**4. Glaucoma mechanisms**

**3. Ocular hypertension – The mechanisms**

274 Glaucoma - Basic and Clinical Aspects

ditis (von Graefe) or a secretory neurosis (Donders).

nea or the obliteration of the space of Fontana."\*

*clearly inapplicable to the human eye.*

veins.

Previously mentioned essence of glaucoma, recognized in the mid-1850s, attributed to exces‐ sive formation of intraocular fluid or hyper secretion and assumed to eider a type of choroi‐

The clear concept of the eye mechanisms that were involved in the intraocular pressure pro‐ duction, in that time, was not plain. German anatomist Schwalbe12 began in 1860s the exper‐ imental study of the fluid exchange of the eye, searching the lymphatics in the anterior segment. When the dye is injected into the anterior chamber of the eye, in aqueous solution or suspension, it appears promptly in veins on the surface of the globe! His conclusion was that the anterior chamber is a lymphatic space in open communication with anterior cilliary

Theodor Leber13 also injected dyes into the anterior chamber of the eye of a rabbit, and dis‐ criminated certain border structures. This disclosure stimulated many investigators of that time, including Leber, to investigate a cannular system and Schwalbe, to investigate the an‐ terior chamber angle in animals. Thus Leber discovered normal outflow (on a fresh enucleated mammalian eye), he presented it as a filtration through the trabecular meshwork and a flow through ciliary and vortex veins.His conclusion was that the rate of outflow was, in principle, proportional to the perfusion pressure, except during an initial period, when the perfusion fluid took up the space occupied in the living eye by blood. He actually deter‐ mined filtration coefficients, the forerunners of today's coefficients of aqueous outflow.

Since this outflow was from fresh enucleated eyes at the pressures prevailing in the living eye, Leber reasoned that the same process of outflow must also take place in the normal liv‐ ing eye. To maintain a stable in vivo pressure, the steady loss of fluid must be compensated for by steady formation of an equal amount of fluid, which Leber believed could also take place through a process of filtration. Thus, the filtration theory of aqueous formation and elimination was born. In a few human eyes enucleated in far-advanced stages of glaucoma, Leber found very low filtration coefficients which indicated abnormal resistance to aqueous outflow[14]. This finding fitted in well with the first detailed pathologic report on the condi‐ tion of the chamber angle in far-advanced glaucoma[15]: "The most important finding in genuine glaucoma is the circular adhesion of the iris periphery to the periphery of the cor‐

*\*Although Kieser of Göttingen had clearly shown in 1804 that the spaces described by Fontana in the eyes of herbivores did not exist in man, the term "Fontana's space" was still used in the 1870s and 1880s for the intertrabecular spaces of the human corneoscleral meshwork. Only the detailed studies of the region begun by Schwalbe in 1870 and continued by others made the term "Fontana's space"*

Considering that in either case glaucoma could result from an inflammatory or an obstruc‐ tive process within the angle or from pressure from behind. It was realized almost immedi‐ ately that the peripheral anterior synechiae could be either the cause or the effect of glaucoma. Pathologic specimens which supported these mechanisms were identified and re‐ During 1880s and 1890s, it was observed that chronic inflammatory glaucomas composed two thirds of all glaucomas. Angle closure glaucomas were dominant. Priestley Smith meas‐ ured the horizontal corneal meridian in normal eyes 11.6mm and in glaucomatous eyes 11.2mm[17], what expressed dominance of the angle closure glaucoma in that period. 1888. Priestley Smith also introduced the concept of a predisposition to glaucoma, which consists in progressive narrowing of the circumlental space with age, due to the steady growth of the lens in eyes with small corneas. Anatomicaly, the ciliary processes in states of hyperaemia are crowded forward, pressing the iris against the anterior angle wall. This based on a Smith's experiment on the animal that a small excess of pressure in the vitreous chamber (as little as 4 mm Hg) makes the lens and the suspensory ligament advance in such a manner as to close the angle of the anterior chamber.

Next step was the discovery of shallowness of the anterior chamber as an important role in the mechanism of the acute glaucoma (in the eyes with acute inflammatory glaucoma)[18]. The description of the mechanism: if the pupil dilates in an eye with shallow anterior cham‐ ber, the iris, particularly with its thicker portion, can occlude the filtration angle and, there‐ by, raise the intraocular pressure. If contraction of the sphincter frees the filtration space, the event remains a prodromal attack. At a certain level of intraocular pressure the ocular veins are compressed at their place of entry into the sclera; venous stasis develops with increased transudation; that, and not inflammation, is the true nature of glaucoma.[18]

The Revolution on this field came in 1920.when Curran [19](Kansas City) and Seidel [16] (Heidelberg), on the basis of astute clinical observations, independently announced the con‐ cept of the relative pupillary block.

Curran's paper[19]: "normally the aqueous passes through the pupil from the posterior to the anterior chamber, but it is here contended that in glaucoma this passage is impeded on account of the iris hugging the lens over too great a surface extent. Some of the aqueous gets through while some passes back, forcing the lens and the iris still more forward. "
