Alcoholic neuropathy: Clinical, electrophysiological, and biopsy findings

Authors

  • F. Behse MD,

    1. Institute of Neurophysiology, University of Copenhagen, and the Laboratory of Clinical Neurophysiology of the Rigshospital, Copenhagen, Denmark
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  • Dr. F. Buchthal MD

    Corresponding author
    1. Institute of Neurophysiology, University of Copenhagen, and the Laboratory of Clinical Neurophysiology of the Rigshospital, Copenhagen, Denmark
    • Institute of Neurophysiology, University of Copenhagen, Juliane Maries Vej 36, DK2100, Copenhagen ϕ, Denmark
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Abstract

Nerve conduction and biopsy findings from the sural nerve in 37 patients with alcohokic neuropathy were compared with findings in 6 patients who had neuropathy associated with postgastrectomy malnutrition. Half the patients with alcoholic neuropathy had both muscle weakness and sensory loss, half had only sensory impairment, but all had electromyographic signs of denervation. Only half the patients, with or without muscle weakness, had signs of malnutrition.

In alcoholics, sural nerve conduction velocity was slowed to at most 60% of normal, correlating with loss of large fibers. These findings, together with a marked reduction in amplitude of the sensory potentials, are consistent with axonal loss. Myelinated fiber counts showed loss of small and large fibers in most nerves, retaining a bimodal distribution. Signs of regeneration were rare. Segmental demyelination was found in only 0.3% of teased fibers. Electron microscopy confirmed axonal degeneration of myelinated and unmyelinated fibers.

Neuropathy after gastrectomy malnutrition was clinically similar to alcoholic neuropathy. Conduction velocities were slower than expected from the diameter of the largest myelinated fibers, however, and teased fibers showed segmental demyelination. The findings are against alcoholic neuropathy being due to malnutrition and suggest a toxic action on peripheral nerve.

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