The auditory nerve is comprised of thousands of tiny nerve fibers responsible for transmitting sound to and from the ear and the brain. Recent discoveries have shown that they are the most vulnerable structures in the inner ear, and they naturally die away throughout the human lifespan due to exposure to noise, medications and aging. Now, a study from researchers at Harvard Medical School has described, for the first time, the adult brain’s ability to compensate for a near-complete loss of auditory nerve fibers that link the ear to the brain. The team state that their findings suggest that the brain’s natural plasticity can compensate for inner ear damage to bring sound detection abilities back within normal limits; however, it does not recover speech recognition. The opensource study is published in the journal Neuron.
Previous studies show patients who describe difficulties understanding speech despite having normal hearing thresholds recorded with an audiogram, and researchers have long hypothesized that the loss of nerve fibers contribute to this condition. Studies show that patients with a substantial depletion of auditory nerve fibers can sit across from a person and hear the sound of their voice without the ability to extract any intelligible information from it. It is thought that the loss of nerve fibers reduces the bandwidth of information that can be transmitted from the inner ear to the brain, which leads to a struggle to process sound information, even if hearing thresholds are normal. The current study shows that the brain’s plasticity, its ability to adapt to its environment, also contributes to this clinical presentation, and may explain why some patients report difficulties understanding speech despite having normal hearing thresholds.
The current study used chemicals to wipe out nearly all of the nerve fibers charged with processing sound in the inner ears of mice. The lab then observed normal responses to sound and increased activity in the cortex, the highest stage of processing in the brain, to determine that the cortex is where the ‘amplifier’ resides. Data findings show that there were limits to what could be recovered by the brain’s natural plasticity. Results show that the increased amplification at higher stages of brain processing could fully recover sensitivity to faint sounds, however the ability to resolve differences in complex sounds, like speech, did not recover to the same degree.
The team explain that findings suggest that plasticity in the adult brain at higher stages of processing acts as an amplifier, similar to an amplifier in a hearing aid. They go on to note that it appears that even just 3% of the normal complement of inputs is enough for the brain to operate on; however, the compensation is incomplete. Results show that the neurons that recover cannot decode complex sounds, such as speech, which are central to a person’s ability to communicate.
The team surmise that their findings show that having too much gain in the system can push neural circuits toward becoming pathologically hyperactive and hypersensitive. They go on to add that by establishing the actual cellular components of the brain’s amplifier, there is potential to reconnect patients to the auditory world without hearing phantom ringing or noise hypersensitivity. For the future, the researchers state that the consequences of not having enough amplification are obvious, however, they now plan to explore whether debilitating auditory conditions such as tinnitus or hyperacusis might also reflect too much amplification in the system.
Source: Massachusetts Eye and Ear
