American Society for Peripheral Nerve

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The Impact Of The Local Neuroma Environment On The Development Of Pain
Alexandra E Halevi, MD1; Deng Pan, BS1; Jesse Hu, BS2; Susan E. Mackinnon, MD3; Matthew Wood, PhD1; Amy M Moore, MD4
1Washington University School of Medicine, St Louis, MO, 2Washington University School of Medicine, Saint Louis, MO, 3Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine, St. Louis, MO, 4Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine, Saint Louis, MO

Background: Neuropathic pain and the development of painful neuromas following peripheral nerve injury are poorly understood and unpredictable. Current surgical treatments focus on resection of the painful neuroma followed by other surgical modalities, such as transposition, and have variable success. Our study evaluated the effect of the local, both physical and chemical, environment of the neuroma on the intensity and onset of pain in rats using a sciatic nerve transection neuroma model.

Methods: Lewis rats (group 1) underwent a sciatic nerve transection proximal to the trifurcation (n=6) and cold allodynia (pain-related) testing for 8 weeks. Lewis rats (group 2) underwent a sciatic transection as above (n=6) with coaptation of the distal 1 cm of the mature neuroma bulb from group 1. The negative control group (group 3) underwent coaptation of a 1 cm isograft to a fresh sciatic transection (n=6). These two groups were tested weekly for acetone cold allodynia. Total flinch time was measured within a 60 second window, including licking of the paw and refusal to bear weight on the affected limb. At 8 weeks, the sciatic nerve tissue was collected. T-cell and macrophage populations were assessed using immunohistochemistry.

Results: There was no difference in either the time to onset of pain or the intensity of pain as measured by cold allodynia in the 2 groups. There is histological confirmation that there was axonal ingrowth into the coapted nerve in both groups. Additionally, there were no clear structural differences or variations in inflammatory cell infiltration at the final time point.

Conclusions: There were no differences in either onset or intensity of pain in the intervention compared to the control groups, nor any structural or inflammatory cell variations. These data suggest that neuroma pain in the rat model is likely mediated by central changes, either in the DRG or in the brain, and not in the local environment of the neuroma itself. These findings support the use of genetic and proteomic studies focused on the central response to nerve injury in order to identify potential mechanisms for modulating neuropathic pain.

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