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. Tinnitus Today I will be talking about the history, epidemiology, classification, pathophysiology, evaluation, and treatment of tinnitus. I will start with history. The first written account of medical treatment of tinnitus is all the way back to the Egyptians. For the bewitched ear and humming in the ears, they would infuse oil, frankincense, tree sap, herbs, and soil; and they would administer it via a reed stalk that they put in the external ear. The Mesopotamians documented on clay tilework their rituals and chants, and they used to chant to get rid of the whispering or singing in the ears. These are two of the chants. "Whoever thou may be, may E restrain me." This is E depicted in the figure. He was the god of water. The other incantation was, "It hath flown against me. It hath attacked me. O seven heavens, seven earths, seven winds, seven fires, by heaven be ye exorcised." I do not think they worked. Early Greco-Roman medicine defined the treatment of tinnitus based on the cause of the disease, so they were the first to really try to relate the two. If it stemmed from a cold, then the ear should be cleaned and the breath held until some humor froths out from it. If the tinnitus stems from the head, then exercise, rubbing, and gargling should be carried out, as well as dieting and placing radish, cucumber juice, honey, and vinegar in the ear. Later, the works of Hippocrates and Aristotle really were the first to introduce the idea of masking. They were fond of saying, "Why is it that buzzing in the ear ceases if one makes a sound. Is it because a greater sound drives out the less?" In the Middle Ages, they continued with this pouring of things into the ear, and a Welsh treatment recommended to take a loaf of hot bread, divide it in two, and put it in each ear as hot as you could take it and thus perspire and by the help of God you would be cured. That sounds like it is from the Middle Ages, but here is a picture of ear candling, which is still done in alternative medicine. A burning candle is put in the ear to try to draw out wax and other debris. But, in addition, some proponents of candling say it is good for tinnitus and sinus problems. In the Renaissance, we saw the introduction of surgery into the treatment of tinnitus. The thought was that wind would become entrapped in the ear and circle around and around inside it, and so they would trephinate the mastoid to allow the wind to escape. In the 19 th century, the work of Frenchman, Jean Marie Gaspard Itard advanced the study of tinnitus with some progressive ideas that we still adhere to today. Most tinnitus is associated with hearing loss. He gave the earliest descriptions of objective versus subjective tinnitus, and he recognized that the treatment often failed but, meanwhile, the physician was to make the tinnitus less unbearable. Usually he did this with masking. Finally, in the 19 th century, we saw advances in technology and in the germ theory and anesthesia. Electrical stimulation evolved as a treatment, and germ-free surgery allowed more attempts at surgical therapy, including ligation of offending blood vessels as well as incudectomy. Today, tinnitus is still affecting a lot of people. It affects 30% of the adult population; however, only 6% of this 30% report incapacitating symptoms. Most of the people who do seek medical care, however, feel that they have been told that there is nothing that can be done about it and that they have to learn to live with it. The prevalence of tinnitus increases with age, and has been shown to be independent of noise exposure. It seems to be more common in men, more common in Caucasians, and more common in lower-income families. It has also been seen in children. Thirteen percent of school-age children experience tinnitus. If we limit that population to those who have failed their hearing screening, that number becomes 59%. It is thought that the increased incidence of otitis media may play a role in this reported higher prevalence. There are several ways to classify tinnitus. This is one way: divide it into subjective and objective. Subjective tinnitus is heard only by the patient, and objective tinnitus is heard by the patient and the examiner. The subjective tinnitus is usually nonpulsatile, and the objective is usually pulsatile. The pulsatile tinnitus can be broken down into vascular and nonvascular causes. Vascular could either be arterial—examples being carotid artery disease, arteriovenous fistulas or malformations, aberrant anatomy, or hypertension—and venous causes, which could be transmission from benign intracranial hypertension, jugular bulb anomaly, glomus tumor, or hydrocephalus. The nonvascular causes include myoclonus of the palatal musculature as well as the stapedius or tensor tympani. Attempts have been made to simplify and standardize the description with a universal classification system, and several people have proposed one. However, few have gained acceptance. The most accepted one is the Nodar classification. It uses the pneumonic ABC C-Clap. This is essentially A, is it unilateral? B, is it bilateral? C, is it centered in the head or does it sound like it is coming from somewhere else? The next C is the cause, which is often unknown, but you can narrow it down to noise or acoustic neuroma. The next C is composition. What does the sound actually sound like? Some people hear crickets, some people hear hissing; loudness, on a scale of 1 to 10; annoyance, on a scale of 1 to 10; and pitch, is it high or is it low? The tinnitus handicap inventory is a self-report questionnaire that is used to evaluate the effects of tinnitus and its treatments on daily life. This and other self-reporting questionnaires are the main objective ways to evaluate tinnitus. So, although these are subject (since the patient is filling it out), these instruments are used to compare tinnitus across patients and before and after treatments. They include questions like: Is it difficult to concentrate or read or work? Is it difficult to hear? Does it make you angry? Are you depressed?—these kinds of things. The etiology of tinnitus: I am going to be focusing mainly on subjective tinnitus. Otologic causes include noise exposure, which is the case with today’s patient. This is the most common cause of hearing loss and associated tinnitus. Presbycusis, Ménière's disease, chronic otitis, otosclerosis, otoacoustic emissions, acoustic neuromas, cerumen impaction and labyrinthitis all can cause tinnitus. Trauma can also cause tinnitus with whiplash and neck injury, or explosion injuries. Also, central nervous system disorders, closed head injuries or temporal bone fracture, MS, meningitis, these metabolic causes, and temporomandibular joint disorders, which can actually be a cause of unilateral tinnitus if the patient just has the symptoms in one ear. We have seen that in our Clinic. Depression/anxiety is a big issue with tinnitus, and we will talk more about that later, but tinnitus is definitely seen more often in people with these problems. Again, the side effect of medications. On this slide is just a short list of the medications that can cause tinnitus, so, as you can see, it is pretty widespread. The pathophysiology of tinnitus: Essentially, you just saw how many etiologies there are, so you can imagine how many different pathways have been suggested. There is also a wide range of severity. It can be a benign sound heard only occasionally, or it can be a devastating roar that is heard 24 hours a day and prevents the patient from functioning. Again, the percentage of patients with tinnitus this severe is very small, but that population is out there. Subjective tinnitus is the perception of sound in the absence of any actual sound. So, it is a phantom sensation that is not unlike the phantom pain when you have an amputated limb. Because it is the perception of sound, it has been accepted that the symptoms originate in the ear. In the ear theory, damage to the outer hair cells results in an alteration of cilia and their stiffness. This causes decoupling from the tectorial membrane, which causes an increase in the baseline output; so the spontaneous discharge rate of the auditory system is elevated and troublesome tinnitus results. The problems with this theory, and I have listed three here, are that deaf people can have tinnitus; tinnitus can persist after sectioning of the auditory nerve; and, not everyone with hair cell damage suffers with symptoms of tinnitus. The primary area of malfunction may be the ear, but it is thought that the location of structures that actually generate the abnormal neuroactivity that is perceived as sound is somewhere else, probably more central. The thoughts here are that abnormal input to the CNS generates altered neural activity in the central auditory system. What is abnormal input? Basically, abnormal input could be outer hair cell dysfunction with normal inner hair cell function, resulting in an imbalance in the type of input to the dorsal cochlear nucleus causing a neuroactivity that causes tinnitus. What other type abnormal inputs could you have? You could have decreased input and this has been seen to cause disinhibition of the dorsal cochlear nucleus and subsequent increased activity with tinnitus. Or, the abnormal input could be that you have too much input and that causes, in a domino effect, persistent hyperactivity in nuclei of the auditory system and tinnitus. Basically, any type of abnormal input into the auditory system can cause more central structures to perceive this as tinnitus. There are functional imaging studies that support the idea that tinnitus is central, and this is just one example. PET scanning, in which a sound was put into the right ear of the patient and he had bilateral lighting up of his PET. When they took away the stimulus, the patients who heard tinnitus just had unilateral uptake in their auditory cortex. This suggests that if it was more of a central peripheral sound then it would have been bilateral. There are several studies that have localized the area of tinnitus as being central. Pathophysiology: This abnormal input to the central nervous system leads to reorganization of the pathways in the central auditory system. We know this as neuroplasticity. These changes may lead to abnormal interactions between auditory and other central pathways that normally do not participate in hearing. So the auditory information gets to areas of the brain that usually do not process sound. This is thought to be the mechanism by which other symptoms of tinnitus are generated, like the depression, the fear, and the anxiety. This coupling of the auditory system with other central systems, like the limbic or the autonomic nervous system, is the basis of the neuron-physiological approach to tinnitus. This approach postulates that the central nervous system detects nonrandom activity in the periphery, and it perceives it as sound: tinnitus. Initially, a person is aware of this sound because it is a new signal and stands out from the baseline neuronal activity. In most people, however, this sound is not interpreted as carrying important information and so it undergoes habituation and it is ignored by our higher centers. If, however, this initial perception of tinnitus is associated with a negative emotion like fear, anxiety, or annoyance, it is interpreted as an important message because our body thinks we need to prepare for danger or attack. This activates the limbic and autonomic systems in order to prepare us to respond. This reaction of the autonomic nervous system is a conditioned response to the tinnitus signal. This was proposed by Jastreboff in 1990. This is a diagram from a 1996 paper, and essentially, this is the sound or the trigger that is associated and you detect it on a subcortical level and it is perceived by auditory cortex. This signal, if not important, is just ignored. We learn that it is not an important signal and that we do not need to pay attention to it, and we ignore it. However, if we have a response to it, it involves the limbic system and the autonomic nervous system, and these interactions potentiate this signal. They make it stronger. Instead of weakening it and making it go away, the involvement of these two systems make it stronger so that we notice it. The effects of tinnitus on an individual depend on the extent of the activation of the limbic and the autonomic nervous systems and not necessarily on the level of activation within the auditory pathways. If the limbic and autonomic systems are not activated by the tentative signal, then the person is experiencing tinnitus without any associated disturbances. How do we evaluate these people? Again, this is the classification ABC C‑CLAP that we went over. Obviously, do a thorough otologic exam—otoscopy, tuning fork, cranial nerve and cerebellar testing—this way you can possibly rule out any causes of pulsatile tinnitus if they have middle ear masses. Also do an audiologic exam, as was done for our patient. Getting an audiogram is important to determine if the tinnitus is symmetric or asymmetric and, again, that would direct further workup for a more central process like a retrocochlear mass. Electrophysiologic evaluation, ABR, ENG, radiologic, MRI, depression screen—this is, again, important. Many patients was depression are essentially predisposed to have more trouble with their tinnitus. So, when patients come in, it is important to try to elicit history of depression from them. Using just one mnemonic, SIG E CAPS, can help you ask a patient. Are you having trouble sleeping? Do you have decreased interest in your activities? Excessive guilt? Decreased energy? Difficulty concentrating? Changed appetite, either increased or decreased? Psychomotor retardation or suicidal thoughts? There are also four tests—the tinnitus clinic tests—which clinically are not as relevant, but seem to be used frequently in the research area of tinnitus: Pitch matching. The patient is presented with two tones and they choose the one closest to their tinnitus. They repeat this until the closest match is identified. Interestingly, in a large group of patients, most of them match their tinnitus pitch at or above 4,000 Hz. Most tinnitus is high pitched. Loudness matching. After the pitch is matched, the intensity of the test is increased until it is equal to the intensity of the tinnitus. And surprisingly, most people match the pitch of their tinnitus to only 9 dB or below. So the tinnitus is not actually that loud relatively. Some people find this surprising, and again, this is because of the involvement of the other centers of the brain that cause the tinnitus, no matter how loud, to be annoying. Minimum masking levels. Most patients are best masked at the frequency of their tinnitus. The masking noise is presented and then it is increased in volume until the patient can hear it. It is then increased at 1-2 dB increments until the patient reports the tinnitus is no longer audible. Again, the idea is that you would increase the volume until the tinnitus is no longer audible; however, if the patient was uncomfortable because the masking sound was so loud, then you would stop. Residual inhibition. This is a phenomenon of reduction or complete absence of the tinnitus after a period of masking. It is basically induced by applying minimum masking level plus 10 dB for 60 seconds. Then you would time the period of residual inhibition. Eighty-eighter percent of patients display some form of this. Treatment: Basically, the main thing to avoid are saying that "there is nothing that can be done and you will just have to learn to live with it." This is hard on patients and, it seems, not true. Reassurance. Most patients do well with plain old reassurance after you have eliminated serious pathology. Like our patient, for whom this was sufficient, they can co on with their lives. You can recommend that they avoid loud noises and offending medications. If they do have TMJ, you can treat that. Suggest home masking techniques such as dehumidifiers and fans and tuning a radio between two stations. Most patients will not require further treatment; however, a small percentage will persist with severe and debilitating systems. What can be done for them? One technique is masking. There are three types of maskers. There are hearing aids, tinnitus maskers, and tinnitus instruments; which one you use essentially depends on the patient. Hearing aids are good for patients who have tinnitus in the 4 kHz and lower range. The hearing aids work by amplifying ambient noise. For a person who has tinnitus in this range, that ambient noise will suffice as a masker. Tinnitus maskers are used to adjust the frequency in the volume to mask the tinnitus, so there is no hearing aid; and there is no amplification in this one. It is just a frequency that the patient tunes to his tinnitus to mask it out. A tinnitus instrument is a combination of these two things. It is a hearing aid and a masker. These work well in patients with high-pitched tinnitus and a high-frequency loss. If the masking sound must be increased to an uncomfortable level in order to mask the tinnitus, this is not a good treatment for that patient, which I alluded to earlier. In approximately 90% of patients, masking devices can reduce tinnitus; and in 70% of these patients, the tinnitus is completely masked. The next treatment is alprozalam or Xanax. Patients who were prescribed this anti-anxiety medication for the treatment of anxiety were calling into the American Tinnitus Society saying it was helping their tinnitus. Researchers were intrigued and did an open study on 40 patients before and after treatment with alprozalam. They used a 10-point scale for patients to rate their symptoms. It was shown that the alprozalam had a direct effect by reducing the perceived loudness of the tinnitus. They went ahead and did a more formal study, a randomized double-blind study, of 40 patients essentially set up the same way. Half of them got placebo, half of them got alprozalam. Their results supported these findings, that, in fact, the Xanax was helping the tinnitus. Depression and tinnitus: Most people with tinnitus are not depressed or seriously bothered by their tinnitus. However, the people who are debilitated by their tinnitus are often found to be suffering from a major depressive disorder. Does tinnitus cause the depression? No, tinnitus is just a stressor that can trigger a psychiatric episode in a susceptible person. Does depression cause tinnitus? Again, probably not; but tinnitus that was barely noticeable can become more intrusive when a depressed person begins to pay attention to it. Treating the depression can relieve the tinnitus. Most studies have been conducted with tricyclic antidepressants. Using a tinnitus handicap questionnaire as their objective measure, these studies show that the tricyclic can be superior to a placebo in treating patients with severe tinnitus. Trials using neuroantidepressants, the SSRIs like Prozac and Paxil, are underway now. This next treatment, tinnitus retraining therapy, is complicated and based on the neurophysiologic approach to tinnitus as described by Jastreboff. Again, the four postulates here are that in addition to the auditory system, the limbic and the autonomic systems are involved in tinnitus. It is the sustained activity of the sympathetic nervous system that causes the anxiety associated with the tinnitus. These conditions between the systems of the brain are governed by conditioned reflexes. By inducing and sustaining habituation of these conditioned reflexes, it is possible to remove the negative impact of the tinnitus. To state it another way, acoustic input that does not carry important information is ignored. That is called habituation. Acoustic information that is classified as important, something that we need to hear for our safety or protection, is enhanced and consciously perceived. So the goal of the tinnitus retraining therapy is to train the central nervous system to interpret the tinnitus as unimportant and to ignore it and habituate it. Essentially that is just taking out these two arms of the diagram and bringing us back to where most people initially have tinnitus, which is on a subcortical and then, fleetingly, cortical level until it is habituated. This is done by enhancing the level of the background noise, and the contrast between the tinnitus and the background signal is decreased. With this decrease in difference between the signals, it is more difficult to detect the tinnitus, and it is not perceived as important; so it is ignored. The background noise is enhanced with a tabletop sound machine or a wearable sound generator or hearing aids, again depending on the patient's particular symptoms. It is, however, important, not to completely mask the tinnitus. To me this sounded initially just like masking, but if you completely mask the tinnitus then you are not going to habituate the signal because you cover it up, you are hiding it from the central nervous system, so you are not forcing the central nervous system to recognize it and then recognize it as not important and ignore it. Patients have to undergo intense counseling. Therapy is not just associated with having the background noise. They also have to undergo intense counseling about the physiology of hearing and how we are trying to uncouple these two centers of the brain. Then, in addition, they have to use this noise generator for at least six hours a day for about 12 to 18 months. There are no published, randomized, or well controlled studies; but, using tinnitus handicap questionnaires to evaluate the efficacy, Jastreboff has reported significant improvement in tinnitus in over 80% of his cases. The goal now is to have other tinnitus centers reproduce these results. Other interesting things happening now: cochlear implants. Tinnitus is often associated with profound hearing loss; and it was noted that a secondary benefit of a cochlear implant was the suppression of tinnitus. Looking across the board at multiple studies, prevalence of pre-op tinnitus is about 80% - 90% and the secondary benefit of tinnitus suppression has been reported from 34% - 93%. The risk of worsening tinnitus is low. This is undergoing further study. Other treatments include transcutaneous electrical stimulation, where there are actual electrical signals given through the skin, around the ear, and on the auricle; cochlear vestibular nerve section, labyrinthectomy. Again it is pretty much 50-50 the number of people this works for as far as relieving the tinnitus or not. Transtympanic therapies are gaining favor. This started with Ménière's disease and using transtympanic therapy to control vertiginous symptoms. Now people are interested in also trying to control tinnitus using this method. Then there are alternative methods. Alternative medicine like acupuncture, ginko biloba, vitamins, hyperbaric oxygen therapy; but there is no hard evidence that any of these work. In summary, many people have tinnitus. Most people are not seriously bothered by it. They are satisfied with a short explanation and reassurance. For those who are severely impaired, consider concurrent depression and be aware that there are multiple options for treatment in a motivated patient. Case Presentation EW is a 65-year-old man who presents with a 3-year history of “ringing” in his ears. The ringing is bilateral, non-pulsatile, and is present all the time. It is worse in quieter environments, but does not interfere with the patient’s daily activities. The patient denies any symptoms of depression. He complains that he has trouble hearing women’s voices, but otherwise thinks his hearing is OK. He has no past otologic history and denies otorrhea, otalgia, and any visual changes. He also denies any history of head trauma. He has no significant past medical or surgical history and is on no regular medications. He takes ibuprofen occasionally for headaches. He was a gunner in the military and was exposed to loud gunfire. There is no family history of hearing loss. On exam, the patient has no abnormal findings. His TM’s are intact, mobile, with no retractions. His tuning fork exam reveals Weber to the midline and Rinne air greater than bone bilaterally. There are no middle ear masses. The patient’s nose is clear and his oral cavity is moist without lesions or masses. His neck is supple with no masses and his cranial nerves II-XII are intact. An audiogram shows bilateral, symmetric, high frequency sensorineural hearing loss. The patient is counseled that his tinnitus is likely a result of his history of noise exposure and that it is very unlikely that he has a brain tumor or other serious problem. He is given some literature on home masking techniques, such as using fans or humidifiers at night. He is also instructed to avoid ibuprofen and aspirin containing medicines. He is given the website address and phone number for the American Tinnitus Association and feels reassured. He feels that his tinnitus is not interfering with his life and is happy that there is not something “more serious” wrong. Bibliography: Andersson G, Lyttkens L, Hirvela C, Furmark T, Tillfors M, Fredrikson M. Regional cerebral blood flow during tinnitus: A PET case study with lidocaine and auditory stimulation. Acta Otolaryngol 2000;120:967-972. Baguley DM, Axon P, Winter IM, Moffat DA. The effect of vestibular nerve section upon tinnitus. Clin Otolaryngol 2002;27:219-226. Dobie RA. Depression and tinnitus. Otolaryngol Clin N Am 2003;36:383-388. Ghossaini SN, Spitzer JB, Mackins CC, Zschommler A, Diamond BE, Wazen JJ. High-frequency pulsed electromagnetic energy in tinnitus treatment. Laryngoscope 2004;114:495-500. Heller AJ. Classification and epidemiology of tinnitus. Otolaryngol Clin N Am 2003;36:239-248. Hoffer ME, Wester D, Kopke RD, Weisskopf P, Gottshall K. Transtympanic management of tinnitus. Otoalryngol Clin N Am 2003;36:353-358. Howard ML. Myths in neurotology, revisited: Smoke and mirrors in tinnitus therapy. Otol Neurotol 2001;22:711-714. Jastreboff PJ, Gray WC, Gold SL. Neurophysiological approach to tinnitus patients. Am J Otol 1996;17:236-240. Jastreboff PJ, Jastreboff MM. Tinnitus retraining therapy for patients with tinnitus and decreased sound tolerance. Otolaryngol Clin N Am 2003;36:321-336. Kaufman IA , Countryman, LLF, Bernstein LH, Shambaugh GE Jr. Vincent’s violent vertigo: An analysis of the original diagnosis of epilepsy vs. current diagnosis of Meniere’s Disease. Acta Otolaryngol (Stockh) 1991;485:84-103. Kitahara M. Tinnitus Pathophysiology and Management. Igaku-Shoin: Tokyo, New York; 1998. Lascaratos J, Assimakopoulos. From the roots of otology: Diseases of the ear and their treatment in Byzatine times (324-1453 A.D.). Am J Otol 1999;20:397-402. Mirz F, Gjedde A, Ishizu K, Pedersen CB. Cortical networks subserving the perception of tinnitus—a PET study. Acta Otolaryngol 2000;Suppl 543:241-243. Mirz F, Pedersen CB, Ishizu K, Johannsen P, Ovesen T, Stodkilde-Jorgensen H, Gjedde A. Positron emission tomography of cortical centes of tinnitus. Hear Res 1999;134:133-144. Miyamoto RT, Bichey BG. Cochlear implantation for tinnitus suppression. Otolaryngol Clin N Am 2003;36:345-352. Moller AR. Pathophysiology of tinnitus. Otolaryngol Clin N Am 2003;36:249-266. Nagler SM. Tinnitus. A patient’s perspective. Otolaryngol Clin N Am 2003;36:235-238. Neher A. Tinnitus: The hidden epidemic. A Patient’s perspective. Ann Otol Rhinol Laryngol 1991;100:327-330. Schwaber MK. Medical evaluation of tinnitus. Otolaryngol Clin N Am 2003;36:287-292. Seidman MD, Babu S. Alternative medications and other treatments for tinnitus: Facts from fiction. Otolaryngol Clin N Am 2003;36:359-381. Steenerson RL, Cronin GW. Tinnitus reduction using transcutaneous electrical stimulation. Otolaryngol Clin N Am 2003;36:337-344. Stephens SDG. The treatment of tinnitus—a historical perspective. J Laryngol Otol 1984;98:963-972. Stool SE. Portrait of an artist with deafness and tinnitus: George Catlin. Am J Otol 1987;8:78-80. Vernon JA, Meikle MB. Masing devices and alprazolam treatment for tinnitus. Otolaryngol Clin N Am 2003;36:307-320. Vernon JA, Meikle MB. Tinnitus: Clinical measurement. Otolaryngol Clin N Am 2003;36:293-305. Weir N. Otolaryngology: An Illustrated History. 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