Acute or subacute alcoholic neuropathy mimicking Guillain-Barré syndrome.
Over the last 10 years we have encountered 8 patients with chronic alcoholism who presented with severe symmetrical polyneuropathy, primarily proximal in 6, which evolved over a period of 24 h to 3 weeks. In 3 cases, artificial ventilation was required. Sensory symptoms were in all instances intense, and tendon reflexes absent. CSF protein levels were normal. The course was one of gradual improvement, often incomplete with residual motor and distal sensory deficits. Three patients died within 2 months to 2 years with multiple and severe pathologies attributable to chronic alcoholism. There was no evidence for disorders other than the alcoholism and malnutrition. Electrophysiological findings were consistent with predominantly axonal lesions and nerve biopsy specimens confirmed acute and severe axonal lesions. Several of these patients had been referred to us with a possible diagnosis of Guillain-Barré syndrome due to the severity of the neuropathy and the rapidity of its onset (Landry syndrome). Acute alcoholic neuropathy is distinguishable, however, on clinical, electrophysiological and morphological grounds.
Department of Neurology, University Hospital, Limoges, France.
F
F
Tabaraud
J M
JM
Vallat
J
J
Hugon
H
H
Ramiandrisoa
M
M
Dumas
J L
JL
Signoret
D000208:Acute Disease; D000328:Adult; D000437:Alcoholism / Q000150:complications*; D003937:Diagnosis, Differential; D004594:Electrophysiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000175:diagnosis* / Q000209:etiology; D011129:Polyradiculoneuropathy / Q000175:diagnosis*