It is common knowledge that it takes a while for the hearing to become ‘normal’ again after listening to music that is too loud. The American Tinnitus Association estimates that there are almost 50 million people in the U.S. and millions more worldwide who suffer from tinnitus, which can range from being intermittent and mildly annoying to chronic, severe and debilitating. There is no cure for tinnitus.

A new study published in the first February issue of The Journal of Neuroscience has shown that researchers at the University of Michigan Health System suggest that over-exposure to noise can actually cause more lasting changes to our auditory circuitry that potentially lead to tinnitus, commonly known as ringing in the ears.

In a previous study, the researchers proved that touch-sensing “somatosensory” nerves in the face and neck could become overactive after hearing damage. The nerves appear to overcompensate for the loss of auditory input, which results in the brain interpreting or rather ‘hearing’ noise that does not really exist.

Findings of the new study that is based on Shore’s previous research, revealed that after exposure to loud noise, the somatosensory neurons, which carry information about touch, vibration, skin temperature and pain, stay highly active even after hearing itself returns to normal.

According to leading researcher Susan E. Shore, Ph.D., of U-M’s Kresge Hearing Research Institute, who is a professor of otolaryngology and molecular and integrative physiology at the U-M Medical School, even though the study was conducted in guinea pigs, the findings play a significant role in finding a potential relief for people who suffer from tinnitus.

She states:

“The animals that developed tinnitus after a temporary loss in their hearing after loud noise exposure were the ones who had sustained increases in activity in these neural pathways. In the future it may be possible to treat tinnitus patients by dampening the hyperactivity by reprogramming these auditory-touch circuits in the brain.”

In normal hearing, the first reception of signals that arrive from the ear via the auditory nerve is the dorsal cochlear nucleus, which is an area in the brain that also functions as the center where “multitasking” neurons process other sensory signals like touch together with hearing information.

According to Shore’s previous research, other sensory signals that enter the dorsal cochlear nucleus are amplified during hearing loss. Scientists believe that in many cases this overcompensation by the somatosensory neurons evokes tinnitus.

Baby boomers are particularly affected by tinnitus. They increasingly find as they reach an age at which their hearing is likely to get worse that they start to suffer from tinnitus, which typically occurs with hearing loss, but can also appear after a head and neck trauma like after a car accident or dental work. It is also the number one disability amongst members of the armed forces.

Shore, who also serves on the scientific advisory committee of the American Tinnitus Association, says that the involvement of somatosensory nerves in the head and neck explains why many tinnitus sufferers are able to change the volume and pitch of the sound by clenching their jaw or moving their head and neck.

She concludes:

“This is the first research to show that, in the animals that developed tinnitus after hearing returned to normal, increased excitation from the somatosensory nerves in the head and neck continued. This dovetails with our previous research, which suggests this somatosensory excitation is a major component of tinnitus. The better we understand the underlying causes of tinnitus, the better we’ll be able to develop new treatments.”

Written by Petra Rattue