Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Subjective Tinnitus
Jayson S. Greenberg, M.D.
March 12, 1998

Tinnitus is defined as the perception of sound or noise without any external stimulation. It can be further subdivided into subjective tinnitus and objective tinnitus. A listener other than the patient can perceive objective tinnitus. The patient alone perceives subjective tinnitus.

Tinnitus has been described as a symptom of ear disease for as long as man has been able to communicate to his fellow man. The first written accounts date to back to the Egyptians of 1600 B.C. They describe the treatment of the bewitched ear, which involves the infusion of balanities oil and frankincense together with two unknown ingredients. There is no documentation of their success rates with this method. Aristotle is credited with one of the earliest statements on masking. He wrote, "Why is it the buzzing in the ears ceases if one makes a sound? Is it because a greater sound drives out the less?" The Greek physician Galen used sedatives, like opium, to dull the brain?s response to tinnitus. Throughout the next several centuries the treatment of tinnitus continued to revolve around the placement of various exotic substances into the ear. The French physician, Itard, is widely recognized as the father of audiology. In his Traie des Maladies de L'oreille, published in 1821, he devotes one chapter to tinnitus, in which he argues that the treatment is generally unsuccessful and in most cases the role of the physician was to make the tinnitus bearable. A technique that rarely failed was to cover the internal sound by an external one. The sound should be matched as far as possible to the tinnitus. For example, a roaring fire should mask a roaring tinnitus. Jones and Knudsen are credited with developing the first commercial masker in 1928. In 1948, Saltzman and Ersner demonstrated that hearing aids can suppress tinnitus.

Approximately 17% of the population in Europe and the United States experience tinnitus and 7% seek medical attention. For 3.5%, tinnitus severely affects the patient?s life, interfering with work, sleep, concentration, and social interactions. For 0.8%, the tinnitus is debilitating and prevents the patient from conducting a normal life. In the United States, these numbers represent 44 million, 18 million, nine million, and 2 million tinnitus sufferers respectively. The percentage of tinnitus sufferers increases with age, as one-third are older than 65 years. Men and women are affected equally.

The most important principle in the evaluation of a patient with tinnitus is to remember it is a symptom, not a disease. When taking a history, it is first important to rule out other medical conditions that may be associated with tinnitus. Certain potentially treatable causes include hypertension, hyperlipidemia, thyroid and electrolyte abnormalities, as well as several medications. Salicylates, quinine, non-steroidals and diuretics are most commonly implicated. Less that 20% of cases are associated with systemic disease. A thorough otologic history is also essential as 7%-80% of patents with otologic disease experience tinnitus. Almost all patients with Meniere's disease experience tinnitus, and 10% of patients with acoustic neuromas have unilateral tinnitus as their presenting symptom. An audiogram is warranted, as patients may complain of hearing loss or have a hearing loss that that they are unaware of. Approximately 80% of patients have varying degrees of high frequency sensorineural hearing loss. Those patients with unilateral tinnitus and unilateral hearing loss need to be further evaluated radiologically to rule out skull base tumors.

As far as history taking, Dr. Nodar from the Cleveland Clinic offers the pneumonic ABC C-CLAP for tinnitus evaluation. ABC is used to evaluate the location. Is it tinnitus aurium- in one ear, binaural - heard in both ears, or cerebri - centered in the head. The next C stands for cause. Dr. Nodar identifies 5 types of stress that can cause or aggravate tinnitus. These include emotional stress, physical stress, acoustic stress, chemical stress, or pathologic stress. The next C stands for composition and represents ringing, buzzing, hissing, roaring, crickets, and single or multiple sounds. L is for loudness, which can be measured on an audiometer and reported in decibels or simply rated on a scale of 1-5. A is for annoyance and is usually the reason precipitating the patient?s office visit. This is a subjective judgment made on a scale of 1-10. Finally P stands for pitch which can be subjectively judged to be high or low, or can be matched with an audiometer and measured in frequency.

Tinnitus is an auditory phantom perception, and thus does not have any external or physical representation that can be analyzed and used as a basis for diagnosis and treatment. However, attempts have been made to objectify subjective tinnitus in order to facilitate treatment. Loudness and pitch can be measured by presenting tones at varying intensities and pitch to identify tinnitus matches. Masking level is another variable that can be measured and can be important for treatment. This is defined as the intensity level of an external sound that masks or covers up tinnitus.

Also for monitoring purposes, varying questionnaires and grading systems have been devised in attempts to measure tinnitus severity and quantify response to treatment. Newman et al developed the Tinnitus Handicap Inventory at Henry Ford Hospital in Detroit. It consists of 25 questions that can be broken into subscales. The functional subscale reflects role limitations in the areas of mental functioning, social/occupational functioning, and physical functioning. Examples of questions include "Because of your tinnitus is it difficult to concentrate?" or " Because of your tinnitus do you have trouble falling asleep at night?" The emotional subscale represents emotions such as anger, frustration, irritability, and depression. The final subscale is the catastrophic subscale, which questions the patient's desperation, inability to cope, and lack of control. Patients check yes, no, or sometimes in response to these questions and receive a total score.

There is no definitive cure for tinnitus. Before describing various treatment options, it is important to explain the varying theories behind the origin of tinnitus. As previously mentioned, tinnitus is a symptom of multiple pathologies. There is no proven theory of the tinnitus mechanism. There is consensus that tinnitus is the result of aberrant neural activity within the auditory pathways, and that activity is mistakenly interpreted as sound within the auditory centers. Based on the anatomy, there are two schools of thought regarding the origin of tinnitus, peripheral versus central.

Initially, theories about the tinnitus mechanism focused on the cochlea or auditory nerve as a tinnitus generator. Perhaps the ringing was the result of actual mechanical oscillations within the ear. If this is the case then a certain fraction of acoustic energy should be radiated out. This energy should then be detectable by sensitive instruments. These active mechanical processes which generate acoustic energy within the cochlea are called otoacoustic emissions. They are thought to result from the motile characteristics of hair cells. Spontaneous otoacoustic emissions may result from feedback oscillations between overactive sensory elements and the middle ear. This excess of mechanical energy could cause oscillation or increased activity of hair cells, which could then be the tinnitus source. However, tinnitus has been found to correlate to otoacoustic emissions in only 5% of cases. Other cochlear mechanisms have been postulated as well. These range from discordant damage to outer and inner hair cells, ionic imbalance within the cochlea, and dysfunction of cochlea neurotransmitter systems.

In an attempt to identify a tinnitus generator, Jastreboff has developed an animal model of tinnitus. There are two scenarios behind this model. First, is to assume an animal will experience tinnitus when exposed to a situation known to induce tinnitus in humans. The other is being able to evaluate an animal's perception while attempting to induce tinnitus. Jastreboff used salicylate, which induces tinnitus in normal hearing humans in 100% of cases. His studies showed an increase in metabolism in the inferior colliculus, which had previously been demonstrated. He then went one step further by showing an increase in spontaneous electrophysiologic activity at the inferior colliculus versus controls that were injected with saline. Although this shows changes in neuronal activity, there is no proof that the guinea pigs experienced tinnitus. At least, they did not complain of tinnitus.

To detect if animals were experiencing tinnitus, Jastreboff used standard behavioral conditioning techniques developed by Pavlov. Briefly, this involves taking a conditioned stimulus, such as noise and associating it with a negatively or positively reinforced unconditional stimulus such as an electrical shock. Through the pairing of these stimuli, an animal reacts to the central stimulus in a manner similar to the unconditional stimulus. Or in simpler terms, simply hearing a certain noise alone will induce the behavioral manifestation of fear. Jastreboff reversed this paradigm to associate silence with danger and the presence of noise with safety. He exposed his animals to around the clock sound and to an electrical shock during the termination of sound. To evaluate animal behavior, he used two opposite motivations, thirst and fear. Rats were placed at a baseline level of water deprivation and learned to lick water from tubes called lickometers, where each lick could be counted. He hypothesized that fear opposes thirst and should decrease the rate of licking. Again, animals were trained to associate offset of background noise as a signal of danger. They then attempted to passively extinguish this behavior by presenting silence without electrical shocks. The control group took 4-5 days to return to pretraining levels. Extinction was also measured in two other groups, one with tinnitus before training, and one with tinnitus after training. As predicted, extinction occurred faster in those animals with post training tinnitus. With external background noise turned off, this group still perceived background noise or tinnitus and returned to pretreatment levels faster. Alternatively, rats were introduced with tinnitus prior to suppression training. When background noise was switched off, these rats perceived tinnitus as their conditioned stimulus. Since tinnitus would be experienced during all extinction days, their extinction, as predicted, took longer.

There indeed may be cochlear involvement, but the mechanism behind tinnitus must extend beyond the cochlea. Based on cochlear testing, there is no prediction of whether tinnitus may be present, will develop or will become troublesome. Even though tinnitus is commonly associated with noise-induced hearing loss, there is a subpopulation of tinnitus sufferers with normal audiograms. In theory, if the source of tinnitus is purely cochlear, then sectioning of the auditory nerve should cure the problem. However, it is well documented that cochlear nerve section fails to relieve tinnitus in approximately half of all cases. Likewise, it has been shown that contralateral masking of unilateral tinnitus is about equally effective as ipsilateral masking. Thus there must be an additional central component.

PET scanning has been used to identify a central component of the tinnitus pathway. In a study published in the January Journal of Neurology, Lockwood et al at SUNY-Buffalo used PET scans to study a unique subset of tinnitus patients who could modulate their tinnitus with orofacial movements. Cerebral blood flow measured during stimulation with external tone bursts presented to just one cochlea produced bilateral activation of auditory cortical regions in controls and patients with tinnitus. Orofacial movement induced loudness changes were observed unilaterally, and not bilaterally, implicating involvement of a more central part of the auditory pathway.

The idea of a tinnitus generator as the sole mechanism and treating the remainder of the auditory system as a prewired cable transmitting the tinnitus signal to the auditory cortex, is probably too narrow. So aside from abnormalities of cochlear function, there is abnormal processing of tinnitus related signals within the central nervous system. Jastreboff in his neurophysiologic model of tinnitus believes tinnitus should be regarded as a disorder of perception and should not be viewed as a perception of signals emerging from a single localized generator. Tinnitus results from the perception of abnormal activity within the auditory pathways, which cannot be evoked by any combination of external sounds. He hypothesizes that the process by which tinnitus emerges can be subdivided into 3 phases: generation, detection, and perception. Generation can occur peripherally and may be associated with disorders involving the cochlea or cochlear nerve. Detection occurs in subcortical centers and is based on pattern recognition. Perception and evaluation occurs in the auditory cortex with involvement of the limbic system, pre-frontal cortex and other cortical areas.

This model is based on five principles. First, for each sensory system, processing of information occurs on several levels, each contributing to the final signal reaching the cortex.

Second, all subsystems within the nervous system are interconnected, resulting in parallel processing of information, while each system determines the type and extent of specific response evoked by the stimulus. This is in contrast to a more traditional hierarchical model of cortical organization. This principle offers the possibility of creating loops that under conditions of a continuous sensory stimulus with significant emotional tone, further amplifies the perception of tinnitus by creating positive feedback loops within the cortical networks.

Third, the nervous system exhibits a high level of plasticity with continuous modifications of connections resulting in enhancement of certain signals and a decrease in response to irrelevant signals. The CNS is oriented towards homeostasis with excitatory and inhibitory influences providing flexibility, control, and balance. Researchers have reported that after sound induced hearing loss, sensitivity of the cochlear nuclei and inferior colliculi neurons to electrical stimulation increased and recruitment emerged. This would explain the phenomenon that when a person with normal hearing is placed in an anechoic chamber deprived of auditory input, the person will experience increased hearing sensitivity and may even experience tinnitus. So in certain cases, tinnitus may be due to increased gain within the subcortical auditory system.

Fourth, detection of sensory signal information occurs on a pattern matching principle, allowing for complete perception of a signal even when it becomes distorted. This would explain how the auditory system can extract signals based on pre-set criteria allowing for detection of important sounds, even at low intensity, while ignoring other louder environmental sounds. This explains the rapid onset of tinnitus and its persistence despite low levels of perceived loudness. Once this abnormal pattern is classified and detected it is very persistent. It is possible to reverse this pattern recognition with low levels of white noise. This noise would interfere with the pattern recognition process making it increasingly difficult to separate the tinnitus signal from background neuronal activity. With no other processes enhancing recognition of the signal, the pattern would no longer be detected.

Fifth, signals that are new or relate to positive or negative reinforcement are treated as significant and evoke an emotional response. Repetition of signals not associated with positive or negative reinforcement result in disappearance of any response to their presence. In the majority of cases, the presence of tinnitus with the lack of any positive or negative reinforcement results in the habituation of the tinnitus signal. This is the cornerstone of treatment. Many of us who have left a concert experience tinnitus. We treat the tinnitus as a natural event and it does not cause any annoyance. Others may treat tinnitus as a signal that something has gone wrong with their hearing or brain. They begin to focus attention to it. Here is where the limbic system becomes involved as the patient develops annoyance and a vicious cycle results. Loudness and pitch are of secondary importance and play a secondary role. This further explains why acoustic parameters do not correlate with treatment outcome, and why people with similar acoustic descriptions of tinnitus may differ radically in their levels of annoyance and impact.

So, the classification of tinnitus as peripheral or central is too superficial. Even if the initial cause of tinnitus can be traced to the cochlea, neuronal processing is dominant. In summary, a weak imbalance of neuronal activity within the auditory system, usually related to cochlear damage, is detected at low levels within the auditory system. Being a new signal, it is further enhanced by subcortical centers, transferred to the auditory cortex, and perceived as sound - tinnitus, and is evaluated.

Based on the neurophysiologic model, the primary goal of tinnitus treatment is to remove its perception from the patent's consciousness and initiate the process of habituation. Treatment is aimed at retraining the subcortical and cortical centers involved in processing tinnitus signals without attempting to suppress the tinnitus generator. It is fundamental to remove the association between tinnitus and the emotional state. Treatment begins with objective counseling revealing to the patient the potential tinnitus mechanisms within a background of the physiology of the auditory system.

Understanding the tinnitus mechanisms should decrease annoyance. Counseling uses the principle that known, unpleasant phenomenon is less frightening than the unknown. To further facilitate habituation, a low-level auditory signal is introduced to interfere with the detection of tinnitus related neuronal activity. However, this is not masking. Masking would be counter-productive. Habituation is a reconditioning of connections within subcortical centers and cannot occur if the stimulus is absent. Habituation is a treatment and not a cure. It usually requires 12 months of therapy and patients are encouraged to continue for another 6 months to ensure that the plastic changes within the brain are firmly established.

Based on the role of patients' emotions and interactions within the limbic system, psychological profiles of tinnitus sufferers have been extensively studied. The majority of tinnitus sufferers never seek professional advice. As a result, help seeking and non-help seeking patients with tinnitus have been contrasted. Help seekers have been found to have less effective coping strategies. A large percentage are externalizers. They feel as if their tinnitus is outside their sphere of influence. Similar research has found that those with an external locus of control may experience higher levels of emotional distress. This lack of control leads to heightened levels of depression and anxiety, which function to increase tinnitus severity. Counseling and reassurance are an essential aspect of tinnitus management.

Before exploring specific treatment regimens, I want to review basic treatment guidelines. Remember that tinnitus is a symptom and not a disease. Any reversible medical or otologic disorder must be treated. Medications should be re-evaluated with avoidance of aspirin, non-steroidals and other implicated medications. Some advocate diet regulation with elimination of caffeine. Up to 50% of patients with severe tinnitus have excessive caffeine intake. Patients should avoid disturbing noise, use noise protection, and are encouraged to employ home masking techniques. These include music at night or tuning the radio in between stations at a level of "white noise."

The concept of masking dates back to the ancient Greeks. Masking is provided in three general classes: tinnitus maskers, conventional hearing aids, or a combination of both. Hearing aids have the most success for low-pitched tinnitus. They amplify ambient environmental noise, which serves to mask the tinnitus. Additionally, hearing aids offer psychological benefit and stress reduction. The associated improvement in hearing relieves patients as they realize their tinnitus was related to hearing impairment. Hearing aids are an excellent initial treatment option as the majority of tinnitus patients have an associated sensorineural hearing loss. They are most effective with low-pitched tinnitus, less than 4000Hz, that is located within the impaired portion of hearing ability.

Masking devices are similar in appearance to hearing aids. Before choosing a masker or hearing aid you should attempt to elicit whether hearing loss or tinnitus is the major complaint. For example, patients may complain that their tinnitus is worse in a crowd of people and they cannot understand what is being said. Patients are instructed to use the lowest masking level possible. The masking sound is completely under the patient?s control. It can be turned up or down or off at will. Studies reveal no evidence of demonstrable hearing loss or interference with speech discrimination with long term use. Jastreboff et al reviewed patients in a prior trial of tinnitus management and found that over half the patients who used a level of noise below that required to completely mask their tinnitus. These patients exhibited a high level of improvement. As far as predictive value for treatment outcome, those patients reporting tinnitus improvement had a decrease in their minimal masking level. Tinnitus maskers are effective in approximately 20% to 30% of cases.

A tinnitus instrument is a combination hearing aid and masking device. Each device has a different volume control that can be adjusted independently. At nighttime or in quiet situations where the tinnitus is more intense, the masking sound can be increased without changing the hearing aid. The tinnitus instrument is effective in one half to two thirds of cases.

Electrical stimulation is another form of tinnitus treatment. There are four subjective responses of a patient to electrical stimulation. These include vibration at lower intensities, followed by auditory sensation, tinnitus suppression and pain at higher intensities. Studies have used up to 100 micro amps at varying frequencies for anywhere from 10 to 60 seconds. Stimulation can be intra or extracochlear. In 1976, House demonstrated an improvement in symptoms in patients receiving cochlear implants. Intracochlear stimulation through cochlear implantation has been found to be effective in up to 75% of patients. This includes patients whose tinnitus was decreased and abolished. Suppression can continue for several hours after the implant has been switched off. Extracochlear stimulation of either the round window, promontory, or transcutaneously can relieve tinnitus in 40% to 60% of cases. The exact mechanism behind the success of electrical stimulation is unclear. Various studies support both cochlear and central effects. For example, cochlear implants can suppress tinnitus in the non-operated ear. Other studies have revealed no differences in efficacy based on age, audiogram, or etiology of tinnitus. The effects are short lived, lasting anywhere from 30 seconds to one week. Side effects include stimulation of other cranial nerves during the procedure and can include vertigo, pharyngeal or nasal discomfort, cough, and facial spasms.

Various alternative treatments including acupuncture, hypnosis, and biofeedback have been researched. Biofeedback is a psychological strategy to voluntarily control internal responses. As attention becomes focused on tinnitus, there is an increase in mental distress. Increases in mental distress are associated with increased muscle contraction. Biofeedback aims at breaking this reinforcement cycle through muscle relaxation. However, biofeedback alone does not address psychological aspects including abnormal coping strategies. Acupuncture is an age-old treatment for chronic pain that has been used to treat tinnitus. Review of the literature finds no evidence for long term effects of acupuncture. Placebo-controlled studies show no specific alleviating effects. Hypnosis helps patients by reducing anxiety and tension through relaxation and improving coping abilities. However, studies are unclear as to whether hypnosis is any better than simple counseling.

There are various pharmacologic therapies that have been evaluated for the treatment of tinnitus. However, one must be extra cautious when evaluating drug trials. There can be a significant placebo effect. One should be skeptical of any studies without controls. Ideal studies should be double blind with crossover design. Tinnitus should be quantified prior to and following treatment. To say tinnitus has decreased by 50% could imply that on a scale of 1-100, tinnitus severity has decreased from 100 to 50 or 10 to 5. The reader should also note how reductions in tinnitus were measured from audiometry, questionnaires, scales, or global change questions.

Lidocaine has been the one medication that has provided a reliable reduction in tinnitus. A number of randomized control studies demonstrate 70%-80% success rate. Generally 2% plain lidocaine is used, and 1.5 mg/kg is injected over 4 minutes. However, the relief is short lived, on the order of minutes to hours. As we all know, there are a number of adverse effects associated with intravenous lidocaine. Since lidocaine is not effective orally, tocainide, the amide analog of lidocaine has been studied. This oral analog has not been nearly as effective. The success of lidocaine supports the role of neural hyperactivity in the control of tinnitus. By blocking sodium channels, lidocaine may be reducing hyperactivity. The exact site of lidocaine?s effect being the cochlea, auditory nerve, or central auditory nervous system remains unknown.

Benzodiazapines have also been studied. Pharmacologically, they bind to GABA receptors, enhancing their effect. GABA receptors are located in the auditory pathway, especially at the level of the inferior colliculus. GABA is an inhibitory neurotransmitter. The theory behind the use of benzodiazepines is that they increase GABA-ergic activity, inhibiting the tinnitus production. Diazepam has been prescribed frequently, but more for its tranquilizing action. Initial studies with alpazolam have been promising. The major side effect is drowsiness, and sample sizes are small. More importantly, benzodiazepines should be used cautiously since their long-term use is not recommended.

Based on increased psychopathology in patients with tinnitus, the role of anti-depressants in treatment has been studied. One classic study by Dobie et al, used nortryptilene, a tri-cyclic antidepressant. This double blind randomized study involved 92 patients who were stratified by the presence of major depression. The two primary outcome variables were two global questions. Has the medication helped you in any way? Has your tinnitus improved? Sixty-seven percent answered yes to question one versus 40% of the placebo group. This result was found to be statistically significant (p=0.008), while 43% answered yes to question 2 versus 30% of the placebo group. They also found that the single best predictor of benefit was insomnia. This is consistent with the fact that adequate antidepressive therapy usually improves sleep. The authors note that their study was limited to patients with severe tinnitus, and may not have as much benefit in less severe cases.

The main surgical option that has been described for tinnitus is selective cochlear nerve section. It is important to note that of the millions of tinnitus sufferers, this operation is rarely indicated or performed. Surgical candidates must have lost all serviceable hearing in the affected ear, have failed to respond to conservative medical management, and have accepted the fact that their tinnitus may persist despite surgery. A selective eighth nerve section versus a total nerve section has the advantage of preserving vestibular function. The risks of the procedure, aside from persistence of tinnitus, are similar to a vestibular nerve section, and include CSF leaks, meningitis, and facial palsies. Studies show improvement in approximately 50% of cases.

In summary, I offer this quote from George Catlin, an 18th century painter and lawyer."If it were only deafness that I have to submit to, I feel as if I could sit down in silence for the rest of my life and be content with my daily employment, but the disease is attended with the sound in the ear not unlike the drawing of a viola bow across one of the strings and not a pulse night or day has been there without the sound. What I wish to hear I cannot hear, and what I do not wish to hear I am compelled to hear." Tinnitus can be a frustrating problem for both the patient and the clinician. The exact mechanism is unknown, and there is no cure. Tinnitus is a symptom, not a disease. Once other medical and otologic etiologies have been evaluated, it is important to reassure patients and introduce them to effective treatment options.

Case Presentation

MA is a 68-year-old female with a several year history of hearing loss and tinnitus. Her tinnitus is bilateral. She describes her tinnitus as a high pitched ringing. She rates it as a 3 on a loudness scale of 1-5. Her tinnitus is annoying to the point that it intermittently interferes with sleep. She noted that her tinnitus improves during the day in noisier environments and is worse at night. She has never used a hearing aid. She has had no history of trauma or chronic noise exposure. She denies any otalgia or otorrhea. She denies any symptoms of vertigo or dizziness. She does not take aspirin or NSAIDS.

Past medical history: diabetes mellitus controlled with diet. Medications: none. Physical exam revealed tympanic membranes that were clear and intact bilaterally. The nasal passage and oral cavity were clear. Neck showed no lymphadenopathy or masses. Cranial nerves II-XII were intact.

The results of the audiogram were explained to the patient. She was counseled that her tinnitus was most likely a result of her hearing loss and was given a hearing aid referral. She was also instructed to use the white noise of a radio at night time to mask her symptoms. This patient was seen back in follow up at one month. She still had tinnitus although it had now decreased to a 1 on the loudness scale. Additionally, she reported decreased difficulty sleeping at night.

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