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قراءة كتاب Glaucoma A Symposium Presented at a Meeting of the Chicago Ophthalmological Society, November 17, 1913

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Glaucoma
A Symposium Presented at a Meeting of the Chicago Ophthalmological Society, November 17, 1913

Glaucoma A Symposium Presented at a Meeting of the Chicago Ophthalmological Society, November 17, 1913

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دار النشر: Project Gutenberg
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atrophies and contracts. There is very little evidence of small-cell infiltration or the formation of cicatrical tissue. Numerous slits may develop in the iris through which the fundus of the eye may be seen (polycoria). The pigment layer does not atrophy in proportion to the stroma of the iris; by the contraction of the stroma of the pigment layer is doubled upon itself at the pupillary margin, forming a black ring of greater or less width (ectropian uveae). The iris becomes attached to the pectinate ligament and to the endothelium of Descemet's membrane. In a very few cases the closure of the angle is not complete at the apex, a small space remaining comparatively free for a long time. The adhesion of the iris to the pectinaform ligament and cornea is not uniform at all parts of the periphery; it varies in width. Portions of the iris angle may remain open while other parts are closed. Where the iris tissue lies in contact with the cornea, the stroma of the iris almost totally disappears. In some cases the iris becomes totally adherent to the cornea.

Ciliary Body and Chorioid. In acute glaucoma there is congestion of the entire uveal tract, the congestion partaking more of a venous stasis than of an active or arterial congestion. The vessels of the ciliary process, which are larger and more tortuous in adults of advanced years than in the young, become enormously distended, causing almost complete obliteration of the perilental space. They press against the root of the iris and the equator of the lens, forcing them forward. There is edema of the ureal tract, apparently from transudation of serum. Many small, and sometimes rather large hemorrhages may occur. There is but little small cell infiltration, indicating almost total absence of what is ordinarily recognized as true inflammation. It is probable that the secretion from the glandular zone of the ciliary body is increased.

On subsidence of the congestion, as after miotics or iridectomy, the tissues may return to very nearly a normal condition. The iris recedes from contact with the ligamentum pectinatum and cornea and the filtration angle is again open. In some cases the iris becomes adherent to the head of the ciliary processes and, when atrophy of the ciliary body occurs, is drawn backward at the base of the iris by the receding tissues. If the hypertension persists or is repeated at varying periods, a slow atrophy of the uveal tract sets in. Eventually the ciliary body becomes very much reduced in thickness, is flattened out, the ciliary processes reduced in size and the blood vessels disappear or are reduced much in caliber. Those that persist possess walls that are much thickened. This is particularly true of hemorrhagic glaucoma.

In advanced absolute glaucoma the chorioid may become reduced to a very thin membrane consisting of connective tissue and pigmented cells, scarcely distinguishable even by moderate powers of the microscope. Atrophy is marked in the vicinity of the venae vorticosae. Czermak and Birnbacher describe proliferation of the endothelium of the large veins with contraction and obliteration of their lumen.

Optic Nerve and Retina. In the acute form the retina and optic nerve present the same condition that is present in the vascular tunic; namely, that of venous stasis with the consequent edema. Frequently minute hemorrhages occur in the retina, particularly in violent acute attacks. Cupping of the discs slowly develops, causing more or less stretching of the nerve fibers over the edge of the cup. The gradual diminution of the field of vision is due in greater part to death of peripheral nervous elements of the retina, those parts of the field farthest removed from the large arterial trunks suffering first. The arrangement of the arteries at the disc, passing out as they do from the nasal side, of necessity make the vessels that pass to the temporal part of the retina longest and of less caliber. These vessels and their terminals are first to suffer marked diminution in size; death of the perceptive elements supplied with nutrition by these vessels follows. For this reason the nasal part of the field of vision is more often the first to disappear. In congestive (inflammatory) glaucoma, the typical field of vision shows most marked contraction on the nasal side. The disturbance of the nutrition of the retina accounts in greater part for the various forms of visual field met with.

Death of all of the perceptive elements of the retina eventually occurs. The loss of nutrition is apparently not the whole cause of blindness. Atrophy of the nerve fibers follows death of retinal neurons, but atrophy of some of the nerve fibers may be, and probably is, due to the pressure and traction exerted upon them at the margin of the disc. It is probable that too much importance has been given to this mode of interference with the nerve fibers. However, the change in the position of the lamina cribrosa must exert a deleterious effect, particularly on those fibers which pass through the peripheral meshes, the shape of which must necessarily be much distorted. In glaucoma simplex, which is largely devoid of marked congestive periods (acute attacks), a surprisingly high degree of acuity of vision may exist with a deep excavation and pale nerve. Careful studies of the retinal vessels in glaucoma (Verhoeff Arch. of Ophth. XLII. p. 145; Opin. Soc. Française d'Ophth. 1908) disclose the fact that an increase in the elastic tissue and connective tissue elements occurs in some cases, also proliferation of the endothelial cells, which serve to irregularly narrow and, in some instances, obliterate the lumen of the vessel. Arteries and veins are both affected. Hyaline degeneration of the media also occurs. The process is not uniform.

Glaucomatous Cup. The excavation of the disc progresses slowly and is due in part to stretching the fibers of the lamina cribrosa pressing this structure outward, and partly to atrophy and disappearance of the nerve tissue and much of the vascular tissues in the nerve head. The displacement backward of the lamina cribrosa may cause that structure to lie behind the outer surface of the sclera. Atrophy and cystic degeneration of the nerve trunk follows destruction of retinal neurons and cupping of the disc. Neuroglia remains in part. Connective tissue elements increase in the optic nerve as the nerve fibers disappear.

Glaucomatous Ring. The development of the pale circle which surrounds the disc, particularly in glaucomatous eyes, is due to a very slight recession of the pigment layer of the retina and of the margin of the chorioid at this point with some atrophy, apparently consequent on the beginning retraction of the lamina cribrosa and slightly increased pressure of the nerve fiber layer on the underlying tissues at the margin of the disc. This permits the sclera to show through a very little at this part. In some eyes in which there is a beginning sclero-chorioiditis posterior, the condition is very similar to that presented by the glaucomatous ring.

Field of Vision. The two pathological processes that operate to destroy the function of the retina suffice to produce scotomata in the field of vision of varying shapes. The typical glaucomatous field in the acute cases shows a defect most pronounced to the nasal side. As has been shown by Bjeraum, the blind spot corresponding with the optic disc is enlarged in glaucoma, a relative scotoma often connecting it with the blind nasal portion of the field either above or below the horizontal meridian (Straub). The field in a simple

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