The effectiveness of a structured educational intervention on disease-related misconception and quality of life in patients with irritable bowel syndrome.

A significant number of patients with irritable bowel syndrome hold misconceptions about their disease and experience more impaired quality of life compared with the general population and people suffering from other chronic diseases. This study was designed to explore the effectiveness of a structured educational intervention on disease-related misconceptions and quality of life in patients with irritable bowel syndrome in Wuhan, China. A convenience sample of 23 patients with irritable bowel syndrome participated in an educational program that consisted of 4 weekly sessions in a group setting. Instruments, including an irritable bowel syndrome-related misconception scale and irritable bowel syndrome quality-of-life scale, were used for evaluation at baseline and 3 months after the sessions. Three months after the structured educational intervention, the score for irritable bowel syndrome-related misconception was significantly decreased (p < .001), and the score for irritable bowel syndrome quality of life was significantly improved (p < .001). We conclude that the structured educational intervention seems to be a proper method to reduce the disease-related misconceptions and improve the quality of life in patients with irritable bowel syndrome. Planning and implementing such clinical education programs will be helpful in decreasing disease-related misconceptions and promoting quality of life in patients with irritable bowel syndrome.

Discrepancies between c-Kit positive and Ano1 positive ICC-SMP in the W/Wv and wild-type mouse colon; relationships with motor patterns and calcium transients.

BACKGROUND: Interstitial cells of Cajal associated with the submuscular plexus (ICC-SMP) generate omnipresent slow-wave activity in the colon and are associated with prominent motor patterns. Our aim was to investigate colon motor dysfunction in W/W(v) mice in which the ICC are reportedly reduced. METHODS: Whole organ colon motility was studied using spatio-temporal mapping; immunohistochemical staining was carried out for c-Kit and Ano1; calcium imaging was applied to ICC-SMP. KEY RESULTS: Discrepancies between Ano1 and c-Kit staining were found in both wild-type and W/W(v) colon. ICC-SMP were reduced to ~50% in the W/W(v) mouse colon according to c-Kit immunohistochemistry, but Ano1 staining indicated a normal network of ICC-SMP. The latter was consistent with rhythmic calcium transients occurring at the submucosal border of the colon in W/W(v) mice, similar to the rhythmic transients in wild-type ICC-SMP. Furthermore, the motor pattern associated with ICC-SMP pacemaking, the so-called 'ripples' were normal in the W/W(v) colon. CONCLUSIONS & INFERENCES: c-Kit is not a reliable marker for quantifying ICC-SMP in the mouse colon. Ano1 staining revealed a normal network of ICC-SMP consistent with the presence of a normal 'ripples' motor pattern. We detected a class of Ano1 positive c-Kit negative cells that do not depend on Kit expression for maintenance, a feature shared with ICC progenitors.

The origin of segmentation motor activity in the intestine.

The segmentation motor activity of the gut that facilitates absorption of nutrients was first described in the late 19th century, but the fundamental mechanisms underlying it remain poorly understood. The dominant theory suggests alternate excitation and inhibition from the enteric nervous system. Here we demonstrate that typical segmentation can occur after total nerve blockade. The segmentation motor pattern emerges when the amplitude of the dominant pacemaker, the slow wave generated by interstitial cells of Cajal associated with the myenteric plexus (ICC-MP), is modulated by the phase of induced lower frequency rhythmic transient depolarizations, generated by ICC associated with the deep muscular plexus (ICC-DMP), resulting in a waxing and waning of the amplitude of the slow wave and a rhythmic checkered pattern of segmentation motor activity. Phase-amplitude modulation of the slow waves points to an underlying system of coupled nonlinear oscillators originating in the networks of ICC.

Neurogenic and myogenic properties of pan-colonic motor patterns and their spatiotemporal organization in rats.

BACKGROUND AND AIMS: Better understanding of intrinsic control mechanisms of colonic motility will lead to better treatment options for colonic dysmotility. The aim was to investigate neurogenic and myogenic control mechanisms underlying pan-colonic motor patterns. METHODS: Analysis of in vitro video recordings of whole rat colon motility was used to explore motor patterns and their spatiotemporal organizations and to identify mechanisms of neurogenic and myogenic control using pharmacological tools. RESULTS: Study of the pan-colonic spatiotemporal organization of motor patterns revealed: fluid-induced or spontaneous rhythmic propulsive long distance contractions (LDCs, 0.4-1.5/min, involving the whole colon), rhythmic propulsive motor complexes (RPMCs) (0.8-2.5/min, dominant in distal colon), ripples (10-14/min, dominant in proximal colon), segmentation and retrograde contractions (0.1-0.8/min, prominent in distal and mid colon). Spontaneous rhythmic LDCs were the dominant pattern, blocked by tetrodotoxin, lidocaine or blockers of cholinergic, nitrergic or serotonergic pathways. Change from propulsion to segmentation and distal retrograde contractions was most prominent after blocking 5-HT3 receptors. In the presence of all neural blockers, bethanechol consistently evoked rhythmic LDC-like propulsive contractions in the same frequency range as the LDCs, indicating the existence of myogenic mechanisms of initiation and propulsion. CONCLUSIONS: Neurogenic and myogenic control systems orchestrate distinct and variable motor patterns at different regions of the pan-colon. Cholinergic, nitrergic and serotonergic pathways are essential for rhythmic LDCs to develop. Rhythmic motor patterns in presence of neural blockade indicate the involvement of myogenic control systems and suggest a role for the networks of interstitial cells of Cajal as pacemakers.

Habitual rapid food intake and ineffective esophageal motility.

AIM: To study non-cardiac chest pain (NCCP) in relation to ineffective esophageal motility (IEM) and rapid food intake. METHODS: NCCP patients with a self-reported habit of fast eating underwent esophageal manometry for the diagnosis of IEM. Telephone interviews identified eating habits of additional IEM patients. Comparison of manometric features was done among IEM patients with and without the habit of rapid food intake and healthy controls. A case study investigated the effect of 6-mo gum chewing on restoration of esophageal motility in an IEM patient. The Valsalva maneuver was performed in IEM patients and healthy controls to assess the compliance of the esophagus in response to abdominal pressure increase. RESULTS: Although most patients diagnosed with NCCP do not exhibit IEM, remarkably, all 12 NCCP patients who were self-reporting fast eaters with a main complaint of chest pain (75.0%) had contraction amplitudes in the mid and distal esophagus that were significantly lower compared with healthy controls [(23.45 mmHg (95%CI: 14.06-32.85) vs 58.80 mmHg (95%CI: 42.56-75.04), P < 0.01 and 28.29 mmHg (95%CI: 21.77-34.81) vs 50.75 mmHg (95%CI: 38.44-63.05), P < 0.01, respectively)]. In 7 normal-eating IEM patients with a main complaint of sensation of obstruction (42.9%), the mid amplitude was smaller than in the controls [30.09 mmHg (95%CI: 19.48-40.70) vs 58.80 mmHg (95%CI: 42.56-75.04), P < 0.05]. There was no statistically significant difference in manometric features between the fast-eating and normal-eating groups. One NCCP patient who self-reported fast eating and was subsequently diagnosed with IEM did not improve with proton-pump inhibition but restored swallow-induced contractions upon 6-mo gum-chewing. The Valsalva maneuver caused a markedly reduced pressure rise in the mid and proximal esophagus in the IEM patients. CONCLUSION: Habitual rapid food intake may lead to IEM. A prospective study is needed to validate this hypothesis. Gum-chewing might strengthen weakened esophageal muscles.