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Alcohol-Related Acute Axonal Polyneuropathy
A Differential Diagnosis of Guillain-Barré Syndrome
Johannes C. Wöhrle, MD;
Konstantinos Spengos, MD;
Wolfgang Steinke, MD;
Hans H. Goebel, MD;
Michael Hennerici, MD
Arch Neurol. 1998;55:1329-1334.
Background Chronic axonal polyneuropathy is a well-known clinical sequela of excessive alcohol consumption; however, acute axonal polyneuropathy related to alcohol abuse is less well recognized.
Objective To describe alcohol-related acute axonal polyneuropathy in 5 chronic alcoholics who developed ascending flaccid tetraparesis and areflexia within 14 days.
Methods Case series with clinical, laboratory, electrophysiological, and, in 1 patient, biopsy data.
Results All 5 patients consumed a daily average of 250 g of alcohol, and 4 had lost a substantial amount of weight recently. Additional 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-Barré syndrome, although the protein level was mildly elevated in 1 patient. Blood laboratory findings were consistent with long-standing alcohol abuse. Compound muscle and sensory nerve action potentials were absent or reduced, while conduction velocities were normal or mildly reduced. Three to 4 weeks after onset, needle electromyography displayed moderate to severe fibrillations and positive sharp waves in addition to normal motor unit potentials, indicating an acute axonal polyneuropathy; this was confirmed by sural nerve biopsy in 1 patient.
Conclusions 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-Barré syndrome is important because treatment requires balanced diet, vitamin supplementation, and abstinence from alcohol, while immunotherapy may not be indicated.
From the Department of Neurology, Klinikum Mannheim of the University of Heidelberg, Mannheim, Germany (Drs Wöhrle, Spengos, Steinke, and Hennerici); and Department of Neuropathology, Klinikum of the Johannes Gutenberg-University, Mainz, Germany (Dr Goebel).
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