A reservoir with a free outlet can only fill during a flood; and then quickly empties itself again. The outflow channels in the normal eye provide for carrying away of the waste products of such an active nutrition, that it is hard to think they will become inadequate in glaucoma until there has been a marked decrease from their normal capacity. Priestley Smith has pointed out that the glaucomatous eye softens more slowly than the normal eye after enucleation, in spite of the fact that a greater force is operating to drive fluid out of the eye. In his recent tonometric studies Schoenberg noted that under manipulation the glaucomatous eye softened more slowly than the normal eye; and suggests this diminished drainage as an important evidence of glaucoma.
Obstructed outflow might begin in an abnormal tendency of the tissues to retain fluid, a tendency that Fischer might locate in the colloids. The increase of intra-ocular pressure noted in cases of uveal inflammation, to be presently referred to, may be due to some such tendency. But it is rational to ascribe to obstruction of the filtration angle of the anterior chamber, the important part it has been supposed to play in the pathology of glaucoma. However this obstruction may be brought about, whether by thickening of the iris root during dilatation of the pupil, pushing forward of the iris root by the larger ciliary processes of age, or the enlarged crystalline lens pressing on the ciliary processes; or by inflammatory adhesion of the iris to the filtration area; ballooning of the iris, or its displacement by traumatic cataract; or adhesion to the cornea after perforating ulcer in the secondary glaucomas; or whether the obstruction is due to the accumulation of experimental precipitates, as shown by Schreiber and Wengler, or possibly of pigment granules into Fontana's space; or a process of sclerosis closing the spaces by contraction of new-formed connective tissue, or the covering over with proliferating implanted epithelium following injury opening the anterior chamber; glaucoma follows impairment of this drainage space, and lessened outflow through it. This blocking of the angle of the anterior chamber must be regarded as an established fact in the etiology of glaucoma. But because it is so definitely established, and because so much work has been done with reference to it, we may attach to it an undue importance.
The escape of the outflow of fluid from the eye is ultimately through the veins. The general venous blood pressure is so low (often negative in the great veins of the neck during inspiration) that no obstacle can come from it to the ocular outflow. The venous blood pressure permits the eyeball to become perfectly soft. We have all seen tension of 5 mm., or even less; and general venous pressure does not rise to the normal intra-ocular tension. Increased intra-ocular pressure requires that there must be some obstacle that keeps the intra-ocular fluid from reaching the general venous system. This may be in the lymph drainage system of the eye; but it may also be in the ocular veins themselves.
Experimentally the eyeball can be made to burst by tying all the venous outlets from it. I have seen very high intra-ocular tension develop in a few hours after general thrombosis of the orbital veins. The absence of the canal of Schlemm is noted in congenital buphthalmos. The enlargement of the anterior perforating veins is an old symptom of chronic glaucoma. Obstruction to outflow of blood through the vorticose veins, by the increased intra-ocular pressure, has long been a recognized explanation of the malignant tendency of glaucoma—a part of the vicious circle established in this disease. There is reason that we should give careful attention to the views of Heerfordt and Zirm, that obstruction to the venous outflow may be the effective cause of the disease. Zirm believes the venous plexus of the choroid is an essential part of the mechanism for the regulation of intra-ocular tension, the necessary vaso-motor control depending on nerve centers situated in the iris.
Nerve Control
The accurate control of normal intra-ocular pressure, by mutual adjustment of inflow and outflow of fluid, is scarcely conceivable without some highly specialized, extremely sensitive nerve mechanism to preside over it. This is suggested by analogy with the regulation of secretion in the lacrimal, salivary, or peptic glands, or the maintenance of blood pressure in the heart and arteries. Clinical observations point the same way. Many patients connect their attacks (especially their earlier ones of ocular discomfort, impaired vision, haloes around the light, and dilated pupil) with social excitement, anxiety, worry, anger or fatigue. A patient of mine gave up her card parties, because an exciting game generally ended in blurred vision, a rainbow around the light, and a dilated pupil, and sometimes an aching eye. Another woman watching beside her dying husband and exposed to extreme cold, had her first attack of glaucoma, so severe as to destroy the sight of one eye. The other eye, also affected at the time, recovered good vision, and has remained several years without a second attack and without treatment.
Laqueur's first attack occurred at the end of a long exhausting morning in the operating room, with luncheon delayed two hours. The connection of his later attacks with anger, worry, embarrassment, even the excitement of watching a play at the theatre, was noted again and again. In Javal's case, the attack fatal to one eye came at the culmination of an exciting electoral campaign. The other eye was stricken at the termination of the Dreyfus case, in which Javal was intensely interested. There seems to be a special liability to glaucoma among those residing at high altitudes, best explained by nerve influence. The frequency of glaucoma among Jews may be due to a small cornea, as suggested by Priestley Smith; but it is quite as reasonable to connect it with a racial excitability or nervous instability. More definite knowledge of the nervous mechanism concerned in the regulation of intra-ocular pressure and the production of glaucoma is much needed.
Alterations of Fluids and Tissues
The influence of increased affinity of the tissues for fluid has already been referred to. That a similar obstacle to the escape of fluid from the eyeball might be due to a change of character in the fluid, is a conception that has been entertained as a working hypothesis, and much experimental and analytical work has been done to test its correctness. This work has been so slightly related to practical ophthalmology, and so contradictory in its results that alterations in the fluids can only be regarded as a possible etiologic factor. Glaucoma secondary to intra-ocular hemorrhage, operations on the lens or its capsule, or severe nutritional disturbance may be capable of such explanation.
Different Kinds of Glaucoma