Massachusetts Eye and Ear and Harvard Medical School announced that researchers have described, for the first time, the brain’s ability to compensate for a near-complete loss of auditory nerve fibers.
The study article, published in a December 2015 online edition of Neuron, suggests 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 intelligibility. This imperfect hearing recovery may explain why some patients report difficulties understanding speech despite having normal hearing thresholds.
“Our findings suggest that plasticity in the adult brain at higher stages of processing acts as an amplifier – the same way that you’d have an amplifier on a hearing aid,” said Daniel B. Polley, PhD, director of the Amelia Peabody Neural Plasticity Laboratory at Massachusetts Eye and Ear, and an associate professor of otolaryngology at Harvard Medical School. “It seems that even just 3% of the normal complement of inputs is enough for the brain to operate on; however, the compensation is incomplete. There is a cost, and the cost is that the neurons that recover cannot decode complex sounds, such as speech, which are central to our ability to communicate.”
As described by the authors, the auditory nerve is comprised of thousands of tiny nerve fibers responsible for transmitting sound information to and from the ear and the brain. Recent discoveries have shown that the sensory nerves 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.
Patients who report difficulties understanding speech despite having normal hearing thresholds on audiograms have long perplexed physicians, and researchers have hypothesized that the loss of nerve fibers contributes to this. The paper’s authors suggest that the brain’s plasticity, or adaptability, contributes to this clinical presentation.
“Someone with a substantial depletion of auditory nerve fibers would be sitting across from you and could hear the sound of your voice but would not be able to extract any intelligible information from it, particularly if other people were talking nearby,” said Polley. “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.”
For their sound processing investigation, the researchers studied lab mice whose inner ear nerve fibers had been wiped out. They observed normal responses to sound and an increased activity in the cortex—the highest stage of processing in the brain—and determined that the cortex is where the “amplifier” resides. They found that there were limits to what could be recovered by the brain’s natural plasticity. They discovered that the increased amplification at higher stages of brain processing could fully recover sensitivity to faint sounds, but that the ability to resolve differences in complex sounds, like speech, did not recover to the same degree.
The researchers undertake further studies to explore whether debilitating auditory conditions such as tinnitus or hyperacusis might reflect too much amplification in the system.
“Like feedback from a microphone, having too much gain in the system can push neural circuits toward becoming pathologically hyperactive and hypersensitive,” said Polley. “By establishing the actual cellular components of the brain’s amplifier, we hope that one day we might be able to turn the volume knob up and down to find that ‘sweet spot’ where people can reconnect to the auditory world without hearing phantom ringing or cringing at a loud noise that most people would shrug off as tolerable.”
Source: Massachusetts Eye and Ear
Image credits: Massachusetts Eye and Ear; © Igor Stramyk | Dreamstime.com