No matter what the cause, the condition interrupts the transmission of sound from the ear to the brain. Some of the neural circuits no longer receive signals. Strangely, this does not cause hearing loss. Instead, when neural circuits don’t receive stimulation, they react by chattering together, alone at first and then synchronous with each other. Once the nerve cells become hyperactive and occur at the same time, they simulate a tone the brain “hears” as tinnitus. Analogous to a piano, the broken “keys” create a permanent tone without a pianist playing the keys.
Hyperactivity and deep brain stimulation. Researchers have observed hyperactivity in neural networks after exposing the ear to intense noise. Understanding specifically where in the brain this hyperactivity begins and how it spreads to other areas could lead to treatments that use deep brain stimulation to calm the neural networks and reduce tinnitus.
^ Langguth B, Goodey R, Azevedo A, et al. (2007). "Consensus for tinnitus patient assessment and treatment outcome measurement: Tinnitus Research Initiative meeting, Regensburg, July 2006". Tinnitus: Pathophysiology and Treatment. Progress in Brain Research. 166. pp. 525–36. doi:10.1016/S0079-6123(07)66050-6. ISBN 978-0444531674. PMC 4283806. PMID 17956816.
Another example of somatic tinnitus is that caused by temperomandibular joint disorder. The temporomandibular joint (TMJ) is where the lower jaw connects to the skull, and is located in front of the ears. Damage to the muscles, ligaments, or cartilage in the TMJ can lead to tinnitus symptoms. The TMJ is adjacent to the auditory system and shares some ligaments and nerve connections with structures in the middle ear.
ABR (ABR) testing may show some subtle abnormalities in otherwise normal persons with tinnitus (Kehrle et al, 2008). The main use of ABR (ABR test) is to assist in diagnosing tinnitus due to a tumor of the 8th nerve or tinnitus due to a central process. A brain MRI is used for the same general purpose and covers far more territory, but is roughly 3 times more expensive. ABRs are generally not different between patients with tinnitus with or without hyperacusis (Shim et al, 2017).
Ask your doctor about experimental therapies. No cure for tinnitus has been found but research is ongoing, so you should be open to experimental therapies. Electronic and magnetic stimulation of the brain and nerves might correct the overactive nerve signals that cause tinnitus. These techniques are still in development, so ask your doctor or hearing specialist if trying one might be right for you.[6]
Muscular tinnitus can be caused by several degenerative diseases that affect the head and neck including amyotrophic lateral sclerosis or multiple sclerosis. Myoclonus can also cause muscular tinnitus, especially palatal myoclonus, which is characterized by abnormal contractions of the muscles of the roof of the mouth. Spasms of the stapedial muscle (which attaches to the stapes bone or stirrup), which is the smallest muscle in the body, and tensor tympani muscle, both of which are located in the middle ear, have also been associated with objective tinnitus. Myoclonus or muscle spasms may be caused by an underlying disorder such as a tumor, tissue death caused by lack of oxygen (infarction), or degenerative disease, but it is most commonly a benign and self-limiting problem.
Exposure to loud noise. Loud noises, such as those from heavy equipment, chain saws and firearms, are common sources of noise-related hearing loss. Portable music devices, such as MP3 players or iPods, also can cause noise-related hearing loss if played loudly for long periods. Tinnitus caused by short-term exposure, such as attending a loud concert, usually goes away; both short- and long-term exposure to loud sound can cause permanent damage.
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