Long after damage has occurred to a person’s hearing, some people still experience persistent tinnitus—the perception of a buzzing, ringing, or hissing sound—that can’t be accounted for by actual sounds. Remarkably, this phenomenon is very similar to bouts of chronic pain that persist after an injury has healed—and sometimes without the precursor of an injury.

Now researchers at Georgetown University Medical Center, in collaboration with Germany’s Technische Universität München, say they've identified a single brain dysfunction that causes both tinnitus and chronic pain. Their study, published in the journal Trends in Cognitive Sciences, revealed a common cause for these conditions, which affect 50 million (tinnitus) and 76.2 million (chronic pain) Americans alone. 

In a normally functioning brain, neural structures such as the nucleus accumbens, the ventromedial prefrontal cortex, and the anterior cingulate cortex act as “gatekeepers” to control noise, pain, and emotional signals and keep them from getting dysfunctional. In people who've suffered hearing loss, “the brain tries to reorganize and make the person hear as well as possible, but the side effect is that tinnitus noise is generated,” says Josef Rauschecker, one of the authors of the study. In people with tinnitus, these gatekeepers don't work as they should, letting through unwanted signals.

Strikingly, says Rauschecker, the brains of people who suffer from tinnitus have similar, measurable neural activity to those who suffer from chronic pain. In both cases this suggests that while there may be no external source of sound or pain—often referred to as “phantom pain”—the brain is receiving signals nonetheless.

“In tinnitus, the sound comes from the structures like the auditory cortex. It signals to the person that it’s a sound,” Rauschecker tells mental_floss. “It’s the same with chronic pain. There’s neuron activity in the brain’s pain system long after the injury has healed.”

Even more intriguing is the fact that those who suffer tinnitus or chronic pain also often suffer from depression or anxiety, says Rauschecker. This may stem from the fact that these brain structures also regulate emotions and interpret sensations. They do so via the nucleus accumbens, the brain’s reward and learning center, using the neurotransmitters dopamine and serotonin.

“The frontal cortex is part of the brain’s executive system—part of the limbic system—which regulates emotions. In tinnitus and chronic pain, we find that when these structures are impaired, there are fewer neurons and hyperactivity in the striatum that controls these emotions,” says Rauschecker. In essence, the brain is no longer able to turn down the volume, or incorrectly overemphasizes the signals, amplifying them and creating noise, pain, depression, or anxiety. 

While researchers don’t yet understand how these neural structures become broken, they are getting closer to understanding how the brain modulates—or fails to modulate—these signals. Now that they've identified the brain structures involved, their next line of research is learning how the neurotransmitters involved, such as glutamate, GABA, serotonin, and dopamine, play a role.

Through a variety of treatments, Rauschecker hopes they can learn to modulate the gatekeepers’ excessive reception and "turn down" signals of noise and pain to normal levels. "The ultimate goal is to get drug treatment and develop something that can mitigate this suffering," he says.

In the meantime, he suggests that we can all limit our potential to develop tinnitus by steering clear of excessively loud noises, or using earplugs and other means to reduce noise when possible. “Once you have tinnitus, it’s much harder to reverse.”