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The relationship of tinnitus, hyperacusis, and hearing loss.


The triad of tinnitus, hyperacusis, and hearing loss remains an often-underdiagnosed combination of symptoms that causes physical, mental, and emotional distress for millions of patients. To the best of our knowledge, no review has heretofore been published in the literature regarding the possible relationship among these three entities. We believe that these symptoms may have a common pathophysiologv. Specifically, improper function of cochlear hair cells may result in a hearing loss secondary to the failure of these cells to propagate proper signals through the auditory centers. In response to an incongruous neural message, higher auditory cortical centers may adapt and remodel transmitted sound. This neuroplasticity may lead to an increased perception of volume in the auditory cortex (hyperacusis) and to the perception of phantom sounds (tinnitus). Awareness of the potential relationship among tinnitus, hyperacusis, and hearing loss may contribute to improved diagnosis, treatment, and follow-up for patients with these conditions.


Tinnitus, hyperacusis, and hearing loss are three unique symptoms that may have a common pathophysiology. Unfortunately, our lack of a definitive understanding of these entities can lead to misdiagnosis or underdiagnosis and therefore to improper clinical management.

There is a paucity of adequate discussion in the literature regarding the potential relationships among these three symptoms. A recent MEDLINE search revealed a scarcity of articles on the possible relationship among tinnitus, hyperacusis, and hearing loss. Although many patients have different forms of these individual disorders, the mechanisms of dysfunction may be the same; all may relate to the malfunction or destruction of parts of the auditory pathway.

In this article, we review the basic mechanics of tinnitus, hyperacusis, and hearing loss, and we discuss the possible similarities among them in an attempt to promote improved diagnosis and treatment.

Sound processing and perception

The intricacies of the nuclei and ascending pathways of the auditory system are beyond the scope of this article, but a general review of auditory processing will help the reader better understand tinnitus, hyperacusis, and hearing loss. The cochlear nerve continues to fire action potentials in the absence of sound; this is called spontaneous activity. Obviously, the auditory cortex does not perceive this as sound, but it is able to decipher this neural message as silence. As we hear audible sound, the activity in the auditory system increases and becomes more regular and synchronized. This activity is processed extensively in subcortical auditory centers before it reaches the cerebral cortex, where the actual perception of sound takes place. (1)

Jastreboff et al have noted that when a person is put into a chamber with a very low sound level, the sensitivity of hearing increases and all sound seems loud; they found that 94% of such subjects developed temporary tinnitus. (2) Background noise thus presents an interesting situation wherein we can actually hear the noise, but we learn, or rather choose, to filter it out before we consciously perceive it. Many people who enjoy background music are able to tune it out and focus on a task at hand when necessary.

Jastreboff et al also found that most sounds do not evoke any emotional response or activate the autonomic nervous system. (2) We know that the limbic system, which helps regulate emotional experience and expression, may play a role in how we hear and react to sounds. However, we know little about how this system may regulate emotion. Much research remains to be done in order to bridge this gap in our knowledge.


Tinnitus encompasses not only ringing and buzzing but a myriad of other types of auditory perceptions in the absence of external sound. Some authors have estimated that more than 35 million Americans suffer from tinnitus. (1) Others have reported that tinnitus may affect as many as 30% of the United States population and that as many as 6% have severe symptoms. (3)

Tinnitus can be divided into two types: objective and subjective. The former may occur as a result of temporomandibular joint dysfunction, vascular bruits, swallowing, and other sources of physiologic sounds that are heard by affected individuals; objective tinnitus can be heard by others and measured. Subjective tinnitus, the focus of our discussion from this point on, takes place without any physical presence of sound, and it can be heard only by the affected individual. Subjective tinnitus can be subdivided into two categories: peripheral, which is related to the cochlea, and central, in which pathology is centered on the brain. (4)

Although the exact mechanism of tinnitus is not known, these phantom sounds are associated with numerous conditions, including acoustic trauma, use of ototoxic drugs, head trauma, otosclerosis, tumors, Meniere's disease, increasing age, stress, psychological disorders, chronic pain syndromes, and genetics among others. Some hypotheses about the mechanisms of peripheral tinnitus center on (1) the involvement of the VIIIth cranial nerve and (2) cochlear receptor function. Perhaps any impetus that alters the level of spontaneous activity in the VIIIth cranial nerve could theoretically result in tinnitus. (4) Bauer proposed that tinnitus is the result of reversible outer hair cell dysfunction and decoupling stereocilia from the tectorial membrane. (5) Schwaber theorized that the basic pathophysiology of tinnitus involves an alteration in stereocilia stiffness that results in an increase in the discharge rate of hair cells. (6) The mechanisms of central tinnitus may be more complicated. Jastreboff et al found that cutting the auditory nerve actually caused tinnitus in close to 60% of patients who had not experienced tinnitus prior to the procedure. (2) On the other hand, Simpson and Davies reported that sectioning the auditory nerve ameliorated symptoms in 45 to 76% of patients. (4) Jastreboff et al wrote that some people will develop tinnitus if they are exposed to low sound levels for an extended period of time. (2)


We know little about the etiology of hyperacusis other than that it involves a direct malfunction of the facial nerve; as a result, the stapedius muscle is unable to dampen sound. Hyperacusis is believed to represent an alteration in the central processing of sound, usually secondary to a central perception of the neural signal. (7,8) This distortion of perceived sound is similar to the distortion that occurs in tinnitus. In fact, some authors contend that tinnitus and hyperacusis are two manifestations of the same internal problem, (2) and that almost all patients with hyperacusis eventually experience tinnitus. (9) Hyperacusis has also been linked to hearing loss, based on the theory that the auditory system "turns up the volume" in an attempt to improve hearing. (l0)

Hearing loss

In this article, we focus primarily on sensorineural rather than conductive hearing loss. Sensorineural hearing loss usually occurs as a result of difficulties in the propagation of neural impulses along the VIIIth cranial nerve. Any disruption of the neural signal transmitted from the hair cells in the cochlea will lead to a less crisp sound. Hearing loss often occurs with acute tinnitus, whereas chronic tinnitus may be the result of a central auditory dysfunction or a cortex reorganization. (11) Overall, damage to the auditory system, especially the hair cells in the cochlea, appears to lead to a decrease in sound sensitivity.

Mechanisms of tinnitus and hyperacusis

There is no known mechanism of subjective tinnitus. Numerous theories have been proposed, and many more are currently under investigation. The literature clearly describes how trauma, Meniere's disease, salicylate intoxication, chemical induction, noise, and other factors are associated with tinnitus, but the exact biochemical source(s) remains to be elucidated. Moller discussed the link between tinnitus and hearing loss and concluded that tinnitus is not directly related to the degree of hearing loss. (12) An accepted theory of tinnitus suggests that the mechanism involves a malfunction or destruction of the cochlear hair cells. (6)

One significant problem with research on tinnitus is that while psychological studies have been primarily performed on humans, anatomic and pathophysiologic studies have been conducted on animal models. (13) Coles postulated that tinnitus is most often related to disorder, damage, or degeneration in the middle ear. (14) On the other hand, Simpson and Davies suggested that anything that alters neural spontaneous activity could theoretically lead to tinnitus. (4) The various potential mechanisms that have been proposed are complex and often controversial, but understanding them will be key to the effectiveness of treatment and management in the future.

Even though some researchers consider tinnitus and hyperacusis to be two aspects of one problem, the mechanism of hyperacusis has been studied even less than that of tinnitus, partly because of the lack of animal models with this disorder.


In addition to measurements of pure-tone average and speech discrimination, other useful diagnostic tests for hearing disorders include loudness-matching and loudness-discomfort-level tests, which determine which specific sound levels cause discomfort. Frequency matching also aids in identifying which frequencies are prominent in hyperacusis. Newer technology is beginning to focus on imaging evidence of tinnitus; for example, positronemission tomography (PET) can demonstrate active areas in the cerebral cortex without the need for any external stimulation. Magnetic resonance imaging, of course, is recommended for evaluating patients with unilateral tinnitus and hearing loss suggestive of an acoustic neuroma. (6)

Numerous self-assessment tools are available to accurately define a patient's auditory perception. The Tinnitus Handicap Inventory has been often recommended because of its ease of administration, its incorporation of functional and emotional constructs, and its internal consistency and reliability. (15) With respect to other questionnaires, Berry et al deemed that the Tinnitus Cognitions Questionnaire and the Tinnitus Reaction Questionnaire are too narrow in scope and the Tinnitus Effect Questionnaire, although broad enough, does not differentiate certain aspects of the tinnitus disability. (15) Researchers who have used these and other psychoacoustical characterizations of tinnitus (intensity, frequency, annoyance, and disturbance levels) have found no relationship between a patient's level of tinnitus and his or her level of annoyance or disturbance. (2)

Classic and nonclassic pathways

Numerous authors in audiology have referred to a classic pathway of hearing in which transmitted sound is passed along the network of auditory nuclei and interpreted in the cerebral cortex as recognizable sound. Moller devised a theory of a nonclassic pathway of hearing, which he likened to the role of the somatosensory system in vision. (12) For example, vision is not the sole input by which we sense where our body is in space. Proprioceptors in muscles, joints, and even our vestibular system to some extent all contribute information to our auditory structures. According to Moller's theory, hearing involves more than the transmission of information along a simple, direct line to the cerebral cortex. Information from other sensory systems also contributes to sound perception, loudness, and localization through a convergence into the auditory centers. Certain portions of this nonclassic pathway may be able to augment and even compensate for errors or damage in auditory regions. (12)


Neuroplasticity refers to the ability of the brain to remodel or change. During the past decade, vast strides have been made toward understanding the brain. For example, in cases of extremity amputation, PET scans have shown how the brain adapts to new input and how it uses the available sensory cortex to achieve expanded sensation in the remaining areas of the damaged extremity. (12) Likewise, patients who have a sensory deficit such as blindness often acquire greater sensation acuity in other areas. As our bodies change and sometimes are damaged, the brain attempts to accommodate to new input and stimuli. Neuroplasticity may even represent a physiologic correlate of learning.

Moller explained how neuroplasticity can be both detrimental and beneficial to a system. (12) It has a negative effect when it leads to the development of new synapses or the unmasking of dormant ones that contribute to hypersensitivity and hyperactivity (e.g., phantom pain). Tinnitus may represent a reorganization of neural circuits that not only results in the generation of sound but in a change in the site where sensory information is processed. (4) Neural remodeling is beneficial when the function of injured structures is shifted to different parts of the central nervous system (CNS) in an attempt to compensate for improper input. Decreased sensory input can activate the process of neuroplasticity and thereby lead to changes in synaptic function, which may be a cortical way of "learning." (12)

Hearing remodeling

The process of neuroplasticity may explain how tinnitus, hyperacusis, and hearing loss may share a common connection. Gerken reported that a hearing loss of as little as 20 dB can lead to a sharp increase in sensitivity to electrical stimulation in the auditory system. (10) The idea of a nonclassic hearing pathway expands our understanding of hearing. Any type of trauma, destruction, or change in the default auditory pathway may trigger the CNS to compensate in response to the novel or reduced input. (12) Increased loudness, ringing in the ears, and a decrease in sound clarity represent the complex nonclassic reaction to the irregularity.

Tinnitus may be caused by an augmented input from other sensory organs that are attempting to counteract a lack of proper stimulation. Many investigators have suggested that tinnitus is caused by an inhibition of central auditory structures that is attributable to a reduced or improper input from the auditory nerve's normal spontaneous activity. (5) The brain may construe this information as a ringing or buzzing in the ears.

Hyperacusis resembles the hyperalgesia of chronic pain except that it is manifested in the auditory cortex. (4,12) During a central sensitization, some neurons may lose their tonic inhibition as they attempt to adapt, and they become disinhibited and overresponsive. Some sort of injury or change may lead to the development of new neuronal connections or to a hyperstimulation of existing connections.

Hearing loss itself may lead to a clouding of the signal, just as turning up a radio's volume too high can lead to excessive static, which decreases clarity. The brain's efforts to make up the difference for a weak signal transmission following hearing loss may lead to symptoms such as tinnitus and hyperacusis. This change in hearing transmission and reception can have serious consequences.


Most reports in the literature contend that there is no cure for tinnitus. Because our understanding of tinnitus and hyperacusis is limited, there may be some temptation to tell our patients that nothing can be done. However, the effects of such a message might be devastating. It is essential to recognize that options do exist to alleviate some of their discomfort and improve their quality of life.

Data are somewhat conflicting as to whether there is an effective treatment for tinnitus, and there are certainly no published data that conclusively demonstrate an effective treatment for the triad of tinnitus, hyperacusis, and hearing loss. Authors of many texts have stated that there is no effective pharmacologic treatment of tinnitus. (4,16) Although this may be true, Seidman and Babu have suggested that several therapeutic options are available that can make tinnitus more manageable. (17) They published a comprehensive review of many studies and current beliefs regarding the effects of different drugs, vitamins, minerals, and herbs on tinnitus. They reported that even a change in diet has reduced tinnitus in some patients.

Pharmacologic therapy. Consistent with the ideas that there are some apparent similarities between tinnitus and chronic pain, Simpson and Davies found that some drugs (e.g., lidocaine, sedatives, and antidepressants) alleviate the symptoms of both conditions. (4)

Many drugs have been used to treat tinnitus, hyperacusis, and hearing loss; anesthetics, antidepressants, anticonvulsants, anxiolytics, antispasmodics, antihistamines, diuretics, vasoactive medications, herbs, and others have been mentioned in the literature. (17) Intravenous lidocaine has been reported to be effective in treating tinnitus, (12,17,18) but it carries serious potential side effects, its half-life is very short, and no effective oral formulation has been found. (12) Transtympanic steroids and aminoglycosides have shown some effectiveness. (19) Antidepressants have often been used in view of the fact that serotonin has been postulated to be involved in the plastic changes in the brain. (20) For example, Gopal et al reported that the selective serotonin reuptake inhibitors were effective in alleviating complaints of hyperacusis. (21)

Complementary medicine. As many patients search for nontraditional methods of alleviating their symptoms, natural remedies have become popular. Ginkgo (made from the dried leaves of the Ginkgo biloba tree) is marketed as a remedy for tinnitus and many other ailments. Ginkgo appears to contain vasoactive substances affecting prostaglandins, which have been reported to ease symptoms in many tinnitus patients. (4) However, other studies failed to demonstrate that ginkgo was any more efficacious than placebo. (17) Other treatments include conventional psychology, hypnosis, and acupuncture.

Electrical stimulation. Electrical stimulation has been employed as a treatment for tinnitus since the 1800s. (22) Owing to the fact that one of the theories proposed to explain the cause of tinnitus and hyperacusis concerns the lack of a proper signal propagation from the cochlear hair cells, exogenous electrical stimulation has been used in an attempt to replace the missing signal. Both direct cochlear stimulation and transcutaneous stimulation have been used with varying degrees of success. (22) Many of the studies of electrical stimulation lacked sufficient statistical power because their patient populations were too small. Steenerson and Cronin wrote that they were not sure why electrical stimulation is efficacious in approximately 50% of patients, but they hypothesized that contributing factors might include the increase in blood flow to the cochlea, the mimicking effects of nerve stimulation, a placebo effect, and the benefits of concomitant psychological support. (22) Little has been written about the duration of relief for these patients, but in the absence of constant electrical stimulus, effects do not appear to be long lasting.

Hearing aids. One report has suggested that hearing aids may inhibit the brain's attempt to amplify sound perceptions and thus diminish tinnitus. (9)

Vibrational therapy. Another approach involves the use of vibrational therapy, in which broadband sound is used to desensitize patients to their hearing abnormalities. (17) Clinical trials of vibrational therapy are under way.

Tinnitus retraining therapy. Tinnitus retraining therapy (TRT) was developed in the late 1980s by Jastreboff. (2) (For the purposes of this article, TRT refers to training in general rather than to any specific type of TRT program.) Patients who undergo TRT learn a process of habituation. This process usually takes 12 to 18 months to complete, (2) but once it is mastered, patients are able to downplay the effects of their auditory challenges. Once this skill is learned, there is no need to continue treatment.

During habituation training, the brain is trained to recognize tinnitus-related neural activity as a neutral, insignificant signal. (2) TRT focuses on removing the negative emotion connection attached to tinnitus perception and preservation of tinnitus detection (but not necessarily perception) during the treatment process. Jastreboff et al argued that because we are unable to erase or correct the source of tinnitus, we should focus our attention on what happens between the source of the tinnitus and the site where it is received in the cerebral cortex. (2) Patients can be taught to ignore the presence of tinnitus instead of actively focusing on it. In a random sample of 150 of 800 patients who completed TRT, more than 80% experienced significant relief of symptoms. (2)

Habituation can be augmented by the use of a device that emits a low-level broadband sound; such a device can be worn throughout the day like a hearing aid. The idea behind this device is that patients will experience downregulation of the hyperstimulation that is associated with increased emotions and increased habituation.

According to Jastreboff et al, masking of tinnitus is not recommended during TRT because retraining can succeed only if the brain recognizes the sound. (2) In time, the brain will begin to ignore these sounds, and the cerebral cortex will not be activated to produce a distress response.

Researchers at the University of Maryland Tinnitus and Hyperacusis Center use a type of habituation TRT that they say has been fairly successful in decreasing the effects of tinnitus and hyperacusis. (7) Note that both conditions appear to be effectively treated by the same habituation training. Likewise, Berry et al studied TRT and found that it resulted in a significant alleviation of both tinnitus and hyperacusis as determined by the Tinnitus Handicap Inventory. (15)These results again suggest a close relationship between tinnitus and hyperacusis. More long-term standardized studies are needed.

Jastreboff et al claimed that TRT does not cause any harm to the patient, but it does have some negative aspects. (2) In addition to the significant amount of time required to complete training, TRT places a financial burden on patients. Also, there may be some question as to whether TRT is any more effective than direct patient education and counseling because there do not appear to be any large randomized placebo-controlled studies designed to make such comparisons; some of the studies that have been performed to assess TRT were conducted on small populations (9 to 30 patients). (15) Finally, more investigation needs to be done on the placebo effect of counseling.

Patient education. Patient education is a major component of treatment for tinnitus, hyperacusis, and even hearing loss because knowledge can dispel fear. Again, telling patients that nothing can be done for their condition (negative counseling) can cause them to worry and intensify their perception of their hearing irregularities. Patients should receive some basic instruction on the pathophysiology of the auditory system as it relates to tinnitus in order to weaken the emotional reactions that exacerbate symptoms. (2)


The authors thank Donald A. Godrey, PhD, for his assistance with the preparation of the manuscript.


(1.) Fortune DS, Haynes DS, Hall JW III. Tinnitus. Current evaluation and management. Med Clin North Am 1999;83:153-62.

(2.) Jastreboff PJ, Gray WC, Gold SL. Neurophysiological approach to tinnitus patients. Am J Otol 1996; 17:236-40.

(3.) Heller AJ. Classification and epidemiology of tinnitus. Otolaryngol Clin North Am 2003;36:239-48.

(4.) Simpson JJ, Davies WE. Recent advances in the pharmacological treatment of tinnitus. Trends Pharmacol Sci 1999;20:12-18.

(5.) Bauer CA. Animal models of tinnitus. Otolaryngol Clin North Am 2003;36:267-85.

(6.) Schwaber MK. Medical evaluation of tinnitus. Otolaryngol Clin North Am 2003;36:287-92.

(7.) University of Maryland Medicine: Tinnitus and Hyperacusis Center. What is hyperacusis?

(8.) Katzenell U, Segal S. Hyperacusis: Review and clinical guidelines. Otol Neurotol 2001;22:321-6.

(9.) The Hyperacusis Network. Hyperacusis. newsletter.htm

(10.) Gerken GM. Central tinnitus and lateral inhibition: An auditory brainstem model. Hear Res 1996;97:75-83.

(11.) Ochi K, Ohashi T, Kenmochi M. Hearing impairment and tinnitus pitch in patients with unilateral tinnitus: Comparison of sudden hearing loss and chronic tinnitus. Laryngoscope 2003;113:427-31.

(12.) Moller AR. Pathophysiology of tinnitus. Otolaryngol Clin North Am 2003;36:249-66.

(13.) Brix R. Psychophysiological dimensions of tinnitus. In: Vernon JA, Moller AR, eds. Mechanisms of Tinnitus. Boston: Allyn and Bacon, 1995:1-5.

(14.) Coles RR. Classification of causes, mechanisms of patient disturbance, and associated counseling. In: Vernon JA, Moller AR, eds. Mechanisms of Tinnitus. Boston: Allyn and Bacon, 1995:11.

(15.) Berry JA, Gold SL, Frederick EA, et al. Patient-based outcomes in patients with primary tinnitus undergoing tinnitus retraining therapy. Arch Otolaryngol Head Neck Surg 2002; 128:1153-7.

(16.) Hain TC, Micco A. Cranial nerve VIII: The vestibulocochlear system. In: Goetz CG, Pappert EJ, eds. Textbook of Clinical Neurology. Philadelphia: W.B. Saunders, 1999:184-200.

(17.) Seidman MD, Babu S. Alternative medications and other treatments for tinnitus: Facts from fiction. Otolaryngol Clin North Am 2003;36:359-81.

(18.) Weinmeister KP. Prolonged suppression of tinnitus alter peripheral nerve block using bupivacaine and lidocaine. Reg Anesth Pain Med 2000;25:67-8.

(19.) Hoffer ME, Wester D, Kopke RD, et al. Transtympanic management of tinnitus. Otolaryngol Clin North Am 2003;36:353-8.

(20.) Simpson JJ, Davies WE. A review of evidence in support of a role for 5-HT in the perception of tinnitus. Hear Res 2000;145:1-7.

(21.) Gopal KV, Daly DM, Daniloff RG, Pennartz L. Effects of selective serotonin reuptake inhibitors on auditory processing: Case study. J Am Acad Audiol 2000; 11:454-63.

(22.) Steenerson RL, Cronin GW. Tinnitus reduction using transcutaneous electrical stimulation. Otolaryngol Clin North Am 2003;36: 337-44.

From the Division of Dentistry/Otolaryngology, Department of Surgery, Medical College of Ohio, Toledo.

Reprint requests: Kejian Chen, MD, Department of Surgery, Medical College of Ohio, Dowling Hall, Room 2464, 3065 Arlington Ave., Toledo, OH 43614-5807. Phone: (419) 383-4547; fax: (419) 383-6127; e-mail:
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Author:Chen, Kejian
Publication:Ear, Nose and Throat Journal
Geographic Code:1U3OH
Date:Jul 1, 2004
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