Abstract
Originally Amiodarone, a diiodated benzofuran derivative, was developed in the year 1960 to treat angina pectoris. Nowadays it is mainly used to maintain a sinus rhythm in patients with atrial fibrillation or ventricular tachycardia. While amiodarone-related optic neuropathy has become a well-recognized entity, its exact cause is still unclear. A possible explanation accuses the intracytoplasmatic lamellar and granular bodies, which develop in multiple parts of the eye as in the cornea [1], lens, retina, and the optic nerve. This process may lead to an optic disc edema and later to optic nerve atrophy [2][3]. The first amiodarone-associated side effects concerning the optic disc were described in 1987 by Feiner et al. as well as by Gittinger et al. [4][5]. Usually, the interval between initiation of orally administered amiodarone treatment and onset of visual loss is several months [6]. No critical dosage and no critical time interval have been defined so far.