Handbook of Pain and Palliative Care by Rhonda J. Moore

Author:Rhonda J. Moore
Language: eng
Format: epub
Publisher: Springer New York, New York, NY

Peripheral Factors

Since neurons are flexible entities, which can grow and change their shapes to some degree, the damage caused to nerve fibers during an amputation can have differing consequences in individual cases. Sometimes, the terminal swelling that is formed and the axonal sprouting that occurs after a nerve cell is cut can lead to the formation of a neuroma. These are tangled knots of nerve tissue that develop because the axons are unable to reconnect properly. The activity of such malformed neurons can be spontaneous and unpredictable (Fried et al. 1991). Ectopic signals produced by these neuromas might also be responsible for some forms of pain in amputees.

Changes in the electrical properties of cell membranes can increase the excitability of damaged nerve cells. The mechanisms responsible for these changes involve the upregulation or novel expression, as well as the trafficking, of voltage-sensitive sodium channels and decreased potassium channel expression (Devor 2006). Another factor are altered transduction molecules for the sensitivities to heat, cold, and mechanical stimulation of the neuroma (Gorodetskaya et al. 2003). These alterations in the firing behavior of injured neurons might lead to the often reported exacerbating effects of changing temperatures on phantom limb pain, as well as the elicitation of phantom limb pain by nonpainful tactile stimulation of the stump (Nikolajsen and Jensen 2005).

However, the formation of neuromas is not instantaneous. Thus, the described effects cannot account for the frequent reports of phantom limb pain immediately after the amputation. Thus, researchers have looked for other sources of ectopic activation and found such activity, which can even summate with the ectopic discharges described earlier, in the dorsal root ganglion (DRG). This is a module on a dorsal root, containing the cell bodies of afferent neurons in the spine. Interactions between neighboring neurons can amplify the overall ectopic signal and thus exacerbate the pain. Moreover, both spontaneous and triggered sympathetic activation can elicit or intensify ectopic discharges (Chen et al. 1996), which might be one reason why the experience of phantom limb pain is generally stronger during times of emotional distress. This sympathetic-sensory coupling occurs both at the level of the neuroma and at the level of the DRG. Recently, it has been shown that there might be a genetically determined disposition to develop ectopic neuroma and DRG discharge (Devor 2005a, b). The genetic influence on the development of phantom limb pain, though understudied at this point in time, could also explain some of the observed differences in the experience of pain between individuals with very similar medical histories and kinds of amputation.

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