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Reappraisal of alcoholic myopathy
  1. Amin A. Faris2,
  2. Marcelino G. Reyes3
  1. Division of Neurology, University of Missouri School of Medicine at Kansas City General Hospital, Missouri, U.S.A.
  2. Department of Pathology, University of Missouri School of Medicine at Kansas City General Hospital, Missouri, U.S.A.
  3. Medical Center, Kansas City, Missouri, U.S.A.


    To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles, we studied 11 chronic alcoholics who had no muscular weakness or wasting. Six patients demonstrated distal hyporeflexic (ankle jerks) sensory neuropathy on clinical examination. Four patients, one of whom was asymptomatic, had slow peroneal motor nerve conduction velocities. Patterns of neuropathy were present in the electromyograms of the proximal muscles of two patients. Muscle biopsy studies with enzyme histochemistry indicated denervation atrophy and myopathic changes in the contralateral quadriceps muscles of eight patients. As denervation atrophy was present, we concluded that these myopathic changes represented the effects of denervation of these muscles. We conclude, therefore, that the proximal subclinical alcoholic myopathy, previously described as primary by ourselves and others, is the result of denervation due to the well-known alcoholic neuropathy.

    Statistics from

    Clinical and biopsy study on chronic alcoholics without muscle weakness or wasting


    • 2 Present address: Baptist Memorial Hospital, Memphis, Tennessee, U.S.A.

    • 3 Present address and for reprints: Department of Neurology, Chicago Medical School, 2020 West Ogden Street, Chicago, Illinois, U.S.A.

    • 1 Supported in part by U.S.P.H.S. grant NB-05457-03 and a grant of the Medical Staff Fund.

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