| OCR Text |
Show Journal of Neuro- Ophlhalmology 17( 1): 29- 32, 1997. © 1997 Lippincoll- Ravcn Publishers, Philadelphia Asymptomatic Optic Disc Edema Richard N. Gordon, M. D., Ronald M. Burde, M. D., and Thomas Slamovits, M. D. Non- arteritic anterior ischemic optic neuropathy ( AION- na) classically presents with visual loss, altitudinal visual field defects, and optic nerve swelling. AION- na presumably occurs secondary to an ischemic event. Two patients are described who were at risk for developing AION- na. Both patients presented with optic disc edema but did not have visual loss or visual field defects. Neither patient developed visual loss or visual field defects in the affected eye throughout one and two years of follow- up respectively. The optic disc edema resolved spontaneously in both affected eyes. The clinical spectrum of AION- na could range from a " full- blown" classic attack to a minimal attack characterized by disc swelling without visual loss. The amount and distribution of disc ischemia determines the individual clinical picture. The failure of either affected eye in this study to develop symptoms likely represents a graded axonal atrophy with mechanical decompression of the optic nerve. Key words: Anterior ischemic optic neuropathy- Axoplasmic flow- Diabetic papillopathy- Luxury perfusion- Optic nerve edema- Relative afferent pupillary defect- Visual field. The classic clinical presentation of nonarteritic anterior ischemic optic neuropathy ( AION- na) is the sudden onset of visual loss with altitudinal visual field defects and optic nerve swelling. AION- na presumably occurs secondary to an ischemic event. We describe two patients who were at risk for developing AION- na and presented with optic disc edema but remained asymptomatic and free of visual field defects. From the Montcfiore Medical Center, Department of Ophthalmology, New York, New York, U. S. A. Address correspondence and reprint requests to Dr. Ronald M. Burde, Department of Ophthalmology, Albert Einstein College of Medicine, Moutefiore Medical Center, 111 East 210 Street, Bronx, NY 10467, U. S. A. CASE REPORTS Case 1 A 53- year- old man with no significant past medical history was seen on 1 December 1992 with the chief complaint of one month of blurred right eye vision, described as a cloud over the inferior visual field. Best corrected visual acuity was 20/ 30 + 2 OD and 20/ 20 - 3 OS. Color vision was right 2/ 15 Ishihara color plates, and left 14/ 15 plates. A right relative afferent pupillary defect was noted. Slit lamp exam was unremarkable. The intraocular pressures were 20 mm Hg OD and 19 mm Hg OS. Dilated fundus exam ( Fig. 1) revealed a swollen right optic nerve with a supero-temporal sector of pallor and " luxury perfusion" present superonasally. The left disc was anomalous with a small central cup. Goldmann perimetry revealed an inferior altitudinal defect OD and a normal visual field OS. Erythrocyte sedimentation rate ( Westergren) was 37 mm/ h and a CBC was normal. It was felt that the patient had a nonarteritic anterior ischemic optic neuropathy ( AION- na) in the right eye. One week later ( 8 December 1992), he noted a further decrease in visual acuity OD. Best corrected visual acuity was 20/ 100 - 1 OD and 20/ 20 - 1 OS. On fundus examination, the tight disc had a new area of pallor inferotemporally. Kinetic visual fields showed new superior altitudinal field loss OD. He underwent right optic nerve sheath fenestration the next day ( 9 December). Two months postoperatively vision was 20/ 200 OD and 20/ 20 - 3 OS with stable superior and inferior visual field defects. Three years later ( 31 January 1995), visual acuity was 20/ 100 - 1 OD and 20/ 20 - 3 OS. He correctly identified 15/ 15 Ishihara color plates with the left eye but only the test plate with the right. Kinetic visual fields were unchanged. The right disc had a wedge of temporal pallor. The left disc had a wedge of inferotemporal swelling 29 30 R. N. GORDON ET AL. FIG. 1. Patient 1, 1 December 1992. Swollen right optic nerve with no central cup, a small superotemporal sector of pallor, and " luxury perfusion" superonasally. A small central cup is present on the left, and both discs have anomalous vascular branching patterns. associated with peripapillary nerve fiber layer hemorrhages ( Fig. 2). Over one year has elapsed ( 14 February 1996) since the left disc swelling was discovered, and the patient remains free of visual loss and visual field defects on the left. Case 2 A 77- year- old man was referred to the neuro-ophthalmology service on 23 August 1990. Five months previously ( March 1990), he had undergone uneventful cataract extraction in the left eye. Optic disc edema was discovered on routine follow- up exam. By report, no disc edema had been observed prior to surgery. The patient denied any episodes of visual loss or blurring of vision and was entirely free of visual symptoms on presenta- FIG. 2. Patient 1, 31 January 1995. The left disc has inferotem-poral swelling associated with peripapillary nerve fiber layer hemorrhages. FIG. 3. Patient 2, 23 August 1990. Left disc elevation with " luxury perfusion" at the superior and inferior poles. ./ Newo- Oplulmlmol, Vol. 17, No. 1. 1997 ASYMPTOMATIC OPTIC DISC EDEMA 31 tion. Past ocular history was significant for iridectomies in both eyes in 1967 for narrow angles. The patient had diabetes mellitus, systemic hypertension, coronary artery disease, and had suffered two myocardial infarctions in the past. Review of systems was unremarkable. His medications were Captoten, Isopten, Diabeta, and Zantac. Best corrected visual acuity was 20/ 25 OD and 20/ 20 - 2 OS. No relative afferent pupillary defect was noted. Color vision was 12/ 15 Ishihara color plates OU. Slit lamp examination on the right showed a patent peripheral iridectomy and mild nuclear sclerotic cataract, and the left eye had a healing limbal wound consistent with prior intraocular surgery, a sector iridectomy, and a well-centered posterior chamber intraocular lens implant. The right disc was flat and pink with a small central cup and an anomalous vascular branching pattern. Minimal diabetic retinopathy was present in the macula. The left disc had 360- degree elevation with dilated peripapillary vessels (" luxury perfusion") at the superior and inferior poles and a small central cup ( Fig. 3). Static full field threshold perimetry was normal on the right and an enlarged blind spot was present on the left. The patient was thought to have asymptomatic ischemic optic neuropathy. The possibility of a diabetic pap-illopathy was also considered even though the patient's age places him in a different risk category. Fluorescein angiography revealed disc edema and cystoid macular edema of the left eye, and an MRI scan of the orbits was unremarkable. He remained asymptomatic and did not develop a visual field defect or relative afferent pupillary defect. The left optic disc swelling slowly resolved and two years later ( July 1992) was only mildly elevated nasally with slight pallor temporally. There was also peripapillary atrophy. COMMENT Nonarteritic anterior ischemic optic neuropathy is characterized by sudden, painless visual loss accompanied by nerve fiber bundle defects, an afferent pupillary defect, and optic disc swelling ( 1- 4). It affects patients between the ages of 45 and 80 years ( 5). Among identified associated risk factors, the one universal feature of this entity is a crowded optic nerve head without a normal physiologic cup ( 6). A 25- 50% incidence of sequential AlON- na affecting the fellow eye within 5 years has been reported ( 5). Furthermore, an increased incidence of AION- na following uncomplicated cataract extraction has been reported ( 7). Hayreh ( 8) described four patients and referred to seven others in the literature who had optic disc edema but were asymptomatic at the time of discovery. They had relatively normal visual fields ( some cases had enlarged blind spots), but classic altitudinal visual field defects followed from days to months later. All patients previously had an episode of AION- na in the fellow eye. Hayreh theorized that different degrees of optic nerve ischemia can occur in AION- na, with mild ischemia disrupting axoplasmic flow, producing disc swelling but not interfering with action potential transmission. However, this mild ischemia may progress to a more severe degree, and at some level visual loss will occur. The amount and distribution of disc ischemia determines the individual clinical picture. We believe that the paucity of similar attacks or the failure of recrudescence of disc swelling in the affected eye reflects the presence of a graded axonal atrophy mechanically decompressing the nerve ( 6,9). Thus, the clinical spectrum of AION- na could range from a " full- blown" classic attack to a minimal attack reflected by disc swelling without visual loss or associated with transient obscuration of vision. These cases are important as they demonstrate a crowded but otherwise normal disc that became swollen under observation ( presumably due to an ischemic event) but remained asymptomatic. Unlike the patients in Hayreh's series, these patients have not developed visual field loss. Both patients were at increased risk for developing AION- na; in case 1, with a previous episode in the fellow eye, and in case 2, following recent cataract extraction. Case 2 may alternatively have had diabetic pap-illopathy. A recent large series by Regillo et al. ( 10) indicates that diabetic papillopathy can also occur in older patients and those with type II diabetes. However, the authors of that paper and Burde et al. ( 6) infer that although the clinical presentation and prognosis for these two entities may differ, the pathophysiologic mechanisms for AION- na and diabetic papillopathy may not be distinct. We believe that the underlying pathophysiology of asymptomatic disc edema is likely to represent a graded ischemic process, and partial axonal atrophy appears to be important prognostically. We also wonder if the finding of luxury perfusion implies any predictive value visa- vis prognosis. REFERENCES 1. Kurz O. Uber Papilliles arteriosclcrotica. Ophlhalmologica 1948; 116: 281- 5. 2. Kurz O. Vascular oplicopalhy. Doc Ophthalmol 1969; 26: 582- 9. 3. Ellenberger C Jr, Kellncr JL, Burdc RM. Acute oplic neuropathy in older patients. Arch Neurol I973; 28: 182. 4. Boghcn DR, Glaser JS. Ischacmic optic neuropathy: the clinical profile and natural history. Brain 1975; 98: 689- 708. 5. Burde RM, Savino PJ, Trobe JD. Clinical decisions in nemo-ophthalmology. Boston: Mosby- Year Book, 1992: 50- 1. 6. Burde RM. Optic disk risk factors for nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1993; 1 16: 759- 62. 7. Carrol FD. Optic nerve complications of cataract exlraclion. Trans Am Acad Ophthalmol Otolaryngol 1973; 77: 623. 8. Hayreh SS. Anterior ischemic optic neuropathy V. Optic disc edema- an early sign. Arch Ophthalmol 1981; 99: 1030- 40. ./ Neiim- Oplltliallliol, Vol. 17, No. 1, 1997 32 R. N. GORDON ET AL. 9. Belirens MM, Odel JG. Other optic nerve disorders. In: Lessel S, 10. Regillo CD, et al. Diabetic papillopathy, patient characteristics and Van Dalcn JTW, cds. Current neuro- ophthalmology, St. Louis: fundus findings. Arch Ophthalmol 1995; 113: 889- 95. Mosby- Year Book, 1991: 40. J Newo- Ophthalmol, Vol. 17. No. 1. 1997 |
