ALCOHOL-RELATED ACUTE AXONAL POLYNEUROPATHY - A DIFFERENTIAL-DIAGNOSIS OF GUILLAIN-BARRE-SYNDROME

Background: Chronic axonal polyneuropathy is a well-known clinical seq uela of excessive alcohol consumption; however, acute axonal polyneuro pathy related to alcohol abuse is less well recognized. Objective: To describe alcohol-related acute axonal polyneuropathy in 5 chronic alco holics who developed ascending flaccid tetraparesis and areflexia with in 14 days. Methods: Case series with clinical, laboratory, electrophy siological, and, in 1 patient, biopsy data. Results: All 5 patients co nsumed a daily average of 250 g of alcohol, and 4 had lost a substanti al amount of weight recently. Additional clinical features included pa inful paresthesia, myalgia, and glove and stocking-type sensory loss. Repeated cerebrospinal fluid examinations failed to show the marked in crease of protein concentration with normal cell count typical of Guil lain-Barre syndrome, although the protein level was mildly elevated in 1 patient. Blood laboratory findings were consistent with longstandin g alcohol abuse, Compound muscle and sensory nerve action potentials w ere absent or reduced, while conduction velocities were normal or mild ly reduced. Three to 4 weeks after onset, needle electromyography disp layed moderate to severe fibrillations and positive sharp waves in add ition to normal motor unit potentials, indicating an acute axonal poly neuropathy; this was confirmed by sural nerve biopsy in 1 patient. Con clusions: Excluding other factors, we assume that in these patients th e combination of alcohol abuse and malnutrition caused severe acute ax onal polyneuropathy. Its distinction from Guillain-Barre syndrome is i mportant because treatment requires balanced diet, vitamin supplementa tion, and abstinence from alcohol, while immunotherapy may not be indi cated.