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Show Journal of Neuro- Ophthalmology 20( 3): 171- 172, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Amiodarone Optic Neuropathy Without Disc Edema Matthew A. Speicher, MD, Michael H. Goldman, MD, FACC, and Georgia A. Chrousos, MD A 48- year- old man presented with bilateral blurred vision and visual field changes while prescribed amiodarone. Improvement of vision and visual field defects was documented within 3 weeks after discontinuation of the medication, and complete resolution occurred at 3 months. A unique feature of this amio-darone- associated optic neuropathy is the absence of any optic nerve edema. Key Words: Amiodarone- Ocular side effects- Optic neuropathy. Multiple reports have described patients with amio-darone- induced optic neuropathy ( 1- 10). Characteristically, patients develop an insidious blurring of vision, a mild to moderate decrease in visual acuity, or visual field loss that is frequently bilateral at onset ( 1). Vision may progressively worsen until discontinuation and systemic clearance of the medication, but it may improve thereafter ( 2- 7). To our knowledge, all previously reported cases, except one, have included optic disc swelling or atrophy. Feiner et al.( 3) described the case of a patient with peripheral neuropathic signs, ataxic pursuit movements, decreased visual acuity, and decreased visual evoked potentials, all of which improved after discontinuation of amiodarone administration. The findings from examination of the optic nerves were normal in this patient. We describe the case of a 48- year- old man who developed bilateral optic neuropathy without optic disc edema while prescribed amiodarone ( Pacerone; Upsher- Smith Laboratories, Inc., Minneapolis, MN). CASE REPORT A 48- year- old man was referred for a neuro-ophthalmic consultation because of a 2- week history of " hazy vision" bilaterally. He denied any other neurologic symptoms. His ocular history was remarkable only for myopia. His medical history was remarkable for atrial fibrillation for which he was prescribed amiodarone 400 Manuscript received February 28, 2000; accepted May 8, 2000. From the Georgetown University Center for Sight ( MAS, GAC), Washington, DC; and private cardiology practice ( MHG), Arlington, Virginia. Address correspondence and reprint requests to Georgia Chrousos, MD, Georgetown University Center for Sight 7PHC, 3800 Reservoir Road NW, Washington, DC 20007. mg and digoxin ( Lanoxin; Glaxo Wellcome, Inc., Research Triangle Park, NC) 0.125 mg daily. The findings from the examination showed best-corrected visual acuity of 20/ 20 bilaterally, normal color vision by Ishihara plates, and normal pupils. Results of slit- lamp biomicroscopy showed diffuse whorl- like mi-crodeposits in the epithelium of both corneas. The unremarkable results of fundus examination included normal optic nerves with sharp margins and a cup- disc ratio of 0.4 ( Fig. 1). Early bilateral visual field defects were shown with automated static perimetry ( Fig. 2, top). The patient was advised to discontinue amiodarone administration after discussion with his cardiologist and to return for repeated visual field testing in several weeks. Two months later, the patient returned, experiencing worsening of his vision; he stated that everything appeared to be " smoky." He had continued taking amiodarone, despite being advised otherwise by his cardiologist. Visual acuity was 20/ 20" OU with difficulty. Results of repeated visual field testing showed marked progression of the previous defects ( Fig. 2, bottom). Again, findings of thorough examination of the optic nerves showed no abnormalities. Amiodarone therapy was discontinued. Results of a blood work- up, including complete blood count, erythrocyte sedimentation rate, rapid plasma reagin, and detailed screening for a hyper-coagulable state, were within normal limits. Results of magnetic resonance imaging of the brain were also normal. At a follow- up visit approximately 3 weeks after discontinuation of amiodarone administration and initiation of propafenone ( Rythmol; Knoll Laboratories, Mount Olive, NJ) 200 mg three times daily, he reported that his vision seemed to be improving markedly over the past week and that he no longer experienced any visual difficulty. Visual acuity was now a clear 20/ 20 OU, and the visual fields were dramatically improved with only trace residual superior scotomata ( Fig. 3, top). He was seen 2 months later, at which time his visual acuity was 20/ 15- OD and 20/ 20+ OS. Results of visual field testing were normal ( Fig. 3, bottom), and his atrial fibrillation was well controlled with administration of propafenone and digoxin. DISCUSSION In 1987, Gittinger et al. ( 2) first reported two cases of optic neuropathy that were thought to be secondary to 171 ^ T 172 M. A. SPEICHER ET AL. & i i.. • i FIG. 2. Humphrey 30- 2 visual fields OS and OD performed during the initial visit ( top) and 2 months later while still being administered amiodarone ( bottom). ". I1-::-.'!:-.: . ' : • : : " . • • : : . " ••• Jam': FIG. 3. Humphrey 30- 2 visual fields OS and OD 3 weeks ( top) and 3 months ( bottom) after discontinuation of amiodarone administration. FIG. 1. Optic nerves OD and OS showing lack of edema or atrophy. administration of amiodarone. Both patients had bilateral optic nerve edema, although only one patient had decreased visual acuity and abnormal visual fields. Since then, multiple authors have described similar cases ( 3- 10). Papillary abnormalities were noted in all but one of these published cases ( 3). Our case is unusual in that the optic discs appeared to be normal at every examination with no apparent edema throughout the course of visual symptoms and no atrophy later. In addition, the patient was a young healthy individual without significant risk factors for anterior ischemic optic neuropathy. We were able to document the time course of his complete recovery with visual field testing. This allowed us to objectively confirm improvement within 3 weeks of discontinuation of amiodarone administration. This case emphasizes the significance of maintaining a high index of suspicion for patients with visual problems while administered amiodarone. Periodic formal visual field testing may be indicated for all patients on this medication because the incidence of optic neuropathy has been reported to be 1.79% for this population versus 0.3% in age- matched individuals not administered amiodarone ( 3). Early diagnosis and prompt discontinuation of the offending agent may offer the best chance for complete recovery. REFERENCES 1. Macaluso DC, Shults WT, Fraunfelder FT. Features of amio-darone- induced optic neuropathy. Am J Ophthalmol 1999; 127: 610- 2. 2. Gittinger JW, Asdourian GK. Papillopathy caused by amiodarone. Arch Ophthalmol 1987; 105: 349- 51. 3. Feiner LA, Younge BR, Kazmier FJ, et al. Optic neuropathy and amiodarone therapy. Mayo Clin Proc 1987; 62: 702- 17. 4. Nazarian SM, Jay WM. Bilateral optic neuropathy associated with amiodarone therapy. J Clin Neuroophthalmol 1988; 8: 25- 8, 5. Dewachter A, Lievens H. Amiodarone and optic neuropathy. Bull Soc Beige Ophthalmol 1988; 227: 47- 50. 6. Sreih AG, Schoenfeld MH, Marieb MA. Optic neuropathy following amiodarone therapy. Pacing Clin Electrophysiol 1999; 22: 1108- 10. 7. Ferreiro JL, Isern Longares J A, Ramon Moya AF. Optic neuropathy caused by amiodarone. Neurologia 1990; 5: 160- 3. 8. Seemongal- Dass RR, Spencer SR. Bilateral optic neuropathy linked with amiodarone. Eye 1998; 12: 474- 7. 9. Palimar P, Cota N. Bilateral anterior ischaemic optic neuropathy following amiodarone. Eye 1998; 12: 894- 6. 10. Belec L, Davila G, Bleibel JM, et al. Bilateral optic neuropathy during prolonged treatment with amiodarone. Ann Med Interne 1992; 143: 349- 50. J Neuro- Ophthalmol, Vol. 20, No. 3, 2000 |
