In recent years, the incidence of hearing impairment and tinnitus has increased due to noise, stress, and lifestyle habits, and hearing impairment and tinnitus are becoming more and more important as a category of common diseases. The number of people visiting hearing clinics is gradually increasing, and about 15% of people will be disturbed by tinnitus to varying degrees throughout their lives.
Understanding this issue begins with an understanding of hearing development, which is largely due to acquired remodeling. Infants begin to respond to sound at about three months of age, and later gradually develop hearing in response to acoustic stimulation, as well as forming our acquired language.
Research suggests that tinnitus may originate in the cochlea, be recognized as an abnormal temporal configuration in the auditory pathway, be reinforced by subcortical centers, and finally form the sensation of tinnitus (including the psychological component).
Among them, the association cortex, limbic system, and prefrontal cortex are closely related to tinnitus-induced sensations and adverse emotions; plastic changes in the brain play an important role in the formation of severe tinnitus, and the brain perceives tinnitus as an important signal and enhances its perception and captures any changes related to tinnitus, forming a vicious circle between adverse emotions and tinnitus.
On the other hand, hearing is formed by insensitivity to static changes in sound and sensitivity to dynamic changes in sound. This is why the phenomenon of “not being able to hear your own heartbeat, but being able to hear the heartbeat of others” occurs. As hearing decreases, the original acoustic stimuli that can be heard in the cerebral cortex no longer exist, and the original signal-to-noise ratio in the cerebral cortex is weakened, so the original auditory memory and signal-to-noise balance cannot be maintained, and tinnitus (noise) may appear.
Therefore, tinnitus is often accompanied by hearing problems, and hearing problems must be diagnosed and treated early. It is important to reconstruct the cortical signal-to-noise ratio early and to highlight the effects of sound. This is where acoustic information therapy is particularly important.
In reality, tinnitus occurs in most cases with hearing loss, but there are also some cases of tinnitus in which the cause cannot be detected by existing conditions, that is, tinnitus without hearing loss.
Current research on tinnitus is at a hypothetical stage, suggesting that the area of the cochlear lesion is not the only factor determining the pitch of tinnitus, but that tinnitus is the result of a combination of peripheral and central lesions. Some retrocochlear lesions present early with tinnitus only, such as auditory neuroma. Others have sudden brain lesions that present with tinnitus. Others, such as: tinnitus on one side gradually changes to bilateral tinnitus with the same pitch on both sides; tinnitus sensation persists despite cutting or destroying the cochlear nerve on the side of the tinnitus; tinnitus can also be present in a deaf ear with almost no hearing.
Matching tests for tinnitus suggest that the loudness of tinnitus should be about 10 dB below the hearing threshold. After pure tone audiometry and tinnitus pitch matching data in a large number of tinnitus cases, it was found that the frequency range of hearing loss correlates with the tinnitus pitch, but does not exactly match.
It may originate in the cochlea, be recognized as an abnormal temporal configuration in the auditory pathway, be reinforced by subcortical centers, and finally form the sensation of tinnitus (including the psychological component). The joint cortex, limbic system and prefrontal cortex are closely related to tinnitus-induced sensations and dysphoria; plastic changes in the brain play an important role in the development of severe tinnitus, and the brain perceives tinnitus as an important signal and enhances its perception and captures any changes associated with it, creating a vicious circle between dysphoria and tinnitus.
Objective clinical detection of tinnitus
Since the 1980s, scholars have tried to find electrophysiological indicators to confirm the presence of tinnitus by recording spontaneous or evoked electrical activity, based on the theory that tinnitus, as an abnormally perceived “sound”, should be reflected at some level of the auditory system, but the results to date have been specious.
The reasons for the ambiguous results of electrophysiological examination of tinnitus may be.
①The test instrument used is not sensitive enough;
(ii) The ratio between the tinnitus signal and the background noise is not large enough to be discriminated.
(iii) Tinnitus may manifest itself in the form of reduced spontaneous activity;
④The loudness of tinnitus is not related to the degree of annoyance it causes;
(5) Tinnitus may represent a dispersed phenomenon, i.e., a reflection of the interrelationship of many brain regions.
In summary, tinnitus involving abnormalities of the auditory system and certain brain regions often causes strong and not easily diluted emotional reactions, accompanied by different subtypes of auditory hypersensitivity. To date, there is no objective method to detect and measure tinnitus, and the mechanisms of tinnitus formation have not yet been fully elucidated. The development of a systematic approach to tinnitus classification will help in future treatment.
It is important to seek medical attention early after the onset of tinnitus, so that the cause of tinnitus can be easily identified and treatment is often effective. For tinnitus that is more than two weeks old, treatment is more difficult, and this is where an important treatment, acoustic information therapy, becomes particularly important, relying on acquired auditory reshaping to repair the irreversible lesions that are already present.