This case was shown to the British Laryngological, Rhinological and Otological Association.

W. M., twenty-eight years, came under my care yesterday on account of a sudden swelling of his eye which had taken place two hours previously, and which had occurred suddenly as he was blowing his nose without a handkerchief, and which gave him the impression as if something were running out of his eye. The swelling crackled in a manner characteristic of emphysema, and the first suspicion was that he must have had some disease of the orbital wall of the anterior ethmoidal cells, and that on examination there would be found some evidence of ethmoidal disease. None such was to be elicited, and the only history obtainable was that he received several kicks on the nose and back of the ear two months ago. This has probably resulted in a fracture of the orbital wall of certain of these cells.

A man, aet. twenty-eight years, complains of nasal obstruction and purulent discharge, with a disagreeable odor in the nose. The polypi having been removed, the pus appeared to flow from under the anterior ends of the middle turbinates. After wiping the discharge away and bending the patient’s head forward, it reappeared in large quantity. On transillumination the cheek on both sides appeared quite dark, and the patient had no subjective sensation of light. The diagnosis of antral suppuration was now considered almost certain, and the patient was advised to have both antra punctured from the alveolar margins. This was accordingly attempted under gas, but although the antrum drill was forced in for its full length, no cavity was reached.

Puncture from the inferior meatus was next attempted, and considerable force was used in two different points; but with no better result. It would seem therefore that the antra must be very small, if not entirely absent.

Discussion.—Mr. Spencer thought it might be one of those convoluted inferior turbinals which form a gutter in which pus collects. The majority considered it suppuration in the ethmoidal region.

The patient was a female child, aged eight years, a hydrocephalic idiot. The history given was that about one year previously a white spot had appeared on the right eye and that the eye began to project. Six months later a growth was first noticed on the right cornea, and this had constantly increased in size. Latterly a white spot had appeared on the left eye. On examination of the eyes there was seen a large conical tuberculated excrescence protruding between the lids of the right eye. It was half an inch in length and its base attached to the cornea covered about four-fifths of its surface. The left cornea exhibited a yellowish infiltration just below the pupil, over which the cornea was bulging; the anterior chamber was deep, the iris was immobile, the tension was slightly raised, and the eye was quite blind. Both globes were very anÆsthetic, and there was considerable muco-purulent discharge from a chronic inflammation of both conjunctival sacs. The growth upon the right eye was accidentally detached a few days after admission into the hospital, and it was then seen to have been attached to the cornea at the apex of a central staphyloma, which was left covered by a fleshy soft core which had formerly been embodied in the center of the growth. The cornea was entirely opaque, and the eye was quite blind. After removal of the right eye a few days later examination of the globe revealed a co-arct retina with evidences of chronic degenerative changes in all the various structures. The anterior chamber was completely abolished, the iris throughout its extent being firmly adherent to the back of the cornea, which was bulging centrally. The apex of the corneal staphyloma had evidently been the site of a large perforation, which was closed by the fleshy granulations which formed the core of the growth. The growth itself measured half an inch from apex to base and one and a half inch around its base.

The interior portion was soft and crumbling, but the external layers were hard and horny and cut with difficulty. A wedge-shaped piece was cut away from the growth and specimens were cut and stained with carmine. The microscope showed that the external layers consisted of several faintly fibrillated strata of a dense, homogeneous nature. The layers occupied about one-quarter of the entire thickness of the walls, the rest being entirely composed of small nucleated cells, those most external being stratified. Adopting Mr. Bland Sutton’s classification of human horns, this growth would be an example of a cicatrix horn, the rarest of all varieties of horn, and one which had been usually found in connection with cicatrices of burns and scalds. The probable Ætiology in this case was an overgrowth of granulation tissue closing the perforation in the cornea, which, owing to an unhealthy condition of the wound and eye, which was anÆsthetic and atrophic, had become exuberant, simulating exactly the condition known as “proud flesh” elsewhere. By a process of accumulation and heaping up, the granulations gradually formed a cap over the cornea, whilst the external layers gradually became stratified and horny from the pressure of fresh growth from the central core and by the action of the air. The nature of the growth was evidence that the corneal epithelium bore no share in its production and discounted the possibility that it might be due to a huge crust of inspissated conjunctival discharges.

W. S., aet. thirty-one years, admitted to Royal Halifax Infirmary May 15, 1899, complaining of pain in right ear and right side of face of six months’ duration. For two months right side face swollen and copious bloody, purulent discharge from right nostril. Nine years ago had syphilis. Insomnia from pain.

On admission: Temperature 100°; skin over right superior maxilla red and oedematous; thick purulent discharge from right superior meatus, sequestrum in region of right cribriform plate; naso-pharynx, chest, and abdomen normal; urine, sp. gr., 1014; trace of albumen. Fundi (of eye) normal.

May 16—No pus found in antrum on exploration and flushing. Patient taking 60 grs. pot. iod. (t. i. d.) and mercurial inunction. Temperature in ear usually higher than that in mouth until just before death. June 8.—Mortuus est.

Post-mortem Examination.—Skull. Base of brain was bathed in thick greenish pus, principally in the neighborhood of the pituitary body, the pus extended back over the pons and medulla. No brain abscess. Ventricles contained more than normal quantity of fluid. Frontal sinuses and cribriform plate of ethmoid and ethmoidal cells normal.

To right of the sella turcica there was some necrosis of the walls of the sphenoidal sinus. Probe readily passed from base of skull through sphenoidal sinus into the nose. Large free opening from said sinus into nose, which sinus was full of muco-pus. Cavernous sinus not thrombosed. Right antrum of Highmore contained about a dram of thick glairy mucus.

There have been recorded two cases of perichondritis of the septum due to alveolar periostitis. Suppuration of dental cyst was cause in the following case.

A young man had pain in second left upper incisor; two days after obstruction of nose supervened, with pain in forehead and high fever. There was a sudden copious discharge of fetid pus from right nostril seven days later. The entire mucosa of the septum was raised from the cartilages, etc. It is considerably swollen over right side of the triangular cartilage, but less so posteriorly. Severe headache in forehead and frontal eminence, and still little fever. The pus was escaping through a small hole into the left nostril. It was freely incised. The triangular cartilage was disintegrated, and the pus had burrowed between the soft tissues and vomer and vertical plate of the ethmoid. The choanÆ were constricted by thickening of the septal mucous membrane. The wound healed in a fortnight without sequestrum, while the toothache lasted but two days.

Six months later the patient had recurrence of pain in the same tooth of two months’ duration; it was extracted and pus continued to exude from the socket. A probe, passed 2½ centimeters to the floor of the nose and septum, showed a cavity covered with membrane in the anterior parts of upper jaw, which was a cyst at the root of the tooth. The anterior cyst walls were removed with bone forceps, and the remainder scraped. The cavity gradually healed.

The cyst probably broke through under the septal mucous membrane. In exceedingly few cases of perichondritis does the process extend to the osseous septum. Only once has the author seen record of a case which was as extensive as this. The offensive odor also points to a dental origin.

It is now generally recognized that the disease known as locomotor ataxia may include among its clinical manifestations symptoms other than those which depend on pathological changes in the spinal cord. A number of these are associated with the functions of the eyeballs. The Argyll-Robertson pupil is universally admitted as valuable confirmatory evidence of a diagnosis of locomotor ataxia; ocular paralyses, if less frequent, are certainly not less significant; and optic nerve atrophy is at least so well known in connection with the disease that its occurrence in any individual case would hardly call for comment.

A further step forward in our knowledge of the clinical possibilities of locomotor ataxia has been the recognition of the fact that ocular disturbances may precede the evidences of any spinal lesion. This advance necessarily means that the occurrence of any one of the ocular events above mentioned must, unless otherwise explained, generate the suspicion that the case may in its later events display the phenomena known to depend upon sclerosis of the posterior columns of the spinal cord.

It is very difficult to collect the evidence necessary to show in what proportion of cases this suspicion is justified by the event. For it is certain that ocular disturbances may long precede the manifestation of spinal symptoms. In the case of optic atrophy the interval may, according to Gowers, extend even to twenty years. Thus it can only be in very exceptional instances that one and the same physician will have the opportunity of observing at least a number of these cases through all the stages of their progress. Yet, if true, it is of manifest importance, for the sake both of exact knowledge and of accurate prognosis, that it should be clearly recognized that an optic-nerve atrophy, an ocular paralysis, or a loss of the pupil light reflex, unless capable of other explanation, belongs in all probability to the order of events incident to locomotor ataxia, and that any one of these may well be the introduction to a more widely-spread manifestation of the disease.

For reasons stated above, the collection of complete histories necessary to afford actual demonstration of the truth of these propositions is difficult; and all the more so as there is reason to believe that in those cases in which the early stress of the disease falls upon the nervous apparatus of the eyeball the spinal symptoms are apt to be slight in degree as well as delayed in development. This is certainly the case when the ocular disturbance takes the form of optic-nerve atrophy. “In a large number of such cases,” says Gowers, “ataxy never comes on, the spinal malady becoming stationary when the nerve suffers.”

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.

(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.

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.

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.

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 oedema 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 oedema 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.

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.

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.

Jonnesco believes that the starting-point of the nervous derangement producing glaucoma is central: “When one removes the ganglion the point of origin of the influence will not be removed, but the communication between this center and the eyeball is destroyed.”

Regardless of the differing views of physiologists concerning the mechanism of the reduction of ocular tension, based on experiments made on the lower animals, there can be no difference of opinion concerning the effect of excision of the superior cervical ganglion in the human subject. The operations made by Jonnesco and others on the Continent, and by myself in America, prove that removal of the superior cervical ganglion causes a marked reduction of intra-ocular tension in glaucomatous cases. That the same effect occurs in eyes with normal tension is evident from my third operation—that done for optic-nerve atrophy.

EXTENT OF SYMPATHECTOMY IN DIFFERENT DISEASES.

Up to the present time excision of the cervical sympathetic has been performed for the following diseases: epilepsy, exophthalmic goiter, glaucoma, and optic-nerve atrophy. The question naturally arises: How extensive an operation is necessary in these affections? This I will attempt to answer:

In epilepsy it is necessary to excise the entire cervical chain on both sides for the reason that, according to Jonnesco’s theory, it is necessary to convert a state of cerebral anÆmia—which he assumes is the condition in epilepsy—into one of cerebral hyperÆmia. Since the carotid plexus is formed by branches from the superior ganglion, and the vertebral plexus arises from branches which have their origin in the inferior cervical ganglion, it is evident that the entire cervical sympathetic must be removed.

In exophthalmic goiter, although Jonnesco in his first operation excised only the superior and middle ganglia, he now believes it necessary to remove the inferior as well, for this reason: from the superior ganglion the ocular fibers arise; from the inferior the vasodilator, cardiac-accelerator, and, probably, the secretory nerves of the thyroid gland. If eye, thyroid, and cardiac symptoms are to be relieved the entire chain must be excised.

In glaucoma removal of the superior ganglion alone is necessary. All of the sympathetic fibers of the eye, with the exception of those which pass directly from the cerebrum by way of the trigeminus, are connected with the superior ganglion.

In optic-nerve atrophy, if it should be proved that noninflammatory atrophy of the optic nerve can be improved by sympathectomy, removal of the superior ganglion alone will be necessary, for reasons already given.

If the glaucoma is unilateral, it is necessary to remove only the corresponding ganglion.

HISTORY OF SYMPATHECTOMY.

In 1889 Alexander of Edinburgh resected the superior ganglion on both sides. In 1892 Jacksh resected the vertebral plexus and cut the cord connecting the middle and inferior ganglion. The third operator was Kummel, who excised the superior ganglion on one side only. In 1893 Bojdanik made a bilateral resection of the middle ganglion. In 1896 Jaboulay made a bilateral section of the sympathetic cord, above and below the middle ganglion. These operations were all made for epilepsy.

In regard to exophthalmic goiter, Jaboulay made a simple section of the sympathetic early in 1896. In September of the same year Jonnesco excised the superior and middle ganglia.

Jonnesco was the first, in 1896, to do a bilateral resection of all three cervical ganglia, though it is claimed by a Polish surgeon, Baracz, that he proposed the same in 1893. To Professor Jonnesco furthermore belongs the credit of having first excised the superior ganglion for glaucoma in September, 1897.

Ball of St. Louis was the first to remove the superior cervical ganglion for optic-nerve atrophy. The date of this operation was June 24, 1899.

Terrier, Guillemain, and Malherbe, in their “Chirurgie du Cou,” 1898, were among the first to give the surgery of the sympathetic a place in a text-book.

Among those who have operated on the cervical sympathetic for the relief either of glaucoma or exophthalmic goiter, or both, are Abadie, RÉclus, Gerard-Marchant, Chauffand and QuÉnu, Jeunet, Bled, Ball, Renaud, and Bartlett.

Panas is opposed to sympathectomy in glaucoma. He reports seeing a patient in whom, three months after the operation, vision was still declining.

FranÇois-Frank, at a meeting of the Paris Academy of Medicine, held May 22, 1899, spoke of the effect of sympathectomy on the circulation of the thyroid gland, brain, and eyes, and on the heart. He believes that the operation can easily produce good results.

Doyon has described the trophic changes produced in the rabbit by excision of the cervical sympathetic.

CONCLUSIONS.

From a study of the cases of sympathectomy made by Jonnesco and others, and from the observation of my own cases, I offer these conclusions:

1. Excision of the superior cervical ganglion is a most valuable procedure in glaucoma.

2. It is of more value in glaucoma simplex than in inflammatory glaucoma.

3. In inflammatory glaucoma, on which iridectomy has been done without benefit, excision of the superior cervical ganglion should certainly be tried.

4. In cases of absolute glaucoma with pain, sympathectomy is to be tried before resorting to any operation on the eyeball.

5. In cases of simple optic-nerve atrophy, sympathectomy may possibly be beneficial if done before vision is entirely lost.

6. In cases of exophthalmic goiter, which do not improve under hygienic medicinal and electric treatment, excision of the cervical sympathetic on both sides is to be advised.

7. In unilateral glaucoma excision of the sympathetic ganglion is to be done only on the corresponding side.

8. In the hands of a careful operator, excision of the superior and middle ganglia is a safe operation, but removal of the inferior ganglion can be done safely only by the most skillful surgeons.

9. The postmastoid route is to be preferred in excision of any part, or all of the cervical sympathetic.

10. The fact that glaucoma is improved by sympathectomy and the finding of pathologic changes in the excised ganglia suggest the conclusion that this affection is due either to a permanent irritation of the cervical sympathetic, or to an irritation located elsewhere and transmitted by means of the cervical sympathetic.

I wish to extend my thanks to Drs. E. C. Renaud and Willard Bartlett for valuable assistance in the preparation of this paper; to Dr. Carl Fisch for the pathologic report.

Case shown at the Lar. Soc. of London:

A woman, Æt. thirty-one years, had suffered several years with discomfort in nose, throat, and mouth, with dyspepsia. Mucosa of nares and pharynx markedly atrophied. Atrophied condition made post-rhinoscopy easy. “The eustachian eminences were seen to be enormous, filling the fossÆ of RosenmÜller, and reaching nearly to the pharyngeal roof. Just behind the upper edges of the choanÆ, on each side, there appeared a transverse elliptical opening, which was about half an inch long and a fifth of an inch across at the widest part on the left side, and slightly less in each dimension on the right; a probe apparently extends about a quarter of an inch into the cavity.” In the discussion following some thought them to be small recesses formed by cicatricial tissues, other formed by peculiar distribution of adenoid tissue, and still genuine sinuses.

We ascertain by interrogation, (a) if the discharge is purulent or muco-purulent; (b) whether it is unilateral or bilateral; (c) whether it is continuous, intermittent, or influenced by change of posture; (d) if there is offensive smell perceived by the patient or by others; (e) pain is not usually complained of unless there is obstruction to drainage, and consequently retention of pus under pressure. Unilateral discharge suggests a foreign body in a child or sinus involvement in an adult. If it is intermittent or influenced by position probably originates in a sinus. Subjective fetor suggests sinusitis; while objective fetor, ozena; and combined subjective and objective is the rule in syphilitic necrosis. Location of pain is of very little, if any, use in diagnosis.

Rhinoscopy.—Attention directed to (a) situation of the pus; (b) polypi; (c) atrophy of the mucous membrane; (d) crusts; (e) ulcerations; (f) adenoids; (g) nasal obstruction; (h) foreign bodies. Under (a) beside usual cleansing of nasal cavities and reexamination to ascertain situation, he recommends “tamponading,” i. e., by blocking up first one part, then another, with pledgets of wool, and noticing whence the discharge reappears. (e) Ulceration may be syphilitic, simple, tubercular, or lupoid in origin. “It must not be forgotten that a perforation” of the septum “may be entirely the work of a misused finger-nail.” (g) The normal mucoid discharge damned up by nasal obstruction frequently becomes purulent.

Special methods of diagnosis as follows are mentioned: transillumination; examination of upper teeth; catheterization of the ostium, maxillares, naso-frontal canal, and outlet of the sphenoidal sinuses; external examination of antrum and frontal sinuses; exploratory puncture of the antrum through the inferior meatus, alveolar process, or canine fossa. Diagnosis of ethmoiditis is principally by exclusion.

Treatment of the accessory sinuses may be summed up under the following indications: (a) removal of the cause; (b) evacuation and drainage of pus; (c) antiseptic irrigation; (d) removal of morbid material, when present. PALMER.

The detection of optic neuritis is of the greatest importance in the diagnosis of cerebral affections. Nevertheless, in certain cases of double optic neuritis with headache considerable caution is necessary before coming to a conclusion as to the exact nature of the disease. Though these two symptoms are present in the majority of cases of brain tumor and are so frequently due to this cause they are also met with in other diseases. In some cases of granular kidney, for example, the patient comes under treatment for headache and failure of vision; and ophthalmoscopic examination may reveal intense optic neuritis like that of cerebral tumor (neuritic form of albuminuric retinitis). At first the symptoms appear to indicate cerebral tumor, but a careful examination of the urine and cardio-vascular system will clearly reveal the cause. Limited space does not permit an enumeration of all the causes of double optic neuritis with headache. The results of the examination of one hundred cases presenting these two symptoms reveal, however, several points of interest. Most of these cases have been seen by us conjointly; some were seen separately, whilst others (in Groups I. to VIII.) were examined by one of us (R. T. W.) whilst holding the post of medical registrar at the Manchester Royal Infirmary. For permission to include the latter amongst our cases we are indebted to the medical board of that hospital.

With respect to the diagnosis and termination these one hundred cases may be grouped as follows:

I. Brain tumor, verified by necropsy, 27.

II. Cases terminating fatally; probably, majority due to brain tumor; but no necropsy obtained, 27.

III. General symptoms of brain tumor; but necropsy revealed distention of the ventricles of the brain with fluid; no tumor (serous meningitis of ventricles), 2.

IV. Cerebral abscess (fatal), 3.

V. Tuberculous meningitis (fatal), 2.

VI. Chronic interstitial nephritis; neuritic form of albuminuric retinitis (fatal), 3.

VII. Toxic conditions and blood diseases: Chronic lead poisoning, 3. Ulcerative endocarditis, (fatal), 1. Purpura hemorrhagica (fatal), 1. Henoch’s purpura (fatal), 1. Chlorosis with cerebral symptoms (recovery), 3.

VIII. Headache and double optic neuritis (without localizing symptoms); probably syphilitic (recovery, with blindness, 2; with impaired vision, 4), 6.

IX. Headache and double optic neuritis (without localizing symptoms); no evidence of syphilis; duration six and two and a quarter years, respectively. Termination still uncertain, 2.

X. Headache and double optic neuritis (without localizing symptoms); no evidence of syphilis; recovery with blindness, 8; with impaired vision, 3; with good vision, 8, 19.

The following are brief abstracts of the notes of the cases in Group X. which have come under our observation and which we have followed for a considerable period of time. The number of years during which each case has been followed is given in parentheses after the brief note.

1. A boy, aged ten years. Double optic neuritis, headache, and vomiting; slight internal strabismus of the left eye. Recovery with normal vision. (Seven years.)

2. A young woman, aged seventeen years. Headache, vomiting, and double optic neuritis. Recovery, but with impaired vision in one eye and blindness in the other. (Five and a half years.)

3. A young woman, aged eighteen years. Double optic neuritis, headache, and vomiting; several epileptic fits. Recovery, with useful vision in one eye; vision in the other is very defective. (Seven years.)

4. A young woman, aged eighteen years. Double optic neuritis, headache, and vomiting. Recovery, but complete blindness followed. (Four years.)

5. A young woman, aged nineteen years. Double optic neuritis, headache, and vomiting. Recovery with good vision. (Three years.)

6. A man, aged twenty years. Double optic neuritis, headache, and vomiting. Recovery, but complete blindness followed. (Two and a half years.)

7. A girl, aged ten years. Double optic neuritis, headache, and vomiting; knee-jerks were absent. Recovery, but complete blindness followed. (Three years.)

8. A boy at the age of thirteen years had double optic neuritis and headache; recovery ensued. At the age of fifteen years he had a return of headache and double optic neuritis; also vomiting. At a later date there was partial anÆsthesia in the distribution of the right fifth cranial nerve; the right cornea was opaque; there was complete blindness in both eyes. Partial anÆsthesia of the face and blindness remained, but otherwise the patient recovered and felt quite well nine months after the second attack.

9. A girl, aged sixteen years. Double optic neuritis, headache, vomiting; slight internal strabismus of the right eye. Recovery with normal vision. (Four and a half years.)

10. A boy, aged ten years. Double optic neuritis, headache, and vomiting. The head had increased in size. Recovery, but with complete blindness. (Three years.)

11. A woman, aged nineteen years. Double optic neuritis, headache, and vomiting. Recovery with normal vision. (Three years.)

12. A boy, aged fifteen years. Double optic neuritis, headache, and vomiting. Recovery. (Two and a half years.)

13. A woman, aged twenty-one years. Double optic neuritis, much swelling of the disks, headache, and vomiting. Complete recovery with normal vision. (Four and three-quarter years.)

14. A girl, aged fifteen years. Double optic neuritis, headache, and vomiting. Recovery with good vision. (Five and a quarter years.)

15. A boy, aged twelve years. Double optic neuritis, headache, and vomiting; slight internal strabismus of the right eye. Recovery with good vision. (Four years.)

16. A man, aged forty years. Double optic neuritis, headache, and vomiting. Recovery, but with complete blindness. (Eighteen months.)

17. A youth, aged seventeen years. Double optic neuritis, headache, and vomiting. Recovery, but with total blindness. (Five years.)

18. A woman, aged twenty-two years. Double optic neuritis, headache, and vomiting. Recovery, but with total blindness. (Two and three-quarter years.)

19. A girl, aged fourteen years. Double optic neuritis, headache, and vomiting; internal strabismus (left) for fourteen days. Recovery, with normal vision. (Two years.)

The following are brief notes of the cases in Group IX.:

20. A girl, aged twelve years. Headache, vomiting, and double optic neuritis in December, 1893. Recovery in twelve months, but vision was much impaired. She remained well with the exception of occasional headache until December, 1899. Then the severe headache returned. She became ataxic and optic neuritis reappeared. In April, 1900, the headache was much less and the patient felt much better, but she was completely blind. (Six and a half years.)

21. A young woman, aged seventeen years. Headache, vomiting, and double optic neuritis. Vision was impaired. Vomiting ceased; the headache continued for over two years, but recently disappeared after lumbar puncture. (Two and a quarter years.)

In all cases of double optic neuritis a systematic and careful examination of the patients should be made. The urine and cardio-vascular system should be examined for signs of chronic interstitial nephritis; the gums should be examined for the lead line and other indications of lead poisoning should be sought for; the question of chlorosis or other “blood disease” should be considered; and the ears should be examined for signs of otitis. But when all these conditions have been excluded and when the symptoms are apparently due to a cerebral affection, there is one group of cases in which localizing brain symptoms are absent and in which the chief indications of disease are headache, double optic neuritis, and often vomiting. In most of these cases syphilis can be also excluded. A diagnosis of brain tumor is given, and the growth is thought to be situated in some region in which the localizing symptoms are at first indefinite—cerebellum, temporo-sphenoidal lobe, or prefrontal region. Such a diagnosis often proves to be correct. Localizing symptoms may develop later and a necropsy may show the accuracy of the opinion expressed. But sometimes, to the surprise of the medical man, a fatal termination does not occur; the symptoms sometimes disappear and the patient recovers, though very often impairment or loss of vision remains. The patient may continue in good health for years or for a lifetime afterwards. Most medical men who have paid much attention to cerebral diseases will have met with a case or cases of this kind. The chief object of our article is to call attention to this class of cases and to indicate the frequency of their occurrence. Nineteen out of one hundred cases of double optic neuritis with headache in the table just given could (after careful examination) be placed in this group (X.).

What is the cause of the symptoms in this group of cases? Possibly in some cases the symptoms are caused by a non-malignant tumor (or tuberculous mass) which ceases to extend and becomes quiescent and encapsuled. One of us has recorded a case in which symptoms of cerebral tumor (including Jacksonian epilepsy and hemiplegia) gradually subsided and temporary recovery ensued; but three years later symptoms of cerebellar tumor developed and death occurred. The necropsy revealed a recent large tuberculous mass in the cerebellum and an old capsuled tuberculous mass just beneath the motor cortex in the right cerebral hemisphere. The latter had evidently been the cause of the early cerebral symptoms from which the patient had recovered. An instructive case has been recorded by Dr. T. K. Monro of Glasgow. The patient, at the age of sixteen years, suffered from severe headache with failure of vision which passed on to complete blindness. For thirty-three years he was an inmate of a blind asylum, ophthalmoscopic examination showing double optic atrophy. He died at the age of sixty-three years, from cancer of the stomach, and the post-mortem examination also revealed a large myxomatous tumor in the left half of the cerebellum. In all probability the early cerebral symptoms had been associated with optic neuritis which had passed on to optic atrophy and the cause had been the myxoma in the cerebellum which had remained quiescent for forty-six years.

In some cases of double optic neuritis with headache and general cerebral symptoms, when recovery occurs the cause is probably distention of the ventricles of the brain with fluid—serous meningitis of the ventricles (Quincke). This condition was present at the necropsy, and no tumor growth could be found in two out of the one hundred cases tabulated. It is probable that a number of the cases in which a diagnosis of cerebral tumor has been made, but in which recovery has occurred, have been due to this condition—serous meningitis of the ventricles. Probably the two cases in Group IX. and possibly some of the cases in Group II., in which death did not occur for several years after the onset of symptoms, were of this nature. Other cases which recover may be due to a basal meningitis.

The table given above is instructive both as regards the diagnosis and prognosis in cases of double optic neuritis with headache. It shows the necessity for careful examination before giving either a diagnosis or prognosis, and the clinical group of cases No. X. ought always to be borne in mind whenever the diagnosis is obscure and localizing symptoms are absent.

There are two other points to which we would draw attention. In ten out of the one hundred cases the patient recovered completely from the headache and general cerebral symptoms and regained perfect health, but the optic neuritis was followed by atrophy and complete blindness. In the face of this terrible termination we cannot help thinking that simple trephining of the skull and the removal of bone, without any interference with the brain, as suggested and practiced by Mr. Victor Horsley for the relief of optic neuritis and pressure symptoms, is a method of treatment worthy of more frequent trial when vision is failing markedly. Dr. James Taylor has published cases which appear to show that this method of treatment may be of service in checking the optic neuritis and failure of vision. In the class of cases in Group X. if there should be a suspicion that the symptoms may be due to serous meningitis of the ventricles, lumbar puncture appears to be worthy of trial, since several cerebral cases are now on record in which this treatment appears to have been of great service, and in which the cause of the cerebral symptoms was probably that just mentioned.

A schoolboy, aged seven years, was admitted into Westminster Hospital on January 28, 1900, the only history obtainable being that on the previous morning he had been brought home in a “fit,” which lasted the greater part of the day. On admission he was perfectly sensible and talked freely, but on being put to bed he passed into a condition of semi-consciousness which lasted for many days. He took no notice when spoken to, and remained absolutely mute. The face and upper extremities exhibited choreiform movements of a slow and coarse type. These movements were apparently purposive in character, and at times he endeavored to clutch at objects within his reach. Sometimes the arms were widely extended, and then slowly flexed, as if performing the act of embracing. Sometimes the movements conveyed the idea that he was feebly endeavoring to strike those around him. There was no paralysis of the face or of the muscles of the limbs. The movements were, as a rule, bilateral, although sometimes the facial movements were unilateral, but not always on the same side. There was no rigidity of the muscles, retraction of the head, or opisthotonos. There was nothing to indicate that the patient suffered from headache, although at times the brows were contracted and the face wore a worried and anxious appearance. The bowels were open twice a day and urine and fÆces were passed in bed. The motions were normal in character. The patient was unable to swallow, and had to be fed by the nasal tube. There was no nystagmus, the pupils were normal in size and contracted well to light. There was well-marked double optic neuritis. The temperature was 99.8° F., and the pulse was 108. There was no tenderness or swelling of the joints, and there was no rash on the skin. No tache cÉrÉbrale could be obtained. There was a little cough, but there was no expectoration. The breath and heart-sounds were normal. The urine was acid, had a specific gravity of 1018, and contained neither albumen nor sugar. The spleen was not enlarged. The patient showed no signs of anÆmia, but the blood was not examined. There was no wasting of the muscles, and the knee-jerks were present, although somewhat sluggish. The tongue was clean, and presented no sign of having been bitten. The patient would not protrude it voluntarily, and it had to be examined with the spatula.

The condition of the patient remained practically unchanged for twelve days. The highest temperature recorded was on the second day, when it reached 100°; on the following day it was 99.8°, and from that time onward it was normal. The double optic neuritis continued, and the disks were observed to be getting paler. On February 13 (the seventeenth day of the illness) the patient was much more sensible, and recognized his mother, putting his arms round her neck. He was still unable to talk, although apparently he endeavored to do so, from time to time uttering a few unintelligible words. On being asked if he would like an orange he nodded his head, and he showed some signs of interest in a watch which was shown to him. The incontinence of urine and fÆces continued, but food was taken with less difficulty. The movements gradually subsided. On the 17th the patient could say his own name, but beyond that could utter only inarticulate sounds, and failed to recognize letters or words, either written or printed. On the 20th he was able to speak plainly, although incoherently. He endeavored to get out of bed, and during the night was so noisy that he had to be removed from the ward. Urine and fÆces were still passed under him. On the 22d he was quieter, and for the first time indicated that he wanted the bed-pan. The optic neuritis was less marked. On March 1 the patient was able to get up, and seemed to be quite well. On the 8th the following note was furnished by Mr. G. Hartridge, who had frequently examined his eyes during the course of his illness: “Pupils five millimeters each. React well to light, to convergence, accommodation, and consensually. Right vision 6
6, left vision 6
9. Right disk getting white; not much swelling of the disk; edges clearing. Retinal vessels, specially veins, very full and tortuous. Left disk pale (less so than right), dim; edges blurred.” The only medical treatment adopted was the administration for a few days of 15 minims of liquor arsenicalis three times a day.

Several years have elapsed since Dr. R. Berlin described a series of cases in which he had observed a peculiar retinal change after the eye had been struck with a blunt object, as, for example, a stick or a stone. Under those circumstances he noticed a cloudiness of portions of the retina, not involving the retinal blood vessels. The milky appearance reached its height in twenty-four to thirty-six hours, and disappeared in two or three days. Berlin pointed out that the rapidity with which the cloudiness developed, and the length of time that it persisted, stood in direct relationship with the severity of the original injury. This curious condition, which Berlin called commotio retinÆ, was associated with some reduction of sight, episcleral congestion, and a difficulty in getting the pupil to dilate when atropine was dropped into the eye. Small retinal hemorrhages were sometimes present. Berlin explained the ophthalmoscopic picture by supposing that a rupture of the choroid was followed by bleeding and oedema of the retina. This theory has recently been opposed by Denig. That observer, as the result of experiments upon rabbits, believes that the blow upon the eyeball causes the vitreous to impinge upon the retina, to tear the internal limiting membrane, and to force the vitreous into the nerve-fiber layer. The alternate elevations and depressions thus brought about in the nerve-fiber layer of the retina are, according to Denig, the cause of the ophthalmoscopic appearances.

Since the publication of Berlin’s original paper few cases of commotio retinÆ have been recorded. Indeed, the retinal changes are of so fleeting a nature that an opportunity for observing them must occur comparatively seldom. This fact leads me to place upon record brief notes of a somewhat interesting case:

E. S., aged eleven years. First seen on July 25, 1899.

History.—At 6.45 P. M., on July 24, the patient was struck in the right eye with a cricket ball, made of cork and covered with rag cloth.

Present State.—Right eye: Small abrasion of the skin of the lower lid, with a surrounding area of redness. Some general conjunctival congestion, with a definite ecchymosis in the ocular conjunctiva, opposite the lower-outer quadrant of the cornea. Tension minus 1. The pupil distinctly sluggish and a trifle larger than the other one. Anterior chamber deep. A narrow line of blood clot lay at the bottom of the anterior chamber. V. 5
9 (ii. letters). Pupil dilates imperfectly to a mydriatic. With the mirror alone some parts of the fundus oculi were seen to be unduly white. When examined more closely with the ophthalmoscope there was found a wide but defective zone of whitish fundus, situated peripherally upward, inward, and outward. No such appearances could be made out in the lower part of the fundus. The retinal vessels, which lay anterior to the affected areas, showed no changes. In most places it was possible to get beyond the whitish patches so as to see the edges of the latter. These margins were irregular, and showed white, tongue-like projections running into normal fundus. Some small islands of cloudiness lay, however, beyond the area of general haziness. Around the yellow-spot region was a white radiating appearance, but no definite white mass was present in that place. Left eye: No fundus changes. V. 5
5 (iv. letters). Tension normal.

Treatment.—Vaseline to abrasion of skin of lid; atropine drops (2 grs. to the ounce—to each eye twice a day); rest in bed.

Progress.—July 26. R. V. 5
12; tension still rather low. The blood clot present in anterior chamber and also on anterior capsule of lens renders it difficult to see the fundus clearly; but no white patches can be made out in the fundus.

July 27. A little blood is still present in the lower part of the anterior chamber. The parts of the retina that were milky have resumed almost their natural appearance, and the changes above mentioned are now represented merely by a faint, whitish, ill-defined stippling of the areas in question. Around the yellow spot is a system of fine radiating lines, which extend for some distance into the surrounding fundus. This is doubtless due to oedema of the retina.

July 28. R. V. 5
6 (i letter); tension still slightly minus. Ecchymosis present in ocular conjunctiva, but the blood has disappeared from the anterior chamber. Pupil not so wide as that of the left eye, although atropine is being used to both. Faint cloudiness lower third of the cornea, made up of almost transparent dots, as may be seen with a +20 lens in certain positions of the eye. Fundus changes have disappeared; faint radiating lines, however, may still be seen around the yellow-spot region.

July 29. R. V. 5
6 (ii letter) T—I. Pupil now as large as that of the other eye. Yellow-spot region still surrounded by a wide band of fine, closely set, radiating gray lines. It may be noted that the corresponding region of the left (unaffected) eye is encircled by an ordinary oval reflex.

August 1. R. V. 5
6; (Tn.). A small ecchymosis still present in the ocular conjunctiva on the outer side of the cornea. No blood in anterior chamber; no corneal cloudiness. Radiating appearance still present around yellow spot of fundus.

August 9. R. V. 5
9, L. V. 5
9; (Tn.).

August 12. Vision unaltered. Radiating lines still present around yellow-spot region of affected eye.

September 5. The right pupil rather larger than its fellow, but no break in the continuity of the edge of the iris can be discovered to account for this. The action, both to light and to accommodation, of the pupils is equal. The radiating lines formerly present around the yellow spot of the right eye have been replaced by an ordinary oval reflex, like that present in the other fundus. Tn.; R. V. 5
6 (i letter), L. V. 5
6 (i letter); No. 1 Jaeger read easily.

September 7. Under atropine. R. V. = 5
18 + 1.5 D. Sph. = 5
5. L. V. = 5
12 + 1.0 D. Sph. = 5
5.