I plan to make a slight alteration in the topic listed on your program today and the reason for this is that lately I have seen very clearly the ease with which tinnitus has been considered as only a local ear disorder. No-one can deny, or even dare to deny, that medical and psychologic factors in a patient's personal make-up greatly effect the severity of the tinnitus and his response to it. And yet, I’ve repeatedly heard over the course of the past month the complaint of non-physicians who have said: ‘Why do you require an otologic evaluation at the University of Oregon; we’re just as qualified to see this patient as anyone else’. I think the reason is clear and irrefutable; that tinnitus is a medical disorder and the evaluation of tinnitus without a medical evaluation is poor medicine. The subtleties of diabetes, and thyroid disease and hyperlipidemia, and hypertension and drug reaction and allergies, are all easily enough overlooked by a physician, not to say how frequently they might be overlooked by others.

A clinical classification of subjective idiopathic tinnitus is presented today as an aid to the clinician in the understanding of the tinnitus complaint; to establish the site of lesion of the tinnitus complaint; and to provide a logical basis for the treatment of subjective idiopathic tinnitus. The problem of subjective idiopathic tinnitus is multi-faceted.

An up-to-date, modern classification of subjective idiopathic tinnitus must be multi-faceted—one based on the relationship of subjective idiopathic tinnitus to:

(a) Parameters of external sound stimulation—objective and subjective, i.e. frequency, intensity, duration, pitch, loudness.

(b) Response of the auditory system to pure tone and masking stimulation.

(c) Correlation of findings of the cochleo-vestibular evaluation.

(d) Evoked response audiometry for early, middle, and late responses.

The classification of subjective idiopathic tinnitus must be a dynamic, expanding one of increasing complexity relating to the advances of the basic sciences; and one in which the clinician plays a vital role.

My interest in tinnitus is very long. It stems, I think, from an interest in the sensory nature of Medicine, if you like in the cultural aspect of it. Imagine my horror when I discovered, starting my training, that I had to do some millions of tonsillectomies and adenoidectomies and submucous resections of the septum, always aiming for an attempt at studying the senses. And, in fact, more than ten years ago, I decided that tinnitus was possibly the one that I could study then. The reason was that I was a very genial person, that we had little equipment available and that not very much was known about that subject; and I felt that if I’d say something, then maybe it would be of note. And here I am. Now the position, as I found it there, was the following: modern medicine is based on a comparison of symptomatology with pathological knowledge.

Galen thought that tinnitus was due to ‘exhalations from the stomach’, and in books written before 1861 you may often read descriptions of Stomach Deafness, an entity well recognized before Menière put his name to it.

I found a monograph by George Field published in 1875 on Tinnitus Aurium in which he puts together an account of the causes of tinnitus that is comprehensive even by the standards of today, from hairs tickling the tympanic membrane to Eustachian catarrh, vascular abnormalities and brain damage. When he comes to treatment: middle ear problems were treated by myringotomy or by patching perforations with damp paper and, for the rest, drugs of various kinds were used—with about as much effect as was described in some of the papers read earlier in this meeting. Belladonna (atropine) seems to have been particularly well thought of. Anti-emetics were used in Menière's disorder and one of Field's patients strongly recommended putting a piece of dead eel in the ear as a reliable cure for tinnitus.

When I offered to speak on this subject I expected to review the literature, extract cases from my hospital's record system, and look for a few points of interest in a topic that had not come my way very often.

First, I found very little on the subject in the medical literature. An exception is a paper in 1972 by Nodar from Syracuse, New York, in which he studied a school population of about 2,000 over three years and found a 13 per cent incidence of tinnitus in normal children and a 59 per cent incidence in those who had failed audiometric screening tests.

There was also a paper by Glanville, Coles and Sullivan (1971) in which a family with objective tinnitus was described. One child of 2½ had narrow-band tones of 5 and 8 kHz. coming from the left and right ears respectively. Pure tone audiometry showed nearly normal hearing for low frequencies, but a notch in each ear at the frequency of the objective tinnitus. Curiously the child did not seem to hear the tinnitus himself.

The purpose of this paper is to report on the clinical experience gained with the use of antihistamine; vasodilator medication—alone and/or in combin- ation in an attempt to control SIT (subjective idiopathic tinnitus). The report is based on 172 consecutive clinical cases seen for the chief complaint of SIT. This report is not a controlled study; however, it is presented to give a clinical impression of the response of the patient to such management based on our case series. Whenever tinnitus is mentioned, we refer to SIT (subjective idiopathic tinnitus).

Of the three methods for the treatment of tinnitus now available, masking, biofeedback and medical, we believe medical treatment has the most promise for the future. The masking treatment substitutes one potentially annoying external noise for the patient's own internal noise and in our experience is of little value. The biofeedback treatment requires a rather sophisticated patient and therapist to begin with, and only helps a limited number of those well suited to the treatment program. The drug therapy is, however, immediate and real, not dependent on the patient, and limited only to the number of drugs having an effect on the end-organ and the central pathways of hearing.

Tinnitus is a problem of enormous proportions. A probability sampling of 6672 adults selected at random in the United States, ranging in age from 18 to 79 years, during the years of 1960 to 1962, revealed that 32 per cent of adults (36 million out of the U.S. population of 220 million) experienced tinnitus, and that 6·4 per cent (7·2 million out of the U.S. population of 220 million) of them complained of severe and at times debilitating tinnitus.

At the Shambaugh Fifth International Workshop on Middle Ear Micro-surgery and Fluctuant Hearing Loss held in Chicago in March 1976, Professor Tamotsu Morimitsu, of Kyushu University in Fukuoka, Japan, reported on the successful treatment of sudden hearing loss (SHL) with diatrizoate meglumine, an iodinated dye used in radiologic studies, which has a trade name of ‘Hypaque’ in this country. The initial case that stimulated Professor Morimitsu's interest involved a patient who had a SHL of 40 days’ duration and a significant improvement in hearing following a 1 cc. test dose of intravenous Hypaque prior to a vertebral angiography study. Subsequently, Professor Morimitsu compared 39 patients treated with Hypaque within two weeks following onset of SHL, to 419 patients, followed by the Sudden Deafness Research Committee of Japan, who were treated with vasodilators within the same time period. Of the patients treated with Hypaque, 54 per cent had complete recovery of hearing compared to 19 per cent of those treated with vasodilators.

I present to you the temporal bones of a patient with a mixed type hearing loss. In his right ear, he had stapedial fixation; he had a conductive hearing loss, and he had some sensori-neural loss. In the opposite (left) ear, he had an almost symmetrical pathological lesion, but there was no stapedial fixation. The stapes on this side was still loose and the patient did not have any conductive loss; the loss was entirely sensori-neural. I guess this set of temporal bones goes as far as any that I have seen to prove the theory that there is such a thing a cochlear otosclerosis. And most of us do believe there is such a thing as cochlear otosclerosis; and although this patient did not have a conductive hearing loss, he did have otosclerosis, he did have a sensori-neural hearing loss only, and he did have tinnitus. So here would be a patient with tinnitus due to a sensori-neural hearing loss only, presumably due to otosclerosis, that might be amenable to some type of therapy such as Sodium Fluoride.

Over the last almost year and a half, a lot of people have offered dissertations on the possible etiology of tinnitus in Menière's disease (everything from changes in DC potential, deformation of the basilar membrane, change relationship between the outer hair cells and the tectorial membrane) so I’m not going to spend a great deal of time reiterating all of that. What I’d like to tell you is that Menière's disease is an unusual disease process. You have to remember that it's subject to spontaneous remissions and exacerbations. And not only are the symptoms of tinnitus subject to those same remissions and exacerbations, but so also are the other symptoms, of vertigo and hearing loss. I think all of you are familiar with the classic audiometric presentation of patients with Menière's disease. We at Temple have been investigating almost all of our patients with uni- laterality of hearing loss with BSER, and it's been our experience that, in patients with endolymphatic hydrops, there is no change in the BSER pattern, particularly with reference to the intra-aural latencies.

I became interested in tinnitus, after a particular observation we made in Bordeaux on a deaf patient, while studying the effects of electrical stimulation of the ear as a means of artificial auditory stimulation (Cazals et al., 1978; Portmann et al., 1979). Indeed such electrical stimulation has been tried many times and was taken over again in about the 1970's by House and Urban (1973), Michelson (1971) and others (Merzenich et al., 1974).

The questions we were asking at the time were whether there were many deaf patients who could eventually benefit from such a procedure and to know whether, for instance, they would have enough, if any, remaining nerve fibers in their cochleas available for their electrical stimulation. So we undertook the simplest way of studying this, by applying, in totally deaf patients, electrical stimulation to the cochlea; and by investigating the sensation evoked in the patient by this electrical stimulation, as it has been done also by many other investigators.

An interesting and unexpected benefit of the cochlear implant is a significant reduction in tinnitus in many patients who use the device.

Dr. William F. House has implanted a single-channel cochlear implant device in 50 patients. The implanted electronics are: an induction coil, which is embedded in the bone in the postauricular area; an active electrode, which is passed through the opened facial recess into the round window and approximately 20 mm. into the scala tympani; and a ground electrode, which is placed into either the attic area or Eustachian tube area.

Tinnitus is a common and often perplexing problem in neurosurgical patients, and post-traumatic tinnitus is the type most often encountered. To put the magnitude of the problem in perspective, it should be noted that neurosurgeons in the United States treat approximately 10,000 to 20,000 patients with brain tumors each year, whereas approximately 500,000 patients with severe head injuries are treated each year. The incidence of tinnitus in association with head injuries is variable, from 5 to 35 per cent in reported series, and in our own experience tends toward the lower percentage. Even using the 5 per cent figure it is apparent that U.S. neurosurgeons see more patients with tinnitus in a year than they do patients with brain tumors.

The post-traumatic tinnitus is usually high-pitched, associated with impaired hearing, and frequently related to temporal-bone injury. Often this is a self-limiting problem. At times there is a question as to whether or not the tinnitus actually disappears, or the patient no longer seeks medical attention.

Because tinnitus is often associated with hearing loss, one could consider its experience as a compounded stress. According to Selye (1956) stress has been described as the ‘rate of wear and tear in the body associated with feelings’ that can be as subjective as the responses to pain and pruritus. In his Stress Syndrome or a General Adaptation Syndrome, Selye stressed homeostatis as the goal of the stages of alarm, resistance, and exhaustion. Selye emphasized that ‘stress is not necessarily morbid, could be curative and associated with changes in structure and in chemistry with the body’ attempting to adapt against the stress. Tinnitus is a stress.

Tinnitus is a noise in the ear with subjective and objective qualities. It can occur normally in everyone, being invariably transient, without untoward emotional or physical effects. Tinnitus has been described as a buzzing, roaring, hissing, or grinding type of noise, located unilaterally or bilaterally.