Correlation between optic disc atrophy and aetiology: anterior ischaemic optic neuropathy vs optic neuritis.

BACKGROUND: The morphologic features of swollen disc in the acute stage of optic neuritis and anterior ischaemic optic neuropathy (AION) have been extensively investigated in contrast to the morphologic features of optic disc atrophy after these events. OBJECTIVE: : A prospective study to evaluate the morphologic features of optic disc atrophy 6 months or more after optic neuritis and nonarteritic AION. PATIENTS AND METHODS: A total of 35 optic discs after nonarteritic AION (n=27) and 24 after optic neuritis (n=19) in otherwise healthy subjects have been evaluated by direct fundoscopic examination with a +90 diopters lens and optic disc photography. The average age of patients at the onset of AION was 57.8 years (range: 38-80) and at the onset of optic neuritis was 32.6 (range: 19-46). The female:male ratio was 18 : 17 in the former and 15 : 9 in the latter. The evaluated parameters included: degree of rim pallor (0 to +3), location of rim pallor, height of rim above the retina, depth and width of cup, peripapillary retinal artery to vein (A : V) ratio, and peripapillary pigment epithelial atrophy. A comparison was made also with 17 age-matched normal discs of 17 patients. Statistical significance was calculated with chi(2) and Fisher's exact test. RESULTS: Most of the discs after AION were paler (+2: 70%, +3: 26%) than after optic neuritis (normal colour: 8%, +1: 58%, P< or =0.007). Rim segmental involvement after AION was usually either superior 'altitudinal' (53%) or inferior 'altitudinal' (29%), whereas after optic neuritis, it was usually either temporal-central (papillomacular) (42%) or diffuse temporal (42%, P<0.0001). Discs had lower A : V ratio (1 : 3, 40%) after AION compared with optic neuritis (1 : 3, 8%) (P=0.007). There were no significant differences between the two groups in height of the rim, cupping, and peripapillary atrophy. CONCLUSIONS: : A combination of the degree of rim pallor, location of rim pallor, and A : V ratio may be of value in assessing the aetiology of optic disc atrophy when no previous clinical data are available and a compressive lesion has been ruled out.

Aggressive systematic treatment for central retinal artery occlusion.

PURPOSE: To report the efficacy of an aggressive systematic regimen for the treatment of acute nonarteritic central retinal artery occlusion (CRAO). METHODS: Eleven patients who had unilateral CRAO with symptoms of fewer than 48 hours' duration were treated with an aggressive stepwise systematic regimen until retinal circulation improved or until all the treatment steps were performed. Five patients with unilateral CRAO and symptoms of fewer than 48 hours' duration were treated in the same institution in an arbitrary nonsystematic manner. The therapeutic steps of the aggressive treatment included ocular massage, sublingual isosorbide dinitrate, intravenous acetazolamide, intravenous mannitol or oral glycerol, anterior chamber paracentesis, intravenous methylprednisolone followed by streptokinase, and retrobulbar tolazoline. After each step, retinal flow was evaluated by three-mirror contact lens. The nonsystematic treatment was arbitrary and included one or several of the above. Visual acuity and complete eye examination data were recorded before and after treatment. RESULTS: Visual acuity and retinal arterial supply were improved in eight (73%) of the 11 patients treated in the stepwise systematic manner. All eight patients in whom visual acuity improved had symptoms for fewer than 12 hours, and the presumed cause was either platelet-derived or cholesterol embolus from atheroma or the patients had glaucoma. Patients in whom visual acuity did not improve had CRAO that was attributed to calcified emboli or primary antiphospholipid antibody syndrome and had symptoms more than 12 hours before treatment. Visual acuity did not improve in all five patients with the nonsystematic treatment regardless of the presumed cause or duration of the occlusion. The success of the treatment in the systematic treatment group was statistically significantly better compared with the outcome of the nonsystematic treated group (Fischer exact test, P = .01). CONCLUSIONS: In the treatment of CRAO, an aggressive systematic regimen including medical and mechanical means may reestablish retinal circulation and improve visual outcome. The cause of arterial occlusion, the nature of occlusive emboli, and the duration of retinal ischemia may determine the visual outcome, but a larger series is warranted to verify the effectiveness of the treatment and the prognostic factors.