Part 5

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.

DEADY.

=Lodge, Jr., M. D., Samuel.—A Case of Fatal Sphenoidal Suppuration.=—_The Laryngoscope_, March, 1900.

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 œdematous; 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.

PALMER.

=Killian, Prof. Gustav.—Case of Acute Perichondritis and Periostitis of the Nasal Septum of Dental Origin.=—_Münch. med. Wochen._, No. 5, 1900.

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.

PALMER.

=Hawthorne, C. O.—The Eye Symptoms for Locomotor Ataxia, with a Clinical Record of Thirty Cases=.—_Brit. Med. Jour._, March 3, 1900.

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.

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

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

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

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

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

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