Ear damage is a trigger for tinnitus
Tinnitus is a common condition often described as a ringing or buzzing sound in the head or ears, in the absence of an actual physical sound. This phantom sensation affects 10 to 15% of the human population, mostly without a problem, but in about 1% of people tinnitus causes severe disruptions of daily life. It can cause problems sleeping, evoke stress and anxiety and result in depression. Unfortunately there is, as yet, no cure for tinnitus. There are several treatments available but they are generally aimed at masking the tinnitus or reducing the anxiety and stress associated with it.
Neuroscientists have shown that perception of a physical stimulus, e.g. sound, touch or light, is caused by activity in specific brain pathways, which are triggered by signals from a peripheral receptor (like the rod and cone cells in the eye or hair cells in the cochlea). Therefore, it is thought that tinnitus, which is a perception without a physical stimulus, is due to abnormal, spontaneous activity (not resulting from an actual stimulus) in the brain.
Tinnitus is also strongly associated with damage to the cochlea. Many scientists now believe that trauma to the cochlea leads to changed input from the ear to the brain which then causes altered patterns of activity in the brain itself. This suggests that damage to the inner ear is the trigger for the development of tinnitus. Exactly which brain changes are responsible for causing tinnitus is still under investigation.
Two phases of tinnitus development
In our laboratory we have been working on an animal model studying the effects of cochlear damage and hearing loss on nerve cell activity in the brain. Using this model we showed that the spontaneous nerve cell activity (not evoked by sound) in a part of the brain which processes sound, the auditory midbrain, increases after inner ear damage caused by a loud sound exposure. Similar observations have been made in other areas of the brain that are involved in the processing of sound as well.
We also found that this increase in spontaneous activity could be suppressed by cutting or silencing the auditory nerve. However, there are two issues with this finding that are important to point out. Firstly, we could only suppress the increased activity in the midbrain if we reduced the auditory nerve activity in the first few weeks after the cochlear trauma and not at any later point in time. Secondly, we do not believe that this means that the auditory nerve itself has increased activity.
Instead, we think that development of increased activity in the brain has two phases. In the first phase, cells in the brain become hyper-excitable i.e. they respond more vigorously to the reduced input from the auditory nerve following damage to the cochlea. In the second phase, the cells in the brain stop needing signals from the auditory nerve to be active and their increased activity is now caused by another mechanism.
If the increased spontaneous activity in the brain after cochlear damage is involved in the generation of tinnitus, our results may well have therapeutic implications. They suggest that early onset tinnitus could be altered by changing the spontaneous activity of the auditory nerve. This might explain why cutting the auditory nerve can have a beneficial effect in some tinnitus sufferers but not in others. The former are still in the first phase of tinnitus development whilst the latter group are in phase 2. However, cutting the auditory nerve leads to complete deafness and therefore is not a desirable therapy.
Could drug treatments supress tinnitus?
A drug that lowers the spontaneous activity of the auditory nerve would be of more use, clinically. One such drug is furosemide, a common diuretic drug used to treat, among other things, high blood pressure. Interestingly, there are already reports that furosemide can suppress tinnitus in some people. Does furosemide perhaps suppress tinnitus of recent onset (phase 1 tinnitus)?
To try to answer this, we used our animal model to investigate whether a single dose of furosemide could block the early behavioural signs of tinnitus. We found that furosemide could indeed block the tinnitus that emerged in the first weeks after cochlear damage. This supports our hypothesis that early onset tinnitus can be reduced by a drug that affects auditory nerve activity. The next step, therefore, is to find out if the same is true in people. We also have no idea about how long the early stage of tinnitus lasts in humans (and it may vary considerably depending on the cause of the tinnitus and other factors) - this needs to be determined.
Whether long-term suppression of tinnitus can be achieved using furosemide is also a question that needs to be answered. And finally, furosemide cannot be administered to all people with tinnitus; it has some potentially serious side effects and needs to be administered under close medical supervision. If it is shown to be effective in treating people with tinnitus, more research would be required to investigate other possible drugs that can affect auditory nerve spontaneous activity without having other side-effects.
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