The increasing number of reports during the past two years1 of the results of heparin therapy in retinal venous occlusion should focus interest again on the various mechanisms by which this condition is produced, of which there are four. As will be shown, these four different types of pathologic change are by no means equally amenable to this anticoagulant therapy. In the present paper, special emphasis is placed on the differential diagnostic points which determine the pathogenesis of the occlusion and hence the success of therapy with heparin and dicoumarin (3,3′-methylene-bis[4-hydroxycoumarin] ). The pathogenesis of the first and perhaps the most frequent type of occlusion of the central retinal vein, that on the basis of systemic angiosclerosis in older persons, has been elucidated by the investigations of Harms,2 Scheerer,3 Verhoeff4 and Hertel.5 In the course of an essentially chronic sclerotic atrophic process, which affects the central