Randomized, Placebo-Controlled Trial of Biofeedback for the Treatment of Rumination.

OBJECTIVES: We previously demonstrated that rumination is produced by an unperceived, somatic response to food ingestion, and we developed an original biofeedback technique based on electromyography (EMG)-guided control of abdomino-thoracic muscular activity. Our aim was to demonstrate the superiority of biofeedback vs. placebo for the treatment of rumination. METHODS: Randomized, placebo-controlled trial performed in a referral center. Consecutive patients who fulfilled the Rome III criteria for rumination (18 women, 6 men; 19-79 years age) were selected and all included in the study; 1 patient assigned to placebo withdrew because of an unrelated accident. Abdomino-thoracic muscle activity after a challenge meal was recorded by EMG. The patients in the biofeedback group were shown the signal and instructed to control muscle activity, whereas the patients in the placebo group were not shown the signal and were given oral simethicone. Each patient underwent 3 sessions over a 10-day period. MAIN OUTCOME: number of rumination events as measured by questionnaires for 10 consecutive days before and after intervention. RESULTS: Patients on biofeedback (n=12) but not on placebo (n=11) effectively learned to reduce intercostal activity (by 51±6% vs. 10±7% increment on placebo; P<0.001) and anterior wall muscle activity (by 52±4% vs. 9±2% increment on placebo; P<0.001). Biofeedback treatment resulted in a 74±6% reduction in rumination activity (from 29±6 before to 7±2 daily events after intervention) vs. 1±14% on placebo; P=0.001 (from 21±2 before to 21±4 daily events after intervention). CONCLUSIONS: Rumination can be effectively corrected by biofeedback-guided control of abdomino-thoracic muscular activity.

Biofeedback-guided control of abdominothoracic muscular activity reduces regurgitation episodes in patients with rumination.

BACKGROUND & AIMS: Rumination syndrome is characterized by effortless recurrent regurgitation of recently ingested food into the mouth, with consequent expulsion or re-chewing and swallowing. We investigated whether rumination is under volitional control and can be reversed by behavioral treatment. METHODS: We performed a prospective study of 28 patients who fulfilled the Rome criteria for rumination and had no organic disorders on the basis of a thorough evaluation. The diagnosis of rumination was confirmed by intestinal manometry (abdominal compression associated with regurgitation). Patients were trained to modulate abdominothoracic muscle activity under visual control of electromyographic recordings. Recordings were made after challenge meals, before training (baseline), and during 3 treatment sessions. Outcome was measured by questionnaires administered daily for 10 days before training, immediately after training, and at 1, 3, and 6 months after training. RESULTS: By the end of the 3 sessions, patients had effectively learned to reduce intercostal activity (by 50% ± 2%; P < .001 vs basal) and anterior wall muscle activity (by 30% ± 6%; P < .001 vs basal). Patients reported 27 ± 1 regurgitation episodes/day at baseline and 8 ± 2 episodes/day immediately after treatment. Regurgitation episodes decreased further to 4 ± 1 episodes at 6 months after training. CONCLUSIONS: Rumination is produced by an unperceived somatic response to food ingestion that disrupts abdominal accommodation and can be effectively corrected by biofeedback-guided control of abdominothoracic muscular activity.

Mechanisms of postprandial abdominal bloating and distension in functional dyspepsia.

OBJECTIVE: Patients with irritable bowel syndrome and abdominal bloating exhibit abnormal responses of the abdominal wall to colonic gas loads. We hypothesised that in patients with postprandial bloating, ingestion of a meal triggers comparable abdominal wall dyssynergia. Our aim was to characterise abdominal accommodation to a meal in patients with postprandial bloating. DESIGN: A test meal (0.8 kcal/ml nutrients plus 27 g/litre polyethylenglycol 4000) was administered at 50 ml/min as long as tolerated in 10 patients with postprandial bloating (fulfilling Rome III criteria for postprandial distress syndrome) and 12 healthy subjects, while electromyographic (EMG) responses of the anterior wall (upper and lower rectus, external and internal oblique via bipolar surface electrodes) and the diaphragm (via six ring electrodes over an oesophageal tube in the hiatus) were measured. Means +/- SD were calculated. RESULTS: Healthy subjects tolerated a meal volume of 913±308 ml; normal abdominal wall accommodation to the meal consisted of diaphragmatic relaxation (EMG activity decreased by 15±6%) and a compensatory contraction (25±9% increase) of the upper abdominal wall muscles (upper rectus and external oblique), with no changes in the lower anterior muscles (lower rectus and internal oblique). Patients tolerated lower volume loads (604±310 ml; p=0.030 vs healthy subjects) and developed a paradoxical response, that is, diaphragmatic contraction (14±3% EMG increment; p<0.01 vs healthy subjects) and upper anterior wall relaxation (9±4% inhibition; p<0.01 vs healthy subjects). CONCLUSIONS: In functional dyspepsia, postprandial abdominal distension is produced by an abnormal viscerosomatic response to meal ingestion that alters normal abdominal accommodation.

Abdomino-phrenic dyssynergia in patients with abdominal bloating and distension.

OBJECTIVES: The abdomen normally accommodates intra-abdominal volume increments. Patients complaining of abdominal distension exhibit abnormal accommodation of colonic gas loads (defective contraction and excessive protrusion of the anterior wall). However, abdominal imaging demonstrated diaphragmatic descent during spontaneous episodes of bloating in patients with functional gut disorders. We aimed to establish the role of the diaphragm in abdominal distension. METHODS: In 20 patients complaining of abdominal bloating and 15 healthy subjects, we increased the volume of the abdominal cavity with a colonic gas load, while measuring abdominal girth and electromyographic activity of the anterior abdominal muscles and of the diaphragm. RESULTS: In healthy subjects, the colonic gas load increased girth, relaxed the diaphragm, and increased anterior wall tone. With the same gas load, patients developed significantly more abdominal distension; this was associated with paradoxical contraction of the diaphragm and relaxation of the internal oblique muscle. CONCLUSIONS: In this experimental provocation model, abnormal accommodation of the diaphragm is involved in abdominal distension.

Abdominal accommodation: a coordinated adaptation of the abdominal wall to its content.

BACKGROUND AND AIM: We previously showed that colonic gas infusion increases the girth and modifies the muscular activity of the anterior abdominal wall. We hypothesized that abdominal accommodation to volume loads is an active process instrumented by the coordinated activity of the anterior wall and the diaphragm. METHODS: To increase intraabdominal volume in healthy subjects, a gas was infused into the colon (1.44 L in 1 h) while measuring girth (by tape measure) and electromyography (EMG) activity of the anterior wall (via four pairs of surface electrodes) and the diaphragm (via six ring electrodes over an esophageal tube in the hiatus). After preliminary feasibility studies (N = 12), postural activity (N = 6) and responses to colonic gas loads, both with the trunk erect (N = 8) and in supine position (N = 8), were studied. A morphometric analysis was performed by computed tomography, image analysis (N = 8). RESULTS: In the erect position, anterior wall tone was higher and diaphragmatic tone was lower than in the supine position. With the trunk erect, gas infusion induced diaphragmatic relaxation (by 21 +/- 3%; P < 0.05) and anterior wall contraction (16 +/- 4% EMG increment; P < 0.05). By contrast, in the supine position, it induced diaphragmatic contraction (15 +/- 6%, P < 0.05), while the anterior wall, in the absence of postural tone, showed no change (3 +/- 2%, NS). Gas infusion was associated with girth increase (7.3 +/- 1.0 mm with the trunk erect and 8.6 +/- 1.4 mm in the supine position) and diaphragmatic ascent (17.6 +/- 5.2 mm; P < 0.05). CONCLUSION: The degree of abdominal distension produced by intraabdominal volume increments results from posture-related abdomino-phrenic muscular responses.