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Organic arsenic‐induced Guillain‐Barré‐like syndrome due to melarsoprol: A clinical, electrophysiological, and pathological study
Author(s) -
Gherardi Romain K.,
Chariot Patrick,
Vanderstigel Muriel,
Malapert Denis,
Verroust Josette,
Astier Alain,
BrunBuisson Christian,
Schaeffer Annette
Publication year - 1990
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880130713
Subject(s) - guillain barre syndrome , medicine , spinal cord , arsenic poisoning , pathology , wallerian degeneration , pathological , anterior horn cell , axonal degeneration , weakness , somatosensory evoked potential , anesthesia , arsenic , anatomy , immunology , amyotrophic lateral sclerosis , chemistry , disease , organic chemistry , psychiatry
A young woman suffering from sleeping sickness was treated with melarsoprol. Thirty‐eight days after the first administration of this organo‐arsenic compound, myalgias, distal paresthesias and rapidly progressive weakness developed in all four limbs. Electrophysiological studies were misleading for Guillain‐Barré syndrome. Neuropathological data included massive distal wallerian degeneration in peripheral nerves and abnormalities in dorsal ganglia and spinal cord where vacuolation of anterior horn cells and axonal neurofilamentous masses were observed. Very high concentrations of arsenic were found in the spinal cord, contrasting with undetectable levels in peripheral nerves. Our findings are consistent with an arsenic neuronopathy manifested by initial proximal demyelination and delayed distal axonal damage. Renal and hepatic dysfunctions, which were implicated in the toxic arsenic accumulation, should be systematically detected before administration of melarsoprol. The diagnosis of Guillain‐Barré syndrome must be considered with caution in patients treated with this compound.