Summary of Study: Scientists think that we might have two distinct pathways for processing sound, one for registering the existence of sounds and their characteristics (such as pitch), and another for registering pain induced by sound.
Say you enter a loud concert. You hear a guitar, harmonica and fans cheering energetically. You may also experience pain as a consequence of the exposure to loud noises. It has long been known that the awareness and ability to identify these sounds is dependent upon a pathway begun at the inner hair cells in the cochlea of the ear, and relayed on to the central nervous system by type I fibers. The processing of sound-induced pain like that experienced at the loud concert, however, may follow a different path. Last March, a team of researchers showed that processing of sound-induced pain seems to originate at outer hair cells in the ear and connect to the central nervous system along type II fibers. When they selectively inactivated type I fibers in mice, deafening the animals and leaving them with only type II fibers functioning, and then exposed them loud sounds, they found that cells in the central nervous system were still activated, but that these were cells in a slightly different place.
Key Outcomes: This study asserts that sound and pain due to sound are carried along separate pathways from the ear to the central nervous system and to somewhat different places within the central nervous system.
Relevance to tinnitus/hyperacusis: Given that pain due to sound is the primary feature associated with hyperacusis, this study suggests that this newly identified “pain due to sound” pathway might be compromised in people with hyperacusis.
Study authors: Emma N. Flores, Anne Duggan, Thomas Madathany, Ann K. Hogan, Freddie G. Ma´rquez, Gagan Kumar, Rebecca P. Seal, Robert H. Edwards, M. Charles Liberman, and Jaime Garcı´a-An˜overos, Current Biology.
