Chronic abdominal pain is characterized by intermittent or persistent pain that occurs over a period longer than 2 months. Chronic or recurrent abdominal pain (RAP) is not a diagnosis but is a descriptive term that applies to intermittent, severe, episodic pain. It is frightening to both families and care providers who are concerned that it is a harbinger of serious disease such as an infectious, inflammatory, metabolic, anatomical, or neoplastic disorder. However, in most cases, the pain is functional, and has no known anatomical, histological, or “organic” etiology. RAP is a central feature of most functional gastrointestinal disorders in children, including functional abdominal pain (FAP), irritable bowel syndrome (IBS), functional dyspepsia, and abdominal migraine. Functional pain disorders can affect school attendance and performance, peer relationships, and participation in organizations, sports, and personal and family activities.
PATHOGENESIS AND EPIDEMIOLOGY
FAP is reported to occur in 10% to 15% of children between the ages of 4 and 16 years. A recent community-based study demonstrated that up to 28% of children complain of abdominal pain at least once per week and only 2% seek medical attention. RAP accounts for 2% to 4% of all pediatric office visits and up to half of the referrals to tertiary care gastroenterology clinics. Most studies suggest 2 peaks in the prevalence of RAP: between ages 4 and 6 years of age and between 7 and 12 years of age. However, a larger survey demonstrated a peak of RAP in adolescents between 12 and 15 years of age. Most studies report a female predominance, in particular beyond the age of 8 years old.
Functional pain disorders are considered to have a multifactorial etiology, resulting from a complex interaction between genetic vulnerability, environmental triggers, early life experiences and psychosocial factors. A unifying theory of all functional gastrointestinal disorders is the alteration of the brain-gut axis that can present with clusters of symptoms related to abnormal signals arising from the gastrointestinal tract or abnormal processing of signals in the central nervous system. An evolving understanding of the mechanisms at play suggests that a transient noxious event or inflammatory insult results in a persistent sensitization of neural pain pathways, altering the conscious awareness of gastrointestinal (GI) sensory input, also described as visceral hyperalgesia or central sensitization. An example of this hyperalgesia is found in a subset of patients with FAP who experience exaggerated pain compared to normal subjects during equal pressures of balloon distension in the rectum. The lower sensory pain threshold observed in patients with FAP may be due to increased responsiveness of intraluminal mechanoreceptors, primary sensory afferent neurons, second-order neurons in the spinal cord, or abnormal processing of sensory information in the brain. Recent advances in functional brain imaging indicate that altered connectivity between large-scale intrinsic brain networks including the amygdala, prefrontal cortex, and hypothalamus, may underlie a central sensitization process. Aberrant connectivity between these networks and cortical and subcortical brain ...