S85 CURRENT RESEARCH SURVEY OF OPHTHALMOLOGY VOLUME 44 • SUPPLEMENT 1 • OCTOBER 1999 © 1999 by Elsevier Science Inc. 0039-6257/99/$19.00 All rights reserved. PII S0039-6257(99)00093-4 Methylprednisolone Therapy for Retinal Laser Injury Yoram Solberg, MD, PhD, Galina Dubinski, PhD, Marina Tchirkov, MSc, Michael Belkin, MD, MA, and Mordechai Rosner, MD, MSc The Goldschleger Eye Institute, Tel-Aviv University and Sheba Medical Center, Tel-Hashomer, Israel Abstract. Objective: Laser photocoagulation treatment of the posterior pole of the retina is often com- plicated by immediate visual impairment, which is caused by the unavoidable laser-induced destruction of the normal tissue adjacent to the lesion. A neuroprotective therapy aimed at salvaging this normal tissue might enhance the benefit obtained from treatment and permit safe perifoveal photocoagula- tion. To determine whether corticosteroids can provide neuroprotection during photocoagulation, we examined the effect of methylprednisolone on laser-induced retinal injury in a rat model. Methods: Argon laser lesions were inflicted on the retinas of 36 rats and were followed immediately by intraperi- toneal injections of high-dose methylprednisolone or saline. The animals were sacrificed after 3, 20, or 60 days, and their retinal lesions were evaluated histologically and morphometrically. Results: No histo- pathologic differences were observed between the treated and control animals. Methylprednisolone treatment was demonstrated to posses some neuroprotective effect for a short time after laser exposure, but was ineffective in ameliorating the long-term results of retinal laser injury. Conclusions: On the basis of our results, we suggest that high-dose methylprednisolone treatment is ineffective in ameliorating laser-induced retinal injury. Other drugs should be investigated for their potential role as neuroprotec- tive agents to prevent the spread of retinal laser damage. (Surv Ophthalmol 44 [Suppl 1]:S85–S92, 1999. © 1999 by Elsevier Science Inc. All rights reserved.) Key words. corticosteroids • laserphotocoagulation • methylprednisolone • neuroprotection The use of lasers is becoming increasingly wide- spread in research, industrial, and military fields, and accordingly, it accounts for a growing number of occupational eye accidents. 18,51,58 Most of these oc- ular injuries lead to retinal destruction with massive photoreceptor loss and severe visual impairment. 34,39 Similar visual impairment is often observed after therapeutic retinal photocoagulation treatments. Ophthalmic laser treatment is the standard ther- apy for many vision-impairing retinal disorders. One such disorder is age-related macular degeneration (AMD), the leading cause of new cases of legal blind- ness in developed countries. 56 Age-related macular degeneration induces pathologic changes in the outer layers of the retina. In advanced stages of the disease, choroidal neovascular elements (CNVs) in- vade the subretinal space, ultimately resulting in the formation of a disciform, fibrovascular membrane. The retina over the membrane gradually degener- ates and loses its photoreceptor cells, 11,21 which even- tually leads to severe impairment of visual acuity. The efficacy of laser photocoagulation treatment for juxtafoveal CNVs in patients suffering from vi- sion-impairing AMD was demonstrated by the Macu- lar Photocoagulation Study in 1990 55 : laser photoco- agulation treatments effectively delayed or prevented the deterioration of different visual parameters. However, most of the laser-treated eyes experienced an immediate decline in visual acuity after treatment (i.e., loss of 3 lines, on average, from baseline on the acuity chart), and 18% of patients suffered from se- vere visual loss (i.e., 6 or more lines from baseline) as a direct result of the treatment. A similar, even more severe, complication was observed when subfoveal macular CNVs were treated with argon laser photo- coagulation. 53,54 Immediately after treatment, 20% of eyes exhibited severe visual loss. This immediate decline in visual acuity is a result of the dynamic expansion of the laser-induced le- sion, which involves destruction of the normal neu- rosensory retinal tissue located in the fovea just in- ternal or adjacent to the treated CNVs. 5,12 Therefore,