A new study from Mass Eye and Ear investigators shows that individuals who report tinnitus, which present as a ringing in the ears in more than one out of ten adults worldwide, are experiencing auditory nerve loss that is not picked up by conventional hearing tests. This work is part of a P50 grant awarded by the National Institutes of Health (NIH) to Mass Eye and Ear researchers within the Eaton-Peabody Laboratories (EPL) for their work on cochlear synaptopathy, which is commonly referred to as “hidden hearing loss.” The results from this study provide a better understanding on the origins of tinnitus and are published November 30th in Scientific Reports.
“Beyond the nuisance of having persistent ringing or other sounds in the ears, tinnitus symptoms are debilitating in many patients, causing sleep deprivation, social isolation, anxiety and depression, adversely affecting work performance, and reducing significantly their quality of life,” said senior author Stéphane F. Maison, PhD, CCC-A, a principal investigator at Mass Eye and Ear, a member of Mass General Brigham, and clinical director of the Mass Eye and Ear Tinnitus Clinic. “We won’t be able to cure tinnitus until we fully understand the mechanisms underlying its genesis. This work is a first step toward our ultimate goal of silencing tinnitus.”
Many individuals with hearing loss report a buzzing, humming, ringing or even roaring sound in their ears. It’s been a longstanding idea that these symptoms, known as tinnitus, arise as a result of a maladaptive plasticity of the brain. In other words, the brain tries to compensate for the loss of hearing by increasing its activity, resulting in the perception of a phantom sound, tinnitus. Until recently though, this idea was disputed as some tinnitus sufferers have normal hearing tests.
However, the discovery of cochlear synaptopathy back in 2009 by Mass Eye and Ear investigators brought back to life this hypothesis as it was evidenced that patients with a normal hearing test can have a significant loss to the auditory nerve. In view of this paradigm shift in the way researchers and clinicians think about hearing loss, Maison and his team sought to determine if such hidden damage could be associated with the tinnitus symptoms experienced by a cohort of normal hearing participants. By measuring the response of their auditory nerve and brainstem, the researchers found that chronic tinnitus was not only associated with a loss of auditory nerve but that participants showed hyperactivity in the brainstem.
“Our work reconciles the idea that tinnitus may be triggered by a loss of auditory nerve, including in people with normal hearing,” said Maison.
In terms of future directions, the investigators aim to capitalize on recent work geared toward the regeneration of auditory nerve via the use of drugs called neurotrophins.
“The idea that, one day, researchers might be able to bring back the missing sound to the brain and, perhaps, reduce its hyperactivity in conjunction with retraining, definitely brings the hope of a cure closer to reality,” Maison added.
Disclosures: The authors declare no competing interests.
Funding: This work was supported by a grant from the NIDCD (P50 DC015857) and the Lauer Tinnitus Research Center at the Mass Eye and Ear.
