It is still an open question whether the tinnitus aurium which occasionally occurs in gradual changes of the external air pressure originates within the organ of hearing, or whether it is due to other causes. The subjective noises heard during balloon ascensions and mountain climbing are naturally attributed to the variations in pressure between the middle ear and the external air. But if we study the clinical picture of so-called mountain sickness, we are struck with the predominance of the circulatory phenomena, the markedly accelerated pulse, the dyspnea, and local symptoms of flashes and subjective noises in the ears; we are irresistibly led to attribute the ocular and aural phenomena to the vascular disturbances, and not to alterations of the special sense organs.

It may be well in this connection to call attention to the fact that similar phenomena, though somewhat milder in character, occur in the treatment of heart and lung diseases with rarefied and compressed air, when the patients are entering or leaving the pneumatic chamber. A certain degree of caution is therefore advisable in the case of individuals whose hearing is not quite perfect, especially such as are troubled with tinnitus aurium.

Schwartze's observation that "many persons with incurable middle-ear sclerosis experience relief during a protracted stay in high Alpine health resorts, on account of their freedom from the distressing tinnitus aurium, and the marked improvement in the hearing" has not been explained. But is it not permissible to assume that the aural symptoms are due to circulatory disturbances? For if the tinnitus is really a vascular murmur within the ear, would it not be relieved by the beneficial effect of the altitude on the heart?

DISTURBANCES OF THE FUNCTION OF THE EUSTACHIAN TUBE DUE TO ALTERATIONS IN THE UPPER

AIR-PASSAGES.

The diseases of the upper air-passages that diminish the permeability of the tubes are principally those which are accompanied by swelling of the mucous membrane. The relation existing between the nose and the postnasal space is a very intimate one, and very few diseases have their

1 66 Die chirurg. Erkr. des Ohres,” p. 169.

origin and exclusive seat in the postnasal space without involving the nose. The great majority of pharyngeal diseases arise, as we have already stated, by extension from the nose, so that the importance of rhinology in the study of diseases of the ear is easily explained.

Any acute catarrh in the upper air-passages may lead to intumescence and occlusion of the pharyngeal orifice, and thereby produce a fall in the pressure of the middle ear. As soon as the swelling subsides and the tube again becomes patulous, the morbid symptoms usually disappear without treatment. In chronic catarrh, on the other hand, as the hypertrophy of the mucous membrane does not, like the hyperemia in acute catarrh, tend to disappear spontaneously, the changes produced in the middle ear by occlusion of the tube are of a more lasting character. The continued tension of the membrana tympani leads to atrophy, and the persistent retraction disturbs the normal relation of the ossicles, which then exert a constant pressure on the fenestra ovalis.

It is fair to assume that, in consequence, the muscles of the ossicles-the tensor tympani and the stapedius-are thrown into a state of permanent contraction, and probably atrophy from disuse; while, as a result of the hyperæmia ex vacuo, a chronic inflammation of the mucous membrane of the tympanum develops, giving rise to morbid conditions. which can not be distinguished clinically from catarrh of the middle ear due to other causes. These conditions are in great need of anatomic and clinical investigation; in fact, the concept of middle-ear disturbance by occlusion or obstruction of the tube has never been clearly differentiated from the idea of inflammatory middle-ear catarrh, and the various views advanced in the text-books descriptive of middle-ear catarrh of inflammatory and noninflammatory origin merely add to the confusion.

Any and all diseases of the nose and postnasal space which are followed by obstruction of the nasal passages lead to passive hyperemia in the mucous membranes, which in turn produces occlusion of the Eustachian canal. The recognition of this important fact is comparatively recent, and since the causal relation between these disturbances and the interference with nasal respiration by the presence of adenoid growths was definitely established the attention of clinicians has been directed to the significance of nasal

stenoses in occlusions of the Eustachian tube. The interference with nasal breathing may be due to a number of conditions within the nose, as hypertrophy of the mucous membrane, mucous polypi, tumors, syphilitic or tuberculous infiltrations, foreign bodies, etc. There may be a congenital narrowing of the nasal cavity from deformity, and hyperplasia of the septum or abnormal curvature of the turbinated bones. The obstruction may be situated in the postnasal space, and may take the form of hypertrophied pharyngeal tonsils, tumors, syphilis, or tuberculosis occluding the posterior nares. Hence the recognition and removal of any obstacle to nasal respiration should constitute an integral part of every examination and treatment of the There can be no hope of curing the ear affection before the causes which are responsible for the congestion of the mucous membrane have been removed and the permeability of the tube has been restored.

ears.

If I have included hypertrophy of the pharyngeal tonsils or adenoid vegetations among the diseases which produce hyperemia and swelling of the mucous membrane, with occlusion of the tube by interfering with nasal respiration, it is because I believe the occlusion is due to a general " adenoid habit" of the nose and pharynx, rather than to the direct mechanical intrusion of the pharyngeal tonsil. The "adenoid habit" manifests itself in the rhinoscopic image as a hyperplasia of the entire lymphatic ring of Waldeyer; the follicles in the posterior pharyngeal wall and in the longitudinal folds on each side of the pharynx are more numerous, and are intensely red and swollen. Hyperplasia of Rosenmüller's crypts and of the anterior fold of the tube may develop as the manifestation of a general hyperplasia of all the lymphatic elements entering into the formation of the so-called pharyngeal lymphatic ring; hyperplasia of these structures necessarily favors the occlusion of the tube by compressing the orifice.

Two forms of adenoid enlargement are distinguished: a diffuse, cushion-like hyperplasia, and a villous variety consisting of finger-like projections or true vegetations. Their usual seat is the roof and upper portion of the posterior wall of the pharynx, so that they fill the upper part of the postnasal space more or less completely, and whenever they hang down below the level of the upper margin of the posterior nares, the latter are obstructed and nasal breath

ing is interfered with. As the vegetations usually spring from the median line, they are not, when at rest, in contact with the lateral walls of the pharynx and therefore do not occlude the orifices, as we are frequently able to demonstrate in the postrhinoscopic image; but whenever the palatal and pharyngeal muscles contract, as in swallowing, retching, and similar movements, the lumen of the postnasal space is constricted and the enlarged growths are forced against the lateral walls of the pharynx, thus giving rise to periodic occlusion of the tube. The adenoid tissue is not the soft, gelatinous mass that it is sometimes compared to, but is comparatively firm, and returns to its normal position of rest, dependent on gravity, as soon as the constrictors of the pharynx and the tensores and levatores palati relax and the postnasal cavity regains its normal volume. But it is not clear to me how a momentary occlusion of the orifice can have the same effect as a permanent one, and I therefore consider the hyperemia of the entire mucous membrane the most important factor in the production of aural complications.

Paralysis of the muscles of the soft palate, especially of the levator veli palatini and tensor veli palatini,—muscles which effect the opening of the Eustachian tube,—is followed by permanent occlusion, with the usual appearances of the membrana tympani. The action of the muscles may be similarly affected by tumors, by syphilitic, tubercular, or other kinds of ulcerations or their scars, and by cleft palate, so that these conditions are also occasionally accompanied by middle-ear disease.

DISEASES OF THE MIDDLE EAR DUE TO INFECTION FROM THE POSTNASAL SPACE.

The cartilaginous portion of the Eustachian tube is lined. with ciliated columnar epithelium, the ciliary current being directed toward the pharynx, which is replaced at the isthmus by cells of the same type as that of the middle ear. Since, therefore, the mucous membrane of the tube is a direct continuation of the epithelium of the postnasal space, we can readily understand that an inflammatory process beginning in the latter is not arrested at the pharyngeal orifice, but is continued into the tube itself, and may be followed by acute inflammation of the mucous membrane

of the middle ear. Next to acute rhinitis and pharyngitis, the most important inflammations in the etiology of otitis media are those which occur in the acute exanthemata. These will be discussed elsewhere.

In addition to the ordinary inflammations of the mucous membrane of the tube and middle ear, we observe acute suppurative otitis media in the train of acute nasal and pharyngeal diseases. As we may have either a simple or a suppurative inflammation without any apparent external reason, we are forced to assume a different behavior of the mucous membrane of the middle ear in regard to the invading pathogenic germs to explain the occurrence of suppuration in the middle ear through the channel of the Eustachian tube.

It is well known, as has been mentioned, that the nose and postnasal space harbor a multitude of microorganisms. Their presence in the healthy organism appears to have no significance, perhaps because of a bactericidal property of the mucous secretion which destroys the virulence of the pathogenic germs and prevents their further development. It may also be assumed-and has, in fact, been practically demonstrated experimentally by Zaufal, Kanthack, Scheibe, and others, in spite of the differences in the individual results that the middle ear normally contains bacteria which may, under favoring circumstances, regain their virulence.

The number of bacteria in the middle ear and the liability of the organ to infection depend on the condition of the epithelium lining the tube and the size of the lumen. If the ciliated epithelium is intact, it enables the tube to rid itself of any deleterious substances, and thus forms a protection against invasions from the pharynx. Since any inflammatory alterations, be they acute or chronic, which destroy the integrity of the epithelium tend to remove this natural protection, they will naturally be accompanied by inflammation and suppuration in the middle ear.

The question whether abnormal dilatations of the tube may produce pathologic conditions in the ear by affording an easier entrance to pathogenic germs deserves passing mention.

In catheterization of the tube the nature of the blowing noise, and the strength of the concussion-note afford a clue to the size of the lumen. But, in addition to this, other