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Show Journal of Clinical N~ uro- ol'hlhulmology 9( 2): 116- 118, 1989. Anterior Ischemic Optic Neuropathy and Increased Intraocular Pressure Robert L. Tomsak, M. D., Ph. D., and Bernd F. Remler, M. D. © 1989 Raven Press, Ltd" New York Five patients were noted to have increased intraocular pressure ( lOP) during evaluation for acute nonarteritic anterior ischemic optic neuropathy ( AlaN), Three of the five had no prior record of lOP elevation; all five had small cup- to- disc ratios. Elevated lOP may be a risk factor for developing AlaN, especially in eyes with structurally congested optic discs, Key Words: Anterior ischemic optic neuropathyIntraocular pressure- Glaucoma- Optic disc structure. From the Division of Ophthalmology, Department of Surgery, and Division of Neuro- ophthalmology, Department of Neurology, University Hospitals of Cleveland and Case Western Reserve University School of Medicine, Cleveland, Ohio. Address correspondence and reprint requests to Dr. R L Tomsak at Division of Neuro- ophthalmology, University Hospitals of Cleveland, Lakeside 3200A, 2074 Abington Rd., Cleveland, OH 44106, US. A This work was presented al II", Cleveland Clinic foundation \ ll1rnni M" din,;, l" n" ] R ] ORE: 116 Anterior ischemic optic neuropathy ( AION) ( 1,2) is characterized by sudden visual loss that is usually nonprogressive. It is accompanied by variable degrees of loss of visual acuity, often in conjunction with altitudinal defects in the visual field. The optic disc has the characteristic appearance of pallid edema, with or without hemorrhages, due to axoplasmic stasis that results from infarction of the laminar portion of the optic nerve. The pathogenesis of nonarteritic AION is believed to correlate with the developmental structure of the optic disc. Presumably, a small scleral canal diameter results in axonal crowding in the region of the lamina cribrosa. This crowding of nerve fibers is associated with small to absent cupto- disc ratios and may make the nerve head more susceptible to infarction if regional blood flow is compromised for any reason ( 1,2). Here we report five patients who suffered nonarteritic AION and who also had mild elevations in intraocular pressure ( lOP) as measured by applanation tonometry; all had small or absent optic cups. METHODS AND RESULTS Five of 56 consecutive patients with acute nonarteritic AION referred to us for neuro- ophthalmic consultation during the period from September 1986 to April 1988 were noted to have increased lOP at the time of our examination ( Table 1). Visual acuities and visual field characteristics are listed in Table 2. The average age was 67 years ( range 46- 81 years). Four of the five had no known cardiovascular disease; one man had insulin- dependent diabetes mellitus ( case 2). The three patients aged 70 or older ( cases 2, 3, and 5) had no clinical symptoms of giant cell arteritis or polymyalgia rheumatica. Westergren sedimentation rates were 15 ( case 2), 5 ( case 3), and 28 ( case 5) mm/ h. ANTERIOR ISCHEMIC OPTIC NEUROPATHY AND INCREASED IOP 117 TABLE 1. Summary of findings Case no. Age ( yrs)/ sex Affected eye lOP ( mmHg) 46/ M O. S. 0.0.22 0. S. 29 2 70/ M O. S. 0026 0. S. 29 3 81/ F 0.0. 0.0.28 0. S. 24 4 57/ F 0.0. 0.0.29 0. S. 25 5 80/ F O. U. 0.0.25 0. S. 26 Three of the five ( cases 2,3, and 5) had increased lOP first noted by us at the time of referral for evaluation of loss of vision. Patient 1 was under treatment for ocular hypertension with 0.5% Timoptic O. U. at the time the ischemic optic neuropathy happened. Patient 4 was noted to have increased lOP when she was first evaluated for sudden visual loss by the referring ophthalmologist 3.5 weeks prior to our examination; when seen by us she was also using 0.5% Timoptic 0.0. twice a day. Four of the five patients ( cases 1- 4) had unilateral AlaN; all these had slightly higher lOPs in the affected eye ( Table 1). In every case the unaffected fellow eye had a cup- to- disc ratio of ~ 0.1 as judged by stereoscopic slit lamp biomicroscopy; thus, none showed evidence of glaucomatous optic nerve damage. DISCUSSION The association between elevated lOP and AlaN has been described before in somewhat different contexts. Foulds ( 3) found that 7 of 24 consecutive patients with ischemic optic neuropathy examined by him had some form of glaucoma as well: Five had chronic simple glaucoma, one had closed angle glaucoma, and one had secondary glaucoma. Begg and colleagues ( 4,5) reported seven similar patients. Three of their subjects ( 5; TABLE 2. Visual acuities and visual field defects in affected eyes Case Description of visual no. Visual acuity field loss 20/ 40 + 3 Inferior altitudinal. denser nasally 2 20/ 40 Inferior altitudinal. denser nasally 3 20/ 300 Generalized constriction with cecocentral scotoma 4 20/ 20 Nasal. denser inferiorly 5 20/ 200 ( 0.0.) Complete inferior altitudinal 20/ 30 + 3 ( O. S.) Upper nasal quadrant cases 5- 7) carried the diagnosis of ocular hypertension prior to developing ischemic optic neuropathy. In contrast to those of our patients, their optic cups were described as " wide," " wide, deep," and " suspicious." All three also had ischemic or valvular heart disease and were 72 years of age or older. In a discussion of AlaN following cataract surgery, Hayreh ( 2) described a group of patients who had elevations in lOP in the affected operated eye. The elevations in lOP noted by him were of the same magnitude observed in our patients. Hayreh stated that the perfusion pressure in the optic nerve is dependent on a balance between systemic blood pressure and lOP. Therefore, a fall in blood pressure or a rise in lOP could result in ischemia to the optic nerve head secondary to a fall in perfusion pressure below a critical level. The occurrence of AlaN during open heart surgery ( 6) and the recent documentation of elevations in lOP during cardiopulmonary bypass ( 7) also make for interesting comparison and conjecture. Other observations link AlaN and lOP elevations. Katz and co- workers ( 8) found that patients who had experienced nonarteritic AlaN tended to have peaks in lOP significantly higher than control subjects. They too suggested that increased lOP may be a predisposing factor for the development of acute optic disc ischemia. Perhaps elevated lOP leads to mechanical distortion of optic disc topography, ultimately resulting in hypoperfusion and infarction of the optic nerve head. In this regard Levy and Crapps ( 9) studied movement of the optic disc in response to controlled increases in lOP in enucleated human eyes and found maximum movement near the center of the disc. The greatest displacement occurred at mild elevations of lOP. They commented that this movement might cause compression of blood vessels secondary to mechanical distortion within the lamina cribrosa. Increased lOP has also been implicated as a predisposing factor for central retinal vein occlusion ( 10). Sludging of blood, endothelial damage within the vein, and subsequent thrombosis might result from stretching or compression of the lamina cribrosa caused by pressure fluctuations ( 10). In summary, our observations suggest that elevations in lOP somehow playa role in the development of AlaN in eyes without significant optic disc cupping. If this relationship holds true, it is likely that these eyes represent a subset of the population at risk for AlaN. Whether or not this observation has any bearing on subsequent involvement of the fellow eye ( 11) is not known. However, the potential for prophylactic treatment with I Clill Neuro- ophthalmol. Vol. 9. No. 2, 1989 118 R. L. TOMSAK AND B. F. REMLER ocular hypotensive agents is intriguing. The role of lOP in the rare cases of progressive AlaN ( 12,13) is also open to question at present. REFERENCES 1. Beck RW, Servais GE, Hayreh SS. Anterior ischemic optic neuropathy IX. Cup- to- disc ratio and its role in pathogenesis. Ophthalmology 1987; 94: 1503- 8. 2. Hayreh SS. Anterior ischemic optic neuropathy IV. Occurrence after cataract extraction. Arch Ophthalmol 1980; 98: 1410- 6. 3. Foulds WS. Visual disturbances in systemic disorders: optic neuropathy and systemic disease. Trans Ophthalmol Soc UK 1969; 89: 125- 46. 4. Begg IS, Drance SM, Sweeney VP. Haemorrhage on the disc- a sign of acute ischaemic optic neuropathy in chronic simple glaucoma. Can JOphthalmoI1970; 5: 321- 30. 5. Begg IS, Drance SM, Sweeney VP. Ischaemic optic neuropathy in chronic simple glaucoma. Br J Ophthalmol 1971; 55: 73-- 90. 6. Sweeney PJ, Breuer AC, Selhorst JB, et al. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology 1982; 32: 560- 2. 7. Larkin DFP, Connolly P, Magner JB, et al. Intraocular pressure during cardiopulmonary bypass. Br J Ophthalmol 1987; 71: 177-- 80. 8. Katz B, Weinreb RN, Wheeler D. Ischemic optic neuropathy and intraocular pressure [ Abstract]. Ophthalmology 1987; 94 ( suppl 10): 92. 9. Levy NS, Crapps EE. Displacement of optic nerve head in response to short- term intraocular pressure elevation in human eyes. Arch OphthalmoI1984; 102: 782-- 6. 10. Chew EY, Trope GE, Mitchell BJ. Diurnal intraocular pressure in young adults with central retinal vein occlusion. Ophthalmology 1987; 94: 1545-- 9. 11. Repka MX, Savino PJ, Schatz NJ, Sergott RC. Clinical profile and long- term implications of anterior ischemic optic neuropathy. Am JOphthalmoI1983; 96: 478-- 83. 12. Kline LB. Progression of visual defects in ischemic optic neuropathy. Am JOphthalmoI1988; 106: 199- 203. 13. Borchert MB, Lessell S. Progressive and recurrent nonarteritic anterior ischemic optic neuropathy. Am JOphthalmol 1988; 106: 443-- 9. |
