ation, and
especially diminished oxidation, are the chief causes of increased
affinity of the colloids for water. Such affinity increased by the
impairment of the intra-ocular circulation, may well constitute a factor
making for malignancy in glaucoma. But it can hardly explain the
original departure from a normal pressure balance.

We must assume that intra-ocular pressure is kept down to the normal
limit, by the prompt response of a regulative mechanism, which
diminishes the flow of fluid into the eye, or permits its more rapid
escape, whenever fluid tends to accumulate in the eye and increase its
tension.

Little has been done to show that increase of fluid entering into the
eye is the cause of glaucoma. A normal, or even a low arterial blood
pressure is sufficiently above the normal intra-ocular pressure to
furnish a source of increased fluid in the eye. Increased arterial
pressure has been found in 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