**1. Introduction**

#### **1.1. Diagnostic criteria**

In the late 1980s, a group of experts met in Rome to establish symptom-based diagnostic criteria for functional gastrointestinal disorders (FGIDs). This first set of "Rome criteria," published in 1989, focused exclusively on adults [1]. In 1999, when these criteria were revised, a pediatric committee established a parallel set of diagnostic criteria for FGIDs in children and adolescents [2]. The Rome II pediatric subcommittee defined four pediatric disorders related to abdominal pain: functional dyspepsia (FD), irritable bowel syndrome (IBS), abdominal migraine, and functional abdominal pain. With Rome II, FD was defined as persistent or recurrent pain or discomfort centered in the upper abdomen (above the umbilicus) that was unrelated to a change in stool frequency or form and not exclusively relieved by defecation. Further, there had to be no evidence of an inflammatory, anatomic, metabolic, or neoplastic process to explain the patient's symptoms. Importantly, the committee determined that mild, chronic inflamma‐ tory changes on mucosal biopsies should not preclude the diagnosis of FD. Similar to the adult criteria on which they were based, the Rome II pediatric criteria for FD included 3 subtypes: 1) ulcer-like, in which pain was the predominant symptom; 2) dysmotility-like, in which discomfort (e.g., bloating, early satiety, postprandial fullness) was the predominant symptom; and, 3) unspecified.

In 2006, the same process of expert committees again revised the criteria, yielding the current Rome III criteria [3,4]. In adults, the previous FD subtypes were eliminated while two new subtypes were identified based on new studies generally utilizing factor analysis. The first subtype, postprandial distress syndrome, was defined as bothersome postprandial fullness occurring after ordinary sized meals and/or early satiation that prevents finishing a regular

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meal. The second subtype, epigastric pain syndrome, was defined as intermittent pain or burning localized to the epigastrium (i.e., not generalized or localized to other abdominal or chest regions) and of at least moderate severity. The Rome III pediatric subcommittee also eliminated the old subtypes, but did not adopt the new adult subtypes because of a lack of existing data to support their existence in children and adolescents. However, recent evidence suggests that the adult subtypes actually may have meaningful associations with mucosal inflammation and psychosocial functioning in pediatric FD [5].

#### **1.2. Prevalence and presentation**

Most pediatric gastroenterologists may not routinely use Rome criteria and differences exist in how the criteria are interpreted. Nevertheless, there is agreement that a strong majority of children with chronic abdominal pain presenting to pediatric gastroenterology practices fulfill criteria for an FGID, with the two most common being FD and IBS [6-9]. Community preva‐ lence for FD is estimated at 3.5-27% in children/adolescents compared to 20-30% in adults [3,4].

In both pediatric and adult gastroenterology practices, FD frequently overlaps with IBS or gastroesophageal reflux [7,10]. Adult IBS overlap is associated with more psychological dysfunction including anxiety and depression, compared to "pure" FD, but this association does not appear to be present in pediatric overlap [11,12]. Pediatric FD is associated with lower quality of life, increased functional disability, and increased likelihood of meeting criteria for an anxiety disorder relative to healthy children [13]. In adults with FD, the association with anxiety appears to be specific to patients with postprandial distress syndrome, with this relationship also apparent in children/adolescents with symptoms consistent with postpran‐ dial distress syndrome [5,14].

#### **1.3. Etiology**

FD, like all FGIDs, is probably best understood through a biopsychosocial model (see Figure 1). This model states that symptoms are likely the result of varying contributions from, and interactions between, biological/physiological factors (e.g. inflammation, mechanical distur‐ bances, hypersensitivity), psychological factors (e.g. anxiety, depression, somatization), and social factors (e.g. interactions with parents, teachers, or peers). Within this model, there is less emphasis on the "cause" of symptoms than on "contributors" to its emergence and mainte‐ nance. This model would suggest that there is value in identifying and targeting all of the factors which might be contributing to symptom generation in children with FD. It also would suggest that there is value in understanding the mechanisms by which the factors interact with one another, as these mechanisms represent additional opportunities for clinical intervention.

and central sensitization of the nervous system, which results in visceral hyperalgesia [15]. Neuroplastic changes may occur that affect the response thresholds of enteric nerves, thereby negatively impacting both sensitivity and motility [16]. Both motility and sensitivity responses to acute inflammation in adults generally are reversible; however, animal model responses suggest that, if inflammation occurs in neonates, neuroplastic changes and sensitivity may persist into adulthood [17,18]. Visceral sensitization may be even more relevant in instances where there is chronic inflammation with ongoing mediator release, as there may be subse‐

Inflammation and the Biopsychosocial Model in Pediatric Dyspepsia

http://dx.doi.org/10.5772/56635

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quent effects on visceral sensitivity that compound and prolong the issue.

**Figure 1.** The Biopsychosocial Model of FD
