Glaucoma : $b A symposium presented at a meeting of the Chicago Ophthalmological Society, November 17, 1913 — John Shaqi
Glaucoma : $b A symposium presented at a meeting of the Chicago Ophthalmological Society, November 17, 1913
Science
Glaucoma : $b A symposium presented at a meeting of the Chicago Ophthalmological Society, November 17, 1913
Glaucoma
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 of the disease. Zirm believes
the venous plexus of the choroid is an essential part of the mechanism
for the regulation of intra-ocular tension, the necessary vaso-motor
control depending on nerve centers situated in the iris.
_Nerve Control_
The accurate control of normal intra-ocular pressure, by mutual
adjustment of inflow and outflow of fluid, is scarcely conceivable
without some highly specialized, extremely sensitive nerve mechanism to
preside over it. This is suggested by analogy with the regulation of
secretion in the lacrimal, salivary, or peptic glands, or the
maintenance of blood pressure in the heart and arteries. Clinical
observations point the same way. Many patients connect their attacks
(especially their earlier ones of ocular discomfort, impaired vision,
haloes around the light, and dilated pupil) with social excitement,
anxiety, worry, anger or fatigue. A patient of mine gave up her card
parties, because an exciting game generally ended in blurred vision, a
rainbow around the light, and a dilated pupil, and sometimes an aching
eye. Another woman watching beside her dying husband and exposed to
extreme cold, had her first attack of glaucoma, so severe as to destroy
the sight of one eye. The other eye, also affected at the time,
recovered good vision, and has remained several years without a second
attack and without treatment.
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