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Alcohol-Related Acute Axonal Polyneuropathy,A Differential Diagnosis of Guillain-Barre Syndrome
Arch Neurol 55:1329-1334, Wohrle,J.C.,et al, 1998
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Article Abstract
All 5 patients consumed a daily average of 250 g of alcohol, and 4 had lost a substantial amount of weight recently. Additionally clinical features included painful paresthesia, myalgia, and glove and stocking-type sensory loss. Repeated cerebrospinal fluid examinations failed to show the marked increase of protein concentration with normal cell count typical of Guillain-Barre syndrome, although the protein level was mildly elevated in 1 patient. Blood laboratory findings were consistent with longstanding alcohol abuse. Compound muscle and sensory nerve action potentials were absent or reduced. Three to 4 weeks after onset, needle electromyography displaced moderate to severe fibrillations and positive sharp waves in additional to normal motor unit potentials, indicating an acute axonal polyneuropathy; this was confirmed by sural nerve biopsy in 1 patient. Excluding other factors, we assume that in these patients the combination of alcohol abuse and malnutrition caused severe acute axonal polyneuropathy. Its distinction from Guillain-Barre syndrome is important because treatment requires balanced diet, vitamin supplementation, and abstinence from alcohol, while immunotherapy may not be indicated.
 
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alcohol
alcohol,neurologic complications with
alcoholic polyneuropathy
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ascending paralysis
axonal degeneration
burning paresthesia
cerebrospinal fluid,elevated protein of
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Guillain Barre syndrome
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nutritional deficiency
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polyneuropathy,acute sensory
quadriparesis
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