Utilizing Neuroscience to Cure Tinnitus

By Abaan Merchant

Hiss. Woosh. Click. Can you find what’s making that noise? These are some of the sounds approximately 50 million Americans hear every hour of their day. Unfortunately, they suffer from varying degrees of tinnitus, a disease that results in perception of sound when there is no external noise present (1). Tinnitus is most likely to affect individuals between the ages of 60 to 69. A person who has endured prolonged exposure to loud noises (such as deafening music, machinery, etc.) is likely to be diagnosed with some form of tinnitus. The issue stems from loss of sensory hair cells in the cochlea of the inner ear (2). The function of these hair cells is to pick up on noise at varying decibels. When exposed to loud sounds, the hair cells become damaged and do not regenerate, rendering the individual unable to hear noise at the corresponding decibel.

It is important to address tinnitus due to the debilitating effect it can have on an individual. While an “annoying ringing” may seem like a minor inconvenience, moderate-to-extreme forms of tinnitus can negatively impact everyday life. For example, some individuals suffer from depression and anxiety because the ringing does not allow them to remain employed or hold social interactions. In many cases, tinnitus only worsens as an individual continues to age.

            Currently, there are no firmly established treatments for cochlea hair cell regeneration. However, neuroscience researcher Hidehiko Okamoto seems to have found an affordable and viable coping strategy to tinnitus (3). Dr. Okamoto based his work on previous research on the auditory cortex (the portion of the brain concerns with receiving and processing sounds). In the experiment. Dr. Heinze et al. (5) tested subjects by having them listen to tones that were missing a specific decibel. After repeated trials, the group observed reduced activity of the neurons associated with carrying the message from the cochlea hair cell to the auditory cortex. When a tone at the missing decibel was played, the test subjects had more difficulty detecting it.

Based on these results, Dr. Okamoto designed a similar experiment involving music. First, the effected decibel level was determined in several patients and music was digitally altered to play exclusively at that level. Next, three groups were tested; the first group was a control (they were simply monitored with no variable). The second group was given edited music, but at the incorrect decibels. The final group was given music that corresponded with the decibel level of their tinnitus. The objective of the experiment was to determine how “replacing” the noise they hear with music would affect their tinnitus. After monitoring all three groups for a year, a clear consensus was reached: there was no improvement in the first two groups, but the final group reported their “ringing” to have become up to 30% quieter.

It was already understood that for some cases of tinnitus, the neurons associated with the hair cell were also damaged. However, what Okamoto proved in his experiment was that the auditory cortex may be playing a more significant role in tinnitus than once assumed. Although his experiment was only on a small sample, two possible conclusions were proposed. It was possible that the music reduced activity in the damaged neurons or that they were suppressed by neighboring neurons when the music played.

While much of the findings are still being evaluated, it is vital to explore the possibility of restoring the damaged neurons as a next step. During a neuroscience seminar at the Loyola University Chicago, Dr. Wei-Ming Yu presented his paper “A Gata3–Mafb transcriptional network directs post-synaptic differentiation in synapses specialized for hearing. (6)” In the paper, Dr. Yu et al. explain how transcription factor Mafb is vital in auditory ribbon synapse formation. The purpose of these synapses is to provide rapid transport of a stimulus signal from the cochlea hair cells to the spiral ganglion nuclei (SGN for short). SGNs are the specific neurons that carry the signal from the hair cell to the auditory cortex for processing. More importantly, tinnitus is most likely to affect the function of these cells. Therefore, if Mafb production/activity is stimulated, neuronal connections can be manipulated to create a new pathway to the auditory cortex (perhaps by linking to another hair cell).

For millions of individuals suffering from tinnitus, hope continues to build as research explores new options for therapy. While experiments are still in their preliminary stages, significant strides to a clinical solution have already been taken in recent years. In addition to attention in research, many social precautions are in place to limit new cases of tinnitus. For example, many workplaces that utilize loud machinery are mandated to provide protective gear to employees. Technology companies limit the volume on headphones and devices to display warning signs when volume is too high. There are several strategies (both clinical and recreational) already available to the public to relieve the stress of tinnitus. With many precautionary efforts coupled with awareness and research, the issue of tinnitus is sure to go out with a whisper.

Works Cited:

1)     Demographics. (n.d.). Retrieved December 04, 2017, from https://www.ata.org/understanding-facts/demographics

2)     Yong, E. (2009, December 29). Treating tinnitus with an individually tailored piece of music. Retrieved December 04, 2017, from http://phenomena.nationalgeographic.com/2009/12/29/treating-tinnitus-with-an-individually-tailored-piece-of-music/?_ga=2.29003836.1659416281.1512262640-1911931344.1512262640

3)     Understanding Tinnitus -- the Basics. (n.d.). Retrieved December 04, 2017, from https://www.webmd.com/a-to-z-guides/understanding-tinnitus-basics

4)     Jäncke, L., Gaab, N., Wüstenberg, T., Scheich, H., & Heinze, H. J. (2001, December). Short-term functional plasticity in the human auditory cortex: an fMRI study. Retrieved December 04, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/11689309

5)     Neuro300 | Powered By Box. (n.d.). Retrieved December 04, 2017, from https://luc.app.box.com/v/neuroseminar/folder/35225444686