Glaucoma | Page 5

for diminished tissue activity; and it is conceivable,
under normal intra-ocular tension, that diminished nutritional activity
may result in the same symptoms as are produced in other eyes by
increased tension. Glaucoma is probably not so much an increase of
tension as a loss of balance between intra-ocular tension and nutritional
activity.
In contrast with the above are the cases marked by sudden elevations of
ocular tension recurring repeatedly over long periods without
permanent visual impairment. Laqueur's case continued of this
character for six years, under the use of miotics, and then was cured by
iridectomy, the cure remaining permanent with normal vision until his
death after 30 years. Millikin has reported the case of a patient who in
five years had "many hundreds" of attacks, in which vision was
impaired, haloes appeared about the light, the pupil dilated, the cornea
became steamy, and tension rose to plus T. 1 or plus T. 2. After
iridectomy the attacks ceased, leaving no pathological cupping of the
disc, full vision, and a good field. I have seen cases of this type in
women under middle age, and of marked nervous instability.
A third type which will come to be more generally recognized, as the
tonometer comes to be more widely used, includes cases in which there
is little beside the increase of intra-ocular tension to justify their
mention in a discussion on glaucoma. A patient, then aged 21, suffered
three years ago from a scotoma almost central; and was first seen six
months after that with a macular choroidal atrophy and abnormal
pigmentation. She suffered, we afterwards concluded, from choroidal
tuberculosis. A recurrence involving adjoining choroid occurred
fourteen months ago. There was at the start pain, slight dilatation of the
pupil, and slight general hyperemia of the globe. The tension of the
eyeball rose to 60 mm., that of the fellow eye being 20 mm. Under

miotics the tension fell at first but slightly. It was 55 mm. at the end of
a week; but after two weeks came down to normal, 20 mm. A month
later the tension rose to 28 mm., but for a year has continued normal;
the eye did well under tuberculin treatment, and without any local
treatment. In September of this year I had two cases of iritis in which
the intra-ocular tension rose to 45 and 52 mm., respectively, and
gradually returned to normal, with the cure of the iritis under atropine.
In one of these cases, a lady of 70, I used atropine also in the other eye,
but the tension of that eye remained normal, 22 to 24 mm., throughout.
After needling the lens in young people I have seen a rise of
intra-ocular tension to 50 and 60 mm., maintained for many days, with
considerable general deep hyperemia, and soreness of the globe,
followed by gradual return to normal tension, and no permanent
impairment of vision or the visual field.
One other type may be mentioned. That of an elderly patient with
marked vascular disease, often renal involvement, and distinctly
impaired nutrition. There may be renal retinitis or retinal hemorrhages.
The case may easily become one of hemorrhagic glaucoma. It may run
a very chronic course. But it may become suddenly worse, or go on to
complete blindness with pain, demanding enucleation, after some
temporary perturbation, as the performance of a glaucoma operation. It
is pre-eminently the kind of a case you would prefer would go to some
one else.
Each of these types illustrate a distinct cause or group of causes. The
first type brings us near to what may be the essential nature of
glaucoma, impairment of ocular nutrition by the intra-ocular tension,
which is generally elevated, but may not be above the usual normal. A
special weakness in the nutrition of nerve tissue may be assumed. It
would help to explain the cavernous atrophy of the optic nerve
associated with simple glaucoma. The second type shows impairment
of the regulative mechanism permitting rapid rise of the intra-ocular
pressure. In persons of good nerve nutrition and strong recuperative
power, it may exist for years without doing permanent damage. But
joined to causes of the first type, lowered nutritive activity, it causes
rapid and permanent loss of sight. The third group are cases associated

with glaucoma only as causes. In eyes with low nutritive power, or
subject to exacerbations of increased intra-ocular pressure, uveal
inflammations may prove disastrous. The fourth type shows the results
of the combination of the causes of the other types; with the elements
of acute or slow malignancy added--the impaired circulation and
lowered oxidation producing some degree of edema of the tissues that
insures a fatal result.
This is no complete presentation of my subject, but a selection of facts
bearing on the etiology, to serve as a foundation for