There is no generally accepted opinion as to the mechanism of divergence in human eyes. Some authors (Duke-Elder,1Pugh, Alfred Graefe and others) have assumed that divergence is merely a passive function resulting from relaxation of convergence. Brouwer's theory of a convergence center located in Perlia's nucleus has almost universally been accepted (Riley2). The majority of observers find it difficult to believe that of all well regulated functions divergence alone should be without a definite innervation. If the limit of divergence were identical with a position of rest due to complete relaxation of convergence, every person who loses the ability of fusion ought to manifest divergent strabismus, whereas only a certain percentage do. Bielschowsky3stated that active divergence innervation is necessary to overcome esophoria. On the basis of neuromuscular physiologic observations, Bruce4stated that his conception of ocular divergence was that of a combined passive (i.