glaucoma is apt to approach concentric limitation; namely, more like the field in simple atrophy. This is consistent with the fact that simple glaucoma in many cases possesses the characteristics of glaucoma plus atrophy of the optic nerve.

Vitreous. During the acute attack, the vitreous may become slightly turbid by transudation of serum from the vessel of the ciliary body and the chorioid and may become filled with fibrin. In some chronic cases in which absolute glaucoma is reached the development of small blood vessels in convoluted loops springing from the vessels of the discs has been observed. Any process that increases the volume of the contents of the vitreous chamber, as hemorrhage, neoplasm, profuse serous or plastic exudation, may by pushing iris and lens forward produce an attack of acute glaucoma.

Buphthalmos. Reis (Graefe's Arch. f. Ophth. V. LX. 1905) states that there is always obliteration of the anterior scleral venous channels (Schlemm's canal) in buphthalmos. Seefelder (Graefe's Arch. V. LXIII. 1906) mentions the abnormal position and abnormal narrowing of Schlemm's canal and the imperfect and insufficient differentiation of the cornea-scleral junction. In all of the cases in which the eye has been examined microscopically obliteration of Schlemm's canal has been reported. This is thought to be a defect in development. Magitot (Ann. d'Oculis CXLVII) suggests that injury to mesoderm which pushes itself between the ectoderm and anterior surface of the lens would account for the failure in development of Schlemm's canal. The changes that occur in the tissues of the eye appear to be largely due to the stretching consequent on the more or less uniform distentions of the globe as a result of hypertension.

Cornea. This portion of the fibrous membrane is enlarged, globous or flattened, irregularly thinned, particularly at the periphery, where it may be as thin as tissue paper, nebulous because of the stretching of its fibers principally, but in some degree (differing in different cases) to edema of the epithelial layer. Fissures occur in Descemet's membrane.

Anterior Chamber. This is very deep in the greater number of cases. However, this rule has many exceptions.

The vascular tunic may be congested in young infants, but atrophy soon develops and may reach an extreme degree. The sclera ordinarily becomes quite thin throughout, but may retain almost a normal thickness at the equator of the globe and posteriorly. Posterior sclera ectasae may develop. The iris, as a rule, hangs free from the cornea, often tremulous because of retraction of the lens beyond the iris plane. In some cases the iris is partly or totally adherent to the posterior surface of the cornea.

The vascular membrane (iris, ciliary body and chorioid) and the retina become atrophic, the atrophy varying in degree in various parts. Detachment of the retina may occur, often preceded by or accompanied by subretinal hemorrhage. The optic disc becomes deeply cupped and the tissues of the optic disc and optic nerve extremely atrophied. The crystalline lens may become cataractous and shrunken. Spontaneous rupture of the suspensory ligament with consequent subluxation of the lens may follow.

Secondary Glaucoma. The pathological conditions that precede secondary glaucoma are many and differ widely. They may be briefly classified as:

1. Those that cause a partial or complete closure of the lymph spaces and Schlemm's canal by cicatrical contraction, as in sclero-keratitis.

2. Those that cause obstruction to the lymph spaces at the filtration angle by the deposition of fibrin or cellular elements, as in iritis, hemorrhage into the anterior chamber, etc.

3. Those that cause obstruction of the filtration angle by advancement of the iris and lens, as occurs when the volume of the contents of the vitreous chamber is increased, as from retinal or chorioidal hemorrhage or neoplasm.

The various changes are so numerous that they need not be described further here. The ultimate changes due to high tension resemble those already described.

Dr. John E. Weeks' Paper on Pathology of Glaucoma

Discussion,
E. V. L. Brown, M.D.,
Chicago.

I would like to emphasize one of the newer features of the pathologic anatomy of glaucoma, one which has received too little attention in this country: the lacunar or cavernous atrophy of the optic nerve.

The name accurately describes the condition. Tiny clear spaces form in the lamina cribrosa and in front and behind it in the nerve tissue. Their exact nature is unknown. Usually they are entirely empty, often they are traversed by fine glial fibers. They seem to be in no relation to the blood vessels. Adjoining lacunae are supposed to fuse to form larger cavernae and these finally merge and constitute the final glaucoma cup. The lamina may then bridge across the space like a cord, or lie back against the end of the nerve trunk.

Schnabel considered all glaucoma cups to be formed in this way, independent of tension. His views were strongly supported by Elschnig, but as vigorously opposed by others. Axenfeld cites the fact that the glaucoma cup may disappear after operation. (I myself have seen a cup of 7 D. reduced to 1 D. in the course of a year after the tension had been lowered from 62 to 12.) Stock found the same lacunae in eight cases of myopia. The last extended study of the subject was made by E. v. Hippel, who found lacunae in 20 of 33 cases (60 per cent); enough certainly to make one look for them carefully in every case. He publishes a large number of excellent photo-micrographs, but none more typical than one I have in my possession.

I have been especially interested in this subject because I have met with a complete and total glaucoma cup, with the typical (ampulliform) undermining of the scleral ring, in a pair of eyes without increased tension. The (Schiotz) tonometer was used daily for 70 consecutive days and never registered more than 12-14 mm. Hg. The man had been blinded by wood alcohol. At the time I could find no other report in the literature, but overlooked a publication by Lewin and Guillery. Friedenberg has since reported cases of the same nature.

If other conditions than increased tension can produce a typical (ampulliform) glaucomatous excavation of the disc, why may not the cavernous atrophy and cup in glaucoma be due in part at least to similar processes, possibly in the nature of a toxic oedema of the nerve, either in association with tension or independent of it, as contended for by Schnabel?