Dr. Edward Jackson's Paper on Etiology and Classification of Glaucoma Discussion, Francis Lane , M.D. Chicago.

Not one of the theories thus far propounded to explain the essential cause of increased intra-ocular tension is satisfactory. Our present day knowledge apparently ceases with a more or less incomplete understanding of the mere circumstance under which increase of tension in general depends.

The question of the source of the normal intra-ocular pressure must first be solved before any discussion of a pathological increase can be engaged in. This question primarily hinges on whether the corneo-sclera is to be regarded as an unelastic capsule with a fixed volume, or as a yielding envelope with an ever changing capacity.

This brings us at once to the consideration of that theory which probably has held our attention for the longest period of time, i. e., the volumetric theory. According to it, the normal intra-ocular tension depends on the volume of fluids within the eyeball. Any variation in the quantity of the contents gives rise to a change in the pressure, therefore, the globe has been regarded as "an elastic capsule, whose capacity, form, and internal pressure depend on the balance struck between a constant inflow, or formation of aqueous, and a proportionate outflow or resorption." (Henderson.)

Hill has satisfactorily demonstrated that, under physiological conditions, the hydrostatic pressure within the eye and the skull is identical; it rises and falls simultaneously; it is the same as the cerebral venous pressure; it is constantly varying, depending directly on the general circulation. Upon these findings Henderson based his opinion that the physiological properties of the tunica fibrosa and the skull are identical, realizing at the same time, that the rigidity of the corneo-sclera, because of its fibrous nature, is not as firm as the cranium. In accepting this belief the inference was that the cubic capacity of both coverings is fixed. Applying these conclusions to the eye, it can be said that the pressure of the fixed intra-ocular volume varies with the venous tension within the bulb, which in turn is influenced by the general circulation. Such a conception, while not strictly in accord with recognized physiological teachings, proves that the normal intra-ocular pressure is not a question of volume content, but that it is purely a question of pressure of a fixed volume within an unyielding capsule. Dr. Jackson virtually puts aside the volumetric theory with his statement, that "the balance of intra-ocular pressure is not maintained by the slight distensibility of the sclero-corneal coat." Further discussion on the inadequacy of the volumetric theory need not detain us.

It is well to recall a few anatomical features because of their bearing on the theories herein considered.

1. The angle of the anterior chamber is a true angle and not an annular sinus.

2. The meshwork of the iris angle (ligamentum pectinatum), a cellular structure at birth, undergoes a progressive and physiological fibrosis with early subsequent sclerosis, until finally it becomes a fibrous structure. The individual strands of this meshwork are more than two times as large at advanced age as at birth, consequently the alveoli of the meshwork becomes markedly reduced in size.

3. The spongy nature of this meshwork affords free access of aqueous to the venous sinus of Schlemm, thence by tributaries into the supra-choroidal space and anterior uveal venous system.

4. Fuchs's iris cripts afford direct access of aqueous to the veins of the iris.

Furthermore, two simple principles are taught by physics: Fluids are incompressible and they seek the lowest hydrostatic level. The application of these perfectly obvious principles to the eyeball makes the intra-ocular pressure the same as that within the elastic venous walls, which is the lowest circulating pressure within the bulb.

To summarize: The aqueous has direct access to the anterior uveal venous system; the physiological thickening of the strands of the meshwork of the iris angle supplies a mechanical obstruction between the anterior chamber and the venous sinus of Schlemm; intra-ocular pressure stands at the same level as the intra-venous, consequently, the hydrostatic pressure is the same on both sides of the iris angle meshwork, because the canal of Schlemm is a secondary venous system; lastly, the outflow of aqueous into the venous sinus is by diffusion, not by filtration, because the pressure is the same on both sides of the meshwork.

These facts and deductions have given rise to the present day circulatory theory of intra-ocular pressure, so we now can approach the predisposing and exciting factors which determine glaucoma.

The central fact to be borne in mind is, if the physiological pressure is vascular in origin and nature, the pathological pressure must likewise be derived from the same source.

Sclerosis of the meshwork of the iris angle is the predisposing factor because it hinders free access of aqueous into the venous sinus of Schlemm. Sclerosis alone, however, will not cause glaucoma so long as access to the iris veins can keep the intra-ocular pressure at the intra-venous level, and, too, as long as the exciting cause is absent.

The exciting cause is vascular, maintained and influenced by the general circulatory pressure. A rise of the general vascular tension alone will not cause glaucoma, because any alteration in intra-ocular pressure resulting would be purely a temporary change, easily taken care of by the extensive access of aqueous to the intra-ocular venous system. When these two factors coexist in their varying combinations, pathological increase of pressure results—in short, glaucoma.

Syphilis, rheumatism, gout, auto-intoxication and many other constitutional disorders are well recognized agencies which induce sclerosis in body tissues, so there can be little doubt that these conditions produce pathological sclerosis of the meshwork of the iris angle. Psychic disturbances, congested portal or renal system, hard mental or muscular work, etc., etc., induce increased pressure of the general circulation, and so simultaneously the intra-ocular pressure.

According to the edema theory advanced by Fischer, glaucoma is "essentially an edema of the eyeball, and for its production we must hold responsible the same circumstances which are responsible for a state of edema in any other part of the body." The magnificent experimental work of this investigator has shown that edema is nothing more or less than an increased capacity of the protein colloid tissues for water; that the most important factor leading to this increased hydration capacity is an abnormal production or accumulation of acid content, effected by those agencies which are instrumental in causing sclerosis and an increase of blood pressure.

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.

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