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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
alcoholism
areflexia
ascending paralysis
axonal degeneration
burning paresthesia
cerebrospinal fluid,elevated protein of
flaccid paralysis
Guillain Barre syndrome
Guillain Barre syndrome,differential diagnosis of
misdiagnosis
muscle pain
nerve conduction studies
neuropathy
neuropathy,acute
neuropathy,peripheral
neuropathy,sensory
nutritional deficiency
polyneuropathy
polyneuropathy,acute sensory
quadriparesis
sensory polyneuropathy
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