The medical term for ringing in the ears is tinnitus, which means noise in Latin. Tinnitus is not limited to ringing but may be perceived as whistling, buzzing, humming, hissing, roaring, chirping or other noise. Its technical definition is the perception of any of these sounds in the absence of an acoustic stimulus in the surrounding environment. Approximately 20 million people in the United States experience tinnitus and as many as two million of them suffer from it to the degree that it interferes substantially with their occupation, social life and other daily activities. (It is not known why this condition affects individuals differently.)
Tinnitus is a symptom that is associated with virtually all disorders of the auditory system and can arise from any of its parts. Although usually associated with a loss of hearing, it may occur without any hearing loss. And even among people with the same type of hearing loss, some may or may not develop tinnitus. Exactly why this is so remains unclear. Many of the causes of this problem are well known, but the mechanisms of its production and its area or areas of generation remain controversial.
There are several types of tinnitus. 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 brain stem, such as the dorsal cochlear nucleus. This loss of input then sometimes leads to increased spontaneous activity in the neurons of the nucleus, as if some inhibition had been removed. Drugs such as aspirin, quinine and aminoglycoside antibiotics, as well as cancer chemotherapeutics and other ototoxic agents can also cause tinnitus, as can infections and head injuries.
Because tinnitus in animals is usually accompanied by hearing loss, it is often difficult to segregate the condition's effects from those 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 way station 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 sound perception generation 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 their brains, 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.