People with tinnitus experience persistent ringing or buzzing in their ears that can significantly impact their quality of life — and now, scientists think they finally know what causes the condition.
A new study revealed that people with tinnitus have damage to specific fibers within their auditory nerve that is not detected by standard hearing tests. In addition, neurons in the brainstem — a region at the bottom of the brain that connects to the spinal cord — are more active in response to noise in people with tinnitus than in those who have never experienced it.
The findings, published in the journal Scientific Reports, support an existing theory that tinnitus is caused by a subtle loss of hearing, which in turn prompts the brain to overcompensate by ramping up the activity of neurons involved in the perception of sound. As a result of them being hyperactive, people hear what seem like “phantom sounds.”
“We’re not talking about a treatment — for the first time, we’re talking about a possible cure,” said Dr. Stéphane F. Maison, clinical director of the Tinnitus Clinic at the Mass Eye and Ear hospital in Boston.
Approximately 1 in 10 adults in the U.S. have experienced tinnitus, which can be triggered by many things, including exposure to loud music at a concert or an ear infection. Tinnitus can last just minutes or become chronic and last for years.
In the new study, the authors recruited 201 people who said they’d never had tinnitus in their lives, 64 who had experienced it “at some point” and 29 who had chronic tinnitus, meaning their symptoms had continued for at least six months. The researchers tested the participants’ hearing using a gold-standard clinical tool called an audiogram.
“In the clinic, we ask patients to raise their hand whenever they hear a tone and what the audiologist does is measure the threshold, or the lowest level at which you can detect those tones, to try to figure out your hearing sensitivity,” Maison said.
All the participants passed this test, so they technically qualified as having “normal hearing.”
However, when the authors placed electrodes in the participants’ ears and measured the electrical activity of the auditory nerve and brainstem in response to clicking sounds, they discovered that people with tinnitus had damage to a specific type of fiber that responds to louder sounds.
Within the inner ear is a snail-shaped chamber called the cochlea, which contains cells that detect vibrations and convert them into electrical signals. These signals are then carried by auditory nerve fibers via the brainstem to the auditory cortex in the brain, which interprets the signals as sounds.
When someone tunes into quiet sounds, such as during a private conversation, they only need to rely on one set of auditory nerve fibers that respond to quiet noises, Maison said. However, if they’re chatting in a noisy environment, they also need input from fibers that respond to louder sounds, he said.
These latter fibers are more likely to become damaged as people age or as a result of excessive noise exposure. However, this specific damage may not be detected by regular hearing tests that only assess a person’s ability to hear quiet sounds, he said.
This may explain “hidden hearing loss” where people are assessed to have normal hearing despite struggling to hear in noisy environments.
In the study, people with tinnitus also had greater activity in the neurons of their brainstem in response to the clicking sounds. Maison believes this reflects how the brain is compensating for a loss in auditory nerve function.
The new study hints that tinnitus could be treated with repairs to the damaged auditory nerve fibers. For example, it may be possible to treat tinnitus by regenerating the auditory nerve using growth factors called neurotrophins, Maison said. That would mean the brain would no longer have to compensate for hearing loss, so the person’s tinnitus may subside.
However, this research is still in its early days, so it’s unlikely such a treatment will be available soon.
Article originally appeared on Live Science
