Investigations of the potential value of cortisone for treating ocular inflammation followed the early and considerable investigations by Wintersteiner and Pfiffner (1935), Mason el al. (1940), and Kendall (1940) on the chemistry of steroid substances produced by the adrenal cortex; the demonstration by Sprague et al. (1948) and Thorne el al. (1949) of the clinical effect upon patients suffering from disorders such as Addison's disease; and the dramatic improvement recorded by Hench et al. (1949) in patients with rheumatoid arthritis. Within a relatively short time, some of the most obvious effects on inflammatory process in the eye were established as they had been for other parts of the body (Gordon and McLean, 1950; Woods, 1951; Scheie el al., 1951; Fitzgerald et al., 1951; Lavery el al., 1951; Duke-Elder et al., 1951;Leopold et al., 1951;and Olson et al., 1950). Capillary permeability was decreased; cellular exudation reduced; and granulation-tissue formation, fibroblastic reaction, and the formation of new vessels were inhibited. The steroid also inhibited the ocular inflammatory response to direct organismal infection, to anaphylactic or allergic reactions, and to the injection into the eyes of nonbacterial irritants such as glycerin, jequirity, trimethylamine, colchicine, or talc (Leopold el d.,