The main difference between superficial and deep or visceral pain is the nature of the pain evoked by noxious stimuli. This is probably due to a relative deficiency of Aδ nerve fibers in deep structures, so there is little rapid, sharp pain. In addition, deep pain and visceral pain are poorly localized, nauseating, and frequently are accompanied by sweating and changes in blood pressure. Pain can be elicited experimentally from the periosteum and ligaments by injecting hypertonic saline into them. The pain produced in this manner initiates reflex contraction of nearby skeletal muscles. This reflex contraction is similar to the muscle spasm associated with injuries to bones, tendons, and joints. The steadily contracting muscles become ischemic, and ischemia stimulates the pain receptors in the muscles. The pain in turn initiates more spasm, setting up a vicious cycle.
In addition to being poorly localized, unpleasant, and associated with nausea and autonomic symptoms, visceral pain often radiates or is referred to other areas. The autonomic nervous system, such as the somatic, has afferent components, central integrating stations, and effector pathways. The receptors for pain and the other sensory modalities present in the viscera are similar to those in skin, but there are marked differences in their distribution. There are no proprioceptors in the viscera, and few temperature and touch receptors. Nociceptors are present, although they are more sparsely distributed than in somatic structures.
Afferent fibers from visceral structures reach the CNS via sympathetic and parasympathetic nerves. Their cell bodies are located in the dorsal root ganglia and the homologous cranial nerve ganglia. Specifically, there are visceral afferents in the facial, glossopharyngeal, and vagus nerves; in the thoracic and upper lumbar dorsal roots; and in the sacral dorsal roots.
As almost everyone knows from personal experience, visceral pain can be very severe. The receptors in the walls of the hollow viscera are especially sensitive to distension of these organs. Such distension can be produced experimentally in the gastrointestinal tract by inflation of a swallowed balloon attached to a tube. This produces pain that waxes and wanes (intestinal colic) as the intestine contracts and relaxes on the balloon. Similar colic is produced in intestinal obstruction by the contractions of the dilated intestine above the obstruction. When a visceral organ is inflamed or hyperemic, relatively minor stimuli cause severe pain, a form of hyperalgesia.
