OCR Text |
Show William Fletcher Hoyt William Fletcher Hoyt, MD, received his medical education at the University of Cal-ifornia, San Francisco (UCSF), followed by a year's study at the Wilmer Institute at The Johns Hopkins University, under the mentorship of Frank B. Walsh, MD. Dr. Hoyt returned to UCSF in 1958 to found the neuro-ophthalmology service. During a 36-year academic career-all of it at UCSF-he authored 266 journal articles, co-authored (with Frank B. Walsh, MD) the third edition of Clinical Neuro-Ophthalmology, and trained 71 neuro-ophthalmology fellows. In 1983, he received the title of Honorary Doctor of Medicine from the Karolinska Institute. At present, he serves as Professor Emeritus of Ophthalmology, Neurology, and Neurosurgery at UCSF. In recognition of his con-tributions, in 2001 the North American Neuro-Ophthalmology Society, in conjunction with the American Academy of Ophthalmology, initiated the Hoyt Lecture to be delivered each year at the Annual Meeting of the American Academy of Ophthalmology. Interventional Neuro-Ophthalmology: Not an Oxymoron Steven A. Newman, MD Journal of Neuro-Ophthalmology 2012;32:177-184 doi: 10.1097/WNO.0b013e318256638e © 2012 by North American Neuro-Ophthalmology Society Iam deeply honored to present the Tenth Annual Hoyt Lecture. No one has had more influence on modern neuro-ophthalmology than William Hoyt, MD. The list of students, residents, and fellows who he directly mentored, or who were indirectly touched by his trainees, is too long to enumerate. In particular, Bill's contributions, including the clinical vignettes in the third edition of Clinical Neuro- Ophthalmology, his meticulous approach to patients, and his ability to adapt to new technology, have served as a model and inspiration for all of us. In ophthalmology, as in other areas of medicine, some people fix things, and others teach those individuals what to fix. Neuro-ophthalmology has as its primary goal the diagnosis of visual system pathology. As such, this "cognitive" branch of ophthalmology has largely been separated from therapeutics. Cogan (1) stated that "Neuro-ophthalmology shares with neu-rology in general, limited therapeutic successes. Its strength is largely diagnostic, rather than therapeutic." Yet, this has changed dramatically with advances in neuroimaging and neu-rotherapeutics. As neuro-ophthalmologists, we are going to be asked increasingly, if not to play a primary interventional role, then to be involved in making decisions about when and how intervention takes place. In the last 3 to 4 decades, there has been a paradigm shift to quantification of the 3 diagnostic pillars of our specialty: anatomy, physiology, and psychophysics. The study of clinical neuroanatomy has been revolutionized with the introduction of neuroimaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI). Optical coherence tomography (OCT) is a revolutionary technology for examining various parts of the eye including the nerve fiber layer and optic disc. Physiology can now be quantitated through a variety of electrophysiologic tests, including electroretinography (ERG) and visual evoked potentials (VEP). In recent years, these technologies have been improved to the point that we can now examine specific areas of the retina or the visual field with the advent of multifocal ERG and VEP. Other examples of quantifying physiologic function are the use of neutral density filters in the assessment of a relative afferent pupillary defect (2), and the quantification of relative movement of the 2 eyes as described by Hess (3), 1 of the 3 ophthalmologists to win the Nobel Prize. Finally, the development of automated perimetry has allowed standardization and greater reproduc-ibility of visual field testing. In addition, new psychophys-ical techniques have been devised to study the visual field in a more rapid and specific fashion, including frequency dou-bling technique and short wavelength automated perimetry. The combination of the neuro-ophthalmologist becom-ing more involved in therapeutics, and the advent of more Department of Ophthalmology, University of Virginia, Charlottes-ville, Virginia. The author declares no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the full text and PDF versions of this article on the journal's Web site (www.jneuro-ophthalmology.com). Address correspondence to Steven A. Newman, MD, Department of Ophthalmology, University of Virginia, Charlottesville, VA 22908; E-mail: san7a@virginia.edu Newman: J Neuro-Ophthalmol 2012; 32: 177-184 177 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. FIG. 1. Thyroid eye disease. Eye movements show a right hypotropia in primary position increasing with gaze up and to the right. FIG. 2. Thyroid eye disease. After left inferior oblique surgery, neither eye goes up to the right well, associated with marked decrease in double vision. FIG. 3. Thyroid eye disease. Binocular visual fields demonstrate an expanded area of binocular single vision (BSV) after inferior oblique surgery. A. Before surgery, B. After surgery. 178 Newman: J Neuro-Ophthalmol 2012; 32: 177-184 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. accurate and reproducible techniques to quantify our clinical findings, form the basis of my lecture. I will approach this in 4 major categories: (1) what the neuro-ophthalmologist can treat; (2) how the neuro-ophthalmologist can assist in diagnosis; (3) how the neuro-ophthalmologist can assist with treatment; (4) how the neuro-ophthalmologist can provide advice for a variety of treatment decisions. In the tradition of Walsh & Hoyt's Clinical Neuro-Ophthalmology, 3rd edition, I will illustrate my presentation with a series of clinical case studies. WHAT THE NEURO-OPHTHALMOLOGIST CAN TREAT Eye muscle surgery often plays a critical role in rehabilita-tion of many of our patients who present with strabismus of restrictive or paretic cause. The goal of any strabismus surgery is not only to give the patient single binocular vision in primary position and down reading gaze but also to maximize the area of binocularity (4,5). At times, it may be impossible to improve the overall excursion of an eye with limited eye movements. This may necessitate surgery on the contralateral eye, limiting its range, but allowing the patient to achieve maximum binocularity (6). A 69-year-old man was evaluated for a 3-month history of vertical diplopia. He was found to have 2 mm of right proptosis and marked limitation of elevation of the right eye (Fig. 1). His only area of single binocular vision was in FIG. 4. Fibrous dysplasia associated with fibrosis in the left superior rectus. Eye movements demonstrate impairment of depression of the left eye. FIG. 5. Fibrous dysplasia. Hess screen measurements before (A) and after (B) eye muscle surgery (right inferior rectus recession with posterior fixation suture) show reduction of left hypertropia in downgaze. FIG. 6. Papilledema. Automated visual fields disclose bilateral arcuate visual field loss, greater in the right eye. Newman: J Neuro-Ophthalmol 2012; 32: 177-184 179 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. extreme downgaze. Orbital CT demonstrated enlargement of the inferior rectus muscles, compatible with thyroid eye disease. Recession of the right inferior rectus muscle might have provided single vision in primary gaze, but probably would have led to diplopia in downgaze. Instead, inferior oblique surgery on the left eye was performed (Fig. 2), which dramatically improved the patient's area of single binocular vision (Fig. 3). A 36-year-old woman was referred for evaluation of double vision. She was known to have fibrous dysplasia of the left orbital roof. Previous cranial reconstructive surgery had left her with restriction of the left superior rectus muscle, making it difficult for her to look down (Fig. 4). Because I realized that it would not be possible to make her left eye move better, I performed a right inferior rectus recession with posterior fixation suture (Faden procedure). This, combined with a left superior rectus recession, reduced her diplopia while reading and achieved single bin-ocular vision in primary gaze as well (Fig. 5). Although many of us spend little time in the operating room, there are some procedures that traditionally have fallen within the purview of neuro-ophthalmology. One such example is optic nerve sheath fenestration. A 34-year-old woman reported that things "look dark." Her visual acuity was 20/30 in the right eye and 20/50 in the left eye, with bilateral papilledema. She was found to have a tuberculum sellae meningioma, but 10 days after neurosurgical resection, her papilledema persisted and her visual fields became more con-stricted (Fig. 6). She underwent right optic nerve sheath fen-estration, and within 1 week, she noted improvement in her visual function. At 2-year follow-up, her bilateral optic disc edema had resolved, and while she was left with optic atrophy and arcuate nerve fiber bundle defects in her visual fields, central acuity was preserved at 20/25 in each eye (Fig. 7). The mechanism of action and indications for optic nerve sheath fenestration remain unclear. Noncontrolled studies suggest that it can protect the optic nerve from progressive damage related to intracranial hypertension (7,8). Although generally accepted as a treatment for chronic papilledema secondary to idiopathic intracranial hypertension, there are no controlled, prospective studies evaluating appropriate surgical indication and timing, and progressive visual loss may occur even after optic nerve sheath fenestration surgery (9-11). HOW THE NEURO-OPHTHALMOLOGIST CAN ASSIST IN DIAGNOSES Although the advent of high-resolution neuroimaging techniques has improved anatomic localization of a disease process, these studies are not specific and obtaining tissue for pathologic examination is often required. A 57-year-old man presented with a 3-week history of periocular pain and horizontal diplopia. He was found to have limited abduc-tion of the right eye, which was presumed due to a right sixth nerve palsy. Quantitative measurement of intraocular pressure in abduction revealed a 10 mm Hg rise suggestive of medial rectus restriction and an orbital CT confirmed a mass involving the right medial rectus muscle. Fine needle aspiration biopsy (FNAB) of the mass was diagnostic of FIG. 7. Papilledema. Two years after right optic nerve sheath fenestration, there is improvement in both visual fields. FIG. 8. Carcinoid tumor. A. Fine needle aspirate reveals clusters of large malignant cells with nuclear molding and scant cytoplasm (·400). B. Immunochemistry for serotonin shows strong expression (·400). 180 Newman: J Neuro-Ophthalmol 2012; 32: 177-184 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. metastatic carcinoid tumor (Fig. 8). The patient was treated with endocrine suppression and radiation therapy. Modifications of the FNAB technique introduced by Kennerdell et al (12-14) permit biopsy of skull base lesions. A 68-year-old woman was referred with a 6-week history of diplopia and was found to have a right sixth nerve palsy. Her MRI demonstrated a suspicious area in the region of the right cavernous sinus (Fig. 9). To reach this area of the skull base, I adapted the technique used in neurosurgery for percutaneous trigeminal rhizotomy. Using the Stealth neu-ronavigation system to access the posterior cavernous sinus through the foramen ovale (Fig. 10), cellular elements were obtained, revealing B cells, which stained for CD10 and CD19. The patient was spared a craniotomy, and her lymphoma was treated with radiation therapy. HOW THE NEURO-OPHTHALMOLOGIST CAN ASSIST WITH TREATMENT The past 30 years have seen a revolution in the endovas-cular approach (transarterial, transvenous) to a variety of intracranial lesions, including aneurysms, arteriovenous malformations, and carotid-cavernous sinus fistulae (15). The neuro-ophthalmologist can play a critical role in pro-viding neurovascular access. A 61-year-old woman reported the acute onset of blurred vision in each eye, and an eye examination was unremarkable. While her symptoms resolved, 1 month later, she complained of double vision. A CT and MRI of the brain were reported as normal. The following month, she noted pulsatile tinnitus and over the next 3 months, her diplopia worsened, and she developed bilateral conjunctival injection and chemosis. The patient was started on systemic antibiotics, but when her vision deterio-rated, she was referred for neuro-ophthalmic evaluation. At the time of examination, her visual acuity was 20/25 in the right eye and 20/400 in the left eye. There was a 1.2 log unit left relative afferent pupillary defect, with bilateral abduction deficits, 2 mm of left proptosis with marked chemosis of the left eye. Visual fields showed a pattern of nerve fiber layer field loss greater in the left eye. The right fundus was normal, whereas the left showed prominent retinal veins. Cerebral angiography confirmed a left carotid-cavernous sinus fistula, with cortical venous hypertension (Fig. 11A). A transvenous approach through the inferior petrosal sinus to embolize the fistula was unsuccessful. I was able to assist in accessing the fistula through the right superior ophthal-mic vein (Fig. 12) (18). The neuroradiology team was able to use detachable coils to embolize the fistula (Fig. 11B), FIG. 9. Lymphoma. A. Contrasted T1 coronal MRI shows an enhancing mass (arrows) in the right cavernous sinus. B. Coronal T1 scan shows loss of fat signal on the right at the skull base. FIG. 10. Lymphoma. Using a Stealth neuronavigation sys-tem, a 20-gauge needle on a 20-mL syringe with a pistol-grip fine needle aspiration biopsy handle is placed directly through the right foramen ovale into the cavernous sinus. Inset: axial and coronal computed tomography images show location of biopsy needle. Newman: J Neuro-Ophthalmol 2012; 32: 177-184 181 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. with resolution of chemosis, diplopia, and improvement in visual acuity. In this case, a transverse approach through the superior ophthalmic vein was successful (19). At times, such access is not available, requiring embolization through the superior orbital fissure via a direct percutaneous orbital puncture (15-17,19-21). Complications may arise in treat-ing carotid-cavernous sinus fistula, many with ophthalmic manifestations (22,23). The neuro-ophthalmologist must remain involved in delivering care to the patients. HOW THE NEURO-OPHTHALMOLOGISTS CAN PROVIDE ADVICE FOR A VARIETY OF TREATMENT DECISIONS Following the observation of Smith (24) , and confirmed by others (25-28), not only can radiation therapy slow pro-gression, but it may also actually improve visual function, in patients with optic nerve sheath meningioma. A 39-year-old woman presented with a 3-year history of decreased vision at 2/200 in the right eye, while vision in the left eye remained at 20/20. She had a 2.1 log unit right afferent papillary defect. MRI confirmed the presence of a right optic nerve sheath meningioma (Fig. 13), and the patient who was treated with 50 Gy of fractionated external beam radiation within 3 months had right visual acuity improved to 20/200, she was able to "see colors." Two years later, her visual acuity in the right eye further improved to 20/40. In a commensurate fashion, the patient's right relative afferent defect improved from 2.1 to 0.9 log units (3 months after radiotherapy) and to 0.3 log units (2 years after radiother-apy), as did her visual fields (Fig. 14). OCT demonstrated moderate bilateral retinal nerve fiber layer thinning (right eye: 75.22 mm; left eye: 82.92 mm). Savino (29) pointed out in the Seventh Annual Hoyt Lecture that OCT might help predict which patients may be expected to experience improved visual acuity following treatment. As our patient demonstrated, thinning of the nerve fiber layer does not preclude improvement in central acuity and visual fields (30,31). In linking the neuro-ophthalmologists' increasing role in treatment with improved methods of quantifying our clinical findings, it will be essential that we obtain class 1 evidence with prospective, randomized double-blind clinical trials. To date, we have completed the Optic Neuritis Treat-ment Trial (ONTT) (32) and the Ischemic Optic Neurop-athy Decompression Trial (IONDT) (33). Both studies provided useful information concerning therapy, but per-haps more importantly, they have delineated the natural history of these 2 optic nerve disorders. The ONTT proved that while intravenous corticosteroids might hasten visual recovery early in the clinical course, over a 15-year follow-up period, there was no difference in recovery of visual function between treated and untreated patients. In fact, oral corticosteroids predispose patients to recurrent attacks of optic neuritis. The ONTT also taught us a great deal about the likelihood of a patient developing multiple scle-rosis after an episode of optic neuritis and demonstrated that MRI of the brain is a powerful predictor of the chances of developing demyelinating disease. The IONDT proved that optic nerve sheath fenestration was not only efficacious FIG. 11. Carotid-cavernous sinus fistula. A. Lateral subtracted view of cerebral angiogram demonstrates carotid-cavernous sinus fistula with dilation of the left superior ophthalmic vein. B. Closure of the fistula following coil embolization. FIG. 12. Carotid-cavernous sinus fistula. An 18-gauge angiocatheter is placed in the superior ophthalmic vein (arrow) allowing access to the cavernous sinus. Platinum coils can be placed directly into the carotid-cavernous sinus fistula. 182 Newman: J Neuro-Ophthalmol 2012; 32: 177-184 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. in the treatment of ischemic optic neuropathy but also found that approximately 40% of patients (with visual acu-ity ,20/60) can experience spontaneous improvement. A third prospective study, the Idiopathic Intracranial Hypertension Treatment Trial is currently underway. Hopefully, it will provide us with a better understanding of the natural history of idiopathic intracranial hypertension and the efficacy of medical therapy. I see the neuro-ophthalmologists role evolving, not only in our ability to establish the correct diagnosis but also in becoming more involved in the treatment of our patients. But every treatment has a risk-benefit ratio or as I teach my residents: "There is no operation that can't make a patient worse." We must always be mindful of the guiding principle in medicine: first do no harm. In conclusion, it is essential that data regarding anatomy, physiology, and psychophysics be obtained in a standardized and quantifiable manner. It is these data that allow us to determine whether our patient's condition is changing and enables us to make better decisions regarding therapy. As neuro-ophthalmologists, we now stand ready to be more involved in patient evaluation, guiding interven-tion, and being there to assist when intervention is necessary. For the full Hoyt Lecture and accompanying figures, please consult Supplemental Digital Content at the fol-lowing links: • Hoyt Lecture Report, http://links.lww.com/WNO/A39. • Figures 1-10, http://links.lww.com/WNO/A40. • Figures 11-20, http://links.lww.com/WNO/A41. • Figures 21-30, http://links.lww.com/WNO/A42. • Figures 31-40, http://links.lww.com/WNO/A43. • Figures 41-49, http://links.lww.com/WNO/A44. FIG. 13. Optic nerve sheath meningioma. Contrast-en-hanced axial T1 magnetic resonance imaging shows a right optic nerve sheath meningioma. FIG. 14. Optic nerve sheath meningioma. Sequential automated visual fields done before treatment (A) with improvement 3 months (B) and 4 years (C) after radiation therapy. Newman: J Neuro-Ophthalmol 2012; 32: 177-184 183 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. REFERENCES 1. Hughes SS. David Glendenning Cogan, MD. Ophthalmology Oral History Series. Berkeley, CA: Foundation of the American Academy of Ophthalmology, 1990:158. 2. Thompson HS. The vitality of the pupil: a history of the clinical use of the pupil as an indicator of visual potential. J Neuroophthalmol. 2003;23:213-224. 3. Hess WR. Eine neve untersuchungsmethode bei doppelbildern. Arch Augenheilk. 1909;62:233-238. 4. Dyer JA. Lesions of the orbit affecting motility. Int Ophthalmol Clin. 1971;11:202-207. 5. Buckley EG. Paralytic strabismus. In: Plager DA, ed. Strabismus Surgery. Basic and Advanced Strategies. New York, NY: Oxford University Press, 2004:83-116. 6. Newman SA. Inferior oblique surgery for restrictive strabismus in patients with thyroid orbitopathy. Trans Am Ophthalmol Soc. 2009;107:72-90. 7. Chandrasekaran S, McCluskey P, Minassian D, Assaad N. Visual outcomes for optic nerve sheath fenestration in pseudotumor cerebri and related conditions. Clin Experiment Ophthalmol. 2006;34:661-665. 8. Milman T, Mirani N, Turbin RE. Optic nerve sheath fenestration in cryptococcal meningitis. Clin Ophthalmol. 2008;2:637-639. 9. Wall M. Idiopathic intracranial hypertension: mechanisms of visual loss and disease management. Semin Neurol. 2000;201:89-95. 10. Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri). Curr Neurol Neurosci Rep. 2008;8:87-93. 11. Wilkes BN, Siatkowski RM. Progressive optic neuropathy in idiopathic intracranial hypertension after optic nerve sheath fenestration. J Neuroophthalmol. 2009;29:281-283. 12. Kennerdell JS, Slamovits TL, Dekker A, Johnson BL. Orbital fine-needle aspiration biopsy. Am J Ophthalmol. 1985;99: 547-551. 13. Kennerdell JS, Slamovits TL, Dekker A, Johnson BL. Orbital fine-needle aspiration biopsy. Am J Ophthalmol. 1985;99: 547-551. 14. Kennerdell JS, Dekker A, Johnson BL, Dubois PJ. Fine-needle aspiration biopsy. Its use in orbital tumors. Arch Ophthalmol. 1979;97:1315-1317. 15. Halbach VV, Higashida RT, Hieshima GB, Hardin CW, Yang PJ. Transvenous embolization of direct carotid cavernous fistulas. AJNR Am J Neuroradiol. 1988;9:741-747. 16. Teng MM, Lirng JF, Chang T, Chen SS, Guo WY, Cheng CC, Shen WC, Lee LS. Emblization of carotid cavernous fistula by means of direct punture through the superior orbital fissure. Radiology. 1995;194:705-711. 17. White JB, Layton KF, Evans AJ, Tong FC, Jensen ME, Kallmes DR, Dion JE, Cloff HJ. Transorbital puncture for the treatment of cavernous sinus dural arteriovenous fistulas. AJNR Am J Neuroradiol. 2007;28:1415-1417. 18. Satchi K, Mitchell PJ, McNab AA. Transorbital puncture of the cavernous sinus to treat a dural carotid-cavernous sinus fistula. Ophthal Plast Reconstr Surg. 2009;25:54-56. 19. Iaccarino V, Spaziante R, Bonavolonta G, Cirillo S, Divitis E. Treatment of carotid-cavernous fistula by trans-venous anterior (trans-orbital) approach. Case report and review of previous report. J Neurosurg Sci. 1993;37:103-112. 20. Spinelli HM, Falcone S, Lee G. Orbital venous approach to the cavernous sinus: an analysis of the facial and orbital venous system. Ann Plast Surg. 1994;33:377-383. 21. Miller NR, Monsein LH, Debrun GM, Tamargo RJ, Nauta HJ. Treatment of carotid-cavernous sinus fistulas using a superior ophthalmic vein approach. J Neurosurg. 1995;83:838-842. 22. Gupta N, Kikkawa DO, Levi L, Weinreb RN. Severe vision loss and neovascular glaucoma complicating superior ophthalmic vein approach to carotid-cavernous sinus fistula. Am J Ophthalmol. 1997;124:853. 23. Leibovitch I, Modjtahedi S, Duckwiler GR, Goldberg RA. Lessons learned from difficult or unsuccessful cannulations of the superior ophthalmic vein in the treatment of cavernous sinus dural fistulas. Ophthalmology. 2006;113:1220-1226. 24. Smith JL, Vuksanovic MM, Yates BM, Bienfang DC. Radiation therapy for primary optic nerve meningiomas. J Clin Neuroophthalmol. 1981;1:85-99. 25. Turbin RE, Thompson CR, Kennerdell JS, et al. A long-term visual outcome comparison in patients with optic nerve sheath meningioma managed with observation, surgery, radiotherapy, or surgery and radiotherapy. Ophthalmology. 2002;109:890-899. 26. Arvold ND, Lessell S, Bussiere M, Beaudette K, Rizzo JF, Loeffler JS, Shih JA. Visual outcome and tumor control after conformal radiotherapy for patients with optic nerve sheath meningioma. Int J Radiant Oncol Biol Phys. 2009;75:1166-1172. 27. Lesser RL, Knisely JP, Wang SL, Yu JB, Kupersmith MJ. Long-term response to fractionated radiotherapy of presumed optic nerve sheath meningioma. Br J Ophthalmol. 2010;94:559- 563. 28. Miller NR. New concepts in the diagnosis and management of optic nerve sheath meningioma. J Neuroophthalmol. 2006;26:200-208. 29. Savino PJ. Evaluation of the retinal nerve fiber layer: descriptive or predictive? J Neuroophthalmol. 2009;29:245- 249. 30. Sergott RC, Savino PJ, Boseley TM. Modified optic nerve sheath decompression provides long-term visual improvement for pseudotumor cerebri. Arch Ophthalmol. 1988;106:1384-1390. 31. Kardon RH. Role of the macular optical coherence tomography scan in neuro-ophthalmology. J Neuroophthalmol. 2011;31:353-361. 32. Beck RW, Cleary PA, Anderson MM Jr, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med. 1992;326:581-588. 33. Ischemic Optic Neuropathy Decompression Trial (IONDT) Research Group. Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. JAMA. 1995;273:625-632. 184 Newman: J Neuro-Ophthalmol 2012; 32: 177-184 The Tenth Annual Hoyt Lecture Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |