1 he Prime Etiological Factor of Glaucoma 
is Constitutional 
BY 
S. O. RICHEY, M.D., 
OF WASHINGTON, D. C. 
FROM 
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 
November, 1892. Extracted from 
The American Journal of the Medical Sciences for November, 1892. 
THE PRIME ETIOLOGICAL FACTOR OF GLAUCOMA IS 
CONSTITUTIONAL.1 
By S. O. Richey, M D., 
OF WASHINGTON, I). C. 
This paper will be occupied with the presentation of one idea, for a 
resume of the literature of glaucoma would unprofitably occupy much 
space, as so much has been written offering diverse views of its different 
features, each with a show of reason. 
Mr. Jonathan Hutchinson, in the Bowman Lecture, 1884, discusses 
the relation between certain diseases of the eye and gout. The tissues 
of an individual long subject to the causes of gout may become modified 
in such a way that they are liable to suffer in a peculiar manner when 
exposed to the ordinary causes of disease; the nervous and vascular sys- 
tems are specially so disposed. Rheumatic gout may have such a rela- 
tion to true gout, and he names “ hot eyes,” calcareous bands of the 
cornea, arthritic iritis, relapsing cyclitis, glaucoma, and retinitis hiemor- 
rhagica as having such connection ; and asks if it can attack any of the 
structures of which the nervous system is composed. 
In the London Lancet, January, 1873, he describes an iritis occurring 
at an early age, differing from other forms of arthritic iritis, in being 
persistent and insidious, rather than paroxysmal. Without any attack 
of acute inflammation, adhesions quietly form between the iris and the 
capsule of the lens. . . . This affection usually begins in but one 
eye, and advances to almost entire loss of vision in it, before attacking 
the other. It is insidious, and for the most part painless, but is liable 
to exacerbations and periods of improvement. It is remarkably intract- 
able, prone to attack both eyes, and to end in blindness. 
Such is the position of an acute observer as to the influence of gout 
upon the eye. 
The question as to the cause of increased tension is still open, whether 
due to too rapid infiltration, or to impeded excretion, with a leaning to 
the latter. 
Opposed to Mr. Priestley Smith’s theory, that “glaucoma of every 
form is essentially a disease of retarded excretion,”2 are the conclusions 
of Schnabel,3 supported by clinical and pathological studies, that “ glau- 
1 Read at the meeting of the American Ophthalmological Society, July 20,1892. 
2 Trans. Seventh International Medical Congress, vol. iii. p. 84. 
3 Archiv Ophthalmol., vol. vii. p. 14. 2 
RICHEY, ETIOLOGY OF GLAUCOMA. 
coma may be present without obliteration of the sinus of the anterior 
chamber; that the latter can exist without glaucoma; that glaucoma 
can be cured without obliteration of the sinus of the chamber being 
removed.” 
“ It has been proved by Mr. Windsor,1 of Manchester, that acute 
glaucoma may occur where there is congenital absence of the iris.” 
A doubt, which reaches almost a denial, is general as to whether 
excavation of the disc is due to pressure, or not. In Rydell’s2 case, 
blind from acute glaucoma of three weeks’ standing, without excavation, 
pain was relieved and tension reduced, but vision was not improved. 
Mauthner3 claims that “ We find in the beginning of an excavation that 
pressure frequently is not increased. I have recently examined the left 
eye of a patient, in which there is the beginning of a pressure excavation, 
of which there was not the slightest sign a year ago, when I saw him for 
paresis of one of the muscles. The functional disturbance is extra- 
ordinary, and shows itself in transitory obscurations ; central S. is less 
than in R. E , which has S = 6/vi, while with L. E. a few letters of 6 
are not seen at 6 m. distance. Without glasses the patient, who is forty- 
five years old, reads with R. E., J. 2, with the left eye J. 3 : F. undis- 
turbed. The well-known appearance of the vessels is very marked at the 
upper lateral edges of the papilla. T. is precisely the same in both eyes, 
and falls even below the physiological maximum. Would such a press- 
ure produce such a picture?” 
“Some morbid process has attacked the intra-ocular end of the 
optic nerve, causing a diminished resistance (softening) of the lamina 
cribrosa, so that it yields to even normal pressure in the eye, but at the 
same time there is going on in the optic nerve an alteration, which has 
the greatest resemblance to that in the lamina cribrosa, and leads to a 
softening, to a giving way of the supporting connective tissue.”4 
Reading these comments on glaucoma with a free mind, our previous 
ideas are subverted, because we must conclude that increased tension is 
not necessary to excavation ; that excavation is not always present, even 
when increased tension has existed sufficiently long to produce it; that 
excavation may result from5 “ some morbid process ” in the nerve, 
1 A Practical Treatise on Diseases of the Eye, by Haynes Walton, London edition, 
p. 1170. See Ophthalmic Review. 
2 Yon Graefe’s Archiv, 1872, vol. xviii. pp. 1-51. 
3 Archiv Ophthalmol., vol. viii. p. 38. 4 Vide supra, p. 39. 
5 Garrod, on “Rheumatoid Arthritis,” Reynolds’ System of Medicine, p. 553 : “In 
the early stage, when swelling is prominent, a considerable increase of synovial fluid 
is found, and the joint exhibits the same appearance as in case of ordinary inflamma- 
tion. The lining membrane is often red from over-injection of the bloodvessels. It 
the bone be sawn through, it is often found spongy, and contains a large amount of 
oily matter, from the occurrence of & species of fatty degeneration.” N.B. All italics are 
iny own. RICHEY, ETIOLOGY OF GLAUCOMA. 
3 
lessening its resistance; that increased tension is not dependent upon 
obstruction of the channels of excretion. 
If the last proposition be true, that increased tension is not dependent 
upon obstruction of the channels of excretion—and Schnabel supports 
his conclusion by dissections of the organ which he had observed while 
affected with the malady—then increased tension must be caused by too 
rapid infiltration, or secretion. Schnabel argues further,1 that glaucoma 
is a disease of the bloodvessels of the eye, which develops either gradu- 
ally, or at once, in the region supplied by the long anterior and posterior 
ciliary arteries, the central bloodvessels, and those of the sclerotic circle; 
that the disturbances of nutrition and function are the direct result of 
these disturbances of circulation, etc. 
Mr. Priestley Smith’s theory was obviously derived from the study of 
glaucoma of local origin ; and yet, as Mr. Brailey, of London,a says, 
“ it fails to account for temporary glaucoma, for glaucoma without the 
characteristic application of the iris, for glaucoma in young persons, for 
one-sided glaucoma, for glaucoma in aphakic eyes, and especially for 
cases where a traumatic dislocation of the lens backward has been 
quickly followed by increased tension. It does not, also, explain the 
invariable inflammation and atrophy of the ciliary body and optic 
nerve.” 
To the theory of increased secretion, or more properly too rapid infil- 
tration, a vis a tergo, some derangement of the general system, is a sine 
qua non. The uric acid diathesis, of which gout is a characteristic 
feature in many instances, offers the most satisfactory explanation: 
true gout, of acute inflammatory glaucoma; rheumatic gout, of chronic 
simple glaucoma. 
In nearly all particulars acute gout of the toe and acute inflammatory 
glaucoma are alike. Observe the points of resemblance : 
Acute Inflammatory Glaucoma. 
1. An inherited tendency. 
2. Most frequent after the period of 
presbyopia. 
3. First attack is usually in cold weather. 
4. Premonitory symptoms: Impaired 
A.; premature presbyopia, increased H.; 
halo, rising clouds or smoke, heaviness of 
brow, shooting pains in the eye, increased 
tension. These may be so slight as to 
cause no anxiety. 
5. Sudden seizure, usually at night. 
Acute Gout op the Great Toe. 
1. An inherited tendency. 
2. Most frequent after the beginning of 
senile changes. 
3. First attack, usually in winter, or 
spring. 
4. Premonitory symptoms may be so 
slight as to pass unnoticed, or may be 
very distressing. 
5. Attack is sudden, usually between 
two and five o’clock in the morning. 
(Garrod.) 
1 Archiv f. Augenheilkunde, vol. xv. p. 311. 
2 Trans. Seventh International Medical Congress, vol. iii. 4 
RICHEY, ETIOLOGY OF GLAUCOMA 
Acute Inflammatory Glaucoma. 
6. Constitutional disturbances; febrile 
excitement, with some nausea and vomit- 
ing. 
7. Circumorbital pain, peri-corneal and 
sub-conjunctival injection, slight protru- 
sion of globe, sluggish, dilated iris; cornea 
dull and anaesthetic, humors greenish, 
ischaemia. 
8. As the attack passes off there is great 
chemosis, lachrymation, and photophobia. 
The cornea becomes roughened. 
9. The inflammatory attack passes off 
in a few days or weeks. 
10. The disease is not arrested: there 
may be a recurrence of acute inflamma- 
tory attacks, chronic inflammatory exa- 
cerbations, or the disease may progress 
insidiously. 
11. No pus. 
12. Urine. ? 
13. No analysis of aqueous humor, so 
far as I know. 
14. The disease may attack first one eye 
and then the other. 
15. Occurs most frequently in women. 
Acute Gout op the Great Toe. 
6. Chilliness, heat of skin and per- 
spiration, thirst, loss of appetite, a white 
tongue, constipation, and restlessness. 
7. Toe is swollen, red, hot, and ex- 
quisitely tender. Veins proceeding from 
the toe are turgid with blood, and the 
joint is stiff. Great tension of the skin. 
8. As the attack passes off there is pit- 
ting of the skin (oedema), then desquama- 
tion. 
9. Duration, from four days to three 
weeks. 
10. Gout recurs, and the frequency of 
the paroxysms increases. 
11. No pus. 
12. Urine scanty, high-colored, and de- 
posits a colored sediment on cooling. 
13. Synovia contains urate of soda. 
14. Gout not uncommonly seizes first 
one great toe, then the other. 
15. Is rare in women. 
Thus, each maybe inherited and have the premonitory symptoms; 
the attack is sudden and at night; in each it is characterized by great 
pain, engorgement, and tension, followed by oedema and exfoliation ; 
duration, from a few days to a few weeks; recurrence of the affection, 
possibly to attack the other side, or to become chronic. No pus. 
Such is the clinical picture. 
That acute inflammatory glaucoma is more frequent in females, and 
gout of the great toe more frequent in males, may be due to the greater 
emotional tendencies of women ; for, according to Schweigger mental 
emotion and loss of sleep favor acute glaucoma.” 
While women derive a certain immunity from podagra by reason of 
menstruation (Hippocrates), yet at the approach of the climacteric, a 
period of greater or less tendency to vascular cerebral disturbance, aris- 
ing from the intermittence of the derivative action of this function, 
acute inflammatory glaucoma is most frequent, and chronic simple 
glaucoma develops. 
“ The great toe1 contains a considerable amount of tissues peculiarly 
liable to become the seat of the deposition of urate of soda; as, for ex- 
ample, the cartilages and ligaments, tissues having either little vascu- 
larity, or nourished independently of bloodvessels ; the great toe being 
1 Garrod, “ Pathology of Gout,” Reynolds’ System of Medicine, vol. i p. 535. RICHEY, ETIOLOGY OF GLAUCOMA. 
5 
very remote from the heart, the circulation is weaker there 
The reasons for the great toe on one side of the body being affected 
apply equally to the other; and hence, the disease not uncommonly 
attacks first one toe and then the other, within the short space of a few 
hours or days.” 
Anatomically, the eye is an extremity of the body, not quite so far 
from the heart as the toe, and is exposed to variations of temperature and 
to injury; the sclerotic, the cornea, and the tendons of the extrinsic 
muscles are of dense fibrous tissue, with little vascularity ; the stroma 
of the choroid and iris is of reticular connective tissue, supporting pig- 
ment cells, bloodvessels, etc., the zonule of Zinn is a fibrous perforated 
membrane, the lens capsule is a structureless membrane, the corpus 
vitrei depends upon bloodvessels not its own for nutrition, and con- 
tains mucin, and (Picard) 0.55 per cent, of urea, and about 0.75 per cent, 
of sodic chloride. The posterior surface of the iris and ciliary body 
secrete the aqueous humor (synovia?) which contains a small amount 
of albumin, sugar, and sodic chloride, equal to -g of its volume. 
With increase of blood-pressure and intra-ocular pressure, there is in- 
crease of albumin and the production of fibrin in the anterior chamber. 
(Jessner and Griinhagen.) 
Taken with the fact that a local derangement, as a dislocated lens, 
does not seem sufficient to cause the whole train of symptoms, general 
as well as local, called glaucoma (though it may precipitate an 'attack 
which would probably have taken place at a later date), the clinical 
history of a seizure and the anatomical peculiarities of the regions under 
consideration present a picture of such mimicry as we find nowhere 
else repeated. The crucial test, the presence of urate of soda, I have 
had no opportunity to apply since recognizing the resemblance. 
To again read Garrod/ “ The impure state of the blood, due to the 
presence of urate of soda, is probably the cause of the disturbance 
which often precedes the gouty paroxysm ; that is, of the so-called pre- 
monitory symptoms. Urate of soda in abnormal quantity in the blood 
is essential to an attack of gout, .... but does not constitute 
gout; .... that the amount of deposited urate of soda is not in 
proportion to the intensity of the inflammation, and that in some the 
infiltration may ensue and give rise to scarcely any inflammatory action. 
. . . The inflammation of the gouty paroxysm tends to the 
destruction of the urate of soda in the blood of the inflamed part, and 
probably of the salt also which is thrown out.” Soelberg Wells2 ob- 
serves that “ males who are attacked by glaucoma frequently suffer from 
gout, or disorders of the digestive organs :” of primary glaucoma, “ when 
1 Reynolds’ System of Medicine, vol. i. p. 533. 
2 A Treatise on Diseases of the Eye, 3d Amer. ed., 1880, p. 589. 6 
RICHEY, ETIOLOGY OF GLAUCOMA. 
once the one eye has become affected by glaucoma there is great ten- 
dency in the disease to invade the other also.” 
Mr. Hutchinson1 asserts that “ all forms of rheumatism, and all forms 
of gout, are included in the common term, arthritic. But we cannot 
limit the term to the joints, as its etymology might seem to require, but 
must allow it also to apply to certain affections of the muscles, fasciae, 
tendons, and other fibrous structures which have been proved to be 
dependent upon the same peculiar state of health Under 
the term rheumatism we include all arthritic maladies which are not 
proved to be gouty I must protest, at once, against any 
attempt to limit the term gout to cases in which attacks of acute in- 
flammation of the great toe occur Rheumatism differs 
from gout in being of nerve origin, and due to reflex disturbance of 
nutrition; .... it is, according to my hypothesis, the basic 
diathesis to which a small minority of cases of gout is superadded.” 
The younger Garrod says that rheumatic gout lacks the distinguish- 
ing feature of gout, urate of soda. 
Many of the manifestations of rheumatic gout are associated with 
chronic glaucoma, viz. : enlarged or distorted joints, a peculiar senile 
pallor, or muddiness of the skin ; periods of mental depression, and other 
symptoms, attributable only to changes in the nervous system. I have 
found nowhere any reference to pathological alteration of nerve tissue 
in gout, although the existence, character, and specific cause of such 
changes, which are presumed to exist because of the nervous symptoms 
present in lithiasis, would have important bearing upon the subject in 
hand, in explaining the structural changes in the lamina cribrosa and 
the intra-ocular end of the optic nerve, the condition of diminished re- 
sistance associated with excavation without increase of tension, in cases 
of chronic glaucoma. 
Dr. W. W. Johnston,2 Washington, D. C., published some thoughts 
“On the Nature and Treatment of Forms of Disease characterized by 
Indigestion, the Presence of Bile, Urates, and Uric Acid in the Urine, 
and by Nervous Symptoms,” which suggest a possible cause and expla- 
nation of the nerve changes in chronic glaucoma. In his own words, 
“ The question of the continuous production of toxic substances in the 
intestinal canal in health, and the protection of the organism by physio- 
logical elimination, as well as the auto-intoxication of the organism by 
the absorption of poisons in alterations of the gastro intestinal tract, 
was developed in detail by Professors Albertoni and Silvia at the meet- 
ing of the Fourth Italian Congress of Internal Medicine, held in Rome. 
Professor Silvia enumerates the following substances as probable 
1 Trans. Seventh International Medical Congress, vol. ii. p. 92. 
2 The Medical News, March 12, 1892. RICHEY, ETIOLOGY OF GLAUCOMA. 
7 
poisons: peptoxine, organic bases (ptomaines and leucomaines), indol, 
phenol, lactic acid, ammonia, sulphuretted hydrogen, acetone, etc. The 
direct proof of the fact that the nervous phenomena in such cases are 
due to the absorption of toxic matters from the intestines is not yet 
found, but the argument is a forcible one. The existence of indigestion 
is known by the symptoms : the presence of toxic matters in the in- 
testine in health is proved The relationship of acute 
indigestion and nervous disturbances, and the association of fermentative 
dyspepsia with nervous symptoms, and an excess of these products in 
the urine and feces, give sufficient grounds for adopting this theory as 
reasonable.” 
Dr. Johnston has given much attention to the subject of digestion, 
and if a reference to his able paper will induce those who have the 
care of cases of chronic glaucoma to read it, it will probably divert 
attention from glaucoma, except as a local manifestation of a general 
malady (although he does not refer to glaucoma), broaden the view of 
the subject, and enable us to comprehend the changes in nerve tissue 
going on elsewhere in the system in rheumatic gout, by that which 
takes place in the intra-ocular end of the optic nerve, exposed to obser- 
vation, in chronic glaucoma. 
Returning to the subject of intra-ocular tension, Mr. Priestley Smith1 
claims that “ high tension depends more upon an excess of blood in the 
eye than upon an excess of intra-ocular fluid,” while Dr. Spender2 has 
observed, as early symptoms of arthritis, increase of pulse rate with 
high arterial tension. 
Mr. Hutchinson3 concludes that “ it is probable that there are many 
different forms of inflammation of the eye, or of parts of it, which are 
in connection with gout. They may be divided into two groups: a, 
those which go with acquired, humoral, or renal gout; b, those which 
depend upon inheritance of structures damaged, or, at any rate special- 
ized, by gout in predecessors. The difference between the two classes of 
affections is very marked. In the one, attacks of a transitory nature are 
the rule, and the attacks are often acute and attended by much pain. 
In the second group, although a tendency to temporary recovery and 
recurrence is often observed, yet, there is a great proneness to chronicity, 
and persistence. The invasion is often insidious, but the disease is 
usually in the end destructive.” 
If the difference between the forms of acute inflammatory and 
chronic simple glaucoma had been in the mind of Mr. Hutchinson the 
description could not have been more effective than in the specification 
of the two groups named above. 
1 Ophth. Rev., vol. vi. p. 196. 
2 Garrod: A Treatise on Rheumatism. Am. ed., 1890, p. 245. 
3 Ophth. Rev., vol. iii. p. 385. 8 
RICHEY, ETIOLOGY OF GLAUCOMA. 
His address will bear reading with this thought. 
Ordinarily, when both eyes are attacked by the same disease process, 
we rationally conclude that the cause is constitutional, and do not treat 
an expression of the dyscrasia, but rather its cause. 
In chronic glaucoma, a local manifestation is treated (for, sooner or 
later, both eyes are attacked), and then we wait to see what “ turns up,” 
with about the results presented by Dr. Bull,1 of New York, to the 
American Ophthalmological Society, in 1889 ; the detailed history of 
ninety cases of chronic simple glaucoma, subjected to the operation of 
iridectomy, during a period of seventeen years. The paper is most inter- 
esting and instructive, especially the summing up : “ One hundred and 
fifty-four operations were done on the one hundred and eighty eyes 
under consideration. Vision was temporarily improved by iridectomy 
in both eyes in two cases, and in one eye in six cases; but in all eight 
cases, after a few months, a steady loss of vision and narrowing of the 
field set in, and continued progressively as long as the patients were 
under observation. 
“ Vision remained unchanged, neither better nor worse, after the oper- 
ation, for a period of one year or longer, in both eyes in eight cases, and 
in one eye in twenty cases. 
“ Vision grew slowly and steadily worse after the operation, in both 
eyes in forty cases, and in one eye in twenty-nine cases. 
“Vision grew rapidly worse after the operation, in both eyes in two 
cases, and in one eye in eight cases.” 
He concludes that “ the health and age of the patient exert a decided 
influence upon the operation, and any marked evidence of senility is 
distinctly unfavorable to the operation.” 
Dr. Gruening,2 of New York : “ In chronic glaucoma with degenerative 
changes, neither iridectomy nor anterior sclerotomy will give the patient 
the desired relief; posterior sclerotomy may do it at times.” 
Mr. Power,3 of London : “ In cases of chronic glaucoma no operation 
is of much service.” This terse statement, it seems to me, covers the 
whole ground. 
The good results of operation in chronic glaucoma are in compara- 
tively small ratio, and are therefore accidental, and not scientific; for 
it often precipitates disaster by additional irritation. So long as the 
two chief clinical characteristics of glaucoma, increase of tension and 
excavation of the disc, are not satisfactorily explained, the management 
of such cases must be empirical. The author of iridectomy for glaucoma 
acknowledged it to be empirical, and only experience has taught us in 
1 Trans. Amer. Ophth. Soc., vol. vi., part 2, pp. 246, 291. 
2 Ibid., 1889. 
3 Trans. Seventh Internat. Med. Congress, vol. iii. p. 106. RICHEY, ETIOLOGY OF GLAUCOMA. 
9 
what cases it is of most value, those of acute inflammatory glaucoma ; 
for here it saves the eye until another time ; it does not cure the disease. 
Dr. Bull’s statistics do not teach us to do iridectomy in chronic glaucoma, 
cases of which form of the disease are in excess of any other, unless 
upon the plea of dernier ressort—because we know of nothing better. 
They indicate that the majority of eyes are worse after an operation; 
in a few the status quo ante is maintained ; in a still smaller percentage 
there is some improvement. With this diversity of result, who, save in 
the occasional case of immediate gain, or loss, to the eye, can say what 
influence is attributable to operation ? Might the case not have done 
just as well without interference? Is the surgeon justified in a feeling 
of certainty that he has done a service ? If all such cases followed 
approximately a given course he would have a guide; but they vary so 
much. If it progresses slowly after an operation, it might have done so 
without it. If it remains stationary for a time, can that be attributed 
to operation ? If the patient goes rapidly blind, has he a right to re- 
proach the surgeon? In operation is possibility, not probability. In 
simple glaucoma it has a questionable rationale, and experience teaches 
that, if done at all, it must be done with caution. It is double-edged, 
and may cut either way. 
It is a prime necessity that a quiet, healthy, out-door life should be 
led, apart from occupations of much nervous excitement, causing loss 
of reserve force ; that a condition of self-possession should be maintained ; 
that the dietary should be regulated as to time, quantity, and quality; 
for over-feeding and bad feeding is a conspicuous vice of the age. In 
adult life the effort should be to preserve the balance between waste and 
repair, and to see that both processes are normal. This is a duty which 
the family physician may share. 
As such cases pursue so chronic a course, it would seem wise to dis- 
cover the constitutional cause, and to begin with that, instead of with 
the last expression of the disease, leaving the cause in action. 
Rational management of the disease involves a study of the general 
condition and a correction of all the habits of the individual. This is 
difficult, but our function is advisory, and each sufferer must “ work out 
his own salvation ” with our guidance. 
By controlling the quantity of food productive of uric acid, and by 
reducing the whole quantity to the possibility of easy digestion and 
assimilation, thus lessening the amount of toxic substances in the in- 
testinal tract; by the regular entire excretion of what is excessive by 
way of the kidneys and bowels, harm in this way is obviated. Tonic 
aperients (not irritants and excitants), which encourage natural action 
of the intestines, serve a good purpose when used with judgment. 
Hunyadi water, taken at bedtime, lies in the tract all night, does not 
purge, but by its solvent power prevents accretions. Nothing should be 10 
RICHEY, ETIOLOGY OF GLAUCOMA. 
done to lessen the digestive power, and a quantity of food should be 
taken, small enough to insure its digestion and proper disposal. Any- 
thing (as coffee) which retards digestion must be rejected for obvious 
reasons. 
Salicylate of phenol, it is claimed, has been found in the joints of gouty 
persons taking it; therefore its purpose is apparent. 
Lithia waters secure the excretion of some uric acid ; piperazine, a 
new synthetical compound, is commended as having twelve times the 
solvent power of lithia upon uric acid. Strychnine acts by stimulating 
the functional activity of all the organs of the physical economy. 
Galvanism, if properly and steadily used, is profitable. After ten 
minutes’ use of two milliamperes direct current to the sympathetic, in an 
ordinary case, ocular tension is lessened, the pupils seem more active, and 
the patient becomes calm, often almost falls to sleep. By the experi- 
ments of Onimus andLegros1 it has been shown that if the direct current 
(positive pole at the nerve centre) be employed, the circulation is aug- 
mented ; within a few moments the arteries have increased in bulk, and 
the whole network of capillaries is seen in great commotion. Faradiza- 
tion contracted the bloodvessels, but after a time contraction ceased, and 
the arteries became larger than before the application. The continuous 
current, on the other hand, renders circulation more active, and reestab- 
lishes it when it has been arrested. The induced current causes spas- 
modic contraction of the unstriped muscle, while the continuous current 
produces a vermicular contraction (Bartholow). The latter thus favors 
the natural movement of the vessel, and while directly increasing the 
amount of blood passing, by reaction the amount of blood in the part 
supplied by the vessel is reduced to the normal. The object to be gained, 
stimulation of the cervical ganglia, the trophic centres of the region of 
the trigeminus, is accomplished as well with the cathode held in the hand 
as in contact with the affected region; yet, when placed on the temple, 
or above the eye, it has some additional mental effect, which is not unde- 
sirable. 
The writer has endeavored to cover the ground as concisely as possible: 
to offer the salient points of a view of the subject he has entertained for 
several years, especially in regard to too much food. He thinks that in 
the hypothesis discussed we find the true etiological factor of the most 
intractable of diseases, chronic glaucoma; that acute inflammatory 
glaucoma is a paroxysmal expression of the same affection ; that local 
irritation, or trauma, excites an attack of glaucoma only in the presence 
of the dyscrasia; that operation saves the eye during a paroxysm ; that 
operation serves little purpose in chronic glaucoma, even when it does 
not, by irritation, hasten the disease process or precipitate a paroxysm ; 
1 Traite d’Electricite Medicate, Paris, 1872. RICHEY, ETIOLOGY OF GLAUCOMA. 
11 
that chronic glaucoma is a neurosis—a progressive atrophy with the 
feature of inflammation with deficient power, varied by periods of seem- 
ing rest; that correcting and controlling individual habits, especially in 
the amount and character of food taken, will do more to preserve vision 
than operation; and that there may be a possibility of aborting chronic 
glaucoma, if the tendency to it be recognized at an early stage. Jotirrjal 
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items. The News, in short, is a crisp medical newspaper, a necessity to every practitioner. 
Its sphere is different from and complementary to that of the ideal medical magazine, The 
American Journal. To lead every reader of either to prove for himself the value of the two 
combined, the commutation rate has been fixed at the rate of $7.50 per annum. 
The Year-Book of Treatment for 1892 
Gives a classified summary and review of the real advances in treatment made during 1891, in all 
departments of the science of medicine. Price $1.50; or in combination with either or both the 
above journals, 75 cents. Ready early in 1892. 
The Medical News Visiting1 List for 1892 
Published in four styles: Weekly, dated, for 30 patients; Monthly, undated, for 120 patients per 
month; Perpetual, undated, for 30 patients weekly per year; Perpetual, for 60 patients weekly 
per year. The first three styles contain 32 pages of important data and 176 pages of assorted 
blanks; the 60-patient perpetual consists of 256 pages of blanks. Price, each, $1.25. In com- 
bination with either or both above periodicals, 75 cents. Or, Journal, News, Visiting List 
and Year-Book, $8.50. Thumb-letter index for Visiting List, 25 cents extra. 
LEA BROTHERS & CO., PUBLISHERS, PHILADELPHIA, 706 & 708 SAN SOM STREET.