The Disease-Process, Glaucoma. 
BY 
S. O. RICHEY, M.D., 
OF WASHINGTON, D. ,C. 
FROM 
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 
June, 1893. Extracted from The American Journal of the Medical Sciences, June, 1893. 
THE DISEASE-PROCESS, GLAUCOMA. 
By S. O. Richey, M.D., 
OF WASHINGTON, D. C. 
A fair hypothesis must be based upon all the known facts of a case, 
and must rationally explain them all. 
" Scleritis1 is more often met with in persons of a rheumatic, or gouty, 
habit than in others." Garrod2 has seen two cases of sclerotitis with 
white deposits of urate of soda on the surface of the tissue; " likewise 
on the tarsal cartilage at the angles of the eyes." Increased tension is 
constantly a symptom in scleral metamorphoses. " During life the ex- 
istence of scleritis is often overlooked, or is first recognized by its results, 
staphyloma or atrophy."3 A chronic hypertrophic condition of the 
sclerotic always precedes total phthisis of an eyeball, and the process 
leading to it begins, without exception, in the posterior parts of the 
sclerotic around the entrance of the optic nerve, and progresses more 
and more toward the corneo-scleral margin.4 Coccius5 saw one case of 
fatty degeneration of the sclerotic in glaucoma, and Cusco and Coccius 
suggest that the starting-point of glaucoma is an inflammation of the 
sclerotic. Lime deposits in the sclerotic at this period of life might 
easily be mistaken for fatty degeneration-the presence of fat globules 
in the tissue would be essential to its proof. The effect of fatty degen- 
eration of the sclerotic would be its friability and diminished resistance 
to intra-ocular pressure, with subsequent lowered tension. The occur- 
rence of this condition in a very limited number of cases is possible, for 
any phase in this "combination of diseases" is conceivable. In nearly 
all cases of glaucoma, however, a state of increased rigidity of the sclera 
is a marked characteristic; high tension and increased rigidity of the 
sclerotic, to some extent, mask each other. 
The sense of the discussion upon this malady at the Heidelberg Con- 
gress, in 1877, is that the apparent teachings of dissections are incon- 
clusive. " Anatomical observations in explanation of this array ot 
symptoms serve little purpose," and yet each one of " this array of 
symptoms " is an evidence of morbid change in some of the ocular 
structures.6 The presence of all the symptoms, or of the most charac- 
1 Soelberg: Wells, Dis. of the Eye, Bull's ed., p. 273. 
2 Reynolds : System of Med., vol. i., p. 517. 
3 Stellwag : Dis. of the Eye. Am. ed., 1873, p. 336. 
4 Alt: Lectures on the Human Eye, 1880, p. 45. 
5 Archiv f. Augenheilk., B. ix., 1, p. 21. 
6 Alt, p. 155. 2 
RICHEY: GLAUCOMA. 
teristic of the observable structure changes, are not essential at any 
given stage, and all cases do not run the same unvaried course; but, 
taking the whole history of two cases to their conclusion, and usually 
the distinguishing symptoms have been present, and the result is much 
the same. If the varying symptoms, the different diseases which are 
included in the name, the natural explanation of the symptoms, and 
the theory of their causation can be made consistent with each other, 
and can be shown to be due to a common cause, the fog surrounding this 
question will be somewhat thinned. 
The accumulated testimony of all observers, interpreted, points to 
morbid changes in the connective, or fibrous, tissues as the initial and 
permanently progressive lesion of the disease, indicating that these 
changes are interstitial, beginning in the sclera; that they consist in 
connective-tissue proliferation, with its usual debasing effect upon the 
higher functional forms of tissue enclosed by the sclera, which, by their 
protests against this inexorable degradation, give rise to the subjective 
symptoms present-the objective symptoms are phases of the progress 
of the disease. 
By a histological consideration of the globe, one is impressed with the 
amount of connective tissue in its construction and its importance to 
the integrity of the eye, for this organ is composed of fibrous and con- 
nective tissue, an elaborate and pervading framework and support to 
vitally functional tissues, surrounding every structure. Because of its 
low vitality and consequent indisposition to resentment, it rarely (about 
1 per cent, of all cases) acts viciously, and then we must look for a 
persistent cause of irritation, of low grade, with a tendency to reversion 
along the lines of evolution. In the inadequacy of the liver to convert 
uric acid into urea we have such a tendency ; in the presence of uric 
acid in the blood and tissues we have such a cause. When a disease 
is bilateral it cannot be purely local in its origin ; in the consideration 
of causes persistent irritation is an essential quality, and acute inflam- 
matory action results when the irritation is increased. Uric acid is 
carried by the blood, and the envelope of an organ receives its first 
effect; hence, it has been observed that the sclerotic is denser and harder 
than normal before any other evidence is in existence of the presence 
of the dread disease, and as this occurs at a period of life when such 
condition, to some extent, is supposed to be natural, it is liable to attract 
little attention. 
The morbid process, to my mind, is a hyperplasia oj connective tissue 
which diffuses itself through the whole organ, possessing the property ot 
pathological connective tissue to always contract. High arterial tension 
promotes the formation of new connective tissue, is present early in 
glaucoma, and is the conservative effort of Nature to relieve the blood 
of uric acid. This product acting mildly for a long time, will usually RICHEY: GLAUCOMA. 
3 
cause connective-tissue proliferation; if the action be intense or if the 
urate of soda is formed in this region, the vascular apparatus chiefly 
is affected and violent inflammatory action results. In this we find the 
difference between chronic and acute glaucoma. The slow, insidious 
progress of simple glaucoma is a point in favor of this view, as all forms 
of glaucoma, including the hemorrhagic, are the outcome of connective- 
tissue growth, varying in degree of acuteness, or in the active func- 
tional tissue first invaded ; it may be that the coats of the bloodvessels 
are first involved, or that there is a binding of nerve fibres by the en- 
croachment of the connective tissue surrounding them, or that there is 
thickening of the stroma of the choroid, or retina, or even of the inner 
layer of the sclerotic, which last would, to some extent, shorten the 
antero-posterior diameter of the eyeball interiorly, producing increas- 
ing1 hypermetropia. 
In interstitial nephritis from the same cause, we have an analogue to 
the condition called glaucoma, with similar constitutional disturbances, 
and a like morbid process of the cortex and parenchyma. It is of low 
grade, insidious, and is often unmarked by positive symptoms until the 
beginning of the end; it always attacks both kidneys, though not 
usually at the same time, and therefore the disease is seldom at the same 
stage of progress in both; the progress of the malady has its interrup- 
tions and exacerbations, or it may be lighted into more acute action ; 
after each exacerbation the disease is more advanced ; step by step, the 
history of simple glaucoma. 
Hyperplasia of the connective tissues offers an unforced explanation 
of all the sympathetic and anatomical phenomena of glaucoma: the 
so-called prodromata-impaired accommodation, premature presbyopia, 
increasing hypermetropia, halo, fogginess of vision, and heaviness of the 
brow ; the local symptoms of an attack-increased intra-ocular tension, 
circumorbital pain, peri-corneal injection, protrusion of the globe, slug- 
gish dilated iris, anaesthetic cornea, lachrymation, photophobia; the 
anatomical peculiarities-excavation of the disk, obstruction of the 
channels of filtration, the white ring of the papilla; the complications- 
1 Within the past few years, I have seen two cases of primary glaucoma in women 
aged fifty-three and seventy-one years), in which, without any observable change in 
the anterior section of the eyeball, myopia, has developed and increased precisely 
as in the progressive myopia of early life. The individuals read more comfort- 
ably without convex lenses, and require concave lenses for distance. There is excava- 
tion and increased intra-ocular tension in both eyes in both cases, the two eyes of each 
person being different in depth of excavation and the degree of myopia. The vitreous 
appears to have receded instead of being advanced, and the eyeball is distended poste- 
riorly, as in staphyloma posticum. Choroidal atrophy has not yet appeared : -3 D' 
on the worse eye gives V. = 20/xx. 
If any operation would serve here, it must be posterior sclerotomy, in which event the 
same operation would serve in staphyloma posticum. 
These cases may be the exceptions which prove the rule. 4 
RICHEY: GLAUCOMA. 
coloboma iridis, total aniridia, nephritic retinitis, detached retina, high 
degrees of staphyloma posticum (with reduced tension). Wells1 is my 
authority for the statement that Bonders claimed inflammation to be 
not an integral part of glaucoma, but an unessential complication. 
The constitutional disturbances are due to the constitutional cause of 
the interstitial process. 
In fulminating glaucoma the irritation has been sudden and violent 
in its action (possibly urate of soda) ; in the hemorrhagic form the walls 
of the bloodvessels have first been affected and rendered brittle; in the 
chronic, irritable form the irritant has been mildly persistent, with 
periodical accessions of intensity. All are forms of one process, due to 
one cause, unless the disease is unilateral and the cause clearly some 
local injury ; even then a predisposition exists. 
Anaesthesia cornea is not so great in degree or in the area involved 
in acute, as in chronic glaucoma; in acute glaucoma it may be limited 
to some one part of the cornea, while in the chronic form the whole 
cornea is about equally affected. If this symptom were due to high 
tension, it would be more pronounced in acute glaucoma; that this is 
not true, favors the idea of an invasion of the canal containing the nerve 
by new tissue in the chronic affection. 
The bluish-gray tint of the media may be caused by the presence of 
an increased number of wandering cells or by exceeding fine fibrillae of 
new-formed connective tissue, or by the presence of uric acid crystals. 
Obstruction of the channels of filtration is not a cause of glaucoma, as 
seems to be understood by those who favor the " filtration theory," nor 
does this obstruction come from the interior of the globe by the advance- 
ment of the iris and its application to the posterior surface of the cornea. 
This may occur, but it is secondary to obstruction of the channels. If 
obstruction took place by application of the iris, the process would 
complete a " vicious circle," and two things would be expected which do 
not happen: (a) the exits being closed, the pressure of fluids would be 
toward the posterior channel of excretion (Leber) near the optic nerve, 
with deepening of the anterior chamber; (6) the channels being closed 
by the application of the iris to the posterior surface of the cornea, "thus 
establishing glaucoma," the obstruction and increased intra-ocular 
tension, in the nature of things, would act and react upon each other, 
and the condition would grow worse until relieved by (mechanical) 
surgical interference. Is this the case ? " These slight attacks of 
glaucoma, often lasting only a few hours, clearly disprove the distention 
theory.2 How is that theory to be reconciled with the fact that the 
attacks occur suddenly, and soon afterward disappear spontaneously ? 
1 Wells, vid. sup., p. 583. 
2 Schweigger: Archiv f. Augenheilkunde, vol. xxiii. RICHEY: GLAUCOMA. 
5 
How can the filtration at the angle of the chamber be so suddenly inter- 
rupted and so wonderfully soon re-established ?" 
Does not reason rather lean toward the following ? 
Scleral changes may be found in all cases of primary glaucoma, 
hypertrophy with increased rigidity, which begins always in the posterior 
portion of the sclerotic, about the entrance of the optic nerve (Alt), 
advances gradually to the corneo-scleral margin and encroaches upon 
the channels of excretion. Such changes, beginning posteriorly, reduce the 
size of the emissaries as they pass through the sclerotic and cause venous 
stasis: this, with the diminution of space in the vitreous chamber by 
hypertrophied sclera, causes advancement of its contents, and may lessen 
the depth of the anterior chamber without increasing the intra-ocular 
tension, as sometimes happens. The neoplastic connective tissue, during 
the interval, invades the optic nerve, and all is prepared for an increase 
of tension as soon as the morbid tissue so occupies the channels as to 
slow excretion. Now, some circumstance (an injury, mental emotion, 
exposure, imprudence in diet) violently disturbs the circulation (local or 
general), and precipitates an attack of glaucoma. Or, no such cause 
acting, simple glaucoma is developed with its whole train of symptoms. 
In case of acute glaucoma, the vascular disturbance over, the engorge- 
ment passes off, leaving the channels much as they were immediately 
before the attack, which could not happen if the obstruction were due to 
the application of the iris to the cornea. Iridectomy probably acts by 
promptly relieving such engorgement; myosis, by creating a diverticulum. 
The narrowing of the channels by hyaline1 and epithelial masses, or by 
cicatricial contraction, is of more permanent character, does not belong 
to the early stage, and cannot be cured by iridectomy, or any other oper- 
ation anterior to the vitreous. Only the result of the operation can, at 
times, decide the character of the obstruction. 
Dilatation of the pupil (which is not always present), which varies 
in degree and regularity with the same degree of tension, depends upon 
constriction of the motor filaments to the iris from the third nerve, 
as they pass through the thickened sclera. 
The shallow anterior chamber is a result of the advancement of the 
corpus vitrei caused by venous stasis and the encroachment by the sclera 
upon the vitreous space (this being possibly a factor in the dilatation of 
the pupil) ; for, by scleral hypertrophy and the resulting atrophy of the 
uveal tract, the secretion of the aqueous humor is diminished and the 
resistance ab fronte is reduced; hence, the very temporary relief from 
paracentesis of the anterior chamber (similia similibus). 
Excavation is rare in a first acute attack, and therefore cannot be 
entirely due to pressure, which is sometimes excessive in such attack. 
As the disease progresses the resistance at the papilla is lessened by 
1 DeWecker: Ocular Therapeutics, English ed., 1879, p. 260. 6 
RICHEY: GLAUCOMA. 
the same agent which so effectually degrades the other tissues and permits 
the effect of pressure to appear; or, the excavation is due to contraction 
of the new morbid tissue. 
" A delicate connective tissue is frequently found in glaucomatous 
excavations, having been formed in the adjacent part of the vitreous 
body."1 " I have not infrequently seen a well-marked glaucomatous 
excavation on one side, and a neuritis of mild but distinct form, with 
stretching (?) of the tissue and beginning excavation, in the other 
eye."2 Is there any difference in appearance between glaucomatous 
excavation and that which follows gray atrophy? 
In event that intra-ocular pressure alone in glaucoma could produce 
excavation in a papilla of normal resistance, it would be JwineZ-shaped. 
This is rarely true ; the excavation is usually shaped like a cup, or trun- 
cated pyramid, the width being often greater than the depth, the structure 
disappearing laterally to a point under a ledge of the sclerotic, which 
protects it from direct pressure. This pathological peculiarity can be 
due, alone, to neither intra-ocular pressure, nor to modification of tissue 
in the papilla, but is the product of the action of both. The atrophic 
process in the optic nerve seems to be caused by the extension and pro- 
liferation of fine connective tissue, and its subsequent contraction. 
" There is a continuity of inner connective tissue of the optic nerve with 
that of the sclerotic and choroid."3 To this same agent is probably due 
the grayish-yellow glaucomatous ring. 
The acuteness and field of vision are controlled by the same influences, 
and pari passu, which modify the appearance and condition of the papilla. 
Arterial pulsation*1 occurs when the normal balance between general 
arterial tension and intra-ocular tension is disturbed. Reduction of 
blood-pressure takes place when the lumen of the arteries is diminished 
by infiltrated new connective tissue, as is common in lithiasis, and thus we 
may have arterial pulsation without increase of intra-ocular tension, or 
excavation of the disk. Impure blood excites spasm of the smaller arteries. 
Mydriasis reduces, and myosis increases the area of vascular dis- 
tribution of the ciliary region. By mydriasis the arterial circulation is 
suddenly obstructed, resulting in temporary engorgement, which may be 
sufficient to excite an acute glaucoma if the channels of excretion are 
narrowed. Hypermetropia favors ciliary engorgement by constant ex- 
cessive demands upon the ciliary muscle. Therefore, " chronic glaucoma5 
is a neurosis (vasomotor)-a progressive atrophy with the feature of 
inflammation with defective power; acute inflammatory glaucoma is a 
paroxysmal expression of the same affection." 
1 Alt, vid. sup., p. 156. 
2 E. G. Loring: Text-book of Ophthalmoscopy, vol. ii., p. 229. 
3 Lbwig: Studien des Phys. Inst. Breslau, 1858, p. 125. 
4 Schweigger: Archiv f. Ophthalmologic, Oct. 1891, p. 491, 492. 
5 Richey: Amer. Journ. Med. Sciences,Nov. 1892; Trans. Amer. Ophthal. Soc., 1892. Yfye JoUrpal 
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