Amiodarone neuropathy

Steven Herskovitz MD (Dr. Herskovitz of the Montefiore Medical Center has no relevant financial relationships to disclose.)
Louis H Weimer MD, editor. (Dr. Weimer of Columbia University has received consulting fees from Roche.)
Originally released September 21, 2001; last updated January 3, 2017; expires January 3, 2020

Overview

The author reviews the clinical neurotoxicity of the antiarrhythmic agent amiodarone, an amphiphilic drug that forms intralysosomal lipid complexes in multiple tissues. The most common amiodarone-related neurotoxicities are tremor, ataxia, and peripheral neuropathy; more infrequent neurotoxicities include myopathy, optic neuropathy, basal ganglia dysfunction, encephalopathy, and pseudotumor cerebri. The neuropathy is usually a subacute to chronic sensorimotor polyneuropathy with axonal, demyelinating, or mixed features.

Key points

 

• The most common amiodarone-related neurotoxicities are tremor, ataxia, and peripheral neuropathy; more infrequent neurotoxicities include myopathy, optic neuropathy, basal ganglia dysfunction, encephalopathy, and pseudotumor cerebri.

 

• The neuropathy is usually a subacute to chronic sensorimotor polyneuropathy with axonal, demyelinating, or mixed features.

 

• Amiodarone is an amphiphilic drug that forms intralysosomal lipid complexes in multiple tissues.

Historical note and terminology

Amiodarone is a di-iodinated benzofuran derivative initially developed in the 1960s as an antianginal agent; it was later used as a cardiac antiarrhythmic agent in the management of supraventricular and ventricular arrhythmias. It is approved in the United States for the treatment of refractory and life-threatening ventricular arrhythmias. Like bretylium and sotalol, it is a class III antiarrhythmic agent and shares the capacity to prolong the duration of action potentials and refractoriness in Purkinje fibers and ventricular muscle (Roden 1996). Neurotoxic side effects were first described in the 1970s and consist principally of a sensorimotor polyneuropathy, tremor, and ataxia and more infrequently, myopathy, optic neuropathy, basal ganglia dysfunction, encephalopathy, and pseudotumor cerebri. Dronedarone, a new drug approved in 2009 for atrial fibrillation, is structurally related to amiodarone, but noniodinated, and it may have a more favorable overall safety profile (Clem 2010).

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