The high-pitched ringing, squealing, hissing, clicking, roaring, buzzing or whistling in the ears that can drive tinnitus sufferers crazy may be a by-product of the brain turning up the volume to cope with subtle hearing loss, a new study suggests. The results, published in the Sept. 21 Journal of Neuroscience, may help scientists understand how the condition arises.
Tinnitus is clearly a disorder of the brain, not the ear, says study coauthor Roland Schaette of the University College London Ear Institute. One convincing piece of evidence: Past attempts to cure the condition by severing the auditory nerve in desperate patients left people completely deaf to the outside world — but didn’t silence the ringing. How the brain creates the maddeningly persistent phantom noise remains a mystery.
Usually, tinnitus is tied to some degree of measurable hearing loss, but not always. “We’ve known for a long time that there are people who report tinnitus whose audiograms are normal,” says auditory neuroscientist Larry Roberts of McMaster University in Canada, who wasn’t involved in the new study. “It has been a puzzle to figure out these exceptions to the rule.”
Schaette and coauthor David McAlpine, also of the UCL Ear Institute, suggest that these exceptions may actually be due to “hidden hearing loss” that shirks detection in standard hearing tests.
The pair focused on the 10 percent of people with tinnitus who seem to have normal hearing. The team recruited 15 women with chronic tinnitus and 18 women who were free of the condition, all of whom had normal hearing tests. The researchers used electrodes to record the brain’s electrical activity as the subjects listened to loud, rapid-fire clicks.
In the people with tinnitus, electrodes picked up a subtle abnormality in one of the brain’s initial electrical response to the clicks. A signal generated by nerve fibers that carry sounds from the ear’s cochlea into the brain was weakened, perhaps because of damage to some of the fibers. This hard-to-detect hearing loss may be driving tinnitus.
A signal generated later in the sound-ear-brain pathway looked normal in people with tinnitus, the team found. In response to the loud clicks, electrical activity in the brainstem was no different between the two groups.
In participants with tinnitus, this seemingly normal signal from the brainstem comes from the brain compensating for its hearing loss by boosting nerve cells’ signal-sending activity in a way that doesn’t depend on the external sounds, Schaette and McAlpine propose. It’s this heightened — and spontaneous — nerve cell activity in the brainstem that leads to the phantom tinnitus sound, they reason.
“The brain cranks up the volume to make up for the pathologically low signal from the auditory nerve, exaggerating everything and creating tinnitus,” Schaette says.
The subtle hearing loss detected in the new study, and its link to tinnitus, is cause for concern, says Roberts. “It does suggest — and frankly, I think, very strongly suggest — that there is more hearing loss in the general population than we realize,” he says. “There is a looming public health risk here, I think of considerable magnitude.”