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Chronic abdominal pain is characterized by intermittent or persistent pain that occurs over a period greater than 2 months. Chronic or recurrent abdominal pain (RAP) is reported to occur in 10% to 15% of children between the ages of 4 and 16 years and accounts for 2% to 4% of all pediatric office visits.1 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, without demonstrable evidence of a pathological condition. Functional pain disorders often impact school attendance and performance, peer relationships, and participation in organizations, sports, and personal and family activities.




An evolving understanding of the mechanisms of functional pain disorders suggests that a transient noxious event or inflammatory event results in a persistent sensitization of neural pain pathways, altering the conscious awareness of gastrointestinal sensory input, also described as visceral hyperalgesia. An example of this hyperalgesia is found in a subset of patients with functional abdominal pain who experience exaggerated pain compared to normal subjects during equal pressures of balloon distension in the rectosigmoid. The lower sensory pain threshold observed in patients with functional abdominal pain (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. Some patients with FAP may also experience headaches, dizziness, motion sickness, pallor, temperature intolerance, and nausea, suggesting a generalized dysfunction of the autonomic nervous system. The central corticotropin-releasing factor system has also been implicated in mediating the effects of early life stress and possibly contributing to the development of abnormal reactivity of the hypothalamic-pituitary-adrenal axis to stress later in life.2


The neuronal circuitry involved in pain sensation develops during the early neonatal period and requires use-dependent activity for appropriate development. Noxious stimuli or stress during this critical period of development appears to decrease the sensory thresholds and increase pain responses. Neonatal rat exposure to either repetitive colorectal distension or colonic irritation results in permanent alterations in spinal dorsal horn neurons and persistence of visceral hyperalgesia in adulthood.3 Several findings in humans suggest that sensitization in early life may not result in persistent symptoms but may predispose a child to develop hyperalgesia in response to later injury or stress. Infants who undergo surgery require higher fentanyl dosages intraoperatively than do infants with no previous surgery.4 Similarly, infants with prenatally diagnosed hydronephrosis demonstrate increased abdominal sensitivity compared to controls.5 Early childhood behavioral experiences may also impact later pain responses. Survivors of child abuse have higher stress vulnerability and are more likely to develop irritable bowel syndrome.


Psychological comorbidities may also increase the likelihood of a child having ...

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