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