Part 6

CASE XXI.—E. S., aged forty-three. Diplopia from paralysis right external rectus, pupils small, each with Argyll-Robertson phenomenon; visual left acuity only 6/12, and small but distinct central scotoma, with some contraction of the peripheral field; knee-jerks distinct, and no ataxia or other evidence of spinal disease. Three early miscarriages, no full-time child. No change while under observation for nine months, but on two occasions severe attack of vomiting and abdominal pain, extending over several days and without recognized cause (? gastric crises).

CASE XXII.—A. M., aged fifty-five. Left ptosis and paralysis of external ocular muscles supplied by third nerve in 1887, the pupils being normal, followed by incomplete recovery. In 1897 development of identical condition on the right side, and pupils found to be small and with Argyll-Robertson phenomenon; knee-jerks very slight and with great difficulty, but no other evidence of spinal disease. No history of syphilis.

CASE XXIII.—H. F., aged thirty-seven. Right ptosis with diplopia (seven days) and defective inward excursion of right eyeball; pupils very small, not quite equal, and with Argyll-Robertson phenomenon; optic disks pale and marked contraction of visual fields, but normal central vision; knee-jerks scarcely to be obtained, but no other evidence of spinal disease. No history of syphilis. Father of four healthy children. Seen after a month’s interval, paralysis of all external right ocular muscles supplied by third nerve, and knee-jerks absent.

(c) _Ocular Paralysis, with More or Less Evidence of Spinal Disease._

CASE XXIV.—G. S., aged forty-one. Ptosis and complete ophthalmoplegia externa on left side, with dilated and immobile pupils and some degree of right ptosis, these conditions or some of them having been present for five years. Knee-jerks distinct, and no ataxic phenomenon, but imperfect control over bladder, and failure of sexual power during last six months. No admitted syphilis.

CASE XXV.—J. L., aged forty-two. Diplopia and drooping left upper eyelid for four years. Ptosis left side, and marked defect of ocular movements in each eye; left pupil dilated and immobile; right small, contracts during convergence, but no light response; no other ocular defect. Knee-jerk scarcely obtained on either side; no ataxia, but attacks of “twitching pains” in lower limbs, and for some time difficulty in starting the flow of urine. Venereal sore in 1882, and subsequent loss of hair, but no other secondary symptoms. Patient watched for twelve months without appreciable change.

CASE XXVI.—L. D., aged forty-four. Crossed diplopia (one month), without obvious ocular paralysis, and pupils small with Argyll-Robertson phenomenon. Knee-jerks absent; no ataxia to usual test, but has noticed tendency to stagger in the dark; is troubled with pains in the knees, has difficulty in commencing the act of micturition, and recent marked failure of sexual power; venereal sore at twenty years, and subsequent sore throat, but no skin eruption or loss of hair. Father of three healthy children.

CASE XXVII.—J. H., aged forty-seven. Double vision of two months’ duration; similar attack three years ago, with complete recovery. Paralysis of right external rectus; pupils, visual acuity, and visual fields normal. Knee-jerks absent, but no other evidence of spinal disease. Patient the subject of albuminuria, and presents physical evidence of an aneurism of the ascending aortic arch. Youngest child has marked evidence of inherited syphilis.

CASE XXVIII.—W. M., aged thirty-five. Paralysis of left third nerve, without iridoplegia or cycloplegia; pupils normal. Knee-jerks absent, but no ataxia or other evidence of spinal disease. Several venereal sores ten years ago, but no recognized secondary syphilis. There is, however, evidence of a former iritis.

CASE XXIX.—M. C., aged fifty-four. Paralysis of left external rectus, with history of two previous attacks of diplopia during last four years; no other ocular defect, unless some imperfect light response in left pupil; knee-jerks absent, and complaint of “sciatica” for two years, but no other evidence of spinal disease. Albuminuria distinct, and physical signs of hypertrophy of left ventricle. No history of syphilis.

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.

=Kyle, M. D., D. Braddon.—Initial Forms of Tubercular Laryngitis.=—_Inter. Med. Mag._, March, 1900.

The enumeration and exact description of these prodromal symptoms are so important that we copy them in full.

The following, which is a translation of an article by Monsarrat of Paris (_Rev. Hebdom. Laryngol., d’Otol., et de Rhinol._, No. 43, October 28, 1899), covers the ground so thoroughly that it is worthy of repetition:

“Laryngeal phthisis completely developed presents multiple and varied symptoms, some more characteristic than others. In one patient are found symptoms functionally grave, out of proportion to the lesions relatively benign. In another, physical signs take first place; there may be an ulceration completely obliterating one cord, or considerable œdema of the arytenoids and vestibule, which closes the opening of the glottis. Having reached the period when tuberculosis is easily recognized, the various patients are able to date their laryngitis from diverse pathologic beginnings. This one will present solely the history of a cough, the other a raucous voice, in another pain will take precedence. In mentioning these various modes of commencement we insist on the connection which may exist between each of them and the localization at the beginning of tuberculosis, on one or the other parts of that complex organ known as the larynx. Let us divide the symptoms into the functional and the laryngoscopic. The connection or antithesis between them will be noticed.

“An initial symptom, quite frequent in tubercular laryngitis, is, without a doubt, cough. This symptom, common to all maladies of the respiratory tract, would have no diagnostic value, except that it is characteristic. On it alone the diagnosis of laryngeal phthisis could never be based. At the beginning, cough puts us on our guard, especially when it is causeless; that is to say, when auscultation of the chest fails to reveal anything abnormal. This cough is always persistent, sometimes violent, hawking, and provoking.

“The physical signs of the chest do not correspond to the tenacity of the cough; it is therefore possible for the larynx to be accused. As regards this cough, the ‘hemming’ so often described, and which draws attention most often to a possible rhinopharyngitis, may cause us to think at the beginning of tuberculosis, but only after examination of the rhinopharynx has established its integrity. There is a cough, well known at the beginning of tubercular laryngitis, a little dry cough, commencing insidiously, often at the moment when the patient is about to speak, which the individual himself does not notice, but to which his friends attach an importance too often justified by the outcome. The cough may be hacking, followed or not by expectoration, and often accompanied by vomiting. It is certainly right to consider it as a symptom of the beginning of the disease.

“The speaking voice is often altered, dysphonia appears, and the patient who is attacked presents little alteration in his larynx; no ulceration, the cords accurately approximate, and they are very slightly congested; the laryngeal image does not reveal anything by which this profound alteration in the voice can be explained. There is no cough. There will come a time in the disease, however, which will cause us to see that this, too, is an initial form, and oblige us to give a prognosis exceedingly guarded.

“The voice may be eunuchoid. Castex has noted it among the tuberculous. The raucosity of the voice should also recall the statistics which demonstrate the fact that a fifth of the cases of this condition are tubercular. But these three symptoms, dysphonia, raucosity, eunuchoid voice, are also found in other maladies of the larynx; conditions, however, easily diagnosticated by the laryngoscope. If nothing justifies these affections of the voice, one should think of tuberculosis. It is these initial forms, apparently paradoxical, but analogous to that, which we are going to mention under the subject of pulmonary lesion not sufficient to provoke cough in the beginning if the larynx has not been initially affected. The forms that are recognized in the mirror are evidently very numerous. We will mention some: Congestion of the cords, monocorditis, recurrent laryngitis, and a nodular form at the free border of the vocal cords. We do not take into consideration any variety of ulceration, no matter how insignificant, as for the most part the velvety aspect of the cords leads us to think at once of laryngeal phthisis. But this has not appeared at the beginning, and we are only considering initial forms. The symptoms which we are attempting to describe are those suggestive of tuberculosis, and we only say that tuberculosis of the larynx may begin by a nodule, by a congestion, by a monocorditis, etc.

“Congestion of the vocal cords, whose ætiology is difficult to explain, often coincides with slight dysphonia, with cough. This congestion, fugacious, if not tuberculous, disappears with rest, if it is not aggravated by a chronic rhinopharyngitis. In the majority of cases the patient returns. Despite a treatment, properly instituted, the congestion persists; it extends on the cords; it may remain there, or it may reach over the ventricular bands to the arytenoidal apophyses; this is a form of commencing laryngeal phthisis, especially if, after a period of calm, there is found in a patient a new congestion. It is recurrent laryngitis, another form of initial tuberculosis more grave than the first. Against laryngitis of this form treatment is of no avail.

“Another variety of initial tuberculosis is monocorditis. The patient becomes suddenly aphonic; laryngoscopic examination shows a cord perfectly red, congestion of which is evident, not only by the color, but by its altered volume. Contrast with the sound cord is often striking. Movements of the affected cord may be observed, but it is generally paretic. Acute monocorditis should cause us to think that it is an initial form of tuberculosis. This monocorditis often corresponds to the side of the lungs which is afterward or at that time attacked by the bacillus. Certain authors admit that this relation is absolutely constant, and their statistics allow no exception to the rule. On the other hand, Bayle’s theory, setting forth the direct penetration of the tubercular infection, becomes less often justified. It is the lymphatic route which most often produces bacillary infection.

“Tubercular laryngitis may often begin by a nodule situated on the border of the vocal cords. It is important not to confound it with singers’ nodules, these latter being more conical and more rounded. The tuberculous nodule may grow slowly, not ulcerate for a long time; interfering so little with the speaking voice that the patient often refuses any intervention. But the day comes when we see this nodule desquamate, and we may observe the evolution of the tuberculous ulceration which displaces it. We make no mention of the other forms of commencement characterized by a congestion of the entire organ, by œdema of the epiglottis, by a lividity quite characteristic which invades the entire endolaryngeal mucosa, forms most usual for the tubercular involvement of the larynx. A form especially noticeable is that which begins with a sensation of a lump in the throat. It is true that this variety is not observed except in the nervous; it is not, however, to be compared to the globus hystericus. Tuberculous patients, in whom the tuberculous process in the larynx begins with a sensation of a lump in the throat, may be in very good health, but this particular impression is often the first symptom which they observe in a laryngitis, which finally becomes tuberculous. At the moment when the patient complains of this symptom it may happen that laryngoscopic examination fails to detect any lesion. It is useless to add that this form is especially met with in the female. It most nearly resembles that form that begins with a dysphagia that persists to the end; but at the beginning of tubercular laryngitis this dysphagia alone is noted without any other symptoms.” So it can be seen that laryngeal phthisis may begin by a variety of symptoms, some common, the others rare. It is needless to insist upon the importance of an early diagnosis.

PALMER.

=Ball, James Moores.—On Removal of the Cervical Sympathetic in Glaucoma and Optic-Nerve Atrophy.=—_Jour. A. M. A._, June 2, 1900.

I propose to consider the surgery of the cervical portion of the great sympathetic nerve in certain ocular diseases. European oculists and surgeons have performed sympathectomy for glaucoma and exophthalmic goiter. I have gone further, and in one instance removed the superior cervical ganglion for simple atrophy of the optic nerve. I have performed sympathectomy four times up to July 20, 1899. First the cases will be reported; then the conclusions will be drawn.

CASE I.—EXCISION OF SYMPATHETIC FOR GLAUCOMA ABSOLUTUM.

Mrs. B. S., aged thirty-six, has had pain in and around the right eye for two months, and examination showed vision in this eye reduced to light perception; tension + 3, and the pupil widely dilated. The anterior chamber was shallow, the cornea cloudy and slightly anæsthetic, the media slightly cloudy, still allowing the fundus to be seen. The episcleral vessels were enlarged. Circumcorneal injection was present and the optic nerve cupped. A diagnosis of chronic irritative glaucoma was made. The left eye presents immature cataract, and vision in this eye is 20/70.

Knowing of the flattering results obtained by Jonnesco and others, by excision of the superior cervical ganglion in absolute glaucoma, I explained the operation to the patient, and obtained permission to operate. On May 15, 1899, the patient was anæsthetized, chloroform being employed. An incision four inches in length was made on the right side downward from the mastoid process, extending along the posterior border of the sterno-cleido-mastoid muscle. The external jugular vein was cut and tied. The sterno-cleido-mastoid was then separated from the trapezius muscle, and the spinal accessory nerve was cut. A deep dissection was then made, exposing the carotid sheath. This was opened to enable us to locate the pneumogastric nerve beyond question. The carotid, internal jugular vein, and pneumogastric nerve were then pulled forward, enabling us to see the rectus capitis anticus major muscle, on which the superior cervical ganglion rests. Tearing through the fascia, the ganglion was found and stripped. The ganglion was then cut high up with curved scissors and all its branches severed. About one inch of the trunk of the sympathetic below the ganglion was removed. The wound was closed with interrupted sutures and the neck placed in a plaster cast. The time required for operation was fifteen minutes, and immediately after it was noticed that the right eye was suffused with tears, the right conjunctiva much injected, and the right nostril moist. The intra-ocular tension was + 2. The patient slept well all night, without medicine, being free from pain for the first time in over two months. Tension had steadily decreased to + 1.

On May 16, slight ptosis was noticed on the right side. This symptom is yet present. On May 19 the circumcorneal injection was much less; the conjunctival hyperæmia and lachrymation were still present, while the ptosis was slightly increased and tension was + 1.

At the present date—July 23, 1899—this patient has no pain. The retinal arteries are increased in size. Tension is + 1. Vision has increased from light perception to ability to count fingers at three feet. The conjunctival injection which followed the operation has disappeared; the optic nerve has a color more approaching the normal. The ptosis is less.

This was the first sympathectomy made in America for glaucoma.

CASE II.—DOUBLE SYMPATHECTOMY FOR GLAUCOMA SIMPLEX.