Pathophysiology
One of the possible mechanisms relies on otoacoustic emissions. The inner ear contains thousands of minute inner hair cells with stereocilia which vibrate in response to sound waves, and outer hair cells which convert neural signals into tension on the vibrating basement membrane. The sensing cells are connected with the vibratory cells through a neural feedback loop, whose gain is regulated by the brain. This loop is normally adjusted just below onset of self-oscillation, which gives the ear spectacular sensitivity and selectivity. If something changes, it is easy for the delicate adjustment to cross the barrier of oscillation, and tinnitus results. Exposure to excessive sound kills hair cells, and studies have shown as hair cells are lost, different neurons are activated, activating auditory parts of the brain and giving the perception of sound.
Another possible mechanism underlying tinnitus is damage to the receptor cells. Although receptor cells can be regenerated from the adjacent supporting Deiters cells after injury in birds, reptiles, and amphibians, in mammals it is believed they can be produced only during embryogenesis. Although mammalian Deiters cells reproduce and position themselves appropriately for regeneration, they have not been observed to transdifferentiate into receptor cells except in tissue culture experiments. Therefore, if these hairs become damaged, through prolonged exposure to excessive sound levels, for instance, then deafness to certain frequencies results. In tinnitus, they may relay information that an externally audible sound is present at a certain frequency when it is not.
The mechanisms of subjective tinnitus are often obscure. While it is not surprising that direct trauma to the inner ear can cause tinnitus, other apparent causes (e.g., temporomandibular joint disorder (TMJD or TMD) and dental disorders) are difficult to explain. Research has proposed there are two distinct categories of subjective tinnitus: otic tinnitus, caused by disorders of the inner ear or the acoustic nerve, and somatic tinnitus, caused by disorders outside the ear and nerve, but still within the head or neck. It is further hypothesized somatic tinnitus may be due to "central crosstalk" within the brain, as certain head and neck nerves enter the brain near regions known to be involved in hearing.
Studies by researchers at the University of Western Australia suggest tinnitus is caused by increased neural activity in the auditory brainstem where the brain processes sounds, causing some auditory nerve cells to become overexcited. The basis of this theory is most people with tinnitus also have hearing loss, and the frequencies they cannot hear are similar to the subjective frequencies of their tinnitus. Models of hearing loss and the brain support the idea a homeostatic response of central dorsal cochlear nucleus neurons could result in them being hyperactive in a compensation process to the loss of hearing input. This, in turn, is related to changes in the genes involved in regulating the activity of those nerve cells. This proposed mechanism suggests possible treatments for the condition, involving the normalization or suppression of overactive neural activity through electrical or chemical means.
While most discussions of tinnitus tend to emphasize physical mechanisms, there is strong evidence that the level of an individual's awareness of her or his tinnitus can be stress-related, and so should be addressed by improving the state of the nervous system generally, using gradual, unobtrusive, long-term treatments.
Since some tinnitus mimics electronic sounds, some recent research is focusing on electronics, the prolonged use of cell phones, and other modern electronic devices as possible causes. These findings are consistent with reviews of older research associating tinnitus with prolonged exposure to electromagnetic radiation.
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