BERKELEY, CA—Tinnitus has long been among the most common, troublesome, mysterious, and intractable conditions related to hearing. While many cases are mild, tinnitus can cause constant torment, sleeplessness, and desperation that may even lead to thought of suicide.
Adding to the frustration over tinnitus is that neither the causes nor the best treatments for the condition are clear. While many people benefit fro various treatments, others do not.
That’s why recent findings by neuroscientists from the University of California, Berkeley, are welcome news to the estimated 10% of the population who suffer from the high-pitched ringing or buzzing in their ears that tinnitus brings.
Writing last week in the online journal Proceedings of the National Academy of Sciences, the researchers suggest several new approaches to treatment, including retraining the brain, and new avenues for developing drugs to suppress the ringing.
ASSOCIATED WITH HAIR CELL DAMAGE
According to co-author Shaowen Bao, adjunct assistant professor in the Helen Wills Neuroscience Institute at UC Berkeley, tinnitus is most commonly related to hearing loss, especially that caused by loud noise or, less often, ototoxic medications, which damage hair cells in the inner ear. Since, each hair cell is tuned to a different frequency, damaged or lost cells leave a gap in hearing, typically in a specific frequency.
Previous experiments have shown that the perceptions of ringing don’t originate in the inner ear, but in regions of the brain, including the auditory cortex, that receive input from the ear.
Research by Bao and four colleagues using rats with induced hearing loss sheds light on how neurons in the auditory cortex generate the phantom sound perceptions known as tinnitus. Neurons that have lost sensory input from the ear become more excitable and fire spontaneously. “With the loss of hearing, you have phantom sounds,” said Bao, who himself has tinnitus.
In an interview with the University of California media relations office, Bao discussed possible treatments. One strategy is to retrain patients so that the brain cells where tinnitus originates receive new input, which should reduce spontaneous firing. This can be done by enhancing the response to frequencies near the lost frequencies.
Bao noted that retraining the ear has been tried before, but with limited success. He said that most retraining is based on the assumption that reorganization of the brain, i.e., changing how frequencies “map” to regions of the auditory cortex, is a cause of the tinnitus. This is the opposite of his conclusion.
Bao explained, “We argue that reorganizing the cortical map should be the goal, so that the nerves get some input and stop their tinnitus activity.” He added, “You don’t want to leave these cells without sensory input.”
Another treatment strategy, Bao said, is to develop drugs that inhibit the spontaneous firing of the idle neurons in the auditory cortex. His experiments showed that tinnitus is correlated with lower levels of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid).
Bao demonstrated that two drugs that increase the level of GABA eliminated tinnitus in rats. Unfortunately, these drugs have serious side effects and cannot be used in humans. He has applied for grants to start screening drugs for their ability to enhance GABA receptor function, increase the synthesis of GABA, slow the re-uptake of GABA around nerve cells, or slow its enzymatic degradation
The research was supported by the American Tinnitus Association and the National Institute on Deafness and other Communicative Disorders.