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DISOPYRAMIDE‐INDUCED NEUROPATHY
Author(s) -
Briani C.,
Zara G.,
Ruggero S.,
Negrin P.
Publication year - 2002
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2002.7011_5.x
Subject(s) - disopyramide , medicine
Neuropathies are well‐known complications of therapy with amiodarone, but other antiarrhythmic drugs are rarely associated with neurological side effects. We report a patient who developed a severe sensory‐motor neuropathy after treatment with disopyramide. A 71 year‐old woman, who had been treated with disopyramide 500 mg/day for 4 years for cardiac arrythmias, presented with fatigue, paresthesias, and pain in her lower limbs. Morning stiffness and arthralgias were also present. On neurological examination, her gait was unsteady, and weakness was present in the 4 limbs; tendon reflexes were reduced in the upper limbs and lost in the lower limbs. C‐reactive protein was increased. Electrodiagnostic studies revealed a sensory‐motor polyneuropathy, with reduced motor conduction velocity (MCV) in peroneal nerves (38 m/sec) with normal compound muscle action potential (CMAP) amplitude. There was some evidence of muscle denervation, with fibrillation at rest and reduced patterns on maximal contraction; no sensitive potential was recorded from sural nerves. Antibodies to peripheral nerve antigens (gangliosides, sulfatides, MAG, glycosaminoglycans) resulted negative. A diagnosis of polymyalgia rheumatica was made and steroid started with a prompt recovery of arthralgias and stiffness. Weakness and dysesthesias in the legs, however, worsened and an electrophysiological study, three months later, evidenced a more severe peripheral neuropathy, with a slower MCV (31 m/sec) and signs of denervation. After excluding other known causes of neuropathy, disopyramide was withdrawn. Four months later, the patient showed a significant improvement of the symptoms and of electrophysiological studies, with peroneal nerve MCVs of 40 m/sec and reappearance of the excitability of the sural nerves (43 m/sec). This is, to our knowledge, the second case of a disopyramide‐induced polyneuropathy so far reported. Although uncommon, it should be considered when polyneuropathy occurs and no other causes are found. If possible, the discontinuation of the therapy might help in clarifying the diagnosis and curing the neuropathy.