of the patch were fairly sharply defined from the surrounding fundus by its color, but there was no pigment ring. I was unable to determine whether the patch lay in the same plane as the choroid or projected forwards.

I again examined the patient on November 7. This time in the left eye there were two patches, in the same region, separated from each other by about two millimeters, and plainly projecting above the niveau of the fundus. A thorough examination of the fundus, so far as it was possible without the use of a mydriatic, revealed nothing further. In the right eye, however, there was now to be seen a focus corresponding to the others in all particulars except in size and position. It was smaller than they, and lay more towards the macula. A fortunate circumstance was its position beneath one of the retinal vessels, which could plainly be seen running over and raised by it.

My next examination was two days later. The left eye showed an increase in the size of the tubercles but not in the number. In the right eye, however, were two new ones. Their positions correspond fairly well to the course of one of the inferior temporal vessels.

Repeated examinations, continued to the day before his death, showed no change in the number of the tubercles, but a gradual increase in their size was noticed. Towards the last, the patient became more difficult to examine, owing to a supervention of a semicomatose condition. Patient died November 21, three weeks after he came under my observation.

The postmortem revealed a general miliary tuberculosis. Only the posterior segments of the eyes were removed. In the right eye were three yellowish nodules, lying subretinally and evidently arising from the choroid. Their positions were the same as I had made out ophthalmoscopically. Only three were macroscopically visible. The left eye contained only two tubercles, each about the size of the optic disc, and lying in the positions I had determined intravitam.

The microscopical examination of the tubercle removed showed it to be a fusiform enlargement with the long diameter from above, downwards, lying wholly within the choroid. The retina was detached from the choroid and the latter from the sclera during the process of removing and hardening. The pigment layer of the retina still adheres to the choroid except over the tubercle itself where it fails entirely. Portions of the choroid are adherent to the sclera. This is especially true of the area beneath the tubercle, where there has been a migration of the choroidal pigment into the sclera, accompanied by a slight degree of small-cell infiltration. A scleral blood-vessel is seen in cross-section, and the surrounding tissue shows a small cell infiltration. Otherwise the sclera is normal.

Opinions differ as to the frequency with which tuberculosis of the choroid is part of a general miliary tuberculosis. Cohnhiem found it in almost every case. I was unable to obtain the exact percentage. On the other hand, Dahl found it absent in all of three cases. Between these extremes are thè findings of the following authors: Bouchert,

ten per cent; Bock, eighty-two and seven-tenths per cent; Demme, twenty-one per cent; Litten, seven and five-tenths per cent; Carpenter and Stephenson, fifty per cent; also in nine and twenty-five one-hundredths per cent of tuberculous affections other than general miliary tuberculosis. From such wide diversity of findings, no fixed conclusions as to the frequency of the occurrence can be drawn, but we may expect to find tuberculosis of the choroid in at least fifty per cent of the cases of general miliary tuberculosis.

LARYNGOLOGY.

BY WILLIS SIDNEY ANDERSON, M. D., DETROIT, MICHIGAN.

ASSISTANT TO THE CHAIR OF LARYNGOLOGY IN THE Detroit COLLEGE OF MEDICINE.

SUPERNUMERARY TEETH IN THE NOSE AND THE MAXILLARY SINUS.

JOHN M. INGERSOLL (The Laryngoscope, September, 1903) calls attention to the possibility that supernumerary teeth may be found in the floor of the nose or in the maxillary sinus. A case is reported of impacted teeth found in the maxillary sinus in a four-year-old boy. The chief point of interest in this case is that the dentigerous cyst occurred in connection with the deciduous teeth. Such cysts occur more frequently with permanent teeth. Several other cases are reported, among which is one occurring in a patient forty years old with a syphilitic history. The tooth was imbedded in the floor of the

nose.

THE HISTOLOGIC STRUCTURE OF BONY CYSTS OF THE NOSE, WITH SOME REMARKS ON THEIR GROWTH AND ORIGIN.

J. KIKUCHI (Archiv für Laryngologic, Band XIV, Heft 2) believes that these cysts are structural abnormalities rather than the results of inflammatory processes. The presence of a well developed mucous lining to the cyst cavity is regarded by the author as an absolute refutation of their inflammatory origin. If the cysts were formed by the rolling in of the middle turbinal, together with a rarifying ostitis, the author believes that, inasmuch as the turbinal is provided with cavernous tissue, we ought to find a similar structure on the inner surface of the cyst. This is not the case.

He draws the following conclusions: (1) The bony cysts may originate in the cartilage of the fetal turbinals. One case shows it in a four-months' old fetus. The author believed this case to be an example of an aberrent ethmoid cell in the middle turbinal. (2) The character of the mucous membrane lining these bony cysts is identical with that of the ethmoid cells. The mucous cells are localized at the opening of the cyst. (3) The enlargement, or thinning of their bony walls, would gradually take place by resorption following an inflammation.

THE IMPORT OF THE SALIVARY GLANDS AND NASAL SECRETIONS IN HAY FEVER.

D. BRADEN KYLE (The Laryngoscope, September, 1903) lays great stress on the chemic changes taking place in the various secretions and believes that much can be learned by the study of the secretions from the mucous glands, as an etiologic factor in the causation of hay fever. He believes that local irritation may be brought about by chemic change in the secretions.

THE COMPLICATIONS OF HYPERTROPHY OF THE PHARYNGEAL TONSIL.

GEORGE B. WOOD (American Medicine, October 3, 1903) believes the pharyngeal tonsil to be a distinct organ, although of no more importance than an ordinary lymph gland, and, therefore, there can be no objection to its removal if hypertrophied. He divides the complications of the hypertrophy of the pharyngeal tonsil into two groups, mechanical and infectious. Mouth breathing is due to the mechanical obstruction and favors infection. He attributes the backwardness of many school children to adenoids, also deformities of the chest and jaws. He gives the following statistics taken from the dispensary records of the Children's Hospital: Of the three hundred sixty-one children with nose and throat affections, eighty-seven were boys and sixty-two were girls. Nasal discharge or recurrent attacks of coryza were present in seventy-eight cases; some form of ear trouble was present in sixty-three, or forty-two per cent; symptoms of nasal obstruction were present in one hundred seventeen, or seventy-eight per cent; headache was present in twenty-eight cases, or nineteen per cent; cough in forty-five cases, or thirty per cent. All these symptoms depend on the adenoid hypertrophy and disappear after removal of the growth. When a number of such symptoms are present he believes a tentative diagnosis can be made in the majority of cases.

THE ARCH OF THE PALATE.

HENRY L. SWAIN (The Laryngoscope, October, 1903) gives a careful review of the influences which modify the growth and development of the arch of the palate and concludes from his study:

(1) That it is possible by deforming processes which artificially alter the shape of the skull to produce a change in the form and shape of the hard palate.

(2) That under these above-mentioned conditions the septum seems to conform itself to the altered development of the rest of the face, rather contrary to our previous ideas regarding the habits of this structure.

(3) That if from arrested or retarded development of the superior maxilla the palate fails to descend to its proper level, a bent septum is liable to be produced, as when the palate is arched too greatly by

an unnatural narrowing process. Hence a palate of perfectly normal height as compared to breadth may produce a bend in the septum.

(4) That in considering the various causes which produce the abnormalities of the palate, we must lay more stress upon the lack of proper aeration of the maxillary sinuses retarding their development and hence that of the whole superior maxilla.

(5) The conservation and general care of the deciduous teeth help to produce a normal horizontal curve in the hard palate and lessen the tendency to narrowing.

THERAPEUTICS.

BY DELOS LEONARD PARKER, PH. B., M. D., DETROIT, MICHIGAN.

LECTURER ON MATERIA MEDICA IN THE DETROIT COLLEGE OF MEDICINE.

THE TREATMENT OF ANGINA PECTORIS.

DOCTOR WILLIAM F. WAUGH (The Therapeutic Gazette, November, 1903) says that while angina pectoris is usually associated with organic disease of the heart, it may occur as a pure neurosis. Whatever the cause, however, the disease itself is one that causes intense physical suffering and places the individual attacked by it in immediate danger of death. Doctor Waugh thinks the prevalence of this disease is more common than formerly.

As to treatment he thinks too little attention is paid to the patient during the intervals between the attacks. As to the paroxysm the best treatment consists of the administration of nitroglycerin in doses of 1-250 grain, repeated every minute until relief is afforded and the face flushes. This effect, he says, is prolonged by the administration of atropin in doses of 1-250 grain repeated every ten minutes until the mouth becomes dry. Doctor Waugh says any salt of atropin will answer for the purpose, but that he personally prefers the valerianate. By repeating the doses of the atropin whenever the dryness of the mouth subsides the paroxysm can be controlled indefinitely.

In addition to this treatment Doctor Waugh advises the exhibition of strychnin, preferably the valerianate, and any stimulant that may be at hand, such as alcohol, ammonia, pepper, ginger or other spice given in concentration and as hot as the stomach will bear.

After the paroxysm has passed the hygiene, diet and habits of the patient should be regulated. Concerning the use of drugs at this stage of the disease, Doctor Waugh says: "Structural lesions of the heart are to some extent amenable to treatment. Rheumatic, syphilitic and other deposits waste away under the influence of such remedies as the following: Mecrury biniodid 1-20 grain, iodoform 1-2 grain, arsenic iodid 1-67 grain, and phytolaccin or stilligin 1-2 grain, given before meals and at bedtime, and continued for months. The arsenic. exerts an action upon the nutrition of the heart that would not be believed by those who give it in maximal doses for a week or two only."

In cases of uric acid manifestations administer colchicine in single

doses at bedtime. Begin with one-sixtieth grain and gradually increase the dose until it causes slight nausea or catharsis in the morning; then continue as long as necessary. An occasional week's use of zinc phosphide, one-sixth grain, is of great value in improving the nutrition of the nervous centers.

EDITORIAL COMMENT.

POINTS IN REGARD TO LOCOMOTOR ATAXIA.

THERE exists a rather common idea that the various lesions of the spinal cord accompanied by sclerosis are in their nature steadily progressive. As a matter of fact the use of the term "progressive" to the patient is a most unfortunate one.

To tell a patient that he has "progressive" muscular atrophy is a needless bit of pessimism. It is bad enough to tell him the known truth that he has a muscular atrophy-but the word progressive makes the future black to him. Not all cases of spinal muscular atrophy are progressive in the sense that the patient takes it. We, none of us, know either how fast, how far, or how long the muscular atrophy will extend. The term should be abandoned.

The same idea of steady progression is pretty generally held of locomotor ataxia. In the Semaine Medicale Marie and Mocquot ask the question "At what age do tabetics die?" and then answer it from statistics of the Bicetre Hospital.

In general, tabes does not materially shorten life. Among twenty blind tabetics fifty per cent were more than sixty years old at death, and all but three were over fifty. Of the whole number of tabetics eighty-three per cent were over fifty and fifty-one and five-tenths per cent were over sixty years of age.

Such figures compel us to modify, somewhat, the common idea that locomotor ataxia, once started, is likely to progress steadily to a fatal termination. In truth, the progress of tabes is exceedingly slow. Were we to include, as we should, the years of so-called "sciatica," or "rheumatic pains," which precede the recognized ataxia, this would be still more evident. Even after ataxia and the more striking features of tabes are developed, progression of the disease is uncertain. Many cases even come to a standstill. The patient may either improve to a very considerable extent or at least become no worse for a period of many years. Were he to follow modern methods of training his muscles instead of, as is so often done, allowing them to become useless from disuse on account of the difficulty in managing them, such remissions. would be still more common. At any rate his chances of dying early are not great.

In connection with the idea of securing remission, or keeping the patient so that he can still be useful and capable, it is worth while.