Visceral afferent nerves differ functionally from non-visceral afferents. Visceral nociceptors (Table 4.1) are:

The principal visceral afferents are anatomically associated with sympathetic and parasympathetic fibers [splanchnic afferents, pelvic nerve afferents]. There are two types of peripheral afferent nerve endings: (a) low threshold; and (b) the largest population—high threshold [reserve, inactive, nonfunctional usually]. Low threshold peripheral organ mechanoreceptors [also called “wide dynamic range”] encode organ distension from low physiologic pressures to high noxious pressures. They are insensitive to touch, cut and generally any form of mechanosensation. The high threshold endings become active upon development of end organ pathological processes such as local inflammation and stimulation by chemokines and interleukins. This capacity for neuroplasticity is the basis of peripheral end organ sensitization, which results in central sensitization and expansion of receptive fields. Furthermore, the ability to localize the source of pain (spatial resolution) in visceral pain is poor due to two factors: (1) Viscera are relatively sparsely innervated in comparison to somatic structures (nearly 1:10 ration in comparison to somatic structures); and (2) Secondary spinal neurons receive convergent input from both viscera and skin. Pain pathways involved in visceral nociception are maintained by both efferent mechanisms [sympathetically maintained] and afferent visceral sensory mechanisms. A study by AK Houghton and colleagues concluded that dorsal column pathways play an important role in the processing and relaying of pancreatic visceral nociceptive information [1].

Neuronal cell types are largely defined by size. Large “light” neurons have A fibers and small “dark” neurons have C-fibers. Fiber size is directly related to the degree of fiber myelination, which is, in turn, directly related to conduction velocity. Thus the large, myelinated A fibers have the fastest conduction velocity whereas the small, unmyelinated C fibers have the slowest conduction velocity [2, 3]. Comparing nociceptive to non-nociceptive afferent neurons [4], nociceptive neurons were found to have longer action potential duration and slower maximum firing rate. These properties appeared to be graded according to the conduction velocity with the slowest (C) fibers having the longest action potential and the least rate of fiber firing (C > A-δ > A-β/α). Up to 80 % of visceral dorsal root ganglia cell somata are C-fibers, and the rest Aδ fibers. Aβ fibers are rarely encountered on viscera. In comparison, only 7–17 % of C-fibers are found at the L4 DRG part of the sciatic nerve. Spinal visceral afferents terminate in the superficial dorsal horn, lamina V and around the central canal (lamina X). Somatic cutaneous afferent neurons terminate in the superficial lamina of the dorsal horn and lamina V which explains the convergence of visceral and somatic stimuli at the level of second order neurons.

As discussed earlier, abdominal viscera receive dual innervation from the afferent and efferent system.

Nearly 80 years ago Gaser & Erlanger demonstrated that less cocaine is needed to stop conduction in thin myelinated A nerve fibers than in thicker ones. Since then, decades of research have documented differential local anesthetic susceptibility of A-, C-, and B fibers. There are two approaches to achieving this differential block of nerve fibers: an anatomic approach and a pharmacologic approach. The anatomic approach is based upon the notion that there is enough anatomic separation of the nerve fibers (afferent and efferent) to allow selective blockade of particular painful abdominal structures. The pharmacologic approach takes advantage of the fact that sympathetic and somatic nerve fibers exhibit different sensitivities to local anesthetics, thus the injection of various concentrations of local anesthetics would allow for a differential blockade of the fibers [5]. By observing the analgesic and anesthetic responses to injections of normal saline (placebo) and different amounts of local anesthetics, pain may be distinguished as visceral or non-visceral in origin.