Studies in autotomy: its pathophysiology and usefulness as a model of chronic pain

Abstract

An interesting behavioral syndrome results in animals from the same or similar types of lesions that lead to deafferentation pain in humans; many neurectomized animals begin to scratch, bite, or self-mutilate their denervated limb, a phenomenon termed autotomy. The proposition that this behavior in animals is a response to the chronic pain of peripheral nerve injury has met with considerable controversy. If this issue were resolved, then a better understanding of the neurophysiology of autotomy might help elucidate the mechanisms of the human conditions. To determine the association between deafferentation and the autotomy behavior, we developed a pharmacologically induced functional deafferentation preparation using chronic perineural lidocaine infusion of the sciatic nerve. This 'chronic lidocaine' model's behavior was compared with that of the neurectomy model. While autotomy was noted in 80% of the latter group, no animal undergoing a chronic perineural infusion of lidocaine autotomized. We thus conclude that autotomy is not a response to non-painful sensory deafferentation, but rather that this behavior is a response to pain. We also studied the development of autotomy in a variety of other focal denervation preparations. On the basis of these data, we conclude that autotomy is not due to loss of sensory input on a functional basis nor to an action potential-mediated process. Rather, nerve damage which coincidentally involves sensory loss is necessary and sufficient for the development of this behavior. We suggest that interruption of a humoral feedback process homeostatically operating within the first order sensory neuron with its effect exerted post-synaptically leads to autotomy. The evidence supports the existence of a loss of a transportable, humoral autotomy inhibitory factor.

The autotomy relief effect of a silicone tube covering the proximal nerve stump

“…Autotomy is the behavior seen in animal models with neuropathic pain such as anethesia dolorosa or phantom limb pain, 23 and the behavior may be dependent on input from a neuroma. 27,28 The degree of autotomy is reduced by the administration of catecholamine reuptake blockers or agonists of GABA that have an effect on human neurogenic pain. 29 In the autotomy pattern, a serious attack on one toe or more is increased at 2 to 4 weeks after nerve section.…”

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

“…There is evidence that autotomy behavior is produced by ongoing pain or dysesthesia, associated with increased neuronal activity, which is referred to the anesthetic region (Coderre et al 1986a;Blumenkopf and Lipman 1991;however, also see Sweet 1981;Rodin and Kruger 1984). Autotomy behavior is dramatically affected by alterations in the level of noxious input present at the time of, or prior to, nerve section.…”

Central Neuroplasticity and Pathological Pain

“…Deafferentation by peripheral neurectomy or dorsal rhizotomy in rodents is followed by self‐mutilation (autotomy) in which the animals bite and scratch the insensate paw to the point of amputation 42. There is evidence that autotomy behavior is produced by ongoing pain or dysesthesia, associated with increased neuronal activity, which is referred to the anesthetic region 43. Autotomy behavior is dramatically affected by alterations in the level of noxious input present at the time of, or prior to, nerve section.…”