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  • Title: Comparison of autotomy behavior induced in rats by various clinically-used neurectomy methods.
    Author: Zeltser R, Beilin BZ, Zaslansky R, Seltzer Z.
    Journal: Pain; 2000 Dec 15; 89(1):19-24. PubMed ID: 11113289.
    Abstract:
    When a peripheral nerve is cut, a neuroma develops at its proximal end. Nerve-end neuromas are known to be a source of ectopic sensory input. In some humans this input may cause spontaneous and evoked neuropathic pain. There is currently no available animal model for developing better methods of cutting nerves that produce less painful neuromas than those currently in clinical use. Transection of the sciatic and saphenous nerves in rats also produces nerve-end neuromas. Afferent fibers in such neuromas spontaneously emit ectopic input that coincides with the outbreak of licking, scratching and self-mutilation of the denervated limb ('autotomy'). This behavior is considered to be the expression of spontaneous disagreeable sensations such as paresthesias, dysesthesias or neuropathic pain. We propose here that the autotomy model can be used as the first step for development of better neurectomy methods. As a demonstration, in this report we compared the course of autotomy expressed by rats following several methods of cutting peripheral nerves that are currently in clinical use. We found that the lowest extent of autotomy was caused by sciatic and saphenous neurectomy with a CO(2) laser. Tight ligation of the nerve, or a simple cut with scissors, also yielded significantly lower autotomy scores compared to cryoneurolysis and electrocut. The differing scores of autotomy caused by these neurectomy methods may derive from different properties of the injury discharge produced by these methods at the time of nerve cut. Our results raise the possibility that a higher incidence of neuropathic pain or related sensory disorders in humans may be expected following cryosurgical and electrocut neurectomies. If validated by further studies, neurectomy methods eliciting lower incidence of autotomy, and sensory disorders in models not based on autotomy may produce lower levels of neuropathic pain in humans.
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