The studies of motility alterations were noted in adults with FGIDs and their symptoms could be explained by this alteration31). The small and large bowel with dysmotility and variations in transit time were also documented in several stuidies32). Especially in irritable bowel syndrome (IBS) patients, it seems to be higher in the amplitude and number of colonic contractions rather than control. Also there is an association between rectal balloon distention and abnormal motor responses33,34). Episodes of abdominal pain frequently coincided with abnormal contractions35). Impaired clearance and propulsion of intestinal gas are present in patients with inflammatory bowel disease (IBD)36). However, it remained unclear that motility alteration in patient could be the cause in patient with IBS in the field of the physiologic and clinical significance. It has been shown that the small and large bowel motility patterns are alike with the contractions noted in control grouop37).

The well-known hypothesis which can explain the clinical features in patient with IBS is visceral hypersensitivity31). It has been documented that the patients with IBS seem to have more sensitivity than control group at the time of balloon distention in colon38~40). The volumes of retained gas in IBS patients who developed pain were retained and well tolerated by healthy individuals41). In functional dyspepsia (FD), it is shown that intolerance to gastric distention exited42,43). Furthermore, high school-aged children with FD showed slower gastric emptying time and feeling of nausea after meal time44).

It is well known that some investigations have proven a familial history of FGIDs45~47). Children with RAP seem to have parents who have the similar symptoms45). It has been documented that the evidences of genetic effects were found in the monozygotic twins as two times as developing IBS in dizygotic twins48). It has also been reported that an independent and stronger predictor is a parent with IBS48). In spite of several investigations of multiple gene studies, the results are still inconclusive. There were researches which have focused on essential element (proteins) which has an effect on the serotonin function and serotonin transporter protein. Link between these proteins showed co-morbid stressful conditions that frequently showed in patient with IBS49~52). Serotonin transporter protein has a function to inactivate serotonin, which act in pain control and connection between the visceral and the central nervous system. The similarity which a different feature of diarrhea and constipation can be existed in patients with IBS was documented53). It is reported that in patients with IBS, the level of serotonin transporter protein mRNA and serotonin transporter protein decreased significantly in the intestinal epithelial cell54). Interestingly, these findings have not been proved in a current study55). But, some studies showed the description of a link between a protein critical to serotonin receptor functions and IBS55). IBD patients showed high level of p11. Recognition of gastric distention of hypersensitive patients with FD can be reduced by 5-HT 1B receptor enhancers56). The modulation of p11 could be responsible for acceleration of serotonergic receptors, including serotonin receptors55), and p11 could be decreased due to involvement of slow colonic transit time from stimulation of serotonergic receptor.

Psychological factors and stress can have effect on the characteristics of symptoms and clinical manifestation, moreover outcome in child with FGIDs31). Familial responses affect the experience of illness, school activities, and hospital visit57). Children whose parents with IBS tend to visit the hospital more than healthy control58). It has been demonstrated that the severity of pain and the level of parental distress were independent factors predicting behavior in children with RAP59). Two samples of social learning were documented as a positive reinforcement and modeling in children with IBS60,61). Furthermore, it has been suggested that parents who give special advantages to children with GI symptoms tend to enhance their complaints62). A model of illness behavior with GI symptoms can be provided by parents evading unpleasant works or looking forward to special consideration when they are sick60,62). It has been reported in retrospective and prospective studies that parents who tend to reinforce their symptoms could make their children's behaviors more severe than healthy control59,61). The higher levels of depression and anxious feeling can be detected in children with RAP rather than healthy control. Also the severity of anxiety and depression was documented in children with long term of GI symptom and signs63). Besides, it is demonstrated that a poor ability to deal with stressful conditions was noted in children with FAP rather than healthy controls64). A recent prospective investigation has been proven that the psychosocial indicators and development of IBS have an association in patient with IBS31). Another research reported that behavior of ill patients, symptoms, sleep discomforts, depression, anxious feeling, psychosocial stress had significant correlation with the onset of IBS65). Although the psychosocial factors have a possibility to predict the onset of IBS, it is impossible to explain the correlation between the development of FGIDs and psychological conditions completely31). Most of the psychological situation can be produced after the development of GI symptoms and it is considered to be the part of the effects of FGIDs31). It is supposed that systemic homeostasis against physical, immune, and psychological stress can be defined paradoxically as a stress. Stress can augment the gut sensitivity and relaxation can reduce its sensitivity. Slow gastric emptying can be leaded by anger, anxiety, and pain66,67) and colonic motional activity can enhance66). The greater physiologic response in FGIDs patients seems to make psychosocial stress66). It have been proven that in the field of pathophysiology, stress plays an important role67) on clinical presentation of IBS68).

In 1984, the XII International Congress of Gastroenterology was held in Lisbon, and adults investigators who had an interest in FGID were requested to develop diagnostic criteria of IBS71,72). Four years after the initial committee73), the recommendations of International Congress of Gastroenterology was presented and named 'Rome criteria'. There were a few published reports to reference to validate the recommendations of criteria. Finally they reviewed several researches and discussed to reach a consensus73). From this effort, production of complete classification system could be formed with criteria for 24 FGIDs as Rome I criteria72). The Rome I criteria was revised with addition of more information about clinical, pathophysiological, diagnostic features and management methods for each FGIDs74). Psychological and social aspects of FGIDs and guideline for managements was also provided by this committees74). From this publication and application of the Rome criteria, a better understanding of childhood FGIDs could be obtained and patient care improved associated with this development4). This recent effort induces the development of the Rome III criteria in April 200675,76). From the introduction of Rome II criteria in 199977), over 200 Medline quotations were developed, but from the introduction of Rome III criteria, over 600 quotations were developed. The neonate/toddler and the child/adolescent committees published the Rome III criteria, separately. In Table 3, pediatric FGIDs were presented from the Rome III criteria75,76,78). Most important changes of the Rome III pediatric criteria were the decline in the duration of symptoms from 3 to 2 months except for cyclic vomiting syndrome and abdominal migrain4).