Symptoms Of Functional Gastrointestinal Disorders Research Articles

Natural history of functional gastrointestinal disorders: Comparison of two longitudinal population-based studies

BackgroundFunctional gastrointestinal disorders are common but information on their natural history is limited. AimsTo document the natural history of functional gastrointestinal disorders in a population based study and to compare with the Olmsted County study. MethodA questionnaire was mailed to the same age- and gender-stratified random sample of the Icelandic population aged 18–75 in 1996 and 2006. Results were compared to the Olmsted County study. ResultsPrevalence of functional gastrointestinal disorder symptoms was stable between these periods in time: 16.9% and 17.2% for irritable bowel syndrome, and 4.8% and 6.1% for functional dyspepsia. Onset of each disorder was more often higher in the Olmsted County study than in Iceland. Disappearance rates were similar for both studies. Transition probabilities varied across the different subgroups and were different between studies. The same proportion had the same symptoms in the initial and final studies. More subjects had no symptoms in Iceland (52% vs. 40%) and different symptoms at follow up (38% vs. 23%). ConclusionPrevalence of functional gastrointestinal disorder symptoms was stable over time but the turnover in symptoms was high. A higher number of subjects had no symptoms in Iceland than in Olmsted County and there was a greater variation in subjects having different symptoms at follow up.

Chronic psychosocial stress induces visceral hyperalgesia in mice

Experimental and clinical evidence has shown that chronic stress plays an important role in the onset and/or exacerbation of symptoms of functional gastrointestinal disorders. Here, we aimed to investigate whether exposure to a chronic and temporally unpredictable psychosocial stressor alters visceral and somatic nociception as well as anxiety-related behaviour. In male C57BL/6J mice, chronic stress was induced by repeated exposure to social defeat (SD, 2 h) and overcrowding (OC, 24 h) during 19 consecutive days. Visceral and somatic nociception was evaluated by colorectal distension and a hot plate, respectively. The social interaction test was used to assess social anxiety. Mice exposed to psychosocial stress developed visceral hyperalgesia and somatic hypoalgesia 24 h following the last stress session. SD/OC mice also exhibited social anxiety-like behaviour. All these changes were also associated with physiological alterations, measured as a decreased faecal pellet output and hypothalamic-pituitary-adrenal (HPA) axis disruption. Taken together, these data confirm that this mouse model of chronic psychosocial stress may be useful for studies on the pathophysiological mechanisms underlying such stress-associated disorders and to further test potential therapies.

Functional gastrointestinal disorders in inflammatory bowel disease: Impact on quality of life and psychological status

In inflammatory bowel disease (IBD), ongoing gastrointestinal (GI) symptoms consistent with coexistent functional GI disorders (FGID) might occur. It is uncertain what effect these symptoms have on health-related quality of life (HRQoL) and psychological comorbidity. The aim of the present study was to identify interrelationships among IBD, symptoms consistent with FGID, HRQoL, and psychological comorbidity. A total of 256 consecutive IBD patients had diagnoses and disease activity verified at case-note review. Patients completed a contemporaneous survey assessing HRQoL, anxiety/depression, and GI symptoms (classified by Rome III criteria). Of 162 respondents (response rate: 63%), 95 (58.6%) had Crohn's disease and 63 (38.8%) had ulcerative colitis. By Rome III criteria, 66% met criteria for at least one FGID. Those with significant (Hospital Anxiety and Depression Scale ≥ 8) anxiety and/or depression were more likely to meet criteria for coexistent FGID (78% vs 22% and 89% vs 11%, respectively; each P < 0.001). A "load effect" was noted, such that the number of symptoms consistent with FGID in each patient correlated positively with anxiety and depression and negatively with HRQoL. Symptoms of any coexistent FGID were highly prevalent, even in those with currently-inactive IBD (57%). Symptoms consistent with FGID are highly prevalent in IBD and correlate with greater psychological comorbidity and poorer HRQoL in a "load-dependent" fashion. Therapy directed either at symptom load or psychological comorbidity might independently improve HRQoL in IBD.

Community‐based study on psychological comorbidity in functional gastrointestinal disorder

Functional gastrointestinal disorder (FGID) is one of the commonest digestive diseases worldwide. Current evidence supports a bio-psycho-social pathophysiological model for FGID, which underscores the importance of psychological and social factors in development of FGID. Concomitant psychological disorders, which include anxiety, depression and somatization, have been shown to be associated with FGID in both specialist and community-based studies. This suggests that the association is genuine rather than biased observation in referral centers. Furthermore, psychological distress such as depression, anxiety and phobia are strongly correlated with severity of FGID symptoms. There are biologically plausible mechanisms that support the causal role of psychological disorders in FGID. Psychological distress, in particular anxiety, can induce aggravation of visceral hyperalgesia as well as hypervigilance in FGID patients. This leads to poorer quality of life and increased utilization of healthcare service in addition to worsening of symptoms. Despite the numerous reports on the potential therapeutic value of psychotropic agents and psychological intervention, the importance of screening for concomitant psychological disorder in FGID patients has not been fully recognized in daily practice. Most FGID patients tend to have very low awareness of their mood symptoms, which lead to delayed diagnosis, deterioration of disease and unnecessary investigations. Many of these patients may be reluctant to accept the diagnosis of concomitant psychological disorders and therefore a good doctor-patient rapport and therapeutic relationship are essential for management of these patients.

46. Increased eosinophils and mast cells in the irritable bowel syndrome

Background Irritable bowel syndrome is a functional bowel disorder, the aetiopathogenesis of which has been poorly understood. It appears to be multifactorial and to involve altered gastrointestinal motor function, enhanced perception of visceral stimuli and psychosocial factors. Only a few studies have analysed the involvement of inflammatory cells in this condition. The aim of this study was to determine whether eosinophils and mast cells were increased in the colonic mucosa in irritable bowel syndrome compared to controls. Method Slides of 20 colonic biopsy materials of patients with irritable bowel syndrome who had endoscopically and histologically normal colonic mucosa were analysed. Twenty normal controls that had random colonic biopsies with macroscopic and histologic normal colonic mucosa and no organic or functional bowel disease were enrolled. Quantification of eosinophils and mast cells was performed on three non-overlapping fields of lamina propria at ×40 magnification. Eosinophil degranulation was semi-quantitatively estimated assessing the extent of free granules within the lamina propria. Results Among the total of 20 tests and 20 controls, the majority were females (75% and 65%, respectively). Diarrhoea predominant irritable bowel syndrome was the most common mode of presentation. Eosinophil number, degranulation and mast cell count were significantly high in colonic biopsies obtained from irritable bowel syndrome compared to control. Comment Elevated mast cells have already been reported in the colonic and ileal biopsies and there were a few proposals predicting the involvement of eosinophils in the pathogenesis of the irritable bowel syndrome. This study supports this finding and explains the possible neural – mast cell – eosinophil interaction in generating the symptoms of functional gastrointestinal disorders including irritable bowel syndrome.

Triple sugar screen breath hydrogen test for sugar intolerance in children with functional abdominal symptoms

Sugar intolerance and functional gastrointestinal disorders are both common in school age children. Both may present with similar complaints such as abdominal pain, diarrhea and bloating. Lactose, fructose and sucrose hydrogen breath tests are widely used to detect sugar malabsorption. To determine the proportion of children with symptoms of functional gastrointestinal disorders (FGID) that have sugar intolerance as determined by using a breath hydrogen test. We prospectively enrolled subjects with chronic abdominal pain, bloating and/or chronic diarrhea. All subjects underwent triple sugar screen hydrogen breath test (TSST) using the combined sugar solution. Breath hydrogen concentration ≥ 20 ppm above baseline was interpreted a positive test for sugar malabsorption. A positive hydrogen breath test consistent with sugar malabsorption was found in 5 out of 31 (16%) subjects. Three of these subjects were confirmed to have lactose malabsorption based on small bowel lactase enzyme analysis or subsequent lactose hydrogen breath test. One subject with positive TSST was diagnosed with fructose malabsorption based on dietary history; he improved on a limited fructose diet, and one was diagnosed to have gastric Crohn's disease. Approximately one in six children with symptoms of FGID had sugar intolerance as determined by the TSST.

Patients With Irritable Bowel Syndrome Exhale More Hydrogen Than Healthy Subjects in Fasting State

Background/AimsIrritable bowel syndrome (IBS) is a common disorder with significant morbidity and impairment of quality of life. Most patients (26%-83%) with IBS from Asia reported bloating. Bloating may result from increased amount or distribution of gas in the gut or exaggerated perception of distension. To evaluate whether patients with IBS produce more hydrogen even in fasting state, we conducted a study with the following aims: (1) to estimate fasting breath hydrogen levels among patients with IBS as compared with healthy controls (HC) and (2) to study relationship between symptoms of IBS and stool frequency and fasting breath hydrogen levels.MethodsEighty-one patients with IBS (Rome III criteria) and 123 HC were included. Hydrogen breath test was performed using a gas analyzer after an overnight (12 hours) fast. Both patients with IBS and HC had similar preparation before breath hydrogen estimation.ResultsOf 93 patients with symptoms of functional gastrointestinal disorders, 81 (87.1%) met Rome III criteria and 12 (12.9%) were negative and hence, excluded from the study. Patients with IBS were comparable in age (35 ± 11.8 years vs 37.5 ± 13.1 years, p = NS) and gender (male 61/81 [75.3%] vs 77/123 [62.6%], p=0.67) with HC. Average fasting breath hydrogen was higher in patients with IBS as compared to HC (mean 10.1 ± 6.5 ppm vs 5.5 ± 6.2 ppm, p < 0.0001). Number of stools per week correlated with average fasting breath hydrogen excretion in patients with IBS (r = 0.26, p = 0.02).ConclusionsInspite of similar preparation for the test, fasting breath hydrogen was higher in patients with IBS as compared to HC. Number of stools per week correlated with fasting breath hydrogen levels among patients with IBS.

Neuropeptide S Receptor Induces Neuropeptide Expression and Associates With Intermediate Phenotypes of Functional Gastrointestinal Disorders (Gastroenterology 2010;138:98-107)

Irritable bowel syndrome (IBS) is the most common gastrointestinal disorder, of largely unknown etiology and pathobiology. There is growing evidence regarding the genetic contribution in IBS, however the precise etiology of IBS is still unknown. Recently, it has been proposed that several genetic markers are associated with some aspect of IBS. Neuropeptide S receptor 1 (NPSR1), the receptor for neuropeptide S (NPS), is expressed on the intestinal epithelium, and is involved in inflammation, anxiety, and nociception. NPSR1 gene was recently found to be genetically associated with inflammatory bowel disease and asthma.1,2 The author wanted to determine whether NPS induces expression of gastrointestinal (GI) neuropeptides; and to associate NPSR1 single nucleotide polymorphisms (SNPs) with symptom phenotype and GI functions in health and functional GI disorders (FGID). The author undertook the present study in vitro and in vivo model together. First, the effect of NPS on messenger RNA expression of neuropeptides was assessed in NPSR1-tranfected HEK293 cells. Second, 17 NPSR1 polymorphisms were compared between 466 FGID patients and 233 healthy controls. They showed that NPS-NPSR1 signaling induced increased expressions of cholecystokinin, vasoactive intestinal peptide, peptide YY, and somatostatin. There were no significant associations with phenotypes of FGID symptoms. However, there were several NPSR1 SNPs associated with individual motor or sensory functions; the associations of SNPs rs2609234, rs6972158, and rs1379928 with colonic transit rate, while the rs1379928 polymorphism was also associated with pain, gas, and urgency sensory ratings at 36 mm Hg distention. The author concluded that the expression of several neuropeptides is induced upon NPS-NPSR1 signaling and NPSR1 variants are associated with colonic transit in FGID.

Are Rice and Spicy Diet Good for Functional Gastrointestinal Disorders?

Rice- and chili-containing foods are common in Asia. Studies suggest that rice is completely absorbed in the small bowel, produces little intestinal gas and has a low allergenicity. Several clinical studies have demonstrated that rice-based meals are well tolerated and may improve gastrointestinal symptoms in functional gastrointestinal disorders (FGID). Chili is a spicy ingredient commonly use throughout Asia. The active component of chili is capsaicin. Capsaicin can mediate a painful, burning sensation in the human gut via the transient receptor potential vanilloid-1 (TRPV1). Recently, the TRPV1 expressing sensory fibers have been reported to increase in the gastrointestinal tract of patients with FGID and visceral hypersensitivity. Acute exposure to capsaicin or chili can aggravate abdominal pain and burning in dyspepsia and IBS patients. Whereas, chronic ingestion of natural capsaicin agonist or chili has been shown to decrease dyspeptic and gastroesophageal reflux disease (GERD) symptoms. The high prevalence of spicy food in Asia may modify gastrointestinal burning symptoms in patients with FGID. Studies in Asia demonstrated a low prevalence of heartburn symptoms in GERD patients in several Asian countries. In conclusion rice is well tolerated and should be advocated as the carbohydrate source of choice for patients with FGID. Although, acute chili ingestion can aggravate abdominal pain and burning symptoms in FGID, chronic ingestion of chili was found to improve functional dyspepsia and GERD symptoms in small randomized, controlled studies.

Psychological Stress and Self-Reported Functional Gastrointestinal Disorders

Functional gastrointestinal disorders (FGID) are common, but despite their relevance in public health care, the etiology of FGID remains essentially unknown. Stress has been suggested as a pathophysiological factor in FGID. The aims of the present study were (a) to determine the prevalence of FGID in a sample of apparently healthy students, and (b) to determine the association of stress and FGID. The prevalence rates of 21 different FGID were assessed using an internet-based design. Subjective experience of chronic stress, individual coping strategies, and dispositional stress reactivity were measured. A total of 668 subjects provided complete data sets (66% women). About 64.2% reported at least one FGID. Symptoms of FGID were significantly predicted by increased levels of perceived chronic stress, dispositional stress reactivity, and use of maladaptive coping strategies. FGID are common in apparently healthy young individuals. The importance of stress-related factors in individuals suffering from FGID indicates that stress-reducing interventions may be beneficial in these patients.

Neuropeptide S Receptor Induces Neuropeptide Expression and Associates With Intermediate Phenotypes of Functional Gastrointestinal Disorders

NPSR1, the receptor for neuropeptide S (NPS), is expressed by gastrointestinal (GI) enteroendocrine cells, and is involved in inflammation, anxiety, and nociception. NPSR1 polymorphisms are associated with asthma and inflammatory bowel disease. We aimed to determine whether NPS induces expression of GI neuropeptides; and to associate NPSR1 single nucleotide polymorphisms (SNPs) with symptom phenotype and GI functions in health and functional GI disorders (FGID). The effect of NPS on messenger RNA expression of neuropeptides was assessed using real-time polymerase chain reaction in NPSR1-tranfected HEK293 cells. Seventeen NPSR1 SNPs were successfully genotyped in 699 subjects from a regional cohort of 466 FGID patients and 233 healthy controls. Associations were sought using gender-adjusted regression analysis and false discovery rate correction. NPS-NPSR1 signaling induced increased expression of cholecystokinin, vasoactive intestinal peptide, peptide YY, and somatostatin. There were no significant associations with phenotypes of FGID symptoms. There were several NPSR1 SNPs associated with individual motor or sensory functions; the associations of SNPs rs2609234, rs6972158, and rs1379928 with colonic transit rate remained significant after false discovery rate correction. The rs1379928 polymorphism was also associated with pain, gas, and urgency sensory ratings at 36 mm Hg distention, the level prespecified for formal testing. Associations with rectal sensory ratings were not significant after false discovery rate correction. Expression of several neuropeptides is induced upon NPS-NPSR1 signaling; NPSR1 variants are associated with colonic transit in FGID. The role of the NPS system in FGID deserves further study.

Recent insights on central processing and psychological processes in functional gastrointestinal disorders

There is increasing evidence for a key role of psychological processes and their central nervous system substrates in functional gastrointestinal disorders, although the exact nature of the relationship remains only partially understood. However, progress in this key area of psychosomatic medicine is rapidly being made. In this review article, we will give an overview of recent advances in understanding the complex mechanisms by which psychological processes and functional gastrointestinal disorder symptoms reciprocally influence each other. Various lines of evidence from different branches of biomedical and psychological science will be discussed, particularly epidemiology, patho- and psychophysiology and functional brain imaging, focusing on the most recent and novel findings. We will conclude this paper with a paragraph on new insights into treatment.

S1034 Symptoms of Functional Gastrointestinal Disorders (FGIDs) in IBD Patients and the Inter-Relationships of Psychological Co-Morbidity, Quality of Life and Disease Activity

S1034 Symptoms of Functional Gastrointestinal Disorders (FGIDs) in IBD Patients and the Inter-Relationships of Psychological Co-Morbidity, Quality of Life and Disease Activity

The effect of functional gastrointestinal disorders on psychological comorbidity and quality of life in patients with inflammatory bowel disease

Symptoms of functional gastrointestinal disorders (FGIDs) are common in patients with inflammatory bowel disease (IBD). Psychological comorbidities of anxiety and depression are also highly prevalent in IBD. To quantify the burden of FGIDs in a hospital-based cohort of patients with IBD and to determine whether there is any inter-relationship between the presence and number of FGIDs and patients' quality of life or psychological status. A cross-sectional survey of 61 out-patients was performed. Data on psychological status, quality of life, disease activity and functional symptoms according to Rome III criteria were collected. Overall, 49 (80%) participants met Rome III criteria for a functional bowel disorder and 52% of participants met criteria for more than one FGID. Participants with no FGID had significantly better physical quality of life than those with more than two FGIDs (P = 0.025). However, there was no relationship among the number of FGIDs, mental quality of life, anxiety or depression. Functional gastrointestinal disorders are highly prevalent in out-patients with IBD. Somewhat unexpectedly, the presence of anxiety and/or depression did not appear to correlate with either the presence or the number of FGIDs.

T1171 Concomitant Symptoms of Functional Gastrointestinal Disorders (FGIDs) in Patients with Inflammatory Bowel Disease (IBD) Are Associated with Decreased Quality of Life (Qol)

T1171 Concomitant Symptoms of Functional Gastrointestinal Disorders (FGIDs) in Patients with Inflammatory Bowel Disease (IBD) Are Associated with Decreased Quality of Life (Qol)

Fundamentals of Neurogastroenterology: Basic Science

The focus of neurogastroenterology in Rome II was the enteric nervous system (ENS). To avoid duplication with Rome II, only advances in ENS neurobiology after Rome II are reviewed together with stronger emphasis on interactions of the brain, spinal cord, and the gut in terms of relevance for abdominal pain and disordered gastrointestinal function. A committee with expertise in selective aspects of neurogastroenterology was invited to evaluate the literature and provide a consensus overview of the Fundamentals of Neurogastroenterology textbook as they relate to functional gastrointestinal disorders (FGIDs). This review is an abbreviated version of a fuller account that appears in the forthcoming book, Rome III. This report reviews current basic science understanding of visceral sensation and its modulation by inflammation and stress and advances in the neurophysiology of the ENS. Many of the concepts are derived from animal studies in which the physiologic mechanisms underlying visceral sensitivity and neural control of motility, secretion, and blood flow are examined. Impact of inflammation and stress in experimental models relative to FGIDs is reviewed as is human brain imaging, which provides a means for translating basic science to understanding FGID symptoms. Investigative evidence and emerging concepts implicate dysfunction in the nervous system as a significant factor underlying patient symptoms in FGIDs. Continued focus on neurogastroenterologic factors that underlie the development of symptoms will lead to mechanistic understanding that is expected to directly benefit the large contingent of patients and care-givers who deal with FGIDs.

Pharmacological and Pharmacokinetic Aspects of Functional Gastrointestinal Disorders

Medications are commonly used for the treatment of patients with functional gastrointestinal disorders. The general goal of this report is to review the pharmacokinetics and pharmacology of medications used in functional gastrointestinal disorders. Methods included literature review, consensus evaluation of the evidence for each topic assigned originally to 1 or 2 authors, and broader review at a harmonization session as part of the Rome III process. This report reviews the animal models that have been validated for the study of effects of pharmacologic agents on sensation and motility; the preclinical pharmacology, pharmacokinetics, and toxicology usually required for introduction of novel therapeutic agents; the biomarkers validated for studies of sensation and motility end points with experimental medications in humans; the pharmacogenomics applied to these medications and disorders; and the pharmacology of agents that are applied or have potential for treatment of functional gastrointestinal disorders, including psychopharmacologic agents. Clinician and basic investigators involved in the treatment or investigation of functional gastrointestinal disorders or disease models need to have a comprehensive understanding of a vast range of medications. It is anticipated that the interaction between investigators of basic science, basic and applied pharmacology, and clinical trials will lead to better treatment of these disorders.

Functional gastrointestinal disorders and mood disorders in patients with inactive inflammatory bowel disease: Prevalence and impact on health

Symptoms of functional gastrointestinal disorders (FGID) associated with mood disorders (MD), such as depression and anxiety, occur in some patients with quiescent inflammatory bowel disease (IBD) and could be caused by changes in gut motility, visceral hypersensitivity, or psychological dysfunction. We assessed the prevalence of FGID symptoms and mood disorders in ambulatory patients with quiescent IBD and examined their impact on health-related quality of life (HRQOL) and use of health resources. Consecutive ambulatory patients with IBD completed a survey of Rome II criteria for FGID, the Hospital Anxiety and Depression Survey, HRQOL indices, and health resource utilization. Logistic and linear regression analyses tested for predictors of FGID and HRQOL. Of 361 patients surveyed, 149 (44 ulcerative colitis [UC] and 105 Crohn's disease [CD]) had inactive IBD during the previous 12 months. Symptoms of at least 1 FGID occurred in 81.9%. Functional anorectal disorders were the most prevalent (53.7%) followed by functional bowel disorders (51.7%), and both were of greater prevalence than in the Canadian population (41.6% and 22.6%, respectively). Irritable bowel syndrome symptoms were more common in inactive CD than in UC (26% versus 9.1%, P = .01) and functional constipation was more common in inactive UC than in CD (26.2% versus 5.8%, P < .01). MD occurred in 27.3% of UC and 31.3% of CD patients. Age > or =40 years and anxiety independently predicted an FGID. Both FGID symptoms and MD were associated with impaired HRQOL and increased use of health services. Many patients with inactive IBD have symptoms compatible with FGID. Both FGID-like symptoms and MD are associated with impaired HRQOL and increased health resource utilization. Recognition and treatment of FGID and MD could potentially improve daily functioning of IBD patients.

Diet and Functional Gastrointestinal Disorders: A Population-Based Case-Control Study

Diet has been implicated to play a role in functional gastrointestinal disorders (FGID) in clinic-based studies. No population-based data comparing food and nutrient consumption between individuals with FGID and without gastrointestinal symptoms are available. The purpose of this study was to compare the dietary consumption of specific food items and nutrients between individuals with FGID and without symptoms in a population-based sample. A validated self-report Bowel Disease Questionnaire was mailed to an age- and gender-stratified random sample of participants aged 20-50 yr from Olmsted County, Minnesota. All patients who reported either FGID symptoms (irritable bowel or dyspepsia) or no gastrointestinal symptoms were invited to undergo a blinded physician interview and physical exam and to complete a validated Harvard Food Frequency Questionnaire. Wilcoxon rank sum tests and logistic regression were used for statistical analysis. In total, 222 of the 260 eligible (85%) subjects participated and 218 provided diet data: 99 were FGID cases and 119 were healthy controls. Cases and controls consumed similar number of servings per week of wheat-containing foods, lactose-containing foods, caffeinated drinks, and fructose-sweetened beverages. Cases were slightly more likely to consume >or=7 servings per week of norepinephrine- and epinephrine-containing foods (57%vs 45%, p= 0.10), but not serotonin- or tryptophan-containing foods. No differences were observed for amount of intake of calories, fiber, protein, iron, calcium, niacin, and vitamins C, D, E, niacin, B(1), B(2), B(6), and B(12). Cases reported consuming more fat (median, 33%vs 31%) and less carbohydrates (median, 49%vs 52%) than controls. No differences were seen in the consumption of frequently suspected "culprit" foods between community residents with and without FGID symptoms. While symptoms may be due to food sensitivity rather than altered diet composition, the role of fat and perhaps norepinephrine and epinephrine in foods in gut symptoms needs to be studied further.

Changes of the neuropeptides content and gene expression in spinal cord and dorsal root ganglion after noxious colorectal distension

Visceral pain/hypersensitivity is a cardinal symptom of functional gastrointestinal disorders. With their peripheral and central (spinal) projections, sensory neurons in the dorsal root ganglia (DRG) are the “gateway” for painful signals emanating from both somatic and visceral structures. In contrast to somatic pain, the neurochemical pathways involved in visceral pain/hypersensitivity have not been well studied. We hypothesized the neuropeptide changes in spinal cord and DRG during visceral pain would mirror similar changes in somatic nociception. Noxious (painful) colorectal distension (CRD) was done by distending a rectal balloon up to 60 mm Hg phasically for 1 h in Sprague–Dawley rats. The spinal content of calcitonin gene-related peptide (CGRP), substance P (SP), galanin and vasoactive intestinal peptide (VIP) as well as their mRNAs in DRG were measured at 0, 4 and 24 h after the CRD. Visceromotor reflex (VMR) was measured by recording the electromyogram at the abdominal muscle in response to CRD. Distal colorectum was removed for evaluating the presence of inflammation. No significant evidence of histological inflammation was seen in the colonic mucosa/submucosa after repeated CRD, which is confirmed by myeloperoxidase assay. The spinal content of CGRP and SP decreased significantly 4 h after CRD, while galanin and VIP levels increased gradually and reached highest level at 24 h ( p < 0.05). The mRNAs in DRG of the neuropeptides were significantly upregulated after CRD ( p < 0.05). VMR recording showed the rat's colon became hypersensitive 4 h after CRD, a sequence parallel to the spinal changes of CGRP and SP in timeframe. Noxious mechanical distension of the colorectum causes an acute change in the spinal levels of excitatory neurotransmitters (CGRP and SP), probably reflecting central release of these peptides from sensory neurons and contributing to the hypersensitivity following the noxious CRD. This is followed by a slower change in the levels of the inhibitory neurotransmitter galanin and VIP. Such stimulation results in significant alternation of the gene expression in DRG, reflecting the plasticity of the neuronal response. In the absence of visceral inflammation, the aforementioned neuropeptides are important mediators in the processing of visceral pain/hypersensitivity.