People suffering from tinnitus hear ringing, buzzing, or hissing in their ears much like an amputee might feel phantom pain in a missing limb. Although exposure to loud noise may contribute, some cases have no apparent trigger.
It’s not known yet exactly where and how tinnitus occurs in the brain, says Richard Salvi, director of the Center for Hearing and Deafness at the University at Buffalo. But functional MRI studies with rats show the abnormal activity underlying tinnitus and a related condition called hyperacusis isn’t confined to a specific brain location, but actually involves a neural network.
Salvi and colleagues induced tinnitus in rats by administering the active ingredient in aspirin, which has long been known to produce tinnitus and hyperacusis symptoms in humans.
Salvi, one of the authors of the study, said:
“Certain brain regions become very active once tinnitus is induced, much more so than it is for an animal with normal hearing. Even though high-dose aspirin induces a hearing loss and less information is being sent from the ear to the brain as a result, the brain responds with greater activity.
It’s paradoxical, like a car getting better gas mileage with a less efficient engine.”
Fight or Flight Response
Tracing the neural network’s course, the investigators identified a major hub within the central auditory pathway, the sound processing center of the brain.
“Other research has shown this activity, but what is novel about the current study is the amygdala pops up. This is the part of the brain that assigns emotion to our perceptions,” says Salvi. “Many patients report the onset of tinnitus after experiencing significant stress or anxiety.
We think it’s not just the hearing loss that’s essential. There are other emotional factors working together with the auditory factors.”
The reticular formation, an arousal center involved in the “fight or flight” response is active too, plus the hippocampus, the memory region of the brain that helps identify where things are located, such as the location of the phantom sound.
So the auditory system is connecting sound to a location, the ear in this case. There is emotion and arousal, but the final puzzling piece to the network is activity in the cerebellum, normally activated during motor planning events like reaching for a cup or catching a ball.
“We were shocked when this part of the brain popped up,” says Salvi. “Almost all parts of the network can be explained: location of sound; the emotional attachment; why people get aroused when they have tinnitus; we’re puzzled by the cerebellum involvement, but it might act like some kind of “gate” that’s allowing the phantom sound to enter the consciousness.”
These findings could lead to a testable model that helps to identify what region or regions of the brain might be responsible for causing the two conditions.
Having conceptualized a broader, more comprehensive neural network, the researchers hope to eventually test the model by deactivating specific segments of the neural network. By the process of elimination they would learn if shutting down one part of that network relieves tinnitus, hyperacusis, or both conditions.
Yu-Chen Chen, Xiaowei Li, Lijie Liu, Jian Wang, Chun-Qiang Lu, Ming Yang, Yun Jiao, Feng-Chao Zang, Kelly Radziwon, Guang-Di Chen, Wei Sun, Vijaya Prakash Krishnan Muthaiah, Richard Salvi, Gao-Jun Teng Tinnitus and hyperacusis involve hyperactivity and enhanced connectivity in auditory-limbic-arousal-cerebellar network eLife 2015; 4:e06576 DOI: http://dx.doi.org/10.7554/eLife.06576
_Photo: Spooky Pooka, Wellcome Images _