Experiments in the past few years have shown that the ringing doesn't originate in the inner ear, though, but rather in regions of the brain including the auditory cortex that receives input from the ear.
Bao's experiments in rats with induced hearing loss explain why the neurons in the auditory cortex generate these phantom perceptions. They showed that neurons that have lost sensory input from the ear become more excitable and fire spontaneously, primarily because these nerves have "homeostatic" mechanisms to keep their overall firing rate constant no matter what.
"With the loss of hearing, you have phantom sounds," said Bao, who himself has tinnitus. In this respect, tinnitus resembles phantom limb pain experienced by many amputees,
One treatment strategy, then, is to retrain patients so that these brain cells get new input, which should reduce spontaneous firing. This can be done by enhancing the response to frequencies near the lost frequencies. Experiments over the past 30 years, including important research by Merzenich, have shown that the brain is plastic enough to reorganize in this way when it loses sensory input. When a finger is amputated, for example, the region of the brain receiving input from that finger may start handling input from neighboring fingers.
Bao noted that retraining the ear has been tried before, but with limited success. Most such attempts have taken patients with some residual hearing and trained their ears to be more sensitive to the affected frequencies. This wouldn't work for patients with profound hearing loss, however.
Most retraining is also based on the assumption that reorganization of the brain that is, changing how frequencies "map" to regions of the auditory cortex is a cause of the tinnitus. This is the opposite of Bao's conclusion.
"We argue that reorganizing the
|Contact: Robert Sanders|
University of California - Berkeley