Researchers take an important step towards silencing tinnitus

New research out of the US has linked tinnitus to a loss of auditory nerve fibres – a type of “hidden” hearing loss not detected in conventional hearing tests.

The new study in Science Advances provides a better understanding of the origin of tinnitus, which affects more than 740 million adults globally.

Dr Stéphane F. Maison, clinical director of the Massachusetts Eye and Ear Tinnitus Clinic and senior author of the study, says in some people tinnitus “reduces significantly (people’s) quality of life”.

“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, and adversely affecting work performance.

“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.”

Tinnitus has long been thought to be caused by maladaptive plasticity of the brain. The brain tries to compensate for a loss of hearing by increasing its activity, resulting in the perception of a phantom sound.

But this idea was disputed until recently because some tinnitus sufferers return normal hearing test results.

In 2009 Massachusetts Eye and Ear researchers found patients with an otherwise normal hearing test – a clinical audiogram which measures the loss of sensory hair cells – can have significant loss to the auditory nerve.

This interrupts communication between hair cells in the inner ear and the auditory nerve fibres that transmit information to the cochlear nucleus in the brainstem. This alters the processing of auditory information.

It is now known as cochlear synaptopathy or “hidden hearing loss”.

In this study, the researchers wanted to know whether hidden hearing loss could be associated with the tinnitus symptoms experienced by people with otherwise normal hearing.

By measuring the auditory nerve and brainstem, Maison and his team 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.

The aim now is to capitalise on recent work on 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.”