Case XXX.—(By permission of Mr. N. M. MacLehose, M. B.) H. Y., aged thirty. Homonymous diplopia observed over a period of six months without appreciable ocular paralysis; pupils of medium size, with definite Argyll-Robertson phenomenon; knee-jerks absent, and in later months decided ataxia and sensory defects in lower limbs; visual acuity unaffected to ordinary test, but gradual contraction of visual fields, especially on right side; chancre and secondary syphilis four years before.
There are in these series of cases many facts which might reasonably be made the subject of remarks, and several of the cases are certainly of great individual interest. But they are here displayed in the above grouping for the purpose of illustrating the clinical order and sequence in which, as a matter of actual experience, the ocular disturbances of locomotor ataxia may manifest themselves in relation to the spinal evidences of that disease. Of course, in those cases in which there exists only a single ocular symptom unaccompanied by any sign of spinal disease, it may be objected that it has yet to be demonstrated that such cases are of the nature of locomotor ataxia. It is doubtless to be desired that such cases should be under exact observation as long as the opportunity for further developments exists—that is, for the entire life of the patient. But to insist upon such a condition is a mere counsel of perfection. One must make reasonable use of such evidence as the brevity of life and the exigencies of practice permit. And the evidence here set forth affords at least a very strong presumption, to say the least of it, of the truth of the doctrines stated in the earlier paragraphs of this paper. Probably the particular proposition which is most likely to be contested is the one which places the Argyll-Robertson pupil equally with optic-nerve atrophy, and an ocular paralysis, as a possible first event in the eruption of the phenomena of locomotor ataxia. But on turning to the records it will be found that the facts support this suggestion almost as strongly as they support the corresponding suggestion in reference to optic-nerve atrophy and ocular paralysis. Attention in this respect may be particularly given to Case XIII. The man complains of a quite recent diplopia, and he has undoubtedly had syphilis; the pupils show the Argyll-Robertson phenomenon. It is in the highest degree probable that, had the patient been under observation a week or two earlier, the condition of the pupils would have been the sole existing ocular abnormality. Yet in the light of the development of an ocular paralysis, it can scarcely be doubted that, whether he develop spinal symptoms or not, his nervous system is the site of diseased processes of the locomotor ataxia order. When to these facts there are added, as in Cases XIV. to XVII., illustrations of the various forms and degrees of evidence of spinal disease that may be associated with the Argyll-Robertson pupil, it seems impossible to resist the conclusions that the condition of the pupil so named may be the first evidence of locomotor ataxia; that it may precede by varying intervals other evidences of the disease; and that at least very probably, in a certain number of cases, the symptomatology of the disease may be permanently restricted to this one event. In some examples of its spinal form locomotor ataxia is undoubtedly an extremely chronic disease, with few and imperfectly developed symptoms; and it is thus not unnatural to expect that similar limitations may obtain in the ocular manifestations of the disease. That evidences of grave nervous disease may be limited to the pupil is well seen in Case XVIII., where a syphilitic patient was under observation for three years without the discovery of any abnormality other than paresis of each sphincter iridis. There is certainly no obvious reason why a similar restriction should not determine the Argyll-Robertson pupil as a purely isolated phenomenon with, it must be added, the same unfortunate possibilities that are undoubtedly attached to the patient whose case has just been quoted. The conclusions above adopted in reference to the Argyll-Robertson pupil are applicable, mutatis mutandis, to optic-nerve atrophy and to ocular paralysis, as is abundantly demonstrated in the corresponding series of the cases recorded in this paper.
Deady.
Menzies, J. Acworth.—Detachment of Corneal Epithelium (?).—British Med. Jour., March 17, 1900.
The following case seems to be worthy of record because of the long duration of the symptoms and the immediate relief ultimately obtained. Mrs. W. consulted me on August 4, 1899, and gave the following history: Five years previously the right eye was struck and “cut” by a cricket ball. Since that time there had been pain exactly as if there was a foreign body under the lid or embedded in the cornea. There was a pricking feeling on winking, and the patient could not bear to have the upper lid touched in its outer half. She could only obtain ease by keeping the eyes closed and perfectly still, or wide open with the lids motionless. On examination no foreign body could be seen, and the lids were normal. In the lower outer quadrant of the cornea careful observation showed that the epithelium was ruffled and freely movable over a small area, and in part of the same area was a tiny circular, slightly opaque, raised patch of the corneal tissue. Nothing more could be made out. I prescribed a bandage and some boric lotion with cocaine. Two months later, on October 6, I again saw the patient, who was then in precisely the same condition as before, and had been so during the two months’ interval. She was in such misery that I decided to adopt surgical measures at once. Accordingly, after instilling cocaine, I carefully explored the painful area with a needle, but could detect no foreign body. I then scraped the part thoroughly with a sharp spoon, removing the epithelium for some little distance around, and a fair amount of corneal tissue in the affected area. The following day there was some smarting, but the eye could be moved freely under the lid, and there was no pain on pressure over the previously tender spot. Progress was uninterrupted. The epithelium grew over the denuded surface, and no opacity resulted. The eye now is perfectly right and the vision is normal.
I should have put the difficulty I had in making a diagnosis down to my having overlooked some detail, had it not been that the patient was for a considerable time under treatment at an eye hospital. The explanation I am inclined to adopt, for want of a better, is this, that the original blow caused the anterior elastic lamina with the epithelium to become detached. The nutrition of the epithelium might thus be kept up, and every movement which pressed upon the surface would bring the detached membrane down on the corneal nerve filaments. But it must be confessed it is not easy to understand how this condition could remain stationary for five years.
Deady.
Hines, M. D., Oliver S.—Iodide of Stannum in Tuberculosis.—The Amer. Hom., March 15, 1900.
The author thinks iodide of stannum often preferable to stannum in tuberculosis. He uses it when the patient has a clear complexion and long eyelashes and where the progress of the disease is rapid. He reports a case for which the 2x trituration was given, in which there was “a marked tubercular affection of the chest, increased vocal fremitus, an abundance of thick yellow and sweetish sputum, sweat at night, and rapid emaciation.” The result was encouraging.
Palmer.