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Neuroma Removal for Neuropathic Pain: Efficacy and Predictive Value of Lidocaine Infusion

Nikolajsen, Lone MD, PhD* †; Black, Joel A. PhD‡ §; Kroner, Karsten MD; Jensen, Troels S. MD, DMSc; Waxman, Stephen G. MD, PhD‡ §

doi: 10.1097/AJP.0b013e3181ed0823
Original Articles

Objective Injury to peripheral nerves associated with trauma, amputation, or surgery may lead to the formation of neuromas that can produce severe pain refractory to pharmacotherapy. Ectopic impulse activity arising in blindly ending axons within the neuroma, which contain abnormal accumulations of sodium channels, is thought to be a major contributor to this pain. The effect of surgical excision has remained controversial. Here we report a prospective study on the effect of neuroma removal on pain.

Methods A series of 6 patients with chronic neuropathic pain owing to neuromas after nerve injury were studied before and 3 months after neuroma excision. Quantitative sensory testing included measurement of areas of brush-evoked allodynia, pinprick hyperalgesia, and mechanical and thermal thresholds. The hypothesis that the analgesic response to a preoperative, intravenous infusion of the sodium channel blocker lidocaine can predict outcome of surgery was also tested.

Results Surgery only relieved spontaneous pain in 2 out of the 6 patients. One of those patients had a prior poor response to neuroma removal. In one patient the pain worsened. Response to surgical removal of neuromas was not predicted by the response to preoperative infusion of intravenous lidocaine.

Discussion Our findings suggest that, as a therapeutic maneuver, surgical excision of neuromas should be reserved for only those patients with intractable pain, who have failed to respond to other therapies. However, prior poor response to neuroma removal does not preclude relief of pain after a new excision.

Departments of *Anesthesiology

Orthopedic Surgery, Aarhus University Hospital

Danish Pain Research Center, University of Aarhus, Denmark

Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven

§Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT

Supported in part by grants from the Medical Research and Rehabilitation Research Services, Department of Veterans Affairs, Washington, DC (S.G.W.), The Erythromelagia Association, Wallingford, PA (S.G.W.), and by the Lundbeck Foundation Copenhagen, Denmark and the Danish Research Council Copenhagen, Denmark (L.N./T.S.J.). The Center for Neuroscience and Regeneration Research is a collaboration of the Paralyzed Veterans of America and the United Spinal Association with Yale University. The authors declare that they do not have a conflict of interest with respect to any of the work presented in this manuscript.

Reprints: Stephen G. Waxman, MD, PhD, Neuroscience Research Center (Building 34), Veterans Administration Connecticut, 127A, 950 Campbell Avenue, West Haven, CT 06517 (e-mail: Stephen.waxman@yale.edu).

Received for publication February 9, 2010; revised April 29, 2010; accepted June 3, 2010

© 2010 Lippincott Williams & Wilkins, Inc.