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From the Departments of Neurology (Drs. England, Happel, and Liu), Neurosurgery (Drs. Happel and Kline), and Anatomy (Ms. Thouron), Louisiana State University School of Medicine, New Orleans, LA; and the Department of Physiology (Drs. Gamboni and Levinson), University of Colorado School of Medicine, Denver, CO.
Supported by grants from the National Institutes of Health (NS15879 to S.R.L.), the United States Department of Defense (DAMD 17-93-V-3013 to J.D.E., L.T.H., and D.G.K.), and a Neuroscience Incentive Grant from the Louisiana State University Neuroscience Center (J.D.E. and L.T.H.).
Presented in part at the 47th Annual Meeting of the American Academy of Neurology, Seattle, WA, May 1995.
Received August 29, 1995. Accepted in final form November 13, 1995.
Address correspondence and reprint requests to Dr. John D. England, Department of Neurology, Louisiana State University School of Medicine, 1542 Tulane Avenue, New Orleans, LA 70112-2822.
Painful neuromas from 16 patients were examined using site-specific antisodium channel antibodies employed in immunocytochemical and radioimmunoassay methods. Normal sural nerves from six of these patients served as controls. Immunocytochemistry showed abnormal segmental accumulation of sodium channels within many axons in the neuromas. Dense immunolocalization was especially apparent within the axonal tips. Radioimmunoassay confirmed a significantly greater density of sodium channels in the neuromas as compared with the sural nerves. Thus, sodium channels accumulate abnormally within the axons of neuromas in humans. This alteration of the sodium channels may underlie the generation of axonal hyperexcitability and the resulting abnormal sensory phenomena (pain and paresthesias), which frequently occur after peripheral nerve injury.
NEUROLOGY 1996;47: 272-276
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