High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial. Comparative evaluation of megadose methylprednisolone with dexamethasone for treatment of primary typical optic neuritis. Effects of intravenous methylprednisolone on outcome in MRI-based prognostic subgroups in acute optic neuritis. Ketorolac versus prednisolone versus combination therapy in the treatment of acute pseudophakic cystoid macular edema.
To compare the effect of high-dose intravenous corticosteroid therapy with placebo in the treatment of recent traumatic optic neuropathy (TON).
                In a double-masked placebo-controlled clinical trial, 31 eyes of 31 patients were randomly assigned to two groups. Patients with history of trauma < or =7 days were included. Unconscious patients, eyes with penetrating trauma and candidates for decompression surgery were excluded. The treatment group (16 eyes) received 250 mg methylprednisolone intravenously every 6 h for 3 days, then 1 mg/kg prednisolone orally for 14 days; the placebo group (15 eyes) received 50 ml normal saline intravenously every 6 h for 3 days, then placebo for 14 days. Visual improvement was considered as a decrease of at least 0.4 logMAR in final visual acuity.
                Mean final BCVA (best corrected visual acuity) in the treatment group was 1.11+/- 1.14 and the placebo group was 1.78 +/- 1.23. This difference was not significant (P = 0.13). Visual acuity was improved in 68.8% of the treatment group and 53.3% of the placebo group, but the difference was not statistically significant (P = 0.38). The difference between initial and final BCVA in both groups was determined to be statistically significant (P < 0.001 and 0.010 respectively).
                Our study confirms earlier findings that there is no difference in visual acuity improvement between intravenous high-dose corticosteroids and placebo in treatment of recent TNO. To compare the efficacy of intravenous methylprednisolone and intravenous dexamethasone on visual recovery and evaluate their side-effects for the treatment of optic neuritis.
                Prospective, randomized case-controlled study including 21 patients of acute optic neuritis presenting within eight days of onset and with visual acuity less then 20/60 in the affected eye who were randomly divided into two groups. Group I received intravenous dexamethasone 200 mg once daily for three days and Group II received intravenous methylprednisolone 250 mg/six-hourly for three days followed by oral prednisolone for 11 days. Parameters tested were pupillary reactions, visual acuity, fundus findings, color vision, contrast sensitivity, Goldmann visual fields and biochemical investigations for all patients at presentation and follow-up.
                Both groups were age and sex-matched. LOGMAR visual acuity at presentation was 1.10 +/- 0.52 in Group I and 1.52 +/- 0.43 in Group II. On day 90 of steroid therapy, visual acuity improved to 0.28 +/- 0.33 in Group I and 0.36 +/- 0.41 in Group II ( P =0.59). At three months there was no statistically significant difference in the color vision, contrast sensitivity, stereoacuity, Goldman fields and the amplitude and latency of visually evoked response between the two groups. The concentration of vitamin C, glucose, sodium, potassium, urea and creatinine were within the reported normal limits.
                Intravenous dexamethasone is an effective treatment for optic neuritis. However, larger studies are required to establish it as a safe, inexpensive and effective modality for the treatment of optic neuritis. Treatment of acute optic neuritis with steroids has been shown to hasten visual recovery without affecting the final degree of recovery. However, MRI-clinical studies indicate that patients with long optic nerve lesions, particularly those that involve the nerve within the optic canal, may have a worse prognosis for recovery of vision. Partly because such lesions could lead to swelling and subsequent ischemic optic nerve damage, steroids could have a selective beneficial effect on this subgroup of patients. The present randomized trial was designed to test this possibility. Sixty-six patients with acute optic neuritis received IV saline or IV methylprednisolone. The clinical, psychophysical, electrophysiologic, and MRI outcomes were assessed after 6 months. Patients with short lesions presented earlier than those with long lesions (involving three or more 5-mm-thick slices of any part of the optic nerve, as well as its intracanalicular portion), and lesion length was significantly less in patients presenting within a week of onset of symptoms. Lesions also tended to lengthen during follow-up in individual patients. Treatment did not limit lesion length in either the long or short lesion subgroup and had no significant effect on final visual outcome. We conclude that steroids do not improve visual outcome or lesion length in patients with acute optic neuritis. To evaluate the efficacy of ketorolac tromethamine 0.5% ophthalmic solution, prednisolone acetate 1.0% ophthalmic solution, and ketorolac and prednisolone combination therapy in the treatment of acute, visually significant, cystoid macular edema (CME) occurring after cataract extraction surgery.
                Randomized, double-masked, prospective trial.
                Twenty-eight patients who had undergone cataract extraction and in whom clinical CME developed within 21 to 90 days after cataract surgery.
                Patients were randomized to topical therapy with ketorolac (group K), prednisolone (group P), or ketorolac and prednisolone combination therapy (group C) four times daily. Treatment was continued until CME resolved or for 3 months, whichever occurred first. Treatment was then tapered over 3 weeks. Examinations were monthly and included Snellen visual acuity, contrast sensitivity, Amsler grid, slit-lamp examination, dilated fundus examination, and fluorescein angiography.
                Twenty-six of 28 patients completed the study. Patients were enrolled an average of 48 days after surgery. The average improvements in Snellen visual acuity were as follows: 1.6 lines in group K, 1.1 lines in group P, and 3.8 lines in group C. This reached statistical significance for all visits when group C was compared with group P, and for visits 4 and 5 when group C was compared with group K. Group C reached a mean change of two lines or more by visit 2; at no time did either group K or P reach a mean two-line improvement. At no time was a significant difference detected between group K and P with regard to visual acuity or change from baseline. A two-line or more improvement in Snellen acuity was achieved in 16 of 26 patients (61%). Analysis by group revealed four of eight patients (50%) in group P, six of nine patients (67%) in group K, and eight of nine patients (89%) in group C who had achieved a two-line or more improvement. In patients who did improve two lines or more, improvement occurred an average of 2.75 months after initiating therapy in group P, 1.43 months in group K, and 1.33 months in group C. Improvements in contrast sensitivity and leakage on fluorescein angiography tended to mirror improvements in Snellen acuity.
                Treatment of acute, visually significant pseudophakic CME with ketorolac and prednisolone combination therapy appears to offer benefits over monotherapy with either agent alone. Patients were more likely to experience recovery of two lines or more of visual acuity. Patients treated with combination therapy or ketorolac monotherapy responded more quickly than did patients treated with prednisolone alone.
There is no conclusive evidence of benefit in terms of recovery to normal visual acuity, visual field or contrast sensitivity with either intravenous or oral corticosteroids at the doses evaluated in trials included in this review.