Tinnitus discovery could lead to new ways to stop the ringing

People with tinnitus -- a constant ringing or buzzing in the ears -- can take heart from a new study by neuroscientists that points to several new strategies for alleviating the problem. 

In experiments on rats, researchers have shown that tinnitus results from decreased inhibition in the auditory cortex. Thus, training that boosts inhibition or drugs that increase the levels of inhibitory neurotransmitter may alleviate the symptoms. 

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Sustained loud noises, as from machinery or music, as well as some drugs can damage the hair cells in the inner ear that detect sounds. Because each hair cell is tuned to a different frequency, damaged or lost cells leave a gap in hearing, typically a specific frequency and anything higher in pitch.

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 neighbouring 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 cortical map should be the goal, so that the nerves get some input and stop their tinnitus activity," he said. "You don't want to leave these cells without sensory input."

"We changed our (brain training) strategy from one where we completely avoided the tinnitus domain to one where we directly engage it and try to redifferentiate or reactivate it, and we seem to be seeing improvement," Merzenich said.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of California - Berkeley. The original article was written by Robert Sanders, Media Relations.

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Journal Reference:

1. S. Yang, B. D. Weiner, L. S. Zhang, S.-J. Cho, S. Bao. Homeostatic plasticity drives tinnitus perception in an animal model. Proceedings of the National Academy of Sciences, 2011; 108 (36): 14974 DOI: 10.1073/pnas.1107998108