Tinnitus refers to the sensation of sound, most often a high-pitched, noisy whistle, in one or both ears in the absence of external stimulation. Like pain, tinnitus is a very subjective phenomenon, and descriptions by sufferers tend to be in terms of a familiar sound such as the roar of the ocean or the ringing of bells. Nearly everyone experiences a mild and transient form of tinnitus. Estimates of the incidence of more severe forms vary, but around 10-14% of adults complain of tinnitus that is either prolonged or present for much of the time, and 0.5% are so affected as to have difficulty in leading a normal life.

The first written record of tinnitus appears to date back to ancient Egyptian medical documents. There are several references in Babylonian medicine to the ‘singing ear’ or the ‘whispering ear’, for which incantation of charms was advocated. Descriptions of noises in the ear and their possible causes were placed on a more scientific footing through the works of the Greek scholar Hippocrates in the fourth and fifth centuries bc and the term tinnitus originates from ancient Rome. Over the subsequent centuries, different types of tinnitus were recognized and described more completely. However, tinnitus remains one of the least understood hearing conditions, for which there is still, in many cases, no specific cure.

Many sounds are generated within the head as a result of muscular activity and by blood rushing through the cranial vessels. However, we are rarely aware of these sounds because the cochlea is shielded by the hard temporal bone. Although people with apparently normal hearing do experience tinnitus, it usually accompanies some form of hearing loss. Indeed, most people who complain to their general practitioners of deafness will also have tinnitus. Although it is often associated with disorders of the ear itself, including blockage of the ear canal by wax, otosclerosis, and Menière’s disease, it is now apparent that neural activity within the brain may be a more important factor. The discovery in the late 1970s that the ear produces sounds that can be detected in the ear canal suggested a possible link between tinnitus and the activity of outer hair cells in the cochlea. However, because drugs such as aspirin both eliminate these emissions and induce tinnitus, this seems to provide an explanation in only a few cases. Moreover, tinnitus is often found in people with severe sensorineural hearing loss or following physical damage to the inner ear, which would argue against a cochlear origin for the condition.

Because of its subjective nature and the paucity of external signs associated with tinnitus, the development of animal models has been problematic. Nevertheless, studies in animals have shown that high doses of aspirin give rise to increased spontaneous activity both in the auditory nerve fibres that leave the inner ear and in the auditory midbrain. We do not yet know the mechanisms underlying central tinnitus or even which areas of the auditory pathway are responsible, but it is possible that a change in the level of inhibitory activity may be involved.

Early remedies for tinnitus usually involved the administration, either orally or into the ear canal, of a variety of substances ranging from oils to ox urine. It was observed in ancient Greece that external noise could mask buzzing in the ears and this was used therapeutically in the nineteenth century. Unless the patient is completely deaf, noise generators are still useful today as a means of providing temporary relief. By amplifying speech or environmental noise, hearing aids can also be effective in many cases. It was claimed at the beginning of the nineteenth century that electrical stimulation of the ear could be used to treat tinnitus. In a similar vein, tinnitus is often reduced after profoundly deaf patients are fitted with a cochlear implant in which sounds are transduced into electrical signals that are delivered to electrodes inserted into the cochlea of the inner ear.

In a small minority of cases tinnitus may be alleviated if the cause of the hearing loss can be treated by surgical or medical means. Because tinnitus is aggravated by stress or fatigue, the most successful treatment involves psychological counselling or some form of relaxation therapy, often in conjunction with devices that use external noise to mask the sounds that are generated within the head.

Measuring tinnitus with auditory evoked response

Tinnitus is the description of a noise inside a person’s head in the absence of auditory stimulation. The noise can be described in many different ways, but the most common description of the tinnitus is a pure tone sound. Over 50 million Americans experience tinnitus to some degree and 12 million have severe enough tinnitus to seek medical attention. About two million people are so seriously disturbed by tinnitus that they cannot function on a day-to-day basis. (American Tinnitus Association, 2010).

Tinnitus can be classified as either subjective or objective. Objective tinnitus can be heard by other people and is usually caused by a medical condition. Subjective tinnitus can only heard by the affected person and in most cases, the cause is unknown. The most common cause of subjective tinnitus is noise exposure which damages hair cells in the inner ear causing tinnitus. Tinnitus can be associated with many emotions and responses from the body. It is best illustrated by Jastreboff’s Neurophysiological model.

The “Edge Effect” theory has been described by many researchers throughout the literature when discussing tinnitus. As hair cells are loss or damaged, afferent neurons generate auditory sensations at frequencies near the impaired region. This theory possibly explains why tinnitus can be associated with and a reflection of hearing loss and why tinnitus can be persistent.

Some researchers believe that spontaneous otoacoustic emissions (SOAEs) may be associated with tinnitus. Processes in the cochlea can cause self oscillation that is perceived as tinnitus, but most studies found that the two phenomena are not related. The evaluation of SOAEs and tinnitus was based on pitch matching and researchers concluded that not enough evidence could be seen to make the conclusion. When the researchers used two specific criteria to evaluate the results, researchers found SOAEs and tinnitus to be related in 2.42% of subjects.

In 2010, Qasem compared the differences in outer hair cell function in normal hearing patients with and without tinnitus. Distortion product OAEs (DPOAEs) were measured and results showed significant differences between groups at all DPOAE frequencies tested. Researchers concluded that decreased DPOAE amplitude can be seen in tinnitus patients due to the association between tinnitus and reduced outer hair cell movement. This study illustrates that the outer hair cells are related to tinnitus.

Moller studied the effects of tinnitus in relation to compound action potentials (CAP) in 1992. Researchers recorded compound action potential components N1 and N2 and found that the latencies of the responses in the tinnitus patients were similar to patients with no tinnitus. This study concludes that tinnitus effects can not be observed in CAP. The effects of tinnitus on auditory brainstem response (ABR) measures have also been evaluated by many researchers. Auditory pathway plays a role in the emotional and physiological response to tinnitus. Research has shown abnormal ABR results (interwave latency delays) in patients with tinnitus. In 2008, Kehrle used ABR testing to evaluate the auditory nerve and brainstem function of tinnitus patients with normal hearing. Results showed delayed wave latencies and interpeak latencies between the tinnitus and non tinnitus patients. Researchers concluded that latency prolongations of wave I and lengthening of III-V IPL found in this study confirmed the findings in previous research. Maurizi in 1985 used ABRs to evaluate the auditory pathway in patients with tinnitus and concluded that patients with tinnitus had abnormal ABR recordings. Peripheral tinnitus was reduced with residual inhibition and recordings returned to normal. However, this method is not valid for all tinnitus patients due to the many different causes of tinnitus. Gerken in 2001 evaluated the influence of tinnitus on auditory evoked potentials. Results showed delayed ABR wave VII latencies in the tinnitus group and about half of the tinnitus patients had MLR amplitudes that were significantly greater than the control group mean. Researchers concluded the latency differences for wave VII only adds more diversity to research findings and should be included in future research. Large MLR waves seen in the tinnitus group may be caused by unknown smaller factors not accounted for in the study.

Tinnitus and auditory evoked cortical potentials have also been studied. It is important to evaluate the primary auditory cortex in relation to Jastrebroff’s model. “ALRs reflect stimulus properties as well as attention and the psychological state of the subjects, both of which are presumed to contribute to tinnitus” -Kadner (2002). Low and colleagues in 2008 concluded that ALRs can be used to evaluate the effectiveness of therapies used to alleviate tinnitus.

Tinnitus has also been studied in relation to event related potentials. In 1991, Shiraishi and colleagues found that the contingent negative variation (CNV) amplitude was significantly enlarged in tinnitus patients. They also found no effect on the latency and amplitude of the N100 and P300 responses. Attias in 1993, found that the amplitudes of N1, P2, and P3 were reduced, P3 latencies delayed, and N1 and N2 had delayed latencies to non-target stimuli.

In 2008, Delb conducted a study that evaluated tinnitus patients with high and low tinnitus related distress and how they differ in respect to focus levels on the tinnitus. Researchers concluded that patients with different levels of distress have differences in their ability to shift attention.

Elbert in 2004 studied the relation between tinnitus and mismatched negativity (MMN). Researchers recorded MMN potentials at stimulus levels at the edge frequency of the patient’s tinnitus and found differences in the recordings. This finding can be applied to tinnitus treatments to monitor progress and show effectiveness.

Tinnitus and long latency auditory evoked potentials (LLAEPs) have also been researched quite frequently. Alterations of LLAEPs have been seen in individuals with tinnitus and indicate problems in the auditory pathway in the cortex which can be concluded by increased latency values. In 2010, Santos Filha measured LLAEP potentials of tinnitus patients with a history of noise exposure. Researchers concluded that LLAEP shifts occur more often in individuals with tinnitus when compared to the control group.

In conclusion, tinnitus can be evaluated with most auditory evoked potentials; however results may be inconsistent. Results must be compared to age and hearing matched control subjects to be reliable. This inconsistently reported may be due to many reasons: differences in the origin of the tinnitus, ABR recording methods, and selection criteria of control groups. Since research shows conflicting evidence, more research on the relationship between tinnitus and auditory evoked potentials should be carried out before these measurements are used clinically.