Visceral pain according to the definition of the IASP ( International Association for the Study of Pain) is:
Pain arising from the internal organs of the body:
• Heart, great vessels, and perivascular structures (e.g., lymph nodes)
• Airway structures (pharynx, trachea, bronchi, lungs, pleura)
• Gastrointestinal tract (esophagus, stomach, small intestine, colon, rectum)
• Upper-abdominal structures (liver, gallbladder, biliary tree, pancreas, spleen)
• Urological structures (kidneys, ureters, urinary bladder, urethra)
• Reproductive organs (uterus, ovaries, vagina, testes, vas deferens, prostate)
• Omentum, visceral peritoneum
What are the clinical characteristics of Visceral Pain?
Again according to the IASP: key features associated with pain from the viscera include:
1. diffuse localization of pain, an unreliable association with organ pathology, together with
2. referred pain sensations,
3. These, most chronic pains, can be triggered or increased due to autonomic and emotional responses.
Referred pain has two components
(1) a localization of the site of pain generation to somatic tissues with pain
processing at the same spinal segments (e.g., chest and arm pain from heart ischemia) and
(2) a sensitization of these segmental tissues (e.g., kidney stones may cause the muscles of the lateral back to become tender to palpation).
These features are in contrast to cutaneous pain, which is well localized and features a graded stimulus-response relationship.
Visceral Sensation have an unreliable nature…
Healthy visceral tissues evoke minimal sensations. Acutely inflamed tissues are more likely to produce painful sensations, but chronic inflammation has unreliable effects.
Chronic inflammation seems to play an increasingly recognized role in many visceral pain syndromes (Irritable bowel disorder, pelvic pain, interstitial cystitis, vulvodynia, etc).
The neurophysiology of visceral pain has become more clear during the last years. Electrophysiological studies have identified primary afferent nerve fibers that encode mechanical and/or chemical stimuli.
Most of these afferent nerve fibers normally are “silent” and unresponsive or minimally responsive to mechanical stimuli at baseline, but they become very mechanically sensitive and highly responsive to other stimuli in the presence of (chronic) inflammation.
Once such a sensitization has taken place, a vicious cycle of chronic inflammation, glia activation and chronic pain emerges.
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