Summary: Hyperacusis refers to a condition in which sounds that are uncomfortably loud to normal people are intolerably loud. This condition is prevalent and affects many people. However, its underlying mechanisms are still not clear and no effective treatments are available. Scientists and clinicians have been searching for the underlying mechanisms. Although there are multiple causes including acoustic trauma and ear infection, a very common theory points to increased central gain in the brain following decreased signal input from the cochlea. However, it remains unclear what special factor in the cochlea might contributes to hyperacusis. Recently, scientists at Johns Hopkins University School of Medicine think that they have discovered the possible role of type II nerve cells, which carry some form of acoustic information from the cochlea of the ear to the central nervous system, in hyperacusis.
Multiple types of nerve cells carry information from the cochlea of the ear to the central nervous system. The predominant type (~95%) is the type I fiber, which carries information about sound that is registered by the inner hair cells inside the cochlea. The sparser (~5%) is the type II fiber, which are activated, albeit weakly, by outer hair cells. Unlike type I cells, the role of type II cells, for decades now, has been somewhat unclear, especially since they have been shown not to be insensitive to sound. However, the recent work of Liu and colleagues may change that, by showing that these cells respond to damage to outer hair cells.
Moreover, they do so in a familiar way. Say you accidentally place your finger on a hot burner. You will recoil instantly, and remove your finger even before you become consciously aware of the pain, though the pain will eventually be perceived. The pathway that allows this to occur is via cells that carry information about temperature from your fingers to your spinal cord, which then activates other muscles in an effort to move the imperiled finger. Dr. Liu and colleagues think that a similar process may be at work in the auditory system, where loud sounds damaging outer hair cells triggers behavior to withdraw from the loud sound. In a cultured inner ear preparation, they found that when damaged outer hair cells release more molecules adenosine triphosphate (ATP) that serve as energy source for these cells to function. They also found that when more ATPs are released, the outer hair cells become more excited and send out more signals that are to be received by the brain. This suggests these nerve cells may act as the ear’s pain sensor and send pain-like signals to the brain that does not tolerate sounds in hyperacusis patients.
Key Outcomes: This study highlights the critical role of type II cells in acoustic damage, and suggests that they operate in a similar way to pain receptors in other parts of the body.
Relevance to tinnitus/hyperacusis: The heightened sensitivity to sound, and in some cases pain associated with sound, that is characteristic of hyperacusis may have a basis in a compromised type II cell system. If type II cells truly respond to acoustic damage, then hyper-sensitivity of these cells could lower the threshold for sounds that cause pain. This could be particularly important for those with hyperacusis, an extreme sensitivity to every day sounds. which in severe cases causes pain.
Study authors: Liu C, Glowatski E, Fuchs PA Proceeds of the National Academy of Science.