CHAPTER XXXVI.

ADHESIVE OR PROLIFERATIVE INFLAMMATION OF THE MIDDLE EAR.

340. The names "adhesive, proliferative, plastic, or hypertrophic" otitis, or "dry catarrh" of the middle ear, refer to an affection of the middle ear which must be considered the analogue and extension of hypertrophic rhinitis. Very rare in early childhood, it cannot be called common until after growth is finished, from which time on its frequency increases until every third or cer tainly every fourth individual in advanced age presents some evidence of this disease. The disease is rarely one-sided-mostly bilateral. But quite often one ear is less affected than the other, sometimes so little that the patient calls his disease one-sided. The progress of the disease is not necessarily parallel in the two ears.

In typical cases it begins so gradually that its exact date of origin can often not be stated. Ringing in the ear, perhaps only occasional at first, may be ignored for a long time until it becomes annoying. Later on it may become the main complaint, more serious to the patient even than the deafness. In neurasthenics tinnitus can cause much suffering and unhappiness. "Stuffy" sensations are usually not present to any distressing extent. except in complicated cases. Dizziness is likewise not a strictly "normal" symptom of adhesive otitis, but it does occur in a small proportion of cases on account of some special localization of the lesion or as a complication, and it may prove very distressing. The hearing becomes affected gradually. Sometimes the patient is not conscious of any impairment for many months; in other cases he is annoyed from the start. The impairment is, of course, most perceptible when listening to

faint sounds-for instance, in the telephone. The disease never ends in absolute deafness. Except in case of ankylosis of the stapes, loud speech can always be understood close to the ear. It may take years before the perception of ordinary conversation becomes embarrassing; but in those instances in which ankylosis between the foot-plate of the stirrup and the oval window takes place, the hearing is much more seriously compromised. This is, on the whole, not a frequent occurrence in adhesive otitis. It may begin early or late in the course, and when begun, it may reach its completion within weeks or within several years. When complete, it practically bars hearing of the voice, except through a speaking tube. It is a common observation in hypertrophic otitis that conversation is better understood in noisy surroundings, like railroad cars, etc., than where silence prevails..

Tests show that a faint whisper is not heard normally even at a time when the patient claims normal hearing. As a rule, the perception of the watch is more impaired in this disease than that of the voice. Tuning-fork tests show air-conduction diminished, especially for low tones, for which bone-conduction is normal, or later on even increased. In Weber's test the sound is localized in the more affected ear, except in cases complicated with lesions in the internal ear. Rinne's test shows impaired air-conduction; later on its normal formula becomes reversed, especially for low tones (Rinne negative).

The course of proliferative otitis is variable. It is only a small minority of cases that continue to get worse steadily. This severe course is favored by pronounced hypertrophic rhinitis with nasal stenosis; but it may happen, too, even without nasal obstruction. On the other hand, a fair majority of patients lose their noises and feeling of stuffiness and retain their hearing for a time without further continuous impairment. The disease has apparently come to a stand-still. The damage done to the hearing is usually permanent, as a rule, even under treatment. This apparent arrest of the disease is

in most cases not permanent. With a fresh "cold" in the nose the symptoms return to a variable degree. Whether or not the loss of hearing power is steadily progressive can be judged only by the history during a period of at least some months. But the presence of other symptoms, tinnitus, fulness, or discomfort of any kind, is evidence of the progressive character of the disease. Yet a permanent arrest of the disease is not so very rare. It can be expected only if the irritative symptoms are either of recent origin, or if of longer duration, have not been continuous. The younger the patient when the disease began, the less probable is a favorable termination.

341. The clinical course of proliferative otitis is complicated in some instances by a slight degree of exudative catarrh. A small number of cases of exudative catarrh change gradually into the plastic form, and thenceforth present the combined lesions of hypertrophy with mucous secretion into the drum cavity. Others do not give the history of acute onset, but pursue a mild, subacute course from the beginning, with considerable variation in the degree of exudative inflammation in consequence of changed environment or as the result of treatment. This "mixed" type of middle-ear disease is aggravated by every fresh "cold" in the nose more so than the purely proliferative form without secretion. But, on the other hand, it is also more readily influenced favorably by treatment. In adhesive otitis, but especially when some exudation is present, the patients claim to hear worse in bad weather. The complaint is not always corroborated by actual test. The patient is at times deceived as to his hearing power by the subjective feeling of fulness or the tinnitus which may be increased by unfavorable weather.

342. The morbid changes in plastic otitis consist of inflammatory swelling, hypertrophy, fibrillary sclerosis, and adhesions of the mucous membrane. In the pure type of proliferative inflammation the lesions are often localized, especially around the articulation of hammer and anvil. When exudation is present, the process is

more likely to be diffuse. The exudate, if present, is scant mucus, sometimes very viscid. Diffuse inflammatory swelling occurs probably only during subacute exacerbations, or in the case of exudative catarrh gradually changing into a plastic otitis. Ordinarily more or less circumscribed hypertrophy of the lining is found, the surface being uneven, sometimes with papillary or villous prominences. The articulations may be imbedded in hypertrophied mucous membrane. As a result of much thickening, the protruding prominences of the lining come into contact and form adhesions, especially between the joint of hammer and anvil and the opposite walls. In other instances the membrane is not hypertrophied, but transformed into relatively rigid fibrous tissue. It has no longer its normal delicacy and pliancy, but binds down the mobile parts which it envelops. Instead of broad adhesions of mucous membrane, narrow rigid adventitious bands are found bridging from one surface to another. There is no good reason to consider this fibrillary sclerosis as the later transformation of hypertrophy of the mucous membrane. It is more likely the result of imperfect involution of inflammation under unknown conditions. The mobility of the hammer is reduced, and its normal position changed into one of increased obliquity, which is maintained partly by adhesions, partly by contraction of the ligaments and of the tensor tympani muscle. The latter may be shortened by fibrillary transformation or bound down by adhesions. The proliferative changes may extend to the round window, thickening its diaphragm. When the disease attacks the vicinity of the oval window, it leads to ankylosis of the foot-plate of the stirrup, the most serious lesion possible in the middle ear so far as sound-conduction is concerned. Even a partial involvement of the articulation by fibrillary transformation of the tissues damages its function. In complete ankylosis the foot-plate is bound down by rigid fibrous tissue, sometimes with interstitial deposition of lime-salts. Bony ankylosis does not often take place in

proliferative otitis; more so, however, in disease of the bony capsule of the vestibule (see ¶ 350).

The Eustachian tube is involved in this disease, at least at its tympanic end. In all probability the Eustachian lesion is the primary one in plastic otitis. Morbid changes are found, as a rule, in the bony (tympanic) portion of the canal, while the cartilaginous part of the tube internal to the isthmus is mostly normal. The lesions correspond to those in the middle ear-viz., diffuse thickening of the mucous lining, or fibrillary sclerosis with concentric narrowing, sometimes adhesions, often valvelike overlapping of the tympanic opening by a fold of mucous membrane. Circumscribed cicatricial strictures like those found in the urethra do not seem to occur in the tube. The pharyngeal portion of the Eustachian lining shows more or less inflammatory swelling (leukocytic infiltration) or permanent hypertrophy, according to the character of the primary nasopharyngeal lesions.

343. Etiology.-Proliferative otitis is the extension of chronic nasal inflammation into the middle ear. It is never observed when seen at the start, except in connection with chronic nasal disease. If the latter heals as the result of changed environment or treatment, the lesions of adhesive otitis may persist in the ear-apparently independently; but the loss of hearing is, as a rule, not progressive. The nasal etiology is illustrated strikingly by the coincidence of the first or more affected ear with the narrower side of the nose in the case of one-sided stenosis. There are, however, some rare exceptions to this rule. Fluctuations in the degree of nasal inflammation are usually accompanied by similar variations of the condition of the ear, especially when we review longer periods in the patient's history. The dependence of the ear disease upon chronic rhinitis is demonstrable in some instances by the arrest of the former by nasal treatment. There are, however, various reasons why this therapeutic test is not always successful. Nasal treatment, even operative, however successful it may be, does not, as a