Tinnitus is the perception of sound in the absence of acoustic stimulus. In most cases, it is directly related to insults to the peripheral auditory system (i.e. the cochlea). The following is a discussion of the most current understanding of tinnitus pathophysiology and is critical for understanding the basis for our tinnitus rehabilitation program.
The auditory system is tonotopically organized, meaning the spatial relations in the cochlea that correspond to specific tones are translated into preserved neural organization patterns that are maintained throughout the auditory cortex. This tonotopic organization is analogous to the keyboard of a piano. If you were to take the cochlear membrane and flatten it out, the location of the low tones would be where the apex of the cochlea is, and the location of the high tones would be where the base of the cochlea is.
In the auditory cortex, the brain receives a constant and steady source of neuronal input from all frequencies. If electrodes were placed in the brain in a person with normal hearing, you would hear the steady crackling of spontaneous neuronal firing. The way that the brain interprets sound is by picking up changes in this steady state of background firing.
There are two things that occur during tinnitus pathogenesis. First, the spontaneous firing rate in the area in the brain that corresponds with the damaged region of the cochlea actually increases. This region has been termed the “lesion projection zone” (LPZ). In the piano analogy, if a set of keys on the keyboard are damaged, the insult would be reflected as a hyperactive spontaneous firing rate in the LPZ. This hyperactivity happens fairly quickly.
The second thing that occurs is that the tones that border the damaged zone in the cochlea become associated with the hyperactivity occurring in the LPZ. Essentially, the tone that people hear when they perceive tinnitus actually corresponds to these border regions, the so-called “lesion edge frequencies” (LEFs). Hence, the hyperactive spontaneous firing rate in the LPZ becomes associated with the LEFs, and the brain interprets this as the apprehension of sound, i.e. tinnitus (Figure 2).
It is noteworthy that both steps are needed for tinnitus to develop. Further, we know that not all people with hearing loss develop tinnitus, despite clear evidence of injury to the auditory periphery. Further, these associations can be transient in the acute setting, but not develop into permanent associations. Most of us have had the experience of tinnitus after exposure to toxic levels of noise, but the apprehension of tinnitus is impermanent. This aspect of tinnitus pathogenesis is the basis for our hypothesis that prompt intervention with customized sound therapy after exposure to toxic noise may actually prevent the development of clinically significant tinnitus.
There is a third component to tinnitus pathogenesis that is equally important to the above events, and this is the creation of pathologic neural networks between the auditory system and the limbic system. It is important to note that while 10% of the population in industrialized countries have tinnitus, in only 25% of these is tinnitus considered clinically significant. Hence, it is this critical development of associations between the auditory cortex and the limbic system that differentiates the simple precept of tinnitus from clinically significant tinnitus. The goal of tinnitus rehabilitation is the eradication of these pathologic neural networks.
Customized Sound Therapy
Sound therapy in tinnitus management (i.e. masking) is the strategy of presenting an external sound to induce suppression of the spontaneous firing in the LPZ, and hence provide tinnitus relief. Traditional (non-customized) masking efforts have presented broadband noises, most typically white noise. However, it is established that targeted (customized) acoustic energy at the LEF provides more effective masking than broad-based acoustic energy. In other words, the more closely the masking sound corresponds with the LEF, the more effective is the tinnitus suppression.
Another disadvantage to traditional “non-customized” masking strategies is that because they use broadband noise, they essentially cripple the subject while the masking therapy is being used. This sets limits on the amount of time a subject is able to have the hyperactivity in the LPZ suppressed, and ultimately, on the rate and degree of tinnitus rehabilitation.
The BeyondTinnitus Therapy Program is designed to address all levels of tinnitus pathology. It is a two stage program.