sham fed unappetizing food. This difference was significant (P < 0.05). In conclusion, we have demonstrated that the cephalic-vagal reflex, as measured by power in the 3 cpm frequency region of the EGG, is sensitive to the subjective palatability of the food.

Electrogastrography: physiological basis and clinical application in diabetic gastropathy.

Electrogastrography is the recording and measurement of gastric myoelectrical activity from electrodes placed on the surface of the epigastrium. Normal electrogastrograms (EGGs) reflect 3 cycles per min (cpm) gastric myoelectrical activity produced by specialized pacemaker cells, the interstitial cells of Cajal, located in the muscular wall of the gastric corpus and antrum. Gastric dysrhythmias (tachygastrias and bradygastrias) are disturbances of the normal gastric pacesetter potentials and are associated with symptoms of nausea, epigastric fullness, and bloating and with hyperglycemia and delayed gastric emptying. In diabetic gastropathy, the normal 3-cpm electrical rhythm is replaced with bradygastrias, tachygastrias, and mixed or nonspecific dysrhythmias. Diagnosis of gastric dysrhythmias identifies an objective neuromuscular abnormality in diabetic patients with upper gastrointestinal (GI) symptoms. Correction of gastric dysrhythmias decreases upper GI symptoms and may improve gastric emptying all of which may enhance glucose control. The EGG diagnosis of gastric dysrhythmias provides new insights into gastric neuromuscular abnormalities and guides therapies to improve upper GI symptoms in patients with diabetes mellitus.

Opioid drugs cause bile duct obstruction during hepatobiliary scans.

Hepatobiliary scans using Tc-IDA are reliable in making the diagnosis of acute cholecystitis. Commonly, opioid drugs are administered in patients with acute cholecystitis to relieve pain. Opioid drugs cause biliary sphincter spasm. Whether these drugs adversely affect hepatobiliary scans is unknown. We studied 13 healthy volunteer subjects, performing three hepatobiliary scans in each one. Scans were performed without opioid drugs and 30 minutes after intramuscularly administered meperidine, morphine, hydroxyzine, hydroxyzine plus meperidine, butorphanol, and nalbuphine. Opioid drugs markedly delayed clearance of Tc-IDA from the common bile duct, simulating common bile duct obstruction. Hydroxyzine alone caused an insignificant delay. We have concluded that opioid drugs cause bile duct obstruction in healthy persons. If opioid drugs are administered before a diagnostic hepatobiliary scan, delayed clearance of Tc-IDA from the common bile duct might lead to an erroneous diagnosis and indicate a potentially unnecessary common bile duct exploration. Opioid drugs should not be administered for several hours before a diagnostic hepatobiliary scan.

Assessment of the multiple dimensions of nausea: the Nausea Profile (NP).

Nausea, unlike emesis, is a subjective experience that is difficult to describe to others, be they clinicians or researchers. Previous research has been limited to examining the frequency, severity, and duration of nausea. The goal of this study was to design a questionnaire that would allow for the evaluation of the characteristics of nausea across individuals and situations. This study consisted of 4 stages: descriptors were generated, categorized into 3 dimensions, and reevaluated to verify their reliability; in the final stage, the developed checklist was compared to a visual-analogue-scale (VAS) report of nausea in subjects exposed to a rotating optokinetic drum to stimulate nausea. The overall nausea checklist score and the VAS score were highly correlated (r = 0.71, p < 0.01). The development and use of the nausea checklist are discussed.

Gastroparesis and neuromuscular disorders of the stomach.

Gastroparesis is the most severe form of gastric neuromuscular dysfunction along a continuum that encompasses gastric visceral hypersensitivity, gastric dysrhythmias, and pylorospasm. Gastroparesis may present with vague dyspepsia symptoms or with vomiting of undigested food and weight loss. A careful history and physical examination may suggest the diagnosis of gastroparesis, but symptoms associated with gastric neuromuscular disorders are non-specific. Gastroparesis in patients with diabetes, particularly type 2 diabetes, is more common than appreciated. If gastroparesis is confirmed, then reversible causes such as mechanical obstruction of stomach and chronic mesenteric ischemia must be excluded. ''Idiopathic'' gastroparesis may follow viral infections or be due to degenerative processes that affect gastric enteric neurons, smooth muscle, and/or interstitial cells of Cajal. An approach to the diagnosis and treatment of gastroparesis and gastric neuromuscular disorders is reviewed including dietary counselling and new medical devices.

Chinese hyper-susceptibility to vection-induced motion sickness.

Little is known about the factors that control individual differences in susceptible to motion sickness. A serendipitous observation in our laboratory that most Chinese subjects become motion sick prompted this study. We used a rotating optokinetic drum to provoke motion sickness and compared gastric responses and symptom reports of Chinese, European-American, and African-American subjects. There was no difference in the responses of European-American and African-American subjects; however, Chinese subjects showed significantly greater disturbances in gastric activity and reported significantly more severe symptoms. We suggest that this hyper-susceptibility presents a natural model for the study of physiological mechanisms of nausea and other symptoms of motion sickness.

Motion sickness and gastric myoelectric activity as a function of speed of rotation of a circular vection drum.

Motion sickness symptoms and electrogastrograms (EGGs) were obtained from 60 healthy subjects while they viewed an optokinetic drum rotated at one of four speeds: 15, 30, 60 or 90 degrees.s-1. All subjects experienced vection, illusory self-motion. Motion sickness symptoms increased as drum speed increased up to 60 degrees.s-1; i.e., symptoms decreased at 90 degrees.s-1. Power, spectral intensity, of the EGG at the tachygastria frequencies (4-9 cpm) was calculated at each drum rotation speed since previous studies have shown a close correspondence between development of tachygastrias and motion sickness symptoms. Power at 4-9 cpm increased as a function of drum speed up to 60 degrees.s-1 and then decreased at 90 degrees.s-1. Power at 4-9 cpm and 60 degrees.s-1 was significantly greater than at 15 degrees.s-1. The correlation between the motion sickness symptoms and the power at 4-9 cpm was significant. Thus, drum rotation speed influenced the spectral power of the EGG at 4-9 cpm, tachygastria, and the intensity of motion sickness symptoms.

Motion sickness severity and physiological correlates during repeated exposures to a rotating optokinetic drum.

Fifty-two subjects were exposed to a rotating optokinetic drum. Ten of these subjects who became motion sick during the first session completed two additional sessions. Subjects' symptoms of motion sickness, perception of self-motion, electrogastrograms (EGGs), heart rate, mean successive differences of R-R intervals (RRI), and skin conductance were recorded for each session. The results from the first session indicated that the development of motion sickness was accompanied by increased EGG 4-9 cpm activity (gastric tachyarrhythmia), decreased mean successive differences of RRI, increased skin conductance levels, and increased self-motion perception. The results from the subjects who had three repeated sessions showed that 4-9 cpm EGG activity, skin conductance levels, perception of self-motion, and symptoms of motion sickness all increased significantly during the drum rotation period of the first session, but increased significantly less during the following sessions. Mean successive differences of RRI decreased significantly during the drum rotation period for the first session, but decreased significantly less during the following sessions. In conclusion, we have demonstrated that the development of motion sickness is accompanied by an increase in gastric tachyarrhythmia, and an increase in sympathetic activity and a decrease in parasympathetic activity, and that adaptation to motion sickness is accompanied by the recovery of autonomic nervous system balance.