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Show Journal of Neuw- Ophthalmology 16( 3): 163- 171, 1996. © 1996 Lippincott- Raven Publishers, Philadelphia Luxury Perfusion Following Anterior Ischemic Optic Neuropathy Shmuel Friedland, M. D., Jacqueline M. S. Winterkorn, Ph. D., M. D., and Ronald M. Burde, M. D. We present five patients who developed luxury perfusion following anterior ischemic optic neuropathy in whom fluorescein angiography was misinterpreted as " capillary hemangioma" or neovascularization of the disc. In each case, the segment of disc hyperemia corresponded to a spared region of visual field. Luxury perfusion represents a reparative autoregulatory reaction to ischemia. Key Words: Luxury perfusion- Anterior ischemic optic neuropathy- Autoregulation. Manuscript received March 2, 1995; accepted August 14, 1995. From the Department of Ophthalmology and Visual Sciences ( S. F., R. M. B.), Albert Einstein College of Medicine and Mon-tefiore Medical Center, Bronx, New York, and Departments of Ophthalmology and Neurology and Neuroscience ( J. M. S. W.), Cornell University Medical College, New York, New York, 10021, U. S. A. Address correspondence and reprint requests to Dr. Jacqueline M. S. Winterkorn, Neuro- Ophthalmology, 900 Northern Boulevard, Suite 210, Great Neck, NY 11021. Luxury perfusion is a vascular response to ischemia characterized by dilation of blood vessels and increased perfusion of tissues in a region surrounding an infarct. It occurs after myocardial infarction in the heart ( 1) and after stroke in the brain ( 2), where it has been visualized by magnetic resonance imaging ( MRI) and by conventional cerebral angiography; both demonstrate dilated blood vessels at the border between infarcted and normal brain. Luxury perfusion of the optic nerve head was first described by J. Lawton Smith ( 3), who observed the phenomenon in patients with anterior ischemic optic neuropathy ( AION). AION, perhaps better understood as an infarction at the optic nerve head, commonly presents as sudden visual field loss in an eye with a pale and swollen optic disc. Ellenberger and Netsky ( 4) described it as disc infarction with surrounding anterior optic nerve head ischemia. The development of segmental hyperemia from dilation of vessels on the disc adjacent to the infarction may reflect vascular reorganization compensating for ischemia and responsible for survival of neurons in that segment. Although the presence of luxury perfusion has been acknowledged by Arnold and Hepler ( 5), Burde ( 6), and Rader et al. ( 7), it is not widely appreciated. We present five patients who developed luxury perfusion following AION in whom fluorescein angiography was misinterpreted as " capillary hemangioma" or neovascularization of the disc. We suspect that luxury perfusion commonly develops after optic nerve head infarction but that both the phenomenon and its significance have been overlooked. CASE REPORTS Case 1 A 69- year- old man with non- insulin- dependent diabetes was evaluated for visual loss in the left 163 164 S. FR1EDLAND ET Ah. eye that had occurred 2 months previously and had not improved. The patient was concerned about gradual deterioration in the left eye. About 20 months earlier, he had noticed a sudden decrease in vision in the right eye that had been stable since then. His ocular history was significant for background diabetic retinopathy. Six years before the visual loss, he had undergone extracapsular cataract extractions with posterior chamber intraocular lens implantation. On examination, visual acuity was 20/ 30 OD and 20/ 200 OS with hyperopic correction. Visual fields on Humphrey central 24- 2 threshold test demonstrated superior altitudinal field defects in both eyes. A left relative afferent pupillary defect of 0.6 log units was present. Funduscopy showed small cups in both eyes. The right disc was pale, especially inferotemporally, while the left disc appeared pale except for a hyperemic segment superiorly that appeared elevated with dilated vessels ( Fig. 1A). Fluorescein angiography of the left disc was reported as showing a " capillary hemangioma" superiorly ( Fig. IB). However, fundus photography ( Fig. 1C) and fluorescein angiography done a year before to evaluate the patient's diabetic retinopathy had not shown any such vascular anomaly. The diagnosis of bilateral sequential anterior ischemic optic neuropathy was made, and the " pseudohemangioma" on the left disc was attributed to luxury perfusion. Three months later, visual acuity was 20/ 30 OD and 20/ 50+ OS, representing a spontaneous improvement by five lines in the left eye. A trace left afferent pupillary defect was present. Funduscopic examination revealed background diabetic retinopathy and disc pallor in both eyes. The hyperemic elevated blood vessels on the left disc had resolved. Case 2 A 67- year- old woman with hypertension treated by enalapril maleate ( Vasotec) experienced sudden blurring of vision in her right eye about a month prior to examination. Her left eye was unaffected. She noted no recovery in her right eye and even suspected slow progression of visual field loss. Visual acuity was 20/ 40 OD and 20/ 20 OS. The left eye was normal, and the patient saw 6 of 6 American Optical Hardy Rand Rittler ( AOHRR) color FIG. 1. Case 1. A: Left optic nerve head about 2 months after AION shows luxury perfusion superiorly. B: Fluorescein angiogram of left eye demonstrates " pseudohemangioma" superiorly in region of luxury perfusion. C: Fundus photograph of left optic nerve head 18 months before patient developed AION shows normal color and vessels and small cup. / Neuro- Ophihalmol, Vol. 16, No. 3, 1996 LUXURY PERFUSION FOLLOWING NEUROPATHY 165 FIG. 2. Case 3. A: Left optic disc shows hyper-emic area of luxury perfusion superiorly in otherwise pale disc after AION. B: Humphrey visual field 24- 2 threshold test of the left eye shows superior altitudinal defect corresponding to inferior disc pallor and spared visual field interiorly corresponding to superior area of disc enjoying luxury perfusion. LEFT AGE 73 FIXATION LOSSES FALSE POS ERRORS FALSE NEC ERRORS QUESTIONS ASKED FOVEA: 25 06 9 4/ 24 0/ 18 1/ 12 478 TEST Tilt 00: 15: 46 I f fl S/ N - 12 -? 1 - 3 - 3 - 10 - 15 - II - 12 -' 22 - 25 - 23 TOTAL DEVIATION - 9 - 2 - 8 - 4 - 4 - 7 - 11 - 10 - 8 - UH- 14 - 3 - 13 - IS - 22 - 14 - 23 - 25 - 18 - 10 - 33 - 32 - 27 ( 14) ' 26 | 6 ( 24) ( 33) J) < fl 8 a i2 *?: a a a a a a a a K a a •£ H a a a a a a - » « . • - s a - B if. a a a s a a fe » 18 ( 12) 2S 22 24 19 ( 13) ( 17) ( ifil) 4 3 m • 25 13 22 ( IS) 20 18 f[ 3. ( 1) 15 ( 11) (?) (!) I^ l- f- ( 11, ( I) PHEfiBILITY SYKB0LE " P < ffi 3Z P < " Z/. » P < l>: a p < O. K .? - 3 - 3 " F 1 - 5 - 3 - 4 PATTERN DEVIATION 1 0 - 12 - 8 - 19 - 22 - 26 - IS - 6 1 - 1 - 1 - 3 - 7 - 5 - 7- S££ - 10 - 14 - 13 - 1! - 20 - 22 - 13 - 7 - 9 - 30 - 29 - 24 - IS - 23 0- 3 0 - 4 - 3 - 2 - 1 - 2 2 4 - 6 0 - 11 - 5 •••• 8 " $ & • a a a a 32 - • tt 8 ••" 8 a s a a a ••: # a a a a a a HD PSD SF CP3S SLOGfiL INDl! - 12.42 OB 10.23 08 3 . 1 ! 0B 3.67 08 P < 0.: P< 0.: p< o.: GEfiYTOME SYMBOLS SYM OSE DB T , W. L'>$ W 10 100 - 94 ?. - 31 G luOO " 343 t r. UG2. 10!.!:.! ( I JU I -- VJ 16 1U / Neuro- Ophtlmlmol, Vol. 16, No. 3, 1996 166 S. FR1EDLAND ET AL. plates and full visual field. With the right eye, the patient identified only 3Vz of 6 AOHRR color plates, and its visual field by Humphrey central 24- 2 threshold test showed an inferior altitudinal defect. A right afferent pupillary defect of 1.8 log units was measured. The right optic disc was pale and swollen except for an elevated hyperemic area temporally. The left eye had a small hyperopic disc with good color and normal vessels. When the patient was examined 2 years later, her visual acuity in the right eye had improved to 20/ 25 OD. The visual fields and right relative afferent pupillary defect were unchanged. The hyperemic area noted temporally on the right disc 2 years earlier had disappeared, and the disc was diffusely pale. Case 3 A 72- year- old woman with hypertension treated for a year on propranolol noted painless loss of vision in her left eye 5 weeks prior to examination. The vision in her right eye had become similarly blurred earlier that year, but she had recovered subjectively and had been reading comfortably. However, she had noted no recovery in the visual loss in her left eye. Visual acuity was 20/ 30+ OD and 20/ 50 OS. With the right eye, the patient identified 5 of 6 AOHRR color plates and had superior and inferior arcuate defects on visual field by Humphrey 24- 2 threshold test. With the left eye, the patient identified only 3V2 of 6 AOHRR color plates. The visual field of the left eye by Humphrey central 24- 2 threshold test showed a dense superior altitudinal defect and a mild inferior arcuate defect. A left afferent pupillary defect of 0.9 log units was measured. The optic discs were of a small and crowded type without cupping. The left optic disc showed resolving inflammation and pallor except for an elevated hyperemic area superiorly where the larger vessels appeared engorged and many small telangiectatic vessels were visible ( Fig. 2A). This region of luxury perfusion corresponded to the area of intact visual field inferiorly ( Fig. 2B). Six months later, the patient's vision was 20/ 25- in each eye and both discs were moderately pale, consistent with a history of bilateral AION. Case 4 A 52- year- old man was examined 4 months after he had experienced an acute decrease in vision in his left eye. His medical history was significant for Grave's disease treated with phenylthiourea. Blood tests showed normal thyroid parameters, blood count, chemistries, and sedimentation rate as well as negative tests for sarcoid and syphilis. Visual acuity was 20/ 30 OU. Visual fields by Humphrey central 30- 2 threshold test were full in the right eye and demonstrated constriction with dense superior and inferior arcuate defects in the left eye ( Fig. 3A). A left relative afferent pupillary defect of 2.1 log units was noted. Funduscopic examination revealed no central cup in either disc. The right disc had normal color. The left disc was pale except for the temporal aspect, which appeared hyperemic with an elevated network of fine vessels ( Fig. 3B). Fluorescein angiography revealed leakage of fluid from the abundant vasculature on the temporal aspect of the disc ( Fig. 3C), which was interpreted as a " capillary hemangioma" of the optic disc. Sequential examinations over the next 6 months revealed stable visual acuity and visual fields. The network of fine telangiectatic vessels on the temporal aspect of the disc regressed and ultimately resolved. Case 5 A 53- year- old man with a 10- year history of diabetes was referred by his internist for possible papilledema because bilateral disc edema was noted. Brain MRI suggested only small- vessel ischemic changes. The patient complained of acute visual loss in the right eye 6 weeks earlier, followed by an acute decrease of vision in the left eye a week prior to examination. A retina specialist had examined him, suspected neovascularization of the right disc, performed fluorescein angiography, and scheduled photocoagulation therapy. The visual acuity with the patient's usual hyperopic correction was 20/ 25 OD and 20/ 100 OS. Visual fields by Humphrey 24- 2 threshold test demonstrated a dense inferior altitudinal defect in the right eye with sparing of the superior hemifield ( Fig. 4A). The visual field of the left eye had superior and FIG. 3. Case 4. A ( facing page, top): Humphrey visual field central 30- 2 threshold test of the left eye shows superior and inferior arcuate defects, with sparing only of the cecocentral region corresponding to the area of luxury perfusion seen on the left disc. B ( facing page, lower left): Left optic nerve head is pale except for a region of elevated telangiectatic vessels involving the temporal disc and representing luxury perfusion ( pseudohemangi-oma). C ( facing page, lower right): Fluorescein angiography of same disc as in a shows hyperfluorescence of the area of luxury perfusion. / Neuro- Ophthalmol, Vol. 16, No. 3, 1996 LEFT AGE 52 QUESTIONS ASKED 447 FIXATION LOSSES 5/ 24 xx Fft. SE POS ERRORS 0/ 12 FALSE NEG ERRORS 1/ 7 TEST T1HE 00: 14: 23 FOVEA: 33 DB : : ( I) < 0 4 ( 2) 15 0 ( 0) 2 » 23 ( 2i) 17 ,26 6 < 0 - 23 - 28 - 12 - 28 - 24 - 10 - 9 - 8 - 4 - 20 - 5 - 8 - 8 - 4- 1 - 31 - 25 - 8 - 21 - 32 - 32 - 24 - 31 - 31 TAL - 16 - 28 - 28 - 31 - 16 - 14 - 17 - 28 - 18 - 5 - 24 - 16 - 15 - 28 - 5 - 19 - 17 - 21 - 19 - 3 - 13 - 30 - 25 - 24 - 23 - 29 [•- 31 - 30 DEVIATION 8 * » m * %?.&.&.••• iff ••• m & ••• • ^ * W Ml W M 4 1 m « • » m m m M « « • * « ! S H i K K 4 4 1 4 Ml' 41 « H 4 4 4 - 41 M < 0F18 i' 4) 4 ( 4) < 0 ( 0) 13 ( 15) 27 ( 27) 27 ( 19) < 0 ( 0) < 0 • 7 < 31X&) 8 123 < 12X23) 11 14 ( 1) ( 8) < 0 KO ( 0) 5 ( 0) < 0 ( 0) PROBABILITY SYfBOLS : : R < K £ P < K » P< I* i i F < 0.5X 2 ( 0) 10 4 ( 12) < 0 -< 0)- ( 15) ( 4) (( 44) - 17 - 23 - 7 - 23 - 19 - 5 - 4 - 2 1 - 15 1 - 3 - 2 1 4 - 28 - 20 - 3 - 18 - 27 - 27 - 19 - 28- 28 PATTERN - LO -! 3 - Z3 - a - 11 - 8 - 11 - 23 - 12 0 - 18 - 10 - 10 - 23 0 - 14 - 12 - 16 - 13 - 3 - 7 - 25 - 19 - 19 - 23 - 24 h- 26 - 25 DEVIATION n m " 4 1 41 f ' ' 41 * i • m Ml 41 41 M m ••••• m m * i & » m m m • M 41 8 41 W8 WB ^ ^ Xtf - MJ m m M * 41 « Ml GLOBAL INDICES MP - 17.73 DB P < O. R PSD 10,67 OB P < 0.55; SF OFF CPSO OFF GRfiYTONE SYMBOLS .1 41 t - r- 50 40 31 t •=• 10 21 : si t •=. 100 20 ' 94 t-=. 31S 11 t .=• 1OOO t •=• 10 ' 34- i UB2 1 0( ii) i) 3YM HSB DB / Ncuw- Ophthaliiiol, Vol. 76, No. 3, 1996 168 S. FR1EDLAND ET AL. inferior defects with a dense superonasal scotoma involving fixation. Examination of the fundus showed resolving edema of the right optic disc with blurring of the disc margin and pallor except interiorly, where there was a hyperemic segment of telangiectatic vessels ( Fig. 4B) corresponding to the spared superior visual field. The left disc showed fresh papillitis with hemorrhage, cotton wool exudation, and pallor except for a suggestion of hyperemia on the disc nasally. Bilateral sequential AION was diagnosed and the telangiectatic hyperemic vascular formation in the right eye was ascribed to luxury perfusion. DISCUSSION Each of these patients with AION, characterized by acute decrease in vision and visual field, developed luxury perfusion on the involved disc with a hyperemic segment formed by richly perfused telangiectatic vessels. Significantly, the vascular formation in each case involved the segment of the optic disc least affected by ischemia and corresponding to spared visual field. Although fluorescein angiography of the vascular formation was reported as capillary hemangioma in two patients, the anomalous blood vessels had not been present prior to disc infarction. In a third patient, lack of awareness of the phenomenon of luxury perfusion led to suspicion of disc neovascularization. In each case, the luxury perfusion resolved within several months. We suspect that dilation of vessels on the optic nerve head adjacent to an infarction reflects a compensatory vascular reorganization responsible for survival of the well- perfused region. However, in more than a decade since Smith ( 3) described luxury perfusion on the optic disc of patients in the acute hyperemic stage of AION, the finding has rarely been mentioned and is not often clinically recognized, even though disc infarction is a common cause of visual loss. We suspect that luxury perfusion is a common phenomenon but that it has been overlooked and its role in limiting the extent of optic nerve head infarction not considered. The pathophysiology of optic nerve infarction involves inadequate perfusion of the disc by the posterior ciliary circulation ( 8,9). Systemic risk factors such as chronic hypertension and diabetes, predisposing to poor perfusion and vascular occlusion, and local factors such as crowding on the optic nerve head play variable roles in the development of optic nerve infarction in the individual patient. Two of our patients had diabetes mellitus and another was under treatment for chronic hypertension, both conditions associated with small-vessel disease. Each of the patients described had no central cupping and a small, crowded disc, of the type considered the " disk- at- risk" ( 6) for AION or optic nerve head infarction. Such a disc has insufficient space to accommodate the swelling caused by ischemia. Local axonal swelling results in compression and death of surrounding axons, accompanied by release of excitatory amino acids, leakage of intracellular potassium, loss of the ability to propagate action potentials, and a destructive increase in intracellular calcium with activation of the prostaglandin and phospholipase cycles. Thus, in such a disc, minor ischemia can precipitate a cascade of further vascular occlusion, axonal swelling, and progressive ischemia, resulting in significant disc infarction. The development of luxury perfusion on the optic nerve head almost certainly reflects a vascular autoregulatory mechanism that dilates blood vessels to increase oxygenation of tissues in response to ischemia. Development of luxury perfusion may be predictive of a good visual prognosis after AION ( 10). Although each of the patients presented here complained of subjective progression of visual loss during intermediate stages of recovery, each one had several lines of improvement in visual acuity by the time the luxury perfusion had resolved, and the final visual acuity was 20/ 40 or better in each case. The disc swelling in young diabetics, which generally has an excellent visual prognosis, is characterized by telangiectasia of superficial vessels on the disc ( 11). These vessels probably represent luxury perfusion and may be responsible for preservation of vision in these young patients. The phenomenon of segmental leakage of the disc after optic nerve infarction was described by Arnold and Hepler ( 5). They studied fundus fluorescein angiograms of 41 patients with AION and found not only delayed disc perfusion reflecting ischemia, but also focal or segmental hyperfluores-cence on the disc in more than half of their patients. In agreement with our observations, the hy-perfluorescent segment was not in the part of the disc associated with the visual field defect. This suggests that the hyperfluorescence does not reflect ischemia, but rather the compensatory shunting of blood to viable disc tissue adjacent to the infarction. Clinically, within the first few days after onset of AION, examination of the optic disc often reveals capillary dilatation and hyperemia, which we believe to be the earliest indications of luxury perfusion. Over time, collateral vessels may fill and dilate. The full- blown appearance of luxury perfusion may take several days or weeks to de- / Ncuw- Ophlhalmol, Vol. 16, No. 3, 1996 LUXURY PERFUSION FOLLOWING NEUROPATHY 169 RIGHT AGE 53 FIXATION LOSSES 6/ 23 xx FALSE PCS ERRORS 1/ 3 FALSE NEG ERRORS 0/ 12 QUESTIONS ASKED 442 FOVEA: 25 TEST TII£ 00 HFflS/ tl B H :: 8 £ H & a • • H • • a • • • • • • • &. • 8 • :: • • * • • - • • • • -• • - 3 1 - 1 - 1 - 1 - 10 - 10 - 2 2 - 3 - 4 0- 4 4 - 26 - 28 - 30 - 31 - 31 - 27 - 29 - 24 - 30 - 28 - 29 - 29 - 27 - 28' PATTERN DEVIATION 41 - 3 - 3 - 4 0 - 6 1 - 8 - 1 0 - 22 - IS - 6 - 11 - 18 - 15 - 3 2 2 - 10 - 3 -? 1 - 14 PROBABILITY STOOLS ••= P< 5X £ P < 2X 38 P< V. • P < 0 . R 32 • • - 1 • • • • • • • • m • • • • M • * :: • • • B " • • • H HD PSO SF CPSO GLOBAL INDICES - 1S. 05 DB P < O . K 13.2? OB P < 0.5X OFF OFF GRfiYTONE SYMBOLS SYM I SB DE . 1 50" :'-: . 5 . 1 36 40 1 ' •-• 31 *" * •;• 10 £ 6 30 73 1 -:• £ 1 • t o MM 100 16 20 llffl 7 34 * •> 3 1 6 11 15 :• 1000 6 t •-• 10 7 3 4 3 t •:- 1 5 Jjj BSM 10000 ••: 0 FIG. 4. Case 5. A: Visual field of the right eye on Humphrey 24- 2 threshold test shows preservation of vision in the superior visual field mediated by optic nerve fibers in the area of luxury perfusion seen in B. B: Fundus photograph of the right eye shows luxury perfusion of the inferior region of the optic nerve head. / Neuro- Ophtlmlmol, Vol. 16, No. 3, 1996 170 S. FR1EDLAND ET AL. velop, as neighboring vasculature shunts blood either toward the ischemic area or toward the salvageable tissues surrounding it, to limit the extent of infarction. It may be significant that each of our patients was seen several weeks or months after the onset of AION. Failure of vascular autoregulatory mechanisms at the optic nerve head has been an hypothesis invoked to explain optic nerve head diseases as varied as AION ( 9), glaucoma ( 12,13), and Leber's hereditary optic neuropathy ( 14). The development of both chronic open- angle glaucoma and low- tension glaucoma is attributed to ischemia that results from defective vascular autoregulation at the disc, resulting in inadequate perfusion of the optic nerve. In patients with chronic open- angle glaucoma, Rader and co- workers ( 7) noted narrowing of branches of the central retinal artery in the region immediately around the optic nerve head. They found proximal constriction in 42% of patients with moderate to severe glaucoma and also in 68% of patients with AION. In patients with glaucoma, the peripapillary constriction corresponded to the sector of the disc with the most cupping and the part of the visual field with the greatest loss. Rader et al. speculated that the proximal local constriction could be explained by loss of axons and reduction in local metabolism, but such vascular constriction might also reflect loss of local autoregulatory control of the circulation. Hayreh and Bains ( 15) showed that experimental occlusion of the posterior ciliary arteries in monkeys produced pale disc swelling, similar to that seen in AION. They suggested the presence of a local mechanism regulating optic nerve head blood flow, enabling the disc to maintain a relatively constant blood flow despite wide fluctuations in perfusion pressure. It is now known that vascular endothelium plays a key regulatory role in modulating perfusion of the eye. This control of local tone is effected by the release of a gamut of relaxing and dilating factors by the microcirculatory endothelium ( 16). AION occurs when the perfusion pressure to the optic nerve head falls below the limits for which the autoregulatory mechanism can adjust. Age, long- standing arterial hypertension, and atherosclerosis as well as a crowded disc structure might all predispose to optic nerve infarction to the extent that they interfere with vascular autoregulation. However, the development of luxury perfusion following optic nerve infarction indicates that autoregulatory mechanisms on the disc are still present, although perhaps insufficient to protect the eye completely from hypoperfusion. Patients with luxury perfusion have sufficiently good autoregulatory capacity to divert blood to the region of the disc adjacent to an infarction and to reverse ischemia in the border zone. Luxury perfusion may be partially responsible for limiting the extent of infarction and maintaining or facilitating recovery of good visual function. A fuller understanding of the mechanisms underlying autoregulation of blood flow at the optic nerve head would certainly contribute to our ability to predict, prevent, and perhaps even treat those optic neuropathies thought to have an ischemic component, including AION, glaucoma, and Leber's optic neuropathy. An appreciation of the time course for development and resolution of luxury perfusion on the optic nerve head after disc infarction might provide insights into those mechanisms as well. We suspect that luxury perfusion is a common reparative phenomenon after infarction in the optic nerve head, just as it is after infarction in the heart and brain. More general recognition of its presence will be an important step toward understanding the pathophysiology of ischemic optic neuropathy. Acknowledgment: Supported in part by an unrestricted grant to the Department of Ophthalmology and Visual Science, Albert Einstein College of Medicine, from RPB, Inc., New York, and a fellowship grant from the American Physicians for Medicine in Israel ( S. F.). REFERENCES 1. Braunwald E, Sobel BR. Coronary blood flow and myocardial ischemia. In: Braunwald E, ed. Heart disease. 4th ed. Philadelphia: Saunders, 1992: 1162. 2. Heiss WD, Graf R. The ischemic penumbra- current opinion. Neurology 1994; 7: 11- 9. 3. Smith JL. Pseudohemangioma of the optic disc following ischemic optic neuropathy. / Clin Neuro Ophthalmol 1981; 5: 81- 9. 4. Ellenberger CJ, Netsky MD. Infarction in the optic nerve. / Neurosurg Psychiatry 1968; 31: 606- 11. 5. Arnold AC, Hepler RS. Fluorescein angiography in acute non- arteritic ischemic optic neuropathy. Am ] Ophthalmol 1974; 117: 220- 30. 6. Burde RM. Optic disc risk factors for non- arteritic anterior ischemic optic neuropathy. 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