Tinnitus

Tinnitus and retraining therapyWhat Causes Tinnitus?

1. EXTERNAL AUDITORY CANAL LESIONS

Obstruction of the external auditory canal by wax or other foreign bodies may cause a sensation of fullness in the ear with decreased hearing and when this is present, the patient may experience tinnitus. Usually, this is resolved once the obstruction in the ear canal is removed.

2. VASCULAR LESIONS

The heart’s pumping and blood circulation normally are only occasionally heard by the patient in the silence of a sound-proofed room. However, if the sounds are heard constantly, they signal a pathologic condition and acquire the properties of real tinnitus. In these instances, the patient perceives a pulsating noise in synchrony with his or her heart rate. When this is present, it needs to be evaluated thoroughly. Vascular noises usually are caused by turbulences within blood vessels. Narrowing of blood vessels as well as vascular tumors may cause type of tinnitus. In addition, other vascular malformations may result in this type of sound. Since most of the vascular lesions associated with pulsating tinnitus can be cured by surgical therapy and since some of the underlying vascular disorders are potentially dangerous, all cases of pulsating tinnitus must undergo a thorough medical work-up before treatment is considered.

3. MUSCULAR LESIONS

Some patients may experience a clicking noise radiating from their ear and this can be heard by another person. This can result in a repetitive type of clicking sound and is due to contractions of a muscle within the middle ear. These are involuntary spasms of one of the two muscles attached to the middle ear bones. There are two muscles in the middle ear: the stapedius attached to the stapes bone (stirrup) and the tensor tympani, attached to the malleus (hammer). These muscles normally contract briefly in response to very loud noise. Spasms of the eustachian tube muscles normally are restricted to one side, resulting in click-like sounds. These contractions do not usually open the eustachian tube, but involve the tensor tympani muscle. Since this muscle attaches to the malleus, it thus directionally pulls at the tympanic membrane. Sometimes one can see the movement of the malleus with the clicking sound when this occurs. On occasion, one or both of these muscles may begin to contact rhythmically for no apparent reason for brief periods of time. Because the muscles are attached to one of the middle ear bones, these contractions may result in repetitive sounds in the ear. This clicking sound, although annoying, is harmless and usually subsides without treatment. Should this muscle spasm continue, medical treatment with muscle relaxants or surgery (cutting the spastic muscle may be necessary).

4. OPENING MOVEMENTS OF THE EUSTACHAIN TUBE

Opening the eustachian tube occurs by coordinating action of the two palatal muscles (levator and tensor palatini). The normal action that opens the eustachian tube and causes this are swallowing and yawning. Some patients are bothered by the clicking sound in the ear which accompanies the action of swallowing and some patients can produce these sounds voluntarily and elicit this type of noise.

5. CENTRAL LESIONS

The hearing nerve has approximately 30 thousand fibers within it. Most of these fibers demonstrate spontaneous activity and certain sound frequencies are associated with certain fibers. It is possible that the alterations in this spontaneous activity may generate tinnitus. It has also been demonstrated that the auditory nerve is covered by myelin, and it is in this area that the nerve is more sensitive to vascular compression by blood vessels in the posterior fossa. It is therefore possible that the tinnitus may be secondary to a vascular compression of the auditory nerve. All the fibers of the auditory nerve end in the cochlear nucleus and each fiber may come in contact with as many as 75 to 100 cells of the nucleus. There is also another pathway which is referred to the efferent pathway which is an inhibitory pathway and may be related to the awareness of tinnitus. Specifically, tinnitus may be perceived because of the inability of the efferent system to suppress the tinnitus.

It has been suggested that even though tinnitus may have originated in the cochlea, retrograde changes may occur within the auditory pathway and the tinnitus then becomes a central phenomenon.

6. MIDDLE EAR LESIONS

Any dysfunction of the structure(s) of the middle ear (i.e. tympanic membrane, ossicular chain problems) can result in tinnitus. Acute and long-standing inflammation of the middle ear sometimes will result in tinnitus. Often when the middle ear abnormalities are corrected by surgery, the tinnitus disappears. Sometimes in otosclerosis there is an additional component of tinnitus present, probably of cochlear origin, which is usually not improved by surgery.

7. COCHLEAR LESIONS

The cochlea is probably the most common site in the origin of tinnitus. The inner and outer hair cells are connected to the central auditory pathway by two systems. Afferent fibers carry information from the inner ear to the central nervous system. Efferent fibers from the brain go to the inner ear. It is felt that abnormalities of the hair cells, efferent or afferent fiber pathways may give rise to tinnitus.

A Summary of the Causes of Tinnitus

Tinnitus may originate from various lesions and from different sites. The auditory system involves highly complicated inner ear structures, many afferent and efferent nerve pathways and a great amount of nuclei that form a complex meshwork. To pinpoint tinnitus to a certain structure becomes questionable. This is demonstrated by patients who have had intractable tinnitus after having surgery on their ear or incurring severe diseases of the ear. In an attempt to relieve the tinnitus, cutting the auditory nerve has been done and yet the tinnitus was persistent, indicating the site of lesion causing the tinnitus must have shifted into the central nervous system.

Tinnitus could be explained by abnormal neural activity in the auditory nerve fibers, which may occur if there is a partial breakdown of the myelin covering of individual fibers. A defect in the hair cell would trigger the discharge of connected nerve fibers. For chronic cochlear disorders, there may also be increased spontaneous activity in the hair cells and neurons resulting in tinnitus. In the auditory nerve there are two different kinds of afferent fibers: Inner hair cell fibers with large diameters and outer hair cells fibers with small diameters. Thus, loss of signals from the cochlea might trigger tinnitus as a manifestation of a functional imbalance between the two sets of fibers. In addition, other abnormal changes of the cochlear fluids may result in tinnitus.

There is not one type, one site or one origin of tinnitus, but a multitude of types, sites, and origins. It is also unlikely that one hypothesis on the cause of tinnitus could explain all the features.

THEORETICAL BASIS OF OUR APPROACH TO TREATING TINNITUS AND HYPERACUSIS

(Taken from the bookchapter, Treatment of Tinnitus Based on a Neurophysiological Model of Tinnitus, P.J Jasterboff and J.W.P. Hazell, in the book Treatment of Tinnitus, 1997, J. Vernon editor, ISBN-020518260. Reprint permission granted by Allyn & Bacon. To order single copies of Treatments of Tinnitus, call Allyn & Bacon publishing 1-800-278-3525.)


Tinnitus is a common phenomenon that affects about 17% of the general population and about 33% of the elderly. Until recently tinnitus did not receive sufficient attention, both in clinical practice and in research. While the perception of tinnitus is very real, there is no external sound corresponding to the patients’ perception of sound; thus, tinnitus can be classified as a phantom auditory perception. Consequently there is no objective measurement of tinnitus.

Much effort has been committed to the psychoacoustical description of tinnitus, such as: its pitch, loudness, whether it is perceived in one ear, both ears, or in the head, the minimal level of noise needed to suppress its perception, "how it sounds," etc. The expectation was that these measurements would establish different categories of tinnitus, where for each category a specific treatment could be applied with a predictable outcome. This expectation has not been fulfilled, but nevertheless the efforts have provided interesting, while counterintuitive, results. One important result was that the psychoacoustical characterization of tinnitus has basically no relation to the level of annoyance evoked by tinnitus. In other words, two people with a very similar psychoacoustical description of tinnitus can differ dramatically in their level of annoyance induced by tinnitus: One person ignores tinnitus and is not aware of it and is not annoyed at all, while the other person is constantly aware of tinnitus and has difficulty focusing their attention on work, falling asleep, and enjoying life.

Approximately 75% of all the people who experience tinnitus are not bothered by it, and they treat tinnitus like any other sound to which they easily habituate. The important aspect is that there is no difference in the psychoacoustical characterization of tinnitus between those who experience tinnitus and those who suffer because of it. This observation is one of the findings responsible for the development of a new model of tinnitus, and based on the model, Tinnitus Retraining Therapy. The model is based on basic, well-established neurophysiological and psychological principles. Mainly:

1. The processing of information occurs on several levels for each sensory system, each level contributing to the final stage when a signal reaches the cortex
2. The auditory system is closely connected with the part of the brain that controls emotions and the automatic response of the body to danger
3. Connections within the nervous system are continuously modified, resulting in the enhancement of significant signals, and a decrease of neuronal response to irrelevant signals
4. Sounds that are new, or associated with a negative experience, are treated as significant, evoke an emotional response that triggers the body to prepare for "fight or flight." The repetition of these sounds results in enhancement of their perception and in a resistance of their perception to be suppressed by other signals. The repetition of signals not associated with positive or negative reinforcement results in the disappearance of a response to their presence, i.e., in habituation
5. The detection of sound occurs on a pattern-matching principle, allowing for nearly complete perception of a signal even when it becomes highly distorted.

Consequently, the main point of the theory of tinnitus based on these neurophysiological principles is the postulate that nonauditory systems, particularly the limbic system (involved in emotion), and the autonomic nervous system, which controls all body functions and triggers the "flight of fight" reaction, are an essential part of each case of troublesome tinnitus. The auditory pathways play a secondary role. According to this model the annoyance of tinnitus is determined exclusively by the limbic and autonomic nervous systems.

The following scenario of the emergence of tinnitus perception has been proposed (Neurosci.Res. 8:221-254, 1990). A weak imbalance of neuronal activity within the auditory system, most frequently related to damage of the inner ear, is detected at low levels in the auditory system, and being a new signal it is further enhanced by subcortical centers, transferred to the auditory cortex and perceived as a sound – tinnitus, and is subsequently evaluated. In the majority of cases the continued presence of tinnitus combined with a lack of any positive or negative association results in habituation of the reaction to the tinnitus signal. Although tinnitus perception may still be possible, there is little or no annoyance or discomfort. This situation is typical for children, or those leaving a loud concert, who tend to treat tinnitus as a natural event, and tinnitus typically does not annoy them.

However, in some cases, the perception of tinnitus is associated with a negative emotion. Patients treat tinnitus as an indicator that something is wrong with their hearing, or their brain, and as a result they start to focus their attention on the tinnitus. Quite frequently this occurs as a result of "negative counseling." All too often healthcare professionals advise patients to check for a brain tumor, or indicate that the tinnitus is basically a psychiatric condition, or tell the patient "nothing can be done with tinnitus" and that the patient has to "learn to live with it." This negative reinforcement of tinnitus perception actually enhances the initial responses of the autonomic nervous system evoked by fear. As tinnitus is commonly continuously present and evokes a strong emotional response, this results in the tuning of the neuronal networks detecting the tinnitus signal itself. Consequently, this increases the time an individual is aware of the tinnitus and further enhances the aversive emotional responses and the reaction of the autonomic nervous system, thus increasing annoyance. Notably, the involvement of the limbic and autonomic nervous systems is responsible for the annoyance evoked by tinnitus; the loudness and pitch of tinnitus are irrelevant to a large degree and normally do not play a significant role.

For a significant proportion of patients the compensatory action of the auditory system results in the emergence of hyperacusis. Research on animals has revealed that after permanent or temporary hearing loss the increased sensitivity of about 25% of the neurons in the subcortical auditory centers. These data are in agreement with human data which showed that if a person is put in a chamber with a very low sound level, the sensitivity of hearing increases, all sounds starts to sound loud, and 94% of the people develop temporary tinnitus. These data indicate that tinnitus can result from enhanced sensitivity of the auditory system, which in turn may lower the maximum sound level that person finds comfortable. For these patients, tinnitus and hyperacusis are two manifestations of the same internal problem. In practice the contribution of the hyperacusis component to tinnitus ranges from none at all to the situation where hyperacusis is the only or dominant problem.

From the patient’s point of view the crucial question is what can be done to remove tinnitus-evoked annoyance. To our knowledge there is no drug, procedure, or surgery that can eliminate the source of tinnitus without profound side effects. As evident from the model, even in cases with significant inner ear contribution, attempts to solve the problem by destroying the cochlea or the auditory nerve would not be consistently helpful while making the patient deaf. To make the situation worse, it has been shown that cutting the auditory nerve, which is still promoted by some as a treatment for tinnitus, actually causes tinnitus in close to 60% of the people who did not experience tinnitus before the operation. Another problem arises from the observation that quite frequently more than one type of tinnitus coexists and therefore we would need to attenuate all various sources of tinnitus.

The Tinnitus Retraining Therapy, which was developed by Dr. Jastreboff in mid ’80s and published in 1990 (Jastreboff, P.J. Phantom auditory perception (tinnitus): mechanisms of generation and perception. Neurosci.Res. 8:221-254, 1990), offers a potential solution to this problem. If we cannot erase the source(s) of tinnitus we should turn our attention to what is happening between the source of tinnitus (most frequently at the periphery) and the level where tinnitus is perceived — the cerebral cortex. The idea is to block tinnitus-related neuronal activity from reaching the level of the cortex where it is perceived, and from activating the limbic and autonomic nervous systems — to habituate tinnitus perception and tinnitus-induced reactions.

Everyday experience and research show that we are consciously aware of only a small portion of incoming sounds. Although other sounds evoke changes in the neuronal activity within the auditory pathways, this activity is filtered out by the neuronal networks before they reach the level of conscious perception. Similarly, most sounds do not evoke any emotional reaction or activate the autonomic nervous system.

To understand how tinnitus emerges, it is helpful to understand how sound is processed in the auditory pathways. In the absence of sound there are high levels of neuronal activity in the auditory nerve, as well as in other neurons in the auditory pathways, but this activity is random. The nervous system filters out this activity and therefore we do not perceive it as sound. This random activity can be considered as "a code for silence."


When we are exposed to a sound the activity within the auditory system increases, and becomes more regular and synchronized. While the patterns of electrical activity within the auditory nerve closely reflect the sound that reaches our ear, this activity undergoes extensive processing in several subcortical centers within the auditory pathways before reaching the cortex, where perception of the sound occurs.

Of consequence is the observation that this processing of information can itself result in changes of the connections within the brain that are involved in transmitting signals from the ear to the cortex. In other words, repeated activation by a sound not associated with anything of significance will result in decreased activation of the cortical and limbic areas, whereas sound associated with a significant event, particularly related to danger, will be enhanced and will strongly activate the cortical areas and emotional response. Our brain sorts sounds according to their significance, giving important sounds high priority to our attention and filtering out (habituating) insignificant sounds. Notably, the rules controlling sorting are changing all our life, and with proper training we can enhance our perception of some sounds, while we can train our brain to filter out other sounds.

Accordingly, if we can train the brain to classify tinnitus-related neuronal activity as representing a neutral, nonsignificant signal, then the process of habituation will occur automatically. To achieve this, it is necessary, however, to fulfill two basic conditions:

1. Removal of the negative association attached to tinnitus perception.
2. Preservation of tinnitus detection (but not necessary perception) during treatment.

The first condition results from the observation that signals that induce fear, indicate danger, or that are associated with any unpleasant situation cannot be habituated. To avoid unpleasant situations we must not habituate sounds that provide warning! The decreased negative association of tinnitus is achieved through directive counseling, with emphasis on teaching the patient the basic function of the auditory system and the brain in relevance to tinnitus. This is performed because a known danger evokes a weaker reaction of the autonomic system than an unknown danger. As it is argued in the listed papers, the reactions of the autonomic nervous system are responsible for tinnitus annoyance and decreasing these reactions is a primary goal of the therapy.

The second condition is less obvious, but equally important. For retraining the neuronal networks involved in processing the tinnitus signal, it is fundamental that tinnitus-related activity can be detected. We cannot, by definition, achieve retraining on something that cannot be detected! Thus, for habituation-oriented therapy "masking" of tinnitus is counterproductive. Indeed, preliminary results of a study presently conducted on patients who used masking for 1015 years fully confirm this statement. In these patients tinnitus and its annoyance did not change in all these years. Once they were switched to a habituation-oriented therapy, they achieved tinnitus habituation within a year.

Low level, broad band sound is used to facilitate tinnitus habituation. It was mentioned previously that 94% of the people placed in a very quiet environment develop temporary tinnitus. Silence actually enhances tinnitus and hyperacusis. All our patients are advised to avoid silence and immerse themselves in a low level, emotionally neutral sound environment. The sound used in Tinnitus Retraining Therapy can be of various origins, but for both theoretical and practical reasons we are using broad band noise generated by devices which are worn behind the ear.

The process of retraining takes 12 to 18 months. However, once tinnitus habituation is achieved there is no need for continuing the treatment. Another important property of Tinnitus Retraining Therapy is that it cannot create any harm. At the moment we have over 800 patients treated at our Center, and the results from evaluating a random sample of 150 patients showed over 80% of significant improvement (Jastreboff, P.J., Gray, W.C., Gold, S.L. Neurophysiological approach to tinnitus patients. Am.J.Otology, 17:236-240, 1996).