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Show J. Lee Villano, MD, PhD Department of Oncology, University of Illinois at Chicago, Chicago, Illinois Dr. Moss receives support from the National Institutes of Health (Grant number K12EY021475). The authors report no conflict of interest. REFERENCES 1. Traynis I, Singer S, Winterkorn K, Rosenblum M, Dinkin M. Infiltration of the optic chiasm, nerve and disc by gliomatosis cerebri. J Neuroophthalmol. 2013 Jan 2(epub ahead of print). 2. Saito R, Kumabe T, Jokura H, Shirane R, Yoshimoto T. Symptomatic spinal dissemination of malignant astrocytoma. J Neurooncol. 2003;61:227-235. 3. Boyle R, Thomas M, Adams JH. Diffuse involvement of the leptomeninges by tumour-a clinical and pathological study of 63 cases. Postgrad Med J. 1980;56:149-158. 4. Kondziolka D, Lunsford DL, Martinez AJ. Unreliability of contemporary neurodiagnostic imaging in evaluating suspected adult supratentorial (low-grade) astrocytoma. J Neurosurg. 1993;79:533-536. 5. Barker FG II, Chang SM, Huhn SL, Davis RL, Gutin PH, McDermott MW, Wilson CB, Prados MD. Age and the risk of anaplasia in magnetic resonance-nonenhancing supratentorial cerebral tumors. Cancer. 1997;80:936-941. 6. Scott JN, Brasher PMA, Sevick RJ, Rewcastle NB, Forsyth PA. How often are nonenhancing supratentorial gliomas malignant? A population study. Neurology. 2002;59:947-949. 7. Zonari P, Baraldi P, Crisi G. Multimodal MRI in the characterization of glial neoplasms: the combined role of single-voxel MR spectroscopy, diffusion imaging and echo-planar perfusion imaging. Neuroradiology. 2007;49:795-803. 8. Batra A, Tripathi RP, Singh AK. Perfusion magnetic resonance imaging and magnetic resonance spectroscopy of cerebral gliomas showing imperceptible contrast enhancement on conventional magnetic resonance imaging. Australas Radiol. 2004;48:324-332. 9. Chaskis C, Stadnik C, Michotte A, Van Rompaey K, D'Haens J. Prognostic value of perfusion-weighted imaging in brain glioma: a prospective study. Acta Neurochir (Wien). 2006;148:277-285. 10. Frazier JL, Johnson MW, Burger PC, Weingart JD, Quinones- Hinojosa A. Rapid malignant transformation of low-grade astrocytomas: report of 2 cases and review of the literature. World Neurosurg. 2010;73:53-62. Linezolid-Associated Optic Neuropathy in a Patient With Drug-Resistant Tuberculosis We enjoyed reading the review article by Wang and Sadun (1) dealing with drug-induced mitochon-drial optic neuropathies. Recently, we evaluated a patient taking linezolid, a synthetic antimicrobial agent effective against gram-positive bacteria, including vancomycin-resistant enterococci and methicillin-resistant staphylo-cocci as well as drug-resistant strains of Mycobacterium tuberculosis (2,3). This antibiotic has been linked to optic neuropathy (4-11). Our patient's presentation appears unusual in that it was not associated with prominent optic disc swelling. A 41-year-old woman was referred for evaluation of visual function. She had a history of pulmonary tuberculosis and had been treated with linezolid for 17 months. Initial visual acuity was 20/20, right eye and 20/20, left eye. No abnormalities were detected in the examination of the FIG. 1. (A) Twenty months after beginning linezolid, automated visual fields demonstrate subtle field loss in the right eye and reduced sensitivity in the left eye. (B) Two months after linezolid was discontinued, visual fields show improvement bilaterally. 316 Letters to the Editor: J Neuro-Ophthalmol 2013; 33: 307-318 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. anterior segment of each eye and the fundi. Visual fields were normal. Additional medications included cycloserine, prothionamide, and p-aminosalicylic calcium. Three months later, the patient complained of visual impairment and tingling in both legs. Visual acuity was 20/ 30, right eye and 20/40, left eye. Pupillary reactions were normal but color vision was reduced bilaterally. Results of visual field testing are shown in Figure 1A and funduscopy demonstrated mild temporal disc pallor in each eye (Fig. 2). Optical coherence tomography (OCT) revealed an increase in retinal nerve fiber layer (RNFL) thickness in the infero-temporal quadrant of each eye (Fig. 3A). Linezolid was stopped, and the patient continued on cycloserine, prothionamide, and p-aminosalicylic calcium. Two months later, visual acuity improved to 20/20 in both eyes with intact color vision. Visual fields returned to near normal (Fig. 1B) and the optic discs were unchanged. The inferotemporal RNFL was no longer thickened on OCT (Fig. 3B). Eight months later, visual function was stable, but the patient reported persistent tingling in both legs. Linezolid is part of the oxazolidinone class of antibiotics that inhibit bacterial protein synthesis by binding to the 70S ribosomal initiation complex (12). Although this complex is not present in mammalian cells, it has been shown to reduce mitochondrial respiratory chain enzyme activity in experi-mental animals and in a patient receiving linezolid therapy who developed optic neuropathy (13). Although the precise mechanism for linezolid-induced optic neuropathy is un-known, impairment of mitochondrial function within reti-nal ganglion cells is likely (9,14). An interesting OCT finding in our case was the increase of RNFL thickness in the temporal and inferior quadrants without visible optic disc swelling. A similar alteration of RNFL was described by Barboni et al (15) in Leber hereditary optic neuropathy (LHON). Since LHON is known to be associated with mitochondrial dysfunction, the similarity in RNFL changes in the 2 disorders further FIG. 3. Optical coherence tomography. A. Initially, there is swelling of the inferotemporal RNFL in both eyes. B. Two months after discontinuation of linezolid, swelling of the inferotemporal RNFL has resolved. FIG. 2. There is temporal pallor of both optic discs. Letters to the Editor: J Neuro-Ophthalmol 2013; 33: 307-318 317 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. links linezolid-induced optic neuropathy to a disturbance in mitochondrial energy production (16). The occurrence of linezolid optic neuropathy may be associated with the duration of therapy. Although recom-mended treatment is for 28 days, linezolid often is given for longer periods of time in patients with high risk or resistant bacterial infections (7-11,14). Such was the case in our patient. However, there are exceptions. Joshi et al (17) de-scribed optic neuropathy occurring 16 days after beginning linezolid in a patient with acute lymphocytic leukemia. Jinu Han, MD Kyungsik Lee, MD Soolienah Rhiu, MD Jong Bok Lee, MD Sueng Han Han, MD, PhD Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea The authors report no conflicts of interest. REFERENCES 1. Wang MY, Sadun AA. Drug-related mitochondrial optic neuropathies. J Neuroophthalmol. 2013;33:172-178. 2. Dietze R, Hadad DJ, McGee B, Molino LP, Maciel EL, Peloquin CA, Johnson DF, Debanne SM, Eiseranch K, Boom WH, Palaci M, Johnson JL. Early and extended early bactericidal activity of linezolid in pulmonary tuberculosis. Am J Respir Crit Care Med. 2008;178:1180-1185. 3. Cynamon MH, Klemens SP, Sharpe CA, Chase S. Activities of several novel oxazolidinones against Mycobacterium tuberculosis in a murine model. Antimicrob Agents Chemother. 1999;43:1189-1191. 4. Narita M, Tsuji BT, Yu VL. Linezolid-associated peripheral and optic neuropathy, lactic acidosis, and serotonin syndrome. Pharmacotherapy. 2007;27:1189-1197. 5. Nambiar S, Rellosa N, Wassel RT, Borders-Hemphill V, Bradley JS. Linezolid-associated peripheral and optic neuropathy in children. Pediatrics. 2011;127:1528-1532. 6. Lloyd MJ, Fraunfelder FW. Drug-induced optic neuropathies. Drugs Today (Barc). 2007;43:827-836. 7. Rucker JC, Hamilton SR, Bardenstein D, Isada CM, Lee MS. Linezolid-associated toxic optic neuropathy. Neurology. 2006;66:595-598. 8. Saijo T, Hayashi K, Yamada H, Wakakura M. Linezolid-induced optic neuropathy. Am J Ophthalmol. 2005;139:1114-1116. 9. McKinley SH, Foroozan R. Optic neuropathy associated with linezolid treatment. J Neuroophthalmol. 2005;25:18-21. 10. Frippiat F, Bergiers C, Michel C, Dujardin JP, Derue G. Severe bilateral optic neuritis associated with prolonged linezolid therapy. J Antimicrob Chemother. 2004;53:1114-1115. 11. Lee E, Burger S, Shah J, Melton C, Mullen M, Warren F, Press R. Linezolid-associated toxic optic neuropathy: a report of 2 cases. Clin Infect Dis. 2003;37:1389-1391. 12. Shinabarger DL, Marotti KR, Murray RW, Lin AH, Melchior EP, Swaney SM, Dunyak DS, Demyan WF, Buysee JM. Mechanism of action of oxazolidinones: effects of linezolid and eperezolid on translation reactions. Antimicrob Agents Chemother. 1997;41:2132-2136. 13. De Vriese AS, Coster RV, Smet J, Seneca S, Lovering A, Van Haute LL, Vanopdenbosch LJ, Martin JJ, Groote CC, Vandecasteele S, Boelaert JR. Linezolid-induced inhibition of mitochondrial protein synthesis. Clin Infect Dis. 2006;42:1111-1117. 14. Javaheri M, Khurana RN, O'Hearn TM, Lai MM, Sadun AA. Linezolid-induced optic neuropathy: a mitochondrial disorder? Br J Ophthalmol. 2007;91:111-115. 15. Barboni P, Carbonelli M, Savini G, Ramos cdo V, Carta A, Berezovsky A, Salomao SR, Carelli V, Sadun AA. Natural history of Leber's hereditary optic neuropathy: longitudinal analysis of the retinal nerve fiber layer by optical coherence tomography. Ophthalmology. 2010;117:623-627. 16. Sadun AA, Win PH, Ross-Cisneros F, Walker SO, Carelli V. Leber's hereditary optic neuropathy differentially affects smaller axons in the optic nerve. Trans Am Ophthalmol. 2000;98:223-232. 17. Joshi L, Taylor SR, Large O, Yacoub S, Lightman S. A case of optic neuropathy after short-term linezolid use in a patient with acute lymphocytic leukemia. Clin Infect Dis. 2009;48:73-74. 318 Letters to the Editor: J Neuro-Ophthalmol 2013; 33: 307-318 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
