Glaucoma | Page 3

a large proportion of cases of glaucoma; and may be
necessary to the production of the highest intra-ocular tension. A
sudden relaxation of the arterial walls, that would permit the arterial
blood pressure to make itself felt in the eye, might cause an important
rise of intra-ocular tension and may be a factor in the etiology of acute
attacks. It affords a possible mechanism through which may be
produced the recognized glaucomatous effects of certain nerve
disturbances. But such attacks are not commonly associated with
noticeable flushing of the head and face generally; and paralysis of the

cervical sympathetic is known to lower the intra-ocular tension.
Capillary blood pressure must lie between the arterial blood pressure
and the venous blood pressure. It must be closely associated with the
nutritional processes like secretion or inflammation; beyond this we
know little about it. The association of increased blood pressure with
glaucoma seems to be generally an indirect one through vascular
lesions and disturbances of nutrition.
Obstructed Outflow
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