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Show 10llmal of Clillical Nellro-ophthalmology 7(4): 198-201. 1987. Chronic Asymptomatic Ischemic Optic Neuropathy A Report of Two Cases in Adults with Diabetes Mellitus Michael L. Slavin, M.D. © 1987 Raven Press, Ltd., New York Two adult diabetic patients with chronic asymptomatic optic neuropathy attributed to an ischemic etiology are reported. In one case the typical syndrome of ischemic optic neuropathy occurred in one eye, while the fellow eye had asymptomatic hyperemic optic disc edema that persisted for 6 months without optic atrophy. A minor visual field defect initially detected in that eye resolved spontaneously in 1 month. In the second case, a recent onset, middle-aged diabetic developed bilateral optic neuropathy and optic disc edema that persisted for 12 months, with minimal signs of visual dysfunction. Axoplasmic transport blockage from low-grade ischemia to the optic nerve may cause acute or chronic optic disc edema with minimal or no visual symptoms. Key Words: Anterior ischemic optic neuropathyChronic ischemic optic neuropathy- Diabetes mellitus, optic neuropathy. From the Division of Neuro-ophthalmology, Department of Ophthalmology, Long Island Jewish Medical Center New Hyde Park, and School of Medicine, Health Sciences Center, State University of ew York at Stony Brook, Stony Brook, ew York. Address correspondence and reprints requests to Dr. Mich."' 1 Sli!\'in, DepMtment til" ()phthalmolllgv Long Island . ',' :".>1 (',""kr ~.Il'\\" H:",J., (\lrfe. NY 110·12, U,S.A. /98 The syndrome of anterior ischemic optic neuropathy (AlaN), which is due to infarction of the anterior portion of the optic nerve, typically presents with acute unilateral visual dysfunction, pallid optic disc edema, and characteristic visual field disturbance. Optic atrophy commonly ensues within weeks, and prognosis for visual recovery is guarded. On the other hand, persistent optic disc edema attributed to ischemia is unusual. Two adult diabetic patients presented with chronic asymptomatic optic neuropathy that was most compatible with an ischemic etiology. In one patient, persistent optic disc edema for 6 months was noted in one eye (without optic atrophy), while the fellow eye suffered the typical syndrome of AlaN. The clinical picture in the second case is reminiscent of the variety of optic neuropathy reported to occur in young patients with juvenile onset diabetes mellitus. CASE REPORTS Case 1 A 55-year-old woman with diabetes mellitus for 30 years noted diminished right eye vision for several days. There were no associated symptoms of headache, jaw claudication, polymyalgia rheumatica, or neurologic abnormalities. Visual acuity was 20/40 right, and 20/20 left. Perimetry (Goldmann) revealed a dense inferior altitudinal defect on the right. There was a 2+ right afferent pupil defect and pallid edema of the superior aspect of the right optic disc; the left optic disc was normal. Bilateral mild, nonproliferative diabetic retinopathy was present. Erythrocyte sedimentation rate (Westergren) was 40 mm/h. Two months later visual acuity was 20/25 right, 20/15 left. The visual field on the right side was ISCHEMIC OPTIC NEUROPATHY /99 FIG. 1. Goldmann perimetry. Note dense inferior altitudinal defect on right. and infero-nasal scotoma on left. unchanged but an asymptomatic infero-nasal scotoma on the left side was detected (Fig. 1). There was atrophy of the superior portion of the right disc, and left optic disc edema (hyperemic) (Fig. 2). A superficial temporal artery biopsy showed no evidence of giant cell arteritis. Examination 1 month after showed only an enlarged left blind spot. Left optic disc edema, however, was unchanged. On 6 month follow-up, moderate optic disc edema was still present, while 2 months later, the left optic disc was minimally edematous. Case 2 A 47-year-old woman with hypertension and recent onset diabetes mellitus, noted vague rightsided visual dysfunction for 2 months. There was right optic disc edema. Computerized tomography of the brain and orbits was unremarkable. On neuro-ophthalmic examination, visual acuity was 20/25 right, and 20/15 left. Visual fields (Goldmann) revealed peripheral nasal constriction on each side with no focal scotomas (Fig. 3). Color vision (AO-HRR) was normal and symmetrical. A 2+ afferent pupil defect on the right was noted. Optic disc edema with telangiectatic capillaries overlying the disc on the right (Fig. 4) was seen, while minimal telangiectatic vessels on the left disc were present. Fluorescein angiography confirmed bilateral optic disc edema. On 1 month follow-up, the visual field on the left was normal, while it was unchanged on the right. Right optic disc edema was again noted with the additional finding of peri-papillary lipid exudates. Left optic disc edema had increased. Examination 2 months later was unchanged. On 6 month follow-up, slight right optic atrophy with retinal nerve fiber layer dropout and diminished left optic disc edema were present. Four months thereafter, the left optic disc was minimally edematous. DISCUSSION Similar to the acute symptomatic neurologic deficit incurred by cerebrovascular infarction (CVA, the "stroke" syndrome), sudden visual loss typically heralds the onset of idiopathic AION. Although stuttering visual loss up to several weeks with AION has been rarely reported (1,2), the clinician, under those circumstances, should exclude more common etiologies of subacute optic neuropathy. Some patients with atypical AION in the first eye have been found to harbor asymptomatic optic disc edema (ODE) in the fellow eye (1,3- 5). Several months later, the classic presentation of 200 M. L. SLAVIN FIG. 2. (A) Resolving right inferior optic disc edema, and superior optic atrophy. (8) Hyperemic left optic disc edema, with normal retinal arterioles. AION developed in the second eye. Hayreh (5) in 1981 reported four such cases in which no objective or subjective visual dysfunction in the fellow eye with ODE was evident. In two cases, asymptomatic ODE was present for 2 months before complete resolution. Several months later, however, ODE recurred and an infero-nasal visual field defect developed in each case. Both ODE and visual field defects notably resolved 2 months thereafter. In Case 1, the typical syndrome of AION developed in one eye while asymptomatic ODE was noted in the fellow eye. Unlike those reported by Hayreh, the ODE persisted for 6 months. The initial visual field disturbance, however, improved spontaneously in 1 month. These cases imply that mild ischemia of the optic nerve could result in ODE due to abnormalities ofaxoplasmic transport without impairing the ability of the axon to conduct the visual signal. The dissociation of optic disc edema and visual loss is often seen in cases of papilledema, in which the cause of impaired axoplasmic transport is most likely compressive. The bilateral optic neuropathy in Case 2 is not typical of an ischemic, inflammatory, or compressive process. ODE persisted for 1 year before minimal optic atrophy ensued in one eye, and a subtle visual field defect remained. The fellow asymptomatic eye with an initial minimal visual field disturbance showed persistent ODE (with telangiectatic vessels overlying the disc) for 6 months despite earlier improvement of visual fields. The clinical picture is similar to the optic neuropathy (? ischemic) described in young patients with juvenile onset diabetes mellitus. Lubow and Makley (6) in 1971 reported three young patients with chronic diabetes mellitus and bilateral ODE. In one case, visual obscurations were the only symptom, while no objective visual dysfunction was demonstrable. Thus, bilateral papilledema from increased intracranial pressure was simulated. ODE persisted for 7 months in one eye. The "intricate capillary network on the disc" was thought to represent diabetic microangiopathy. In their second case, minimal acuity and visual field impairment developed, but spontaneous improvement of ODE and visual function occurred 6 months after. Twelve cases were described by Barr and associates (7) in 1980 with a similar theme. Bilateral ODE, minimal visual acuity, and visual field abnormalities, with excellent recovery, presented in long-standing juvenile diabetes in the second or third decades of life. There was no positive corre- ISCHEMIC OPTIC NEUROPATHY 201 FIG. 3. Goldmann perimetry showing bilateral peripheral nasal depression. lation of ODE with background diabetic retinopathy. In some of those cases and those reported by Pavan and associates (8) also dilation of the superficial radial capillaries on the surface of the optic disc were noted. FIG. 4. Right optic disc edema with overlying telangiectatic capillaries. Case 2, a 47-year-old with recently diagnosed diabetes presented with features of the optic neuropathy described in juvenile onset diabetes. I believe that this case falls into the spectrum of clinical AlaN ranging from asymptomatic ODE with chronic persistent axoplasmic transport blockage to frank acute optic disc infarction and severe irreversible visual loss. Presumably in juvenile diabetes and, in those patients with AlaN and minimal visual dysfunction, a sufficient optic nerve collateral circulation exists that spares the axons from irreversible injury that would impair vision. REFERENCES 1. Boghen DR, Glaser jS. Ischaemic optic neuropathv. The clinical profile and natural historv. Braill 1975;98:689-708. 2. Knox DL, Duke JR. Slowlv progressive ischemic optic neuropathy. TrailS Am Acad Ophthalmol Otoian/Ilgol 1971;75: 1065-8. 3. Georgiades G. Konstas P, Stangos N. Relexions issues de i'etude de nombreux cas de pseudo-papilite vasculaire. BI/II Soc Ophtha/mol Fr 1966;79:505-36. 4. Eagling EM, Sanders MD, Miller SjH. Ischaemic papiIIopathy. Brl OphthalIl1011974;58:990-1008. 5. Hayreh SS. Anterior ischemic optic neuropathy: V Optic disc edema as early sign. Arch OplzthalllwI198l;99:1030-40. 6. Lubow M, Makley TA. Pseudopapilledema of juvenile diabetes mellitus. Arclz OphthalllwI197l;85:417-22. 7. Barr CC, Glaser jS, Blankenship G. Acute disc swelling in juvenile diabetes. Arch Ophthalmol 1980;98:2185-92. 8. Pavan PR, Aiello LM, Wafai Z, Briones }C, Sebestyen jG, Bradbury Mj. Optic disc edema in juvenile-onset diabetes. Arch OphthalmoI1980;98:2193-5 1(11Il Nc"ro-ophtlwlllloi. \'01. '. ,\;0 4. ]98~ |
