Chapter III: Part 3

Of course, in a given case of optic-nerve atrophy without spinal symptoms the question may fairly be raised whether it is right to place such a case in the locomotor ataxia group. All that can be said in reply is (1) that from cases of optic atrophy pure and simple one passes by an unbroken series of steps through cases with more and more distinct evidence of locomotor ataxia to, at the end of the series, optic atrophy in association with characteristic ataxic symptoms, and (2) that, as already stated, a simple case of optic atrophy may remain unchanged for many years, and yet in the end display undoubted evidence of the development of a spinal lesion. But if optic-nerve atrophy may be the primary symptom in the disease, if the occurrence of spinal symptoms may follow it after an interval of many years, and if again it may remain without at any time any existing ataxia, it is not unreasonable to presume that both the Argyll-Robertson pupil and an ocular paralysis may each have exactly corresponding relations to the development of the spinal evidences of locomotor ataxia. The collection of evidence to support this suggestion is even more difficult than in the case of optic-nerve atrophy. The latter condition must ere long compel the patient to seek medical advice, and thus the opportunity for a complete investigation of the state of his nervous apparatus is afforded at a relatively early date. But an Argyll-Robertson pupil may exist, and presumably exist for years, without any inconvenience to the patient. Such a patient, therefore, will not consult his medical adviser until spinal or other symptoms display themselves, and thus the precedence of the pupillary condition cannot be determined. In the case of an ocular paralysis medical assistance is, no doubt, usually promptly invoked. But such an occurrence is open to a number of ætiological explanations, for example, rheumatism, cold, etc., which it is difficult to exclude with confidence. Hence it is much less precise in its significance than either a double optic atrophy or the Argyll-Robertson pupil. It must be by the collection of observations extending over a long term of years that actual demonstration of the relationship of the ocular disturbances now in question to the occurrence of spinal disease can be established. But while falling short of the merit of actual demonstration, the presentation of the facts displayed by a number of cases which could only be observed over relatively brief periods is not without value. If no one case affords a complete history of all the stages of the disease the picture presented may none the less be fairly complete, provided the cases are sufficiently numerous, and they are seen at different points of development. It is believed that in the present series these conditions are fulfilled. The conclusions they afford, as far as the present purpose is concerned, are: (1) That an optic-nerve atrophy, an ocular paralysis, or an Argyll-Robertson pupil may exist as an isolated symptom for a considerable time, presumably for years; (2) that any two of these may be associated together, with a correspondingly increased presumption that the diseased process causing them is of the locomotor ataxia order; (3) that any one of the three, or a combination of two or all of them, may exist in conjunction with a greater or less degree of evidence of spinal disease; and (4) that occasionally a case which commences with purely ocular symptoms may be seen to develop with comparative rapidity characteristic symptoms of the spinal lesion of locomotor ataxia. The cases therefore may be held to justify the view that an optic-nerve atrophy, an ocular paralysis, or the Argyll-Robertson pupil (not capable of other explanation) must be regarded as affording a definite basis for suspicion in reference to a possible development of spinal disease. On the other hand, it must be admitted that the prognostic indication, so far as spinal disease is concerned, is not an absolute one, for the ocular defect may exist certainly for many years without any evidence whatever of the involvement of the spinal cord.

The cases here recorded have all been the subject of detailed and in most cases repeated examination, and unless the contrary is stated, it may be taken for granted that the thoracic and abdominal viscera are normal, to physical and other methods of examination. In all cases, too, in which no specific statement is made, it is to be understood that the visual acuity, the visual fields (both for white and colors), and the fundus oculi have been proved to be normal. This last statement of course does not apply to cases in which optic atrophy exists. Particular care has been taken to be accurate in regard to the condition of the pupils and the knee-jerks. In nearly, if not absolutely in every instance where a departure from the normal is chronicled, the record has been confirmed by more than one observer, and in the case of a deficient knee-jerk the conclusion stated has never been formulated until the conditions insisted on by Gowers, Buzzard, and Jendrassik have been fulfilled. With a few exceptions in which only a single observation was possible, the patients have been watched for months, and in some instances for several years. The cases are arranged in series, with a view to show how, from a purely ocular condition, one may pass through gradually accumulating evidence to the same ocular condition in association with the characteristic signs of the spinal lesion of locomotor ataxia.

I.—CASES IN WHICH OPTIC-NERVE ATROPHY IS THE PRIMARY OR DOMINATING
CONDITION.

(_a_) _Optic Atrophy, without Other Evidence of Disease._

CASE I.—W. T., aged twenty-five. Failure of vision extending over two years, with reduction of visual acuity to the power of counting fingers at three feet. Double optic atrophy; pupils medium, with distinct light response; knee-jerks distinct and no evidence of spinal disease, and no cerebral symptoms other than one or two attacks of giddiness. Urethritis, but no syphilis.

CASE II.—F. R., aged thirty-eight. Double optic atrophy, with almost complete loss of vision, the defective sight having been observed for at least eighteen months; pupils dilated and immobile; no evidence of spinal disease, unless possibly some degree of failure of sexual power; no cerebral incidents; no history or evidence of syphilis.

(_b_) _Optic Atrophy, with Other Ocular Evidence Suggestive of Locomotor
Ataxy._

CASE III.—(By permission of Mr. Ernest Clarke, F. R. C. S.) R. C., aged thirty-nine. Double optic atrophy, reducing right visual acuity to the power to count fingers at four feet, and left to mere perception of light; right pupil dilated and three times the size of the left; neither any light response, but free movement on convergence; entire absence of symptoms and objective signs of spinal disease; “gleet” twenty years before, no syphilis.

CASE IV.—A. S., aged twenty-five. Double optic atrophy, with observed failure of vision for twelve months. V. A. right-hand movements only; left, 6/18 part; pupils 2.5 mm., no light response, but contract on convergence; knee-jerks difficult to obtain, but movement, though possibly wanting in promptness, is normal in extent; no ataxia or other evidence of spinal disease; mother of three healthy children, no miscarriages.

(_c_) _Optic Atrophy, with Some Evidence of Spinal Disease._

CASE V.—W. A., aged thirty-seven. Double optic atrophy, with reduction of visual acuteness to “hand movements;” pupils dilated and immobile; knee-jerks absent, but no other evidence of spinal disease; venereal sore when aged twenty; no recognized secondaries, and father of four healthy children.

CASE VI.—J. G., aged thirty-five. Failure of sight (six months); optic atrophy, gradually increasing whilst under observation of twelve months; pupils not definitely abnormal; knee-jerks absent throughout, but no further appearance of spinal disturbance; urethritis, but no history of syphilis; father of two healthy children, wife no miscarriages.

CASE VII.—F. L., aged thirty-nine. Double optic atrophy, reducing visual acuteness to 6/24, pupils very small, and with Argyll-Robertson phenomenon; subsequent to failure of sight (twelve months) has had shooting pains in thighs, and failure in retention power of bladder; knee-jerks distinct; no ataxia or sensory defect in lower limbs; venereal sore twenty years before; no recognized secondary syphilis; wife healthy: seven pregnancies, five miscarriages.

(_d_) _Optic Atrophy, with Distinctive Evidence of Spinal Disease._

CASE VIII.—C. H., aged thirty-eight. Failure of sight (two years) from double optic atrophy; pupils medium, with Argyll-Robertson phenomenon; moderate double ptosis, but no ocular paralysis; shooting pains in lower limbs (eight years); knee-jerks absent; considerable ataxia and failure of control over bladder; syphilis at nineteen years.

CASE IX.—G. S., aged forty. Pallor of disks and peripheral contraction of visual fields; four months later loss of knee-jerks and gradual development of ataxia; pupils normal throughout; death at the end of twelve months with symptoms of meningitis; syphilis at twenty-five years.

II.—CASES WITH ARGYLL-ROBERTSON PHENOMENON.

(_a_) _Argyll-Robertson Phenomenon, without Other Evidence of Disease._

CASE X.—A. L., aged thirty-three, the subject of slight hypermetropic astigmatism. Pupils small, not quite circular, with Argyll-Robertson phenomenon; no other ocular defect, and no evidence of a spinal lesion. No history of syphilis.

CASE XI.—K. S., aged forty-three. Pupils rather small, unequal, quite destitute of light response, though moving freely in convergence; no other ocular defect except some presbyopia; no evidence of spinal disease, though left knee-jerk not easily obtained. Unmarried; syphilis seems highly improbable.

CASE XII.—G. G., aged sixty. Pupils small, with distinct Argyll-Robertson phenomenon. Knee-jerks, not easily obtained, but not definitely abnormal, and no other evidence of spinal disease. Patient suffers from defective vision, probably from tobacco poisoning (central scotoma for red); no history or evidence of syphilis.

(_b_) _Argyll-Robertson Phenomenon, with Other Ocular Disturbance
Suggestive of Locomotor Ataxia._

CASE XIII.—D. T., aged forty-two. Pupils below medium size, destitute of light response, with free movement in convergence; had for seven days suffered from diplopia, and under observation gradual development of complete paralysis of right external rectus; no other ocular defect. Knee-jerks distinct, and no suggestion of spinal disease; chancre of lip and secondary syphilis nine years before.

(_c_) _Argyll-Robertson Pupils, with More or Less Evidence of Spinal
Disease._

CASE XIV.—T. F., aged fifty-five. Right pupil 2mm., left 3 mm., each with Argyll-Robertson phenomenon; no other ocular defect except presbyopia. Ten years ago had difficulty in passing urine, and since then occasionally voids it involuntarily, and for eighteen years has been liable to seizures of pain in calves, insteps, and heels; knee-jerks normal, and no objective signs of spinal disease. Venereal sore when aged twenty, but no secondary symptoms, and father of six healthy children.

CASE XV.—H. W., aged thirty-eight, is the subject of hypermetropia, 4.5 D. Pupils very small, especially left; neither moves under light, but distinct contraction during convergence. Admits recent difficulty in descending stairs, saying he “frequently misses the bottom step,” and has suffered from “sciatica” for two years. No objective evidence of spinal disease, and urinary and sexual functions undisturbed. Admits gonorrhea, but denies syphilis. Wife miscarried eight months after marriage; no further pregnancies.

CASE XVI.—R. S., aged forty-three. Hypermetropic and presbyopic. Pupils small, unequal, not quite circular, and with definite Argyll-Robertson phenomenon. Knee-jerks cannot be obtained (confirmed on three different dates), but no other sign or symptom of tabes dorsalis, unless “rheumatic pains” in lower limbs for several years. Unmarried; no history of syphilis. Four years ago had, after “catching cold,” to have urine withdrawn by a catheter, but no subsequent disturbance of bladder function.

CASE XVII.—E. W., aged forty-eight. Myosis with Argyll-Robertson phenomenon; right ptosis and crossed diplopia (one month), without obvious ocular paresis; absence of right knee-jerk (confirmed on two occasions), and failure in retention power of bladder (six months), but no other evidence of spinal disease; vulvar sores and skin eruption six years before.

III.—CASES IN WHICH AN OCULAR PARALYSIS IS THE EARLIEST OR DOMINATING
SYMPTOM.

(a) _Ocular Paralysis, without Other Evidence of Disease._

CASE XVIII.—(By permission of Mr. J. T. James, F. R. C. S.) F. D., aged thirty-seven. Dilated and immobile pupils, without any other ocular defect. No evidence of spinal disease; syphilis nine years ago; no change while under observation for three years.

CASE XIX.—K. K., aged twenty-eight. Iridoplegia, double, followed by paralysis of left external rectus, the condition being under observation for nearly a year, but without the discovery of any satisfactory explanation. No evidence of spinal disease. Married, four healthy children, no miscarriage; during one pregnancy very free loss of hair (now grown again), but no other occurrence to suggest syphilis. No family or personal history of gout or rheumatism.

CASE XX.—G. H., aged thirty-three. Dilated and immobile pupils, with incomplete ptosis and divergence of eyeball on each side. Present condition of four years’ duration, and separated by an interval of three years from venereal sore and skin eruption. No other ocular defect; no evidence of spinal disease, and general health good throughout. No change while under observation for three months.

(b) _Ocular Paralysis, with Other Ocular Evidence Suggestive of
Locomotor Ataxia._

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.

Miss M. E., a German, aged forty-three, was sent to me on June 14, 1899. For two years sight had been failing, until at this time vision was as follows: R. E. = 0; L. E = light perception. Tension was + 3. Both optic nerves showed marked cupping of the disk; the vessels were pushed to the nasal side. She stated that she had never had pain in the eyes, and had not consulted an ophthalmic surgeon.

I advised her to submit to an excision of the left superior cervical ganglion; she consented, and on June 15 the operation was performed by myself, assisted by Dr. E. C. Renaud, at St. Joseph’s Sanatorium, in the presence of Drs. J. C. Murphy, A. R. Kieffer, and S. A. Grantham. The operation was difficult, owing to the abnormal position of the vagus nerve. This was outside of and external to the carotid sheath, and was much smaller than normal; it was not larger in diameter than the head of a pin. It was identified by irritating it and watching the effect on the heart. The superior cervical ganglion was removed and one-half inch of the trunk of the sympathetic below. Shortly after the operation there were lachrymation, ocular congestion, and contraction of the pupil on the corresponding side. On the second day she counted fingers at 2½, and on the third at 3½ feet. Slight ptosis was present.

She left the hospital on the eighth day. At this time she counted fingers at four feet. There was only slight, if any, reduction of tension during the eight days she was in the hospital. In counting fingers she saw with the nasal side of the retina—temporal field. I did not see her again until June 30, and she was then counting fingers at five feet. Tension on that day was normal. She had light perception in the right eye.

On July 16 I excised the right superior cervical ganglion without difficulty, and on July 7 she counted fingers at seven feet with the left eye, and could see the hand at four inches with the right. I examined her on July 20, when vision remained the same, the tension of the right eye was + 1, and of the left + 2. She was well pleased to have the small amount of vision she possessed.

CASE III.—SYMPATHECTOMY FOR OPTIC-NERVE ATROPHY.

T. J., aged forty-six, an inmate of the St. Louis City Hospital, a laborer, was admitted on account of blindness. There was no history of syphilis, rheumatism, nor any systemic disease. The patient was of limited mentality. No history of his family could be obtained. He claimed to have had good health all his life, with the exception of an attack of malarial fever several years ago. The patient had been a moderate drinker of alcoholic beverages. In appearance he was robust, and he complained only of loss of vision which, in the left eye, had been failing for eleven months, in the right for seventeen weeks, according to his statement. Until seventeen weeks before this he could see enough with the right eye to get around. Since then vision had steadily declined until he had light perception only—and this only apparent when light was concentrated on the eye by the ophthalmoscopic mirror. Vision of the left eye = 0.

The pupils were widely dilated. The ophthalmoscope showed, in the right eye, a white disk, particularly on the temporal side; the arteries slightly reduced in caliber, veins normal. There was shallow, atrophic cupping of the nerve head. The retina and choroid were normal, the vitreous and lens clear. The left eye showed a disk of a dead white color throughout the whole area, arteries very small, atrophic excavation pronounced, veins reduced in caliber, and choroid normal. The macula was not visible in this eye, owing to the much-reduced blood-supply. The vitreous and lens were clear. Vision was as follows: R. E. = perception of concentrated light. L. E. = 0.

_Diagnosis._—R. E. = optic-nerve atrophy. L. E. = complete atrophy of optic nerve and retina.

_Treatment_: Resection of the right superior cervical ganglion of the sympathetic was done. The operation was followed by conjunctival congestion, lachrymation and contraction of the pupil, slight ptosis and hypotonia.

No appreciable change in the patient’s vision followed, and ophthalmoscopic examination made two weeks after operation showed no change in the appearance of the fundus, except that a cilioretinal artery in the upper part of the disk had doubled in caliber.

So far as I know, Case III. is the first instance in the history of medicine of an excision of the superior cervical ganglion, or of any part of the sympathetic system, for the relief of optic-nerve atrophy. Although the operation was not of benefit in this particular instance, yet I am not willing to concede that it will prove valueless in cases of non-inflammatory atrophy in which vision is not entirely lost. In truth, I expect it to prove beneficial in such cases, sufficiently often to justify the procedure.

I was led to make this experimental operation for several reasons: 1. The use of glonoin is often followed by an improvement in vision in cases of simple atrophy of the optic nerve. 2. Glonoin enlarges the retinal vessels, as has been proved by ophthalmoscopic examination. 3. There is no question that in glaucoma simplex—a disease in which there is an atrophy of the optic nerve—improvement in vision follows sympathectomy. 4. Excision of the cervical sympathetic is followed by an increase in the blood-supply of the orbital contents.

PATHOLOGIC CHANGES IN THE EXCISED GANGLIA.

The microscopic examination of three of the excised ganglia was made by my friend, Dr. Carl Fisch, of St. Louis. The specimens were those from Cases I., II., and III. Of the two ganglia removed from Case II. only the first one—the left—was examined.

Transverse and longitudinal sections of the three specimens were studied microscopically, by means of a great number of different staining methods. Owing to the method by which the ganglia had been preserved—weak formalin solution—the employment of the Golgi—Marchi—and the more delicate Nissl stains was rendered impossible. In general it may be said that the pathologic changes found were the same in the three cases, although a little less pronounced in No. 2 than in 1 and 3.

Most striking of all was a very marked hyperplasia of the connective tissue, which in some places resulted in dividing up the ganglion into small groups of nervous elements separated by broad bands of fibrous elements. The walls of the vascular structures showed decided sclerosis; the connective-tissue sheaths of the ganglionic cells were much increased in thickness. In Case I. small foci of round-cell infiltration were seen in this hyperplastic growth, of an inflammatory character. No plasma nor mast cells could be demonstrated.

The ganglionic cells were markedly pigmented. Together with a number of cells normal to all appearance there were great numbers showing different stages of degeneration. As a rule the nucleus, besides having lost part of its peculiar staining property, had assumed the parietal position; the nucleus was reduced in size or even missing in a large percentage of the cells. While in some cells the chromatic elements were well preserved, in others the process of chromatorhexis and chromatolysis could be followed up through all of its stages. Only comparatively few cells were seen showing the normal dendriform processes; very often the processes were short, ending bluntly, or they had even disappeared altogether. The general peripheral network of processes was much reduced in volume and compressed by the pressure of the connective-tissue formation. Only very few medullated fibers were seen. Unfortunately it was impossible to study their structure with the Marchi method.

The general pathologic aspect was that of a decided sclerosis, originating in inflammatory processes going on in, and starting out from, the walls of the vascular structures. The changes of the nervous elements were most likely not idiopathic, but due to pressure and inhibited nutrition.

The plates accompanying this paper have been made from drawings of sections of superior cervical ganglia.

TECHNIQUE OF THE OPERATION.

The ordinary precautions for surgical cleanliness are to be observed, and general anæsthesia employed. The incision should be made along the posterior border of the sterno-cleidomastoid muscle, starting at the mastoid process and running downward to within an inch of the clavicle. The sternomastoid is separated from the adjacent muscles, the spinal accessory nerve cut, and the carotid sheath reached. This dissection is made with the fingers. The carotid sheath should always be opened in order to locate the pneumogastric nerve. I consider this very important because: 1. The nerve is sometimes outside the sheath, as happened in my second case, in which the pneumogastric was much atrophied and was external to the sheath. 2. Differentiation of the cervical sympathetic from the vagus is sometimes difficult. Often, in operating on the cadaver, I have found both nerves inclosed in the same fascia. It is needless to say that excision of the vagus instead of the sympathetic would not only defeat the object of the operation, but would add a serious complication. Differentiation of these nerves after opening the carotid sheath is not usually difficult, for in working upward the operator comes upon the ganglionic expansion of the sympathetic. The ganglion is seized with forceps and stripped. Its branches are cut first, then the cord passing below is severed, and lastly the ganglion is cut above, as high as possible. It is best to use curved scissors and to have the finger under the ganglion while traction is made, thus cutting on the finger and avoiding injury to the underlying structures.

If the middle ganglion is to be removed, it will be best to excise it first and then work upward. If the entire chain of the sympathetic is to be removed, as is done for epilepsy, and as is now advised in exophthalmic goiter by Jonnesco, the operation is one of great difficulty, owing to the location of the inferior ganglion. This is situated near the neck of the first rib. One of my friends, who is a skillful surgeon, in removing this ganglion ruptured the vertebral artery near its origin and was obliged to tie the subclavian to check the hemorrhage. After the latter has ceased the wound is closed with superficial sutures. The hemorrhage in removal of the superior ganglion is usually trifling, only a few small vessels being cut. The external jugular vein was cut in my first case, but not in the others. The patient leaves the hospital on the eighth or ninth day.

Jonnesco’s method, according to his latest communication on the subject, is different. He always employs the premastoid route where only the superior ganglion is to be removed, reserving the postmastoid for the excision of the entire chain. The carotid sheath is split, the internal jugular vein and sternomastoid drawn outward by a retractor; a second retractor draws the vagus and internal carotid inward. In the space made the superior ganglion is found. The deep vertebral fascia is opened, all the branches of the ganglion isolated and cut by blunt, curved scissors; when this has been done the ganglion is attached only by nerve strands above, a strong pull is made, and the ganglion gives way. The excision is then completed by cutting the inferior strands. In closing the wound, he uses both deep and superficial sutures.

He mentions a transient dysphagia and pain in the cranio-mandibular joint as occurring after this operation.

EFFECTS OF EXCISION OF SUPERIOR CERVICAL GANGLION.

The effects of removal of this ganglion are immediate and remote: The immediate are relief of pain, lachrymation and conjunctival injection, together with a discharge from the corresponding nostril, unilateral sweating, and contraction of the pupil. Often there is an immediate reduction in intra-ocular tension. These effects are noted within five minutes after the excision.

The remote effects are ptosis, which appears on the third or fourth day, improvement of vision, and in some instances a tardy contraction of the pupil and a tardy reduction of the intra-ocular tension. To these there must also be added a slight sinking of the eyeball into the orbit, and a feeling of heaviness in the head. What I have just written applies particularly to cases of glaucoma.

In exophthalmic goiter, after the excision of the ganglia, the exophthalmus and tachycardia are said to improve almost immediately and a reduction of the goiter soon follows.

Although Jonnesco speaks of the immediate reduction of the intra-ocular tension, yet this does not always occur. In my second case, at the end of eight days the tension was + 2. On the sixteenth day the tension was normal. In my first case reduction of the tension was immediate. The relief from pain in the first case was immediate and lasting. This patient had not been free from pain for two months previously. The slight ptosis following sympathectomy is to be attributed to paralysis of Müller’s muscle. Sinking of the eyeball is no doubt due to paralysis of the unstriped peribulbar fibers found in Tenon’s capsule. Contraction of the pupil is usually an immediate result; it may, however, appear tardily. Thus in my first case the pupil was unchanged until the fourth day after the operation; and it did not become at any time as markedly contracted as in the other two patients. In the third case—that of optic-nerve atrophy—the pupil was markedly contracted within five minutes after the excision.

The lachrymation, conjunctival injection, and nasal moisture are transient symptoms which are usually absent after the first day.

In this connection it is interesting to note that Mr. Jonathan Hutchinson, as early as 1866, recognized many of the ocular symptoms of paralysis of the cervical sympathetic, and wrote a paper thereon.

HOW DOES EXCISION OF THE CERVICAL SYMPATHETIC REDUCE INTRA-OCULAR
TENSION?

This is a question difficult to answer—difficult for the reason that we are not sufficiently acquainted with the physiology of the production of aqueous humor under normal surroundings. Panas and Duvigneaud have assumed rightfully that “If the nervous mechanism of intra-ocular secretion or, to speak without hypothesis, the action of the nervous system on intra-ocular tension can be known, the pathology of glaucoma will be cleared up, iridectomy will be explained, and perhaps a new and scientific basis for the treatment of glaucoma will be established.” Many observers have sought to solve the problem. Donders attributed the hypertension to a neuro-secretory cause and believed the trigeminus to be the agent of excessive secretion. He held that section of the trigeminus should relieve intra-ocular tension, while section of the cervical sympathetic could have no particular influence.

His views were overthrown by experiments made by Wegner in 1866, on rabbits. By means of manometers placed in the anterior chamber, he sought to record variations in the intraocular tension. He proved to his own satisfaction that the trigeminus takes no part, while section of the cervical sympathetic produces hypotonia, and irritation of its upper end and causes hypertonia. He held that section of the cervical sympathetic enlarges the blood vessels of the eye; the blood then flows under reduced pressure, and intra-ocular secretion is lessened. Almost identical results were obtained by Adamück—1866‒68—who experimented on cats.

Von Hippel and Gruenhagen believed that the cervical sympathetic contains vasoconstrictor fibers for the eye. Their experiments were made on cats and dogs. They found that irritation of the upper end of the cervical sympathetic causes in the cat hypertonia, while its extirpation increases intra-ocular tension. While, according to Wegner, the hypertonic action proceeds from the enlargement of vessels caused by cutting the cervical sympathetic, and the contraction of the blood vessels caused by the irritation of the nerve causes a hypertonic action, the contrary view is held by Adamück, Von Hippel, and Gruenhagen.

However this may be, there is no doubt that the trigeminus plays no great part in the production of ocular tension. Furthermore, the inefficiency of Bedal’s operation—stretching the nasal nerve—is explained by the fact that it is the cervical sympathetic, and not the trigeminus, which influences intra-ocular tension.

Jonnesco believes that the ocular sympathetic fibers from the brain and spinal cord pass through the superior cervical ganglion; permanent or intermittent irritation of these is accompanied by dilatation of the pupil, narrowing of the small intra-ocular arteries, contraction of the peribulbar muscular fibers, and probably an increased action of the elements which produce the aqueous humor. “As a matter of fact,” says Jonnesco, “any increase of the blood pressure will produce a permanent or intermittent narrowing of the arteries and cause the extravasation and increase in aqueous humor; then it is probable, although not definitely settled, that a permanent or intermittent irritation of the excito-secretory fibers is followed by an increase in the secretion of aqueous humor; the permanent or intermittent dilatation of the pupil pushes the iris into the iris-angle, closes the canals of the filtration zone, and hinders or prolongs the exit of aqueous humor from the eye; the permanent or intermittent contraction of the unstriped peribulbar muscular fibers closes the efferent veins of the eyeball, and hinders the venous circulation of the eye—hence the dilatation of the intra-ocular veins.”

He holds that excision of the superior cervical ganglion destroys all vasoconstrictor fibers of the eye. The arteries relax, the blood pressure is lowered, and extravasation is reduced. This operation destroys the excito-secretory fibers, thus limiting the amount of aqueous produced. The fibers which dilate the iris are destroyed, hence the contraction of the pupil reopens the iris-angle and removes the obstacle to the outflow of aqueous. The nerve-fibers supplying the unstriped muscular apparatus contained in Tenon’s capsule are destroyed, hence the pressure on the efferent veins is removed and ocular circulation is reestablished.