Brain Mechanisms in Tinnitus, Hearing Loss, and Hyperacusis: Differences and Similarities
Tinnitus, hyperacusis, and hearing loss are, in a way, interconnected or related—like in cases of recruitment, where all three conditions are present. This is what Beethoven, for example, is believed to have suffered.
All three conditions can be caused by the death or damage of certain hair cells. When the cells are damaged, they may remain alive but function abnormally. In hearing loss, this would mean that these cells are unable to send sound signals to the auditory nerve. If the damage is due to aging, it is usually the high frequencies that are most affected.
These three auditory conditions can also be caused by damage
to the auditory nerve—especially to the nerve fibers that process loud sounds.
Damage to these fibers could also explain the presence of hidden hearing loss
in some people with tinnitus, even when their audiograms show normal hearing (a
loss that prevents them from understanding conversations in noisy
environments). In general, these nerve fibers are more vulnerable to
noise-induced damage than hair cells. They can even be damaged before the hair cells
themselves.
It has been discovered that damaged hair cells can be
reactivated to restore hearing. However, it also seems quite feasible—or even
more attainable—that the nerve fiber could be repaired to resume sending sound
signals to the brain, since the damage usually occurs only in part of the fiber
and not in the entire nerve cell (which includes the cell body and the other
section of the fiber—see image). In either case, both actions could restore
normal hearing and, in the case of hearing loss, also reverse tinnitus, since
the brain would no longer need to compensate for any missing signal (as one
widely accepted theory suggests).
Source: NewScientist (https://archive.is/EFMSO)
Another possibility under study is that both hair cells and
nerve fibers (and their synapses) could regrow through certain types of gene
therapy.
Another approach is to increase inhibitory neuronal activity
in both hyperacusis and hearing loss, in order to reduce the hyperactivity,
hypersynchrony (responses to sounds that aren’t even audible in the
environment), and/or hypersensitivity (to sounds that are not very intense) of
the neural networks involved in sound processing. Research is exploring how
this could be achieved through gene therapy and also through optogenetics,
which has already produced remarkable results in mice.
When it comes to the brain areas involved in these auditory
disorders, it is known that in the case of tinnitus, multiple regions are
affected, forming a wide network across the brain. In contrast, hearing loss
mainly involves localized damage in the cochlea and the auditory cortex.
On the other hand, tinnitus and hyperacusis differ from
hearing loss because they are defined by what people cannot stop hearing,
rather than what they cannot hear. This also makes a significant
difference when trying to explain why tinnitus occurs alongside hearing loss—or
alongside hyperacusis.
In the first case, the most widespread theory suggests that
tinnitus appears because the brain attempts to compensate for the lack of sound
signals caused by hearing loss. In the second case (that of hyperacusis), this
theory would no longer apply, since tinnitus would appear despite the
absence of hearing loss—and in fact, in the opposite situation: an
over-sensitivity to sound (hyperacusis). Here, tinnitus occurs even though the
brain does not need to compensate for any missing auditory signal.
There are several explanations for this, and most of them
relate to changes in neural or brain plasticity. That is, one or several brain
systems could start malfunctioning as a result of the auditory damage that gave
rise to hyperacusis. One explanation suggests that the neural networks in the
brain’s sound-processing centers become hyperactive, hypersynchronized in their
firing patterns (responding to sounds that aren’t even audible in the
environment), and hyperreactive (to sounds that aren’t very intense).
It’s worth mentioning that, with the discovery of cochlear
synaptopathy in 2009, it was confirmed that in some patients with tinnitus, it
is indeed possible for them to experience what is known as “hidden hearing
loss” even when their audiograms appear normal—thus reinforcing the
compensation theory mentioned earlier. However, if hearing loss were always
the cause of tinnitus, how could we explain that many people with hearing loss do
not experience tinnitus? According to some specialists (such as Dr. Fatima
Husain), tinnitus should be considered independently from the impact of hearing
loss. Her research indicates that around 90% of tinnitus patients have some
degree of hearing loss, but roughly 50% of people with hearing loss never
develop tinnitus.
Finally, another difference between tinnitus and hyperacusis
compared with hearing loss is that, in the first two, there are still no direct
objective tests to measure their presence in a patient.
Sources:
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