Approximately 20 million people in the United States experience tinnitus, and as many as 2 million of them suffer from tinnitus that interferes substantially with their occupation, social life and other activities of daily life. (It is not known why tinnitus affects individuals differently.)

Tinnitus is a symptom that is associated with virtually all disorders affecting the auditory system and can arise from any part of the auditory system. Although it is usually associated with a loss of hearing, it may occur without any hearing loss. And even among people with the same hearing loss, some may develop tinnitus and others won't. Exactly why this is so remains unclear. Many of the causes of tinnitus are well known, but the mechanisms of its production and its area or areas of generation remain controversial.
There are several types of tinnitus, depending on the cause. The most common form arises from damage to the inner ear or cochlea caused by exposure to intense noise. Loud noise can damage the hair cells responsible for receiving auditory stimuli. This results in a decrease in input from the cochlea through the auditory nerve to the auditory centers in the brainstem such as the dorsal cochlear nucleus. This loss of input then sometimes leads to increased spontaneous activity in the neurons of the dorsal cochlear nucleus, as if some inhibition had been removed. Drugs such as aspirin, quinine, aminoglycoside antibiotics, cancer chemotherapeutic agents and other ototoxic agents, as well as infections and head injuries, can also cause tinnitus.

Because tinnitus in animals is usually accompanied by hearing loss, it is often difficult to segregate the effects of tinnitus from the effects of hearing loss. Increased spontaneous activity in the dorsal cochlear nucleus is transmitted to auditory centers in the midbrain such as the inferior colliculus and the medial geniculate body of the thalamus (the common sensory waystation en route to the cerebral cortex), and then on to the auditory cortex of the cerebrum. In animals, increased spontaneous activity in the cortex has been shown to be associated with neurons being activated synchronously, and the synchrony increases as the spontaneous activity increases. Hence, the site or sites of generation of the sound perception known as tinnitus are in the central auditory pathways even if the initial damage is to the inner ear.
Functional magnetic resonance imaging (fMRI) and positron emission tomographic (PET) studies of tinnitus sufferers have shown increased neural activity in their auditory cortices. There is also evidence of the brain reorganizing itself whereby cells in the auditory cortex respond to different frequencies than they had originally. Recent research has further found that individuals with tinnitus have increased activity in the limbic structures of the brain, which is associated with emotional processing. Other symptoms that sometimes occur alongside tinnitus--such as emotional distress, depression and insomnia--may have a common basis in some limbic structure such as the nucleus accumbens.

In summary, the perception of a ringing in the ear in the absence of a sound is thought to result ultimately from the cortices of the brain spontaneously increasing their activity and is associated with changes in the organization of the auditory cortex. But many aspects of tinnitus remain mysterious.

By J. Giambrone
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