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Show visual acuity was 20/20 in each eye, and repeat Humphrey visual field was stable. Her right optic disc was diffusely pale with minimal residual edema. Given the paucity of cases, the potential role of TNF-a antagonists in the treatment of GCA is unclear. Interestingly, vasculitis has been reported to occur with use of TNF antag-onists, mainly in the form of leukocytoclastic vasculitis (10-12). One postulated mechanism for the development of vasculitis during the use of anti-TNF agents is direct drug toxicity to the vasculature. Other mechanisms include deposi-tion of anti-TNF/TNF immune complexes in the vessel wall with induction of a type III hypersensitivity reaction, reaction of autoantibodies with endothelial cells, paradoxical increased vulnerability to granulomatous vasculitis due to TNF defi-ciency, and a TNF antagonist-induced switch from a Th1 to a Th2 T-lymphocyte response (11). Whether any of these proposed mechanisms of vascular destruction underlie the development of GCA during use of TNF-a antagonists is un-known. While on long-term treatment with etanercept except for a 3-week drug holiday, our patient developed symptoms that, in retrospect, were most likely due to GCA. Although we cannot exclude the gap in therapy as a precipitating event of the patient's ischemic optic neuropathy, we believe this most likely was due to natural evolution of her disease process. Katharine Liegel, MD Steven Feldon, MD, MBA Zoë Williams, MD Department of Ophthalmology, Flaum Eye Institute, University of Rochester Medical Center, Rochester, New York Supported, in part, by an unrestricted grant from Research to Prevent Blindness. The authors report no conflicts of interest. ACKNOWLEDGMENTS The authors thank Haodong Xu, MD, of the Department of Pathology, University of Rochester Medical Center. REFERENCES 1. Weyand C, Liao YJ, Goronzy J. The immunopathology of giant cell arteritis: diagnostic and therapeutic implications. J Neuroophthalmol. 2012;32:259-265. 2. Tan A, Holdsworth J, Pease C, Emery P, McGonagle D. Successful treatment of resistant giant cell arteritis with etanercept. Ann Rheum Dis. 2003;62:373-374. 3. Uthman I, Kanj N, Atweh S. Infliximab as monotherapy in giant cell arteritis. Clin Rheumatol. 2006;25:109-110. 4. Airó P, Antonioli CM, Vianelli M, Toniati P. Anti-tumour necrosis factor treatment with infliximab in a case of giant cell arteritis resistant to steroid and immunosuppressive drugs. Rheumatology (Oxford). 2002;41:347-349. 5. Martínez-Toboada VM, Rodríguez-Valverde V, Carreño L, López- Longo J, Figueroa M, Belzunegui J, Mola EM, Bonilla G. A double-blind placebo controlled trial of etanercept in patients with giant cell arteritis and corticosteroid side effects. Ann Rheum Dis. 2008;67:625-630. 6. Cantini F, Niccoli L, Salvarani C, Padula A, Olivieri I. Treatment of longstanding active giant cell arteritis with infliximab: report of four cases. Arthritis Rheum. 2001;44:2933-2935. 7. Andonopoulos AP, Meimaris N, Daoussis D, Bounas A, Giannopoulos G. Experience with infliximab (anti-TNFa monoclonal antibody) as monotherapy for giant cell arteritis. Ann Rheum Dis. 2003;62:1116. 8. Leydet-Quilici H, Luc M, Armingeat T, Pham T, Lafforgue P. Giant cell arteritis during adalimumab treatment for rheumatoid arthritis. Joint Bone Spine. 2007;74:303-304. 9. Seton M. Giant cell arteritis in a patient taking etanercept and methotrexate. J Rheumatol. 2004;31:1467. 10. Mohan N, Edwards ET, Cupps TR, Slifman N, Lee JH, Siegel JN, Bruan MM. Leukocytoclastic vasculitis associated with tumour necrosis factor-a blocking agents. J Rheumatol. 2004;31:1955-1958. 11. Jarrett S, Cunnane G, Conaghan PG, Bingham SJ, Buch MH, Quinn MA, Emery P. Anti-tumour necrosis factor-a therapy-induced vasculitis: case series. J Rheumatol. 2003;30:2287-2291. 12. Cunnane G, Warnock M, Eye KH, Daikh DI. Accelerated nodulosis and vasculitis following etanercept therapy for rheumatoid arthritis. Arthritis Rheum. 2002;47:445-449. Radiation Optic Neuropathy After Proton Beam Therapy for Optic Nerve Sheath Meningioma I enjoyed reading the recent article regarding radia-tion optic neuropathy after proton beam therapy for optic nerve sheath meningioma by Siddiqui et al (1). The authors state "magnetic resonance imaging revealed enhancement of the right optic nerve consistent with radiation optic neuropathy." It is my experience that the optic nerve enhancement, as pictured in Figure 3B, also can result from a multitude of etiologies including extension of optic nerve sheath meningioma (2). Often it is difficult to differentiate the 2 on the fat-suppressed gadolinium-enhanced orbital magnetic resonance imaging. So, how do we know that the optic nerve enhancement was indeed from the radiation and not from progression of the optic nerve sheath meningioma? Michael Vaphiades, DO Departments of Ophthalmology, Neurology, and Neurosurgery, Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 95-104 101 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. University of Alabama at Birmingham, Birmingham, Alabama Supported in part by an unrestricted grant from the Research to Prevent Blindness, Inc, New York, NY. The author report no conflicts of interest. REFERENCES 1. Siddiqui JD, Loeffler JS, Murphy MA. Radiation optic neuropathy after proton beam therapy for optic nerve sheath meningioma. J Neuroophthalmol 2013;33: 165-168. 2. Vaphiades MS. Disk edema and cranial MRI optic nerve enhancement: how long is too long? Surv Ophthalmol. 2001;46:56-58. Response We thank Dr. Vaphiades for his interest in our article and agree that the etiology of optic nerve enhance-ment may be difficult to distinguish based on magnetic resonance imaging (MRI) findings alone. With an optic nerve sheath meningioma (ONSM), the tumor typically shows gadolinium enhancement rather than the nerve itself, giving rise to the typical tram-track sign, while with radi-ation optic neuropathy (RON), the optic nerve itself enhances and may therefore be indistinguishable from the enhancement of the surrounding ONSM. In our patient, we noted several features that supported the diagnosis of RON. Radiographically, the area of new optic nerve enhancement corresponded to the exact location of the highest proton beam radiation dose. Although the optic nerve showed normal short T1 inversion recovery signal at the time of the initial ONSM diagnosis, it showed increased signal with proximal enhancement at the time the patient presented with visual loss, which began 27 months after completion of radiation therapy. Diffuse enhancement of the nerve was noted such that it could not be separated from the surrounding sheath, as opposed to clear tram-track enhance-ment of the remaining distal nerve. Clinically, it would be unusual for an ONSM to grow rapidly, causing progressive visual loss over a period of days to weeks, and then remain stable for the next year, as in our patient. The onset of symptoms in our patient likewise fell within the typical time course for RON. We hope that these details help to further clarify the diagnosis of RON in our patient. The above findings were included in our original submission but were then omitted through the editing process. Jamal D. Siddiqui, MD Department of Ophthalmology, Rhode Island Hospital, Providence, RI Jay S. Loeffler, MD Department of Radiation Oncology, Massachusetts General Hospital, Boston, MA Marjorie A. Murphy, MD Department of Ophthalmology, Providence Veterans Affairs Medical Center, Providence, RI Recurrent Third Nerve Palsy as the Presenting Feature of Neurofibromatosis 2 We read with interest the case report (1) describing recurrent third nerve palsy as the presenting feature of neurofibromatosis type 2 (NF2). We evaluated a child with similar clinical findings. Our patient, whose mother has NF2, presented at age 5 years with painless, right-sided ptosis, and upgaze palsy, with normal pupils that evolved over several days. There was no history of preceding illness or trauma. The remainder of the general and neurological examinations was normal. Hema-tological and biochemical screening as well as inflammatory markers were negative. Magnetic resonance imaging (MRI) of the brain with contrast was normal. The child remained otherwise well and his findings completely resolved over 6 weeks. Over the next 3 years, he had 3 identical spontaneous episodes all involving the same eye, with good but incomplete recovery, in that mild ptosis (1-2 mm) and diplopia on upgaze persisted. Repeat contrast-enhanced brain MRI with each episode was normal, as were blood studies including acetylcholine receptor antibodies for myasthenia gravis. 102 Letters to the Editor: J Neuro-Ophthalmol 2014; 34: 95-104 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
