Understanding tinnitus: computer models might give rise to new treatment strategies

"A spider's web is hidden in one ear, and in the other, a cricket sings throughout the night." This is how Michelangelo described his experience of hearing loss and tinnitus. Like millions of other people, he suffered from this phantom auditory sensation, perceiving a sound when there was no corresponding noise. Tinnitus sounds can be tone-like or noise-like, and common descriptions are 'ringing', 'whistling', 'humming', 'buzzing', 'hissing', or 'roaring'. In severe cases, the tinnitus can be heard even when there is loud ambient sound - on a busy street, for example - seriously degrading the quality of life.

The majority of people with tinnitus also have hearing loss, and the pitch of the tinnitus that they 'hear' is the same as the pitch at which hearing is impaired; for example, someone who is unable to hear high-pitched sounds might describe their tinnitus as a high-pitched ringing noise. Scientists therefore assume that tinnitus can be caused by hearing loss. The unsolved questions are why and how.

Inside the ear, sound is converted into electrical signals that travel along a nerve to the brain, where the sound is perceived - in other words, we become aware of a sound when these signals reach our brain. The ear and the nerve that connects the ear to the brain can be ruled out as the source of tinnitus because tinnitus continues even if the nerve is severed. It must therefore be generated somewhere in the brain. In animals, scientists have discovered that after the inner ear has been damaged, the brain's auditory system becomes more active even when there is no sound. Moreover, the patterns of this spontaneous activity resemble those that are normally evoked by sound when the inner ear is intact. After damage to the inner ear, the normal hearing process therefore seems to be hyperactive, possibly tricking the brain into 'hearing' tinnitus.

The goal our research is to unravel the functional mechanisms that lead to the development of tinnitus. The better we understand the roots of this phenomenon, the stronger our chances of finding a cure. To address the question of how hearing loss can lead to tinnitus, we have used a simplified computer model of the auditory system. In the model, we study how hearing loss changes the activity of the nerve cells in the auditory system. After hearing loss, the nerve cells react only to loud sounds, whereas soft sounds do not activate them. As a consequence, many nerve cells are less active, overall.

This could trigger an adaptive mechanism to ensure that the nerve cells operate within the right range of activity, neither inactive nor too active. When the activity of a nerve cell is strongly decreased after hearing loss, the adaptive mechanism increases its activity level by making it react more strongly to input signals. However, this can also amplify the spontaneous activity of the nerve cells so that they become hyperactive even in silence. As a consequence, the brain might then perceive sound when there is none. Tinnitus could therefore be a side effect of the brain's attempt to compensate for hearing loss. We have tested the model by applying it to the patterns of hearing loss of patients with tone-like tinnitus. The resulting hyperactivity patterns of the model nerve cells are consistent with the tinnitus pitch perceived by the patients. Based on the model predictions, we can derive acoustic or electrical stimulation strategies that might reduce hyperactivity and thus also tinnitus. We hope that this will provide a basis for new treatments for tinnitus.

Roland Schaette, Humboldt-Universität zu Berlin. www.atomiumculture.eu