IT WAS in 1883 that Becker1 gave the first anatomical description of posterior lenticonus in the rabbit, while the first clinical observation in man, by Meyer,2 dates from 1888. As far as the pathogenesis of posterior lenticonus is concerned, it was von Hess * who, on the basis of similar findings in the rabbit and the pig, put forward the theory that the condition was primarily the result of rupture of the posterior capsule of the lens, probably occurring at the embryonic stage, while he admitted that traction of the hyaloid artery might also play an important role. Even though many authors have accepted this hypothesis, others have wondered whether the rupture of the capsule were not, in certain cases at least, an artifact produced by fixation.† This point of view is supported by the fact that 30 cases of posterior lenticonus in animals were described between 1883 and