Glaucoma | Page 7

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.

Pathology of Glaucoma
BY
JOHN E. WEEKS, M.D.,
New York City.
In reviewing the pathology of glaucoma it seems proper to consider the
various structures and tissues of the eye in logical order.
Lids and Conjunctiva. "The only change observed in these tissues is a
reflex edema, excited apparently by pressure on the ciliary nerves and,
probably, irritation of the vaso-motor fibers of the sympathetic."
Lachrymal Gland. Hyper secretion due to reflex irritation.
Cornea. As has been shown by Priestley Smith, the cornea in
glaucomatous eyes is, as a rule, smaller than in non-glaucomatous eyes,
the mean of a series of measurements being 11.1 mm. horizontally and
10.3 mm. vertically in glaucomatous and 11.6 mm. horizontally and 11
mm. vertically in non-glaucomatous eyes. In cases of considerable
increase of tension, particularly if the onset is sudden, the circulation of
lymph in the cornea is interfered with, the anterior layers of the cornea
become edematous, the spaces between the lamellae filled with
albuminous fluid. Some of this fluid finds its way through Bowman's
membrane, apparently by way of the minute channels which permit the
passage of small nerve twigs, and enters the epithelial cell layer. The

fluid finds its way between the epithelial cells in the deeper layers,
apparently being taken into some of the superficial cells by imbibition.
Some of the swollen surface cells open spontaneously and discharge
their contents, others drop off. The process causes a roughening of the
surface of the cornea and produces a faint haziness. There is another
form of haziness that develops on sudden rise in tension and
completely disappears on subsidence of the tension. This is due, as has
been shown by V. Fleischl (Sitzungsberichle d. Weiner Akad. d.
Wissensch, 1880) and others, to increased tension on the fibrillae of the
cornea, a double refraction being induced. In cases of long continued
increase of tension minute permanent vesicles form in the epithelial
layers, particularly in the superficial portion. Anaesthesia of the cornea
develops, due to pressure on the nerve fibers that are distributed to the
epithelium, the compression probably occurring along the course of the
long ciliary nerves, from which the corneal nerves are derived, as they
pass between the choroid