It seems that both of these theories afford an explanation for many of the secondary pathological manifestations which characterize the intra-ocular tissues during a glaucomatous onset. Fischer criticizes the Henderson theory on the ground that increased blood pressure alone does not lead to edema--edema is thwarted by high blood pressure. On the other hand, if Fischer believes that sclerosis of the meshwork of the iris angle is a result and not a cause of glaucoma, then it would seem that Henderson has the better of the argument. The physiological changes in this structure, which take place with advancing age, can rightfully be looked upon as a predisposing factor in glaucoma. Dr. Jackson has presented all other phases of this part of the symposium in such a comprehensive manner that nothing further remains to be said. Pathology of Glaucoma BY JOHN E. WEEKS, M.D., New York City. In reviewing the pathology of glaucoma it seems proper to consider the various structures and tissues of the eye in logical order. _Lids and Conjunctiva._ "The only change observed in these tissues is a reflex edema, excited apparently by pressure on the ciliary nerves and, probably, irritation of the vaso-motor fibers of the sympathetic." _Lachrymal Gland._ Hyper secretion due to reflex irritation. _Cornea._ As has been shown by Priestley Smith, the cornea in glaucomatous eyes is, as a rule, smaller than in non-glaucomatous eyes, the mean of a series of measurements being 11.1 mm. horizontally and 10.3 mm. vertically in glaucomatous and 11.6 mm. horizontally and 11 mm. vertically in non-glaucomatous eyes. In cases of considerable increase of tension, particularly if the onset is sudden, the circulation of lymph in the cornea is interfered with, the anterior layers of the cornea become edematous, the spaces between the lamellae filled with albuminous fluid. Some of this fluid finds its way through Bowman's membrane, apparently by way of the minute channels which permit the passage of small nerve twigs, and enters the epithelial cell layer. The fluid finds its way between the epithelial cells in the deeper layers, apparently being taken into some of the superficial cells by imbibition. Some of the swollen surface cells open spontaneously and discharge their contents, others drop off. The process causes a roughening of the surface of the cornea and produces a faint haziness. There is another form of haziness that develops on sudden rise in tension and completely disappears on subsidence of the tension. This is due, as has been shown by V. Fleischl (Sitzungsberichle d. Weiner Akad. d. Wissensch, 1880) and others, to increased tension on the fibrillae of the cornea, a double refraction being induced. In cases of long continued increase of tension minute permanent vesicles form in the epithelial layers, particularly in the superficial portion. Anaesthesia of the cornea develops, due to pressure on the nerve fibers that are