A CASE OF N EURO-PARALYTIC KERATITIS 
WITH MICROSCOPICAL EXAMINATION 
OF THE DISEASED EYE 
BY 
G. E. De SCHWEINH Z, M.D. 
OPHTHALMIC SURGEON TO THE PHILADELPHIA AND CHILDREN'S HOSPITALS ; OPHTHALMOLOGIST 
TO THE INFIRMARY FOR NERVOUS DISEASES 
[Reprinted^rom the Archives of Ophthalmology, Vol. xx., No. i, 1891] A CASE OF NEURO-PARALYTIC KERATITIS, 
WITH MICROSCOPICAL EXAMINATION 
OF THE DISEASED EYE. 
By G. E. De SCHWEINITZ, M.D., 
OPHTHALMIC SURGEON TO THE PHILADELPHIA AND CHILDREN'S HOSPITALS ; OPHTHALMOLOGIST 
TO THE INFIRMARY FOR NERVOUS DISEASES. 
SINCE the days when Herbert Mayo showed that sec- 
tion of the trigeminus within the cranium produced 
insensibility of the eye, and Magendie, in 1824, demonstrated 
that division of this nerve in rabbits resulted in anaesthesia 
of the globe, with inflammation and sloughing of the cornea, 
physiologists, ophthalmologists, and neurologists have un- 
dertaken a large amount of experimental research in the 
endeavor to definitely prove the cause of the corneal lesion. 
Even at the present day experimenters and clinicians are 
not in accord, and an examination of the statements in 
regard to the etiology of neuro-paralytic keratitis found in 
the standard text-books leaves the reader in doubt whether 
to accept that theory which ascribes the disease to a trophic 
change, or that which attributes it to the lessened power of 
resistance which the cornea, in its insensitive condition, 
presents to external injuries, or to believe, with Gowers 
(" Diseases of the Brain," p. 90), that " this neuro-paralytic 
ophthalmia, as it has been termed, probably depends on the 
irritation of the nerve by the lesion rather than on the 
anaesthesia, or on the mere loss of nerve influence." 
The case which I am about to detail presents certain 
interesting features, both in regard to the probable situation 
of the lesion and the results of the microscopic examination. 
Reprinted from the Archives of Ophthalmology, Vol. xx., No. I, 1891. 27 
Neuro-Paralytic Keratitis. 
William S., a German, aged fifty-eight, was free from disease 
until the year 1863 (perhaps 1866), when he was attacked, accord- 
ing to his own statement, with a bubo of the right side. He 
denied having had a chancre, but shortly after the appearance of 
the bubo his hair fell out. He continued to be in good health 
until three years later, when he contracted rheumatism, and at the 
same time iritis, which was double. These conditions were cured, 
and we have no further record of the disease until March, 1884, 
when he suffered from left hemiplegia, the arm and leg being in- 
volved in the paralysis, with a cure in twelve weeks. In 1885 he 
had a second apoplectiform seizure, unaccompanied by palsy, and 
followed by a rapid restoration to health. In January, 1888, he 
had left facial palsy, at which time the eye was said to have been 
inflamed, but there is no definite record as to the character of 
the inflammation, which evidently was not that which subse- 
quently destroyed his sight. In midsummer of the same year he 
left the hospital without any evident inflammation of either eye, 
according to the statement of the trained nurses in attendance. 
In January of the next year I made the following note : 
Right eye-Round pupil ; light reflex preserved ; large, oval, gray 
optic disc, with dish-like, shallow excavation ; arteries as compared 
with veins smaller than normal ; spots of pigment on the anterior 
capsule of the lens indicating the presence of a former iritis. Left 
eye-Pupil nearly occluded by the former iritis, and preventing 
any view of the fundus ; no evidence of disease of the cornea. 
About this time various examinations made by Drs. J. Hendrie 
Lloyd and Charles K. Mills developed the following facts in re- 
gard to this patient's general condition : The left side of the fore- 
head was absolutely smooth, the left angle of the mouth drawn 
upward, probably due to a spastic condition. There was twitch- 
ing of the eyelids and muscles of the left side of the face, 
inability to protrude the tongue, whistle, or dilate the left nostril. 
The left platysma was weakened, and the masseter and temporal 
muscles atrophied. The lower jaw could not be protruded to 
perform grinding movements, sensation was practically lost over 
the left side of the face, and degeneration reaction present in the 
muscles supplied by the seventh and fifth nerves. The left arm 
was paralyzed, with marked atrophy in the extensor and su- 
pinator muscles, together with advanced degeneration-reaction 
and wrist-drop upon this side. The muscles of the left thigh and 
leg were impaired in power, the extensors and abductors having G. E. De Schweinitz. 
28 
suffered more than their antagonists, but no atrophy was present, 
and there was ready response to both faradism and galvanism. Ex- 
periments with the tuning-fork seemed to prove the partial deaf- 
ness which was present to be due to paralysis of the tensor tympani 
rather than to disease of the auditory nerve. 
In March the type of keratitis which caused the destruction of 
his eye began to develop, and speedily the following conditions 
obtained, in spite of all treatment: Coarse episcleral injection, 
perforation of the lower half of the cornea with hernia of the 
iris, and a filling of the remains of the anterior chamber with 
blood, and absolute anaesthesia of the cornea and conjunctiva. 
Lessened intraocular tension. 
To sum up, it will be seen that this patient suffered from an 
atrophic paralysis with degeneration in the left forearm ; a paraly- 
sis not complete and not atrophic in the entire left leg ; paralysis 
of the facial nerve and of the motor branches of the fifth nerve, 
involving some of the sensory fibres, producing anaesthesia of the 
left side of the face and of the left eyeball. 
Dr. Mills, after an exhaustive study of this case, which has been 
reported in the Tinies and Register of December 7, 188g, and from 
which the facts in regard to the examinations other than those of 
the eye have been quoted, came to the conclusion that this man 
suffered from a lesion in the anterior horn of the left side, in the 
seventh cervical segment, and that it reached out to the adjoining 
segments, and also to the white matter of the crossed pyramidal 
tracts. The condition of the facial muscle's was probably ex- 
plainable by the presence of a lesion of the same character as that 
in the cord, destroying the cell groups of both the facial and 
trigeminal nerves. 
The left eye, which caused the man great inconvenience and 
some pain, and the cornea of which had sloughed, was removed, 
placed in Mueller's fluid, and submitted to microscopic examina- 
tion. The following lesions were found : 
Below the centre of the cornea there is complete perforation of 
the cornea, the aperture being occupied by the stump of the pro- 
lapsed iris, which is granulating and crowded with numerous 
inflammatory and large, granular, pigmented cells. This central 
necrosis, which appears to have begun in the true corneal tissue 
and spread forward until the slough separated and perforation 
and prolapse followed, is sharply limited on either side, beyond 
which the cornea is quite free from inflammatory infiltration. As 29 
Neuro-Paralytic Keratitis. 
the periphery of the cornea is reached we find the epithelial layer 
and overlying conjunctiva much swollen and separated by col- 
lections of deeply stained small cells, which have also invaded the 
corneal tissue, in places massed in pit-like depressions-evidently 
the earlier stages of abscesses. These lesions do not penetrate 
the entire thickness of the cornea, and beyond them, passing 
inward, comparatively healthy tissue remains. 
Immediately in the neighborhood of, and surrounding the 
entrance to, Schlemm's canal, there is a collection of small round 
cells, apparently extending directly into the lumen of this sinus. 
Following the iris from the position of its prolapse toward the 
ciliary body, this is seen to be swollen, inflamed, and infiltrated 
with inflammatory cells, a condition which repeats itself in the 
ciliary body. Of special interest are the vessels in these struc- 
tures, particularly in the latter. They present one of the forms of 
obliterating arteritis. Taking as the type a small ciliary arteriole, 
it reveals in cross-section the following characteristics : An 
asymmetrically placed lumen contracted out of proportion to the 
size of the vessel ; unusually prominent endothelial plates pushing 
their way into the central aperture, bounded externally by badly 
stained fibrous elements that have practically substituted the 
middle coat, which can still be seen in the periphery as a narrow 
circle of poorly developed muscular fibres, beyond which the in- 
definite tissue of the adventitia is apparent. The condition is 
analogous to that which has been described under the term 
mesarteritis. 
The choroid, retina, and optic nerve are free from disease. 
The ciliary nerves, where they pass through the sclerotic coat, 
were carefully sought out, but do not present, in the carmine 
sections, any evidence of inflammation or infiltration, and in those 
stained by Weigert's method any sign of degeneration. Their 
reaction to these reagents was in all particulars such as is seen in 
nerves of normal constitution. 
The principal appearances as found microscopically are 
hence: A sharply-defined, central slough of the cornea, 
separated by nearly normal corneal tissue from a periph- 
erally situated, secondary keratitis, having inflammatory 
connection with overlying diseased conjunctiva, but bounded 
below by reasonably healthy cornea ; small-celled infiltration 
surrounding Schlemm's canal ; inflamed iris and ciliary G. E. De Schweinitz. 
30 
body, through which tissues the arterioles present a form of 
arteritis of the type known as mesarteritis ; normal choroid, 
retina, and optic nerve; and unaffected ciliary nerves. 
The keratitis present in the eye under consideration, apart 
from its etiology, is interesting on account of its apparent 
mode of development. It bears a strong resemblance to the 
type described by Senftleben {Virchow's Archiv, Bd. 65, p. 
69), and which he produced in animals in whom the tri- 
geminus had been divided. Under these circumstances this 
investigator found that the primary affection of the cornea 
appeared as a necrosis originated by the repeated trauma- 
tisms which the eye encountered owing to its anaesthesia. 
This circumscribed necrosis of the cornea then acted as a 
seat of inflammatory irritation, and brought into existence 
a secondary keratitis proceeding from the periphery of the 
membrane. 
The obliterating arteritis evident in the vessels of the 
ciliary body, in the study of which I have had the advantage 
of the assistance of Dr. Meigs, presents an inviting oppor- 
tunity to construct a theory in regard to the etiology of 
neuro-paralytic keratitis. As, however, was originally pointed 
out byC. Friedlaender {Centralblatt f. die med. Wissenschaft., 
1876, p. 69) arteritis obliterans is found in specimens from 
clinical and experimental phthisis, in tumors, and in chronic 
inflammations, especially if accompanied by tuberculosis, an 
observation which Dr. Meigs has confirmed in his studies of 
the vessels in various diseased tissues. The existence, then, 
of this lesion in the present instance is to be explained 
as the result of a chronic inflammation, and in no sense as a 
cause of its existence. 
The entire absence of disease of the ciliary nerves is a 
noteworthy fact, and demonstrates that although the nuclei 
of the fifth pair were affected, there was no degeneration or 
inflammation in the course of the peripheral distribution of 
this nerve. 
It may be interesting briefly to refer to the various theories 
which, from time to time, have been advanced to explain 
the existence of neuro-paralytic keratitis. The earlier 
experimenters, Magendie, Claude Bernard, and von Graefe, 31 
Neuro-Paralytic Keratitis. 
maintained that the destructive changes in the eye were 
largely due to the section of a trophic nerve. Snellen con- 
cluded that the disease was nothing more than a traumatic 
inflammation provoked by the presence of undetected in- 
juries and foreign bodies. Schiff, noticing that section was 
followed by paralysis of the nerves of the vessels, together 
with widening of their calibre and later inflammation, rele- 
gated the cause to the nerve itself through a vaso-motor in- 
fluence, but afterward modified this opinion by stating that a 
neuro-paralytic hyperaemia was conditioned by the develop- 
ment of an inflammation stirred up by outside influences. 
The experiments of Samuel, Buettner, Meissner, Eckhard 
and others gave rise to the tropho-traumatic theory, Meiss- 
ner especially holding that the inner fibres of the nerve are 
more important in the trophic influence than any others. 
According to Buettner and Meissner the division of these 
fibres deprived the eye of its capacity to resist external 
influences. Among other theories is that one elaborated by 
Eberth, in which a mycotic influence was invoked to explain 
the disease. The pure traumatic theory, developed origin- 
ally by Snellen, has found many advocates, notably Senft- 
leben and v. Gudden. 
The most recent elaborate work upon this subject is by E. 
v. Hippel ^Archiv f. Ophthalmologie, Bd. xxxv., 2, p. 217), 
from whose paper I have abstracted the facts just quoted. 
This author cannot accept the presence of medially placed 
trophic fibres in the trigeminus, believes the pure traumatic 
theory to be untenable, denies the existence of an impaired 
power of resisting traumatisms on the part of the affected 
eye, which, however, is more exposed on account of the 
anaesthesia to desiccation than is the case with a normal one, 
rejects micro-organisms as etiological factors, and holds that 
the theory of increased evaporation is sufficient to explain 
the development of the inflammation, showing experiment- 
ally how a moist atmosphere can prevent the disease. G. P. PUTNAM'S SONS, PRINTERS 
NEW YORK