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The course of alcoholic‐nutritional peripheral neuropathy
Author(s) -
Hawley Rollin J.,
Kurtzke John F.,
Armbrustmacher Ver W.,
Saini Nirmal,
Manz Herbert
Publication year - 1982
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1982.tb03146.x
Subject(s) - medicine , peripheral neuropathy , nerve conduction velocity , malnutrition , alcohol intake , peripheral , anesthesia , surgery , alcohol , endocrinology , diabetes mellitus , biochemistry , chemistry
63 patients with alcoholic‐nutritional peripheral neuropathy were given neurologic, electrophysiologic and nutritional examinations. 24 of these patients were reexamined later in the course of their disease, after from 2 to 72 months (mean 33). Alcoholic‐nutritional neuropathy appeared and worsened after bouts of heavy alcohol intake and malnutrition. Initially it was sensory and symmetric in character, with prominent involvement of the posterior tibial nerves. With repeated attacks it became more proximal, more motor, and associated with more severe slowing of nerve conduction velocity. 11 of the patients were able to stop drinking alcohol. Initial subjective improvement was seen within the first week or two, but substantial improvement was not seen for 5 to 6 months. Most leg motor nerve velocity improved at a mean rate of increase of 0.12 M/sec per abstinent month. Large motor units and slowed nerve conduction persisted in «cured» patients. The largest motor units detected in the legs grew, despite alcohol intake.