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Updated: 12/29/06 08:31 AM |
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Authors: D.R. Saunders and A.J. Thompson ♦
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"Pain has an Element of Blank
It cannot recollect
When it begun - or if there were
A time when it was not -"
Emily Dickinson
It cannot recollect
When it begun - or if there were
A time when it was not -"
Emily Dickinson
A. Objectives
- Be able to describe the differences between pain of somatic, and of visceral origin. What is the anatomic explanation for the differences? What is the segmental arrangement of visceral afferents? Which nerves serve pelvic pain?
- Know the common locations to which pain from visceral organs is referred.
- Learn about the accessory phenomena to visceral pain. How might a diseased intra-abdominal organ cause somatic pain?
- Learn that visceral hypersensitivity may explain puzzling abdominal pain in some patients.
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B. Introduction
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Visceral = deep aching Cutaneous =sharp, bright |
Most noxious sensations perceived from the digestive organs are
directly channeled from the originating organ to the CNS via afferent visceral pain fibers. Such visceral pain characteristically has the qualities of deep aching, boring, gnawing, vague burning, deep grinding, etc., in contrast to the sharp, “bright,” pricking and knifing qualities of cutaneous pain. Vague digestive rumblings may be perceived from the activities of the normal hollow gut. When motility is greatly exaggerated, the prolonged intense contractions (spasms) or hyper-peristalsis may be intensely painful (intestinal cramps, colic).
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| Distension, traction |
The stimuli initiating pain messages are appropriate for the source organ: In the hollow gut local distention, traction (especially upon mesentery), direct pressure, and ischemia are prime stimuli. For example, following local anesthesia of the abdominal wall, the normal stomach may be cut with a sharp scalpel or pricked with a pin without eliciting pain; but squeezing it, distending it or tugging on its mesenteric attachments will cause pain.
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| Inflammation lowers pain threshold |
The condition of an organ determines its sensitivity to painful stimuli. Lowering of its pain threshold is induced by local inflammation or ischemia. For example, touching, pricking, cutting, or dripping 0.1 N HCl upon the mucosal surface of the opened normal stomach, whose pain afferent nerves are unanesthetized, will not produce noxious sensation. But these small stimuli applied to an active gastric ulcer, or to its immediate mucosal vicinity, will produce pain.
Evolution did not design a central processing system unique to visceral pain. Visceral sensation is vague and poorly localized because, unlike somatic sensation afferent fibers are fewer in number, peripheral visceral sense organs are poorly defined, visceral afferents diverge over several (up to eight) segments of the spinal cord, and afferents from different abdominal locations converge on the same dorsal nerve roots, which may be shared with the better developed somatic sensory pathways. An evolving concept involves enterochromaffin cells signaling nerve terminals by paracrine communication. |
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Next Section (C): Neuroanatomic Organization » |
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