Abstract

At least four mechanisms of branch or central retinal vein obstruction are known. 1 They are (1) venous endothelial proliferation, (2) periphlebitis leading to obstruction, (3) stagnation thrombosis, and (4) pressure from without as in branch arteriovenous nicking or central thickening of the intermediate connective tissue strand at the lamina cribrosa. The usual clinical picture which initially follows the obstruction is too well known to require description. It suffices to say that this is the clinical picture usually erroneously called venous branch or central vein thrombosis. In view of recent work 1 showing the small part actually played by thrombosis in this syndrome, branch venous or central vein obstruction would be a much more accurate term to use. Verhoeff's original fight for this contention should be noted. 2 The myriad fundus changes seen six months to many years after branch or central retinal vein obstruction have been neglected both clinically and

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